In 2015, researchers in California found bovine leukemia virus (BLV) stitched into the DNA of human breast cancer tumors from mastectomies. The virus was found at much higher rates than in normal breast tissue obtained from breast reduction surgeries. Based on this difference, they calculated that as many as 37% of breast cancer cases may be attributable to exposure to BLV, likely through consuming milk or meat from infected animals.

In response, the milk and meat industries seemed more concerned about consumer confidence than consumer cancer. But scientifically, the research priority turned to the question: Could the California results be replicated? The answer, it turns out, was yes. They were replicated among women in Iran. Replicated in Brazil. In Australia, the link was even stronger. In Texas, they found the same thing. Women diagnosed with breast cancer were found to be so much more likely to have bovine leukemia virus DNA in their breast tissue compared with women without cancer, that the attributable risk was calculated at 51.82%, indicating that this meat and dairy virus may be responsible for at least half of the breast cancer cases among the women in Texas they studied.

All in all, six of the eight studies performed to date found the virus in human breast tissues, which “suggests strongly that BLV does infect humans, and breasts can be targets of infection.” Four of the five studies that compared infection rates in cancerous versus normal breast tissue found that the odds of detecting the virus in tumors were, on average, four times higher. How does that compare to other breast cancer risk factors? If you go on hormone replacement for five years, you can bump up your breast cancer risk by 30%. If you take birth control pills for more than a dozen years, your risk may go up by 40%. If you’re obese when you’re older, your risk can go up by 60%. Having a first-degree relative with breast cancer may double your risk. But having your breast infected with bovine leukemia virus may quadruple your risk, as you can see below and at 2:16 in my video Breast Cancer and the Bovine Leukemia Virus in Meat and Dairy.The only risk factors more potent than BLV infection were having the BRCA gene mutation, like Angelina Jolie has, or a high dose of ionizing radiation, like being in the wrong place at decidedly the wrong time, like Hiroshima and Nagasaki during World War II.

Beyond confirmation, one study suggested that older patients had a greater likelihood of testing positive for bovine leukemia virus. That makes sense if BLV is from exposure to dairy and meat. The older we get, the more meals we’ve had—and the more opportunities to become infected over time. Researchers also discovered that the virus comes first, before the cancer diagnosis; they found it was present in some breast tissues 3 to 10 years before cancer was found. “This argues against the idea of viral invasion of already malignant cells,” quashing the theory that maybe the virus is somehow just attracted to the cancer after the fact. Could this explain the consistent findings that breast cancer tissue is more likely to harbor infection? Again, the data showed no — the virus appeared to come first. While the review doesn’t provide absolute proof that BLV is a cause of breast cancer, based on the best available balance of evidence, BLV infection does indeed appear to be a risk factor for breast cancer.

The latest revelation is that BLV has now been found in human blood, too. This has a number of potential ramifications. Blood banks, for example, don’t screen for it. So, it’s possible you can get it from consuming meat or dairy, as well as from getting blood from someone who consumed meat or dairy. This could also mean that BLV could cause leukemia in people. It does in chimpanzees. Two infant chimps were fed milk from cows naturally infected with BLV, and both died of leukemia. We didn’t even know chimps could get leukemia. This certainly suggests the possibility of transmission or induction of leukemia through the ingestion of milk from BLV-infected cows, or blood-borne spread could carry the virus to other organs. In cattle, the virus causes blood cancers, but this may be just because dairy cattle are slaughtered and turned into hamburger when they are still so young, so maybe they don’t have time for tumors to grow in other organs.

How concerned should we be about bovine leukemia virus? “It is not clear whether this is a good news story or a bad news story.” If future studies show that BLV does cause breast cancer in people, there will be significant repercussions for the dairy and cattle industries. But that means there is something we can do about it. Perhaps action should be taken now to eradicate the infection from cattle, rather than waiting for a final verdict. Twenty-one nations have already eradicated BLV from their dairy cattle. In contrast, the BLV prevalence in the United States just keeps increasing. If industries are not going to step up and try to eliminate the disease, then the least they could do is eliminate some of the practices that spread the disease between animals.

BLV is spread via blood through contaminated needles, saw or gouge dehorners, ear taggers, hoof knives, tattoo pliers, nose tongs, and other tools of the agribusiness trade. Though “in view of the emerging information about BLV in human breast cancer, it is prudent to encourage the elimination of BLV in cattle, particularly in the dairy industry.” The hope is that, either way, it may help reduce the scourge of breast cancer.

Doctor’s Note

If you missed the previous video, see Bovine Leukemia Virus as a Cause of Breast Cancer.

Avoiding infectious risks like BLV is another advantage of making meat without animals. See my video, The Human Health Effects of Cultivated Meat: Food Safety.

The incidence of breast cancer continues to increase worldwide. In the United States, this amounted to a 40% increase in the incidence by the turn of the century. Presently, the main approach to preventing mortality is early detection and treatment. That’s important, but why not focus more on primary prevention—protecting people from risk factors so they don’t develop breast cancer at all?

“Overall, it is estimated that 20% of all human cancers have an infectious origin.” Viruses can trigger cancer by turning on cancer genes or turning off cancer-suppressing genes, but they can also contribute to tumor formation just by causing chronic inflammation. Currently, cancer-causing viruses are considered “the major plausible hypothesis for a direct cause of human breast cancer.” How did we get here?

It all started about 40 years ago when a professor of virology at UC Berkeley learned how the mammary tumor virus was discovered in mice. Scientists switched baby mouse pups from mothers with a high incidence of mammary cancer with the babies from mouse strains with a low incidence and found that the cancer incidence in pups matched their foster mothers’—not their biological ones’—showing it wasn’t genetic. “It occurred to me that humans are foster nursed on the cow,” the professor said.

Bovine leukemia virus (BLV) had just been identified as a cancer-causing cow virus. At the time, only about 10% of U.S. dairy cows were infected, but now it’s closer to half. Initially, 66% of herds were affected. Then, it was more like 80%, based on their milk testing positive for the virus, and 100% of the herds in the larger industrial farms. And now, more than 94% of U.S. herds are affected, continuing the historical trend of BLV persistently proliferating within U.S. dairy herds.

We’ve long known that people in countries that consume the most milk have the highest breast cancer incidence. But, as you can see below and at 2:32 in my video, Bovine Leukemia Virus as a Cause of Breast Cancer, the link between dairy consumption and breast cancer incidence isn’t only on the country level.Individual women who are lactose intolerant and consume less dairy also seem to have decreased risk of breast cancer. Milk contains many things that could be contributing to the cancer risk, such as saturated fat and the presence of cancer-promoting growth hormones like IGF-1.

Yes, we know bovine leukemia virus is present in beef and dairy products. About half of the milk and meat samples turn up positive for the virus. In fact, you can sample the virus straight out of the air on dairy farms, on surfaces, and in the milk itself. Most milk is pasteurized, but many dairy products, like raw, aged cheeses, are not. And who hasn’t eaten a pink-in-the-middle hamburger at some point in their life?

Yes, we have evidence that people are exposed to the virus. Yes, we have evidence that people are actively infected with the virus. But it wasn’t until 2015 that we learned infection rates were highest in cancerous breast tissue, as you can see below and at 3:30 in my video.So much so that as many as 37% of breast cancer cases may be attributable to exposure to the bovine leukemia virus.

That was enough for me to make a whole series of videos on the role the virus plays in breast cancer and how the meat and dairy industries responded to the news. What’s the latest update? That’s what I’ll cover next.

Doctor’s Note

You may remember that I’ve previously discussed The Role of Bovine Leukemia in Breast Cancer and the Industry Response to Bovine Leukemia Virus in Breast Cancer.

Stay tuned for the next video: Breast Cancer and the Bovine Leukemia Virus in Meat and Dairy.

In 2018, one of the bestselling blood pressure drugs, valsartan—sold as Diovan—was found to be contaminated by the “probably carcinogenic” nitrosamine known as N-nitrosodimethylamine (NDMA). It’s believed that about 20 million people worldwide were prescribed the drug tainted with this contaminant, which has a cancer risk shown to exceed that of many known potent carcinogens, such as asbestos, PCBs, and benzo[a]pyrene.

As I discuss in my video Cancer-Causing NDMA in Medications (Zantac, Metformin) and Meat, the U.S. Food and Drug Administration (FDA) estimated that taking the drug for a few years could cause cancer in as many as 1 in 8,000 people, whereas the European equivalent of the FDA estimated the cancer risk could be as high as 1 in 5,000. It is unlikely, researchers wrote in this 2019 paper, that drugs like valsartan are “a unique case.” And indeed, a few months later, the FDA announced it had found NDMA in ranitidine. Ranitidine, the acid reflux drug sold as Zantac, is one of the most prescribed drugs on the planet, in addition to being sold over the counter.

Then in 2020, some formulations of metformin, a popular diabetes drug sold as Glucophage, were found to be contaminated. The finding of NDMA in common medicines led the FDA to call for the immediate withdrawal of all Zantac from store shelves, yanking the drug from the market because its testing showed NDMA levels could, in some circumstances, exceed the acceptable daily intake limit of 96 nanograms per day. It was so bad that the FDA found levels of this carcinogenic contaminant in Zantac are similar to the exposure levels you would experience if you ate grilled or smoked meats!

Wait, what?

NDMA has not only been found in contaminated drugs. It is a known byproduct of tire plants, pesticide manufacturing, and leather tanning, and it is found in food and beverages, including processed meat and beer. Now that we know NDMA can transfer through the placenta, this may explain the relationship between maternal cured meat consumption during pregnancy and the risk of childhood brain tumors. For example, eating hot dogs while pregnant may increase childhood brain tumor risk by 33%, and sausages by 44%. Bacon consumption may increase childhood brain tumor odds by 60 or 70%. But it’s not just processed meat. Researchers have found it in poultry products as well. A single serving of chicken contains more than 100 nanograms of NDMA, as you can see below and at 3:02 in my video.

Remember how the FDA said the acceptable daily intake limit is 96 nanograms? Just half a chicken breast contains 110 nanograms.

Now, raw poultry doesn’t have any NDMA; it comes from the cooking process. In fact, the dry-heat cooking of meat, like broiling or grilling, even creates airborne NDMA, releasing this very potent carcinogenic compound into the air. So, even if you’re getting a salad at a charcoal grill restaurant, just being indoors where meat is being grilled could be a significant cancer risk.

Nitrosamines are also found in cigarette smoke, and pressure was put on the tobacco industry to try to remove them, arguing “there is simply no logical reason why a removable carcinogen should be allowed to remain in a consumer product….” That’s the same reason Zantac was yanked from store shelves.

Okay, so let’s get this straight. Zantac—which is one of the best-selling drugs in history, bringing in billions of dollars—was pulled from the market because it contained a probable carcinogen that exceeded the acceptable daily limit, but there may be more of the contaminant in a single serving of chicken?! So, my question is: Why aren’t they pulling poultry off the shelves, too?

Doctor’s Note

NDMA is a nitrosamine, a class of carcinogens also found in processed meat. See, for example, How Much Cancer Does Lunch Meat Cause?.

How can you make meat less cancer-causing? See Carcinogens in Meat.

Is Organic Meat Less Carcinogenic? Check out the video to find out.

Note: The article shown at minute 1:04 of the video I reference has since been retracted due to analytical artifact.

Onions are potentially a good source of antioxidants, which, interestingly, are concentrated in the outer layers just beneath the papery peel. White onions, for example, contain more than ten times the antioxidants in the outer layer compared to the inner core. Unfortunately, most people discard the most nutrient-rich outermost layers, “thus losing a valuable part of the antioxidant-rich material.” In general, yellow onions have more antioxidants than white onions. Red onions beat them both, based on three different antioxidant testing methods, as seen at 0:39 in my video Are Onions Beneficial for Testosterone, Osteoporosis, Allergies, and Cancer?

Though red onions are indeed slightly better, yellow and white onions are no slouches, containing considerable levels of antioxidant activity. We know they’re nutritious, but are there any particular clinical benefits to eating onions? There are all sorts of headlines in the medical literature touting miraculous benefits, but what are these claims based on?

For example, there’s a review purporting to have evidence that testosterone levels in males are enhanced by onion, but the researchers were referring to studies like one on the effects of onion juice after testicular torsion in rats. Who cares what happens after a rat’s testicle is rotated 720 degrees counterclockwise? (Except, of course, the rat.) You don’t know what happens in people until you put human testes to the test. Only then was it discovered that onion extract doesn’t appear to affect men’s testosterone.

What about bone health? Evidently, older white women who ate onions at least once a day had an overall bone density that was 5% greater than women who ate onions no more than once a month. Now, 5% might not sound like a lot, but that improvement in bone density could potentially mean decreasing their hip fracture risk by more than 20% if, indeed, it is cause and effect.

Daily administration of onion for four weeks did cause a big bump in bone density. This could lead to a safe, effective, and low-cost approach to osteoporosis in—you guessed it—rats. Another rodent study!

Great strides have been made in treating osteoporosis with drugs, but they have the potential for serious adverse side effects, so scientists have turned their attention to natural remedies. In one study, researchers randomized people to drink onion juice or placebo onion juice for 8 weeks. Improvement was noted for a marker of bone health; however, they didn’t actually follow participants long enough to compare osteoporosis rates.

Do shallots exhibit anti-allergy activity or offer any therapeutic effects for relieving allergic runny noses? Sixteen patients were randomized equally into an antihistamine group or a group that got antihistamines and capsules containing dried shallot powder. It looked like the shallot group did better after four weeks, but there was no statistically significant difference in total symptoms between the two groups. So, another #onionfail.

What about testing the effects of eating fresh yellow onion to try to decrease the toxic effects of a chemotherapy drug called doxorubicin in breast cancer patients? Unfortunately, no significant benefit was found in decreasing damage to the liver or heart. But eating fresh yellow onion was found to help reduce high blood sugar levels and insulin resistance in breast cancer patients during doxorubicin-based chemotherapy. The drug isn’t just toxic to the liver and heart—it may also contribute to insulin resistance.

So, researchers performed a randomized, triple-blind, controlled clinical trial, randomizing patients to eat a whole onion a day or a third of an onion a day for eight weeks. What happened? The higher-dose onion group experienced a significant decrease in blood sugars and insulin resistance compared to the lower-dose group. Levels rose in the lower-dose group but fell in the higher-dose group, as you can see below and at 4:28 in my video.

So, make onions your friend. What’s the worst that can happen—a little onion breath and body odor?

Doctor’s Note

What else can we do for breast cancer? See related posts below.

What can physicians do to promote healthy, life-extending lifestyle changes?

A pivotal paper published in Europe more than a decade ago entitled “Healthy Living Is the Best Revenge” found that practicing just four simple, healthy lifestyle factors compared to none could potentially have a strong impact on preventing chronic diseases. We’re talking nearly 80% less chronic disease risk, slashing diabetes risk by 93%, dropping heart attack risk by 81%, and cutting stroke risk in half and cancer risk by 36%. Think about what that means. The potential for preventing disease and death is enormous. In the United States alone every year, there are a half million first heart attacks, a half million first strokes, a million new cases of diabetes, and a million new cancer diagnoses. The message is clear: Practicing a few healthy behaviors can have a huge impact.

What are those four fabled factors?

• never smoking
• not being obese
• averaging about a half hour of exercise a day
• following healthful dietary principles, including a lot of fruits, vegetables, and whole grains, and less meat

Follow those four simple rules and boom! Enjoy nearly 80% reduced risk of major chronic diseases.

What does that mean for mortality risk? As I discuss in my video How to Increase Your Life Expectancy 12 to 14 Years, a similar combination of four healthy behaviors predicted “a 4-fold difference in total mortality in men and women, with an estimated impact equivalent to 14 y[ears] in chronological age,” meaning the individuals were dying at such a reduced rate that it was as if they were 14 years younger. “Finally, a Regimen to Extend Human Life Expectancy,” proclaimed a commentary in reference to a study that had made a similar analysis of the impact of healthy lifestyle behaviors on life expectancies. But this time, it looked directly at the U.S. population, which is particularly important, since Americans have a shorter life expectancy compared to people living in nearly all other higher-income countries. The researchers concluded that a healthy lifestyle could substantially reduce premature mortality and increase life expectancy in U.S. adults. Okay, but by how much? They estimated that adhering to a low-risk lifestyle could extend life expectancy at age 50 by 14 years in women and 12.2 years in men. So, if you’re 50 right now, instead of only living to 79 if you’re a woman and 75½ if you’re a man in the United States, taking even just basic care of yourself could propel you to an average life expectancy of 93 if you’re a woman and 87½ if you’re a man.

The bottom line is it’s never too late to turn back the clock. A midlife switch just to the basics—at least five daily servings of fruits and vegetables, walking 20 minutes a day, not smoking, and maintaining a healthy weight—leads to a substantial reduction in mortality even in the following few years. We’re talking a 40% lower risk of dying in the subsequent four years. Indeed, “making the necessary changes to adhere to a healthy lifestyle is extremely worthwhile, and…middle-age is not too late to act.”

As an aside, when I realized the 12 to 14 years of added life expectancy were based on data from health professionals, I got excited about all the potential ripple effects. If health professionals start getting healthier, they can become role models for more healthful living and potentially save more lives than just their own. But that may have been wishful thinking. Practicing what you preach can sometimes backfire. Evidently, “displays of excellence can paradoxically turn off the very people they are trying to inspire.”

It’s reasonable to assume that not being a hypocrite and trying to walk the walk would lead to positive consequences, inspiring confidence in others. Don’t you want a dance instructor who can dance, a music teacher who can play, and a health professional who’s healthy? But “this simple intuition fails to take into account the concerns about devaluation than an expert’s superior behavior elicits in others”—that is, that may make people feel inadequate. For example, you know how vegetarians often become targets of ridicule and hostility? That’s because they may come off as morally superior and make other people feel like they’re being looked down upon.

There was an elegant demonstration of this phenomenon in a study where “principled deviants who take the high road threaten others’ moral self-worth.” Participants were asked to complete “a racist task,” and those “moral rebels” who refused to do so were cheered on by observers but disparaged by their fellow participants who had done the task. Why? Because the rebels’ stance was “an implied indictment of their spinelessness.” Isn’t that interesting?

So, when doctors portray themselves as “the picture of health,” patients might think they’re being holier-than-thou, which can unintentionally alienate those who need the doctors’ help the most. It’s easy to imagine how someone with a weight issue might feel threatened and judged by a physician triathlete. But what are we supposed to do? We want healthy practitioners. Physicians who smoke are less likely to tell their patients to quit smoking, physicians who are overweight are less likely to advise about weight loss, and physicians who don’t work out are less likely to talk about exercise. What doctors can do to make patients more comfortable is emphasize that their role is to help people meet their own personal health goals, whatever they may be. Studies show that when doctors take this approach, it increases the appeal of “fitness-focused” physicians to overweight patients. So, doctors can then display model behavior without inadvertently alienating those who would most benefit from their counsel.

Doctor’s Note

For more on lifestyle medicine, see related posts below. 

“In adults, emerging evidence suggests that higher daily intake of fiber-rich fruit and vegetable servings is associated with lower incidences of anxiety, greater happiness, higher life satisfaction, and greater social-emotional well-being,” says a review in the journal Nutrients. So, “persuading people to consume more fruits and vegetables may not only benefit their physical health in the long-run, but also their mental well-being in the short-run,” concluded a study in Social Science & Medicine. Fruit consumption, for example, has a protective association with leading killers like heart disease, stroke, diabetes, and cancer, as well as depression. The question is why?

Several mechanisms have been proposed. For example, one posits it’s the antioxidant and anti-inflammatory properties of produce, which scavenge the free radicals that are involved in some of the inflammation associated with depression. If that’s the case, what about simply taking vitamin C supplements? The brain has some of the highest levels of vitamin C in the body, so it’s thought that if extra vitamin C is consumed, it may have some sort of therapeutic role in brain diseases, especially given that it is not just an antioxidant, but also has other critical functions in the brain, such as helping to build neurotransmitters like dopamine. But you don’t know whether it actually helps until you put it to the test.

One study found a beneficial effect of adding vitamin C as an adjunct treatment to an antidepressant, while another study found no benefit from vitamin C supplementation.

So, there are mixed results for vitamin C and depression. Another study found no benefit when it came to depression, but those randomized to vitamin C instead of placebo pills did show a significant decrease in anxiety level. And this wasn’t only seen in that study.

The effects of oral vitamin C supplementation on anxiety in high school students were studied in a double-blind, randomized, placebo-controlled trial. The teens were given 500 mg a day of vitamin C or a placebo. That daily amount of vitamin C is about what you’d find in five oranges, four yellow kiwifruit or guavas, or one and a half yellow bell peppers. Within just two weeks, the vitamin C reduced anxiety levels compared to placebo, as well as provided a significant drop in heart rate.

Given these data showing that vitamin C may have an anxiety-reducing effect, researchers sought to find out if a single dose could acutely affect emotional states. And indeed, within only two hours of taking some vitamin C, study participants experienced a significant drop in anxiety compared to placebo, though only among those who started out the most anxious in the first place, as you can see below and at 2:42 in my video Do Vitamin C Supplements Help With Anxiety?.

As a bonus, vitamin C supplementation may lower our blood pressure a few points, but whole fruits and vegetables can do the same thing—and may even do it better for those who need it the most, as shown below and at 2:53 in my video.

As I’ve shown previously, simply adding just two servings of fruits and vegetables a day can have psychological well-being benefits within only two weeks—and without the kidney stone risk associated with vitamin C supplements, though that appears to be only a problem in men.

Doctor’s Note

For more on vitamin C and on anxiety, check out related posts below.

The high glycemic impact of potatoes may increase the risk of type 2 diabetes, perhaps by chronically overstimulating the insulin-producing cells in the pancreas. In my last two blogs, I explained how you can decrease the glycemic impact of white potatoes by eating them cold, chilling then reheating them, or adding broccoli, lemon juice, or vinegar. What else can we do?

Well, the pigments in brightly colored berries can act as starch blockers, as you can see below and at 0:38 in my video The Healthiest Type of Potato.

So, if you’re going to eat a high glycemic food, you may be able to moderate its impact by, for example, spreading raspberries on your toast, adding strawberries to your cornflakes, or sprinkling blueberries into your pancake batter. I’m not saying you have to put blackberries in your baked potato, but given that the natural color compounds in fruits can slow down starch digestion, what about pigmented potatoes?

Even regular yellow potatoes like Yukon gold may be preferable to white, but the best may be purple potatoes—not just purple-skinned potatoes but purple-fleshed potatoes. If you’ve never seen purple potatoes, they are remarkable—they have almost a neon-blue glow, which you can see below and at 1:14 in my video.

And not only do they look cool, but purple potatoes cause less of an insulin spike and less of a blood sugar spike compared to even the yellow-fleshed potatoes, suggesting that switching from yellow or white potatoes to purple ones “could have large potential in maintaining public health.”

How do we know the pigments themselves are responsible, rather than other differences between the different potato varieties? Researchers tried using a control made of berries in a potato starch jelly, but that approach would seem to add even more variables. In a test tube, extracts of purple- and red-fleshed potatoes can act as starch blockers. So, if you extract and purify the purple potato pigments, you could remove any other effects of the different potato varieties by adding those purple pigments to yellow potatoes. And lo and behold, compared to plain yellow potatoes, this results in suppressions of blood sugar and insulin spikes. Instead of an overshoot reaction, where blood sugars can actually drop below fasting levels, you get the gentler rise and fall in blood sugars you’d expect from a lower glycemic food, as you can see below and at 2:25 in my video.

The authors suggest purple potato extracts could be produced to make supplements or fancy functional foods, but it might be more cost-effective to get these compounds from consuming purple potatoes themselves.

The purple potato pigments may also affect inflammation. The Potato Association of America likes to paint potatoes as an anti-inflammatory food, but what it doesn’t tell you is that this benefit may be limited to pigmented potatoes. When study participants were randomized to eat a small white potato every day for six weeks versus a yellow- or purple-fleshed potato, those in the purple potato group achieved significantly lower levels of inflammation compared to those in the white potato group, measuring both C-reactive protein and interleukin-6, shown below and at 3:13 in my video.

Pigmented potato consumption also alters oxidative stress. Within hours of eating a large purple potato, you get a nice 60% bump in the antioxidant power of your bloodstream, and this translates into less free radical DNA damage. If you compare the antioxidant activity of white potatoes, yellow potatoes, and purple potatoes, Yukon gold has about twice the antioxidant power as white, but purple has 20 times the antioxidants. That’s comparable to what you might see in berries. Half a purple potato has about the same polyphenol antioxidant content as half a cup of blueberries.

Purple potatoes can increase the antioxidant capacity of our bloodstream, whereas straight white potato starch can act as a pro-oxidant and decrease it. Eat a purple potato, and, over the next eight hours, the antioxidant capacity of your bloodstream goes up. In contrast, if you eat white potato starch devoid of any pigment, you can end up worse off than where you started, as you can see below and at 4:12 in my video.

Okay, but does this translate into different physiological effects? Yes, indeed. When people ate either purple potatoes or white potatoes for two weeks, the purple potatoes improved a measure of arterial stiffness, whereas the white potatoes did not. And this translates into a drop in blood pressure, even in those already taking high blood pressure drugs, suggesting purple potatoes are an effective blood pressure–lowering agent.

But what about the toxic glycoalkaloid compounds found in potatoes? The toxic human dose starts around 2 to 5 mg/kg of body weight, and the lethal dose is not too far behind. But the average amount of total glycoalkaloids found in most potatoes, however, is less than 100 mg/kg; so, at the average American weight of 180 pounds, a toxic dose is like four to nine pounds of potatoes. What happens when you approach that amount? It’s possible you can get nausea, vomiting, or diarrhea that could be easily confused with something like gastroenteritis or food poisoning. Some people can start to get sick at just 1.25 mg/kg of body weight or even experience symptoms at 1 mg/kg. That would only be about two pounds of potatoes at the average American weight. It’s also possible that the glycoalkaloids could start accumulating if you eat potatoes day in and day out. But what about those people who go on a fad potato diet and eat three or four pounds a day? They can do that without risking getting sick if they peel their potatoes, which removes nearly all of the glycoalkaloids.

Doctor’s Note

This is the last in a five-video series on potatoes. If you missed any of the others, see:

• Do Potatoes Increase the Risk of Diabetes?
• Do Potatoes Increase the Risk of High Blood Pressure and Death?
• Glycemic Index of Potatoes: Why You Should Chill and Reheat Them
• How to Reduce the Glycemic Impact of Potatoes
• I previously highlighted purple potatoes in Anti-Inflammatory Effects of Purple Potatoes.

You may also be interested in The Best Way to Cook Sweet Potatoes.

The video on berries I mentioned is Getting Starch to Take the Path of Most Resistance.

White potatoes have a high glycemic index, and consumption of high glycemic impact foods may increase the risk of diabetes. Normally, after a meal, we’d like our blood sugars to rise and fall gently and naturally. But with high glycemic foods like potatoes, we get an exaggerated blood sugar spike. This leads our body to over-compensate with insulin, forcing our blood sugars lower than when we started, which results in negative metabolic consequences, such as a rise in triglyceride fats in the blood, as you can see below and at 0:34 in my video How to Reduce the Glycemic Impact of Potatoes.

However, potatoes are a good source of vitamin C, potassium, and polyphenols, which may counterbalance their glycemic impact. This may explain why potatoes appear to have a neutral effect when it comes to lifespan, unlike other whole plant foods that have been associated with actively living longer.

In my last blog, I explained how the act of chilling cooked potatoes can dramatically lower their glycemic index, even if you then reheat them in a microwave. How else might we reduce the glycemic impact of white potatoes? The same way you make anything better in your nutritional life—add broccoli. Eating two servings of cooked broccoli with your mashed potatoes would certainly do it, immediately cutting the insulin demand by nearly 40%. In contrast, adding chicken breast makes things worse, and adding tuna fish makes things even worse still, nearly doubling the amount of insulin your body has to pump out, as shown below and at 1:31 in my video.

Why does plant protein make things better, but animal protein makes things worse? Because decreased consumption of branched-chain amino acids improves metabolic health. I cover this in my book How Not to Diet, as well as in my video on the topic.

Speaking of How Not to Diet, remember the section on vinegar? The graph below illustrates the blood sugar and insulin spikes that someone with prediabetes may experience after eating a bagel. When that same bagel is consumed alongside a tablespoon or so of apple cider vinegar diluted in about a quarter cup of water, though, the spikes are significantly reduced, as you can see below and at 2:10 in my video.

Does it work for potatoes, too? Simply chilling potatoes may cut down on the blood sugar and insulin spikes, but to get significant drops in both, you just have to add about a tablespoon of vinegar to drop levels by 30% to 40%. And that was just plain white distilled vinegar.

Is it the vinegar itself, or would any acidic condiment do? In a test tube, lemon juice appeared to have a remarkable starch-blocking effect, but you can’t know if it works in people until you put it to the test. And indeed, lemon juice reduces the glycemic responses to bread. And not just by a little, but by about 30%, as you can see below and at 2:50 in my video.

Now, the study participants were drinking a half cup of lemon juice, but that makes it even more remarkable that it was helpful because that added an extra half teaspoon of sugar, yet they still had a better blood sugar response. Vinegar is more potent, though. Just one to two tablespoons a day of vinegar diluted in water can significantly improve both short- and long-term blood sugar control in people with diabetes, which is why clinicians may want to include vinegar consumption as part of their dietary recommendations for their patients with diabetes.

Doctor’s Note

This is the fourth video in a five-part series on potatoes. Missed the first three? See:

• Do Potatoes Increase the Risk of Diabetes?
• Do Potatoes Increase the Risk of High Blood Pressure and Death?
• Glycemic Index of Potatoes: Why You Should Chill and Reheat Them

What about the glycoalkaloid toxins in potatoes? I cover that and discuss the best kind of potato in my upcoming final video in the series: The Healthiest Type of Potato.

If you systematically pull together all the best studies on potato consumption and chronic disease risk, an association is found for the risk of type 2 diabetes and hypertension—but that’s for French fries. Consumption of boiled, baked, or mashed potatoes was not associated with the risk of high blood pressure, but there was still a pesky link with diabetes. Overall, eating potatoes is not related to risk for many chronic diseases, but boiled potatoes could potentially pose a small increase in risk for diabetes. That’s one of the reasons some question whether they should be counted as vegetables when you’re trying to reach your recommended daily servings of fruits and vegetables.

If you look at other whole plant foods—nuts, vegetables, fruits, and legumes (which are beans, split peas, chickpeas, and lentils)—they’re associated with living a longer life. Significantly less risk of dying from cancer, dying from cardiovascular diseases like heart attacks, and 25% less chance of dying prematurely from all causes put together. But no such protection is gained from potatoes for cancer, heart disease, or overall mortality. So, the fact that potatoes don’t seem to affect mortality can be seen as a downside. Now, it’s not like meat, which may actually actively shorten your life, as you can see below and at 1:28 in my video Glycemic Index of Potatoes: Why You Should Chill and Reheat Them.

But there may be an opportunity cost to eating white potatoes, since every bite of a potato is a lost opportunity to put something even healthier in your mouth—something that may actively make you live longer.

So, potatoes are kind of “a double-edged sword.” The reason that potato consumption may have just a neutral impact on mortality risk is that all the fiber, vitamin C, and potassium in white potatoes might be counterbalanced by the adverse effects of their high glycemic index. Not only are high glycemic impact diets “robustly associated” with developing type 2 diabetes, but current evidence suggests that this relationship is cause and effect.

A front group for the potato industry called the Alliance for Potato Research and Education funded a study that found that intake of non-fried potatoes does not affect blood sugar markers, when compared with the likes of Wonder Bread, that is, so that isn’t really saying very much. Foods with a glycemic index (GI) higher than 70 are classified as high-GI foods (high glycemic index foods), and those lower than 55 are low-GI foods. Pure sugar water, for example, is often standardized at 100, and white bread and white potatoes are also way up there as high glycemic index foods. But when you compare them to an intact grain, like barley groats (also known as pot barley), which is a super-low GI food, you can see how refined grains and potatoes are simply no match. Check out the numbers below or at 2:47 in my video.

Is there any way we can have our potatoes and eat them too, by somehow lowering their glycemic index? Well, if you boil potatoes and then put them in the fridge to cool, some of the starch crystallizes into a form that can no longer be broken down by the starch-munching enzymes in your gut, as you can see below and at 3:06 in my video.

However, the amounts of this so-called resistant starch that are formed are relatively small, making it hard to recommend cold potatoes as a solution. But when put to the test, you actually see a dramatic drop in glycemic index in cold versus hot potatoes, shown below and at 3:23 in my video.

So, by consuming potatoes as potato salad, for instance, you can get nearly a 40% lower glycemic impact. The chilling effect might, therefore, also slow the rate at which the starch is broken down and absorbed. So, people who want to minimize dietary glycemic index may consider precooking potatoes and having them chilled or reheated. The downside of eating potatoes cold is that they might not be as satiating as eating hot potatoes. But you may get the best of both worlds by first cooling them and then reheating them, which is exactly what was done in that famous study I profiled in my book How Not to Diet. The single most satiating food out of the dozens tested was boiled-then-cooled-then-reheated potatoes, as you can see below and at 4:09 in my video.

There is actually an appetite-suppressing protein in potatoes called potato protease inhibitor II, but the way you prepare your potatoes makes a difference. Both boiled and mashed potatoes are significantly more satiating than French fries, as shown below and at 4:26 in my video.

That was for fried French fries, though. What about baked French fries? Folks had a big drop in appetite after eating boiled mashed potatoes, compared to white rice or white pasta, which is right where fried French fries were stuck, as well as baked French fries. So, though baked fries may be your BFF, they’re not very satiating.

Doctor’s Note

Just to be clear, you don’t have to reheat. Chilling is the crucial step to dramatically lower the glycemic index, so you can certainly enjoy a cold potato salad. If you’re trying to control your weight, though, you may want to avoid even baked fries.

This is the third in a five-video series on potatoes. If you missed the first two, see Do Potatoes Increase the Risk of Diabetes? and Do Potatoes Increase the Risk of High Blood Pressure and Death?.

Chilling isn’t the only trick to blunt the glycemic impact. You can also add vinegar, lemon, or broccoli.

Stay tuned for the final two videos in this series: How to Reduce the Glycemic Impact of Potatoes and The Healthiest Type of Potato.

Join the resistance! Check out related posts below.

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Is there a link between potato intake and the incidence of hypertension? Harvard researchers followed the diets and diseases of more than 100,000 men and women for decades and found that those who ate potatoes on most days—not only French fries and potato chips, but even mashed, boiled, or baked—appeared to be at higher risk of developing high blood pressure. But what do people put on potatoes? Salt, not to mention butter, so might the potatoes just be innocent bystanders? The researchers made attempts to tease out the effects of salt and saturated fat, and there still seemed to be a link between potato consumption and high blood pressure.

Maybe potato eaters are meat-and-potatoes people. After all, these same Harvard researchers found that meat, including poultry, seemed to be associated on its own with an increased risk of hypertension, and the same goes for even a moderate amount of canned tuna. So, in the potato study, they were careful to try to factor out any effects from the consumption of all types of animal flesh. Yet, they still found an increased risk and became concerned that associating potato intake with hypertension could be a “critical public health problem.” It was assumed potatoes might actually decrease high blood pressure, given their high potassium content, but they found evidence of the opposite effect.

As I discuss in my video Do Potatoes Increase the Risk of High Blood Pressure and Death?, two similar studies performed in Mediterranean Europe did not find any association between potato consumption and high blood pressure, though. Perhaps this is because they don’t smother their potatoes in butter and sour cream in that neck of the woods and instead eat potatoes with other vegetables. Now, the Harvard researchers tried to control for the salty and fatty dietary components associated with eating potatoes in the West, just like these researchers tried to factor out all the extra vegetables, but you can’t control for everything.

One of the main reasons we care about blood pressure is because we care about the consequences. In two studies done in Sweden, where they primarily eat their potatoes boiled, no evidence was found that potato consumption was associated with the risk of major cardiovascular disease. No relationship between potato consumption and risk of premature death was found in Southern Italy either. In the United States, however, potato consumption was associated with increased mortality: a whopping 65% increased risk of dying from heart disease, a 26% increased risk of fatal stroke, a 50% increased risk of dying from cancer, and an increased risk of dying from all causes put together. However, this association disappeared after adjusting for confounding factors. In other words, it wasn’t the potatoes at all. Potato eaters must just smoke more, drink more, or eat more saturated fat or something. Once you control for all these other factors, the link between potatoes and death disappears.

This was confirmed in the NIH-AARP study, the largest such study of diet and health in human history. If you separate out just the potatoes, researchers find they are not associated with increased risk of death, with the possible exception of French fries, which are associated with an increased risk of dying from cancer. Put all the studies together—20 in all—and no significant association has been found between potato consumption and mortality, though again, fried potatoes may be the exception. Even just twice a week, fries may double one’s risk of dying prematurely, independently of other factors, but the consumption of unfried potatoes seemed to be neutral.

I’ve talked a lot about how all plant foods are not created equal, as well as healthy versus unhealthy plant-based diets. To this end, researchers created not only an overall plant-based diet index (PDI)—just scoring plant versus animal foods—but also a healthy plant-based diet index (hPDI) and an unhealthy plant-based diet index (uPDI). The healthy index puts a greater emphasis on whole plant foods, whereas the unhealthy index scores how much low-quality plant foods you’re eating, grouping potatoes along with soda, cake, and Wonder Bread. When you run the numbers, the more plant-based you eat, the longer you live, and the lower your risk of cardiovascular disease. In other words, more plant foods and less animal foods are associated with a significantly lower risk of dying prematurely. This benefit was limited, though, to those eating the healthier plant-food diets. However, the researchers were surprised that those eating the less healthy plant-based diets with processed plant-based junk did not live significantly shorter lives. Maybe that’s just because they were eating fewer animal products, and that’s really the primary determinant of lifespan here, or maybe the lack of an association between less healthy plant-based diets and mortality is because potatoes were kind of coming to the rescue. And indeed, higher intake of potatoes did appear protective; so, given these conflicting results, future studies may consider just resigning fried potatoes to the unhealthy list.

Now, in terms of mortality, fried potatoes may not be as bad as fried meat—fried chicken and fried fish—but that’s not really saying much. The French fry/death data gave the industry trade group Potatoes USA a bit of a chip on its shoulder, reminding readers that observational studies can only prove correlation, not causation, to which the authors replied, “Our data add to the pressing public health calls to limit fried potato consumption.” French fries may be so bad for you that it wouldn’t be ethical to do an interventional study and randomize people to eat them.

Doctor’s Note

This is the second in a five-part series on potatoes. The first installment was Do Potatoes Increase the Risk of Diabetes?.

Aside from French fries, potato consumption is not associated with mortality. Potato eaters tend to live just as long as non-potato eaters. That’s actually bad news. A whole plant food that’s not associated with living longer? One that has a neutral effect on lifespan? That’s a lost opportunity. But what if you really like white potatoes? Then you should chill and reheat them, as I explain in my next video.

Coming up:

• Glycemic Index of Potatoes: Why You Should Chill and Reheat Them
• How to Reduce the Glycemic Impact of Potatoes
• The Healthiest Type of Potato

For more on preventing and treating high blood pressure, see related posts below.

The trouble for white potatoes began in 2006, when the Harvard Nurses’ Health Study, which had followed the diets and diseases of tens of thousands of women for 20 years, found that greater potato intake was associated with a greater likelihood of getting type 2 diabetes. However, of the hundred or so pounds of potatoes Americans eat every year, most are in the deep-fried forms of potato chips, french fries, or other processed products. What happened when they looked specifically at mashed or baked potatoes? They found the same link with diabetes. Okay, but what might potato eaters eat more of? Maybe I should rephrase that: What might meat-and-potatoes people eat more of? Indeed, people who ate more potatoes ate more meat, and we know that animal protein may be associated with increased diabetes risk. But the researchers tried to statistically adjust for that and still found increased risk with potatoes.

Well, what do people put on baked and mashed potatoes? Butter and sour cream. Again, the researchers tried to adjust for other dietary factors like these as well as effectively looking at the ratio between plant and animal fats and whether potato eaters drank more soda or maybe skimped on other vegetables. Yet, still, there seemed to be this association between potatoes and diabetes.

Okay, but that was just one study. By 2015, Harvard researchers had also looked into other cohorts, including the all-male Health Professionals Follow-up Study to complement the all-female Nurses’ studies, and they continued to find a small increased diabetes risk associated with baked, boiled, or mashed potatoes, though french fries do indeed appear nearly five times worse. The authors concluded that potatoes are considered to be a healthy vegetable in dietary guidelines, but the current evidence “casts serious doubts on this classification.” Walter Willett, the chair of Harvard’s nutrition department at the time, went a step further, suggesting potatoes should be siloed up there with candy, as you can see below and at 2:18 in my video Do Potatoes Increase the Risk of Diabetes?.

A meta-analysis of potato consumption and risk of type 2 diabetes published in 2018 combined all six of the prospective studies that had been done to date, and the researchers found about a 20% increase in diabetes risk associated with each serving of potatoes a day, concluding “[l]ong-term high consumption of potato…may be strongly associated with increased risk of diabetes.” But, again, the great majority of the potatoes consumed were fried, and we know deep-fried foods contain all sorts of nasty things, like advanced glycation end-products. The researchers weren’t able to assess french fries versus non-fried potatoes. Even just three servings of fries a week is associated with nearly 20% greater risk of type 2 diabetes, whereas there was only a tiny associated risk with potatoes in general, and that included the fries mixed in.

The world’s largest manufacturer of frozen french fries took issue with this conclusion. Claiming to make one in three fries eaten on planet Earth to the tune of billions of dollars, the company has the money to fund reviews to cast doubt on the science. One review said that the scientific literature should be read with caution because the impact of potatoes on disease risk factors may depend on the foods they’re grouped with as part of a dietary pattern. Indeed, they do have an actual point. Observational studies can never prove cause and effect, and maybe potato consumption—even baked potato consumption—may just be a marker for an unhealthy diet in general. As much as researchers try to adjust for these other factors, as the journal of the Potato Association of America is quick to remind us, it’s not possible to separate the effects of potatoes and fries from the effects of the overall crappy Standard American Diet.

Is there a country where potato consumption is associated with a healthy diet? If potato consumption was still associated with diabetes there, then that would be concerning. Enter a seventh study, but this time out of Iran, where most potato consumption is of boiled potatoes. In fact, those who ate potatoes had the healthiest diets and ate the most whole plant foods—fruits, vegetables, legumes, and whole grains. And though the researchers tried to tease out those other dietary factors, those eating the most boiled potatoes had only half the odds of developing diabetes. This supports the notion that it may be hard to completely separate out just the potatoes. The bottom line, this systematic review concluded, is that we really don’t have “convincing evidence” that the intake of potatoes in general is linked to type 2 diabetes, but we should still probably hold the fries.

Doctor’s Note

This is the first in a five-part series on potatoes. Stay tuned for:

• Do Potatoes Increase the Risk of High Blood Pressure and Death?
• Glycemic Index of Potatoes: Why You Should Chill and Reheat Them
• How to Reduce the Glycemic Impact of Potatoes
• The Healthiest Type of Potato

Interested in a sampling of diabetes videos? Check out the related posts below.

The act of defecation is very private and the object of cultural taboos, so much so that it’s rarely thought of, even by physicians—but it should be. Constipation accounts for three million annual visits to doctors in the United States and 800,000 emergency room visits. Depending on how you define it, up to 80% of the population may be suffering. Even people who don’t think they’re constipated may very well be clinically constipated. A quarter of so-called healthy study participants reported experiencing “incomplete emptying,” and about half “indicated increased straining.” In fact, more than half had found blood on their toilet paper within the past year. In severe cases, the blood pressure spike associated with straining while passing stool can even trigger a heart attack or a stroke.

There are drugs for it. There are always drugs, resulting in side effects like nausea, diarrhea, headache, and abdominal pain, leaving most patients unsatisfied. So why not instead just try to treat the cause? Common causes of chronic constipation include a lack of whole plant foods containing fiber or insufficient water intake, so changing one’s diet and lifestyle is the preferred method for constipation relief. Such nonpharmacological, clinically effective interventions include engaging in physical activity for about 30 minutes a day.

A systematic review and meta-analysis found that aerobic exercise interventions help, starting at about 140 minutes a week. And then, of course, a diet centered around whole plant foods—the only naturally concentrated sources of fiber—helps as well. Any plants in particular?

When elderly women with severe constipation were given about a dozen prunes a day, they experienced significant improvement within the first week. The control group in the study wasn’t told to do anything, though. When one group does something while the other does nothing at all, you can’t discount the placebo effect. And, indeed, the placebo effect for constipation trials can range up to 44%, meaning up to nearly half of the people given a sugar pill claimed to experience an improvement.

That’s why we need studies like this: Participants were randomized to about 8 prunes a day plus a large glass of water, 12 prunes and water, or just the water alone. So, even the control group got an intervention (the water), which might help with constipation. Previous studies mostly assigned about 10 prunes a day, so the researchers wanted to see if more prunes provided greater benefit or whether fewer would work just as well. They found a significant improvement in stool bulk on the prunes and a significant increase in bowel movement frequency, as you can see below and at 2:45 in my video Prunes: A Natural Remedy for Constipation, though there was no real difference between 8 and 12 prunes. So, 8 a day seems sufficient.

Prunes even seem superior to psyllium, sold as Metamucil, beating it out in terms of improved stool frequency and consistency.

We used to think it was just all the fiber in prunes that was helping, but prune juice evidently works too, which, like most juices, has had the fiber removed. Other potential active components include a natural sugar alcohol known as sorbitol that’s used in some sugar-free gums. Once you eat more than a dozen or so large prunes a day, however, the dose of sorbitol could start reaching laxative levels in susceptible individuals. So, be careful.

If you don’t have constipation, should you avoid prunes? That question has been put to the test, and the answer appears to be no—most people should be able to eat a dozen or so a day without any issues. In fact, it’s interesting to note that prunes have been traditionally used as a laxative and an antidiarrheal remedy.

What about dried figs, one of the few medicinal plants mentioned explicitly in the Bible? Researchers took patients with the type of irritable bowel syndrome (IBS) characterized by constipation and randomized them to one fig with breakfast and one fig with lunch, each with a glass of water, and there was a significant improvement in frequency of defecation and a significant drop in the frequency of hard stools, compared to the control. But what was the control? The control group was just asked to continue their normal diet. In other words, do nothing special. The placebo response for irritable bowel is infamous. Give people with IBS a fake sugar pill, and sometimes 72% say they magically feel better.

That’s why we need this kind of study: a randomized, double-blind, placebo-controlled trial. Researchers made a gross-sounding fake fig paste placebo that supposedly had the same taste, smell, and appearance as the real deal. Those who got the real figs, about six a day, seemed to experience “a significant reduction in colon transit time and a significant improvement in stool type [consistency] and abdominal discomfort,” compared to the placebo. Researchers measured transit time by having people swallow little beads that would show up on X-rays so they could track the progress through their digestive system. They found that those eating the real figs sped up their gut movement by a full 24 hours. Defecation frequency per week didn’t beat out placebo, though. In fact, they tested so many different outcomes, even the stool consistency and abdominal discomfort results may have been statistical flukes. So, it looks like prunes would be the better treatment choice.

Doctor’s Note

What about carbonated drinks? See Club Soda for Stomach Pain and Constipation.

I previously discussed prunes and constipation in Prunes vs. Metamucil vs. Vegan Diet.

What else can prunes do? See Prunes for Osteoporosis.

Can we do anything else for IBS? Check out the related posts below.

“The main purpose of frying is to produce foods with good consumer acceptability. However, not all acceptable foods are safe.” Food chemists have been very interested in the newly discovered toxic compounds produced by frying.

We’ve been refining vegetable oils for more than a century, but only recently have we discovered that this can produce concerning compounds such as 3-MCPD and, even worse, glycidol. 3-MCPD is considered a nongenotoxic carcinogen with a tolerable daily intake, while glycidol is a known genotoxic carcinogen, meaning it can cause cancer by directly damaging our DNA, as I discuss in my video The Carcinogen Glycidol in Cooking Oils.

If a compound is not directly DNA-damaging, it’s assumed that it acts through a mechanism that exhibits a threshold; a so-called no-effect level may exist, a level below which it may not be harmful. But if a compound does damage DNA, it’s generally assumed to follow “a non-threshold mechanism…and no ‘safe level of intake’ can be derived,” because it may only take DNA mutation to start the march towards cancer. So, such substances are not allowed to be added intentionally to foods. For so-called unavoidable contaminants, the “ALARA” principle is followed, meaning that the level should be as low as reasonably achievable or as low as reasonably practicable. Since that’s what glycidol appears to be, we should try to avoid it as much as possible.

A lifetime cancer risk of 1 in 100,000 is “often used as a figure for acceptable risk in the population.” Based on lab animal data, this might be exceeded if someone weighing about 150 pounds consumed less than a microgram a day. However, thanks to the use of refined oils in so many food products, the average glycidol exposure may be more than 50 micrograms. And in children, the level of intake may exceed acceptable cancer risk by 200-fold.

So, do people who eat more fried food get more cancer? There is said to be strong evidence that there may be a higher risk of developing chronic disease among frequent consumers of fried foods, but that’s talking largely about cardiovascular health. For example, in a study of more than 100,000 women, frequently consuming fried foods, especially fried chicken and fried fish, was associated with a higher risk of all-cause mortality, meaning such consumers lived, on average, significantly shorter lives. But that was due largely to cardiovascular mortality, whereas fried food consumption was not generally associated with dying from cancer. In men, however, a larger intake of fried food was associated with a 35% increased risk of prostate cancer. Therefore, perhaps men with an increased risk of prostate cancer should, as a precaution, limit their consumption of fried foods.

These refined oils are also used in infant formulas, which presents a problem for babies who aren’t breastfed. The German Federal Institute for Risk Assessment has come to the conclusion that “infants who are fed exclusively industrially prepared infant milk formula would take in harmful levels of glycidol.” It should be noted that U.S. formulas contain levels of glycidol contamination comparable to those found in Europe—yet another reason that breast is absolutely best. Meanwhile, there are calls on the manufacturers of these products to do everything they can to reduce levels as low as possible.

But, evidently, the industry has yet to find a way to refine vegetable oils without creating these kinds of by-products, “while at the same time maintaining the quality of the refined product.” It was therefore concluded that this problem has no simple solutions, but I disagree. We can choose to avoid the use of oils and fried foods.

Doctor’s Note

I previously talked about 3-MCPD in The Side Effects of 3-MCPD in Bragg’s Liquid Aminos and 3-MCPD in Refined Cooking Oils.

There is no substitute for human breast milk. Adoptive families or those who use surrogates may want to look for a nearby milk bank.

“Intervention studies to enhance healthy ageing need appropriate outcome measures, such as blood-borne biomarkers, which are easily obtainable, cost-effective, and widely accepted.” We need blood-borne biomarkers of mortality risk. For example, having higher levels of C-reactive protein in your blood may increase your risk of dying prematurely by 42%. C-reactive protein is one of the most widely used inflammatory biomarkers for predicting mortality, but those with the highest levels of interleukin-6 (IL-6), another marker of inflammation, may increase premature death risk by 49%. What can we do to bring it down?

I’ve previously talked about foods that can contribute to inflammation, like meat and sugar, versus foods like nuts that don’t. But what about anti-inflammatory foods that actually attenuate that inflammation?

What happens when blueberries are added to a high-fat, high-glycemic-load meal consisting of white potatoes, white bread, ham, cheese, and butter? Adding a single cup of blueberries caused a significant drop in IL-6 from that meal, as you can see below and at 1:15 in my video Which Foods Are Anti-Inflammatory?.

What about raspberries? People were fed eggs, butter, white potatoes, white flour biscuits, and sausage with or without two cups of frozen raspberries blended with water into a smoothie, compared to giving others the same amount of calories and carbs in banana form. Bananas were no match for meat, eggs, dairy, and crappy carbohydrates; that meal resulted in a tripling of IL-6 levels within four hours. But by drinking those two cups of raspberries instead, their bodies were able to hold the line, as you can see below and at 1:45 in my video.

Why did raspberries work but bananas didn’t? Maybe it’s the antioxidants.

Well, antioxidant supplements failed miserably. There was no benefit from antioxidant vitamins and minerals like vitamins C or E, beta-carotene, or selenium. Maybe it’s those special antioxidant pigments, the anthocyanins, that give berries those bright red, blue, and purple colors? Indeed, that’s what dozens of randomized controlled trials have demonstrated, whereas a half-dozen studies combined show pomegranates, a fruit packed with anthocyanin pigments, can bring down inflammation over time.

What about adding spices to meals as an approach to cool down inflammation? Supplementation with grape and turmeric extracts did not affect the inflammatory response to a milkshake. But giving people one teaspoon a day of actual turmeric—that is, the whole spice, not purified curcumin supplements—resulted in a significant drop in IL-6 levels.

Garlic powder reduced IL-6 levels as well, starting at about half a teaspoon a day. Ginger powder (ground ginger) had the same results with doses ranging from half a teaspoon to one and a half teaspoons.

Of course, another way to mediate the inflammation caused by a Sausage and Egg McMuffin is to not eat it in the first place. What about just eating a plant-based diet? To my surprise, the drop in IL-6 did not reach statistical significance. Whenever a dietary intervention doesn’t have the result you expect, you always have to ask, “What exactly was the diet they actually ate?” The study mostly looked at the Mediterranean diet, which certainly has more plants, but maybe the diets didn’t go far enough? For more clarity, we turn to Dr. Turner-McGrievy’s famous New DIETs study, where people either continued to eat their fully omnivorous diets or were randomized to eat a vegan diet, a vegetarian diet, a pesco-vegetarian diet, or a semi-vegetarian diet that, for example, limited red meat. So, whereas the vegan might eat red beans and brown rice with chopped tomatoes and roasted peppers for dinner, the vegetarian might add some cheese, the pesco-vegetarian might add shrimp, and the semi-vegetarian might add some turkey sausage. Below is a more in-depth look at the five diet patterns, which you can also see at 4:01 in my video.

What happened within two months to their Dietary Inflammatory Index scores? The Dietary Inflammatory Index is a measure of how inflammatory your diet is. Negative scores mean your overall diet is anti-inflammatory, and the lower, the better, whereas positive scores mean your overall diet is on balance pro-inflammatory, which is exactly where the people in the study started. That comes as no surprise, given that they were eating regular diets and our nation is awash with inflammation-related disease.

But when the study participants switched to strictly plant-based nutrition, their diet flipped to become an anti-inflammatory diet. That was the case even if they just cut out meat or all meat except fish. But if they instead switched mostly to poultry or only limited their meat intake, their diet remained inflammatory. You can see the results below or at 4:47 in my video.

Now, not all plant foods are anti-inflammatory. If all you do is boost your intake of less healthy plant foods, like juice, white bread, white potatoes, soda, and cake, you can end up even more inflamed. But if you eat a really clean diet of whole plant foods, you get significant reductions in lipoprotein(a)—Lp(a)—which we didn’t even think was possible with diet—as well as drops in LDL cholesterol and even the most dangerous form of LDL cholesterol. Also, nearly across the board, you get a drop in inflammatory markers; we’re talking a 30% drop in C-reactive protein and a 20% drop in IL-6. So, maybe previous studies with plant-centered diets were unsuccessful because they weren’t plant-based enough, with animal products still being substantially consumed. Therefore, the total “elimination of animal products and processed foods…may be a more prudent dietary strategy” to combat inflammation.

Doctor’s Note

Hungry for more? See Foods That Cause Inflammation.

For more on plant-based diets, see related posts below.

Excessive inflammation may play a role in a number of leading causes of death and disability, including type 2 diabetes, obesity, and heart disease. “But what are the stimuli that jumpstart the destructive inflammatory cascade?” You typically hear about the pro-inflammatory nature of a chronic high-fat diet, but the inflammatory effect “may not be limited to chronic intake but may be evident after the consumption of a single meal.”

Within hours after eating an unhealthy meal, inflammatory markers like interleukin-6 (IL-6) can skyrocket, doubling within six hours. The majority of studies show an increase in IL-6 after consuming a high-fat meal. But the meals they tested weren’t just filled with meat, eggs, dairy, and oil, but also junky refined carbohydrates like white flour and added sugar.

When people are given essentially straight butter fat and no carbs, they can still get a spike in inflammation within hours, proving the added fat itself is pro-inflammatory. But when people are given straight sugar water without any fat, the result is the same, proving the added sugar is pro-inflammatory, too, as you can see below and at 1:26 in my video Foods That Cause Inflammation.

Why should we be concerned with the inflammatory responses after unhealthy meal ingestion? Because extensive research points to the idea that “persistent low-grade inflammation is an underlying factor in several high-mortality chronic diseases and that diet can contribute to, or attenuate, that inflammation.”

You’ll note in the graph below that IL-6 levels jumped up to about 3 pg/mL after the meal. (You can also check it out at 1:55 in my video.)

When levels start regularly getting up to about 3 pg/mL, that’s associated with twice the risk of death. That increased risk was found across the board, compiling eight other similar studies, likely because it’s linked with increased risk of heart disease, the number one killer of men and women, even as strongly as some other major well-known risk factors like high cholesterol.

Now, not all high-fat foods cause inflammation. More than a dozen studies combined show that whole plant foods such as nuts do not increase inflammatory markers, even when eating up to handfuls of nuts a day. In fact, spread half an avocado on a beef burger, and you may be able to blunt some of the inflammation caused by the meat—even lean meat—as you can see below and at 2:35 in my video.

There are reviews purporting to show a drop in inflammatory markers after eating wild game, which is about as lean a meat as you can get, but that’s only compared to store-bought meat. Give people some really fatty meat and their IL-6 shoots up, as do their tumor-necrosis factor and C-reactive protein. Inflammatory, inflammatory, inflammatory—within hours of consumption. But what if you instead eat a kangaroo steak, which is extremely low in fat, similar to elk or moose? You’ll get the same strong inflammatory response within hours of eating it, as you can see below and at 3:15 in my video.

Now, certainly less inflammatory than conventional meat you might get at the store, but pro-inflammatory nonetheless, increasing markers of inflammation within mere hours.

Doctor’s Note

Stay tuned for Which Foods Are Anti-Inflammatory?, up next.

For more on diet and inflammation, see related posts below.

The case of POM Wonderful (the pomegranate juice company) vs. Federal Trade Commission made it all the way up to the U.S. Court of Appeals before being denied review by the Supreme Court. In that landmark case, a panel of judges concluded that many of POM’s ads made false or misleading claims and the company “touted medical studies ostensibly showing that daily consumption of its products could treat, prevent, or reduce the risk of various ailments, including heart disease, prostate cancer, and erectile dysfunction.” The U.S. First Amendment does not protect misleading and deceptive ads. Striking a blow to its billionaire owners, the Court ruled that at least one randomized clinical trial would be required to substantiate claims of treating or preventing disease.

If you look at the medical literature on pomegranate in general, you’ll see reviews touting its many benefits, with diagrams like the one below on the medicinal effects of pomegranates (which you can also see at 1:01 in my video Pomegranate: A Natural Treatment for Rheumatoid Arthritis).

But if you dig a little deeper, you see this is based on studies like one that talks about the “antiobesity effects of pomegranate leaf extract in a mouse model.” First of all, who eats pomegranate leaves? And second, who’s a mouse?

Does pomegranate consumption affect weight in humans? If you look at all the randomized controlled clinical trials (meaning human trials), pomegranates have no significant effect on body weight, BMI, belly fat, or even body fat percentage in those randomized to consume pomegranate products. What about the prevention and treatment of cardiovascular diseases? Researchers reviewed 25 clinical trials, looking at cholesterol, blood pressure, artery function, atherosclerotic plaque formation, and platelet function, and did not find significant indications of benefit even in the best studies.

POM Wonderful helped fund a study on pomegranate juice and erectile dysfunction, but it failed as well. Other studies found no benefit for diabetes markers and observed no benefit for chronic obstructive pulmonary diseases, such as emphysema. They were banking on the antioxidant activity of pomegranate juice to help, but that’s antioxidant activity in vitro (meaning in a test tube or petri dish). To my surprise, a meta-analysis of data from 11 randomized controlled trials “did not support convincing evidence” of pomegranate intake having a significant effect on increasing the total antioxidant capacity in the bloodstream because some of the most potent antioxidants don’t even seem to be absorbed into the human body. No wonder pomegranate supplementation didn’t seem to affect oxidative stress in tissue samples taken from prostate cancer patients. But, of course, what we care about is whether it affects the cancer itself.

The strongest evidence for the anticancer activity of pomegranates is said to come from studies on prostate cancer. Unfortunately, early promising results were not confirmed when they were actually put to the test. For example, daily pomegranate intake was found in a randomized controlled trial to have no impact on PSA levels, a marker of tumor progression. Additionally, a randomized, double-blind, placebo-controlled trial found essentially no difference when it came to prostate cancer disease progression, as you can see below and at 3:19 in my video.

They were banking on the anti-inflammatory activity of pomegranate juice to help, but again, that had been demonstrated in vitro. In people, a meta-analysis based on five randomized controlled trials published in 2016 concluded that pomegranate juice did not have a significant effect on C-reactive protein levels, a key marker of inflammation. If you look at the forest plot, though, you’ll see all five trials tended towards lower C-reactive protein levels such that the data combined almost reached statistical significance, as you can see below and at 3:53 in my video.

Indeed, an updated meta-analysis published in 2020 based on seven studies crossed the threshold into statistical significance and found a significant drop in two other inflammatory markers as well.

Perhaps pomegranate juice could help in the control of inflammatory diseases after all. But you don’t know until you put it to the test.

Osteoarthritis involves the degeneration of the cushioning cartilage within joints, particularly the knees. Dripping a pomegranate extract on human osteoarthritic cartilage samples appears to show cartilage-protective effects. As you can see below and at 4:43 in my video, compared to baseline levels of cartilage disintegration, adding inflammation triples the damage. However, with increasing amounts of pomegranate extract, the breakdown starts to calm down.

But again, that’s in a petri dish. How do we know that when we eat pomegranates, the active components actually get into our bloodstream so they can find their way into our joints? Cartilage-protecting components were found to be bioavailable (at least in rabbits), raising the possibility that pomegranates could be a safe and non-toxic treatment with no side effects, as opposed to the drugs currently in use. But is it effective?

The first clinical trial on pomegranate juice and osteoarthritis was not a placebo-controlled trial, but instead randomized people to pomegranate juice or nothing at all. Those drinking the juice did report less stiffness and impairment of physical function, but not significantly better than just doing nothing. Shoot.

Just as I was about to give up on pomegranates, I saw a study titled “Consumption of Hydrolyzable Tannins-Rich Pomegranate Extract Suppresses Inflammation and Joint Damage in Rheumatoid Arthritis.” But it turned out to be from the POM “Not-So-Wonderful” company, inducing joint damage in a mouse as a model of rheumatoid arthritis. Come on!

There was an open-label study, where the patients knew what they were getting. Eight people with active rheumatoid arthritis took pomegranate extract every day, and the six who stuck with it reported fewer tender joints. But as we learned from the osteoarthritis study, if you don’t have a control group, you have no sense of what role, if any, the treatment actually plays.

Finally, we come to this randomized, double-blind, placebo-controlled trial. It’s about time! Half the study participants unknowingly got some pomegranate extracts; the other half unknowingly got the equivalent of a sugar pill. There appeared to be a significant improvement in the number of swollen joints, tender joints, pain intensity, a disease activity score, a health assessment questionnaire, and morning stiffness compared to placebo. So, if you have rheumatoid arthritis, I would indeed recommend you start eating pomegranates. Why not just pop pomegranate pills? After all, it was a pomegranate extract that alleviated disease activity. One good reason to stick to the fruit is that when 19 pomegranate supplements were tested in a laboratory, most didn’t actually appear to have any pomegranate in them at all! Only 6 out of 19 appeared to be authentic.

Doctor’s Note

I previously reported on POM Wonderful back in 2011 in my video Is Pomegranate Juice That Wonderful?. My other video on this fruit is Flashback Friday: Pomegranate vs. Placebo for Prostate Cancer.

What’s one way you can eat them? Check out my cooking video for Cran-Chocolate Pomegranate BROL Bowl.

“The vast majority of cancer research is devoted to finding cures, rather than finding new ways to prevent disease. The results of these skewed priorities are plain to see.” It’s been nearly 55 years since President Richard Nixon declared war on cancer, yet deaths from the most common cancers in the United States have continued unabated.

“We have been looking at the very nature of cancer in the wrong way. Breast cancer doesn’t begin when a lump is first felt or detected by a mammogram. All the common epithelial cancers (lung, colorectal, breast, prostate, pancreas and ovary), which account for the majority of deaths, have a long latency period—often 20 years or more.” So, it’s not like you were healthy one day, then got cancer the next. You haven’t been healthy—you’ve had cancer growing in you for decades. Indeed, there’s a “bizarre misperception that people are ‘healthy’ until they have actual symptoms of invasive cancer,” but “the barn in which hay is smoldering before it bursts into flames is not a safe place.”

So, what does this professor of pharmacology I’ve been quoting recommend? Drugs, of course. Chemoprevention—putting people on drugs to prevent cancer. The pharmaceutical industry spends tons of money promoting chemoprevention of heart disease and strokes with statins and blood thinners, so why shouldn’t people take drugs every day for the rest of their lives to protect against cancer?

There has to be a better way.

What about using diet and nutrition to prevent and treat cancer? Well, what kind of cancer? There are more than 200 types. But here’s the key: They all share the same hallmarks. In a series of papers cited more than 40,000 times in the biomedical literature, 10 hallmarks of cancer have been identified:

• Increased sensitivity to growth factors
• Evading your body’s tumor suppressors
• Dodging your immune system
• Being able to grow forever
• Tumor-promoting inflammation
• The ability to invade and spread
• The ability to hook up its own blood supply
• The accumulation of DNA mutations
• Disarming the self-destruct mechanisms in place
• Hijacking the cell’s metabolism

And, of course, there are classes of drugs to try to counter each one—chemotherapy agents designed to target each piece of the cancer puzzle. You can see them below and at 2:27 in my video Fighting the Ten Hallmarks of Cancer with Food.

Now, ideally, there would be drugs able to target multiple hallmarks at one time, but that’s not how drugs tend to work. Indeed, “this need to target multiple hallmarks is one of the major reasons why, in the context of cancer research, there are many proponents of investigating plant foods as they can deliver a cocktail of bioactive compounds” that may target most, if not all, of the hallmarks of cancer. Below and at 3:00 in my video, you can see a sampling of compounds found in fruits and vegetables—such as berries, greens, and broccoli—shown to be able to target each of the 10 hallmarks of cancer, at least in a petri dish.

Furthermore, they have the qualities of an ideal chemopreventive agent. If you were to design the perfect candidate, you’d want them to be selective to cancerous or precancerous cells while leaving normal cells alone, be side-effect-free, target most types of cancers, be able to be consumed in a daily diet, be conveniently available almost everywhere, and be relatively inexpensive to boot. Plants meet all these criteria. No wonder people who eat more plant-based foods tend to have lower cancer rates.

To be clear, we aren’t talking about taking supplements containing extracts or purified phytochemicals, but rather eating whole plant foods themselves—more of a food system–based approach to targeting the hallmarks of cancer. Foods contain thousands of substances that result in vast numbers of possible interactions, yet much of nutritional science “has long been directed towards the impact of single dietary components.” Yes, this kind of reductionist approach can uncover the role of foods or even individual nutrients in disease development, but let’s think about what the optimal research strategy would be to study the effects of bioactive natural plant compounds on disease prevention. Instead of using isolated phytochemicals to manage cancer, why not try whole foods? Sometimes the whole can be greater than the sum of its parts, a concept known as food synergy.

Check out this study involving the simultaneous inhibition of a series of cancer stages in breast cancer cells using a phytochemical supercocktail. Two breast cancer cell lines were treated with six different plant compounds individually, and then all together, at levels typically found in the bloodstream after eating foods like broccoli, grapes, soybeans, and turmeric. And while the compounds were ineffective individually, together they significantly suppressed breast cancer cell proliferation by more than 80%, inhibited cancer cell invasion and migration, stopped the cancer cells in their tracks, and eventually killed them all off. The plant compounds did all this without having any deleterious effects on the normal noncancerous cells used as control.

No wonder the foundation of cancer prevention—based on an update of the most extensive report on diet and cancer ever published—is not pills, but plants, as you can see below and at 5:28 in my video.

In other words, cut down on alcohol, soda, meat, and processed junk, and center your diet around whole grains, vegetables, fruits, and beans.

Doctor’s Note

I have dozens of videos on cancer prevention and treatment. Check the related posts below. 

In a review updating the evidence on human exposure and toxicity of pesticides, the body of evidence linking pesticide exposure and cancer is said to be so massive that pesticides’ role in the development of cancer “cannot be doubted.” However, most of the evidence that shows DNA damage from pesticides is from occupational exposure among farmers and workers in the fields, the pesticide industry itself, or those living in high-spray areas, as you can see at 0:35 in my video Pesticides and Cancer Risk.

There is evidence linking non-occupational pesticide exposure to DNA damage—in this case, single- and double-stranded DNA fragmentation in the sperm of men with higher levels of pesticides flowing through their bodies—but that was in China, where the average pesticide concentrations are as much as four times higher than in some other parts of the world.

Another way pesticides could potentially facilitate tumor growth is through adverse effects on anticancer immunity. Natural killer (NK) cells are our body’s first line of white blood cell defense against cancer cells and virus-infected cells. Pesticides have been shown to induce harmful effects on these defender cells, reducing their ability to kill off tumor cells. For example, if you put a bunch of NK cells in a petri dish along with human leukemia cells without any pesticide, your natural killer cells can clean house and wipe out more than half the cancer. But if you drip a tiny bit of pesticide on them, the NK cells are so disabled that the cancer wins the day, as you can see below and at 1:37 in my video.

But how much pesticide are we talking about? The researchers used the maximum level found in people actively spraying pesticides. But what about looking at just the residual pesticides left on conventional produce? Is choosing organic for cancer prevention worth the investment?

Pesticides are detectable in the blood and urine of more than 90% of the U.S. population, regardless of where they work or live. We know it’s from the food we eat because crossover trials where people are switched between consuming conventionally grown foods and organic foods show you can turn on and off urinary concentrations of pesticide metabolites like a light switch. But that doesn’t necessarily mean the pesticides are harming us.

The health consequences of ingesting pesticide residues from conventionally grown foods remain unknown, but a recent study did find that people who self-reported the highest frequency of organic food consumption had about a 25% lower risk of getting cancer. The study is the first of its kind to evaluate the association between frequency of organic food consumption and cancer risk, controlling for a wide array of other factors. Doesn’t it matter that consumers eating organic are younger? The researchers controlled for that and still found significantly lower cancer risk. But maybe organic consumers get less cancer because they are more affluent or more highly educated or skinnier, or maybe they exercise more or eat less meat or smoke less. No, the researchers controlled for all that and still found significantly lower cancer risk in organic consumers. Maybe their diets were different in other ways, though—more fruits and vegetables overall, or less junk food? No, they still found significantly lower cancer risk. The researchers concluded, “Our results indicate that higher organic food consumption is associated with a reduction in the risk of overall cancer.”

That was the most sophisticated study of its type to date, but there was an earlier study that was even bigger, and little evidence was found for a decrease in the incidence of all cancers except for perhaps one kind of blood cancer—non-Hodgkin lymphoma. You can see the data below and at 3:59 in my video.

The data show no difference in cancer overall between those who never choose organic and those who usually or always do; the only significant findings were a lower risk of non-Hodgkin lymphoma and an increased risk of breast cancer. Is it possible that women who choose organic food are more conscientious about getting screened for breast cancer, and that explains the higher diagnosis rate? We really don’t know.

Of course, what we care about the most is not just cancer but all-cause mortality—the risk of dying prematurely. As it turns out, higher blood levels of a pesticide known as beta-hexachlorocyclohexane are associated with living a significantly shorter life. How do we cut down on our levels? Decades ago, there was a study that found that the breast milk of a vegetarian mother had less beta-hexachlorocyclohexane than the milk of her non-vegetarian sister, who was also breastfeeding at the time. The vegetarian sister apparently had levels of that pesticide that were lower by about a third, compared with her omnivorous sibling, as you can see below and at 4:48 in my video.

That’s no surprise, since this class of chlorinated pesticides is fat-soluble, so they’re found most frequently in foods of animal origin.

A more recent study failed to look at beta-hexachlorocyclohexane, but it examined polychlorinated biphenyls (PCBs) and found that they were linked to increased mortality risk. Again, the toxins were found in the same kinds of foods: eggs, dairy products, and animal fats. So, it’s no surprise that the blood of those eating vegan was found to be “significantly less polluted than omnivores” in terms of a whole series of PCBs, including those found in the study to be associated with increased mortality; but the vegans did not have lower levels of beta-hexachlorocyclohexane.

The bottom line: If you’re worried about the adverse health effects of pesticides and pesticide-type compounds, you may want to lower your intake of animal products. But when it comes to fruits and vegetables, the benefits of eating conventionally grown produce likely outweigh any possible risks from pesticide exposure. So, concerns about pesticide risks shouldn’t discourage us from stuffing our faces with as many fruits and vegetables as possible. That would give us a huge health benefit, whereas the potential lifelong damage of any pesticides on those same fruits and veggies has been estimated to cut only a few minutes off a person’s life, on average, which is nothing compared to the nutritional benefits of eating more fruits and vegetables.

Doctor’s Note

For more on organic foods, see related posts below.

“Personalized nutrition (PN) is rooted in the concept that one size does not fit all,” and who doesn’t want to think they’re special? The idea of personalized nutrition is inherently appealing to our ego; that’s why simple messages recognizing individuality deeply resonate with us and why such messages are popular in marketing and sales. This focus on uniqueness has spurred the creation of personalized foods, along with the suggestion that “3D Food Printing seems to be a good candidate for food customization.”

Now, there certainly are some legitimate differences between people. Some have a peanut allergy and keel over if they eat a peanut, others have celiac disease and need to avoid gluten, and some are genetically lactose-intolerant. There’s an enzyme mutation common in some parts of Asia that protects against alcoholism because people with the altered enzyme don’t metabolize alcohol as efficiently, so toxic metabolites build up. I published a fascinating video about fast versus slow caffeine metabolizers and the difference in health benefits that actually extends to athletic performance. Caffeine is ergogenic—performance-enhancing—but only in fast metabolizers, shaving more than a minute off 10 kilometers (about 6 miles) of cycling, whereas slower metabolizers either got no benefit or the caffeine actually slowed them down, adding two minutes to their cycling time, depending on which kinds of genes they have that code the enzyme that breaks it down. You can see these results below and at 1:24 in my video How Useful Is Personalized Nutrition?.

But for most people, in most situations, we are more similar than different.

While there is a specific minority of people who need a more personalized approach to nutrition, there is currently insufficient evidence to support truly personalized nutrition for most people. Yet a surprising number of direct-to-consumer genetic testing companies have proliferated, offering personalized nutrition advice. For example, there are supplement-hawking companies that claim to help consumers optimize micronutrient status based on a handful of genetic variants, even though most variants explain just a few percent of the difference in levels between people.

Personalized nutrition is part of a broader push towards personalized medicine, also known as precision medicine. There is a “massive cultural allure” of personal control over diagnosis, treatment of disease, and prevention, spurring demand and intense commercialization. But unlike monogenetic diseases—which are rare genetic diseases caused by a single malfunctioning gene, like hemophilia or sickle cell anemia—most diseases are caused by a complex interaction between multiple genes and environmental factors, which pose a “major challenge for the realization of personalized medicine.”

Take something like adult stature, for example. Researchers have found at least 40 locations on our chromosomes that have been associated with human height, which is strongly inherited. The genes from parents account for about 80% of the difference in height between people, yet those dozens of identified genes explain only about 5% of height variation between individuals.

Researchers find those genetic links by using genome-wide association studies, in which all the chromosomes are scanned to look for statistical associations between diseases and any particular stretches of DNA. That’s interesting, but companies marketing genetic susceptibility tests are reinterpreting these data as if they predict individual risks. But all you’re really getting are modest genetic associations with a slight increase in disease risk and with little predictive power when compared to more significant contributions of things we already know, like lifestyle behaviors. Currently, the practice of using a person’s DNA to predict disease “has been judged to provide little to no useful information.”

For example, let’s say a person’s genetic analysis says they’re at slightly greater risk for some grave condition compared to others in their ancestral group. This person was advised to exercise, keep their weight down, not drink too much alcohol, and eat fruits, vegetables, and whole grains. It’s sound advice, but we should be living this way regardless of our genetic risk. And we know—at least we should know—these simple, basic strategies to reduce risks of common chronic diseases. “The problem, of course, is that very few individuals live this way. Actually, to be more precise, almost nobody lives this way.” That’s not just hyperbole—nationwide surveys show that nearly everyone in the United States consumes a diet that’s not on par with even the wimpy recommendations of the Dietary Guidelines.

Indeed, almost “no one in the United States is eating a healthy diet.” Findings like that remind us that when it comes to public health, “worrying about personalizing our preventive strategies based on genetic risk information borders on the absurd.”

Doctor’s Note

Here’s the video I mentioned about fast versus slow caffeine metabolizers and the difference in health benefits extending to athletic performance: Friday Favorites: Do the Health Benefits of Coffee Apply to Everyone?.

For more about lifestyle approaches, check out related posts below.

Parkinson’s disease is a neurodegenerative brain disorder that affects millions of people. What causes it? Well, if you look at lifestyle factors associated with Parkinson’s disease, dairy consumption is the strongest dietary factor associated with an increased risk of Parkinson’s disease. In fact, dairy products are the only food group consistently linked with a high risk of developing Parkinson’s. Five large prospective studies have confirmed the link. This includes the two Harvard cohorts, the Nurses’ Health Study and the Health Professionals Follow-up Study, which followed more than 100,000 people combined for decades in “the largest analysis of dairy and PD [Parkinson’s disease] to date,” analyzing more than 1,000 newly diagnosed cases. All the studies found a link between dairy and Parkinson’s, with most finding a significant link—about a 50% increase in risk overall in those drinking the most milk compared to those drinking the least, at a p-value below 0.00001, meaning there’s less than a 1 in 100,000 chance you’d randomly get a finding that extreme. You can see this in the chart below and at 1:13 in my video, The Role Milk May Play in Triggering Parkinson’s Disease.

Okay, but why is there a link at all? “Despite clear-cut associations between milk intake and” incidence of Parkinson’s, “there is no rational explanation,” concluded one review. A year later, though, we got a clue: “Midlife milk consumption and substantia nigra neuron density at death.” What does that mean? Parkinson’s is caused primarily by the loss of a certain type of nerve cells in a critical part of the brain, with symptoms first appearing once most of these neurons have died. So one study looked at how much milk people drank when they were in their 40s, 50s, and 60s, and then examined their brains at autopsy and counted how many of those critical neurons they had left. In every single quadrant, neuron density was highest “in those who consumed no milk and lowest in those who consumed the most milk.” Even after removing the Parkinson’s cases, those drinking two cups (473 mL) of milk a day had up to 40% fewer nerve cells in most quadrants of that critical brain region. What’s in milk that could be wiping out brain cells? Among the people who drank the most milk, residues of the pesticide “heptachlor epoxide were found in 9 out of 10 brains.” So, maybe the finding of pesticide residues more commonly in the brains of those who drank the most milk could explain how milk could be cause-and-effect related to Parkinson’s disease risk.

Now, that’s not the only potential explanation. In one of my videos, I talked about how meat contains that clumpy neurotoxic protein alpha-synuclein. Well, dairy products may contain trace amounts as well, but we don’t have confirmation of that. Could the milk sugar “galactose be the missing link?” Galactose is what the lactose in milk breaks down into once it’s in the body. It’s also what’s used to induce aging—to experimentally cause aging—in the brain. When you drink it, the galactose is picked up by your brain within a few hours, and for doses above 100 mg/kg, it appears that galactose can cause pathological alterations in brain cells, similar to those observed in Parkinson’s disease. This amount “can be reached and surpassed” by simply drinking two glasses (473 mL) of milk (the main dietary source of galactose) each day. And of all your brain cells, those dopaminergic neurons—the ones that you need to retain to prevent Parkinson’s—may be more vulnerable to galactose-induced damage because they are more vulnerable to oxidative stress.

Galactose may also explain the findings linking milk drinking with higher death rates. You may be thinking, “Well, duh—the saturated butterfat is just cutting people’s lives short,” but higher mortality with high milk consumption has been observed regardless of the milk fat content. Skim milk might be fat-free, but it’s not lactose-free.

Can’t you just drink lactose-free milk, like Lactaid? That has the lactase enzyme added to make lactose-free milk. But it just breaks down lactose into galactose in the carton rather than in your gut, so you’re still ingesting the same amount of galactose. Perhaps it’s no wonder that more milk intake at midlife may be linked to a greater rate of cognitive decline. Remember, researchers use galactose to create brain aging in the laboratory. D-galactose, a metabolic derivative of lactose, has been extensively used in animal models “to mimic cognitive aging” through oxidative stress. Compared to those who said they “almost never” drink milk, those drinking more than one glass (237 mL) a day appear more likely to suffer a decline in global cognitive function.

Doctor’s Note

Here’s the meat video I mentioned: The Role Meat May Play in Triggering Parkinson’s Disease.

You may remember that I’ve explored this before in Could Lactose Explain the Milk and Parkinson’s Disease Link?. Uric acid may also be a contender—see Parkinson’s Disease and the Uric Acid Sweet Spot.

For more on Parkinson’s disease, check out related posts below.

In one of my previous videos about onions, I talked about the data supporting—or not supporting—the role of onions in boosting testosterone in men, protecting bone health, controlling allergies, and dealing with the side effects of chemotherapy. What about weight loss? Enter the “Effect of Steamed Onion (ONIRO) Consumption on Body Fat and Metabolic Profiles in Overweight Subjects.” Researchers used steamed onions, which aren’t as spicy and have a weaker smell, so they could better disguise them as a placebo. They dried them into onion powder and gave people a minuscule amount—about an eighth of a teaspoon (300 mg) a day. Surely, a little daily dusting of onion powder wouldn’t affect people’s weight. But check out the results reported in the abstract: Measurements using a DEXA scan showed a significant reduction in body fat mass, and a CT scan revealed a significant decrease in whole, visceral, and subcutaneous fat areas.

Hold on. If a little onion powder is so effective for weight loss, why wasn’t it featured in my book How Not to Diet? Because, as so often happens in studies, the spin in the abstract doesn’t accurately represent the actual data. The DEXA scan results measured no significant change of fat in the group that got the placebo capsules. They only appeared to lose about a spoonful (7 g) of fat, whereas the group unknowingly taking an eighth of a teaspoon of onion powder stuffed into capsules lost nearly one and a half pounds (0.64 kg) of body fat—a significant drop from baseline, but not a statistically significant drop compared to the placebo group, meaning the loss could have just been due to chance. Same thing with the CT scan results: 5 times more loss of overall fat and over 30 times more loss of the dangerous visceral fat, but the results did not reach statistical significance compared to placebo.

A more recent study tried four teaspoons (9 g) of onion powder a day and similarly failed to accelerate the loss of visceral, total, or subcutaneous fat compared to placebo—but the placebo was also four teaspoons (9 g) of onion powder a day. They used yellow onions versus white onions, and it seems they both may have caused a loss of abdominal body fat, without a significant difference between them. Either way, you might look at these two studies and think, sure, but what are the downsides? It’s only an eighth of a teaspoon of onion powder a day, so why not give it a try? It can’t hurt, but we just don’t have enough evidence to be confident it will actually help.

Let’s talk about polycystic ovary syndrome, also known as PCOS. It’s one of the most common hormone disorders, affecting 5% to 10% of reproductive-aged women. In addition to causing symptoms like irregular periods, “PCOS is a pre-diabetic state, with decreased insulin sensitivity.” PCOS treatment is challenging due to medication side effects. So, are there dietary options? How about a randomized controlled clinical trial of raw red onion intake?

Why onions? Well, onion extracts can evidently improve blood sugar and insulin sensitivity in rats with diabetes and, more importantly, were found to reduce blood sugar levels in humans with diabetes, but evidently not in non-diabetic humans. People with PCOS are kind of pre-diabetic, so would it work for them? First, let’s look at those other two studies. To study the “Metabolic Effects of Onion and Green Beans,” people with diabetes spent a week eating either a small onion (60 g) each day or the same diet with about six cups (600 g) of green beans instead—and both approaches worked. The onion lowered people’s blood sugar levels by about 10% compared to a non-onion control diet, while the green beans lowered them by roughly 15% compared to the control.

Here’s the study that supposedly shows no blood sugar benefits for people without diabetes. It’s true—onions don’t seem to lower normal blood sugar levels, which is a good thing, but check out what happens when you feed people sugar. Have people consume about two and a half tablespoons (50 g) of corn syrup, and their blood sugar levels shoot up over the next two hours before their body can tamp it back down. But give people the exact same amount of sugar along with more and more onion extract, and the blood sugar spike is significantly dampened, almost as much as if you had instead given them an antidiabetic drug, as you can see below and at 4:00 in my video Onions Put to the Test for Weight Loss, Cholesterol, and PCOS Treatment.

We see the same blunting effect on blood sugar when people get a shot of adrenaline and eat onion extract, compared to receiving adrenaline without the onion extract, as you can see below and at 4:11 in my video.

So, are there blood sugar benefits for both people with and without diabetes? No difference was found in blood sugar levels or other markers of insulin resistance between the high-onion and low-onion groups of PCOS patients, nor were there any differences in a marker of inflammation between the two groups. But women with PCOS aren’t just at higher risk for diabetes and inflammation—they are also at higher risk for high cholesterol.

Women with PCOS are over seven times more likely to have a heart attack and develop heart disease, the number one killer of women. But consuming raw red onion appears to be effective in lowering cholesterol, though the group that ate more onions only dropped their LDL cholesterol about 5 points (5 mg/dL), which was not significantly different than the group that ate fewer onions.

I did find this study from 50 years ago where researchers fed people nearly an entire stick (100 g) of butter, and their cholesterol shot up about 30 points within hours of consumption but by only 9 points or 3 points when combined with about a third of a cup (50 g) of raw or boiled onion. The moral of the story: Don’t eat a stick of butter.

Doctor’s Note

Check out the previous video I mentioned: Friday Favorites: Are Onions Beneficial for Testosterone, Osteoporosis, Allergies, and Cancer?.

A moderately obese person doing moderately intense physical activity, like biking or brisk walking, would burn off approximately 350 calories an hour, but most drinks, snacks, and other processed junk are consumed at a rate of about 70 calories (293 kJ) per minute. Therefore, it only takes five minutes to wipe out a whole hour of exercise.

Enter the AspireAssist siphon assembly.

It’s a percutaneous gastrostomy device, meaning surgeons cut a hole in a person’s stomach and tunnel a fistula out through the abdominal wall. So, after each meal, the person can attach a suction gadget to the hole and directly drain out their stomach contents, as you can see below and at 0:47 in my video Extreme Weight-Loss Devices.

This means you could gorge on donuts, spew them out through the hole in your stomach, then gorge on more donuts. Have your cake, and eat it, too…and two, three, and four times!

It seems to be the quintessential American invention, straight from the land that brought us Jell-O salads, spray cheese, and deep-fried Snickers bars. Patients do lose weight, perhaps in part because the fistula may interfere with the relaxation of the stomach wall during a meal. The process also requires drinking lots of water and thoroughly chewing food, both of which may help with weight loss by increasing hydration and slowing the eating rate. Patients also started making healthier choices to avoid the unpleasant sight of gastric aspirate from unhealthy foods. (The tubing is clear, and, evidently, fried foods look particularly gross as they are pumped out.)

All patients need to take supplemental potassium, since it’s sucked out in stomach juices. Otherwise, they risk becoming potassium-deficient (a common complication in bulimia), but most side effects are just minor wound complications. Serious adverse effects, like abdominal abscesses, are rare. The big selling point is that the siphon device doesn’t change the gastrointestinal tract’s anatomy. That seems like a low bar, but in today’s Wild West world of weight-loss procedures, you can’t take anything for granted. Take the duodenal-jejunal bypass liner, for example.

Gastric bypass surgery works in part by cutting out a portion of the small intestine so it’s no longer in the flow of food, thereby helping to prevent the absorption of calories. Instead of major surgery, how about just dropping down a couple of feet of plastic tubing to line the intestinal walls? The problem with the EndoBarrier is that it has to be anchored in the digestive tract. This is accomplished with 10 barbed hooks that cause lacerations, accounting for the majority of the 891 adverse effects reported in 1,056 patients—nearly 9 out of 10 people. Severe penetrating trauma, resulting in esophageal perforation or liver abscesses, is rarer (occurring in only about 1 in 27 patients).

Concern has been raised about the “palatability” of the AspireAssist stomach pump, but the most cringeworthy endoscopic procedure I discovered in my research was intestinal “resurfacing.” Why cover the inside of your intestines with plastic to prevent absorption when you can just “thermally ablate the superficial duodenal mucosa”? In other words, have your intestinal lining burned off—or rather, “resurfaced.”

Surgeons have tried injecting Botox into the stomach walls of obese individuals, hoping it would partially paralyze their gastric muscles, slow stomach emptying, make people feel fuller longer, and lose weight. It didn’t work.

Researchers in Sweden tried randomizing people to wear corsets for 12 to 16 hours a day, seven days a week, for nine months. And it didn’t work. The study participants just didn’t wear the corsets—they were “perceived as uncomfortable.” Duh.

“Sanitized tapeworms” have evidently been widely advertised as a weight-loss remedy since back in the early 1900s. The fact that living tapeworms have been discovered during bariatric surgery operations suggests that infesting yourself with parasites may not be particularly effective either.

Speaking of disgusting strategies, how about disgust itself? A study entitled “Harnessing the Power of Disgust: A Randomized Trial to Reduce High-Calorie Food Appeal Through Implicit Priming” tried using subliminal messages to ruin people’s appetite. Just before showing images of healthy foods, researchers briefly flashed happy images—such as a group of kittens—for 20 milliseconds. That’s too quick to consciously register, but the hope was to plant a positive imprint on the brain. Before showing images of high-calorie foods like ice cream, they flashed negative scenes, like a cockroach on a pizza slice, vomit in a dirty bathroom, and a burn wound. Apparently, it worked! Subjects subsequently reported a reduced desire to eat high-calorie foods, though this wasn’t tested directly. The researchers concluded that subliminal revulsion might be “a successful tactic to combat the onslaught of food cues that promote unhealthy eating….”

The rest of the world looks on, bemused by American machinations, penning commentaries like “Don’t Let Them Eat Cake! A View from Across the Pond.” A paper in the journal Obesity Surgery entitled “What Are the Yanks Doing?” reviewed “The U.S. Experience with Implantable Gastric Stimulation,” inserting electrodes into the muscular layer of the stomach wall. When that didn’t work, colon electrical stimulation was tried.

Even more shocking were studies like “Repetitive electric brain stimulation reduces food intake in humans.” Though placing deep-brain electrodes is considered a complication-prone operation, scientists have long pondered whether “placing an electrode somewhere in the brain could make people eat less.” Holes were drilled through the skulls of five obese individuals, and wires were pushed into their brains for “electrostimulatory exploration.” Once the researchers poked around and found spots where they were able to elicit convincing hunger responses, they sent in enough juice to fry out electro-coagulatory lesions. It seemed to work in cats and monkeys, but the researchers found that burning holes in people’s brains did not result in weight loss in obese humans. Thankfully, as I explained in my book How Not to Diet, healthy, sustainable weight loss isn’t brain surgery.

Doctor’s Note

Check out Is Gastric Balloon Surgery Safe and Effective for Weight Loss?.

What about drugs? See Are Weight Loss Pills Safe? and Are Weight Loss Pills Effective?.

So, what’s the best way to lose weight? I wrote a whole book about it! How Not to Diet is focused exclusively on sustainable weight loss. Borrow it from your local library or pick up a copy from your favorite bookseller. (All proceeds from my books are donated to charity.) To whet your appetite, take a peek: Trailer for How Not to Diet: Dr. Greger’s Guide to Weight Loss.

For more on this topic, check out related posts below.

Intragastric balloons “arrived with much fanfare in the 1980s,” since they could be implanted into the stomach and inflated with air or water to fill much of the space. Unfortunately, surgical devices are often brought to the market before there is adequate evidence of effectiveness and safety, and the balloons were no exception.

The “gastric bubble” had its bubble burst when a study at the Mayo Clinic found that 8 out of 10 balloons “spontaneously deflated,” which is potentially dangerous because they could pass into the intestines and cause an obstruction, as you can see below and at 0:40 in my video Is Gastric Balloon Surgery Safe and Effective for Weight Loss?.

Before balloons deflated, however, they apparently caused gastric erosions in half the patients, damaging their stomach lining. The kicker is that, in terms of inducing weight loss, they didn’t even work when compared to diet and other behavior modification strategies. Eventually, intragastric balloons were pulled from the market. But now, balloons are back.

After a 33-year hiatus, the U.S. Food and Drug Administration started approving a new slew of intragastric balloons in 2015, which immediately resulted in the placement of more than 5,000 devices. By then, the Sunshine Act had passed. It forced drug companies and the surgical and medical device industry to disclose any payments made to physicians, shining a disinfecting light on industry enticements. By now, most people know about the overly cozy financial relationships doctors can have with Big Pharma, but fewer may realize that surgeons can also get payments from the companies for the devices they use. The 100 top physician recipients of industry payments received an unbelievable $12 million from device companies in a single year. Yet outrageously, when they published papers, only a minority disclosed the blatant conflict of interest.

The benefit of balloons over most types of bariatric surgery is that they’re reversible, but that doesn’t mean they’re benign. The FDA has released a series of advisories about the risks, which include death. But how could someone suffer a stomach perforation with a smooth, rounded object? By that smooth, rounded object causing the patient to vomit so much that they rupture their stomach and die. Nausea and vomiting are unsurprisingly “very common side effects,” affecting the majority of those who have balloons placed inside of them. Persistent vomiting likely also explains cases of life-threatening nutrient deficiencies after balloon implantation.

Some complications, such as bowel obstruction, are due to the balloons deflating, but others, oddly enough, are due to the balloons suddenly overinflating, causing pain, vomiting, and abdominal distention, as you can see below and at 2:45 in my video.

This issue was first noticed in breast implants, as documented in reports such as “The Phenomenon of the Spontaneously Autoinflating Breast Implant.” Out of nowhere, the implants can just start growing, increasing breast volume by an average of more than 50%. “It remains an underreported and poorly understood phenomenon,” one review noted. (Interestingly, breast implants were actually used as some of the first failed experimental intragastric balloons.)

As with any medical decision, though, it’s all about risks versus benefits. Industry-funded trials display “notable weight loss,” but it’s hard to tease out the effect of the balloon on its own from the accompanying “supervised diet and lifestyle changes” prescribed in the studies. In drug trials, you can randomize study participants to sugar pills, but how do you eliminate the placebo effect of undergoing a procedure? Perform sham surgery.

In 2002, a courageous study was published in The New England Journal of Medicine. The most common orthopedic surgery—arthroscopic surgery of the knee—was put to the test. Billions of dollars are spent on sticking scopes into knee joints and cutting away damaged tissue in osteoarthritis and knee injuries, but does that actually work? People suffering from knee pain were randomized to get the actual surgery versus a sham surgery, in which surgeons sliced into people’s knees and pretended to perform the procedure—even splashing saline—without actually treating the joint.

The trial caused an uproar. How could anyone randomize people to get cut open for fake surgery? Professional medical associations questioned the ethics of the surgeons as well as “the sanity” of the patients who agreed to be part of the trial. Guess what happened? The surgical patients got better, but so did the placebo patients, as you can see below and at 4:42 in my video.

The surgeries had no actual effect. Currently, rotator cuff shoulder surgery is facing the same crisis of confidence.

When intragastric balloons were put to the test, sham-controlled trials showed that both older and newer devices sometimes fail to offer any weight-loss benefit. Even when they do work, the weight loss may be temporary because balloons are only allowed to stay in for six months (at which point the deflation risk gets too great). Why can’t you keep putting new ones in? That’s been tried; it failed to improve long-term weight outcomes. A sham-controlled trial showed that any effects of the balloon on appetite and satiety may vanish with time, perhaps as your body gets used to the new normal.

What sham surgery trials have shown us is that some of our most popular surgeries are themselves shams. Doctors like to pride themselves on being men and women of science. For example, we rightly rail against the anti-vaccination movement. Many of us in medicine have been troubled by the political trend in which people “choose their own facts.” But when I read that some of these still-popular surgeries are not only useless but may actually make matters worse (for example, increasing the risk of progression to a total knee replacement), I can’t help but think we are hardly immune to our own versions of fake news and alternative facts.

Doctor’s Note

Next in this two-part series is Extreme Weight-Loss Devices.

For more on bariatric surgery, check out related posts below.

My book How Not to Diet is focused exclusively on sustainable weight loss. Borrow it from your local library or pick up a copy from your favorite bookseller. (All proceeds from my books are donated to charity.)

In 2013, I posted a video based on a study that found that men with erectile dysfunction who ate 100 grams of pistachios (a little more than three handsful) a day for three weeks had “a significant improvement in erectile function.” It’s always nice to see a whole-food intervention have clinical effects, and I was curious to revisit the topic and see what’s been published since.

Even if you ignore all the lab animal studies on hazelnuts improving the function of rat testicles—really, there’s a study titled “Hazelnut Consumption Improves Testicular Antioxidant Function and Semen Quality in Young and Old Male Rats”—you still never know what you’ll find searching the medical literature for nuts and sexual function. I found “a case of penile strangulation with a metal hex nut” in which someone put one on his penis “for sexual pleasure” but couldn’t remove it. (I guess some kinds of nuts can sometimes make things worse.) They tried the Dundee technique, which involves creating 20 puncture holes to relieve the pressure, but that didn’t work, so then they tried a diamond disk cutter. It slipped a few times, but the hex nut was successfully removed. All’s well that ends well.

That got me curious. Evidently, penile entrapment is so common that there is an entire grading system that emergency room doctors can use, as you can see here and at 1:21 in my video Mixed Nuts Put to the Test for Erectile Dysfunction. If a drill isn’t available, the surgeons advised, “a hammer and chisel may be used to remove nuts.”

A drill? Oh, they mean a dental drill. Doctors describing one case bragged about the “precisely cut edges,” but it looks pretty jagged to me. You can see for yourself below and at 1:38 in my video.

To “preserve the penis from fatal outcomes” (that’s a strange way to put it), urologists should be aware of all the available tools and approaches, and if you don’t know how to operate the saw, you can always call in the local blacksmith—but only if “special consent [is] taken from the patient”!

But how are you going to remove an iron barbell or steel sledgehammer head? “With a heavy-duty air grinder provided by the fire department,” requiring six hours of cutting and fire coats to protect the patient from the sparks. Use whatever it takes—hack saw, “cement eater.” You can even use the silk winding method pioneered by Dong et al.

Back to the task at hand! Consuming “at least one serving of vegetables a day and more than two servings of nuts a week was associated with a more than 50% decrease in the probability of ED” [erectile dysfunction] in a snapshot-in-time cross-sectional study. But such observational studies can’t prove cause and effect. It’s like finding that men who eat healthier have better sperm motility. Maybe men who eat nuts are just health nuts, and the improvement is due to some other factor, like exercise. What we need is an interventional trial.

And there is one: a randomized controlled trial studied the “effect of nut consumption on semen quality and functionality.” Healthy men were fed the standard American diet with or without a mixture of nuts—a handful (30 grams) of walnuts and half a handful (15 grams) each of almonds and hazelnuts. Individuals in the nut group experienced significant improvements in their total sperm count, vitality, motility, and shape, perhaps because those “in the nut group showed a significant reduction in SDF”—sperm DNA fragmentation. The nuts appeared to protect their sperm DNA. It’s too bad that the researchers didn’t measure the men’s erectile and sexual dysfunction while they were at it. Oh, but they did!

What is the effect of nut consumption on erectile and sexual function from that same study? The researchers report that those in the nut group saw a significant increase in orgasmic function and sexual desire, but what about erectile function? Any time you see this kind of selective glass-half-full reporting, you suspect some kind of industry funding, and, indeed, that was the case here; the study was partially funded by the International Nut and Dried Fruit Council. Yes, there was a marginal increase in orgasmic function and sexual desire of questionable clinical significance, but there was no improvement in erectile function, intercourse satisfaction, or overall satisfaction. As with so many comparisons, even the so-called significant findings may not even be statistically significant.

But why did the pistachios I talked about back in 2013 work, while these other nuts didn’t? Well, the original study was done on men mostly in their 40s and 50s who already had chronic erectile dysfunction for at least one year, whereas the average age of participants in the newer study was 24. So, the individuals in the later study may have started out with near-maximum circulation, not leaving much room for the nuts to work any magic.

Doctor’s Note

Sorry for that crazy tangent! I just wanted to give people a taste of what it can be like when you dive deep into the medical literature.

The 2013 video I mentioned is Pistachio Nuts for Erectile Dysfunction.

What about walnuts for arterial blood flow? See Walnuts and Artery Function.

More on fertility and sexual function in the related posts below.

Our intestinal tract is the largest barrier between us and the environment. More than what we touch or breathe, what we eat is our largest exposure to the outside world. Normally, our entire gastrointestinal tract is impermeable to what’s inside of it, allowing our body to pick and choose what goes in or out. But there are things that may make our gut leaky, and the chief among them is our diet.

The standard American or Western diet can cause gut dysbiosis, meaning a disruption in our gut microbiome, which can lead to intestinal inflammation and a leaky intestinal barrier. Then, tiny bits of undigested food, microbes, and toxins can slip uninvited through our gut lining into our bloodstream and trigger chronic systemic inflammation.

“To avoid this dysbiosis and intestinal inflammation, a predominantly vegetarian diet”—in other words, eating plants—“should be preferred.” The gut bacteria of people eating a vegetarian diet are associated with intestinal microbiome balance, high bacterial biodiversity, and integrity of the intestinal barrier. Vegetarians tend to have markedly less uremic toxins, like indole and p-cresol, and because fiber is the primary food for our gut microbiome, the gut bacteria of those eating plant-based diets have been found to produce more of the good stuff—namely short-chain fatty acids that play “a protective and nourishing role” for the cells lining our gut, “ensuring the preservation” of our intestinal barrier. Plant fiber is of “prime importance” to preserving the integrity of our intestinal barrier, but you can’t know for sure until you put it to the test.

When people with non-alcoholic fatty liver disease were given whole grains, beans, lentils, fruits, vegetables, nuts, and seeds for six months, they had a significant reduction in zonulin levels.

Zonulin is a protein responsible for the disassembly of the tight junctions between gut-lining cells and is “considered to be the only measurable biomarker that reflects an impairment of the intestinal barrier.” In other words, zonulin is a useful marker of a leaky gut. But since adding all those plants seemed to lower levels, that may “imply that appropriate fiber intake helps to maintain the proper structure and function of the intestinal barrier.” But whole healthy plant foods have a lot more than fiber. How do we know it’s the fiber? And the study didn’t even have a control group. That’s why the researchers said “gut permeability might be improved by dietary fiber” [emphasis added]. To prove cause and effect, it’d be nice to have a randomized, double-blind, crossover study where you compare the effect of the same food with or without fiber.

Such a study does, in fact, exist! A group of healthy young men was randomized to eat pasta with or without added fiber, and there was a significant drop in zonulin levels in the added-fiber group compared to both pre-intervention levels and those of the control group, as you can see below and at 2:51 in my video How to Heal a Leaky Gut with Diet.

So, fiber does indeed appear to improve gut leakiness.

Are there any plant foods in particular that may help? Curcumin, the yellow pigment in the spice turmeric, can help prevent the intestinal damage caused by ibuprofen-type drugs in rats. Similar protection was noted for the broccoli compound sulforaphane in mice. There are no human studies on broccoli yet, but there was a study on three days of the equivalent of about 2 to 3 teaspoons a day of turmeric, which did reduce markers of gastrointestinal barrier damage and inflammation caused by exercise compared to a placebo. Less turmeric may work, too, but no smaller doses have been put to the test.

If you ask alternative medicine practitioners what treatments they use for a leaky gut, number one on the list—after reducing alcohol consumption—is zinc. You can see the list below and at 3:42 in my video.

Zinc doesn’t just protect against aspirin-like drug-induced intestinal damage in rats; when put to the test in a randomized trial of healthy adults, the same thing was found. Five days of 250 mg of indomethacin, an NSAID drug, “caused a threefold rise in gut permeability,” as one would expect from that class of drugs. But this rise in permeability did not occur when participants also took zinc, “strongly suggesting a small-intestinal protective effect.” The dose they used was massive, though—75 mg a day, which is nearly twice the tolerable upper daily limit for zinc. What about getting zinc just at regular doses from food?

A significant improvement in gut leakiness was found even with a dose of just 3 mg of zinc, suggesting that even relatively low zinc supplementation may work. You can get an extra 3 mg of zinc in your daily diet by eating a cup (200g) of cooked lentils.

Doctor’s Note

For more on preventing gut dysbiosis and leaky gut, check out Flashback Friday: Gut Dysbiosis: Starving Our Microbial Self and Avoid These Foods to Prevent a Leaky Gut.

Intestinal permeability, the leakiness of our gut, may be a new target for both disease prevention and therapy. With all its tiny folds, our intestinal barrier covers a surface of more than 4,000 square feet—that’s bigger than a tennis court—and requires about 40% of our body’s total energy expenditure to maintain.

There is growing evidence implicating “the disruption of intestinal barrier integrity” in the development of a number of conditions, including celiac disease and inflammatory bowel disease. Researchers measured intestinal permeability using blue food coloring. It remained in the gut of healthy participants but was detected in the blood of extremely sick patients with sepsis with a damaged gut barrier. You don’t have to end up in the ICU to develop a leaky gut, though. Simply taking some aspirin or ibuprofen can do the trick.

Indeed, taking two regular aspirin (325 mg tablets) or two extra-strength aspirin (500 mg tablets) just once can increase the leakiness of our gut. These results suggest that even healthy people should be cautious when using aspirin, as it may cause gastrointestinal barrier dysfunction.

What about buffered aspirin, an aspirin-antacid combination which theoretically “buffers” gastrointestinal irritation? It apparently doesn’t make any difference: Regular aspirin and Bufferin both produced multiple erosions in the inner lining of the stomach and intestine. Researchers put a scope down people’s throats and saw extensive erosions and redness inside 90% of those who took aspirin or Bufferin at their recommended doses. How many hours does it take for the damage to occur? None. It can happen within just five minutes. Acetaminophen, sold as Tylenol in the United States, may not lead to gastrointestinal damage and could be a better choice, unless you have problems with your liver. And rather than making things better, vitamin C supplements appeared to make the aspirin-induced increase in gut leakiness even worse.

Interestingly, this may be why NSAID drugs like aspirin, ibuprofen, and naproxen “are involved in up to 25% of food-induced anaphylaxis.” In other words, they are associated with over 10-fold higher odds of life-threatening food allergy attacks, presumably because these drugs increase the leakiness of the intestinal barrier, causing tiny food particles to slip into the bloodstream. But can exercise increase risk, too?

Strenuous exercise—for instance, an hour at 70% maximum capacity—may divert so much blood to the muscles and away from our internal organs that it may cause transient injury to our intestines, causing mild gut leakiness. But this can be aggravated if athletes take ibuprofen or any other NSAID drugs, which is unfortunately all too common.

Alcohol can also be a risk factor for food allergy attacks for the same reason—increasing gut leakiness. But cut out the alcohol, and our gut might heal up.

What other dietary components can make a difference? Elevated consumption of saturated fat, which is found in meat, dairy, and junk food, can cause the growth of bad bacteria that make the rotten-egg gas hydrogen sulfide, which can degrade the protective mucus layer. You can see the process below and at 3:21 in my video Avoid These Foods to Prevent a Leaky Gut.

It is said to be clear that high-fat diets in general have a negative impact on intestinal health by “disrupting the intestinal barrier system through a variety of mechanisms,” but most of the vast array of studies that cited the negative effects were done on lab animals or in a petri dish. Are people affected the same way? You don’t know for sure until you put it to the test.

Rates of obesity and other cardiometabolic disorders have increased rapidly alongside a transition from traditional lower-fat diets to higher-fat diets. We know a disturbance in our good gut flora has been shown to be associated with a high risk of many of these same diseases, and studies using rodents suggest that a high-fat diet “unbalances” the microbiome while impairing the gut barrier, resulting in disease. To connect all the dots, though, we need a human interventional trial—and we got one: a six-month randomized controlled-feeding trial on the effects of dietary fat on gut microbiota. It found that, indeed, higher fat consumption was associated with unfavorable changes in the gut microbiome and proinflammatory factors in the blood. Note that this wasn’t even primarily saturated fat, such as from meat and dairy. The researchers just replaced refined carbohydrates with refined fats—swapping out white rice and wheat flour for soybean oil. These findings suggest that countries westernizing their diets should advise against increasing dietary fat intake, while countries that have already adopted such diets should consider cutting down.

Doctor’s Note

For more on leaky gut, check out The Leaky Gut Theory of Why Animal Products Cause Inflammation and How to Heal a Leaky Gut with Diet.

I also talked about gut leakiness in my SIBO video: Friday Favorites: Tests, Fiber, and Low FODMAP for Small Intestinal Bacterial Overgrowth (SIBO).

How do you rate the quality of people’s diets? Well, “what could be more nutrient-dense than a vegetarian diet?” Indeed, if you compare the quality of vegetarian diets with non-vegetarian diets, the more plant-based diets do tend to win out, and the higher diet quality in vegetarian diets may help explain greater improvements in health outcomes. However, vegetarians appear to have a higher intake of refined grains, eating more foods like white rice and white bread that have been stripped of much of their nutrition. So, just because you’re eating a vegetarian diet doesn’t mean you’re necessarily eating as healthfully as possible.

Those familiar with the science know the primary health importance of eating whole plant foods. So, how about a scoring system that simply adds up how many cups of fruits, vegetables, whole grains, beans, chickpeas, split peas, and lentils, and how many ounces of nuts and seeds per 1,000 calories (with or without counting white potatoes)? Looking only at the total intake of whole plant foods doesn’t mean you aren’t also stuffing donuts into your mouth. So, you could imagine proportional intake measures, based on calories or weight, to determine the proportion of your diet that’s whole plant foods. In that case, you’d get docked points if you eat things like animal-derived foods—meat, dairy, or eggs—or added sugars and fats.

My favorite proportional intake measure is McCarty’s “phytochemical index,” which I’ve profiled previously. I love it because of its sheer simplicity, “defined as the percent of dietary calories derived from foods rich in phytochemicals.” It assigns a score from 0 to 100, based on the percentage of your calories that are derived from foods rich in phytochemicals, which are biologically active substances naturally found in plants that may be contributing to many of the health benefits obtained from eating whole plant foods. “Monitoring phytochemical intake in the clinical setting could have great utility” in helping people optimize their diet for optimal health and disease prevention. However, quantifying phytochemicals in foods or tissue samples is impractical, laborious, and expensive. But this concept of a phytochemical index score could be a simple alternative method to monitor phytochemical intake.

Theoretically, a whole food, plant-based or vegan diet that excluded refined grains, white potatoes, hard liquors, added oils, and added sugars could achieve a perfect score of 100. Lamentably, most Americans’ diets today might be lucky to score just 20. What’s going on? In 1998, our shopping baskets were filled with about 20% whole plant foods; more recently, that has actually shrunk, as you can see below and at 2:49 in my video Plant-Based Eating Score Put to the Test.

Wouldn’t it be interesting if researchers used this phytochemical index to try to correlate it with health outcomes? That’s exactly what they did. We know that studies have demonstrated that vegetarian diets have a protective association with weight and body mass index. For instance, a meta-analysis of five dozen studies has shown that vegetarians had significantly lower weight and BMI compared with non-vegetarians. And even more studies show that high intakes of fruits, vegetables, whole grains, and legumes may be protective regardless of meat consumption. So, researchers wanted to use an index that gave points for whole plant foods. They used the phytochemical index and, as you may recall from an earlier video, tracked people’s weight over a few years, using a scale of 0 to 100 to simply reflect what percentage of a person’s diet is whole plant foods. And even though the healthiest-eating tier only averaged a score of about 40, which meant the bulk of their diet was still made up of processed foods and animal products, just making whole plant foods a substantial portion of the diet may help prevent weight gain and decrease body fat. So, it’s not all or nothing. Any steps we can take to increase our whole plant food intake may be beneficial.

Many more studies have since been performed, with most pointing in the same direction for a variety of health outcomes—indicating, for instance, higher healthy plant intake is associated with about a third of the odds of abdominal obesity and significantly lower odds of high triglycerides. So, the index may be “a useful dietary target for weight loss,” where there is less focus on calorie intake and more on increasing consumption of these high-nutrient, lower-calorie foods over time. Other studies also suggest the same is true for childhood obesity.

Even at the same weight, with the same amount of belly fat, those eating plant-based diets tend to have higher insulin sensitivity, meaning the insulin they make works better in their body, perhaps thanks to the compounds in plants that alleviate inflammation and quench free radicals. Indeed, the odds of hyperinsulinemia—an indicator of insulin resistance—were progressively lower with greater plant consumption. No wonder researchers found 91% lower odds of prediabetes for people getting more than half their calories from healthy plant foods.

They also found significantly lower odds of metabolic syndrome and high blood pressure. There were only about half the odds of being diagnosed with hypertension over a three-year period among those eating more healthy plants. Even mental health may be impacted—about 80% less depression, 2/3 less anxiety, and 70% less psychological distress, as you can see below and at 5:15 in my video.

Is there a link between the dietary phytochemical index and benign breast diseases, such as fibrocystic diseases, fatty necrosis, ductal ectasia, and all sorts of benign tumors? Yes—70% lower odds were observed in those with the highest scores. But what about breast cancer? A higher intake of healthy plant foods was indeed associated with a lower risk of breast cancer, even after controlling for a long list of other factors. And not just by a little bit. Eating twice the proportion of plants compared to the standard American diet was linked to more than 90% lower odds of breast cancer.

Doctor’s Note

You can learn more about the phytochemical index in Calculate Your Healthy Eating Score.

If you’re worried about protein, check out Flashback Friday: Do Vegetarians Get Enough Protein?

It doesn’t have to be all or nothing, though. Do Flexitarians Live Longer?

For more on plant-based junk, check out Friday Favorites: Is Vegan Food Always Healthy?.

Data extrapolated from large cholesterol-lowering trials using statin drugs suggest that the incidence of cardiovascular events like heart attacks would approach zero if LDL cholesterol could be forced down below 60 mg/dL for first-time prevention and around 30 mg/dL for those trying to prevent another one. But is lower actually better? And is it even safe to have LDL cholesterol levels that low?

We didn’t know until PCSK9 inhibitors were invented. Are PCSK9 Inhibitors for LDL Cholesterol Safe and Effective? I explore that issue in my video of the same name. PCSK9 is a gene that mutated to give people such low LDL cholesterol, and that’s how Big Pharma thought of trying to cripple PCSK9 with drugs. After a heart attack, intensive lowering of an individual’s LDL cholesterol beyond a target of 70 mg/dL does seem to work better than more moderate lowering. There were fewer cardiovascular deaths, heart attacks, or strokes at an LDL less than 30 mg/dL compared with 70 mg/dL or higher, and even compared to less than 70 mg/dL. There is a consistent risk reduction even when starting as low as an average of 63 mg/dL, and pushing LDL down to 21 mg/dL, remarkably, showed “no observed offsetting” of adverse side effects.

Maybe that shouldn’t be so surprising, since that’s about the level at which we start life. And there’s another type of genetic mutation that leaves people with LDL levels of about 30 mg/dL their whole lives, and they are known to have an exceptionally long life expectancy. So, where did we get this idea that cholesterol could fall too low?

The common claim that lowering cholesterol can be dangerous due to depletion of cell cholesterol is unsupported by evidence and does not consider the exquisite balancing mechanisms our body uses. After all, that’s how we evolved. Until recently, most of us used to have LDL levels around 50 mg/dL, so that’s pretty normal for the human species. The absence of evidence that low or lowered cholesterol levels are somehow bad for us contrasts with the overwhelming evidence that cholesterol reduction decreases risk for coronary artery disease, our number one killer.

What about hormone production, though? Since the body needs cholesterol for the synthesis of steroid hormones—like adrenal hormones and sex hormones—there’s a concern that there wouldn’t be enough. You don’t know, though, until you put it to the test. For decades, we’ve known that women on cholesterol-lowering drugs don’t have a problem with estrogen production and that lowering cholesterol doesn’t affect adrenal gland function. As well, it doesn’t impair testicular function in terms of causing testosterone levels to fall below normal. If anything, statin drugs can improve erectile function in men, which is what you’d expect from lowering cholesterol. But you’ll notice these studies only looked at lowering LDL to 70 mg/dL or below. What about really low LDL?

On PCSK9 inhibitors, you can get most people under an LDL of 40 mg/dL and some under 15 mg/dL! And there is no evidence that adrenal, ovarian, or testicular hormone production is impaired, even in patients with LDL levels below 15 mg/dL. The risk of heart attacks falls in a straight line as LDL gets lower and lower, even below 10 mg/dL, for example, without apparent safety concerns, but that’s over the duration of exposure to these drugs. The longest follow-up to date of those whose LDL, by way of using multiple medications, was kept less than 30 mg/dL is six years.

Now, we can take comfort in the fact that those with extreme PCSK9 mutations, leading to a lifelong reduction in levels of LDL to under 20 mg/dL their whole lives, remain healthy and have healthy kids. Cholesterol-affecting mutations are what cause the so-called “longevity syndromes,” but that doesn’t necessarily mean the drugs are safe. The bottom line is we should try to get our LDL cholesterol down as low as we can, but much longer follow-up data are necessary anytime a new class of drugs is introduced. So far, so good, but we’ve only been following the data for about 10 years. For example, we didn’t know statins increased diabetes risk until decades after they were approved and millions had been exposed. Also worth noting: PCSK9 inhibitors cost about $14,000 a year.

Doctor’s Note

How can we decrease cholesterol with diet? See Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

For more on statin drugs, see the related posts below. 

On the standard American diet, atherosclerosis—hardening of the arteries, the number one killer of men and women—has been found to start in our teens. Investigators collected about 3,000 sets of coronary arteries and aortas (the aorta is the main artery in the body) from victims of accidents, homicides, and suicides who were 15 to 34 years old and found that the fatty streaks in arteries can begin forming in our teens, which turn into atherosclerotic plaques in our 20s that get worse in our 30s and can then become deadly. In the heart, atherosclerosis can cause a heart attack. In the brain, it can cause a stroke. See the progression below and at 0:35 in my video Can Cholesterol Get Too Low?.

How common is this? All of the teens they looked at—100% of them—already had fatty streaks building up inside their arteries. By their early 30s, most already had those streaks blossoming into atherosclerotic plaques that bulged into their arteries. From ages 15 through 19, their aortas had fatty streaks building up throughout them, but no plaques yet, on average, as seen below and at 1:15 in my video.

The plaques started appearing in their abdominal aorta in their early 20s and worsened by their late 20s, by which time fatty streaks had infiltrated throughout. By their early 30s, their arteries were in bad shape, as seen below and at 1:25 in my video.

But that’s just the abdominal aorta, the main artery running through the torso that splits off into our legs. What about the coronary arteries that feed the heart?

Researchers found the same pattern: fatty streaks in teens, early signs of plaque in early 20s that progress with age, and by the early 30s, most people already had plaques in their coronary arteries, as seen below and at 1:47 in my video.

Atherosclerosis starts as early as adolescence.

That’s why we shouldn’t wait until heart disease becomes symptomatic to treat it. If it starts in our youth, we should start treating it when we’re youths. If you knew you had a cancerous tumor, you wouldn’t want to wait until it grew to a certain size to treat it. If you had diabetes, you wouldn’t want to wait until you started going blind before you did something about it. So, how do you treat atherosclerosis? You lower LDL cholesterol through a diet low in saturated fat and cholesterol—a diet that’s low in eggs, meat, dairy, and junk.

If we want to stop this epidemic, we have to “alter our lifestyle accordingly, beginning in infancy or early childhood. Is such a radical proposal totally impractical?” (Eating more healthfully? Radical?!) It would take serious dedication to change our behavior, but atherosclerosis is our number one cause of death. In the case of cigarettes, we did pretty well, slashing smoking rates and dropping lung cancer rates. And, yes, healthy eating is safe. According to the Academy of Nutrition and Dietetics, the largest and oldest association of nutrition professionals in the world, even strictly plant-based diets are appropriate for all stages of life, starting from pregnancy. (NutritionFacts.org is among the websites recommended by the Academy for more information.)

The title of an important study published in the Journal of the American College of Cardiology declares: “Curing Atherosclerosis Should Be the Next Major Cardiovascular Prevention Goal.” What evidence do we have that a lifelong suppression of LDL will do it? There is a genetic mutation of a gene called PCSK9 that about 1 in 50 African Americans are lucky to be born with because it gives them about a 40% lower LDL cholesterol level their whole lives. Indeed, they were found to have dramatically lower rates of coronary heart disease—an 88% drop in risk compared to those without the genetic mutation, despite otherwise terrible cardiovascular risk factors on average. Most had high blood pressure and were overweight, almost a third smoked, and nearly 20% had diabetes, but that highlights how a lifelong history of low LDL cholesterol levels can substantially reduce the risk of coronary heart disease, even when there are multiple risk factors.

This near-90% drop in events like heart attacks or sudden death occurred at an average LDL level of 100 mg/dL, compared to 138 mg/dL in those without the genetic mutation. This means LDL can drop below even 100 mg/dL. Why does a drop in LDL cholesterol by about 40 mg/dL from a lucky genetic mutation lower the risk of coronary heart disease by nearly 90%, while the same reduction with statin drugs lowers it by only about 20%? The most probable explanation? Duration. When it comes to lowering LDL cholesterol, it’s not only about how low it is, but how long it’s been low.

That’s why healthy lifestyle choices may wipe out about 90% of our risk for having a heart attack, while drugs may reduce it by only 20% to 30%. If you’re getting treated with drugs later in life, you may have to get your LDL under 70 mg/dL to halt the progression of coronary atherosclerosis. But if we start making healthier choices earlier, it may be enough to lower LDL cholesterol just to 100 mg/dL, which should be achievable for most of us. That’s consistent with country-by-country data that suggested death from heart disease would bottom out at a population average of about 100 mg/dL, as seen below and at 5:21 in my video.

But that’s only if you can keep your LDL cholesterol down your whole life.

If you’re relying on medication later in life to halt disease progression, you may need to get your LDL below 70 mg/dL, and if you’re trying to use drugs to reverse a lifetime of bad food choices, you may not get to zero coronary heart disease events until your LDL drops to about 55 mg/dL. If your heart disease is so bad that you’ve already had a heart attack but you’re trying not to die from another one, ideally, you might want to push your LDL down to about 30 mg/dL. Once you get that low, not only would you likely prevent any new atherosclerotic plaques, but you’d also help stabilize the plaques you already have so they’re less likely to burst open and kill you.

Is it even safe to have cholesterol levels that low, though? In other words, can LDL cholesterol ever be too low? We’ll find out next.

Doctor’s Note

Didn’t know atherosclerosis could start at such a young age? See Heart Disease Starts in Childhood.

For more on drugs versus lifestyle, check out my video The Actual Benefit of Diet vs. Drugs.

Want to learn more about so-called primordial prevention? See When Low Risk Means High Risk.

Does Cholesterol Size Matter? Watch the video to find out.

Currently, more than half a billion adults have diabetes, and about a 50% increase is expected in another generation. I’ve got tons of videos on the best diets for diabetes, but what about no diet at all?

More than a century ago, fasting was said to cure diabetes, quickly halting its progression and eliminating all signs of the disease within days or weeks. Even so, starvation is guaranteed to lead to the complete disappearance of you if kept up long enough. What’s the point of fasting away the pounds if they’re just going to return as soon as you restart the diet that created them in the first place? Might it be useful to kickstart a healthier diet? Let’s see what the science says.

Type 2 diabetes has long been recognized as a disease of excess, once thought to afflict only “the idle rich…anyone whose environment and self-support does not require of him some sustained vigorous bodily exertion every day, and whose earnings or income permit him, and whose inclination tempts him, to eat regularly more than he needs.” Diabetes is preventable, so might it also be treatable? If we’re dying from overeating, maybe we can be saved by undereating. Remarkably, this idea was proposed about 2,000 years ago in an Ayurvedic text:

“Poor diabetic people’s medicine
He should live like a saint (Munni);
He should walk for 800–900 miles.
Or he shall dig a pond;
Or he shall live only on cow dung and cow urine.”

That reminds me of the Rollo diet for diabetes proposed in 1797, which was composed of rancid meat. That was on top of the ipecac-like drugs he used to induce severe sickness and vomiting. Anything that makes people sick has only “a temporary effect in relieving diabetes” because it reduces the amount of food eaten. His diet plan—which included congealed blood for lunch and spoiled meat for dinner—certainly had that effect.

Similar benefits were seen in people with diabetes during the siege of Paris in the Franco‐Prussian War, leading to the advice to mangez le moins possible, which translates to “eat as little as possible.” This was formalized into the Allen starvation treatment, considered to be “the greatest advance in the treatment of diabetes prior to the discovery of insulin.” Before insulin, there was “The Allen Era.”

Dr. Allen noted that there are clinical reports of even severe diabetes cases clearing up after the onset of a “wasting condition” like tuberculosis or cancer, so he decided to put it to the test. He found that even in the most severe type of diabetes, he could clear sugar from people’s urine within ten days. Of course, that’s the easy part; it’s harder to maintain once they start eating again. To manage patients’ diabetes, he stuck to two principles: Keep them underweight and restrict the fat in their diet. A person with severe diabetes can be symptom-free for days or weeks, but eating butter or olive oil can make the disease come raging back.

As I’ve said before, diabetes is a disease of fat toxicity. Infuse fat into people’s veins through an IV, and, by using a high-tech type of MRI scanner, you can show in real time the buildup of fat in muscle cells within hours, accompanied by an increase in insulin resistance. The same thing happens when you put people on a high-fat diet for three days. It can even happen in just one day. Even a single meal can increase insulin resistance within six hours. Acute dietary fat intake rapidly increases insulin resistance. Why do we care? Insulin resistance in our muscles, in the context of too many calories, can lead to a buildup of liver fat, followed by fat accumulation in the pancreas, and eventually full-blown diabetes. “Type 2 diabetes can now be understood as a state of excess fat in the liver and pancreas, and remains reversible for at least 10 years in most individuals.”

When people are put on a very low-calorie diet—700 calories a day—fat can get pulled out of their muscle cells, accompanied by a corresponding boost in insulin sensitivity, as shown below and at 4:43 in my video Fasting to Reverse Diabetes.

The fat buildup in the liver has then been shown to decrease substantially, and if the diet is continued, the excess fat in the pancreas also reduces. If caught early enough, reversing type 2 diabetes is possible, which would mean sustained healthy blood sugar levels on a healthy diet.

With the loss of 15% of body weight, nearly 90% of individuals who have had type 2 diabetes for less than four years can achieve non-diabetic blood sugar levels, whereas it may only be reversible in 50% of those who’ve lived with the disease for longer than eight years. That’s better than bariatric surgery, where those losing even more weight had lower remission rates of 62% and 26%, respectively. Your forks are better than surgeons’ knives. Indeed, most people who have had their type 2 diabetes diagnosis for an average of three years can reverse their disease after losing about 30 pounds, as you can see below and at 5:37 in my video.

Of course, an extended bout of physician-supervised, water-only fasting could also get you there, but you would have to maintain that weight loss. One of the things that has been said with “certainty” is that if you regain the weight, you regain your diabetes.

To bring it full circle, “the initial euphoria about ‘medicine’s greatest miracle’”—the discovery of insulin in 1921—“soon gave way to the realisation” that, while it was literally life-saving for people with type 1 diabetes, insulin alone wasn’t enough to prevent such complications as blindness, kidney failure, stroke, and amputations in people with type 2 diabetes. That’s why one of the most renowned pioneers in diabetes care, Elliott Joslin, “argued that self-discipline on diet and exercise, as it was in the days prior to the availability of the drug [insulin], should be central to the management of diabetes….”

Doctor’s Note

Check out Diabetes as a Disease of Fat Toxicity for more on the underlying cause of the disease.

For more on fasting for disease reversal, see:

• Friday Favorites: Fasting to Treat Depression
• Friday Favorites: Fasting for Irritable Bowel Syndrome
• Fasting for Post-Traumatic Brain Injury Headache

Fasting is not the best way to lose weight. To learn more, see related posts below.

What is the best way to lose weight? See Friday Favorites: The Best Diet for Weight Loss and Disease Prevention.

What Is Allulose?

Allulose is a natural, so-called rare sugar, present in limited quantities in nature. “Recent technological advances, such as enzymatic engineering using genetically modified microorganisms, now allow [manufacturers] to produce otherwise rare sugars” like allulose in substantial quantities.

Allulose and Weight Loss

What happened when researchers evaluated the effect of allulose on fat mass reduction in people? As I discuss in my video Is Allulose a Healthy Sweetener?, more than a hundred individuals were randomized to a placebo control (0.012 grams of sucralose twice a day), a teaspoon (4 g) of allulose twice a day, or 1¾ teaspoons (7 g) of allulose twice a day for 12 weeks. Despite no changes in physical activity or calorie consumption in the groups, body fat significantly decreased following allulose supplementation. There weren’t any significant changes in LDL cholesterol levels in either of the allulose groups, though.

What about the purported anti-diabetes effects?

Does Allulose Help with Diabetes?

In a randomized, double-blind, placebo-controlled crossover experiment, people with borderline diabetes consumed a cup of tea containing either 1¼ teaspoons (5 g) of allulose or no allulose (control) with a meal. There was a significant reduction in blood sugar levels 30 and 60 minutes after consumption, but it was only about 15% lower compared to the control group and didn’t last beyond the first hour. To test long-term safety, the same researchers then randomized healthy people to a little over a teaspoon (5 g) of allulose three times a day with meals for 12 weeks. There didn’t appear to be any adverse side effects, but there weren’t any effects on weight or blood sugar levels either. So, it turns out the body fat data are mixed, as are the sugar data.

Another study found no effects of allulose on blood sugar levels in healthy participants tested up to two hours after consumption, though a similar study on individuals with diabetes did. And a systematic review and meta-analysis of all such controlled feeding trials suggested that the acute benefit on blood sugars was of “borderline significance.” It’s unclear whether this small and apparently inconsistent effect could translate into meaningful improvements in long-term blood sugar control. It may not be enough just to add allulose—you might also have to cut out junk food.

Is Allulose Good or Bad for You?

As I discuss in my video Does the Sweetener Allulose Have Side Effects?, unlike table sugar, allulose is safe for our teeth; it apparently isn’t metabolized by cavity-causing bacteria to produce acid and promote plaque buildup. It doesn’t raise blood sugar levels either, even in people with diabetes. Allulose is considered a “relatively nontoxic” sugar, but what does that mean?

How Much Allulose Is Too Much?

In one study, researchers gave healthy adults beverages containing gradually higher doses of allulose “to identify the maximum single dose for occasional ingestion.” No cases of severe gastrointestinal symptoms were noted until a dose of 0.4 g per kg of bodyweight was reached, which is about eight teaspoons for the average American. Severe symptoms of diarrhea were noted at a dose of 0.5 g per kg of bodyweight, or about ten teaspoons.

In terms of a daily upper limit given in smaller doses throughout the day, once participants reached around 17 teaspoons (1.0 g/kg bodyweight) a day, depending on weight, some experienced severe nausea, abdominal pain, headache, or diarrhea. So, most adults in the United States should probably stay under single doses of about 8 teaspoons (0.4 g per kg of bodyweight) and not exceed about 18 teaspoons (0.9 g per kg of bodyweight) for the whole day.

So, What’s the Verdict on Allulose?

Are rare sugars like allulose a healthy alternative for traditional sweeteners? Well, considering the variety of potentially beneficial effects of allulose “without known disadvantages from metabolic and toxicological studies, allulose may currently be the most promising rare sugar.” But how much is that saying? We just don’t have a lot of good human data. “As a result of the absence of these studies, it may be too early to recommend rare sugars for human consumption.” This is especially true given the erythritol debacle.

Fifty million Americans suffer from arthritis, and osteoarthritis of the knee is the most common form, making it a leading cause of disability. There are several inflammatory pathways that underlie the disease’s onset and progression, so various anti-inflammatory foods have been put to the test. Strawberries can decrease circulating blood levels of an inflammatory mediator known as tumor necrosis factor, but that doesn’t necessarily translate into clinical improvement. For example, drinking cherry juice may lower a marker of inflammation known as C-reactive protein, but it failed to help treat pain and other symptoms of knee osteoarthritis. However, researchers claimed it “provided symptom relief.” Yes, it did when comparing symptoms before and after six weeks of drinking cherry juice, but not any better than a placebo, meaning drinking it was essentially no better than doing nothing. Cherries may help with another kind of arthritis called gout, but they failed when it came to osteoarthritis.

However, strawberries did decrease inflammation. In fact, in a randomized, double-blind, crossover trial, dietary strawberries were indeed found to have a significant analgesic effect, causing a significant decrease in pain. There are tumor necrosis factor inhibitor drugs on the market now available for the low, low cost of only about $40,000 a year. For that kind of money, you’d want some really juicy side effects, and they do not disappoint—like an especially fatal lymphoma. I think I’ll stick with the strawberries.

One reason we suspected berries might be helpful is that when people consumed the equivalent of a cup of blueberries or two cups of strawberries daily, and their blood was then applied to cells in a petri dish, it significantly reduced inflammation compared to blood from those who consumed placebo berries, as you can see below and at 2:02 in my video Extra Virgin Olive Oil for Arthritis.

Interestingly, the anti-inflammatory effect increased over time, suggesting that the longer you eat berries, the better. Are there any other foods that have been tested in this way?

Researchers in France collected cartilage from knee replacement surgeries and then exposed it to blood samples from volunteers who had taken a whopping dose of a grapeseed and olive extract. They saw a significant drop in inflammation, as shown below and at 2:30 in my video.

There haven’t been any human studies putting grapeseeds to the test for arthritis, but an olive extract was shown to decrease pain and improve daily activities in osteoarthritis sufferers. So, does this mean adding olive oil to one’s diet may help? No, because the researchers used freeze-dried olive vegetation water. That’s basically what’s left over after you extract the oil from olives; it’s all the water-soluble components. In other words, it’s all the stuff that’s in an olive that‘s missing from olive oil.

If you give people actual olives, a dozen large green olives a day, you may see a drop in an inflammatory mediator. But according to a systematic review and meta-analysis, olive oil—on its own—does not appear to offer any anti-inflammatory benefits. What about papers that ascribe “remarkable anti-inflammatory activity” to extra virgin olive oil? Their evidence is from rodents. In people, extra virgin olive oil may be no better than butter when it comes to inflammation and worse than even coconut oil.

So, should we just stick to olives? Sadly, a dozen olives could take up nearly half your sodium limit for the entire day, as you can see below and at 3:47 in my video.

When put to the test, extra virgin olive oil did not appear to help with fibromyalgia symptoms either, but it did work better than canola oil in alleviating symptoms of inflammatory bowel disease. Unfortunately, I couldn’t find any studies putting olive oil intake to the test for arthritis. But why then is this blog entitled “Can Olive Oil Compete with Arthritis Drugs?” Because—are you ready for this?—it appears to work topically.

Topical virgin olive oil went up against a gel containing an ibuprofen-type drug for osteoarthritis of the knee in a double-blind, randomized, clinical trial. Just a gram of oil, which is less than a quarter teaspoon, three times a day, costing less than three cents a day, worked! Topical olive oil was significantly better than the drug in reducing pain, as you can see below and at 4:37 in my video.

The study only lasted a month, so is it possible that the olive oil would have continued to work better and better over time?

Is olive oil effective in controlling morning inflammatory pain in the fingers and knees among women with rheumatoid arthritis? The researchers went all out, comparing the use of extra virgin olive oil to rubbing on nothing and also to rubbing on that ibuprofen-type gel, and, evidently, the decrease in the disease activity score in the olive oil group beat out the others.

Doctor’s Note

For more on joint health, see related posts below.

What about eating olive oil? See Olive Oil and Artery Function.

How Sustainable Is the Weight Loss After Bariatric Surgery? I explore that issue in my video of the same name. Most gastric bypass patients end up regaining some of the fat they lose by the third year after surgery, but after seven years, 75% of patients followed at 10 U.S. hospitals maintained at least a 20% weight loss.

The typical trajectory for someone who starts out obese at 285 pounds, for example, would be to drop to an overweight 178 pounds two years after bariatric surgery, but then regain weight up to an obese 207 pounds. This has been chalked up to “grazing” behavior, where compulsive eaters may shift from bingeing (which becomes more difficult post-surgery) to eating smaller amounts constantly throughout the day. In a group of women followed for eight years after gastric bypass surgery, about half continued to describe episodes of disordered eating. As one pediatric obesity specialist described, “I have seen many patients who put chocolate bars into a blender with some cream, just to pass technically installed obstacles [e.g., a gastric band].”

Bariatric surgery advertising is filled with “happily-ever-after” fairytale narratives of cherry-picked outcomes offering, as one ad analysis put it, “the full Cinderella-romance happy ending.” This may contribute to the finding that patients often overestimate the amount of weight they’ll lose with the procedure and underestimate the difficulty of the recovery process. Surgery forces profound changes in eating habits, requiring slow, small bites that have been thoroughly chewed. Your stomach goes from the volume of two softballs down to the size of half a tennis ball in stomach stapling and half a ping-pong ball in the case of gastric bypass or banding.

As you can imagine, “weight regain after bariatric surgery can have a devastating effect psychologically as patients feel that they have failed their last option”—their last resort. This may explain why bariatric surgery patients face a high risk of depression. They also have an increased risk of suicide.

Severe obesity alone may increase the risk of suicidal depression, but even at the same weight, those going through surgery appear to be at a higher risk. At the same BMI (body mass index), age, and gender, bariatric surgery patients have nearly four times the odds of self-harm or attempted suicide compared with those who did not undergo the procedure. Most convincingly, so-called “mirror-image analysis” comparing patients’ pre- and post-surgery events showed the odds of serious self-harm increased after surgery.

About 1 in 50 bariatric surgery patients end up killing themselves or being hospitalized for self-harm or attempted suicide. And this only includes confirmed suicides, excluding masked attempts such as overdoses classified as having “undetermined intention.” Bariatric surgery patients may also have an elevated risk of accidental death, though some of this could be due to changes in alcohol metabolism. When individuals who have had a gastric bypass were given two shots of vodka, their blood alcohol level surpassed the legal driving limit within minutes due to their altered anatomy. It’s unclear whether this plays a role in the 25% increase in prevalence of alcohol problems noted during the second postoperative year.

Even those who successfully lose their excess weight and keep it off appear to have a hard time coping. Ten years out, though physical health-related quality of life may improve, general mental health can significantly deteriorate compared to pre-surgical levels, even among those who lost the most weight. Ironically, there’s a common notion that bariatric surgery is for “cheaters” who take the easy way out by choosing the “low-effort” method of weight loss.

Shedding the weight may not shed the stigma of prior obesity. Studies suggest that “in the eyes of others, knowing that an individual was at one time fat will lead him/her to always be treated like a fat person.” And there can be a strong anti-surgery bias on top of that—those who chose the scalpel to lose weight over diet or exercise were rated more negatively (for example, being considered less physically attractive). One can imagine how remaining a target of prejudice even after joining the “in-group” could potentially undercut psychological well-being.

There can also be unexpected physical consequences of massive weight loss, like large hanging flaps of excess skin. Beyond being heavy and uncomfortable and interfering with movement, the skin flaps can result in itching, irritation, dermatitis, and skin infections. Getting a panniculectomy (removing the abdominal “apron” of hanging skin) can be expensive, and its complication rate can exceed 50%, with dehiscence (rupturing of the surgical wound) one of the most common complications.

“Even if surgery proves sustainably effective,” wrote the founding director of Yale University’s Prevention Research Center, “the need to rely on the rearrangement of natural gastrointestinal anatomy as an alternative to better use of feet and forks [exercise and diet] seems a societal travesty.”

In the Middle Ages, starving peasants dreamed of gastronomic utopias where food just rained down from the sky. The English called it the Kingdom of Cockaigne. Little could medieval fabulists predict that many of their descendants would not only take permanent residence there but also cut out parts of their stomachs and intestines to combat the abundance. Critics have pointed out the irony of surgically altering healthy organs to make them dysfunctional—malabsorptive—on purpose, especially when it comes to operating on children. Bariatric surgery for kids and teens has become widespread and is being performed on children as young as five years old. Surgeons defend the practice by arguing that growing up fat can leave “‘emotional scars’ and lifelong social retardation.”

Promoters of preventive medicine may argue that bariatric surgery is the proverbial “ambulance at the bottom of the cliff.” In response, proponents of pediatric bariatric surgery have written: “It is often pointed out that we should focus on prevention. Of course, I agree. However, if someone is drowning, I don’t tell them, ‘You should learn how to swim’; no, I rescue them.”

A strong case can be made that the benefits of bariatric surgery far outweigh the risks if the alternative is remaining morbidly obese, which is estimated to shave up to a dozen or more years off one’s life. Although there haven’t been any data from randomized trials yet to back it up, compared to non-operated obese individuals, those getting bariatric surgery would be expected to live significantly longer on average. No wonder surgeons have consistently framed the elective surgery as a life-or-death necessity. This is a false dichotomy, though. The benefits only outweigh the risks if there are no other alternatives. Might there be a way to lose weight healthfully without resorting to the operating table? That’s what my book How Not to Diet is all about.

Doctor’s Note

My book How Not to Diet is focused exclusively on sustainable weight loss. Check it out from your library or pick it up from wherever you get your books. (All proceeds from my books are donated to charity.)

This is the final segment in a four-part series on bariatric surgery, which includes:

• The Mortality Rate of Bariatric Weight-Loss Surgery
• The Complications of Bariatric Weight-Loss Surgery
• Bariatric Surgery vs. Diet to Reverse Diabetes

This blog contains information regarding suicide. If you or anyone you know is exhibiting suicide warning signs, please get help. Go to https://988lifeline.org for more information.

The surgical community objects to the characterization of bariatric surgery as internal jaw wiring and cutting into healthy organs just to discipline people’s behavior. They’ve even renamed it “metabolic surgery,” suggesting the anatomical rearrangements cause changes in digestive hormones that offer unique physiological benefits. As evidence, they point to the remarkable remission rates for type 2 diabetes.

After bariatric surgery, about 50% of obese people with diabetes and 75% of “super-obese” diabetics go into remission, meaning they have normal blood sugar levels on a regular diet without any diabetes medication. The normalization of blood sugar can happen within days after the surgery. And 15 years after the surgery, 30% remained free from their diabetes, compared to a 7% remission rate in a nonsurgical control group. Are we sure it was the surgery, though?

One of the most challenging parts of bariatric surgery is lifting the liver. Since obese individuals tend to have such large, fatty livers, there is a risk of liver injury and bleeding. An enlarged liver is one of the most common reasons a less invasive laparoscopic surgery can turn into a fully invasive open surgery, leaving the patient with a large belly scar, along with an increased risk of wound infections, complications, and recovery time. But lose even just 5% of your body weight, and your fatty liver may shrink by 10%. That’s why those awaiting bariatric surgery are put on a diet. After surgery, patients are typically placed on an extremely low-calorie liquid diet for weeks. Could their improvement in blood sugar levels just be from the caloric restriction, rather than some sort of surgical metabolic magic? Researchers decided to put it to the test.

At a bariatric surgery clinic at the University of Texas, patients with type 2 diabetes scheduled for a gastric bypass volunteered to stay in the hospital for 10 days to follow the same extremely low-calorie diet—less than 500 calories a day—that they would be placed on before and after surgery, but without undergoing the procedure itself. After a few months, once they had regained the weight, the same patients then had the actual surgery and repeated their diet, matched day to day. This allowed researchers to compare the effects of caloric restriction with and without the surgical procedure—the same patients, the same diet, just with or without the surgery. If there were some sort of metabolic benefit to the anatomical rearrangement, the patients would have done better after the surgery, but, in some ways, they actually did worse.

The caloric restriction alone resulted in similar improvements in blood sugar levels, pancreatic function, and insulin sensitivity, but several measures of diabetic control improved significantly more without the surgery. The surgery seemed to put them at a metabolic disadvantage.

Caloric restriction works by first mobilizing fat out of the liver. Type 2 diabetes is thought to be caused by fat building up in the liver and spilling over into the pancreas. Everyone may have a “personal fat threshold” for the safe storage of excess fat. When that limit is exceeded, fat gets deposited in the liver, where it can cause insulin resistance. The liver may then offload some of the fat (in the form of a fat transport molecule called VLDL), which can then accumulate in the pancreas and kill off the cells that produce insulin. By the time diabetes is diagnosed, half of our insulin-producing cells may have been destroyed, as seen below and at 3:36 in my video Bariatric Surgery vs. Diet to Reverse Diabetes. Put people on a low-calorie diet, though, and this entire process can be reversed.

A large enough calorie deficit can cause a profound drop in liver fat sufficient to resurrect liver insulin sensitivity within seven days. Keep it up, and the calorie deficit can decrease liver fat enough to help normalize pancreatic fat levels and function within just eight weeks. Once you drop below your personal fat threshold, you should then be able to resume normal caloric intake and still keep your diabetes at bay, as seen below and at 4:05 in my video. 

The bottom line: Type 2 diabetes is reversible with weight loss, if you catch it early enough.

Lose more than 30 pounds (13.6 kilograms), and nearly 90% of those who have had type 2 diabetes for less than four years can achieve non-diabetic blood sugar levels (suggesting diabetes remission), whereas it may only be reversible in 50% of those who’ve lived with the disease for eight or more years. That’s by losing weight with diet alone, though. For people with diabetes, losing more than twice as much weight with bariatric surgery, diabetes remission may only be around 75% of those who’ve had the disease for up to six years and only about 40% for those who’ve had diabetes longer, as seen below and at 4:41 in my video.

Losing weight without surgery may offer other benefits as well. Individuals with diabetes who lose weight with diet alone can significantly improve markers of systemic inflammation, such as tumor necrosis factor, whereas levels significantly worsened when about the same amount of weight was lost from a gastric bypass.

What about diabetic complications? One reason to avoid diabetes is to avoid its associated conditions, like blindness or kidney failure requiring dialysis. Reversing diabetes with bariatric surgery can improve kidney function, but, surprisingly, it may not prevent the occurrence or progression of diabetic vision loss—perhaps because bariatric surgery affects quantity but not necessarily quality when it comes to diet. This reminds me of a famous study published in The New England Journal of Medicine that randomized thousands of people with diabetes to an intensive lifestyle program focused on weight loss. Ten years in, the study was stopped prematurely because the participants weren’t living any longer or having any fewer heart attacks. This may be because they remained on the same heart-clogging diet but just in smaller portions.

Doctor’s Note

This is the third blog in a four-part series on bariatric surgery. If you missed the first two, check out The Mortality Rate of Bariatric Weight-Loss Surgery and The Complications of Bariatric Weight-Loss Surgery.

My book How Not to Diet is focused exclusively on sustainable weight loss. Check it out from your local library, or pick it up from wherever you get your books. (All proceeds from my books are donated to charity.)

In 2025, I covered a wide variety of hot topics. I released an extensive series on Ozempic, updates on vitamin B12, and, of course, a lot on aging and anti-aging based on my research for How Not to Age. Which videos floated to the top last year? 

#10 How Much Vitamin B12 Do We Need Each Day?

How are the recommended daily and weekly doses of vitamin B12 derived?

#9 The Best Way to Boost NAD+: Supplements vs. Diet (webinar recording)

This webinar wrapped up the pros and cons of all the NAD+ supplements and the ways to naturally boost NAD+ with diet and lifestyle. (Did you know we now offer a growing library of on-demand webinars for CME credits? To learn more and to register, visit us on the LearnWorlds platform.)

#8 How to Improve Your Heart Rate Variability

A healthy heart doesn’t beat like a metronome.

#7 The Best Foods for Your Skin

Greens, apples, tomato paste, and grapes are put to the test as edible skin care candidates.

#6 Friday Favorites: Foods That Cause Inflammation and Those That Reduce It

This is a popular combination of two earlier videos, exploring which foods are the worst when it comes to triggering inflammation within hours of consumption and what an anti-inflammatory diet looks like?

#5 The Healthiest Way to Drink Coffee

Why do those who drink filtered coffee tend to live longer than those who drink unfiltered coffee?

#4 Is One Egg a Day Too Much?

*Spoiler alert*: Meta-analyses of studies involving more than 10 million participants confirm that greater egg consumption confers a higher risk of premature death from all causes.

#3 Do Not Eat Pawpaws

Pawpaw fruits, like soursop, guanabana, sweetsop, sugar apple, cherimoya, and custard apple, contain neurotoxins that may cause a neurodegenerative disease. 

#2 The Highest Antioxidant: Apple, Bean, Berry, Lentil, or Nut?

Remember these kinds of videos from way back when? I brought them back! Of course, the best apple, bean, berry, lentil, and nut are the ones you’ll eat the most of, but if you don’t have a strong preference, which ones have the highest antioxidant power? 

#1 How to Slow Cancer Growth

The fact that this video was so popular is validation for my plan to take on cancer after How Not to Hurt, my upcoming book on lifestyle approaches to pain management, which should be out in (fingers crossed) December 2026. This video explains how, at this very moment, many of us have tumors growing inside our bodies, so we cannot wait to start eating and living more healthfully.

Thank you for being a part of this community. We gained more than 170,000 new subscribers on YouTube in 2025, and the number of people we can reach with this life-saving, life-changing information continues to grow.

What makes these goals stick? Small, enjoyable changes rooted in real food and tradition — not extreme diets or expensive gadgets. Pakistani cuisine already excels here: think fiber-packed lentils, anti-inflammatory spices, fermented yogurt sides, and one-pot meals that warm the body and soul without excess oil.

At Nutric Food Show, we’re all about realistic, flavorful wellness that bridges Pakistani roots with global kitchens. Drawing from 2026’s big trends — fiber-first eating, gut health as the new priority, balanced (not obsessive) protein, fermented foods for microbiome support, and global flavor fusions — here are 7 practical habits to carry you into the new year. Start with just one or two; build from there.

1. Begin Mornings with Jeera-Haldi Water or a Simple Golden Tea (Gut Reset & Immunity Kick)

Why it aligns with 2026 trends Fiber and anti-inflammatory spices are exploding in popularity. Cumin (jeera) stimulates digestion and reduces bloating; turmeric (haldi) modulates immunity and lowers inflammation markers like CRP. Together, they support the gut-immune axis (where ~70% of your immune system lives) without any supplements.

How to make it a habit

• Boil 1 tsp cumin seeds + ½ tsp turmeric powder + a pinch of black pepper in 2 cups water for 5–7 minutes.
• Strain, add fresh lemon and a touch of honey or jaggery. Drink warm on an empty stomach.
• Time: 10 minutes total. Prep a thermos batch the night before.

Swedish/UK/US adaptations

• Swedish twist: Stir in a spoonful of lingonberry jam for tart antioxidants and Nordic flair — perfect for dark vintermorgon.
• UK/US: Add fresh ginger for extra warmth and use oat milk for a creamy “golden latte” version.

Bonus benefit This replaces pricey probiotic drinks while naturally feeding good gut bacteria. Many readers report less morning bloating after 2 weeks.

2. Make High-Fiber Daal Your Weekly Anchor Meal

Why it’s trending Fiber is being called “the new protein” for 2026 — linked to better satiety, stable blood sugar, metabolic health, and gut microbiome diversity. Lentils deliver 15–20g fiber per serving plus plant protein.

Easy implementation

• Cook moong masoor daal (yellow + red split lentils) once or twice a week.
• Sauté onions, garlic, ginger, cumin, turmeric in 1–2 tsp oil. Add rinsed lentils, tomatoes, water/stock; simmer 20–30 min.
• Finish with a light tadka of cumin seeds. Serve with brown rice, quinoa, or whole-wheat roti.

Fusion ideas

• Swedish: Stir in diced carrots, parsnips, potatoes — turns it into a hearty rotfruktsgryta-style stew.
• UK/US: Add spinach or kale for extra greens; top with a dollop of yogurt for creaminess.

Pro tip Batch-cook on Sunday; reheat portions for lunches. This habit alone can push your daily fiber toward the recommended 25–38g.

3. Incorporate Fermented Foods Daily for Microbiome Magic

Why it’s huge in 2026 Fermented foods (probiotics + prebiotics) top gut-health lists, supporting digestion, mood, and immunity. They’re moving mainstream beyond kimchi/kefir.

Simple habit

• Add a small serving of dahi (yogurt) raita or achaar (pickle) to lunch/dinner most days.
• Make quick raita: Whisk plain yogurt with grated cucumber, cumin powder, mint, salt.
• Or temper a pinch of achar masala into veggies for fermented tang.

Global twists

• Swedish: Mix dahi with filmjölk or skyr; add pickled lingonberries or surkål (fermented cabbage).
• UK/US: Use Greek yogurt base; swirl in mango chutney for sweet-heat contrast.

Start small Aim for 1–2 tbsp daily — enough to introduce beneficial bacteria without overwhelming your system.

4. Build 2–3 Warming One-Pot Meals Around Spices Each Week

Why it works Global flavors + anti-inflammatory spices are key. Ginger, garlic, cumin, coriander reduce inflammation and support respiratory health — ideal post-holidays.

Practical routine

• Rotate low-oil classics: vegetable pulao, chicken/veg karahi, or mixed-lentil stew.
• Always start with a light spice temper (1 tsp oil max). Add seasonal veggies for bulk.

Fusion examples

• Swedish vintermat: Root-heavy karahi with cabbage or kale.
• UK/US: Spice it like a curry but serve over quinoa or with naan alternatives.

Time-saver Use a pressure cooker/instant pot for 15-min cook time. Freeze portions for busy weeks.

5. Swap Evening Snacks for Spice-Infused Herbal Drinks

Why it’s smart Mindful eating and non-alcoholic “functional” drinks rise in 2026 — great for digestion and curbing sugar cravings.

Easy ritual

• Brew adrak (ginger) chai, saunf (fennel) water, or elaichi (cardamom) tea after dinner.
• Boil fresh ginger slices + cardamom pods; strain, add milk/honey to taste.

Cozy adaptations

• Swedish: Add cinnamon (kanel) for glögg-like warmth without alcohol.
• UK/US: Use rooibos base for caffeine-free evenings.

Benefit Aids overnight digestion and promotes better sleep — key for energy in January.

6. Add More Colorful Veggies & Fruits to Every Plate (Fiber & Micronutrient Boost)

Why it’s essential 2026 emphasizes whole foods and plant diversity for gut health and longevity. Aim for 5–7 colors daily.

Simple rule

• At every meal, fill half your plate with veggies/fruits.
• Pakistani favorites: Okra bhindi, palak saag, tomato-onion salads, seasonal carrots/beets.

Fusion ideas

• Swedish: Pair with pickled beets or fresh berries.
• UK/US: Add avocado or pomegranate for creaminess/tartness.

Quick win Keep chopped veggies ready in the fridge — makes it effortless.

7. End the Day with 10 Minutes of Mindful Movement or Breathing

Why it matters Movement + stress reduction support everything else. Short walks after meals stabilize blood sugar; breathing calms the nervous system.

Doable habit

• Walk 10–15 minutes post-dinner (a Pakistani tradition called “saair”).
• Or practice 4-7-8 breathing: Inhale 4, hold 7, exhale 8 — repeat 4 times.

Adaptations

• Swedish: Bundle up for a snowy evening stroll.
• UK/US: Indoor yoga or stretch while chai brews.

Wrapping Up: Make 2026 Sustainable & Joyful

These habits aren’t about perfection — they’re about progress through food you already love. Start small: Pick one for January (jeera-haldi water is the easiest win). Track how you feel after 2 weeks — more energy? Better digestion? Less cravings? That’s the real motivation.

In 2026, wellness isn’t about extremes; it’s about balance, flavor, and feeling good in your body. Pakistani cooking gives you the perfect toolkit: affordable, nutrient-dense, warming, and endlessly adaptable.

What’s your starting habit for tomorrow? Drop it in the comments — let’s cheer each other on! Share your tweaks or fusions too. Wishing you a vibrant, healthy, delicious 2026 filled with good food and good feelings.

Stay nourished & strong!

After sleeve gastrectomy and Roux-en-Y gastric bypass, the third most common bariatric procedure is a revision to fix a previous bariatric procedure, as you can see below and at 0:16 in my video The Complications of Bariatric Weight-Loss Surgery.

Up to 25% of bariatric patients have to go back into the operating room for problems caused by their first bariatric surgery. Reoperations are even riskier, with up to 10 times the mortality rate, and there is “no guarantee of success.” Complications include leaks, fistulas, ulcers, strictures, erosions, obstructions, and severe acid reflux.

The extent of risk may depend on the skill of the surgeon. In a study published in The New England Journal of Medicine, bariatric surgeons voluntarily submitted videos of themselves performing surgery to a panel of their peers for evaluation. Technical proficiency varied widely and was related to the rates of complications, hospital readmissions, reoperations, and death. Patients operated on by less competent surgeons suffered nearly three times the complications and five times the rate of death.

“As with musicians or athletes, some surgeons may simply be more talented than others”—but practice may help make them perfect. Gastric bypass is such a complicated procedure that the learning curve may require 500 cases for a surgeon to master the procedure. Risk for complications appears to plateau after about 500 cases, with the lowest risk found among surgeons who had performed more than 600 bypasses. The odds of not making it out alive may be double under the knife of those who had performed less than 75 compared to more than 450, as seen below and at 1:47 in my video.

So, if you do choose to undergo the operation, I’d recommend asking your surgeon how many procedures they’ve done, as well as choosing an accredited bariatric “Center of Excellence,” where surgical mortality appears to be two to three times lower than non-accredited institutions.

It’s not always the surgeon’s fault, though. In a report entitled “The Dangers of Broccoli,” a surgeon described a case in which a woman went to an all-you-can-eat buffet three months after a gastric bypass operation. She chose really healthy foods—good for her!—but evidently forgot to chew. Her staples ruptured, and she ended up in the emergency room, then the operating room. They opened her up and found “full chunks of broccoli, whole lima beans, and other green leafy vegetables” inside her abdominal cavity. A cautionary tale to be sure, but perhaps one that’s less about chewing food better after surgery than about chewing better foods before surgery—to keep all your internal organs intact in the first place.

Even if the surgical procedure goes perfectly, lifelong nutritional replacement and monitoring are required to avoid vitamin and mineral deficits. We’re talking about more than anemia, osteoporosis, or hair loss. Such deficits can cause full-blown cases of life-threatening deficiencies, such as beriberi, pellagra, kwashiorkor, and nerve damage that can manifest as vision loss years or even decades after surgery in the case of copper deficiency. Tragically, in reported cases of severe deficiency of a B vitamin called thiamine, nearly one in three patients progressed to permanent brain damage before the condition was caught.

The malabsorption of nutrients is intentional for procedures like gastric bypass. By cutting out segments of the intestines, you can successfully impair the absorption of calories—at the expense of impairing the absorption of necessary nutrition. Even people who just undergo restrictive procedures like stomach stapling can be at risk for life-threatening nutrient deficiencies because of persistent vomiting. Vomiting is reported by up to 60% of patients after bariatric surgery due to “inappropriate eating behaviors.” (In other words, trying to eat normally.) The vomiting helps with weight loss, similar to the way a drug for alcoholics called Antabuse can be used to make them so violently ill after a drink that they eventually learn their lesson.

“Dumping syndrome” can work the same way. A large percentage of gastric bypass patients can suffer from abdominal pain, diarrhea, nausea, bloating, fatigue, or palpitations after eating calorie-rich foods, as they bypass your stomach and dump straight into your intestines. As surgeons describe it, this is a feature, not a bug: “Dumping syndrome is an expected and desired part of the behavior modification caused by gastric bypass surgery; it can deter patients from consuming energy-dense food.

Doctor’s Note

This is the second in a four-part series on bariatric surgery. If you missed the first one, see The Mortality Rate of Bariatric Weight-Loss Surgery.

Up next: Bariatric Surgery vs. Diet to Reverse Diabetes and How Sustainable Is the Weight Loss After Bariatric Surgery?.

My book How Not to Diet is focused exclusively on sustainable weight loss. Check it out from your local library, or pick it up from wherever you get your books. (All proceeds from my books are donated to charity.)

The treatment of obesity has long been stained by the snake-oil swindling of profiteers, hustlers, and quacks. Even the modern field of bariatric medicine (derived from the Greek word baros, meaning “weight”) is pervaded by an “insidious image of sleaze.” Beguiled by advertising for fairy tale magic bullets of rapid, effortless weight loss, people blame themselves for failing to manifest the miracle or imagine themselves metabolically broken. On the other end of the spectrum are overly pessimistic practitioners of the opinion that “people who are fat are born fat, and nothing much can be done about it.” The truth lies somewhere in between.

The difficulty of curing obesity has been compared to learning a foreign language. It’s an achievement virtually anyone can attain with a sufficient investment of energies, “but it always takes a considerable amount of time and trouble.” And, of those who do stick with it, most will regain much of the weight lost. To me, this speaks to the difficulty, rather than the futility. It may take smokers an average of 30 attempts to finally kick the habit. Like quitting smoking, curing obesity is just something that has to be done. As the chair of the Association for the Study of Obesity put it, it doesn’t take “will power” to do essential tasks like getting up at night to feed a baby; it’s just something that has to be done.

Our collective response doesn’t seem to match the rhetoric or reality. If obesity is such a “national crisis” reaching alarming proportions, dubbed by the post-9/11 Surgeon General as “every bit as devastating as terrorism,” why has our reaction been so tepid? For example, governments meekly suggest the food industry take “voluntary initiatives to restrict the marketing of less healthy food options to children….” Have we just given up and ceded control?

Our timid response to the obesity epidemic is encapsulated by a national initiative promulgated by a Joint Task Force of the American Society for Nutrition, Institute of Food Technologists, and International Food Information Council: the “small-changes approach.” Since “small changes are more feasible to achieve,” suggestions include “using mustard instead of mayonnaise” and “eating 1 rather than 2 doughnuts in the morning.” Seems a bit like bringing a butter knife to a gunfight. Proponents of the small-changes approach lament that, unlike other addictions—for example, alcohol, cocaine, gambling, or tobacco—we can’t counsel our obese patients to give up the addictive element completely, as “[n]o one can give up eating.” But just because we have to breathe, doesn’t mean it has to be through the end of a cigarette. And just because we have to eat doesn’t mean we have to eat junk.

What about bringing a scalpel to the gunfight instead? The use of bariatric surgery has exploded from about 40,000 procedures noted in the first international survey in 1998 to hundreds of thousands performed now every year in the United States alone. The first technique that was developed, the intestinal bypass, involved carving out about 19 feet of intestines. More than 30,000 intestinal bypass operations were performed before we recognized “catastrophic” and “disastrous outcomes” resulted from these procedures. This included protein deficiency-induced liver disease, “which often progressed to liver failure and death.” This inauspicious start is remembered as “one of the dark blots in the history of surgery,” as I discuss in my video The Mortality Rate of Bariatric Weight-Loss Surgery.

Today, death rates after bariatric surgery are considered “very low,” occurring on average in perhaps 1 in 300 to impacting 1 in 500 patients. The most common procedure is stomach stapling, also known as sleeve gastrectomy, in which most of the stomach is permanently removed. Only a narrow tube of the stomach is left so as to restrict how much food people can eat at any one time. It’s ironic that many patients choose bariatric surgery convinced that, “for them, ‘diets do not work,’” when, in reality, that’s all the surgery may be—an enforced diet. Bariatric surgery can be thought of as a form of internal jaw wiring.

Gastric bypass, known as Roux-en-Y gastric bypass, is the second most common bariatric surgery. It combines restriction—stapling the stomach into a pouch smaller than a golf ball—with malabsorption by rearranging one’s anatomy to bypass the first part of the small intestine. It appears to be more effective than just cutting out most of the stomach, resulting in a loss of about 63% of excess weight compared to 53% with a gastric sleeve. But gastric bypass carries a greater risk of serious complications. Many are surprised to learn that new “surgical procedures…do not require premarket testing and approval by the Food and Drug Administration (FDA)” and are largely exempt from rigorous regulatory scrutiny.

Doctor’s Note

I didn’t know there wasn’t some kind of approval process for new surgical procedures!

This is the first video in a four-part series on bariatric surgery. Coming up are:

• The Complications of Bariatric Weight-Loss Surgery
• Bariatric Surgery vs. Diet to Reverse Diabetes
• How Sustainable Is the Weight Loss After Bariatric Surgery?

My book How Not to Diet is focused exclusively on sustainable weight loss. Check it out from your local public library or pick it up from wherever you get your books. (All proceeds from my books are donated to charity.)

There is a new nut on the market called baru almonds, branded as “barukas” or baru nuts. Technically, it isn’t a nut but a seed native to the Brazilian Savannah, known as the Cerrado, which is now among the most threatened ecosystems on the planet. Over the last 30 years, much of the Cerrado’s ecosystem has been destroyed by extensive cattle ranching and feed crop production to fatten said cattle. If it were profitable not to cut down the native trees and instead sell baru nuts, for example, that could be good for the ecosystem’s health. But what about our health?

“Although baru nuts are popular and widely consumed, few studies report on their biological properties.” They do have a lot of polyphenol phytonutrients, presumably accounting for their high antioxidant activity. (About 90% of their phytonutrients are present in the peel.) Are they nutritious? Yes, but do they have any special health benefits—beyond treating chubby mice?

Researchers found that individuals fed baru nuts showed lower cholesterol, supposedly indicating the nuts “have great potential for dietary use” in preventing and controlling cholesterol problems. But the individuals were rats, not humans, and the baru nuts were compared to lard. Pretty much everything lowers cholesterol compared to lard. Nevertheless, there haven’t been any reports about the effect of baru nut consumption on human health, until this: A randomized, controlled study of humans found that eating less than an ounce a day for six weeks led to a 9% drop in LDL cholesterol. Twenty grams would be about 15 nuts or a palmful.

Like many other nut studies, even though the research subjects were told to add nuts to their regular diets, there was no weight gain, presumably because nuts are so filling that we inadvertently cut down on other foods throughout the day. How good is a 9.4% drop in LDL? It’s the kind of drop we can get from regular almonds, though macadamias and pistachios may work even better, but those were at much higher doses. It appears that 20 grams of baru nuts work as well as 73 grams of almonds. So, on a per-serving basis or a per-calorie basis, baru nuts really did seem to be special.

There are lower-dose nut studies that show similar or even better results. In this one, for instance, people were given 25 grams of almonds for just four weeks and got about a 6% drop in their LDL cholesterol. In another study, after consuming just 10 grams of almonds a day, or just seven individual almonds a day, study participants got more like a 30% drop in LDL during the same time frame as the baru nuts. Three times better LDL at half the dose with regular almonds, as you can see below and at 2:47 in my video Are Baruka Nuts the Healthiest Nut?.

The biggest reason we are more confident in regular almonds than baru almonds is that studies have been done over and over in more than a dozen randomized controlled trials, whereas in the only other cholesterol trial of baru nuts, researchers found no significant benefit for LDL cholesterol, even at the same 20-gram dose given for even longer—a period of eight weeks.

That’s disappointing, but it isn’t the primary reason I would suggest choosing other nuts instead of baru nuts. I would do so because we can’t get raw baru nuts. They contain certain compounds that must be inactivated by heat before we can eat them. The reason raw nuts are preferable is because of advanced glycation end-products (AGEs), so-called glycotoxins, which are known to contribute to increased oxidative stress and inflammation.

Glycotoxins are naturally present in uncooked animal-derived foods, and dry-heat cooking like grilling can make things worse. The three highest recorded levels have been in bacon, broiled hot dogs, and roasted barbecued chicken skin—nothing even comes close to that, not even Chicken McNuggets, as you can see below and at 3:50 in my video.

However, any foods high in fat and protein can create AGEs at high enough temperatures. So, although plant foods tend to “contain relatively few AGEs, even after cooking,” there are some high-fat, high-protein plant foods. But, again, AGEs aren’t a problem at all with most plant foods. See the AGE content in boiled tofu (in a soup, for instance), broiled tofu, a raw apple, a baked apple, a veggie burger—I was surprised that veggie burgers are so low in AGEs, even when baked or fried—and nuts and seeds, which are up in tofu territory, especially when roasted, which is why I would recommend raw nuts and seeds and nut and seed butters whenever you have a choice. See below and at 4:33 in my video.

Doctor’s Note

In my Daily Dozen checklist, I recommend eating a quarter cup of nuts or seeds or two tablespoons of nut or seed butter each day. Why? See related posts below. 

For those unfamiliar with advanced glycation end-products (AGEs), check out the first two videos I did on them way back when: Glycotoxins and Avoiding Glycotoxins in Food.

As winter grips the Northern Hemisphere — bringing frosty Swedish mornings, chilly UK evenings, and even cooler vibes in the US — our bodies crave natural defenses against colds, flu, and that nagging fatigue from shorter days. In Pakistani homes, this is no new battle. For centuries, spices like turmeric (haldi) and cumin (jeera) have been the unsung heroes of winter wellness, woven into daily rituals like haldi doodh (golden milk) and jeera water.

These aren’t just flavor boosters; they’re potent winter superfoods backed by both tradition and modern science for immune support, anti-inflammation, and digestive resilience. At Nutric Food Show, we specialize in low-oil Pakistani recipes that adapt these gems for global kitchens—whether you’re fusing them into a Swedish rotfruktsgryta (root vegetable stew) or a simple UK curry, turmeric and cumin deliver warmth without the calories. Let’s unpack their science, traditions, and practical tips—perfect timing for Christmas Eve coziness on your julbord table.

The Science Behind Turmeric: Nature’s Golden Immune Shield

Turmeric’s magic lies in curcumin, its primary bioactive compound (up to 5% in high-quality roots). This polyphenol is a powerhouse: antioxidant, anti-inflammatory, and immunomodulatory—meaning it fine-tunes your immune response rather than just revving it up.

Winter-Specific Benefits (Backed by Studies):

• Immune Modulation Curcumin activates T cells, B cells, macrophages, neutrophils, natural killer cells, and dendritic cells while downregulating proinflammatory cytokines like TNF-α, IL-1, IL-6, and IL-12 (often via NF-κB inhibition). A 2007 review in Journal of Clinical Immunology called it a “potent immunomodulatory agent,” enhancing antibody responses at low doses—ideal for flu season. Recent 2021–2025 studies (e.g., Frontiers in Pharmacology) confirm it balances overactive immunity, reducing sepsis risk and supporting COVID-19 vaccine efficacy by boosting IgG antibodies.
• Respiratory Relief Reduces airway inflammation, eases congestion, and fights sore throats—key for winter ills. Human trials show it lowers acute-phase proteins (e.g., CRP) that spike during infections.
• Gut-Immune Link ~70% of immunity resides in the gut. Curcumin promotes beneficial bacteria (prebiotic effects), aiding nutrient absorption in cold-weather diets heavy on roots and stews.
• Warming & Mood Boost Creates internal heat (thermogenic), combats seasonal blues via dopamine support, and fights oxidative stress from less sunlight.

Bioavailability Hack: Pair with black pepper (piperine boosts absorption by up to 2000%) and a healthy fat—crucial for low-oil cooking.

Cumin: The Earthy Digestive & Antimicrobial Ally

Cumin seeds (Cuminum cyminum) pack cuminaldehyde, flavonoids (apigenin, luteolin), and terpenes—delivering antioxidant, antimicrobial, and carminative punch. Earthy and nutty, it’s a winter staple for gut health (where immunity thrives).

Key Winter Perks (Evidence-Based):

• Immunity Fortress Antioxidants neutralize free radicals; antimicrobial effects kill bacteria/fungi (e.g., H. pylori). Boosts white blood cells via vitamins A/C/E; animal studies show anti-cancer potential (stomach/cervix). Human trials link it to better insulin sensitivity and reduced inflammation—vital for winter metabolic slowdown.
• Digestion Dynamo Stimulates enzymes (amylase, lipase), bile flow; relieves IBS, bloating, gas from holiday feasts. Studies (e.g., 57 IBS patients) confirm symptom relief in 2 weeks. Fiber/minerals (iron, Mg) prevent constipation in cold, low-fiber months.
• Warming Thermogenic Improves circulation, metabolism; aids weight management (overweight trials: reduced BMI/waist).

Pakistani Winter Traditions Jeera water (boil seeds) starts mornings for detox/immunity; haldi doodh (turmeric milk with a pinch of cumin) fights coughs—grandma’s flu buster, now a global “golden milk” trend.

Synergy in Low-Oil Pakistani Cooking: Maximize Nutrients

These spices shine in desi dishes (biryani, karahi, haleem)—low-oil versions preserve actives (heat-stable curcumin/cuminaldehyde).

Pro Tips for US/UK/Swedish Kitchens:

1. Daily Tonics Haldi doodh (½ tsp turmeric + pinch cumin/black pepper in warm milk, jaggery-sweetened). Vegan? Use oat/almond milk. Swedish twist: Add lingonberry for tart julmys.
2. One-Pots Temper cumin seeds (1 tsp) in 1 tsp olive oil (vs ghee for lower sat fat—studies favor olive’s MUFAs for heart health, ghee for high-heat stability). Add turmeric to root vegetable stews—Nordic fusion!
3. Dose ½–1 tsp/day each. Roast whole seeds for potency (low/no oil).
4. Storage Cool, dark jars—retains volatiles.

Ghee vs Olive Oil Quick Note For tadka (tempering), ghee’s high smoke point (485°F) beats olive (375–410°F), but olive’s antioxidants/MUFAs edge for heart/low-oil. Alternate: 1:1 mix.

Air Fryer Bonus Retains more antioxidants vs deep-frying (less oxidation)—perfect for samosas/pakoras (studies show 20–50% nutrient loss in oil-frying).

Why Fusion Works for Sweden/US/UK Winters

Swedish vintermat (root veggies, oats) pairs seamlessly: Turmeric-cumin in gryta boosts beta-carotene absorption. Diaspora communities (large in UK) already love it; US health trends (keto/paleo) embrace golden lattes. Science + culture = unbeatable.

These spices are affordable (~$5/month supply), safe (up to 6g/day curcumin), and versatile—your low-oil Pakistani edge for resilient winters.

Try Tonight Jeera-haldi tea post-julbord. Felt the warmth? Comment your fusions! Tag us on social media with #WinterSuperfoods #HaldiDoodh #JeeraPower #mat #hälsosamt #julmys #godmat #vintermat #healthyfood

Stay fortified!

“Almost 2,500 years ago, Hippocrates stated that ‘All disease begins in the gut.’” When we feed our gut bacteria right with whole plant foods, they feed us right back with beneficial compounds like butyrate, which our gut bugs make from fiber. On the other hand, if we feed them wrong, they can produce detrimental compounds like TMAO, which they make from cheese, eggs, seafood, and other meat.

We used to think that TMAO only contributed to cardiovascular diseases, like heart disease and stroke, but, more recently, it has been linked to psoriatic arthritis, associated with polycystic ovary syndrome, and everything in between. I’m most concerned about our leading killers, though. Of the top ten causes of death in the United States, we’ve known about its association with increased risk of heart disease and stroke, killers number one and five, but recently, an association has also been found between blood levels of TMAO and the risks of various cancers, which are our killer number two. The link between TMAO and cancer could be attributed to the inflammation caused by TMAO, but it could also be oxidative stress (free radicals), DNA damage, or a disruption in protein folding.

What about our fourth leading killer, chronic obstructive pulmonary disease (COPD), like emphysema? TMAO is associated with premature death in patients with exacerbated COPD, though it’s suspected that it’s due to them dying from more cardiovascular disease.

The link to stroke is a no-brainer—no pun intended. It is due to the higher blood pressure associated with higher TMAO levels, as well as the greater likelihood of clots forming in those with atrial fibrillation. Those with higher TMAO levels also appear to have worse strokes and four times the odds of death.

Killer number six is Alzheimer’s disease. Can TMAO even get up into our brains? Yes, TMAO is present in human cerebrospinal fluid, which bathes the brain, and TMAO levels are higher in those with mild cognitive dysfunction and those with Alzheimer’s disease dementia. “In the brain, TMAO has been shown to induce neuronal senescence [meaning, deterioration with age], increase oxidative stress, impair mitochondrial function, and inhibit mTOR signaling, all of which contribute to brain aging and cognitive impairment.”

Killer number seven is diabetes, and people with higher TMAO levels are about 50% more likely to have diabetes. Killer number eight is pneumonia, and TMAO predicts fatal outcomes in pneumonia patients even without evident heart disease. Kidney disease is killer number nine, and TMAO is strongly related to kidney function and predicts fatal outcomes there as well. Over a period of five years, more than half of chronic kidney disease patients who started out with average or higher TMAO levels were dead, whereas among those in the lowest third of levels, nearly 90% remained alive.

How can we lower the TMAO levels in our blood? Because TMAO originates from dietary sources, we could limit our intake of choline- and carnitine-rich foods. They’re so widespread in foods,” though we’re talking about meat, eggs, and dairy. “Therefore, restriction of foods rich in TMA-containing nutrients may not be practical.” Can we just get a vegan fecal transplant? “Vegan donors provided the investigators with a fresh morning fecal sample…”

If you remember, if you give a vegan a steak, despite all that carnitine, they make almost no TMAO compared to a meat-eater, presumably because the vegan hasn’t been fostering steak-eating bugs in their gut. See below and at 3:40 in my video Can Vegan Fecal Transplants Lower TMAO Levels?.

Remarkably, even if you give plant-based eaters the equivalent of a 20-ounce steak every day for two months, only about half start ramping up production of TMAO, showing just how far their gut flora has to change. The capacity of veggie feces to churn out TMAO is almost nonexistent. Instead of eating healthier, what about getting some vegan poop?

In a double-blind, randomized, controlled trial, research subjects either got vegan poop or their own poop back through a hose snaked down their nose, and it didn’t work.

First of all, the vegans recruited for the study started out making TMAO themselves, in contrast to the other study, where they didn’t make any at all. This may be because the earlier study required the vegans to have been vegan for at least a year, and this study didn’t. So, there wasn’t much of a change in TMAO running through their bodies two weeks after getting the vegan poop, but the vegan poop they got seemed to start out with some capacity to produce TMAO in the first place.

So, the failure to improve after the vegan fecal transplant “could be related to limited baseline microbiome differences and continuation of an omnivorous diet” after the vegan-donor transplant. What’s the point of trying to reset your microbiome if you’re just going to eat meat? Well, the researchers didn’t want to switch people to a plant-based diet since they knew that alone can change our microbiome, and they didn’t want to introduce any extra factors. The bottom line is that it seems there may not be any shortcuts. We may just have to eat a healthier diet.

Doctor’s Note

Want to become a donor? Find out How to Become a Fecal Transplant Super Donor.

For more on TMAO, check out related posts below. 

See the microbiome topic page for even more.

In recent years, mold has been blamed for all sorts of “vague and subjective” symptoms, but we have little scientific evidence that mold should be implicated. However, this “concept of toxic mold syndrome has permeated the public consciousness,” perpetuated by disreputable predatory practices of those making money testing homes for mold spores or testing people’s urine or blood. But all these tests are said to “further propagate misinformation and inflict unnecessary and often exorbitant costs on patients desperate for a clinical diagnosis, right or wrong, for their constellation of maladies…The continued belief in this myth is perpetuated by those charlatans who believe that measles vaccines cause autism, that homeopathy works, that fluoride in the water should be removed….”

Mold toxin contamination of food, however, has emerged as a legitimate issue of serious concern, and mycotoxins are perhaps even more important than other contaminants that might make their way into the food supply. Hundreds of different types have been identified, but only one has been classified as a known human carcinogen, and that’s aflatoxin. The ochratoxin I’ve previously discussed is a possible human carcinogen, but we know aflatoxin causes cancer in human beings. In fact, aflatoxins are amongst the most powerful known carcinogens.

It has been estimated that about a fifth of all liver cancer cases may be attributable to aflatoxins. “Since liver cancer is the third-leading cause of cancer deaths worldwide, and mortality rapidly follows diagnosis, the contribution of aflatoxins to this deadly cancer is significant.” And once aflatoxin makes it into the food, there is almost nothing we can do to remove it. Cooking, for example, doesn’t help. Indeed, as shown below and at 1:50 in my video Should We Be Concerned About Aflatoxin?, once it makes it into crops or into the meat, dairy, and eggs from animals consuming those crops, it’s too late. So, we have to prevent contamination in the first place, which is what we’ve been doing for decades in the United States. Because of government regulations, “companies in developed countries…are ‘always sampling’ for aflatoxin,” resulting in nearly $1 billion in losses every year. That may get even worse if climate change exacerbates aflatoxin contamination in the Midwest Corn Belt.

So, on a consumer level, it is more of a public health problem in the less industrialized world, such as in African countries, where conditions are ripe and farmers can’t afford to throw away $1 billion in contaminated crops. Aflatoxin remains a public health threat in Africa, Southeast Asia, and rural China, affecting more than half of humanity. This explains why the prevalence of liver cancer in those areas may be 30 times higher, yet it is not a major problem in the United States or Europe.

Only about 1% of Americans have detectable levels of aflatoxins in their bloodstream. Why not 0%? The U.S. Food and Drug Administration works to ensure that levels of exposure to these toxins are kept as low as practical, not as low as possible. In California, for instance, there has been an increase in “unacceptable aflatoxin levels” in pistachios, almonds, and figs. Unacceptable in Europe, that is, so it affects our ability to export, but not necessarily unacceptable for U.S. consumers, as we allow twice as much aflatoxin contamination.

Figs are unique since they’re “allowed to fully ripen and semidry on the tree.” This makes them “particularly susceptible to aflatoxin production.” It would be interesting to know about the fig-consuming habits of the 1% of Americans who were positive for the toxin. If figs were to blame, I’d encourage people to diversify their dried fruit consumption, but nuts are so good for us that we really want to keep them in our diets. The cardiovascular health benefits we get from nuts outweigh their carcinogenic effects; nut consumption prevents thousands of strokes and heart attacks for every one case of liver cancer. “Thus, the population health benefits provided by increased nut consumption clearly outweigh the risks associated with increased aflatoxin B1 exposure.”

So, we’re left with aflatoxin being mostly a problem in the developing world, and, because of that, it “remains a largely and rather shamefully ignored global health issue….” Where attention has been paid, it has been largely driven by the need to meet stringent import regulations on mycotoxin contamination in the richer nations of the world, rather than to protect the billions of people exposed on a daily basis.

Doctor’s Note

This is the last video in a four-part series on mold toxins. If you missed the others, check the related posts below. 

Ochratoxin has been described as toxic to the immune system, developing fetus, kidneys, and nervous system, as well as being carcinogenic, but that is in animal studies. Ochratoxin “causes kidney toxicity in certain animal species, but there is little documented evidence of adverse effects in humans.” That’s why it’s only considered a possible human carcinogen.

Big Ag assures that current ochratoxin levels are safe, even among those who eat a lot of contaminated foods. The worst-case scenario may be young children eating a lot of oat-based cereals, but, even then, “their lifetime cancer risk is negligible.” Individuals arguing against regulatory standards suggest we can eat more than 42 cups of oatmeal a day and not worry about it. Where do they get these kinds of estimates?

They determine the so-called benchmark dose in animals—the dose of the toxin that gives a 10% increase in pathology—then, because one would want to err on the side of caution, divide that dose by 500 as a kind of safety fudge factor to develop the tolerable daily intake. For cancer risk, you can find the tumor dose—the dose that increases tumor incidence in lab animals by 5%—and extrapolate down to the ”negligible cancer risk intake,” effectively incorporating a 5,000-fold safety factor, as seen below and at 1:28 in my video Should We Be Concerned About the Effects of Ochratoxin?.

It seems kind of arbitrary, right? But what else are you going to do? You can’t just intentionally feed people the stuff and see what happens—but people eat it regularly. Can we just follow people and their diets over time and see if those who eat more whole grains, like oats, for example, are more likely to have cancer or live shorter lives?

What is the association between whole grain intake and all-cause, cardiovascular, and cancer mortality? Every additional ounce of whole grains eaten a day is associated with not only a lower risk for cancer mortality but also a lower risk of dying from all causes put together. Below and at 2:05 in my video are findings from all the big cancer studies. Every single one trended towards lower cancer risk.

The bottom line is that you don’t find adverse effects confirmed in these population studies. This is not to say ochratoxin is necessarily harmless, but “any such risk does not outweigh the known benefits of wholegrain consumption.” In fact, healthy constituents of the whole grains themselves, like their antioxidants, may directly reduce the impacts of mycotoxins by protecting cells from damage. So, eating lots of fruits and vegetables may also help. Either way, “an overall healthy diet can play a significant role in mitigating the risk of contaminants in grain.”

In summary, healthy foods like whole grains are good, but just not as good as they could be because of ochratoxin, whereas less healthful foods, like wine and pork, are worse because of the mycotoxin, as shown below and at 2:52 in my video. Ochratoxin was detected, for example, in 44% of tested pork.

Doctor’s Note

This is the third video in a four-part series on mold toxins. If you missed the first two, see Ochratoxin in Breakfast Cereals and Friday Favorites: Ochratoxin and Breakfast Cereals, Herbs, Spices, and Wine.

Should We Be Concerned About Aflatoxin? is coming up next.

Whether you’re preparing for julbord (Swedish Christmas table), holiday gatherings, or just needing a cozy energy booster, this winter panjeeri fuses authentic Pakistani flavors with Scandinavian touches like lingonberries or filmjölk. It’s nutrient-dense, anti-inflammatory, and incredibly easy to make!

Why Panjeeri is Perfect for Winter (Health Benefits)

In Pakistan, panjeeri is a staple winter sweet and postpartum tonic, loaded with:

• Healthy fats from nuts and seeds for sustained energy
• Anti-inflammatory spices like ginger, cardamom, and turmeric to fight colds
• Iron and protein for immunity during dark months
• Natural sweeteners like jaggery for blood sugar stability

This low-oil panjeeri version uses minimal fat (dry roasting where possible) while keeping all the flavor. It’s vegan-adaptable, gluten-free (with oat flour), and a great alternative to sugary holiday treats.

Perfect for Swedish julmys (Christmas coziness) or as a healthy snack in the US/UK!

Ingredients (Makes about 10-12 servings)

• 1 cup whole wheat flour (atta) – or oat flour for gluten-free
• ½ cup almonds, roughly chopped
• ½ cup mixed nuts (cashews, walnuts, pistachios)
• ¼ cup edible gum (gond/gondh) – optional for extra crunch
• ¼ cup mixed seeds (pumpkin seeds, flaxseeds – a Swedish superfood boost!)
• 2 tbsp shredded dry coconut
• 1 tsp ground dry ginger (sonth)
• ½ tsp ground cardamom (kardemumma)
• ¼ tsp ground cinnamon (kanel)
• Pinch of nutmeg
• 2-3 tbsp olive oil or coconut oil (minimal for low-oil)
• Sweetener: ½ cup grated jaggery (gur) or honey to taste

Swedish Fusion Twists:

• Add ¼ cup dried lingonberries or cranberries for tartness
• Stir in a handful of dried blueberries for Nordic flair

Step-by-Step Instructions

1. Dry Roast the Flour: In a heavy-bottom pan on low heat, roast the whole wheat flour for 10-15 minutes until it turns golden and releases a nutty aroma. Stir constantly – no oil needed here!
2. Roast Nuts & Seeds: In the same pan, lightly roast the chopped nuts, seeds, and coconut until fragrant (5-7 minutes). Set aside.
3. Fry the Gond (Optional): Heat 1 tbsp oil and fry the edible gum until it puffs up like popcorn. Remove and crush lightly.
4. Bloom Spices: Add remaining oil to the pan, then stir in ground ginger, cardamom, cinnamon, and nutmeg for 30 seconds.
5. Combine Everything: Turn off heat. Mix in the roasted flour, nuts, seeds, gond, and grated jaggery. Stir well until the jaggery melts and coats everything evenly.
6. Cool & Store: Let it cool completely, then store in an airtight jar. It stays fresh for weeks!

Serving Ideas:

• Enjoy warm with a glass of milk or chai
• Top with Swedish filmjölk or yogurt for breakfast
• Sprinkle over oatmeal for a fusion twist
• Gift jars for holiday presents!

Oats can be thought of as “uniquely nutritious.” One route by which they improve human health is by providing prebiotics that “increase the growth of beneficial gut microbiota.” There are all manner of oats, ranging from steel-cut oats to, even better, intact oat groats (their form before being cut), all the way down to highly processed cereals, like Honey Nut Cheerios.

“Rolling crushes the grain, which may disrupt cell walls and damage starch granules, making them more available for digestion.” This is bad because we want the starch to make it all the way down to our colon to feed our good gut bacteria. Grinding oats into oat flour to make breakfast cereals is even worse. When you compare blood sugar and insulin responses, you can see significantly lower spikes with the more intact steel-cut oats, as shown below and at 0:54 in my video Ochratoxin in Certain Herbs, Spices, and Wine.

What about ochratoxin? As seen here and at 1:01 in my video, oats are the leading source of dietary exposure to this mold contaminant, but they aren’t the only source.

There is a global contamination of food crops with mycotoxins, with some experts estimating as much as 25% of the world’s crops being affected. That statistic is attributed to the Food and Agriculture Organization of the United Nations, but it turns out the stat is bogus. It isn’t 25%. Instead, it may be more like 60% to 80%. “The high occurrence is likely explained by a combination of the improved sensitivity of analytical [testing] methods and the impact of climate change.”

Spices have been found to have some of the highest concentrations of mycotoxins, but because they are ingested in such small quantities, they aren’t considered to be a significant source. We can certainly do our part to minimize our risk, though. For instance, we should keep spices dry after opening sealed containers or packages.

What about dried herbs? In “Mycotoxins in Plant-Based Dietary Supplements: Hidden Health Risk for Consumers,” researchers found that milk thistle–based supplements had the highest mycotoxin concentrations. It turns out that humid, wet weather is needed during milk thistle harvest, which is evidently why they get so moldy. “Considering the fact that milk thistle preparations are mainly used by people who suffer from liver disease,” such a high intake of compounds toxic to the liver may present some concern.

Wine sourced from the United States also appears to have particularly high levels. In fact, the single highest level found to date around the world is in a U.S. wine, but there’s contamination in wine in general. In fact, some suggest that’s why we see such consistent levels in people’s blood—perhaps because a lot of people are regular wine drinkers.

Ochratoxin is said to be a kidney toxin with immunosuppressive, birth defect–causing, and carcinogenic properties. So, what about ochratoxin decontamination in wine? That is, removing the toxin? Ideally, we’d try to prevent the contamination in the first place, but since this isn’t always practical, there is increased focus on finding effective methods of detoxification of mycotoxins already present in foods. This is where yeast enters as “a promising and friendly solution,” because the mycotoxins bind to the yeast cell wall. The thought is that we could strain out the yeast. Another approach is to eat something like nutritional yeast to prevent the absorption.

It works in chickens. Give yeast along with aflatoxin (another mycotoxin), and the severity of the resulting disease is diminished. However, using something like nutritional yeast as a binder “depends on stability of the yeast-mycotoxin complex through the passage of the gastrointestinal tract.” We know yeasts can remove ochratoxin in foods, but we didn’t have a clue if it would work in the gut until 2016. Yeast was found to bind up to 44% of the ochratoxin, but, in actuality, it was probably closer to only about a third, since some of the bindings weren’t stable. So, if you’re trying to stay under the maximum daily intake and you drink a single glass of wine, even if your bar snack is popcorn seasoned with nutritional yeast, you’d still probably exceed the tolerable intake. But what does that mean? How bad is this ochratoxin? We’ll find out next.

Doctor’s Note

This is the second video in a four-part series on mold toxins. The first one was Ochratoxin in Breakfast Cereals.

Stay tuned for Should We Be Concerned About the Effects of Ochratoxin? and Should We Be Concerned About Aflatoxin?. You can also check: Friday Favorites: Should We Be Concerned About Ochratoxin and Aflatoxin?.

Along with fever, decreased food consumption is one of the most common signs of infection. Often regarded as an undesirable manifestation of sickness, it’s actually an active, beneficial defense mechanism. As I discuss in my video Fasting for Cancer: What about Cachexia, chronic under-nutrition can impair our defenses, but data suggest that, in the short-term, immune function can be enhanced by lowering food intake.

Researchers have shown that the blood from starved mice was nearly eight times better at killing off the invading bacteria in a petri dish, dramatically boosting the capacity of their white blood cells to kill off the pathogens. What about people? And what about cancer?

Does Fasting Help Our Natural Killer Cells Fight Cancer Cells?

When study participants fasted for two weeks on an 80-calorie-a-day diet, not only did their white blood cells show the same kind of boost in bacteria-killing ability and antibody production, but their natural killer cell activity increased by an average of 24%. This is especially interesting because our natural killer cells don’t just help clear infections, but they also kill cancer cells. In fact, that’s how the researchers measured natural killer cell activity; they pitted them against K562 cells, which are human leukemia cells.

Fasting is said to improve anticancer immunosurveillance, or, more poetically, by “stimulating the appetite of the immune system for cancer.” So, why isn’t fasting used more to treat cancer? Because so much about cancer care revolves around keeping people’s weight up to try to counteract the cancer-wasting syndrome.

What Causes Cancer Cachexia?

Until recently, fasting therapy was not considered to be a treatment option in cancer, related to the fact that a common therapeutic goal in palliative cancer treatment is to avoid weight loss and counteract the wasting syndrome known as cachexia, which is the ultimate cause of death in many cancer cases.

Tumors are voracious, rapidly expanding and in need of a lot of energy and protein, so cancer metabolically reprograms the body to start breaking down to feed its tumors. It does this by triggering inflammation throughout the body. It’s not just that people lose their appetite. “The fundamental difference between the weight loss observed in CC [cancer cachexia] and that seen in simple starvation is the lack of reversibility with feeding alone.”

Therapeutic nutritional interventions to correct or reverse cachexia frequently fail. The best treatment for cancer cachexia, therefore, is to treat the cause and cure the cancer. In fact, maybe forcing extra nutrition on cancer patients could be playing right into the tumor’s hands. Like in pregnancy when the fetus gets first dibs on nutrients even at the mother’s expense, the tumor may be first in the feeding line. Maybe our loss of appetite when we get cancer is even a protective response.

Is Chemotherapy Enough?

As I discuss in my video Fasting Before and After Chemotherapy and Radiation, for the past 50 years, chemotherapy has been a major medical treatment for a wide range of cancers. Its main strategy has been largely based on targeting cancer cells, by means of DNA damage caused in part by the production of free radicals. Although these drugs were first believed to be very selective for tumor cells, we eventually learned that normal cells also experience severe chemotherapy-dependent damage, which can lead to dose-limiting side effects, including bone marrow and immune system suppression, fatigue, vomiting, diarrhea, and in some cases, even death.

If you do survive chemotherapy, the DNA damage to normal cells can even lead to new cancers down the road. There are cell-protecting drugs that have been tried to reduce the side effects so you can pump in higher chemo doses, but these drugs have not been shown to increase survival––in part because they may also be protecting the cancer cells. What about instead fasting for cellular protection during cancer treatment?

Fasting and Chemotherapy

Many may not recognize the role fasting can play in cancer prevention and treatment. Short-term fasting before and immediately after chemotherapy may minimize side effects, while, at the same time, it may actually make cancer cells more sensitive to treatment. That’s exciting! 

During deprivation, healthy cells switch from growth to maintenance and repair, but tumor cells are unable to slow down their unbridled growth, due to growth-promoting mutations that led them to become cancer cells in the first place. This inability to adapt to starvation may represent an important Achilles’ heel for many types of cancer cells.

As a consequence of these differential responses of healthy cells versus cancer cells to short-term fasting, chemotherapy causes more DNA damage and cell suicide in tumor cells, while potentially leaving healthy cells unharmed. Thus, short-term fasting may protect healthy cells against the toxic assault of chemotherapy and cause tumor cells to be more sensitive––or at least that’s the theory.

Researchers found that, in rodents, fasting alone appears to work as well as chemotherapy. What’s more, unbridled tumor growth was also knocked down by radiation therapy—and even more so after the combination of radiation and alternate-day fasting. However, alternate-day fasting alone seemed to do as well as radiation. These data are exciting, but for mice with breast cancer. What about people?

Fasting Put to the Test Against Cancers

As I discuss in my video Fasting Before and After Chemotherapy Put to the Test, several patients diagnosed with a wide variety of cancers elected to undertake fasting prior to chemotherapy and share their experiences. They reported a reduction in fatigue, weakness, and gastrointestinal side effects while fasting and felt better across the board, with zero vomiting. The weight lost during the few days of fasting was quickly recovered by most of the patients and did not lead to any discernable harm. So, overall, fasting under care seems safe and potentially able to ameliorate side effects.

In a randomized clinical study, breast and ovarian cancer patients fasted from 36 hours before chemotherapy until 24 hours after, and fasting did appear to improve quality of life and fatigue. However, another study found no such beneficial effects. There did appear to perhaps be less bone marrow toxicity, given the higher counts of red blood cells and platelet-making cells. But no benefit when it came to saving white blood cells—the immune system cells—so that was a disappointment. Perhaps they didn’t fast long enough?

A systematic review of 22 studies found that, overall, fasting may not only reduce chemotherapy side effects (like organ damage, immune suppression, and chemotherapy-induced death), but it may also suppress tumor progression, including tumor growth and metastasis, resulting in improved survival. But, nearly all the studies were on mice and dogs. The studies on humans were limited to evaluating safety and side effects. The tumor-suppression effects of fasting––for example, its influence on tumor growth, metastasis and prognosis––sadly, were not evaluated.

Does Fasting Make Chemo More Effective?

As I discuss in my video Fasting-Mimicking Diet Before and After Chemotherapy, short-term food withdrawal during chemotherapy may begin to solve the long-standing problem with most cancer treatments: how to kill the tumor without killing the patient. Short-term fasting––for example, for 48 hours before chemo and 24 hours afterwards––may reduce side effects, so-called “chemotherapy-induced toxicity.” However, the potential tumor-suppressing effects of fasting have still not been thoroughly evaluated.

Some argue that reducing chemo’s side effects alone could improve efficacy, since patients could withstand higher doses. For example, the heart and kidney damage associated with the widely prescribed anti-cancer drugs limit their full therapeutic potential. It’s not clear, though, that maximizing the tolerated chemo dose would achieve longer survival or better quality of life. For now, I think we should just be satisfied with the fewer side effects for fewer side effects’ sake.

How Does Fasting Work?

Fasting can reduce the levels of insulin-like growth factor-1 (IGF-1), a cancer-promoting growth hormone. The reduced levels of IGF-1 mediate the differential protection of normal cells and cancer cells in response to fasting and improve chemo’s ability to kill cancer but spare normal cells.

So, reducing IGF-1 signaling may provide dual benefits by protecting normal tissues while reducing tumor progression. It may even help prevent the cancer in the first place. But fasting isn’t the only way to drop IGF-1 levels: A few days of fasting can cut levels in half, but that’s largely because protein intake is being cut. Protein is a key determinant of circulating IGF-1 levels in humans––suggesting that “reduced protein intake may become an important component of anticancer and antiaging dietary interventions,” particularly a reduction in animal protein.

Lowering Protein Intake to Lower IGF-1

If you compare those who eat strictly plant-based diets and get about the recommended daily intake of protein (0.8 grams per kg of body weight) to individuals who are just as slender but consume the higher amount of protein more typical to Americans, going on a calorie-restricted diet may lower IGF-1 a little, but eating a plant-based diet can lower it even more than going low calorie. 

So, not only may a diet centered around whole plant foods down-regulate IGF-1 activity, potentially slowing the aging process, but it may be a way of turning anti-aging genes against cancer.

In France, exposure to dietary contaminants was compared between vegetarians and meat-eaters, and the results showed that exposures to persistent organic pollutants like PCBs and dioxins were dramatically lower among those eating more plant-based foods. This was due to their avoidance of foods of animal origin, though they did have higher estimated exposure to some mycotoxins, fungal toxins present in moldy food.

There are many types of mold on the planet, possibly millions, and the vast majority are harmless. However, over the last several years, certain mold toxins, such as aflatoxin and ochratoxin, have been popping up in breakfast cereals. Hundreds of samples were taken off store shelves, and about half were found to be contaminated with ochratoxin, but those store shelves were in Pakistan, which has a sub-tropical climate with monsoons and flash floods, leading to fungal propagation. Similar results have since popped up in Europe, in Serbia, for instance. They’ve also been found in Spain and seen in Portugal. Then, mycotoxins were discovered in breakfast cereals in Canada. What about breakfast cereals sold in the United States?

Researchers collected 144 samples and, similar to other countries, found that about half contained ochratoxin, but only about 7% exceeded the maximum limit established by the European Commission. What is the significance of finding ochratoxin in U.S. breakfast cereals? In the largest study to date, which included nearly 500 samples of cereal off store shelves across the United States, overall detection rates were about 40%, though only 16 of the samples violated the European standards. All the cereals with ochratoxin were oat-based; however, about 1 in 13 of the oat-based cereal samples tested were contaminated.

Ochratoxin has become increasingly regulated by many countries to minimize chronic exposure. Shown below and at 2:23 in my video Ochratoxin in Breakfast Cereals are the current regulations for mycotoxins in cereal-based baby foods, for example, worldwide.

Some countries are very strict, like in the European Union; other countries are less so, and one country in particular has no standards at all. Ochratoxin is not currently regulated at all in the United States.

What about sticking to organic products? One might expect them to be worse due to the fact that fungicides are not allowed in organic production. However, “mycotoxin concentrations are usually similar or reduced in organic compared with conventional products.” For example, in one of the breakfast cereal studies, researchers found similar contamination, and the same was found for infant foods. It cannot be concluded that organic is better than conventional from a mycotoxin perspective. “Despite no use of fungicides, an organic system appears generally able to maintain mycotoxin contamination at low levels.” But how much is that saying, given how widespread it is? How concerned should we be about the public health effects from “long-term exposure to this potent mycotoxin”?

If you look at blood samples taken from populations going back decades, sometimes 100% of people turn up positive for ochratoxin circulating in their bloodstream. In some sense, mycotoxins “are unavoidable contaminants of food,” since they are not easy to detect and many of them can remain hidden. And, once foods have become contaminated, mycotoxins aren’t destroyed by cooking. So, are there some foods we should simply try to avoid due to a higher risk of contamination? That’s exactly the question I’m going to address next.

Doctor’s Note

This is the first video in a four-part series on mold toxins. Check related posts below for the other three.

Hello from Pakistan! We may know sun, but we master warmth from within. As darkness falls and the craving for authentic  vintermat grows, let us introduce you to a new kitchen ritual. This isn’t just a stew; it’s a culinary hug that turns simplepalsternacka, morot, and potatis  into an aromatic journey. Welcome to your new favorite vegetarisk gryta or köttgryta med twist.

Why This Fusion is Your Best Winter Investment

Swedish rotfrukter are nature’s perfect winter pantry. Pakistani spices like turmeric (gurkmeja), cumin (spiskummin), and cinnamon (kanel) are ancient tools for warmth and wellness. Together in a single en gryta, they create a nyttig gryta that is deeply satisfying. This is hemmakok meets global adventure — a true fusion recept for the curious cook.

Recipe 1: Vinter Dahl – Your New Favorite Rotfruktsgryta (Vegetarisk)

This linsgryta med rotfrukter is aklimatsmart powerhouse: vegan, packed with protein , and effortlessly delicious.

For this enkla gryta, you need:

• 3 cups Swedish rotfrukter (diced carrots/morot, parsnips/palsternacka, potatoes/potatis)
• 1.5 cups röda linser (red lentils)
• 1 large onion, 3 garlic cloves, 1 tbsp fresh ginger
• The Spice Mix: 2 tsp turmeric (gurkmeja), 2 tsp cumin (spiskummin), 1 tsp coriander, ½ tsp cinnamon (kanel).
• 1.5L vegetable broth, 2 tbsp tomato puree (tomatpuré)
• Butter (smör) or oil, salt, pepper (peppar)
• To serve: A dollop of gräddfil and fresh herbs.

Så här gör du (The Method):

1. In your largest pot, sauté the onion in smör until soft.
2. Add garlic, ginger, and all spices. Stir for 60 seconds until fragrant—this “blooms” them.
3. Add the rotfrukter and rinsed röda linser. Stir to coat.
4. Pour in broth and tomato puree. Bring to a boil, then lower heat.
5. Cover and let simmer for 35-40 minutes (långkok) until tender.
6. Season. Serve with gräddfil for the perfect cozy bowl.

This vegetarisk gryta vinter is perfect for meal prep and makes a wonderful enkel middag.

Recipe 2: Punjabi Potatis Pytt – A Kryddig Köttgryta

Think of this as a köttgryta with a soulful Pakistani twist. It’s a mättande and deeply flavorful one-pot meal.

Ingredients for this kryddig gryta:

• 500g köttfärs (minced beef/lamb) or grytbitar.
• 4-5 potatoes/potatis, 2-3 carrots/morot (in chunks).
• 1 onion, roughly chopped.
• Spice Blend: 1 tbsp garam masala, 1 tsp smoked paprika, 2 tsp cumin.
• 1 can (400g) krossade tomater (crushed tomatoes).
• 1 cup water or broth. A handful of russin (raisins).
• Butter/oil, salt, pepper.

The enkel Method:

1. Brown the kött in your pot. Remove and set aside.
2. In the same pot, sear the potato and carrot chunks until golden.
3. Add onion and the spice blend. Stir well.
4. Return the meat. Add krossade tomater and water.
5. Cover and simmer on low (långkok) for 45-50 minutes.
6. Stir in russin at the end for a sweet contrast.

How To Make YOUR Recipe Go Viral in Sweden (Your Organic Reach Toolkit)

Since you found this, please help a Pakistani kitchen share warmth with Sweden! Engagement is our only SEO. Here’s how you can join the movement:

1. THE CHALLENGE: #MinRotfruktChallenge 

   • Do this: Cook the recipe. Post your photo/video and ask your followers: “Vilken svensk rotfrukt ska jag krydda näst? Ge mig ett pakistanskt krydda att testa!” (Which Swedish root veg should I spice next? Give me one Pakistani spice to try!)

   • Tag us: @NutricFoodShow & use #MinRotfruktChallenge. We will share every single post and declare a weekly winner!

2. The “Hygge vs. Hug” Debate:

   • In your post, ask: “Är det här gryta svensk hygge eller ett pakistanskt kram? Diskutera.” (Is this stew Swedish hygge or a Pakistani hug? Discuss.) This prompts comments and shares.

3. Practical Swedish Sharing Hooks:

   • Frame it practically: Title your social post: “Sparad: En enkel gryta som gör 4 portioner och värmar hela kvällen.” (Saved: An easy stew that makes 4 portions and warms the whole evening.)

   • Appeal to values: Call it “Den perfekta klimatsmarta och mättande vintermiddagen.”

4. Collaborate Micro-Influencers:

   • Find Swedish food bloggers focused on enkel matlagning, vintermat, or vegetarisk. Offer them the recipe to try. A single feature on a Swedish matblogg can drive massive traffic.

By cooking, sharing, and tagging, you’re not just making dinner—you’re helping build a delicious bridge between our kitchens. Tack för att du hjälper till!

If you search for heavy metal in the National Library of Medicine database, most of what you find is on heavy metal contamination in fish, which “makes it difficult to establish clearly the role of fish consumption on a healthy diet” and perhaps helps to explain the quintupling of odds of autoimmune diseases, such as juvenile arthritis. But searching for the hazards of heavy metal also pops up entries on the “risks from heavy metal music.” In this study, researchers were talking about traumatic injuries from slamming around “during a moshing session,” but you’re more likely to get injured at an alternative rock concert. (Check out some of the artists below and at 0:50 in my video The Dangerous Effects of Heavy Metal Music.)

Certainly, music-induced hearing loss is a serious problem, but that can result from any loud music. Clinical recommendations include the “80–90 rule”—no more than 80% of the maximum volume on personal listening devices for no more than 90 minutes a day. That’s not what the science shows, however. “Do not exceed 60% of the maximum volume” may be more evidence-based, but researchers figure teens would just ignore that, so they came up with more “acceptable” advice.

I assumed I’d see a lot of satanic panic nonsense from the 1980s, when “parents bereaved by suicide…accused Heavy Metal groups of promoting suicidal behaviours and…proceeded to sue musicians.” What kind of evidence did the parents present? There has been “little scholarly research” published until the “The Heavy Metal Subculture and Suicide” paper that tried to correlate the number of statewide heavy metal magazine subscriptions to youth suicide rates. Seriously?

It got really wild, though, when researchers called psychiatric institutions, pretending to be parents worried because their son started listening to heavy metal music, even though they made it clear that their son didn’t exhibit any symptoms of mental illness, didn’t do drugs or drink alcohol, and was doing fine at school. Ten of the twelve facilities believed the son required psychiatric hospitalization. Imagine what that would do to a kid! Researchers found that, decades later, metalheads “were significantly happier in their youth and better adjusted” than their peers.

Some studies were strange. Do Parkinson’s patients walk better listening to The Beatles’ “Yellow Submarine” or Metallica’s “Master of Puppets”? (See below and at 2:32 in my video.)

Others were pretty nondescript. Heavy metal musicians exhibit a higher heart rate than those performing “contemporary Christian,” which isn’t so surprising, as you can see  here and at 2:40.

Some others were kind of cute, like one that investigated the influence of music on promoting patient safety during surgery—veterinary patients, that is. Kittens got spayed with little earphones on their heads. It turns out that “Adagio for Strings” may be more relaxing than AC/DC.

A review on music therapy for human patients warned: “Caution should be exercised…when guiding patients in selecting their music. ‘Chaotic music, such us [sic] hip-hop and metal, is not healing to human cells.’” That even had three citations, though two of them don’t say anything and the third is a nursing newsletter merely quoting someone’s opinion. I did some digging, and it turns out that stomach cancer cells like metal. If you play them Cannibal Corpse versus Beethoven, 12 hours of death metal increases their growth in a petri dish, as you can see below and at 3:28 in my video. (That’s so metal.)

But who puts headphones on their stomach? Or their chests, for that matter? In one study, Mozart killed off one type of breast cancer cell line but not another; in another study, only Beethoven’s 5th Symphony seemed to work, and Mozart flopped when the petri dishes were surrounded by speakers. How does this stuff even get published?

Anyway, the true danger from heavy metal is headbanging. “Headbanging is a contemporary dance form consisting of abrupt flexion–extension movements of the head to the rhythm of rock music, most commonly seen in the heavy metal genre.” Although the “number of avid aficionados is unknown…some fans might be endangered by indulging excessive headbanging.” Despite headbanging generally being “considered harmless,” several health complications have been attributed to this practice, including ripping your carotid artery, rupturing your lung, whiplash injury, neck fracture, or subdural hematoma. One man reported headbanging at a Motörhead concert, and all that “brisk forward and backward acceleration and deceleration forces” might have ruptured his bridging veins and caused him to bleed into his skull.

As shown here and at 4:47 in my video, bridging veins bridge the gap between the brain and the covering that lines the inside of our skull, and if the veins tear, blood can build up under our skull and compress our brain.

This bridging vein rupture has been demonstrated on headbanging cadavers (another very metal study). See below and at 5:02 in my video. It’s been likened to a “pseudo shaken-baby syndrome” in adults.

The researchers conclude that their “case serves as evidence in support of Motörhead’s reputation as one of the most hardcore rock’n’roll acts on earth,” but I think the real takeaway is that a potentially dangerous complication like subdural hematoma can result from “a seemingly benign activity like head banging.” And some of the brain bleeds can be massive. One man complained of a “headache after headbanging at a party.” Why? As you can see in his CT scan below and at 5:35, circled in red is all blood, squishing over his brain. Amazingly, he survived; another man didn’t, headbanging and losing his life to a fatal subdural hemorrhage.

We can tear more than just veins. There are two sets of arteries that tunnel into the skull—the carotid arteries in the front and the vertebral arteries in the back—and we can tear both sets. A 15-year-old boy “indulged in headbanging” and ripped his carotid artery, which led to a massive stroke. He presented as half-paralyzed and unable to speak, and he died in a coma within a week.

What about the vertebral arteries in the back? They’re wedged into our skull, rendering them susceptible to shearing forces from extremes of neck motion, and that’s exactly what appeared to happen when a heavy metal drummer tore the wall of the artery. All of this is really rare, probably afflicting less than one in a thousand or so. What can metalheads do to reduce their risk? “To prevent injury due to such head-banging, the range of head and neck motion should be reduced, slower-tempo music should replace heavy metal rock, the frequency of head-banging should be only on every second beat, or personal protective equipment should be used”—like a neck brace?

“Little formal injury research has been conducted on the worldwide phenomenon of head banging,” so researchers constructed “a theoretical head banging model” with enough physics terms to make any nerd happy: “angular displacement,” “sinusoidal motion in the sagittal plane,” and “amplitude of the displacement curve.” The study participants? Headbangers. The control group? That’s easy with easy listening music.

The head injury curves and neck injury curves, based on headbanging tempo and angular sweep, are shown below and at 7:23.

“An average head-banging song has a tempo of about 146 beats per minute, which is predicted to cause mild head injury when the range of motion is greater than 75º,” so something like what’s seen below and at 7:34 in my video.

The researchers conclude: “To minimise the risk of head and neck injury, head bangers should decrease their range of head and neck motion, head bang to slower tempo songs by replacing heavy metal with adult-oriented rock, only head bang to every second beat, or use personal protective equipment.”

“Unfortunately, it is difficult, if not impossible, to change the habits of heavy metal aficionados.” Maybe what we need are metal-studded neck braces.

Doctor’s Note

What about the healing potential of music? Check out Music as Medicine and Music for Anxiety: Mozart vs. Metal.

“A regular intake of mushrooms can make us healthier, fitter, and happier, and help us live longer,” but what is the evidence for all that? “Mushrooms are widely cited for their medicinal qualities, yet very few human intervention studies have been done using contemporary guidelines.”

There is a compound called lentinan, extracted from shiitake mushrooms. To get about an ounce, you have to distill around 400 pounds of shiitakes, about 2,000 cups of mushrooms. Researchers injected the compound into cancer patients to see what happens. The pooled response from a dozen small clinical trials found that the objective response rate was significantly improved when lentinan was added to chemotherapy regimens for lung cancer. “Objective response rate” means, for example, tumor shrinkage, but what we really care about is survival and quality of life. Does it actually make cancer patients live any longer or any better? Well, those in the lentinan group suffered less chemo-related toxicity to their gut and bone marrow, so that alone might be reason enough to use it. But what about improving survival?

I was excited to see that lentinan may significantly improve survival rates for a type of leukemia. Indeed, researchers found that adding lentinan to the standards of care increased average survival, reduced cachexia (cancer-associated muscle wasting), and improved cage-side health. Wait, what? This was improved survival for brown Norwegian rats, so that the so-called clinical benefit only applies if you’re a rat or a veterinarian.

A compilation of 17 actual human clinical studies did find improvements in one-year survival in advanced cancer patients but no significant difference in the likelihood of living out to two years. Even the compilations of studies that purport that lentinan offers a significant advantage in terms of survival are just talking about statistical significance. As you can see below and at 2:15 in my video White Button Mushrooms for Prostate Cancer, it’s hard to even tell these survival curves apart.

Lentinan improved survival by an average of 25 days. Now, 25 days is 25 days, but we “should evaluate assertions made by companies about the miraculous properties of medicinal mushrooms very critically.”

Lentinan has to be injected intravenously. What about mushroom extract supplements you can just take yourself? Researchers have noted that shiitake mushroom extract is available online for the treatment of prostate cancer for approximately $300 a month, so it’s got to be good, right? Men who regularly eat mushrooms do seem to be at lower risk for getting prostate cancer—and apparently not just because they eat less meat or consume more fruits and vegetables in general. So, why not give a shiitake mushroom extract a try? Because it doesn’t work. On its own, it is “ineffective in the treatment of clinical prostate cancer.” Researchers wrote that “the results demonstrate that claims for CAM [complementary and alternative medicine], particularly for herbal and food supplement remedies, can be easily and quickly tested.” Put something to the test? What a concept! Maybe it should be required before individuals spend large amounts of money on unproven treatments, or, in this case, a disproven treatment.

What about God’s mushroom (also known as the mushroom of life) or reishi mushrooms? “Conclusions: No significant anticancer effects were observed”—not even a single partial response. Are we overthinking it? Plain white button mushroom extracts can kill off prostate cancer cells, at least in a petri dish, but so could the fancy God’s mushroom, but that didn’t end up working in people. You don’t know if plain white button mushrooms work on real people until you put them to the test.

What I like about this study is that the researchers didn’t use a proprietary extract. They just used regular whole mushrooms, dried and powdered, the equivalent of a half cup to a cup and a half of fresh white button mushrooms a day, in other words, a totally doable amount. The researchers gave them to men with “biochemically recurrent prostate cancer”—the men had already gotten a prostatectomy or radiation in an attempt to cut or burn out all the cancer, but it returned and started growing, as evidenced by a rise in PSA levels, an indicator of prostate cancer progression.

Of the 26 patients who had gotten the button mushroom powder, 4 appeared to respond, meaning they got a drop in PSA levels by more than 50% after starting the mushrooms, as you can see here and at 4:31 in my video.

In the next graphic, below and at 4:22, you can see where the four men who responded started out in the months leading up to starting the mushrooms. Patient 2 (“Pt 2”) was my favorite. He had an exponential increase in PSA levels for a year, then he started some plain white mushrooms, and boom! His PSA level dropped to zero and stayed down. A similar response was seen with Patient 1. Patient 4 had a partial response, before his cancer took off again, and Patient 3 appeared to have a delayed partial response.

Now, in the majority of cases, PSA levels continued to rise, not dipping at all. But even if there is only a 1-in-18 chance you’ll be like Patients 1 and 2, seen below and at 5:12, you may get a prolonged, complete response that continues.

We aren’t talking about weighing the risks of some toxic chemotherapy for the small chance of benefit, but just eating some inexpensive, easy, tasty plain white mushrooms every day. Yes, the study didn’t have a control group, so it may have just been a coincidence, but rising PSAs in post-prostatectomy patients are almost always indicators of cancer progression. And, what’s the downside of adding white button mushrooms to your diet?

In these two patients, their PSA levels became undetectable, suggesting that the cancer disappeared altogether. They had already gone through surgery, had gotten their primary tumor removed, along with their entire prostate, and had already gone through radiation to try to clean up any cancer that remained, and yet the cancer appeared to be surging back—until, that is, they started a little plain mushroom powder.

Doctor’s Note

If you missed the previous blog, check out Medicinal Mushrooms for Cancer Survival.

Also check out Friday Favorites: Mushrooms for Prostate Cancer and Cancer Survival.

For more on mushrooms, see Breast Cancer vs. Mushrooms and Is It Safe to Eat Raw Mushrooms?.

For more videos on prostate cancer, check the related posts below. 

Can mushrooms be medicinal? Mushroom-based products make up a sizable chunk of the $50 billion supplement market. “This profitable trade provides a powerful incentive for companies to test the credulity of their customers and unsupported assertions have come to define the medical mushroom business.” For example, companies marketing herbal medicines “exploit references to studies on mice in their promotion of mushroom capsules and throat sprays for treating all kinds of ailments”—but we aren’t mice.

It wouldn’t be surprising if mushrooms had some potent properties. After all, fungi are where we’ve gotten a number of drugs, not the least of which is penicillin, as well as the cholesterol-lowering drug lovastatin and the powerful immunosuppressant drug cyclosporin. Still don’t think a little mushroom can have pharmacological effects? Don’t forget they can produce some of our most powerful poisons, too, like the toxic Carolina false morel that looks rather toadstooly, while others, as you can see here and at 1:15 in my video Medicinal Mushrooms for Cancer Survival, have a more angelic look like the destroying angel—that is its actual name—and as little as a single teaspoon can cause a lingering, painful death.

We should have respect for the pharmacological potential of mushrooms, but what can they do that’s good for us? Well, consuming shiitake mushrooms each day improves human immunity. Giving people just one or two dried shiitake mushrooms a day (about the weight-equivalent of five to ten fresh ones) for four weeks resulted in an increase in proliferation of gamma-delta T lymphocytes and doubled the proliferation of natural killer cells. Gamma-delta T cells act as a first line of immunological defense, and, even better, natural killer cells kill cancer. Shiitake mushrooms did all this while lowering markers of systemic inflammation.

Oyster mushroom extracts don’t seem to work as well, but what we care about is whether mushrooms can actually affect cancer outcomes. Shiitakes have yet to show a cancer survival benefit, but what about reishi mushrooms, which have been used as a cancer treatment throughout Asia for centuries?

What does the science say about reishi mushrooms for cancer treatment? A meta-analysis of five randomized controlled trials showed that patients who had been given reishi mushroom supplements along with chemotherapy and radiation were more likely to respond favorably,  compared to chemotherapy/radiotherapy on its own. Although adding a reishi mushroom extract improved tumor response rates, “the data failed to demonstrate a significant effect on tumour shrinkage when it was used alone,” without chemo and radiation. So, they aren’t recommended as a single treatment, but rather an adjunct treatment for patients with advanced cancer.

“Response rate” just means the tumor shrinks. Do reishi mushrooms actually improve survival or quality of life? We don’t have convincing data suggesting reishi mushroom products improve survival, but those randomized to reishi were found to have “a relatively better quality of life after treatment than those in the control group.” That’s a win as far as I’m concerned.

What about other mushrooms? Although whole shiitake mushrooms haven’t been put to the test for cancer yet, researchers have said that lentinan, a compound extracted from shiitakes, “completely inhibits” the growth of a certain kind of sarcoma in mice. But, in actuality, it only worked in one strain of mice and failed in nine others. So, are we more like the 90% of mouse strains in which it didn’t work? We need human trials—and we finally got them. There are data on nearly 10,000 cancer patients who have been treated with the shiitake mushroom extract injected right into their veins. What did the researchers find? We’ll find out next.

Doctor’s Note

Stay tuned for White Button Mushrooms for Prostate Cancer.

Also check out Friday Favorites: Mushrooms for Prostate Cancer and Cancer Survival.

For more on mushrooms, see Breast Cancer vs. Mushrooms and Is It Safe to Eat Raw Mushrooms?.

For more about Chef Lois, check out this interview.

“Navajo Nation President Jonathan Nez and First Lady Phefelia Nez have been vocal proponents of healthy eating. President Nez found that plant-based eating shortened his recovery time after long-distance runs and helps him to maintain his weight loss. First Lady Nez provided us with one of her family-favorite soup recipes that we modified. We used the modified version for a course called Native Food for Life Online, offered through the American Indian Institute (AII) and the Physicians Committee for Responsible Medicine (PCRM). Minestrone is its Italian name, but the ingredients in this soup originated in the Americas. Chef Walter Whitewater said that growing up on the Navajo Nation, he used to harvest wild onions, carrots, garlic, and spinach. With the addition of frozen corn, canned beans, and zucchini squash, as well as the pasta, all foods that most community members have on hand or receive as part of the Food Distribution Program on Indian Reservations (FDPIR), our version of this recipe is a favorite of Chef Walter. Serve with No Fry Frybread, No Fry Blue Corn Frybread, Homemade White Corn Tortillas, or Blue Corn Tortillas.” – Chef Lois Ellen Frank

Navajo Minestrone Soup

Ingredients Makes approximately 2 quarts 2 cups cooked whole-grain pasta, such as mini farfalle (bow-tie pasta), penne, or elbows (approx. 1 cup uncooked) 1 tablespoon bean juice or water 1 small yellow onion, diced (approx. 1 cup) 3 carrots, peeled, cut into ⅛-inch-thick sticks, and halved into half-moon slices (approx. 1 cup) 2 stalks celery, sliced (approx. 1 cup) ½ cup frozen sweet corn kernels 1 tablespoon roasted garlic  1 zucchini, cut into ½-inch cubes (approx. 1 cup) 1 (15 oz.) can diced tomatoes, organic and no salt added, if possible 2 tablespoons tomato paste 1 cup spinach, fresh or frozen 5 cups water 1 (15 oz.) can dark red kidney beans, drained and rinsed (approx. 1½ cups) 1 (15 oz.) can pinto beans, drained and rinsed (approx. 1½ cups) 1 tablespoon fresh basil, finely chopped ½ teaspoon fresh oregano, finely chopped ½ teaspoon fresh thyme, finely chopped 2 teaspoons New Mexico red chile powder, mild 1 tablespoon flat leaf parsley, finely chopped ¼ teaspoon black pepper, or to taste (optional)

Instructions

In a large, cook the pasta according to the package directions. Remove from heat, drain the cooking water, rinse with cold water to stop the pasta from cooking, and set aside.

In a separate soup pot, heat the bean juice over medium-high heat until hot but not smoking. Sauté the onion for approximately 4 minutes, stirring occasionally to prevent burning. Add the carrots and the celery, and cook for an additional 5 to 6 minutes, stirring but letting the vegetables begin to caramelize. Add the corn and cook for another 2 minutes, stirring once to prevent burning. Add the roasted garlic and cook for another minute, stirring constantly to mix the garlic into the other ingredients. (The bottom of your pan will turn brown, and the vegetables should begin to caramelize.) Add the zucchini and cook for another 3 minutes, stirring to prevent burning. Add the diced tomatoes and tomato paste, stirring to completely mix into the other vegetables and deglaze the bottom of the pan. Add the spinach and water and bring to a boil. Then cover, reduce the heat to medium low, and let simmer, covered, for 10 minutes, stirring once or twice.

Add the canned kidney and pinto beans, stirring them to blend with all the ingredients, then add the basil, oregano, thyme, red chile powder, flat leaf parsley, and black pepper, if using. Return to a boil, then reduce the heat and let simmer for another 10 minutes.

Taste, season with more of any of the spices, if desired. Add the cooked pasta, stir, and bring to a boil. Cook for an additional 1 to 2 minutes until the soup is completely hot. (Do not cook the soup too long, as the cooked pasta may become overcooked.) Remove from heat. Serve.

Recipe adapted from Seed to Plate, Soil to Sky: Modern Plant-Based Recipes Using Native American Ingredients by Lois Ellen Frank with Culinary Advisor Walter Whitewater. Copyright © 2023 by Lois Ellen Frank. Published by Balance Publishing, an imprint of Hachette Book Group. All rights reserved.

You can find Chef Lois Ellen Frank here.

“Globally, 11 million deaths annually are attributable to dietary factors, placing poor diet ahead of any other risk factor for death in the world.” Given that diet is our leading killer, you’d think that nutrition education would be emphasized during medical school and training, but there is a deficiency. A systematic review found that, “despite the centrality of nutrition to a healthy lifestyle, graduating medical students are not supported through their education to provide high-quality, effective nutrition care to patients…”

It could start in undergrad. What’s more important? Learning about humanity’s leading killer or organic chemistry?

In medical school, students may average only 19 hours of nutrition out of thousands of hours of instruction, and they aren’t even being taught what’s most useful. How many cases of scurvy and beriberi, diseases of dietary deficiency, will they encounter in clinical practice? In contrast, how many of their future patients will be suffering from dietary excesses—obesity, diabetes, hypertension, and heart disease? Those are probably a little more common than scurvy or beriberi. “Nevertheless, fully 95% of cardiologists [surveyed] believe that their role includes personally providing patients with at least basic nutrition information,” yet not even one in ten feels they have an “expert” grasp on the subject.

If you look at the clinical guidelines for what we should do for our patients with regard to our number one killer, atherosclerotic cardiovascular disease, all treatment begins with a healthy lifestyle, as shown below and at 1:50 in my video Hospitals with 100-Percent Plant-Based Menus.

“Yet, how can clinicians put these guidelines into practice without adequate training in nutrition?”

Less than half of medical schools report teaching any nutrition in clinical practice. In fact, they may be effectively teaching anti-nutrition, as “students typically begin medical school with a greater appreciation for the role of nutrition in health than when they leave.” Below and at 2:36 in my video is a figure entitled “Percentage of Medical Students Indicating that Nutrition is Important to Their Careers.” Upon entry to different medical schools, about three-quarters on average felt that nutrition is important to their careers. Smart bunch. Then, after two years of instruction, they were asked the same question, and the numbers plummeted. In fact, at most schools, it fell to 0%. Instead of being educated, they got de-educated. They had the notion that nutrition is important washed right out of their brains. “Thus, preclinical teaching”— the first two years of medical school—“engenders a loss of a sense of the relevance of the applied discipline of nutrition.”

Following medical school, during residency, nutrition education is “minimal or, more typically, absent.” “Major updates” were released in 2018 for residency and fellowship training requirements, and there were zero requirements for nutrition. “So you could have an internal medicine graduate who comes out of a terrific program and has learned nothing—literally nothing—about nutrition.”

“Why is diet not routinely addressed in both medical education and practice already, and what should be done about that?” One of the “reasons for the medical silence in nutrition” is that, “sadly…nutrition takes a back seat…because there are few financial incentives to support it.” What can we do about that? The Food Law and Policy Clinic at Harvard Law School identified a dozen different policy levers at all stages of medical education and the kinds of policy recommendations there could be for the decision-makers, as you can see here and at 3:48 in my video.

For instance, the government could require doctors working for Veterans Affairs (VA) to get at least some courses in nutrition, or we could put questions about nutrition on the board exams so schools would be pressured to teach it. As we are now, even patients who have just had a heart attack aren’t changing their diet. Doctors may not be telling them to do so, and hospitals may be actively undermining their future with the food they serve.

The good news is that the American Medical Association (AMA) has passed a resolution encouraging hospitals to offer healthy food options. What a concept! “Our AMA hereby calls on [U.S.] Health Care Facilities to improve the health of patients, staff, and visitors by: (a) providing a variety of healthy food, including plant-based meals, and meals that are low in saturated and trans fat, sodium, and added sugars; (b) eliminating processed meats from menus; and (c) providing and promoting healthy beverages.” Nice!

“Similarly, in 2018, the State of California mandated the availability of plant-based meals for hospital patients,” and there are hospitals in Gainesville (FL), the Bronx, Manhattan, Denver, and Tampa (FL) that “all provide 100% plant-based meals to their patients on a separate menu and provide educational materials to inpatients to improve education on the role of diet, especially plant-based diets, in chronic illness.”

Let’s check out some of their menu offerings: How about some lentil Bolognese? Or a cauliflower scramble with baked hash browns for breakfast, mushroom ragu for lunch, and, for supper, white bean stew, salad, and fruit for dessert. (This is the first time a hospital menu has ever made me hungry!)

The key to these transformations was “having a physician advocate and increasing education of staff and patients on the benefits of eating more plant-based foods.” A single clinician can spark change in a whole system, because science is on their side. “Doctors have a unique position in society” to influence policy at all levels; it’s about time we used it.

For more on the ingrained ignorance of basic clinical nutrition in medicine, see the related posts below.

The most commonly used vegetable oil in the world today is palm oil. Pick up any package of processed food in a box, bag, bottle, or jar, and the odds are it will have palm oil. Palm oil not only contains the primary cholesterol-raising saturated fat found mostly in meat and dairy, but concerns have been raised about its safety, given the finding that it may contain a potentially toxic chemical contaminant known as 3-monochloropropane-1,2-diol, otherwise known as 3-MCPD, which is formed during the heat treatment involved in the refining of vegetable oils. So, these contaminants end up being “widespread in refined vegetable oils and fats and have been detected in vegetable fat-containing products, including infant formulas.”

Although 3-MCPD has been found in all refined vegetable oils, some are worse than others. The lowest levels of the toxic contaminants were found in canola oil, and the highest levels were in palm oil. Based on the available data, this may result in “a significant amount of human exposure,” especially when used to deep-fry salty foods, like french fries. In fact, just five fries could blow through the tolerable daily intake set by the European Food Safety Authority. If you only eat such foods once in a while, it shouldn’t be a problem, but if you’re eating fries every day or so, this could definitely be a health concern.

Because the daily upper limit is based on body weight, particularly high exposure values were calculated for infants who were on formula rather than breast milk, since formula is made from refined oils, which—according to the European Food Safety Authority—may present a health risk. Estimated U.S. infant exposures may be three to four times worse.

If infants don’t get breast milk, “there is basically no alternative to industrially produced infant formula.” As such, the vegetable oil industry needs to find a way to reduce the levels of these contaminants. This is yet another reason that breastfeeding is best whenever possible.

What can adults do to avoid exposure? Since these chemicals are created in the refining process of oils, what about sticking to unrefined oils? Refined oils have up to 32 times the 3-MCPD compared to their unrefined counterparts, but there is an exception: toasted sesame oil. Sesame oil is unrefined; manufacturers just squeeze the sesame seeds. But, because they are squeezing toasted sesame seeds, the 3-MCPD may have come pre-formed.

Virgin oils are, by definition, unrefined. They haven’t been deodorized, the process by which most of the 3-MCPD is formed. In fact, that’s how you can discriminate between the various processing grades of olive oil. If your so-called extra virgin olive oil contains MCPD, then it must have been diluted with some refined olive oil. The ease of adulterating extra virgin olive oil, the difficulty of detection, the economic drivers, and the lack of control measures all contribute to extra virgin olive oil’s susceptibility to fraud. How widespread a problem is it?

Researchers tested 88 bottles labeled as extra virgin olive oil and found that only 33 were found to be authentic. Does it help to stick to the top-selling imported brands of extra virgin olive oil? In that case, 73% of those samples failed. Only about one in four appeared to be genuine, and not a single brand had even half its samples pass the test, as you can see here and at 3:32 in my video 3-MCPD in Refined Cooking Oils.

Doctor’s Note

If you missed the previous post where I introduced 3-MCPD, see The Side Effects of 3-MCPD in Bragg’s Liquid Aminos.

There is no substitute for human breast milk. We understand this may not be possible for adoptive families or those who use surrogates, though. In those cases, look for a nearby milk bank.

We had the pleasure of talking with Ronnie Penn about his military service, his work as a chef and a coach, and what Veterans Day means to him. We hope you enjoy this interview. 

Thank you for your service, Ronnie. We’re honored to speak with you today. Can you start by sharing a bit about your background? What inspired you to enlist, and when did your military journey begin?

I grew up wanting to serve something bigger than myself, and the Marine Corps gave me that opportunity. I enlisted in 2004 and deployed to Iraq during Operation Iraqi Freedom and to Afghanistan from 2012 to 2014. Later, I served in the Coast Guard as a chef, which opened a whole new chapter in how I looked deeper into nutrition. Service taught me discipline, resilience, and the importance of teamwork—qualities I carry into everything I do today.

How did your time in the military shape who you are today? Is there anything in particular about your service that you would like to share?

The military taught me to stay calm under pressure and adapt quickly. Whether it was on deployment overseas or working with my shipmates in the galley, I learned how much impact food, mindset, and discipline can have on performance and morale. Those lessons shaped who I am now—not only as a veteran, but also as a coach who helps others take control of their health.

Were there any habits or disciplines from your military experience that helped in your transition to plant-based living or in your work today as a coach?

Two habits stuck with me: structure and accountability. In the Marines, every detail mattered. That same mindset helps me stick to meal prep, training schedules, and coaching clients. It also made the transition to plant-based eating easier because I was already used to planning ahead and being intentional about what I put into my body.

You’ve spoken about health issues that arose during competition prep, which ultimately led you to switch to a plant-based diet. What symptoms were you experiencing at the time, and what physical or medical changes did you notice after the transition?

When I was competing in bodybuilding, I pushed my body hard—lots of animal protein, supplements, and restrictive dieting. Over time, I developed digestive issues and constant fatigue. Switching to a whole food, plant-based diet changed everything. My digestion improved, and my energy came back. It was eye-opening to see how quickly the body can heal when you give it the right fuel.

Did you encounter any challenges accessing or preparing plant-based foods during active service? How did you make it work in that environment?

Back then, plant-based options were limited, especially on deployment. I loaded up on oatmeal, beans, rice, fruits, and vegetables whenever I could, and I had to get creative, too. I learned how to make simple meals with what was available, and that creativity carried into my role as a chef in the Coast Guard.

Were there any particularly memorable reactions from your shipmates or peers when you introduced them to plant-based meals as a chef in the Coast Guard?

At first, my shipmates were skeptical. But once I started cooking hearty meals, like lentil stews, veggie burritos, or black bean burgers, they were surprised by how satisfying plant-based food could be. I still remember one crew member saying, “I didn’t even miss the meat.” Moments like that showed me how powerful food can be in changing perceptions.

You’ve become a vocal advocate for plant-based eating in high-performance settings. Are there any particular studies or sources that informed or reinforced your choices?

The work of Dr. Greger and NutritionFacts.org has had a huge impact on me. I also leaned on research from the Physicians Committee for Responsible Medicine (PCRM) and books like The China Study. Seeing the science laid out gave me confidence that a plant-based diet wasn’t just personal preference; it was evidence-based. Also, the Netflix documentaries What the Health and Forks Over Knives were also extremely effective influences.

In your opinion, how can education about preparing whole plant foods be a path forward for people to achieve better health?

Education is the key. When people learn how to prepare whole plant foods in simple, tasty ways, it removes the intimidation factor. Once they see how it can lower blood pressure, improve energy, and even prevent chronic disease, it clicks. Food literacy is one of the most powerful tools we have for better health.

Please tell us about your online personal training program and app. What inspired you to start these projects, and how do they help you reach more people with your message?

I started my online fitness coaching because I wanted to reach people beyond the gym. Not everyone can afford a trainer, but most people have a smartphone. Through my training app, I provide meal plans, workout routines, and a grocery list with accountability check-ins. It’s a way to scale what I do—helping people take small, daily steps toward a healthier life.

Lastly, what does Veterans Day mean to you? Is there anything you would like to share with your fellow veterans?

Veterans Day is a moment of reflection for me. It’s about honoring the sacrifices of those who served, as well as reminding myself to live in a way that makes that service meaningful. I want to encourage other veterans to take care of themselves, not just physically, but mentally and emotionally, too. We served our country; now it’s time to serve ourselves by living healthy and purposeful lives.

To learn more about Ronnie, visit his website: https://www.ronniepenn.com/

In 1978, chlorohydrins were found in protein hydrolysates. What does that mean? Proteins can be broken down into amino acids using a chemical process called hydrolysis, and free amino acids (like glutamate) can have taste-enhancing qualities. That’s how inexpensive soy sauce and seasonings like Bragg’s Liquid Aminos are made. This process requires high heat, high pressure, and hydrochloric acid to break apart the protein. The problem is that when any residual fat is exposed to these conditions, it can form toxic compounds called chlorohydrins, which are toxic at least to mice and rats.

Chlorohydrins like 3-MCPD are considered “a worldwide problem of food chemistry,” but no long-term clinical studies on people have been reported to date. The concern is about the detrimental effects on the kidneys and fertility. In fact, there was a time 3-MCPD was considered as a potential male contraceptive because it could so affect sperm production, but research funding was withdrawn after “unacceptable side effects [were] observed in primates.” Researchers found flaccid testes in rats, which is what they were going for, but it caused neurological scars in monkeys.

What do you do when there are no studies in humans? How do you set some kind of safety factor? It isn’t easy, but you can take the lowest observed adverse effect level (LOAEL) in animal studies, which, in this case, was kidney damage, add in some kind of fudge factor, and then arrive at an estimated tolerable daily intake (TDI). For 3-MCPD, this means that high-level consumers of soy sauce may exceed the limit. This was based on extraordinarily high contamination levels, though. Since that study, Europe introduced a regulatory limit of 20 parts per billion (ppb) of 3-MCPD in hydrolyzed vegetable protein products like liquid aminos and soy sauce. The U.S. standards are much laxer, though, setting a “guidance level” of up to 50 times more, 1,000 parts per billion.

I called Bragg’s to see where it fell, and the good news is that it is doing an independent, third-party analysis of its liquid aminos for 3-MCPD. The bad news is that, despite my pleas that it be fully transparent, Bragg’s wouldn’t let me share the results with you. I have seen them, though, but I’m only allowed to confirm they comfortably meet the U.S. standards but fail to meet the European standards.

This is just the start of the 3-MCPD story, though. A study in Italy tested individuals’ urine for 3-MCPD or its metabolites, and 100% of the people turned up positive, confirming that it’s “a widespread food contaminant.” But 100% of people aren’t consuming soy sauce or liquid aminos every day. Remember, the chemical results from a reaction with residual vegetable oil. When vegetable oil itself is refined, when it’s deodorized and bleached, those conditions also lead to the formation of 3-MCPD.

Indeed, we’ve known for years that various foods are contaminated. In what kinds of foods have these kinds of chemicals been detected? Well, if they’re in oils and fats, then they’re in greasy foods made from them: margarine, baked goods, pastries, deep-fried foods, fatty snacks like potato and corn chips, as well as infant formula.

The U.S. Food and Drug Administration’s limit for soy sauce is 1,000 ppb, but donuts can have more than 1,200 ppb, salami more than 1,500 ppb, ham nearly 3,000 ppb, and French fries in excess of 6,000 ppb, as seen here and at 4:03 in my video The Side Effects of 3-MCPD in Bragg’s Liquid Aminos.

Most of us don’t have to worry about this problem, unless we’re consumers of fried food. Someone weighing about 150 pounds, for example, who eats 116 grams of donuts, would exceed the European Food Safety Authority’s TDI, even if those donuts were the person’s only source of exposure. That’s about two donuts, but the same limit-blowing amount of 3-MCPD could be found in only five French fries.

Doctor’s Note

Believe me, I pleaded with the Bragg’s folks over and over. It’s curious to me that Bragg’s allowed me to talk about where its level of 3-MCPD fell compared to the standards but not say the number itself. At least it’s doing third-party testing.

Learn more about this topic in my video 3-MCPD in Refined Cooking Oils.

You can also check out Friday Favorites: The Side Effects of 3-MCPD in Bragg’s Liquid Aminos and Refined Cooking Oils.

It’s been said that more than 2,000 years ago, Hippocrates declared, “Let food be thy medicine and medicine be thy food.” In actuality, it appears that he never actually said those words, but there’s “no doubt about the relevance of food…and its role in health and disease states” in his writings. Regardless, 2,000 years ago, disease was thought to arise from a bad sense of “humors,” as you can see here and at 0:32 in my video Lifestyle and Disease Prevention: Your DNA Is Not Your Destiny.

Now, we have science, and there is “an overwhelming body of clinical and epidemiological evidence illustrating the dramatic impact of a healthy lifestyle on reducing all-cause mortality”—meaning death from all causes put together—“and preventing chronic diseases such as coronary heart disease, stroke, diabetes, and cancer.” But don’t those diseases just run in our family? What if we just have bad genes?

According to the esteemed former chair of nutrition at Harvard, for most of the diseases that have contributed “importantly” to mortality in Western peoples, we’ve long known that non-genetic factors often account for at least 80% to 90% of risk. We know this because rates of the leading killers, like major cancers and cardiovascular diseases, vary up to 100-fold around the world, and, “when groups migrate from low- to high-risk countries, their disease rates almost always change to those of the new environment.” Modifiable behavioral factors have been identified, “including specific aspects of diet, overweight, inactivity, and smoking that account for over 70% of stroke and colon cancer, over 80% of coronary heart disease, and over 90% of adult-onset [type 2] diabetes”—diseases that can largely be prevented by our own actions.

If most of the power is in our own hands, why do we allocate massively more resources to treatment than prevention? And speaking of prevention, “even preventive strategies are heavily biased towards pharmacology rather than supporting improvements in diet and lifestyle that could be more cost-effective. For example, treatment of [high] serum cholesterol with statins alone could cost approximately 30 billion dollars per year in the United States and would have only a modest impact on coronary heart disease incidence. The inherent problem is that most pharmacologic strategies don’t address the underlying causes of ill health in Western countries, which are not drug deficiencies.”

Ironically, the chronic diseases that are most amenable to lifestyle treatment are the same ones most profitably treated by drugs. Why? If you don’t change your diet, you have to pop the pills every day for the rest of your life. So, the cash-cow drugs are the very drugs we need the least. “Even though the most widely accepted, well-established chronic disease practice guidelines uniformly call for lifestyle change as the first line of therapy, physicians often do not follow these recommendations.” “By ignoring the root causes of disease and neglecting to prioritize lifestyle measures for prevention, the medical community is placing people at harm.”

“Traditional medical care relies primarily on the application of pharmacologic and surgical interventions after the development of illness,” whereas lifestyle medicine relies primarily on “the use of optimal nutrition (a whole foods, plant-based diet) and exercise in the prevention, arrest, and reversal of chronic conditions leading to premature disability and death. It looks in a holistic way at the underlying causes of illness.”

Dr. Adriane Fugh-Berman, director of PharmedOut, a wonderful organization I’m proud to support, wrote a great editorial entitled “Doctors Must Not Be Lapdogs to Drug Firms.” “The illusion that the relationship between medicine and the drug industry is collegial, professional, and personal is carefully maintained by the drug industry, which actually views all transactions with physicians in finely calculated financial terms…The drug industry is happy to play the generous and genial uncle until physicians want to discuss subjects that are off limits, such as the benefits of diet or exercise, or the relationship between medicine and pharmaceutical companies…Let us not be a lapdog to Big Pharma. Rather than sitting contentedly in our master’s lap, let us turn around and bite something tender.”

Doctor’s Note

The organization I mentioned, PharmedOut, is a project of Georgetown University Medical Center.

For more on Lifestyle Medicine, see related videos below.

“Consistent evidence” from a variety of sources “unequivocally establishes” that so-called bad LDL cholesterol causes atherosclerotic cardiovascular disease—strokes and heart attacks, our leading cause of death. This evidence base includes hundreds of studies involving millions of people. “Cholesterol is the cause of atherosclerosis,” the hardening of the arteries, and “the message is loud and clear.” “It’s the Cholesterol, Stupid!” noted the editor of the American Journal of Cardiology, William Clifford Roberts, whose CV is more than 100 pages long as he has published about 1,700 articles in peer-reviewed medical literature. Yes, there are at least ten traditional risk factors for atherosclerosis, as seen below and at 1:11 in my video How Low Should You Go for Ideal LDL Cholesterol?, but, as Dr. Roberts noted, only one is required for the progression of the disease: elevated cholesterol.

Your doctor may have just told you that your cholesterol is normal, so you’re relieved. Thank goodness! But, having a “normal” cholesterol level in a society where it’s normal to have a fatal heart attack isn’t necessarily good. With heart disease, the number one killer of men and women, we definitely don’t want to have normal cholesterol levels; we want to have optimal levels—and not optimal by current laboratory standards, but optimal for human health.

Normal LDL cholesterol levels are associated with the hidden buildup of atherosclerotic plaques in our arteries, even in those who have so-called “optimal risk factors by current standards”: blood pressure under 120/80, normal blood sugars, and total cholesterol under 200 mg/dL. If you went to your doctor with those kinds of numbers, you’d likely get a gold star and a lollipop. But, if your doctor used ultrasound and CT scans to actually peek inside your body, atherosclerotic plaques would be detected in about 38% of individuals with those kinds of “optimal” numbers.

Maybe we should define an LDL cholesterol level as optimal only when it no longer causes disease. What a concept! When more than a thousand men and women in their 40s were scanned, having an LDL level under 130 mg/dL left them with atherosclerosis throughout their body, and that’s a cholesterol level at which most lab tests would consider normal.

In fact, atherosclerotic plaques were not found with LDL levels down around 50 or 60, which just so happens to be the levels most people had “before the introduction of western lifestyles.” Indeed, before we started eating a typical American diet, “the majority of the adult population of the world had LDLs of around 50 mg per deciliter (mg/dL)”—so that’s the true normal. “Present average values…should not be regarded as ‘normal.’” We don’t want to have a normal cholesterol based on a sick society; we want a cholesterol that is normal for the human species, which may be down around 30 to 70 mg/dL or 0.8 to 1.8 mmol/L.

“Although an LDL level of 50 to 70 mg/dl seems excessively low by modern American standards, it is precisely the normal range for individuals living the lifestyle and eating the diet for which we are genetically adapted.” Over millions of years, “through the evolution of the ancestors of man,” we’ve consumed a diet centered around whole plant foods. No wonder we have a killer epidemic of atherosclerosis, given the LDL level “we were ‘genetically designed for’ is less than half of what is presently considered ‘normal.’”

In medicine, “there is an inappropriate tendency to accept small changes in reversible risk factors,” but “the goal is not to decrease risk but to prevent atherosclerotic plaques!” So, how low should you go? “In light of the latest evidence from trials exploring the benefits and risks of profound LDLc lowering, the answer to the question ‘How low do you go?’ is, arguably, a straightforward ‘As low as you can!’” “‘Lower’ may indeed be better,” but if you’re going to do it with drugs, then you have to balance that with the risk of the drug’s side effects.

Why don’t we just drug everyone with statins, by putting them in the water supply, for instance? Although it would be great if everyone’s cholesterol were lower, there are the countervailing risks of the drugs. So, doctors aim to use statin drugs at the highest dose possible, achieving the largest LDL cholesterol reduction possible without increasing risk of the muscle damage the drugs may cause. But when you’re using lifestyle changes to bring down your cholesterol, all you get are the benefits.

Can we get our LDL low enough with diet alone? Ask some of the country’s top cholesterol experts what they shoot for, “and the odds are good that many will say 70 or so.” So, yes, we should try to avoid the saturated fats and trans fats found in junk foods and meat, and the dietary cholesterol found mostly in eggs, but “it is unlikely anyone can achieve an LDL cholesterol level of 70 mg/dL with a low-fat, low-cholesterol diet alone.” Really? Many doctors have this mistaken impression. An LDL of 70 isn’t only possible on a healthy enough diet, but it may be normal. Those eating strictly plant-based diets can average an LDL that low, as you can see here and at 5:28 in my video.

No wonder plant-based diets are the only dietary patterns ever proven to reverse coronary heart disease in a majority of patients. And their side effects? You get to feel better, too! Several randomized clinical trials have demonstrated that more plant-based dietary patterns significantly improve psychological well-being and quality of life, with improvements in depression, anxiety, emotional well-being, physical well-being, and general health.

For more on cholesterol, see the related posts below.

An uncontrolled and unpublished study purported to show a beneficial effect of fasting on migraine headaches, but fasting may be more likely to trigger a migraine than help it. In fact, “skipped meals are among the most consistently identified dietary triggers” of headaches in general. In a review of hundreds of fasts at the TrueNorth Health Center in California, the incidence of headache was nearly one in three, but TrueNorth also published a remarkable case report on post-traumatic headache.

The U.S. Centers for Disease Control and Prevention (CDC) estimates that more than a million Americans sustain traumatic brain injuries (TBIs) every year. Chronic pain is a common complication, affecting perhaps three-quarters of those who suffer such an injury. There are drugs, of course, to treat post-traumatic headache. There are always drugs. And if drugs don’t work, there is surgery, cutting the nerves to the head to stop the pain.

What about fasting and plants? A 52-year-old woman presented with a highly debilitating, difficult-to-manage, unremitting, chronic post-traumatic headache. And when I say chronic, I mean chronic; she experienced pain for 16 years. She then achieved long-term relief after fasting, followed by an exclusively plant-foods diet, free of added sugar, oil, or salt.

Before then, she had tried drug after drug after drug after drug after drug—with no relief, suffering in constant pain for years. Before the fast, she started out in constant pain. Then, after the fast, the intensity of the pain was cut in half, and though she was still having daily headaches, at least there were some pain-free periods. Six months later, she tried again, and eventually her headaches became mild, lasting less than ten minutes, and infrequent. She continued that way for months and even years, as you can see below and at 1:45 in my video Fasting for Post-Traumatic Brain Injury Headache. 

Now, of course, it’s hard to disentangle the effects of the fasting from the effects of the whole food, plant-based diet she remained on for those ensuing years. You’ve heard of analgesics (painkillers). Well, there are some foods that may be pro-algesic (pain-promoting), such as foods high in arachidonic acid, including meats, dairy, and eggs. So, the lowering of arachidonic acid—from which our body makes a range of pro-inflammatory compounds—may be accomplished by eating a more plant-based diet. So, maybe that contributed to the benefit in the fasting case, since many plant foods are high in anti-inflammatory components. In terms of migraine headaches, more plant foods and less animal foods may help, but you don’t know until you put it to the test.

Researchers figured a plant-based diet may offer the best of both worlds, so they designed a randomized, controlled, crossover study where those with recurrent migraines were randomized to eat a strictly plant-based diet or take a placebo pill. Then, the groups switched. During the placebo phase, half of the participants said their pain improved, and the other half said their pain remained the same or got worse. But, during the dietary phase, they almost all got better, as you can see here and at 3:11 in my video.

During that first phase, the diet group experienced significant improvements in the number of headaches, pain intensity, and days with headaches, as well as a reduction in the amount of painkillers they needed to take. In fact, it worked a little too well. Many individuals were unwilling to return to their previous diets after they completed the diet phase of the trial, thereby refusing to complete the study. Remember, the participants were supposed to go back to their regular diets and take a placebo pill, but they felt so much better on the plant-based diet that they refused. We’ve seen this with other trials, where those trying plant-based diets felt so good, they often refused to abandon them, harming the study. So, plant-based diets can sometimes work a little too well.

All my videos on fasting are available in a digital download here.  

A chronic gastrointestinal disorder, irritable bowel syndrome affects about one in ten people. You may have heard about low-FODMAP diets, but they don’t appear to work any better than the standard advice to avoid things like coffee or spicy and fatty foods. In fact, you can hardly tell which is which, as shown below and at 0:27 in my video Friday Favorites: Fasting for Irritable Bowel Syndrome.

Most IBS patients, however, do seem to react to specific foods, such as eggs, wheat, dairy, or soy sauce, but when they’re tested with skin prick tests for typical food allergies, they may come up negative. We want to know what happens inside their gut when they eat those things, though, not what happens on their skin. Enter confocal laser endomicroscopy.

You can snake a microscope down the throat, into the gut, and watch in real-time as the gut wall becomes inflamed and leaky after foods are dripped in. Isn’t that fascinating? You can actually see cracks forming within minutes, as shown below and at 1:03 in my video. This had never been tested on a large group of IBS patients, though, until now.

Using this new technology, researchers found that more than half of IBS sufferers have this kind of reaction to various foods—“an atypical food allergy” that flies under the radar of traditional allergy tests. As you can see below and at 1:28 in my video, when you exclude those foods from the diet, there is a significant alleviation of symptoms.

However, outside a research setting, there’s no way to know which foods are the culprit without trying an exclusion diet, and there’s no greater exclusion diet than excluding everything. A 25-year-old woman had complained of abdominal pain, bloating, and diarrhea for a year, and drugs didn’t seem to help. But, after fasting for ten days, her symptoms improved considerably and appeared to stay that way at least 18 months later. It wasn’t just subjective improvement either. Biopsies were taken that showed the inflammation had gone down, her bowel irritability was measured directly, and expanding balloons and electrodes were inserted in her rectum to measure changes in her sensitivity to pressure and electrical stimulation. Fasting seemed to reboot her gut in a way, but just because it worked for her doesn’t mean it works for others. Case reports are most useful when they inspire researchers to put them to the test.

“Despite research efforts to develop a cure for IBS, medical treatment for this condition is still unsatisfactory.” We can try to suppress the symptoms with drugs, but what do we do when even that doesn’t work? In a study of 84 IBS patients, 58 of whom failed basic treatment (consisting of pharmacotherapy and brief psychotherapy), 36 of the 58 who were still suffering underwent ten days of fasting, whereas the other 22 stuck with the basic treatment. The findings? Those in the fasting group experienced significant improvements in abdominal pain, bloating, diarrhea, loss of appetite, nausea, anxiety, and interference with life in general, which were significantly better than those of the control group. The researchers concluded that fasting therapy “could be useful for treating moderate to severe patients with IBS.”

Unfortunately, patient allocation was neither blinded nor randomized in the study, so the comparison to the control group doesn’t mean much. They were also given vitamins B1 and C via IV, which seems typical of Japanese fasting trials, even though one would not expect vitamin-deficiency syndromes—beriberi or scurvy—to present within just ten days of fasting. The study participants were also isolated; might that make the psychotherapy work better? It’s hard to tease out just the fasting effects.

Psychotherapy alone can provide lasting benefits. Researchers randomized 101 outpatients with irritable bowel syndrome to medical treatment or medical treatment with three months of psychotherapy. After three months, the psychotherapy group did better, and the difference was even more pronounced a year later, a year after the psychotherapy ended. Better at three months, and even better at 15 months, as you can see here and at 3:58 in my video.

Psychological approaches appear to work about as well as antidepressant drugs for IBS, but the placebo response for IBS is on the order of 40%, whether psychological interventions, drugs, or alternative medicine approaches. So, doing essentially nothing—taking a sugar pill—improves symptoms 40% of the time. In that case, I figure one might as well choose a therapy that’s cheap, safe, simple, and free of side effects, which extended fasting is most certainly not. But, if all else fails, it may be worth exploring fasting under close physician supervision.

All my fasting videos are available in a digital download here.

Check the videos on the topic that are already on the site here. 

For more on IBS, see related posts below. 

Parkinson’s disease is an ever-worsening neurodegenerative disorder that results in death and affects about 1 in 50 people as they get older. A small minority of cases are genetic, running in families, but 85% to 90% of cases are sporadic, meaning they seem to pop up out of nowhere. Parkinson’s is caused by the death of a certain kind of nerve cell in the brain. Once about 70% of them are gone, the symptoms start. What kills off those cells? It still isn’t completely clear, but the abnormal clumping of a protein called alpha-synuclein or α-synuclein is thought to be involved. Why? Researchers injected blended Parkinson’s brains into the heads of rats and monkeys, and Parkinson’s pathology and symptoms were induced. It can even happen when injecting just the pure, clumped α-synuclein strands themselves. How, though, do these clumps naturally end up in the brain?

As I discuss in my video The Role Meat May Play in Triggering Parkinson’s Disease, it all seems to start in the gut. The part of the brain where the pathology often first appears is directly connected to the gut, and we have direct evidence of the spread of Parkinson’s pathology from the gastrointestinal (GI) tract to the brain: α-synuclein from brains of Parkinson’s patients is taken up in the gut wall and creeps up the vagal nerves from the gut into the brain—at least that was the case in rats. If only we could go back and look at people’s colons before they got Parkinson’s. Indeed, we can. Old colon biopsies from people who would later develop Parkinson’s were dredged up, and, years before symptoms arose, you could see the α-synuclein in their gut.

Research supported by the Michael J. Fox Foundation has found that you can reliably distinguish the colons of patients from controls by the presence of this Parkinson’s protein lodged in the gut wall. But how did it get there in the first place? Are “vertebrate food products…a potential source of prion-like α-synuclein”? Indeed, nearly all the animals with backbones that we consume—cows, chickens, pigs, and fish—express the protein α-synuclein. So, when we eat common meat products, when we eat skeletal muscle, we’re eating nerves, blood cells, and the muscle cells themselves. Every pound of meat contains, on average, half a teaspoon of blood, and that alone could be an α-synuclein source to potentially trigger a clumping cascade of our own α-synuclein in the gut. Though “it may seem intuitive that dietary α-synuclein could seed aggregation in the gut,” this kind of buildup, what evidence do we have that it’s actually happening?

We have some pretty interesting data. There’s a surgical procedure called a vagotomy, in which the big nerve that goes from our gut to our brain—the vagus nerve—is cut as an old-timey treatment for stomach ulcers. Would cutting communication between the gut and the brain reduce Parkinson’s risk? Apparently so, suggesting that the gut to brain’s vagal nerve may be critically involved in the development of Parkinson’s disease.

Of course, “many people regularly consume meat and dairy products, but only a small fraction of the general population will develop PD,” Parkinson’s disease. So, there must be other factors at play that “may provide an opportunity for unwanted dietary α-synuclein to enter the host, and initiate disease.” For example, our gut becomes leakier as we age, so might that play a role? What else makes our gut leaky? “Dietary fiber deprivation has also been shown to degrade the intestinal barrier and enhance pathogen entry.” So, this raises “possibilities for food-based therapies.”

Parkinson’s patients have significantly less Prevotella in their gut, a friendly fiber-eating flora that bolsters our intestinal barrier function. So, low levels of Prevotella are linked to a leaky gut, which has been linked to intestinal α-synuclein deposition, but fiber-rich foods may bring Prevotella levels back up. “Therefore, it is possible that by adopting a plant-based diet, in addition to the beneficial effects of phytonutrients, increasing overall fiber intake may modify gut microbiota and gut permeability [leakiness] in beneficial ways for people with PD.”

So, does a vegan diet—one with lots of fiber and no meat—reduce risk for Parkinson’s? Parkinson’s “appears to be rare in quasi-vegan cultures,” with rates that are about five times lower in rural sub-Saharan Africa, for instance. All this time, we were thinking the benefits seen for Parkinson’s from plant-based diets were due to the antioxidants and anti-inflammatory nature of the animal-free diets, but maybe it’s also due to the increased intestinal exposure to fiber and decreased intestinal exposure to ingested nerves, muscles, and blood.

Wasn’t that fascinating? For more on Parkinson’s, see the related posts below.

In my video Friday Favorites: Benefits of Black Cumin for Weight Loss, I discussed how a total of 17 randomized controlled trials showed that the simple spice could reduce cholesterol and triglyceride levels. And its side effects? A weight-loss effect.

Saffron is another spice found to be effective for treating a major cause of suffering—depression, in this study, with a side effect of decreased appetite. Indeed, when put to the test in a randomized, double-blind, placebo-controlled trial, saffron was found to lead to significant weight loss, five pounds more than placebo, and an extra inch off the waist in eight weeks. The dose of saffron used in the study was the equivalent of drinking a cup of tea made from a large pinch of saffron threads.

Suspecting the active ingredient might be crocin, the pigment in saffron that accounts for its crimson color, as shown here and at 0:59 in my video Friday Favorites: Benefits of Cumin and Saffron for Weight Loss, researchers also tried giving people just the purified pigment.

That also led to weight loss, but it didn’t do as well as the full saffron extract and only beat the placebo by two pounds and half an inch off the waist. The mechanism appeared to be appetite suppression, as the crocin group ended up averaging about 80 fewer calories a day, whereas the full saffron group consumed an average of 170 fewer daily calories, as you can see below and at 1:21 in my video.

A similar study looked specifically at snacking frequency. The researchers thought that the mood-boosting effects of saffron might cut down on stress-related eating. Indeed, eight weeks of a saffron extract halved snack intake, compared to a placebo. There was also a slight but statistically significant weight loss of about two pounds, as you can see here and at 1:41 in my video, which is pretty remarkable, given that tiny doses were utilized—about 100 milligrams, which is equivalent to about an eighth of a teaspoon of the spice.

The problem is that saffron is the most expensive spice in the world. It’s composed of delicate threads sticking out of the saffron crocus flower. Each flower produces only a few threads, so about 50,000 flowers are needed to make a single pound of spice. That’s enough flowers to cover a football field. So, that pinch of saffron could cost a dollar a day.

That’s why, in my 21 Tweaks to accelerate weight loss in How Not to Diet, I include black cumin, instead of saffron, as you can see here and at 2:30 in my video. And, at a quarter teaspoon a day, the daily dose of black cumin would only cost three cents.

What about just regular cumin? Used in cuisines around the world from Tex-Mex to South Asian, cumin is the second most popular spice on Earth after black pepper. It is one of the oldest cultivated plants with a range of purported medicinal uses, but only recently has it been put to the test for weight loss. Those randomized to a half teaspoon at both lunch and dinner over three months lost about four more pounds and an extra inch off their waist. The spice was found to be comparable to the obesity drug known as orlistat.

If you remember, orlistat is the “anal leakage” drug sold under the brand names Alli and Xenical. The drug company apparently prefers the term “faecal spotting” to describe the rectal discharge it causes, though. The drug company’s website offered some helpful tips, including: “It’s probably a smart idea to wear dark pants, and bring a change of clothes with you to work.” You know, just in case their drug causes you to poop in your pants at the office.

I think I’ll stick with the cumin, thank you very much.

Doctor’s Note

The video on black cumin that I mentioned is Friday Favorites: Benefits of Black Cumin Seed (Nigella Sativa) for Weight Loss.

My other videos on saffron are in the related posts below.

For an in-depth dive into weight loss, see my book How Not to Diet. 

“Recent reports of medical students performing pelvic exams for training purposes on anesthetized women without their consent”—or their knowledge—“have produced a firestorm of controversy and calls for greater regulation.” However, that “burst of public outcry” was in the mid-1990s. California was the first state to make the practice illegal, but the “early gains quickly petered out.”

As I discuss in my video Ending the Hidden Practice of Pelvic Exams on Unconscious Women Without Their Consent, “This practice, common since the late 1800s, was largely unchallenged until a 2003 study reported that 90 percent of medical students who completed obstetrics and gynecology (ob-gyn) rotations at four Philadelphia-area medical schools performed pelvic exams on anesthetized women for educational purposes.” (A subsequent study found the percentage to be lower than that in other areas of the country.) The bottom line? “Pelvic Exams Done on Anesthetized Women Without Consent: Still Happening.” How can this continue into 2025? Medical ethicists have called such practices “immoral and indefensible.” “At the end of the day, this is a practice that should come to an abrupt and immediate halt.” Some schools vowed they’d end the practice, but, unfortunately, these early victories quickly stalled. At the same time, a handful of schools revamped their policies, an equal number of hospitals and medical schools publicly dug in, defending the practice.

The Association of Professors of Gynecology and Obstetrics wrote: “As medical educators, we must balance our obligation to develop the next generation of physicians with women’s freedom to decide from whom they receive treatment and what aspects of their care are performed by learners.” “Some especially blunt teaching faculty contend that ‘public’ patients”—those without health insurance—“owe it to the facility and society to participate since they receive free or subsidized care.” Regulations to curb this practice are said to be “placing inappropriate and unnecessary barriers in the way of medical students who need to learn fundamental medical skills” and therefore “should be resisted.” Unsurprisingly, medical students still perform pelvic exams on anesthetized women.

Professional medical societies have given lip service to the concept of asking for explicit consent, but despite the recommendations, “evidence…suggests that the practice is alive and well.” And the “unauthorized use of women is not a localized phenomenon confined to a handful of errant medical schools,” a few bad med school apples, but an international problem.

Even with the emergence of the #MeToo movement and even after Larry Nasser, the infamous USA gymnastics doctor, was sentenced to 40 to 175 years in prison for touching women’s genitalia without their consent, “there are still women who are being used as teaching subjects for these exams without their permission, without their consent.”

A 2020 update from Yale’s Center for Bioethics was entitled: “A Pot Ignored Boils On: Sustained Calls for Explicit Consent of Intimate Medical Exams.” It reads, “Over the last 30 years, several parties—both within and external to medicine—have increasingly voiced opposition to these exams. Arguments from medical associations, legal scholars, ethicists, nurses, and some physicians have not compelled meaningful institutional change.” Yes, there is the lip service paid by medical associations recommending bans on pelvic exams without consent, but those statements are “advisory and incomplete. Associations simply do not have the capacity to compel systemic change, as evidenced by institutions’ inaction.” In response to the medical profession’s inability to police itself, many states have passed legislation to protect patients from this practice.

But, of course, if you are anesthetized, how would you even know if medical students are lining up or not? “Teaching hospitals take patients who are in the worst position to know what’s occurring—they are unconscious—and use them in ways that leave no physical signs and are often undocumented in the patients’ medical records.” So, when the media loses interest, as it has decade after decade, “what incentive is there for teaching faculty or hospitals to voluntarily change?” Perhaps, “when physicians start being threatened with litigation, they’ll start obtaining informed consent.” As one commentator wrote, “Hospital administrators who allow medical students in their facilities to perform pelvic examinations on unconsenting anesthetized women ought to consult with their legal counsel concerning the definition of rape in their jurisdiction.”

“The solution is simple: Just ask.” Ask women for permission. It’s their body, their choice. “But recent experience has shown that meaningful and complete hospital-by-hospital change is unlikely to come until a hospital or doctor pays a substantial award [in some lawsuit] for this error in ethical judgment. We believe that day is coming soon, lest that ignored pot finally boil over. 
 
“Some defend it as harmless and say asking for consent would make it more likely that patients would say no, denying students a crucial part of their training.” When I first wrote about this practice more than 20 years ago in my book Heart Failure about my time in medical school, I talked about how I had gotten the same comments from my classmates: “A well-then-how-are-we-going-to-learn response. To even present such a question is to lose a bit of one’s humanity. The answer, of course, is we should learn from women who give their consent! And to do that—God forbid—we might actually have to first establish a relationship with the patient, a trust—talk to them even. We may have to treat them like human beings.”

It’s unconscionable that medical students are legally allowed to practice pelvic exams on anesthetized women without their consent. Even if you live in one of the states where this practice is technically illegal, how do you know the law will be respected once you’re unconscious? Maybe medical students should wear bodycams.

If you missed the related video, see Medical Students Practice Pelvic Exams on Anesthetized Women Without Their Consent. 

No Pakistani gathering feels complete without biryani. Whether it’s a wedding, Eid, or a simple Sunday lunch, the aroma of spices rising from a steaming pot of biryani defines celebration.
But few realize that biryani isn’t a single dish — it’s a culinary universe. Across Pakistan, each region has its own signature twist — from Karachi’s spicy red biryani to Lahore’s aromatic chicken pulao-biryani, and Hyderabadi-inspired layered biryani from Sindh.

This blog explores the art, science, and soul of Chicken Biryani, revealing not just one, but three authentic and healthy versions you can cook at home — whether you love fiery spice or mild fragrance.

The Secret of a Perfect Chicken Biryani

Before diving into recipes, understand what makes biryani truly “biryani”:

1. Perfectly cooked basmati rice – fluffy, separate grains that don’t clump.
2. A rich masala base – slow-cooked onions, tomatoes, and spices.
3. Layering and steaming (dum) – this step locks in aroma and infuses flavor.
4. Balanced spice and salt – neither too fiery nor bland.

Once you master these foundations, you can customize your biryani to your heart’s content.

1. Karachi-Style Chicken Biryani — Bold, Fiery, and Aromatic

Karachi biryani is famous for its spicy kick and orange hue. It’s layered with masala, potatoes, and juicy chicken pieces.

Ingredients

• 500g chicken (bone-in)
• 2 cups basmati rice (soaked 30 mins)
• 3 onions (thinly sliced)
• 2 tomatoes (chopped)
• ½ cup low-fat yogurt
• 3 medium potatoes (parboiled and cubed)
• 2 tbsp olive oil or ghee
• 1 tbsp ginger-garlic paste
• Spices: cumin seeds, coriander powder, red chili, turmeric, biryani masala
• Herbs: fresh coriander, mint leaves, green chilies
• Food color (orange), lemon juice

Step-by-Step Recipe

1. Fry the Onions: Heat 1 tbsp oil; sauté onions until golden brown. Remove half for garnish.
2. Cook Chicken Masala: Add ginger-garlic paste, tomatoes, yogurt, and spices. Cook till oil separates.
3. Add Potatoes: Stir in boiled potatoes; cook for 5 minutes.
4. Boil Rice: Cook rice with salt, bay leaf, and cloves till 70% done.
5. Layer: In a large pot, spread chicken masala, then rice. Sprinkle fried onions, herbs, lemon juice, and food color.
6. Steam (Dum): Cover tightly and steam for 20 minutes on low heat.

Result: Fiery, flavorful biryani with Karachi’s signature spicy punch and perfectly balanced layers.

2. Lahore-Style Chicken Biryani — Fragrant and Mildly Spiced

Lahori biryani is milder, richer in aroma, and slightly creamy thanks to yogurt and milk. It’s perfect for those who enjoy deep flavors without too much spice.

Ingredients

• 500g chicken
• 2 cups long-grain basmati rice
• 1 cup yogurt
• 1 large onion
• 1 tbsp ginger-garlic paste
• Whole spices: cinnamon stick, cloves, bay leaf, green cardamom
• Saffron or food color soaked in 2 tbsp milk
• 2 tbsp olive oil or butter
• Fresh coriander and mint

Step-by-Step Recipe

1. Prepare Masala: Heat oil, sauté onions until golden. Add ginger-garlic paste and chicken; cook until browned.
2. Add Yogurt & Spices: Stir in yogurt and dry spices. Simmer till thick gravy forms.
3. Boil Rice: Cook rice with whole spices until 80% done.
4. Layer and Steam: In a large pan, layer chicken and rice. Drizzle saffron milk, sprinkle herbs, and cover tightly.
5. Dum Cook: Steam for 15–20 minutes on low heat.

Result: A rich, aromatic biryani with mild spice and royal fragrance.

3. Sindhi Biryani — Tangy, Spicy, and Loaded with Flavor

Sindhi biryani is known for its unique tanginess — a result of dried plums and yogurt — and deep spices that create layers of complexity.

Ingredients

• 500g chicken
• 2 cups basmati rice
• 3 onions, sliced
• 2 tomatoes, chopped
• ½ cup yogurt
• 4 dried plums (alu bukhara)
• 2 green chilies
• 1 tbsp ginger-garlic paste
• Spices: cumin, black pepper, coriander, cinnamon, cardamom
• 2 tbsp olive oil

Step-by-Step Recipe

1. Prepare Masala: Fry onions till golden, add tomatoes, yogurt, and spices.
2. Add Chicken: Cook till tender and masala thickens.
3. Add Dried Plums: Mix in for that signature tangy depth.
4. Boil Rice: Cook rice till 70% done, drain.
5. Layer: Alternate rice and chicken masala, sprinkle mint and green chilies.
6. Steam: Cook on low heat for 20 minutes.

Result: A perfectly tangy, spicy, and irresistibly fragrant Sindhi biryani.

4. Healthy Low-Oil Biryani — A Modern, Nutritious Twist

For health-conscious food lovers, you can make biryani lighter and heart-friendly without losing its authentic flavor.

Healthy Swaps

Use olive oil instead of ghee.
Steam or air-fry onions instead of deep frying.
Use skinless chicken.
Add vegetables like peas, carrots, and spinach for fiber.
Use brown basmati rice for whole-grain nutrition.

Step-by-Step Recipe

1. Cook Chicken in Its Own Juices: Add tomatoes and yogurt to form gravy naturally.
2. Use Less Oil: Just 1–2 tablespoons are enough to coat spices.
3. Layer as Usual: Herbs, rice, and masala — then dum cook for 20 minutes.

Result: A flavorful, fragrant, and guilt-free biryani with 60–70% less oil.

Perfect Sides to Serve With Chicken Biryani

• Cucumber Raita: Yogurt, cucumber, mint, and cumin powder.
• Kachumber Salad: Onion, tomato, lemon, and green chili mix.
• Papad and Pickles: Add crunch and tang to balance spice.

Pro Tips for Restaurant-Style Biryani at Home

1. Always use aged basmati rice for longer grains.
2. Let the biryani rest for 10 minutes before serving.
3. Never stir biryani after dum — it breaks the layers.
4. Use earthen pots (matka) for authentic aroma and slow heat.
5. Adjust chili and salt before final layering; you can’t fix it later!

Final Thought: The Taste That Unites Pakistan

From Karachi to Kashmir, biryani connects us all. It’s more than just food — it’s a feeling of home, celebration, and shared joy. Whether you’re cooking a low-oil version or a rich festive one, every grain tells a story.

At Nutric Food Show, we celebrate not just the recipe, but the culture, the aroma, and the love that goes into every pot of biryani!

As someone who creates Mexican dishes with a plant-based twist, how is food an important part of your culture and how you share your culture with others?

Food is so much more than nourishment—it’s how we love, connect, and remember who we are. For Mexicans, food is truly part of our DNA. From ancient times, when our ancestors offered food to the gods, to modern-day sobremesas with family and friends, sharing food is how we express love. I grew up surrounded by women who talked about recipes the way others talk about dreams. My mother, grandmother, and aunts were always planning the next meal or discovering a new dish. Now I do the same with my siblings. Even though my food today is mostly plant-based, its essence is the same: to bring people together. Through my recipes, I want to recreate that sense of belonging, of always having enough to share and always leaving room for one more at the table. That’s what comemos means to me. It’s not about nostalgia; it’s about showing what being Mexican really looks and tastes like today.

When did you start cooking and developing your own recipes? How do you educate people about making beautiful Mexican dishes using plant-based ingredients? Are people ever surprised to learn your recipes are plant-based?

I started 23 years ago, right after my son was diagnosed with a dairy allergy. That moment changed everything. I had to relearn how to cook. I leaned into spices, explored new vegetables, and discovered different cooking methods. What began as a necessity quickly turned into a passion. I even enrolled in an online course to get certified as a plant-based cook. As my kids grew, so did my curiosity and creativity in the kitchen. Educating others has always been fun for me. I don’t lead with “plant-based” or “vegan”; I lead with flavor. I’ll serve someone a bowl of bean soup, and, after they’ve devoured it, I’ll smile and say, “Congrats, you just had your first vegan meal.” It’s always a surprise for them, and that’s the magic— showing how beautiful, satisfying, and deeply Mexican plant-based food can be.

What are some plant-based ingredients and/or vegan dishes that you’d like to highlight as part of Mexican food traditions? Anything you’d especially like people to know about these foods?

Masa, hands down. It’s the heart of so many beloved Mexican dishes—sopes, huaraches, tlacoyos—and it’s naturally plant-based. What I love most is how versatile it is. You can shape masa into antojitos, but you can also use it to make dumplings and cakes, or get creative and reinterpret global dishes with a Mexican twist. Take a good sope and layer it with mashed potatoes or creamy refried beans, top with salsa, guacamole, shredded lettuce, pickled onions—whatever you love. That’s the beauty of Mexican food; it’s endlessly customizable. You can set up a spread with all kinds of toppings and let everyone build their own plate. It’s not just delicious. It’s inclusive, joyful, and rooted in sharing.

What do you envision as the way forward to encourage people to eat more fruits and vegetables and return to traditional Hispanic eating patterns?

I think the real barrier is the labels and the absolutes. When we frame eating habits as all-or-nothing, people tune out. But if we shift the focus to just one healthy, vibrant meal at a time—one that’s full of colorful fruits and vegetables that add texture, flavor, and joy—then it feels more approachable and exciting. Traditional Hispanic food already celebrates plant-forward ingredients like chiles, tomatoes, squash, beans, and corn. If we bring those foods back to the center of the plate in a way that feels natural, not forced, people will reconnect with them. It’s about showing how beautiful and delicious these meals can be, not preaching about what they “should” eat.

What does National Hispanic Heritage Month mean to you?

To me, National Hispanic Heritage Month is a time to learn, grow, and open our hearts to other cultures. It’s a reminder that the Hispanic community is not monolithic. We come from so many different countries, regions, and traditions, each with its own stories, flavors, and rhythms. This month is about recognizing that richness and also embracing how much we can learn from one another. It’s a time to celebrate our shared values and our differences, and, ultimately, a time to shine a light on how much more we have in common than we often realize.

Please tell us a little bit about your work and career.

I’m a published cookbook author and food blogger passionate about creating healthy, plant-forward meals, some Mexican, that bring people together. My journey started 23 years ago when my son was diagnosed with a dairy allergy. That experience led me to explore plant-based cooking, earn a certification, and eventually launch my blog Piloncillo & Vainilla in 2013, followed by Ale Cooks in English.

I live in Houston with my family, where I continue to cook, create, and celebrate food as the heart of connection.

Hibiscus Chamoy

Originally published here. Ingredients 2 cups hydrated hibiscus flowers 1 cup dried cherries or dried cranberries 3 tablespoons ground chile ancho subs or any other chili powder (or to taste) 1 tablespoon date syrup or date sugar 1 cup water or hibiscus water ¼ cup lime juice (or to taste) Pinch of Tajin (optional)

Instructions

1. Simmer the Ingredients: Start by adding the hibiscus flowers, dried fruit, chiles, and date syrup or date sugar to a blender, then add 1 cup of boiling water. (You can use a glass or stainless-steel bowl.)
2. Blend to Perfection: Blend until smooth. If needed, add ¼ cup water to adjust the consistency.
3. Season and Adjust: Finish with the lime juice, and add a pinch of Tajin if you’d like.
4. Store and Serve: Pour into a clean jar, seal tightly, and refrigerate. It keeps well for up to a month in the fridge, so you’ll have plenty of time to experiment with it on different dishes!

You can find Ale on her blog alecooks.com and piloncilloyvainilla.com, Instagram, Facebook, and Pinterest.

From Heart Failure, a book I wrote about my time at Tufts University School of Medicine: “I am all gloved up, fifth in line. At Tufts, medical students—particularly male students—practice pelvic exams on anesthetized women without their consent and without their knowledge. Women come in for surgery and, once they’re asleep, we all gather around; line forms to the left…We learn more than examination skills. Taking advantage of the woman’s vulnerability—as she lay naked on a table unconscious—we learn that patients are tools to exploit for our education.”

Using female patients to teach pelvic exams without their consent or knowledge remains “a dirty little secret about medical schools.” It is an “age-old” practice that continues to this day in med schools around the world. It’s been referred to as “the ‘vending machine’ model of pelvic exams, in which medical students line up to take their turn…” “Only it’s not a vending machine; it’s a woman’s vagina.”

It’s been called “an outrageous assault upon the dignity and autonomy of the patient…The practice shows a lack of respect for these patients as persons, revealing a moral insensitivity and a misuse of power.” Indeed, “it is yet another example of the way in which physicians abuse their power and have shown themselves unwilling to police themselves in matters of ethics, especially with regard to female patients.” Said a residency-program director at the Johns Hopkins University School of Medicine, “I don’t think any of us even think about it. It’s just so standard as to how you train medical students.”

What happened when this practice came to light in New Zealand? The chair of the New Zealand Medical Association got on television and said: “‘Until recently it wasn’t an issue…I’m very sorry that women feel they’ve been assaulted and violated in this way. That was never our intention.’ He had no idea then, asked the [TV] presenter, that women might object? ‘All I can say is that there have been no objections…’ ‘Could the reason be,’ asked the interviewer logically, “that it’s very hard for an anesthetized woman to know what’s going on?’”

The practice has been defended publicly by many medical schools and hospitals, contending “this touching is entirely appropriate and clearly falls well within the patient’s ‘implied consent’ to carry out the operation.” After all, “patients are aware they are entering a teaching hospital and therefore know that trainees will be actively participating in their care.” However, “researchers have found that many patients do not know when they have interacted with medical students, or even whether they are in a teaching hospital.” How can this be? “Deliberate lies and deception.”

“A survey of medical students found that 100% of them had been introduced to patients as ‘doctor’ by members of the clinical team,” and, as they go through training, there is, as a journal article is titled, an “Erosion in Medical Students’ Attitudes About Telling Patients They Are Students.” “Additionally, as medical students complete their clinical years of training, their sense of responsibility to inform patients that they are students is found to decrease,” especially if there is an opportunity to perform an invasive procedure. That may be why medical students seem to develop a “don’t ask, don’t tell” policy when it comes to seeking consent for pelvic examinations on anesthetized patients. More than a third of 1,600 medical students surveyed across the country strongly disagreed with the statement “Hospitals should obtain explicit permission for student involvement in pelvic exams,” as seen below and at 4:03 of my video Medical Students Practice Pelvic Exams on Anesthetized Women Without Their Consent.

After all, doctors “argue that performing a pelvic examination is no more intimate than placing one’s hands inside an abdomen during general surgery or attempting to intubate a patient” and assert that sticking your fingers in a woman’s vagina is “just as intimate” as an ophthalmologist looking into the back of your eye; any claim to the contrary is just “another attempt to justify the obsession with political correctness.” Said one medical school professor, “Personally, I would prefer to see a new generation of well-trained doctors…rather than a nation of women whose vaginas are protected from battery by medical students.”

The national survey concluded: “Patients admitted to teaching hospitals do not, however, by the mere act of admission relinquish their rights as human beings to have ultimate control over their own body and to be involved in decisions concerning their health care.”

Is it possible that women just don’t care? Studies show that up to 100% of women asked said they would want to know that vaginal exams were being performed by medical students. Since patients care deeply about being asked, why can’t we at least ask their permission? “We can’t ask women,” the medical school faculty replied. “If we do, they might say no.”

It’s jaw-dropping to me that I’m still trying to expose this practice more than 20 years after I first wrote about it. What’s to be done? Ending the Hidden Practice of Pelvic Exams on Unconscious Women Without Their Consent. 

Pakistani cuisine is rich, flavorful, and diverse — from the spicy curries of Punjab to the slow-cooked dishes of Sindh and the meaty kebabs of Khyber Pakhtunkhwa. But there’s one common ingredient in almost every kitchen: oil, and often a lot of it.

While oil enhances flavor and texture, excess consumption is linked to heart disease, obesity, and diabetes, which are rising health concerns in Pakistan. The good news? You don’t have to give up your favorite dishes. By making simple low-oil swaps, you can enjoy the same beloved flavors with far more nutrition and much less guilt.

This blog explores healthy, low-oil versions of Pakistani classics like biryani, chicken karahi, nihari, parathas, and kebabs — showing you how to keep the taste alive while cutting down on unnecessary fats.

Low-Oil Chicken Biryani: Flavorful Without the Grease

Biryani is perhaps the most iconic Pakistani dish. But the traditional version can be heavy with ghee, fried onions, and oil-soaked rice. Here’s how to make it healthier:

Ingredients

• 500g chicken (skinless, trimmed of visible fat)
• 2 cups basmati rice (soaked 30 minutes)
• 2 medium onions, thinly sliced
• 2 tomatoes, chopped
• ½ cup low-fat yogurt
• 2 tbsp olive oil (instead of ½ cup traditional oil)
• Spices: cumin, coriander, turmeric, chili powder, cinnamon stick, bay leaf, cloves
• Fresh coriander and mint leaves

Step-by-Step Recipe

1. Heat 1 tbsp olive oil and sauté onions until golden (air-fryer or oven caramelization works too).
2. Add tomatoes, yogurt, and spices. Stir until a thick masala forms.
3. Add chicken and cook until tender, letting the natural juices form the base instead of extra oil.
4. Boil rice separately with spices until 70% done.
5. Layer rice and chicken masala in a pot. Sprinkle herbs. Steam (“dum”) on low heat for 20 minutes.

Result: Fluffy, aromatic biryani with 70% less oil but full authentic flavor.

Light Chicken Karahi: The Fresh Tomato Trick

Karahi is loved for its fiery, rich masala. Traditionally, it uses almost half a cup of oil to fry chicken and spices. The healthier version uses fresh tomatoes and yogurt to create a rich base without excess oil.

Ingredients

• 500g chicken pieces
• 3 medium fresh tomatoes (blended to puree)
• 1 tbsp olive oil
• 1 tbsp ginger-garlic paste
• Green chilies, fresh coriander, and garam masala for garnish

Step-by-Step Recipe

1. Heat olive oil in a wok. Add ginger-garlic paste.
2. Add chicken, searing until lightly browned.
3. Pour in tomato puree, cook on medium heat until natural oils separate (takes longer but avoids adding fat).
4. Sprinkle garam masala, garnish with coriander and green chilies.

Result: A tangy, spicy karahi with fresh tomato richness instead of heavy oil.

Healthy Nihari: Slow-Cooked Goodness, Less Grease

Nihari is known for its deep, oily surface. But with careful cooking, you can preserve its richness while cutting out unnecessary fat.

Ingredients

• 500g beef shank (trimmed)
• 2 tbsp whole-wheat flour (instead of refined atta for thickening)
• 1 tbsp olive oil
• Spices: fennel, cumin, ginger, garlic, cinnamon, bay leaf, star anise, chili powder

Step-by-Step Recipe

1. Heat oil, add whole spices and meat.
2. Cook until meat browns, then add ginger-garlic paste.
3. Dissolve flour in water, add to pot for natural thickening.
4. Slow simmer for 3–4 hours until meat is tender.
5. Garnish with lemon, ginger slices, and coriander.

Result: A flavorful nihari without a thick oil layer floating on top.

Whole-Wheat Parathas: Crispy Without the Oil Pool

Parathas are a breakfast favorite but often soak in oil or ghee. You can still enjoy crispy, flaky parathas with just a few drops of oil.

Ingredients

• 2 cups whole-wheat flour
• 1 tsp salt
• 1 tsp olive oil
• Water to knead
• 1 tsp ghee or oil for brushing (optional)

Step-by-Step Recipe

1. Knead flour, salt, and water into a soft dough. Rest 20 minutes.
2. Roll out thin, brush lightly with oil, fold, and roll again.
3. Cook on a nonstick tawa, brushing lightly with ghee or oil spray.

Result: Crisp parathas with whole grains and 90% less oil.

Low-Fat Seekh Kebabs: Grill Over Fry

Seekh kebabs are often shallow fried or cooked with dripping fat. By grilling or baking them, you keep the smoky flavor with much less oil.

Ingredients

• 500g lean ground beef or chicken
• 1 onion, grated
• 1 tbsp ginger-garlic paste
• Spices: cumin, coriander, chili powder, garam masala
• Fresh coriander and green chilies

Step-by-Step Recipe

1. Mix all ingredients, shape into kebabs.
2. Grill in oven or air fryer, brushing lightly with olive oil.
3. Serve with mint chutney and salad.

Result: Juicy, smoky kebabs with reduced fat and calories.

Smart Cooking Hacks for Healthier Desi Food

• Use Olive Oil or Mustard Oil – Both are healthier and stable for cooking.
• Air-Fry Instead of Deep Frying – Works well for pakoras, samosas, and kebabs.
• Caramelize Onions Without Frying – Bake or air-fry for biryani and qorma bases.
• Bulk Up with Vegetables – Add spinach, peas, carrots, or beans to reduce meat-fat load.
• Practice Portion Control – Even healthier versions should be eaten in balance.

Final Word: Taste Without the Guilt

Healthy eating doesn’t mean giving up your roots. It means honoring your heritage with smarter choices. Whether it’s biryani, karahi, or kebabs, you can enjoy all the flavor and tradition of Pakistani food with far less oil and more nutrition.

At Nutric Food Show, we’re here to prove that healthy can be delicious — and desi!

In response to the charge that describing the benefits of statin drugs only in terms of relative risk reduction is a “statistical deception” created to give the appearance that statins are more effective than they really are, it was pointed out that describing things in terms of absolute risk reduction or number needed to treat can depend on the duration of the study.

For example, let’s say a disease has a 2% chance of killing you every year, but some drug cuts that risk by 50%. That sounds amazing, until you realize that, at the end of a year, your risk will only have fallen from 2% to 1%, so the absolute reduction of risk is only 1%. If a hundred people were treated with the drug, instead of two people dying, one person would die, so a hundred people would have to be treated to save one life, as shown below and at 1:01 in my video How Much Longer Do You Live on Statins?.

But there’s about a 99% chance that taking the drug all year would have no effect either way. So, to say the drug cuts the risk of dying by 50% seems like an overstatement. But think about it: Benefits accrue over time. If there’s a 2% chance of dying every year, year after year, after a few decades, the majority of those who refused the drug would be dead, whereas the majority who took the drug would be alive. So, yes, perhaps during the first year on the drug, there was only about a 1% chance it would be life-saving, but, eventually, you could end up with a decent chance the drug would save your life after all.

“This is actually the very reason why the usage of relative risk makes sense…” Absolute risk changes depending on the time frame being discussed, but with relative risk, you know that whatever risk you have, you can cut it in half by taking the drug. On average, statins only cut the risk of a cardiovascular “event” by 25%, but since cardiovascular disease is the number one killer of men and women, if you’re unwilling to change your diet, that’s a powerful argument in favor of taking these kinds of drugs. You can see the same kind of dependency on trial duration, looking at the “postponement of death” by taking a statin. How much longer might you live if you take statins?

The average postponement of death has some advantages over other statistics because it may offer “a better intuitive understanding among lay persons,” whereas a stat like a number needed to treat has more of a win-or-lose “lottery-like” quality. So, when a statin drug prevents, say, one heart attack out of a hundred people treated over five years, it’s not as though the other 99 completely lost out. Their cholesterol also dropped, and their heart disease progression presumably slowed down, too, just not enough to catch a heart attack within that narrow time frame.

So, what’s the effect of statins on average survival? According to an early estimate, if you put all the randomized trials together, the average postponement of death was calculated at maybe three or four days. Three or four days? Who would take a drug every day for years just to live a few more days? Well, let’s try to put that into context. Three or four days is comparable to the gains in life expectancy from other medical interventions. For example, it’s nearly identical to what you’d get from “highly effective childhood vaccines.” Because vaccines have been so effective in wiping out infectious diseases, these days, they only add an average of three extra days to a child’s life. But, of course, “those whose deaths are averted gain virtually their whole lifetimes.” That’s why we vaccinate. It just seems like such a small average benefit because it gets distributed over the many millions of kids who get the vaccine. Is that the same with statins?

An updated estimate was published in 2019, which explained that the prior estimate of three or four days was plagued by “important weaknesses,” and the actual average postponement of death was actually ten days. Headline writers went giddy from these data, but what they didn’t understand was that this was only for the duration of the trial. So, if your life expectancy is only five years, then, yes, statins may increase your lifespan by only ten days, but statins are meant to be taken a lot longer than five years. What you want to know is how much longer you might get to live if you stick with the drugs your whole life.

In that case, it isn’t an extra ten days, but living up to ten extra years. Taking statins can enable you to live years longer. That’s because, for every millimole per liter you lower your bad LDL cholesterol, you may live three years longer and maybe even six more years, depending on which study you’re reading. A millimole in U.S. units is 39 points. Drop your LDL cholesterol by about 39 points, and you could live years longer. Exercise your whole life, and you may only increase your lifespan by six months, and stopping smoking may net you nine months. But if you drop your LDL cholesterol by about 39 points, you could live years longer. You can accomplish that by taking drugs, or you can achieve that within just two weeks of eating a diet packed with fruits, vegetables, and nuts, as seen here and at 5:30 in my video. 

Want to know what’s better than drugs? “Something important and fundamental has been lost in the controversy around this broad expansion of statin therapy.…It is imperative that physicians (and drug labels) inform patients that not only their lipid [cholesterol] levels but also their cardiovascular risk can be reduced substantially by adoption of a plant-based dietary pattern, and without drugs. Dietary modifications for cardiovascular risk reduction, including plant-based diets, have been shown to improve not only lipid status, but also obesity, hypertension, systemic inflammation, insulin sensitivity, oxidative stress, endothelial function, thrombosis, and cardiovascular event risk…The importance of this [plant-based] approach is magnified when one considers that, in contrast to statins, the ‘side effects’ of plant-based diets—weight loss, more energy, and improved quality of life—are beneficial.” 

“Physicians have a duty to inform their patients about the risks and benefits of the interventions available to them. However, physicians rarely communicate with methods that convey absolute information, such as numbers needed to treat, numbers needed to harm, or prolongation of life, despite patients wanting this information.” That is, for example, how many people are actually helped by a particular drug, how many are actually hurt by it, or how much longer the drug will enable you to live, respectively.

If doctors inform patients only about the relative risk reduction—for example, telling them a pill will cut their risk of heart attacks by 34 percent—nine out of ten agree to take it. However, give them the same information framed as absolute risk reduction—“1.4% fewer patients had heart attacks”—then those agreeing to take the drug drops to only four out of ten. And, if they use the number needed to treat, only three in ten patients would agree to take the pill. So, if you’re a doctor and you really want your patient to take the drug, which statistic are you going to use?

The use of relative risk stats to inflate the benefits and absolute risk stats to downplay any side effects has been referred to as “statistical deception.” To see how one might spin a study to accomplish this, let’s look at an example. As you can see below and at 1:49 in my video, The True Benefits vs. Side Effects of Statins, there is a significantly lower risk of the incidence of heart attack over five years in study participants randomized to a placebo compared to those getting the drug. If you wanted statins to sound good, you’d use the relative risk reduction (24 percent lower risk). If you wanted statins to sound bad, you’d use the absolute risk reduction (3 percent fewer heart attacks).

Then you could flip it for side effects. For example, the researchers found that 0.3 percent (1 out of 290 women in the placebo group) got breast cancer over five years, compared to 4.1 percent (12 out of 286) in the statin group. So, a pro-statin spin might be a 24 percent drop in heart attack risk and only 3.8 percent more breast cancers, whereas an anti-statin spin might be only 3 percent fewer heart attacks compared to a 1,267 percent higher risk of breast cancer. Both portrayals are technically true, but you can see how easily you could manipulate people if you picked and chose how you were presenting the risks and benefits. So, ideally, you’d use both the relative risk reduction stat and the absolute risk reduction stat.

In terms of benefits, when you compile many statin trials, it looks like the relative risk reduction is 25 percent. So, if your ten-year risk of a heart attack or stroke is 5 percent, then taking a statin could lower that from 5 percent to 3.75 percent, for an absolute risk reduction of 1.25 percent, or a number needed to treat of 80, meaning there’s about a 1 in 80 chance that you’d avoid a heart attack or stroke by taking the drug for the next ten years. As you can see, as your baseline risk gets higher and higher, even though you have that same 25 percent risk reduction, your absolute risk reduction gets bigger and bigger. And, with a 20 percent baseline risk, that means you have a 1 in 20 chance of avoiding a heart attack or stroke over the subsequent decade if you take the drug, as seen below and at 3:31 in my video.

So, those are the benefits. In terms of risk, that breast cancer finding appears to be a fluke. Put together all the studies, and “there was no association between use of statins and the risk of cancer.” In terms of muscle problems, estimates of risk range from approximately 1 in 1,000 to closer to 1 in 50.

If all those numbers just blur together, the Mayo Clinic developed a great visualization tool, seen below and at 4:39 in my video.

For those at average risk, 10 people out of 100 who do not take a statin may have a heart attack over the next ten years. If, however, all 100 people took a statin every day for those ten years, 8 would still have a heart attack, but 2 would be spared, so there’s about a 1 in 50 chance that taking the drug would help avert a heart attack over the next decade. What are the downsides? The cost and inconvenience of taking a pill every day, which can cause some gastrointestinal side effects, muscle aching, and stiffness in about 5 percent, reversible liver inflammation in 2 percent, and more serious damage in perhaps 1 in 20,000 patients.

Note that the two happy faces in the bottom left row of the YES STATIN chart represent heart attacks averted, not lives saved. The chance that a few years of statins will actually save your life if you have no known heart disease is about 1 in 250.

If you want a more personalized approach, the Mayo Clinic has an interactive tool that lets you calculate your ten-year risk. You can get there directly by going to bit.ly/statindecision.

From the crispy pakoras of Punjab to reheated curries in microwaves and slow-simmering pots of nihari, our cooking methods play a huge role in how much nutrition actually ends up on our plate. Vitamin C, B-complex, and antioxidants are particularly sensitive to heat and cooking style, and the wrong method can destroy up to 50–90% of these nutrients.

This article uncovers the science of nutrient loss in cooking, explains how frying, microwaving, and overcooking impact your food, and offers smarter cooking alternatives rooted in both modern nutrition research and traditional wisdom.

Frying: Crispy Flavor, Hidden Nutrient Damage

In Pakistan, frying is almost a cultural identity — whether it’s samosas during Ramadan, parathas at breakfast, or fried chicken on weekends. The aroma is irresistible, but here’s the hidden truth: frying can turn nutrient-rich foods into calorie-heavy, nutrient-poor meals.

The Science of Nutrient Loss in Frying

• Vitamin Breakdown – Vitamins like Vitamin C (important for immunity) and B-vitamins (needed for energy and brain health) are water-soluble and highly heat-sensitive. At frying temperatures (160–190°C), they quickly degrade.

• Mineral Retention vs. Oil Absorption – While minerals like iron and calcium survive better, they get overshadowed by the oil absorption, which increases fat and calorie content.

• Toxic Compounds – Continuous reheating of oil leads to trans fats and acrylamides, linked with cardiovascular risks and inflammation.

Real-Life Example

Think about baingan (eggplant) fritters. Raw baingan is rich in antioxidants like nasunin, but when deep-fried, much of this antioxidant breaks down, and the eggplant absorbs large amounts of oil. What should have been a nutrient-rich side dish becomes an oily calorie bomb.

Healthier Alternatives to Frying

• Shallow Frying – Cook with minimal oil in a heavy-bottomed pan to reduce nutrient damage.

• Air-Frying – Keeps food crisp without drowning it in oil.

• Right Oil Choice – Use mustard oil or olive oil for high-heat stability. For traditional taste, desi ghee in moderation is far better than repeatedly reused cooking oil.

Microwaving: Fast but Not Always Nutrient-Friendly

Microwaves have become the go-to appliance for busy Pakistani families. From reheating leftover daal to defrosting chicken, they are quick and convenient. But are microwaves destroying nutrients in your food? The answer is nuanced.

The Science of Microwaving and Nutrients

• Short Bursts Preserve Nutrients – Microwaving for short times actually retains more nutrients than boiling, because less water is used and cooking time is shorter.

• Reheating Risks – Constant reheating, especially of vegetables, reduces antioxidants like flavonoids and polyphenols that protect against chronic diseases.

• Container Safety – Microwaving food in plastic containers can release harmful phthalates and BPA, which mimic hormones in the body and may cause long-term health risks.

Real-Life Example

Leftover chicken curry reheated in the microwave once is generally safe, but reheating it three times across two days means repeated vitamin breakdown and potential bacterial growth if not cooled properly.

Healthier Alternatives to Microwaving

• Use glass or ceramic dishes, never thin plastics.

• Microwave with a splash of water and cover the food to trap steam — this helps preserve nutrients.

• Avoid reheating the same dish more than once; instead, reheat only the portion you’ll eat.

Overcooking: The Silent Nutrient Killer

Desi cuisine is famous for its slow-cooked richness — from haleem in Karachi to paya in Lahore. While the flavors intensify, overcooking quietly robs your meal of its nutritional strength.

The Science of Overcooking

• Vitamin C Depletion – Found in green chilies, tomatoes, and coriander, Vitamin C begins breaking down after just 10 minutes of continuous heat. Long cooking destroys it almost completely.

• Loss of Polyphenols – Vegetables like spinach, okra, and beans lose polyphenols (plant antioxidants) when boiled or cooked excessively.

• Texture-Nutrition Trade-Off – Soft textures appeal to taste, but nutrients leach out, especially into cooking water that is often drained.

Real-Life Example

Think of daal simmering for hours until creamy. While the flavor deepens, many B-vitamins dissolve into the water, and prolonged heat destroys them further. Unless the liquid is consumed, most vitamins are gone.

Healthier Alternatives

• Pressure Cooking – Reduces cooking time while retaining more vitamins.

• Add Veggies Last – Toss spinach, coriander, or peas at the end to lock in their nutrition.

• Gentle Simmering – Keep flame low and avoid excessive stirring to preserve structure and nutrients.

Smarter Cooking Techniques That Preserve Nutrition

Pakistani kitchens don’t need to lose nutrition for the sake of taste. Traditional methods already offer healthier approaches:

1. Steaming – Best for vegetables like carrots, cauliflower, and beans. It locks in Vitamin C and antioxidants while preserving crunch.

2. Clay Pot Cooking – A heritage method still used in villages. Clay distributes heat evenly and cooks slowly at lower temperatures, protecting delicate vitamins.

3. Stir-Frying – Quick cooking at high heat with little oil. Perfect for chicken vegetable mix or okra stir-fry, keeping nutrition intact.

4. Pressure Cooking – Cuts cooking time, reduces water exposure, and preserves Vitamin B-complex in daals and meats.

5. Blanching – Briefly boiling then cooling vegetables keeps colors vibrant and nutrients intact, making them ideal for salads and side dishes.

Practical Tips for Every Home Kitchen

• Don’t Over-Peel – Potato and cucumber peels contain fiber and minerals.

• Use Less Water – Cook rice, daal, or vegetables with minimal water to prevent nutrient leaching.

• Cook Small Batches – Fresh food retains more vitamins than refrigerated, reheated meals.

• Herbs at the End – Garnishing with fresh mint, coriander, and curry leaves adds both flavor and preserved antioxidants.

• Balance Tradition with Science – It’s okay to enjoy fried samosas occasionally — just balance them with steamed sabzi or fresh salad.

Final Word: Cooking That Heals, Not Just Fills

Our food culture is rich and diverse, but modern cooking shortcuts and overuse of oil and heat are silently depleting the very nutrients that make food life-giving. By shifting to smarter methods — less frying, mindful microwaving, and avoiding overcooking — we can keep both flavor and nutrition alive in our kitchens.

At Nutric Food Show, our mission is to help every Pakistani household rediscover the joy of cooking that heals, not just fills. After all, a stronger nation begins with stronger kitchens.

Drug companies go out of their way—in direct-to-consumer ads, for example—to “present pharmaceutical drugs as a preferred solution to cholesterol management while downplaying lifestyle change.” You see this echoed in the medical literature, as in this editorial in the Journal of the American Medical Association: “Despite decades of exhortation for improvement, the high prevalence of poor lifestyle behaviors leading to elevated cardiovascular disease risk factors persists, with myocardial infarction [heart attack] and stroke remaining the leading causes of death in the United States. Clearly, many more adults could benefit from…statins for primary prevention.” Do we really need to put more people on drugs? A reply was published in the British Medical Journal: “Once again, doctors are implored to ‘get real’—stop hoping that efforts to help their patients and communities adopt healthy lifestyle habits will succeed, and start prescribing more statins. This is a self-fulfilling prophecy. Note that the author of these comments [the pro-statin editorial] disclosed receipt of funding from 11 drug companies, at least four of which produce or are developing new classes of cholesterol-lowering agents,” which make billions of dollars a year in annual sales.

Every time the cholesterol guidelines expand the number of people eligible for statins, they’re decried as a “big kiss to big pharma.” This is understandable, since the majority of guideline panel members “had industry ties,” financial conflicts of interest. But these days, all the major statins are off-patent, so there are inexpensive generic versions. For example, the safest, most effective statin is generic Lipitor, sold as atorvastatin for as little as a few dollars a month. So, nowadays, the cholesterol guidelines are not necessarily “part of an industry plot.”

“The US way of life is the problem, not the guidelines…” The reason so many people are candidates for cholesterol- and blood-pressure-lowering medications is that so many people are taking such terrible care of themselves. The bottom line is that “individuals must take more responsibility for their own health behaviors.” What if you are unwilling or unable to improve your diet and make lifestyle changes to bring down that risk? If your ten-year risk of having a heart attack is 7.5 percent or more and going to stay that way, then the benefits of taking a statin drug likely outweigh the risk. That’s really for you to decide, though. It’s your body, your choice.

“Whether or not the overall benefit-harm balance justifies the use of a medication for an individual patient cannot be determined by a guidelines committee, a health care system, or even the attending physician. Instead, it is the individual patient who has a fundamental right to decide whether or not taking a drug is worthwhile.” This was recognized by some of medicine’s “historical luminaries such as Hippocrates,” but “only in recent decades has the medical profession begun to shift from a paternalistic ‘doctor knows best’ stance towards one explicitly endorsing patient-centered, evidence-based, shared decision-making.” One of the problems with communicating statin evidence to support this shared decision-making is that most doctors “have a poor understanding of concepts of risk and probability and…increasing exposure to statistics in undergraduate and postgraduate education hasn’t made much difference.” But that understanding is critical for preventive medicine. When doctors offer a cholesterol-lowering drug, “they’re doing something quite different from treating a patient who has sought help because she is sick. They’re not so much doctors as life insurance salespeople, peddling deferred benefits in exchange for a small (but certainly not negligible) ongoing inconvenience and cost. In this new kind of medicine, not understanding risk is the equivalent of not knowing about the circulation of the blood or basic anatomy. So, let’s dive in and see exactly what’s at stake.

Below and at 3:55 in my video Are Doctors Misleading Patients About Statin Risks and Benefits? is an ad for Lipitor. When drug companies say a statin reduces the risk of a heart attack by 36 percent, that’s the relative risk.

If you follow the asterisk I’ve circled after the “36%” in the ad, you can see how they came up with that. I’ve included it here and at 3:56 in my video. In a large clinical study, 3 percent of patients not taking the statin had a heart attack within a certain amount of time, compared to 2 percent of patients who did take the drug. So, the drug dropped heart attack risk from 3 percent to 2 percent; that’s about a one-third drop, hence the 36 percent reduced relative risk statistic. But another way to look at going from 3 percent to 2 percent is that the absolute risk only dropped by 1 percent. So, in effect, “your chance to avoid a nonfatal heart attack during the next 2 years is about 97% without treatment, but you can increase it to about 98% by taking a Crestor [a statin] every day.” Another way to say that is that you’d have to treat 100 people with the drug to prevent a single heart attack. That statistic may shock a lot of people.

If you ask patients what they’ve been led to believe, they don’t think the chance of avoiding a heart attack within a few years on statins is 1 in 100, but 1 in 2. “On average, it was believed that most patients (53.1%) using statins would avoid a heart attack after statin treatment for 5 years.” Most patients, not just 1 percent of patients. And this “disparity between actual and expected effect could be viewed as a dilemma. On the one hand, it is not ethically acceptable for caregivers to deliberately support and maintain illusive treatment expectations by patients.” We cannot mislead people into thinking a drug works better than it really does, but on the other hand, how else are we going to get people to take their pills?

When asked, people want an absolute risk reduction of at least about 30 percent to take a cholesterol-lowering drug every day, whereas the actual absolute risk reduction is only about 1 percent. So, the dirty little secret is that, if patients knew the truth about how little these drugs actually worked, almost no one would agree to take them. Doctors are either not educating their patients or actively misinforming them. Given that the majority of patients expect a much larger benefit from statins than they’d get, “there is a tension between the patient’s right to know about benefiting from a preventive drug and the likely reduction in uptake [willingness to take the drugs] if they are so informed,” and learn the truth. This sounds terribly paternalistic, but hundreds of thousands of lives may be at stake.

If patients were fully informed, people would die. About 20 million Americans are on statins. Even if the drugs saved 1 in 100, that could mean hundreds of thousands of lives lost if everyone stopped taking their statins. “It is ironic that informing patients about statins would increase the very outcomes they were designed to prevent.”

The muscle-related side effects from cholesterol-lowering statins “are often severe enough for patients to stop taking the drug. Of course, these side effects could be coincidental or psychosomatic and have nothing to do with the drug,” given that many clinical trials show such side effects are rare. “It is also possible that previous clinical trials”—funded by the drug companies themselves—“under-recorded the side effects of statins.” The bottom line is that there’s an urgent need to establish the true incidence of statin side effects.

“What proportion of symptomatic side effects in patients taking statins are genuinely caused by the drug?” That’s the title of a journal article that reports that, even in trials funded by Big Pharma, “only a small minority of symptoms reported on statins are genuinely due to the statins,” and those taking statins are significantly more likely to develop type 2 diabetes than those randomized to placebo sugar pills. Why? We’re still not exactly sure, but statins may have the double-whammy effect of impairing insulin secretion from the pancreas while also diminishing insulin’s effectiveness by increasing insulin resistance.

Even short-term use of statins may “approximately double the odds of developing diabetes and diabetic complications.” As shown below and at 1:49 in my video Who Should Take Statins?, fewer people develop diabetes and diabetic complications off statins over a period of about five years than those who do develop diabetes while on statins. “Of more concern, this increased risk persisted for at least 5 years after statin use stopped.”

“In view of the overwhelming benefit of statins in the reduction of cardiovascular events,” the number one killer of men and women, any increase in risk of diabetes, our seventh leading cause of death, would be outweighed by any cardiovascular benefits, right? That’s a false dichotomy. We don’t have to choose between heart disease and diabetes. We can treat the cause of both with the same diet and lifestyle changes. The diet that can not only stop heart disease, but also reverse it, is the same one that can reverse type 2 diabetes. But what if, for whatever reason, you refuse to change your diet and lifestyle? In that case, what are the risks and benefits of starting statins? Don’t expect to get the full scoop from your doctor, as most seemed clueless about statins’ causal link with diabetes, so only a small fraction even bring it up with their patients.

“Overall, in patients for whom statin treatment is recommended by current guidelines, the benefits greatly outweigh the risks.” But that’s for you to decide. Before we quantify exactly what the risks and benefits are, what exactly are the recommendations of current guidelines?

How should you decide if a statin is right for you? “If you have a history of heart disease or stroke, taking a statin medication is recommended, without considering your cholesterol levels.” Period. Full stop. No discussion needed. “If you do not yet have any known cardiovascular disease,” then the decision should be based on calculating your own personal risk. If you know your cholesterol and blood pressure numbers, it’s easy to do that online with the American College of Cardiology risk estimator or the Framingham risk profiler.

My favorite is the American College of Cardiology’s estimator because it gives you your current ten-year risk and also your lifetime risk. So, for a person with a 5.8 percent risk of having a heart attack or stroke within the next decade, if they don’t clean up their act, that lifetime risk jumps to 46 percent, nearly a flip of the coin. If they improved their cholesterol and blood pressure, though, they could reduce that risk by more than tenfold, down to 3.9 percent, as shown below and at 4:11 in my video.

Since the statin decision is based on your ten-year risk, what do you do with that number? As you can see here and at 4:48 in my video, under the current guidelines, if your ten-year risk is under 5 percent, then, unless there are extenuating circumstances, you should just stick to diet, exercise, and smoking cessation to bring down your numbers. In contrast, if your ten-year risk hits 20 percent, then the recommendation is to add a statin drug on top of making lifestyle modifications. Unless there are risk-enhancing factors, the tendency is to stick with lifestyle changes if risk is less than 7.5 percent and to move towards adding drugs if above 7.5 percent.

Risk-enhancing factors that your doctor should take into account when helping you make the decision include a bad family history, really high LDL cholesterol, metabolic syndrome, chronic kidney or inflammatory conditions, or persistently high triglycerides, C-reactive protein, or LP(a). You can see the whole list here and at 4:54 in my video.

If you’re still uncertain, guidelines suggest you consider getting a coronary artery calcium (CAC) score, but even though the radiation exposure from that test is relatively low these days, the U.S. Preventive Services Task Force has explicitly concluded that the current evidence is insufficient to conclude that the benefits outweigh the harms.

“A poor diet now outranks smoking as the leading cause of death globally and in the United States, according to the latest data.” The top killer of Americans is the American diet, as you can see below and at 0:23 in my video How Much Do Doctors Actually Know About Nutrition?.

If diet is humanity’s number one killer, then, obviously, nutrition is the number one subject taught in medical school, right? Sadly, “medical students around the world [are] poorly trained in nutrition.” It isn’t that medical students aren’t interested in learning about it. In fact, “interest in nutrition was ‘uniformly high’ among medical students,” but medical schools just aren’t teaching it. “Without a solid foundation of clinical nutrition knowledge and skills, physicians worldwide are generally not equipped to even begin to have an informed nutrition conversation with their patients….”

How bad is it? One study, “Assessing the clinical nutrition knowledge of medical doctors,” found the majority of participants got 70 percent of the questions wrong—and they were multiple choice questions, so they should have gotten about a fifth of them right just by chance. “Wrong answers in the…knowledge test were not limited to difficult or demanding questions” either. For example, less than half of the doctors were able to guess how many calories are in fat, carbohydrates, and protein; only one in ten knew the recommended protein intake; and only about one in three knew what a healthy body mass index (BMI) was. We’re talking about really basic nutrition knowledge.

Even worse, not only did the majority of medical doctors get a failing grade, but 30 percent of those who failed had “a high self-perception of their CN [clinical nutrition] expertise.” They weren’t only clueless about nutrition; they were clueless that they were clueless about nutrition, a particularly bad combination given that doctors are “trusted and influential sources” of healthy eating advice. “For those consumers who get information from their personal healthcare professional, 78% indicate making a change in their eating habits as a result of those conversations.” So, if the doctor got everything they know from some article in a magazine while waiting in the grocery store checkout aisle, that’s what the patients will be following.

Of doctors surveyed, “only 25% correctly identified the American Heart Association recommended number of fruit and vegetable servings per day, and fewer still (20%) were aware of the recommended daily added sugar limit for adults.” So how are they going to counsel their patients? And get ready for this: Of the doctors who perceived themselves as having high nutrition knowledge, 93 percent couldn’t answer those two basic multiple-choice questions, as seen here and at 2:39 in my video.

“Physicians with no genuine expertise in, say, neurosurgery [brain surgery] are neither likely to broadcast detailed opinions on that topic nor to have their ‘expert’ opinions solicited by the media. Most topical domains in medicine enjoy such respect: we defer expert opinion and commentary to actual experts. Not so nutrition, where the common knowledge that physicians are generally ill-trained in this area is conjoined to routine invitations to physicians for their expert opinions on the matter. All too many are willing to provide theirs, absent any basis for actual expertise…” Or worse, they’re “often made on the basis of native bias and personal preference, at times directly tethered to personal gain—such as diet book sales—and so arises yet another ethical challenge.” That’s one of the reasons all the proceeds I receive from my books are donated directly to charity. I don’t want even the appearance of any conflicts of interest.

“In a culture that routinely fails to distinguish expertise from mere opinion or personal anecdote, we physicians should be doing all we can to establish relevant barriers to entry for expert opinion in this [diet and nutrition], as in all other matters of genuine medical significance.” I mean, we aren’t talking celebrity gossip. Lives are at stake. “Entire industries are devoted to marketing messages that may conspire directly against well-informed medical advice in this area.”

“Medical education must be brought up to date. For physicians to be ill-trained in the very area most impactful on the rate of premature death at the population level is an absurd anachronism….The mission of medicine is to protect, defend, and advance the human condition. That mission cannot be fulfilled if the diet is neglected.”

A possible starting place? “Physicians and health care organizations can collectively begin to emphasize their seriousness about nutrition in health care by practicing what they (theoretically) preach. Is it appropriate to serve pizza and soft drinks at a resident conference while bemoaning the high prevalence of obesity and encouraging patients to eat healthier? A similarly poor example exists in medical conferences, including national meetings, where some morning sessions are accompanied by foods such as donuts and sausage.”

When researchers tested more than a thousand patients suffering for longer than six months from symptoms typical with irritable bowel syndrome (IBS), such as excess gas, bloating, diarrhea, and abdominal pain, but who do not appear to have anything more serious going on, like inflammatory bowel disease, a significant percentage were found to be suffering from lactose intolerance—intolerance to the milk sugar lactose. In infancy, we have an enzyme called lactase in our small intestine that digests milk sugar, but, understandably, most of us lose it after weaning. “Although genetic mutation has led to persistence of lactase in adults, about 75% of the world’s population malabsorbs lactose after age 30” and have lactose intolerance. However, a third of the patients were diagnosed with small intestinal bacterial overgrowth (SIBO).

“The evidence for SIBO and IBS is shrouded in controversy, predominantly because of the fact that the [breath] tests used in clinical practice to diagnose SIBO are not valid,” as I’ve explored before. As well, the implications of having more versus fewer bacteria growing in the small intestine are unclear since the number doesn’t seem to correlate with the symptoms. It turns out it isn’t the number of bugs growing in the small intestine, but the type of bugs. So, it’s “small intestinal microbial dysbiosis”—not overgrowth in general, but the wrong kind of growth—that appears to underlie symptoms associated with functional gastrointestinal disorders, like IBS.

How can we prevent this from happening? The symptoms appear to be correlated with a significant drop in the number of Prevotella. Remember them? Prevotella are healthy fiber feeders, “suggestive of a higher fiber intake in healthy individuals,” while the bugs found more in symptomatic patients ate sugar, which “may reflect a higher dietary intake of simple sugars.” However, correlation doesn’t mean causation. To prove cause and effect, we have to put it to the test, which is exactly what researchers did.

“Switching a group of healthy individuals who habitually ate a high­-fibre diet (>11g per 1,000 calories) to a low­-fibre diet (<10g per day) containing a high concentration of simple sugars for 7 days produced striking results. First, 80% developed de novo [new] gastrointestinal symptoms such as bloating and abdominal pain that resolved on resumption of their habitual high-fibre diet. Second, diet­-related changes in the small intestinal microbiome were predictive of symptoms (such as bloating and abdominal discomfort) and linked to an alteration in duodenal [intestinal] permeability.” In other words, they developed a leaky gut within seven days. And, while some went from SIBO positive to SIBO negative and others from SIBO negative to SIBO positive, it didn’t matter because the number of bacteria growing didn’t correlate with symptoms. It was the type of bacteria growing, as you can see below, and at 3:12 in my video Fiber vs. Low FODMAP for SIBO Symptoms.

No wonder their guts got leaky. Levels of short-chain fatty acids plummeted. Those are the magical by-products our good gut bugs make from fiber, which “play an important role in epithelial [intestinal] barrier integrity,” meaning they keep our gut from getting leaky.

So, while we don’t have sound data to suggest that something like a low FODMAP diet has any benefit for patients with SIBO symptoms, there have been more than a dozen randomized controlled trials that have put fiber to the test. Overall, researchers found there was a significant improvement in symptoms among those randomized to increase their fiber intake. That may help explain why “high-fiber, plant-based diets can prevent many diseases common in industrialized societies.” Such diets have this effect “on the composition and metabolic activity of the colonic microbiota.” Our good gut bugs take plant residues like fiber and produce “health-promoting and cancer-suppressing metabolites” like short-chain fatty acids, which have profound anti-inflammatory properties. “All the evidence points to a physiological need for ~50 g fiber per day, which is the amount contained in the traditional African diet and associated with the prevention of westernized diseases.” That is approximately twice the typical recommendation and three times more than what most people get on a daily basis. Perhaps it should be no surprise that we need so much. Even though we split from chimpanzees millions of years ago, “there is still broad congruency” in the composition of our respective microbiomes to this day. While they’re still eating their 98 to 99 percent plant-based diets to feed their friendly flora with fiber, we’ve largely removed fiber-rich foods from our food supply. 

Gastrointestinal symptoms like abdominal pain and bloating account for millions of doctor visits every year. One of the conditions that may be considered for such a “nonspecific presentation” of symptoms is SIBO, a concept that “has gained popularity on the internet in addition to certain clinical and research circles.” SIBO is “broadly defined as excessive bacteria in the small intestine” and typically treated with antibiotics, but “dispensing antibiotics to patients with the nonspecific, common symptoms associated with SIBO is not without risks,” such as the fostering of antibiotic resistance, the emergence of side effects, and the elimination of our good bacteria that could set us up for an invasion of bad bugs like C. diff—all for a condition that may not even be real.

Even alternative medicine journals admit that SIBO is being overdiagnosed, creating “confusion and fear.” SIBO testing “is overused and overly relied upon. Diagnoses are often handed out quickly and without adequate substantiation. Patients can be indoctrinated into thinking SIBO is a chronic condition that can not be cleared and will require lifelong management. This is simply not true for most and is an example of the damage done by overzealousness.” “The ‘monster’ that we now perceive SIBO to be may be no more than a phantom.”

The traditional method for a diagnosis was a small bowel aspiration, an invasive test where a long tube is snaked down the throat to take a sample and count the bugs down there, as you can see at 2:10 in my video Are Small Intestinal Bacterial Overgrowth (SIBO) Tests Valid?.

This method has been almost entirely replaced with breath tests. Normally, a sugar called glucose is almost entirely absorbed in the small intestine, so it never makes it down to the colon. So, the presence of bacterial fermentation of that sugar suggests there are bacteria in the small intestine. Fermentation can be detected because the bacteria produce specific gases that get absorbed in our bloodstream before being exhaled from our lungs, which can then be detected with a breathalyzer-type machine.

Previously, the sugar lactulose was used, but “lactulose breath tests do not reliably detect the overgrowth of bacteria,” so researchers switched to glucose. However, when glucose was finally put to the test, it didn’t work. The bacterial load in the small intestine was similar for those testing positive or negative, so that wasn’t a useful test either. It turns out that glucose can make it down to the colon after all.

Researchers labeled the glucose dose with a tracer and found that nearly half of the positive results from glucose breath tests were false positives because individuals were just fermenting it down in their colon, where our bacteria are supposed to be. So, “patients who are incorrectly labeled with SIBO may be prescribed multiple courses of antibiotics” for a condition they don’t even have.

Why do experts continue to recommend breath testing? Could it be because the “experts” were at a conference supported by a breath testing company, and most had personally received funds from SIBO testing or antibiotic companies?

Even if we could properly diagnose SIBO, does it matter? For those with digestive symptoms, there is a massive range of positivity for SIBO from approximately 4 percent to 84 percent. Researchers “found there to be no difference in overall symptom scores between those testing positive against those testing negative for SIBO…” So, a positive test result could mean anything. Who cares if some people have bacteria growing in their small intestines if it doesn’t correlate with symptoms?

Now, antibiotics can make people with irritable bowel-type symptoms who have been diagnosed with SIBO feel better. Does that prove SIBO was the cause? No, because antibiotics can make just as many people feel better who are negative for SIBO. Currently, the antibiotic rifaximin is most often used for SIBO, but it is “not currently FDA-approved for use in this indication, and its cost can be prohibitive.” (The FDA is the U.S. Food and Drug Administration.) In fact, no drug has been approved for SIBO in the United States or Europe, so even with good insurance, it may cost as much as $50 a day in out-of-pocket expenses, and the course is typically two weeks.

What’s more, while antibiotics may help in the short term, they may make matters worse in the long term. Those “who are given a course of antibiotics are more than three times as likely to report more bowel symptoms 4 months later than controls.” So, what can we do for these kinds of symptoms? That’s exactly what I’m going to turn to next.

What Causes Hair Loss?

As I discuss in my video Supplements for Hair Growth, we don’t lose our hair by washing or brushing it too much––two of the many myths out there. The majority of hair loss with age is genetic for both women and men. Based on twin studies, the heritability of baldness in men is 79%, meaning about 80% of the differences in hair loss between men is genetically determined, but that leaves some wiggle room.

Look at identical twins, for instance: Identical twin sisters with the same DNA had different amounts of hair loss, thanks to increased stress, increased smoking, having more children, or having a history of high blood pressure or cancer.

Indeed, smoking can contribute to the development of both male and female pattern baldness because the genotoxic compounds in cigarettes may damage the DNA in our hair follicles and cause microvascular poisoning in their base.

Other toxic agents associated with hair loss include mercury; it seems to concentrate about 250-fold in growing scalp hair. William Shakespeare may have started losing his hair due to mercury poisoning from syphilis treatment. Thankfully, doctors don’t give their patients mercury anymore. These days, as the Centers for Disease Control and Prevention point out, mercury mainly enters the body through seafood consumption.

Consider this: A woman went to her physician, concerned about her hair loss. Blood tests indicated elevated mercury levels, which makes sense as her diet was high in tuna. When she stopped eating tuna, her mercury levels fell and her hair started to grow back within two months. After seven months on a fish-free diet, her hair completely regrew. Doctors should consider screening for mercury toxicity when they see hair loss.

How to Prevent Hair Loss

In addition to not smoking, managing our stress, and avoiding seafood, is there anything else we can do to prevent hair loss?

We can make sure we don’t have scurvy, severe vitamin C deficiency. We’ve known for centuries that scurvy can cause hair loss, but once we have enough vitamin C so our gums aren’t bleeding, there are no data correlating vitamin C levels and hair loss. So, make sure you have a certain baseline sufficiency.

Foods for Our Hair

What about foods for hair loss? What role might diet play in the treatment of hair loss?

As I discuss in my video Food for Hair Growth, population studies have found that male pattern baldness is associated with poor sleeping habits and the consumption of meat and junk food, whereas protective associations were found for the consumption of raw vegetables, fresh herbs, and soy milk. Drinking soy beverages on a weekly basis was associated with 62% lower odds of moderate to severe hair loss, raising the possibility that there may be compounds in plants that may be protective.

A randomized, double-blind, placebo-controlled study of compounds in hot peppers and soy found significantly higher promotion of hair growth, and the doses used were reasonable: 6 milligrams of capsaicin a day and 75 milligrams of isoflavones. How does that translate into actual food? We can get 6 milligrams of capsaicin in just a quarter of a fresh jalapeño pepper a day and 75 milligrams of isoflavones eating just three-quarter cup of tempeh or soybeans.

Researchers also investigated pumpkin seeds and hair loss. For a few months, 76 men with male pattern baldness received 400 milligrams of pumpkin seed oil a day hidden in capsules (the equivalent of eating about two and a half pumpkin seeds a day) or took placebo capsules. After 24 weeks of treatment, self-rated improvement and satisfaction scores in the pumpkin group were higher, and they objectively had more hair—a 40% increase in hair counts, compared to only 10% in the placebo group. In the pumpkin group, 95% remained either unchanged or improved, whereas in the control group, more than 90% remained unchanged or worsened. Given such a pronounced effect, there was concern about sexual side effects, but researchers looked before and after at an index of erectile dysfunction and found no evidence of adverse effects.

The Best Vitamin for Hair Growth?

The most common ingredient in top-selling hair loss products is vitamin B7, also known as biotin. Biotin deficiency causes hair loss, but there are no evidence-based data that supplementing biotin promotes hair growth. And severe biotin deficiency in healthy individuals eating a normal diet has never been reported. However, if you eat raw egg whites, you can acquire a biotin deficiency, since there are compounds that attach to biotin and prevent it from being absorbed. Other than rare deficiency syndromes, though, it’s a myth that biotin supplements increase hair growth.

Can we just adopt the attitude that it can’t hurt, so we might as well see if it helps? No, because there is a lack of regulatory oversight of the supplement industry and, in the case of biotin, interference with lab tests. Many dietary supplements promoted for hair health contain biotin levels up to 650 times the recommended daily intake of biotin. And excess biotin in the blood can play haywire on a bunch of different blood tests, including thyroid function, other hormone tests (including pregnancy), and the test performed to determine if you’ve had a heart attack––so it could potentially even be life or death.

Do Hair Growth Pills Really Work?

What about drugs? We only have good evidence for efficacy for the two drugs approved by the U.S. Food and Drug Administration: finasteride, sold as Propecia, and minoxidil, sold as Rogaine. It’s considered a myth that all the patented hair-loss supplements on the market will increase hair growth. And they may actually be more expensive, with over-the-counter supplement regimens costing up to more than $1,000 a year, whereas the drugs may cost only $100 to $300 a year. As I discuss in my video Pills for Hair Growth, the drugs can help, but they can also cause side effects. Propecia can diminish libido, cause sexual disfunction, and have been associated with impotence, testicular pain, and breast enlargement, while the topical Minoxidil can cause itching, for example.

How do they work (if they work at all)? Androgens are the principal drivers of hair growth in both men and women. Testosterone is the primary androgen circulating in the blood, and it can be converted to dihydrotestosterone, which is even more powerful, by an enzyme called 5-alpha reductase. That’s the enzyme that is blocked by Propecia, so it inhibits the souping up of testosterone. This is why pre-menopausal women are not supposed to take it, since it could feminize male fetuses, whereas for men, it has sexual side effects like erectile dysfunction, which can affect men for years even after stopping the medication and may even be permanent. Indeed, up to 20% of people reporting persistent sexual dysfunction for six or more years after stopping the drug, suggesting the possibility that it may never go away.

Pass on the Pills and Reach for a Fork

Given the side effects of the current drug options, I encourage you to incorporate hair-friendly foods in your daily routine.

These recipes not only save precious time but also reduce kitchen cleanup. Plus, they carry the rich heritage of Pakistani cooking traditions while fitting seamlessly into modern, fast-paced lifestyles.

Why One-Pot Meals Are Perfect for Weeknights

• Quick Cooking: Most one-pot meals are ready within 45 minutes or less.
• Less Cleanup: Just one pot, fewer dishes, and no mess.
• Balanced Nutrition: Proteins, vegetables, and carbs all in one wholesome meal.
• Authentic Flavors: Retain the slow-cooked taste of desi spices without extra effort.
• Versatile Options: From rice-based to lentil stews, there’s something for every taste.

1. Chicken Yakhni Pulao – Comfort in Every Grain

Fragrant, soothing, and rich in nutrients, yakhni pulao is an all-time family favorite.

Ingredients: Chicken, basmati rice, ginger-garlic, onion, black peppercorns, cinnamon, cloves, bay leaf, cumin, salt, and green chilies.

Step-by-Step Recipe:

1. Boil chicken with spices (peppercorns, cloves, cinnamon, bay leaf) to make yakhni (broth).
2. Strain the broth and separate chicken pieces.
3. In the same pot, sauté onions and ginger-garlic paste until golden.
4. Add chicken, green chilies, and rice.
5. Pour in the yakhni, cover, and cook until rice is fluffy.
6. Serve with raita or fresh salad.

Perfect for weeknights because it’s light on the stomach yet filling.

2. Khichdi – Healing Comfort in a Bowl

A nourishing, humble dish made with rice and lentils—easy, quick, and soul-warming.

Ingredients: Basmati rice, moong dal, cumin seeds, onion, turmeric, ginger-garlic paste, ghee, and salt.

Steps:

1. Wash and soak rice and lentils.
2. In a pot, heat ghee, add cumin and onions until light brown.
3. Add ginger-garlic, turmeric, rice, and lentils.
4. Pour in water, cover, and cook until mushy.
5. Garnish with fried onions and serve with achar or papad.

Packed with protein and perfect for days when you need quick nourishment.

3. Mutton Tahari – The Royal One-Pot Rice

Tahari is a spiced rice dish with roots in Mughlai cuisine, often made with mutton or beef.

Ingredients: Mutton, rice, onions, yogurt, ginger-garlic paste, turmeric, chili powder, garam masala, potatoes, and green chilies.

Steps:

1. Heat oil and fry onions until golden.
2. Add mutton, spices, yogurt, and cook until oil separates.
3. Toss in diced potatoes and sauté.
4. Add soaked rice and water, cover, and simmer until rice is done.
5. Fluff with a fork and serve hot.

A hearty option for meat lovers who crave rich, spicy flavors.

4. Daal Mash with Rice – Protein-Packed Simplicity

When time is short, daal mash with plain rice is unbeatable.

Ingredients: White lentils (mash daal), onions, ginger-garlic paste, tomatoes, green chilies, turmeric, red chili powder, salt, and ghee.

Steps:

1. Boil lentils until soft but not mushy.
2. In the same pot, fry onions in ghee until golden.
3. Add tomatoes, spices, and green chilies.
4. Stir in lentils, simmer for 10 minutes.
5. Serve with plain rice, achar, or salad.

Quick, healthy, and loved by students, professionals, and families alike.

5. Vegetable Pulao – A Wholesome Vegetarian Delight

Great for when you want something light but full of flavor.

Ingredients: Basmati rice, peas, carrots, potatoes, onions, ginger-garlic paste, cumin seeds, green chilies, and salt.

Steps:

1. Heat oil, add cumin and onions until golden.
2. Add ginger-garlic paste, chopped vegetables, and sauté.
3. Add rice, salt, and water.
4. Cover and cook until fluffy.
5. Serve with yogurt raita.

Perfect for weeknights when you want to eat healthy and light.

6. Chicken Karahi with Chapati – One-Pot Shortcut

Although traditionally cooked in a wok, this can be adapted as a one-pot meal.

Ingredients: Chicken, tomatoes, ginger, garlic, green chilies, coriander, salt, and black pepper.

Steps:

1. Heat oil in a karahi, fry ginger-garlic paste.
2. Add chicken and cook until slightly browned.
3. Add chopped tomatoes, salt, pepper, and green chilies.
4. Cook until oil separates and chicken is tender.
5. Garnish with coriander and ginger slices.

Pair with instant chapati or paratha for a quick, filling dinner.

Pro Tips for Perfect One-Pot Meals

• Always soak rice for at least 20 minutes for fluffy grains.
• Balance spice levels depending on family preference.
• Use ghee or olive oil for richer taste and health benefits.
• Add seasonal vegetables for extra nutrition.
• Double portions to store leftovers for next day’s lunch.

Final Thoughts

One-pot Pakistani meals are more than convenience—they’re a lifestyle choice that blends tradition with practicality. Whether it’s a comforting khichdi, a rich tahari, or a hearty yakhni pulao, these dishes keep your evenings stress-free and your stomach happy.

Next time your weeknight feels rushed, let your pot do the magic.

“Psychological health can be broadly conceptualized as comprising 2 key components: mental health (i.e., the presence of absence of mental health disorders such as depression) and psychological well-being (i.e., a positive psychological state, which is more than the absence of a mental health disorder,” and that is the focus of an “emerging field of positive psychology [that] focuses on the positive facts of life, including happiness, life satisfaction, personal strengths, and flourishing.” This may translate to physical “benefits of enhanced well-being, including improvements in blood pressure, immune competence, longevity, career success, and satisfaction with personal relationships.”

What is “The Contribution of Food Consumption to Well-Being,” the title of an article in Annals of Nutrition & Metabolism? Studies have “linked the consumption of fruits and vegetables with enhanced well-being.” A systematic review of research found evidence that fruit and vegetable intake “was associated with increased psychological well-being.” Only an association?

There is “a famous criticism in this area of research—namely, that deep-down personality or family upbringing might lead people simultaneously to eat in a healthy way and also to have better mental well-being, so that diet is then merely correlated with, but incorrectly gives the appearance of helping to cause, the level of well-being.” However, recent research circumvented this problem by examining if “changes in diet are correlated with changes in mental well-being”—in effect, studying the “Evolution of Well-Being and Happiness After Increases in Consumption of Fruit and Vegetables.” As you can see below and at 1:37 in my video Fruits and Vegetables Put to the Test for Boosting Mood, as individuals began eating more fruits and veggies, there was a straight-line increase in their change in life satisfaction over time.

“Increased fruit and vegetable consumption was predictive of increased happiness, life satisfaction, and well-being. They were up to 0.24 life-satisfaction points (for an increase of 8 portions a day), which is equal in size to the psychological gain of going from unemployment to employment.” (My Daily Dozen recommendation is for at least nine servings of fruits and veggies a day.)

That study was done in Australia. It was repeated in the United Kingdom, and researchers found the same results, though Brits may need to bump up their daily minimum consumption of fruits and vegetables to more like 10 or 11 servings a day.

As researchers asked in the title of their paper, “Does eating fruit and vegetables also reduce the longitudinal risk of depression and anxiety?” Improved well-being is nice, but “governments and medical authorities are often interested in the determinants of major mental ill-health conditions, such as depression and high levels of anxiety, and not solely in a more typical citizen’s level of well-being”—for instance, not just life satisfaction. And, indeed, using the same dataset but instead looking for mental illness, researchers found that “eating fruit and vegetables may help to protect against future risk of clinical depression and anxiety,” as well.

A systematic review and meta-analysis of dozens of studies found “an inverse linear association between fruit or vegetable intake and risk of depression, such that every 100-gram increased intake of fruit was associated with a 3% reduced risk of depression,” about half an apple. Yet, “less than 10% of most Western populations consume adequate levels of whole fruits and dietary fiber, with typical intake being about half of the recommended levels.” Maybe the problem is we’re just telling people about the long-term benefits of fruit intake for chronic disease prevention, rather than the near-immediate improvements in well-being. Maybe we should be advertising the “happiness’ gains.” Perhaps, but we first need to make sure they’re real.

We’ve been talking about associations. Yes, “a healthy diet may reduce the risk of future depression or anxiety, but being diagnosed with depression or anxiety today could also lead to lower fruit and vegetable intake in the future.” Now, in these studies, we can indeed show that the increase in fruit and vegetable consumption came first, and not the other way around, but as the great enlightenment philosopher David Hume pointed out, just because the rooster crows before the dawn doesn’t mean the rooster caused the sun to rise.

To prove cause and effect, we need to put it to the test with an interventional study. Unfortunately, to date, many studies have compared fruit to chocolate and chips, for instance. Indeed, study participants randomized to eat fruit showed significant improvements in anxiety, depression, fatigue, and emotional distress, which is amazing, but that was compared to chocolate and potato chips, as you can see below and at 4:26 in my video. Apples, clementines, and bananas making people feel better than assorted potato chips and chunky chocolate wafers is not exactly a revelation.

This is the kind of study I’ve been waiting for: a randomized controlled trial in which young adults were randomized to one of three groups—a diet-as-usual group, a group encouraged to eat more fruits and vegetables, or a third group given two servings of fruits and vegetables a day to eat in addition to their regular diet. Those in the third group “showed improvements to their psychological well-being with increases in vitality, flourishing, and motivation” within just two weeks. However, simply educating people to eat their fruits and vegetables may not be enough to reap the full rewards, so perhaps greater emphasis needs to be placed on providing people with fresh produce—for example, offering free fruit for people when they shop. I know that would certainly make me happy!

When we eat the same foods over and over, we become habituated to them and end up liking them less. That’s why the “10th bite of chocolate, for example, is desired less than the first bite.” We have a built-in biological drive to keep changing up our foods so we’ll be more likely to hit all our nutritional requirements. The drive is so powerful that even “imagined consumption reduces actual consumption.” When study participants imagined again and again that they were eating cheese and were then given actual cheese, they ate less of it than those who repeatedly imagined eating that food fewer times, imagined eating a different food (such as candy), or did not imagine eating the food at all.

Ironically, habituation may be one of the reasons fad “mono diets,” like the cabbage soup diet, the oatmeal diet, or meal replacement shakes, can actually result in better adherence and lower hunger ratings compared to less restrictive diets.

In the landmark study “A Satiety Index of Common Foods,” in which dozens of foods were put to the test, boiled potatoes were found to be the most satiating food. Two hundred and forty calories of boiled potatoes were found to be more satisfying in terms of quelling hunger than the same number of calories of any other food tested. In fact, no other food even came close, as you can see below and at 1:14 in my video Exploiting Sensory-Specific Satiety for Weight Loss.

No doubt the low calorie density of potatoes plays a role. In order to consume 240 calories, nearly one pound of potatoes must be eaten, compared to just a few cookies, and even more apples, grapes, and oranges must be consumed. Each fruit was about 40 percent less satiating than potatoes, though, as shown here and at 1:45 in my video. So, an all-potato diet would probably take the gold—the Yukon gold—for the most bland, monotonous, and satiating diet.

A mono diet, where only one food is eaten, is the poster child for unsustainability—and thank goodness for that. Over time, they can lead to serious nutrient deficiencies, such as blindness from vitamin A deficiency in the case of white potatoes.

The satiating power of potatoes can still be brought to bear, though. Boiled potatoes beat out rice and pasta in terms of a satiating side dish, cutting as many as about 200 calories of intake off a meal. Compared to boiled and mashed potatoes, fried french fries or even baked fries do not appear to have the same satiating impact.

To exploit habituation for weight loss while maintaining nutrient abundance, we could limit the variety of unhealthy foods we eat while expanding the variety of healthy foods. In that way, we can simultaneously take advantage of the appetite-suppressing effects of monotony while diversifying our fruit and vegetable portfolio. Studies have shown that a greater variety of calorie-dense foods, like sweets and snacks, is associated with excess body fat, but a greater variety of vegetables appears protective. When presented with a greater variety of fruit, offered a greater variety of vegetables, or given a greater variety of vegetable seasonings, people may consume a greater quantity, crowding out less healthy options.

The first 20 years of the official Dietary Guidelines for Americans recommended generally eating “a variety of foods.” In the new millennium, they started getting more precise, specifying a diversity of healthier foods, as seen below and at 3:30 in my video. 

A pair of Harvard and New York University dietitians concluded in their paper “Dietary Variety: An Overlooked Strategy for Obesity and Chronic Disease Control”: “Choose and prepare a greater variety of plant-based foods,” recognizing that a greater variety of less healthy options could be counterproductive.

So, how can we respond to industry attempts to lure us into temptation by turning our natural biological drives against us? Should we never eat really delicious food? No, but it may help to recognize the effects hyperpalatable foods can have on hijacking our appetites and undermining our body’s better judgment. We can also use some of those same primitive impulses to our advantage by minimizing our choices of the bad and diversifying our choices of the good. In How Not to Diet, I call this “Meatball Monotony and Veggie Variety.” Try picking out a new fruit or vegetable every time you shop.

In my own family’s home, we always have a wide array of healthy snacks on hand to entice the finickiest of tastes. The contrasting collage of colors and shapes in fruit baskets and vegetable platters beat out boring bowls of a single fruit because they make you want to mix it up and try a little of each. And with different healthy dipping sauces, the possibilities are endless.

How did we evolve to solve the daunting task of selecting a diet that supplies all the essential nutrients? Dietary diversity. By eating a variety of foods, we increase our chances of hitting all the bases. If we only ate for pleasure, we might just stick with our favorite food to the exclusion of all others, but we have an innate tendency to switch things up.

Researchers found that study participants ended up eating more calories when provided with three different yogurt flavors than just one, even if that one is the chosen favorite. So, variation can trump sensation. They don’t call it the spice of life for nothing.

It appears to be something we’re born with. Studies on newly weaned infants dating back nearly a century show that babies naturally choose a variety of foods even over their preferred food. This tendency seems to be driven by a phenomenon known as sensory-specific satiety.

Researchers found that, “within 2 minutes after eating the test meal, the pleasantness of the taste, smell, texture, and appearance of the eaten food decreased significantly more than for the uneaten foods.” Think about how the first bite of chocolate tastes better than the last bite. Our body tires of the same sensations and seeks out novelty by rekindling our appetite every time we’re presented with new foods. This helps explain the “dessert effect,” where we can be stuffed to the gills but gain a second wind when dessert arrives. What was adaptive for our ancient ancestors to maintain nutritional adequacy may be maladaptive in the age of obesity.

When study participants ate a “varied four-course meal,” they consumed 60 percent more calories than those given the same food for each course. It’s not only that we get bored; our body has a different physiological reaction.

As you can see below and at 2:13 in my video How Variation Can Trump Sensation and Lead to Overeating, researchers gave people a squirt of lemon juice, and their salivary glands responded with a squirt of saliva. But when they were given lemon juice ten times in a row, they salivated less and less each time. When they got the same amount of lime juice, though, their salivation jumped right back up. We’re hard-wired to respond differently to new foods. 
Whether foods are on the same plate, are at the same meal, or are even eaten on subsequent days, the greater the variety, the more we tend to eat. When kids had the same mac and cheese dinner five days in a row, they ended up eating hundreds fewer calories by the fifth day, compared to kids who got a variety of different meals, as you can see below and at 2:35 in my video.

Even just switching the shape of food can lead to overeating. When kids had a second bowl of mac and cheese, they ate significantly more when the noodles were changed from elbow macaroni to spirals. People allegedly eat up to 77 percent more M&Ms if they’re presented with ten different colors instead of seven, even though all the colors taste the same. “Thus, it is clear that the greater the differences between foods, the greater the enhancement of intake,” the greater the effect. Alternating between sweet and savory foods can have a particularly appetite-stimulating effect. Do you see how, in this way, adding a diet soda, for instance, to a fast-food meal can lead to overconsumption?

The staggering array of modern food choices may be one of the factors conspiring to undermine our appetite control. There are now tens of thousands of different foods being sold.

The so-called supermarket diet is one of the most successful ways to make rats fat. Researchers tried high-calorie food pellets, but the rats just ate less to compensate. So, they “therefore used a more extreme diet…[and] fed rats an assortment of palatable foods purchased at a nearby supermarket,” including such fare as cookies, candy, bacon, and cheese, and the animals ballooned. The human equivalent to maximize experimental weight gain has been dubbed the cafeteria diet.

It’s kind of the opposite of the original food dispensing device I’ve talked about before. Instead of all-you-can-eat bland liquid, researchers offered free all-you-can-eat access to elaborate vending machines stocked with 40 trays with a dizzying array of foods, like pastries and French fries. Participants found it impossible to maintain energy balance, consistently consuming more than 120 percent of their calorie requirements.

Our understanding of sensory-specific satiety can be used to help people gain weight, but how can we use it to our advantage? For example, would limiting the variety of unhealthy snacks help people lose weight? Two randomized controlled trials made the attempt and failed to show significantly more weight loss in the reduced variety diet, but they also failed to get people to make much of a dent in their diets. Just cutting down on one or two snack types seems insufficient to make much of a difference, as seen below and at 4:44 in my video. A more drastic change may be needed, which we’ll cover next.

The importance of satiety is underscored by a rare genetic condition known as Prader-Willi syndrome. Children with the disorder are born with impaired signaling between their digestive system and their brain, so they don’t know when they’re full. “Because no sensation of satiety tells them to stop eating or alerts their body to throw up, they can accidentally consume enough in a single binge to fatally rupture their stomach.” Without satiety, food can be “a death sentence.”

Protein is often described as the most satiating macronutrient. People tend to report feeling fuller after eating a protein-rich meal, compared to a carbohydrate- or fat-rich one. The question is: Does that feeling of fullness last? From a weight-loss standpoint, satiety ratings only matter if they end up cutting down on subsequent calorie intake, and even a review funded by the meat, dairy, and egg industries acknowledges that this does not seem to be the case for protein. Hours later, protein consumed earlier doesn’t tend to end up cutting calories later on.

Fiber-rich foods, on the other hand, can suppress appetite and reduce subsequent meal intake more than ten hours after consumption—even the next day—because their site of action is 20 feet down in the lower intestine. Remember the ileal brake from my Evidence-Based Weight Loss lecture? When researchers secretly infused nutrients into the end of the small intestine, study participants spontaneously ate as many as hundreds fewer calories at a meal. Our brain gets the signal that we are full, from head to tail.

We were built for gluttony. “It is a wonderful instinct, developed over millions of years, for times of scarcity.” Stumbling across a rare bounty, those who could fill themselves the most to build up the greatest reserves would be more likely to pass along their genes. So, we are hard-wired not just to eat until our stomach is full, but until our entire digestive tract is occupied. Only when our brain senses food all the way down at the end does our appetite fully dial down.

Fiber-depleted foods get rapidly absorbed early on, though, so much of it never makes it down to the lower gut. As such, if our diet is low in fiber, no wonder we’re constantly hungry and overeating; our brain keeps waiting for the food that never arrives. That’s why people who even undergo stomach-stapling surgeries that leave them with a tiny two-tablespoon-sized stomach pouch can still eat enough to regain most of the weight they initially lost. Without sufficient fiber, transporting nutrients down our digestive tract, we may never be fully satiated. But, as I described in my last video, one of the most successful experimental weight-loss interventions ever reported in the medical literature involved no fiber at all, as you can see here and at 2:47 in my video Foods Designed to Hijack Our Appetites.

At first glance, it might seem obvious that removing the pleasurable aspects of eating would cause people to eat less, but remember, that’s not what happened. The lean participants continued to eat the same amount, taking in thousands of calories a day of the bland goop. Only those who were obese went from eating thousands of calories a day down to hundreds, as shown below and at 3:22 in my video. And, again, this happened inadvertently without them apparently even feeling a difference. Only after eating was disconnected from the reward was the body able to start rapidly reining in the weight.

We appear to have two separate appetite control systems: “the homeostatic and hedonic pathways.” The homeostatic pathway maintains our calorie balance by making us hungry when energy reserves are low and abolishes our appetite when energy reserves are high. “In contrast, hedonic or reward-based regulation can override the homeostatic pathway” in the face of highly palatable foods. This makes total sense from an evolutionary standpoint. In the rare situations in our ancestral history when we’d stumble across some calorie-dense food, like a cache of unguarded honey, it would make sense for our hedonic drive to jump into the driver’s seat to consume the scarce commodity. Even if we didn’t need the extra calories at the time, our body wouldn’t want us to pass up that rare opportunity. Such opportunities aren’t so rare anymore, though. With sugary, fatty foods around every corner, our hedonic drive may end up in perpetual control, overwhelming the intuitive wisdom of our bodies.

So, what’s the answer? Never eat really tasty food? No, but it may help to recognize the effects hyperpalatable foods can have on hijacking our appetites and undermining our body’s better judgment.

Ironically, some researchers have suggested a counterbalancing evolutionary strategy for combating the lure of artificially concentrated calories. Just as pleasure can overrule our appetite regulation, so can pain. “Conditioned food aversions” are when we avoid foods that made us sick in the past. That may just seem like common sense, but it is actually a deep-seated evolutionary drive that can defy rationality. Even if we know for a fact a particular food was not the cause of an episode of nausea and vomiting, our body can inextricably tie the two together. This happens, for example, with cancer patients undergoing chemotherapy. Consoling themselves with a favorite treat before treatment can lead to an aversion to their favorite food if their body tries to connect the dots. That’s why oncologists may advise the “scapegoat strategy” of only eating foods before treatment that you are okay with, never wanting to eat again.

Researchers have experimented with inducing food aversions by having people taste something before spinning them in a rotating chair to cause motion sickness. Eureka! A group of psychologists suggested: “A possible strategy for encouraging people to eat less unhealthy food is to make them sick of the food, by making them sick from the food.” What about using disgust to promote eating more healthfully? Children as young as two-and-a-half years old will throw out a piece of previously preferred candy scooped out of the bottom of a clean toilet.

Thankfully, there’s a way to exploit our instinctual drives without resorting to revulsion, aversion, or bland food, which we’ll explore next.

Anyone can lose weight by eating less food. Anyone can be starved thin. Starvation diets are rarely sustainable, though, since hunger pangs drive us to eat. We feel unsatisfied and unsatiated on low-calorie diets. We do have some level of voluntary control, of course, but our deep-seated instinctual drives may win out in the end.

For example, we can consciously hold our breath. Try it right now. How long can you go before your body’s self-preservation mechanisms take over and overwhelm your deliberate intent not to breathe? Our body has our best interests at heart and is too smart to allow us to suffocate ourselves—or starve ourselves, for that matter. If our body were really that smart, though, how could it let us become obese? Why doesn’t our body realize when we’re too heavy and allow us the leeway to slim down? Maybe our body is very aware and actively trying to help, but we’re somehow undermining those efforts. How could we test this theory to see if that’s true?

So many variables go into choosing what we eat and how much. “The eating process involves an intricate mixture of physiologic, psychologic, cultural, and esthetic considerations.” To strip all that away and stick just to the physiologic variable, Columbia University researchers designed a series of famous experiments using a “food dispensing device.” The term “food” is used very loosely here. As you can see at 2:02 in my video 200-Pound Weight Loss Without Hunger, the researchers’ feeding machine was a tube hooked up to a pump that delivered a mouthful of bland liquid formula every time a button was pushed. Research participants were instructed to eat as much or as little as they wanted at any time. In this way, eating was reduced to just the rudimentary hunger drive. Without the usual trappings of “sociability,” meal ceremony, and the pleasures of the palate, how much would people be driven to eat? 
Put a normal-weight person in this scenario, and something remarkable happens. Day after day, week after week, with nothing more than their hunger to guide them, they eat exactly as much as they need, perfectly maintaining their weight, as shown below and at 2:36 in my video.

They needed about 3,000 calories a day, and that’s just how much they unknowingly gave themselves. Their body just intuitively seemed to know how many times to press that button, as seen here and at 2:48 in my video.

Put a person with obesity in that same scenario, and something even more remarkable happens. Driven by hunger alone, with the enjoyment of eating stripped away, they wildly undershoot, giving themselves a mere 275 calories a day, total. They could eat as much as they wanted, but they just weren’t hungry. It’s as if their body knew how massively overweight they were, so it dialed down their natural hunger drive to almost nothing. One participant started the study at 400 pounds and steadily lost weight. After 252 days of sipping the bland liquid, he lost 200 pounds, as you can see here and at 3:35 in my video.

This groundbreaking discovery was initially interpreted to mean that obesity is not caused by some sort of metabolic disturbance that drives people to overeat. In fact, the study suggested quite the opposite. Instead, overeating appeared to be a function of the meaning people attached to food, “aside from its use as fuel,” whether as a source of pleasure or perhaps as relief from boredom or stress. In this way, obesity seemed more psychological than physical. Subsequent experiments with the feeding machine, though, flipped such conceptions on their head once again.

When researchers covertly doubled the calorie concentration of the formula given to lean study participants, they unconsciously cut their consumption in half to continue to perfectly maintain their weight, as seen here and at 4:24 in my video. Their body somehow detected the change in calorie load and sent signals to the brain to press the button half as often to compensate. Amazing!

When the same was done with people with obesity, though, nothing changed. They continued to drastically undereat just as much as before. Their body seems incapable of detecting or reacting to the change in calorie load, suggesting a physiological inability to regulate intake, as shown below and at 4:40 in my video. 
Might the brains of persons with obesity somehow be insensitive to internal satiety signals? We don’t know if it’s cause or effect. Maybe that’s why they’re obese in the first place, or maybe the body knows how obese it is and shuts down its hunger drive regardless of the calorie concentration. Indeed, the participants with obesity continued to steadily lose weight eating out of the machine, regardless of the calorie concentration and the food being dispensed, as you can see here and at 5:19 in my video. 
It would be interesting to see if they regained the ability to respond to changing calorie intake once they reached their ideal weight. Regardless, what can we apply from these remarkable studies to facilitate weight loss out in the real world? We’ll explore just that question next.

The reason I make pesto with walnuts instead of the more traditional pine nuts isn’t only because walnuts are probably healthier with 20 times more polyphenols, but also because of a mysterious phenomenon known as PMS. Not that PMS. Pine mouth syndrome is characterized by what has become my favorite word of the week: cacogeusia, meaning a bad taste in your mouth. You can get cacogeusia from heavy metal toxicity, seafood toxins, certain nutritional and neurologic disorders, or the wrong kind of pine nuts. “Termed ‘Pine Mouth’ by the public, cases present in a roughly similar fashion: a persistent metallic or bitter taste beginning 1–3 days following ingestion of pine nuts lasting for up to 2 weeks.”

As I discuss in my video Pine Mouth Syndrome: Prolonged Bitter Taste from Certain Pine Nuts, thousands of cases have been reported, and it doesn’t seem to matter if the pine nuts are raw or cooked. Could the cause be an unidentified toxin present in some varieties of non-edible pine nuts? Indeed, “out of more than 100 species of the Pinus genus, [only] 30 are considered to be edible by the Food and Agriculture Organisation of the United Nations.”

Researchers analyzed pine nut samples from consumers who had fallen ill and found that, indeed, they all contained nuts from Chinese white pine, which is not reported to be edible. That tree is typically used only for lumber. You can see photos of inedible and edible pine nuts below and at 1:36 in my video.

More photos can be seen here and at 1:40.

We don’t know it’s the Chinese white pine nuts, though, until we put it to the test. Researchers gave study participants six to eight Chinese white pine nuts. Most hadn’t ever heard of pine mouth syndrome, and they all developed symptoms. We still don’t know exactly what it is in those nuts that causes such a bizarre reaction. We know to stay away from those kinds of pine nuts.

So, what kinds of pine nuts are on shelves in the United States? All kinds, apparently, “including those associated with pine mouth.” You can see more examples below and at 2:19 in my video.

Unsurprisingly, hundreds of cases of PMS have been reported in the United States. Most of the implicated nuts “were predominantly reported to be labeled from or originating from Asia, and in most cases China,” as seen here and at 2:30 in my video.

The European Union demanded that China stop sending them toxic nuts, which they did beginning in 2011. “This export restriction likely resulted in a global export restriction of these species to the US as well,” given the decline in cases going into 2012, as shown below and at 2:47. 

Rare cases still occur, though, as evidenced by an active Facebook group entitled “Damn you, Pine Nuts.” The primary reason I made this video is to allay fears should this ever happen to you. “There are no proven therapies for PMS. The only treatment is to cease ingesting implicated nuts and to wait for symptoms to abate.” Thankfully, pine mouth syndrome appears to be benign and goes away on its own.

There is a toxin in plain white button mushrooms called agaritine, which may be carcinogenic. Plain white button mushrooms grow to be cremini (brown) mushrooms, and cremini mushrooms grow to be portobello mushrooms. They’re all the very same mushroom, similar to how green bell peppers are just unripe red bell peppers. The amount of agaritine in these mushrooms can be reduced through cooking: Frying, microwaving, boiling, and even just freezing and thawing lower the levels. “It is therefore recommended to process/cook Button Mushroom before consumption,” something I noted in a video that’s now more than a decade old.

However, as shown below and at 0:51 in my video Is It Safe to Eat Raw Mushrooms?, if you look at the various cooking methods, the agaritine in these mushrooms isn’t completely destroyed. Take dry baking, for example: Baking for ten minutes at about 400° Fahrenheit (“a process similar to pizza baking”) only cuts the agaritine levels by about a quarter, so 77 percent still remains.

Boiling looks better, appearing to wipe out more than half the toxin after just five minutes, but the agaritine isn’t actually eliminated. Instead, it’s just transferred to the cooking water. So, levels within the mushrooms drop by about half at five minutes and by 90 percent after an hour, but that’s mostly because the agartine is leaching into the broth. So, if you’re making soup, for instance, five minutes of boiling is no more effective than dry baking for ten minutes, and, even after an hour, about half still remains.

Frying for five to ten minutes eliminates a lot of agartine, but microwaving is not only a more healthful way to cook, but it works even better, as you can see here and at 1:39 in my video. Researchers found that just one minute in the microwave “reduced the agaritine content of the mushrooms by 65%,” and only 30 seconds of microwaving eliminated more than 50 percent. So, microwaving is probably the easiest way to reduce agaritine levels in fresh mushrooms. 
My technique is to add dried mushrooms into the pasta water when I’m making spaghetti. Between the reductions of 20 percent or so from the drying and 60 percent or so from boiling for ten minutes and straining, more than 90 percent of agaritine is eliminated.

Should we be concerned about the residual agaritine? According to a review funded by the mushroom industry, not at all. “The available evidence to date suggests that agaritine from consumption of…mushrooms poses no known toxicological risk to healthy humans.” The researchers acknowledge agartine is considered a potential carcinogen in mice, but then that data needs to be extrapolated to human health outcomes.

The Swiss Institute of Technology, for example, estimated that the average mushroom consumption in the country would be expected to cause about two cases of cancer per one hundred thousand people. That is similar to consumption in the United States, as seen below and at 3:00 in my video, so “one could theoretically expect about 20 cancer deaths per 1 x 106 [one million] lives from mushroom consumption.” In comparison, typically, with a new chemical, pesticide, or food additive, we’d like to see the cancer risk lower than one in a million. “By this approach, the average mushroom consumption of Switzerland is 20-fold too high to be acceptable. To remain under the limit”—and keep risk down to one in a million—“‘mushroom lovers’ would have to restrict their consumption of mushrooms to one 50-g serving every 250 days!” That’s about a half-cup serving once in just over eight months. To put that into perspective, even if you were eating a single serving every single day, the resulting additional cancer risk would only be about one in ten thousand. “Put another way, if 10,000 people consumed a mushroom meal daily for 70 years, then in addition to the 3000 cancer cases arising from other factors, one more case could be attributed to consuming mushrooms.” 
But, again, this is all based “on the presumption that results in such mouse models are equally valid in humans.” Indeed, this is all just extrapolating from mice data. What we need is a huge prospective study to examine the association between mushroom consumption and cancer risk in humans, but there weren’t any such studies—until now.

Researchers titled their paper: “Mushroom Consumption and Risk of Total and Site-Specific Cancer in Two Large U.S. [Harvard] Prospective Cohorts” and found “no association between mushroom consumption and total and site-specific cancers in U.S. women and men.”

Eating raw or undercooked shiitake mushrooms can cause something else, though: shiitake mushroom flagellate dermatitis. Flagellate as in flagellation, whipping, flogging. Below and at 4:48 in my video, you can see a rash that makes it look as if you’ve been whipped.

Here and at 4:58 in my video is another photo of the rash. It’s thought to be caused by a compound in shiitake mushrooms called lentinan, but because heat denatures it, it only seems to be a problem with raw or undercooked mushrooms.

Now, it is rare. Only about 1 in 50 people are even susceptible, and it goes away on its own in a week or two. Interestingly, it can strike as many as ten days after eating shiitake mushrooms, which is why people may not make the connection. One unfortunate man suffered on and off for 16 years before a diagnosis. Hopefully, a lot of doctors will watch this video, and if they ever see a rash like this, they’ll tell their patients to cook their shiitakes.

The most promising appears to be moringa’s effects on blood sugar control. Below and at 0:55 in my video The Efficacy and Side Effects of Moringa Leaf Powder, you can see the blood sugar spikes after study participants ate about five control cookies each (top line labeled “a”), compared with cookies containing about two teaspoons of moringa leaf powder into the batter (bottom line labeled “b”). Even with the same amount of sugar and carbohydrates as the control cookies, the moringa-containing cookies resulted in a dampening of the surge in blood sugar.

Researchers found that drinking just one or two cups of moringa leaf tea before a sugar challenge “suppressed the elevation in blood glucose [sugar] in all cases compared to controls that did not receive the tea initially” and instead drank plain water. As you can see here and at 1:16 in my video, drinking moringa tea with sugar dampened blood sugar spikes after 30 minutes of consumption of the same amount of sugar without moringa tea. It’s no wonder that moringa is used in traditional medicine practice for diabetes, but we don’t really know if it can help until we put it to the test. 
People with diabetes were given about three-quarters of a teaspoon of moringa leaf powder every day for 12 weeks and had significant improvements in measures of inflammation and long-term blood sugar control. The researchers called it a “quasi-experimental study” because there was no control group. They just took measurements before and after the study participants took moringa powder, and we know that simply being in a dietary study can lead some to eat more healthfully, whether consciously or unconsciously, so we don’t know what effect the moringa itself had. However, even in a moringa study with a control group, it’s not clear if the participants were randomly allocated. The researchers didn’t even specify how much moringa people were given—just that they took “two tablets daily with one tablet each after breakfast and dinner,” but what does “one tablet” mean? There was no significant improvement in this study, but perhaps the participants weren’t given enough moringa. Another study used a tablespoon a day and not only saw a significant drop in fasting blood sugars, but a significant drop in LDL cholesterol as well, as seen below and at 2:27 in my video. 

Two teaspoons of moringa a day didn’t seem to help, but what about a third, making it a whole tablespoon? Apparently not, since, finally, a randomized, placebo-controlled study using one tablespoon of moringa a day failed to show any benefit on blood sugar control in people with type 2 diabetes.

So, we’re left with a couple of studies showing potential, but most failing to show benefit. Why not just give moringa a try to see for yourself? That’s a legitimate course of action in the face of conflicting data when we’re talking about safe, simple, side–effect–free solutions, but is moringa safe? Probably not during pregnancy, as “about 80% of women folk” in some areas of the world use it to abort pregnancies, and its effectiveness for that purpose has been confirmed (at least in rats), though breastfeeding women may get a boost of about half a cup in milk production based on six randomized, blinded, placebo-controlled clinical trials.

Just because moringa has “long been used in traditional medicine” does not in any way prove that the plant is safe to consume. A lot of horribly toxic substances, like mercury and lead, have been used in traditional medical systems the world over, but at least “no major harmful effects of M. oleifera [moringa]…have been reported by the scientific community.” More accurately, “no adverse effects were reported in any of the human studies that have been conducted to date.” In other words, no harmful effects had been reported until now. 

Stevens-Johnson syndrome (SJS) is probably the most dreaded drug side effect, “a rare but potentially fatal condition characterized by…epidermal detachment and mucous membrane erosions.” In other words, your skin may fall off. Fourteen hours after consuming moringa, a man broke out in a rash. The same thing had happened three months earlier, the last time he had eaten moringa, causing him to suffer “extensive mucocutaneous lesions with blister formation over face, mouth, chest, abdomen, and genitalia.” “This case report suggests that consumption of Moringa leaf is better avoided by individuals who are at risk of developing SJS.” Although it can happen to anyone, HIV is a risk factor.

My take on moringa is that the evidence of benefit isn’t compelling enough to justify shopping online for something special when you can get healthy vegetables in your local market, like broccoli, which has yet to be implicated in any genital blistering. 

Moringa (Moringa oleifera) is a plant commonly known as the “miracle” tree due to its purported healing powers across a spectrum of diseases. If “miracle” isn’t hyperbolic enough for you, “on the Internet,” it’s also known as “God’s Gift to Man.” Is moringa a miracle or just a mirage? “The enthusiasm for the health benefits of M. oleifera is in dire contrast with the scarcity of strong experimental and clinical evidence supporting them. Fortunately, the chasm is slowly being filled.” There has been a surge in scientific publications on moringa. In just the last ten years, the number of articles is closer to a thousand, as shown here and at 1:02 in my video The Benefits of Moringa: Is It the Most Nutritious Food?.

What got my attention was the presence of glucosinolates, compounds that boost our liver’s detoxifying enzymes. I thought they were only found in cruciferous vegetables, such as cabbage, broccoli, kale, collards, and cauliflower. Still, it turns out they’re also present in the moringa family, with a potency comparable to broccoli. But rather than mail-ordering exotic moringa powder, why not just eat broccoli?Is there something special about moringa?

“Moringa oleifera has been described as the most nutritious tree yet discovered,” but who eats trees? Moringa supposedly “contains higher amounts of elemental nutrients than most conventional vegetable sources,” such as featuring 10 times more vitamin A than carrots, 12 times more vitamin C than oranges, 17 times more calcium than milk, 15 times more potassium than bananas, 25 times more iron than spinach, and 9 times more protein than yogurt, as shown here and at 2:08 in my video. 
Sounds impressive, but first of all, even if this were true, it is relevant for 100 grams of dry moringa leaf, which is about 14 tablespoons, almost a whole cup of leaf powder. Researchers have had trouble getting people to eat even 20 grams, so anything more would likely “result in excessively unpleasant taste, due to the bitterness of the leaves.”

Secondly, the nutritional claims in these papers are “adapted from Fuglie,” which is evidently a lay publication. If you go to the nutrient database of the U.S. Department of Agriculture, and enter a more reasonable dose, such as the amount that might be in a smoothie, about a tablespoon, for instance, a serving of moringa powder has as much vitamin A as a quarter of one baby carrot and as much vitamin C as one one-hundredth of an orange. So, an orange has as much vitamin C as a hundred tablespoons of moringa. A serving of moringa powder has the calcium of half a cup of milk, the potassium of not fifteen bananas but a quarter of one banana, the iron of a quarter cup of spinach, and the protein of a third of a container of yogurt, as seen below and at 3:15 in my video. So, it may be nutritious, but not off the charts and certainly not what’s commonly touted. So, again, why not just eat broccoli?

Moringa does seem to have anticancer activity—in a petri dish—against cell lines of breast cancer, lung cancer, skin cancer, and fibrosarcoma, while tending to leave normal cells relatively alone, but there haven’t been any clinical studies. What’s the point in finding out that “Moringa oleifera extract enhances sexual performance in stressed rats,” as one study was titled?

Studies like “Effect of supplementation of drumstick (Moringa oleifera) and amaranth (Amaranthus tricolor) leaves powder on antioxidant profile and oxidative status among postmenopausal women” started to make things a little interesting. When researchers were testing the effects of a tablespoon of moringa leaf powder once a day for three months on antioxidant status, they saw a drop in oxidative stress, as one might expect from eating any healthy plant food. However, they also saw a drop in fasting blood sugars from prediabetic levels exceeding 100 to more normal levels. Now, that’s interesting. Should we start recommending a daily tablespoon of moringa powder to people with diabetes, or was it just a fluke? I’ll discuss the study “Moringa oleifera and glycemic [blood sugar] control: A review of the current evidence” next.

When grocery shopping these days, unless you’re sticking to the produce aisle, “it is nearly impossible to avoid processed foods, particularly in the consumption of a typical Western diet,” which is characterized by insufficient plant foods, too much meat, dairy, and eggs, and a lot of processed junk, “along with increased exposure to additives due to their use in processed foods.”

The artificial sweetener sucralose, for example, which is sold as Splenda, “irrefutably disrupts the gut microbiome at doses relevant to human use” and “induces glucose intolerance.” In other words, it can make our blood sugars worse instead of better. It’s relatively easy to avoid artificial sweeteners, but “it may be much more difficult to avoid ingestion of emulsifiers…because they are commonly added to a wide variety of foods within the modern Western diet.” In fact, “emulsifiers are the most widely used additives,” and “most processed foods contain one or more emulsifiers that allow such foods to maintain desired textures and avoid separation into distinct parts (e.g, oil and water layers).” We now consume emulsifiers by the megaton every year, thanks to a multibillion-dollar industry, as you can see below and at 1:03 in my video Are Emulsifiers Like Carboxymethylcellulose and Polysorbate 80 Safe?.

Emulsifiers are commonly found in fatty dressings, breads and other baked goods, mayonnaise and other fatty spreads, candy, and beverages. “Like all authorized food additives, emulsifiers have been evaluated by risk assessors, who consider them safe. However, there are growing concerns among scientists about their possible harmful effects on our intestinal barriers and microbiota,” in terms of causing a leaky gut. As well, they could possibly “increase the absorption of several environmental toxins, including endocrine disruptors and carcinogens” present in the food.

We know that the consumption of ultra-processed foods may contribute to weight gain. Healthier, longer-lived populations not only have low meat intake and high plant intake, but they also eat minimally processed foods and “have far less chronic diseases, obesity rates, and live longer disease-free.” Based on a number of preclinical studies, it may be that the emulsifiers found in processed foods are playing a role, but who cares if “emulsifiers make rats gain weight”? When we read that “emulsifiers can cause striking changes in the microbiota,” they aren’t talking about the microbiota of humans.

Often, mice are used to study the impact on the microbiome, but “only a few percent of the bacterial genes are shared between mice and humans.” Even the gut flora of different strains of mice can be considerably different from each other, so if we can’t even extrapolate from one type of mouse to another, how are we supposed to translate results from mice to humans? “Remarkably, there has been little study of the potential harmful effects of ingested…emulsifiers in humans.”

Take lecithin, for example, which is “perhaps best known as a key component of egg yolks.” Lecithin was found to be worse than polysorbate 80 in terms of allowing bacteria to leak through the gut wall into the bloodstream. However, it’s yet to be determined whether lecithin consumption in humans causes the same problem. “There is certainly a paucity in the data of human trials with the effects of emulsifiers in processed foods,” but we at least have data on human tissue, cells, and gut flora.

A study was titled: “Dietary emulsifiers directly alter the human microbiota composition and gene expression ex vivo potentiating intestinal inflammation.” Ex vivo means outside the body. Researchers inoculated an artificial gut with fresh human feces until a stable culture was established, then added carboxymethylcellulose (CMC) or polysorbate 80 (P80), resulting in boosts in proinflammatory potential starting within one day with the carboxymethylcellulose and within the first week with polysorbate 80, as you can see below and at 3:39 in my video.

“This approach revealed that both P80 and CMC acted directly upon human microbiota to increase its proinflammatory potential…” When researchers then tested the effect of these emulsifiers on the protective mucus layer in petri dish cultures of human gut lining cells, they found that they can partially disrupt the protective layer. As you can see below and at 4:00 in my video, the green staining is the mucus. Both emulsifiers cut down the levels.

However, this study and the last both used emulsifier concentrations that were far in excess of what people might typically get day-to-day. 

“Translocation of Crohn’s disease Escherichia coli across M-cells: contrasting effects of soluble plant fibres and emulsifiers” is probably the study that raised the greatest potential concern. The researchers surgically obtained cells, as well as actual intestinal wall tissue, and found that polysorbate 80 could double the invasion of E. coli through the intestinal lining tissue, as shown here and at 4:27 in my video.

In contrast, adding fiber—in this case, fiber from plantains—could seal up the gut wall tissue twice as tightly, as seen below and at 4:33.

About a decade ago, the American Heart Association (AHA) expressed concern that its “2020 target of improving cardiovascular health by 20% by 2020 will not be reached if current trends continue.” By 2006, most people were already not smoking and had nearly achieved their goal for exercise. But when it came to healthy diet score, only about 1 percent got a 4 or 5 out of its diet quality score of 0 to 5, as you can see below and at 0:35 in my video, Friday Favorites: The Scientific Consensus on a Healthy Diet. And that’s with such “ideal” criteria as drinking less than four and a half cups of soda a week.

In the last decade, the AHA saw a bump in the prevalence of the ideal healthy diet score to about 1 percent of Americans reaching those kinds of basic criteria, but, given its “aggressive” goal of reaching a “20% target” by 2020, it hoped to turn that 1 percent into about 1.2 percent. (Really, as you can see here and at 1:01 in my video.)

So, how’d we do? According to the 2019 update, it seems we’ve slipped down to as low as one in a thousand, and American teens scored a big fat zero. No wonder, perhaps, that “for all mortality-based metrics, the US rank declined…to 27th or 28th among 34 OECD [industrialized] countries. Citizens living in countries with a substantially lower gross domestic product and health expenditure per capita…have lower mortality rates than those in the United States.” Slovenia, for example, beat the United States, ranking 24th in life expectancy. More recently, the United States’s life expectancy slipped further, down to 43rd in the world, although the United States spent the most ($3.0 trillion) on health care…”

What is the leading risk factor for death in the United States? As seen below and at 2:04 in my video, it is the standard American diet. Those trillions in health care spending aren’t addressing the root cause of disease, disability, and death. 

Here are some of the lung cancer death curves, below and at 2:08 in my video:

It took decades to finally turn the corner, but it’s so nice to finally see those drops. When will we see the same with diet?

“Approximately 80% of chronic disease and premature death could be prevented by not smoking, being physically active, and adhering to a healthful dietary pattern.” What exactly is meant by “healthy diet”? “Unfortunately, media messages surrounding nutrition are often inconsistent, confusing, and do not enable the public to make positive changes in health behaviors….Certainly, there is pressure within today’s competitive journalism market for sensationalism. There may even be a disincentive to present the facts in the context of the total body of information consumers need to act on dietary recommendations.” And there’s an incentive to sell more magazines and newspapers. The paper I’m quoting was written in 1997, before the lure of clickbait headlines. In fact, about three-quarters of a century ago, it was noted: “It is unfortunate that the subject of nutrition seems to have a special appeal to the credulous, the social zealot and, in the commercial field, the unscrupulous….The combination is one calculated to strike despair in the hearts of the sober, objective scientist.”

Indeed, the most important health care problem we face may be “our poor lifestyle choices based on misinformation.” It is like the climate change deniers: “Analogous to outspoken cynics denying climate change and influencing public opinion, healthy lifestyle and dietary advice are overshadowed by critics, diet books, the food industry, and misguided information in the media.” Maybe we need an entity like the Intergovernmental Panel on Climate Change (IPCC)—but for nutrition.

These days, “no single expert, regardless of academic stature or reputation, has the prominence to overcome the obstacles created by confusing media messages and deliver the fundamental principles of healthy living effectively to the public.”

What if there were “a global coalition consisting of a variety of nutrition experts, who collectively represent the views held by the majority of scientists, physicians, and health practitioners” that could “serve as the guiding resource of sound nutrition information for improved health and prevention of disease”?

Enter the True Health Initiative, which “was conceived for that very purpose.” A nonprofit coalition of hundreds of experts from dozens of countries has agreed to a consensus statement on the fundamentals of healthy living. See www.truehealthinitiative.org.

Spoiler alert: The healthiest diet is one generally comprised mostly of minimally processed plants.

In a recent review entitled “Damaging Effects of Household Cleaning Products on the Lungs,” researchers noted: “Adverse respiratory effects of cleaning products were first observed in populations experiencing high levels of exposure at the workplace, such as cleaners and health-care workers, with a primary focus on asthma.” Occupational use of disinfectants has also been linked to a higher risk of developing chronic obstructive pulmonary disease, such as emphysema.

As I discuss in my video Friday Favorites: The Effects of Cleaning Products and Air Fresheners on Lung Function, we now know that, in addition to workplace exposures, “exposure to household cleaning products has also emerged as a risk factor for respiratory disorders in childhood,” as well potentially being “an important risk factor for adult asthma.” Common household cleaning spray use accounts for as many as one in seven adult asthma cases. The thought is that inhaling chemical irritants may cause injury to the airways, leading to oxidative stress and inflammation. What can we do about it?

Well, it may be limited to sprays. Researchers found that cleaning products that were not sprayed were not associated with asthma. It’s also possible that environmentally friendly cleaning products “may represent a safer alternative,” though they may still present some risk.

Ideally, safer cleaning products should be available. Unfortunately, the research suggesting harm has “seldom been heeded by manufacturers, vendors, and commercial cleaning companies.” I wonder how much of that is because “most of the workers exposed to cleaning products are women”—both occupationally and, perhaps, domestically.

One of the problems may be the fragrance chemicals. One in three Americans surveyed “reported health problems, such as migraine headaches and respiratory difficulties, when exposed to fragranced products.” And, for about half of them, the problems were so bad they actually lost work over it, either “workdays or a job due to fragranced product exposure in the workplace.”

“Results from this study reveal that over one-third of Americans suffer adverse health effects, such as respiratory difficulties and migraine headaches, from exposure to fragranced products. Of those individuals, half reported that the effects can be disabling. Yet over 99% of Americans are exposed to fragranced products at least once a week, from their own or others’ use.”

The effect on asthmatics may be even worse, affecting closer to two-thirds of Americans. One compound that may be of particular concern is called 1,4-dichlorobenzene, also known as para-dichlorobenzene, which is found in many air fresheners, toilet bowl deodorants, and mothballs. It breaks down in the body into a compound called 2,5-dichlorophenol, which we pee out, giving researchers a reliable measure of our dichlorobenzene exposure. Not only may it make respiratory problems worse for those already suffering from compromised airways, but exposure to dichlorobenzene “at [blood] levels found in the U.S. general population, may result in reduced pulmonary [lung] function” in people who start out with normal breathing. What’s worse, higher exposures “were associated with greater prevalence of CVD [cardiovascular disease] and all cancers combined,” another reason to avoid it. We’d better read labels, right?

Surprisingly, “no law in the US requires the disclosure of all ingredients in fragranced consumer products.” In fact, for laundry supplies, cleaning products, and air fresheners, manufacturers “do not need to list the presence of a ‘fragrance’ on either the label or MSDS,” the material safety data sheet. We won’t know until we smell it.

I support the U.S. Centers for Disease Control and Prevention’s ban. Not only is “the use of tobacco products (including cigarettes, cigars, pipes, smokeless tobacco, or other tobacco products)…prohibited at all times,” but “scented or fragranced products are prohibited at all times in all interior space owned, rented, or leased by CDC.” I wish rideshare services like Uber and Lyft would have a similar policy. I’d even be happy with just a fragrance-free option. About one in five of more than a thousand Americans surveyed said they “would enter a business but then leave as quickly as possible if they smelled air fresheners or some fragranced product,” so it’s in the best interest of businesses, too. “Over 50% of the population would prefer that workplaces, health care facilities and professionals, hotels, and airplanes were fragrance-free.”

There is accumulating evidence that brain-derived neurotrophic factor (BDNF) may be playing a role in human depression. BDNF controls the growth of new nerve cells. “So, low levels of this peptide could lead to an atrophy of specific brain areas such as the amygdala and the hippocampus, as it has been observed among depressed patients.” That may be one of the reasons that exercise is so good for our brains. Start an hour-a-day exercise regimen, and, within three months, there can be a quadrupling of BDNF release from our brain, as seen below and at 0:35 in my video How to Boost Brain BDNF Levels for Depression Treatment.

This makes sense. Any time we were desperate to catch prey (or desperate not to become prey ourselves), we needed to be cognitively sharp. So, when we’re fasting, exercising, or in a negative calorie balance, our brain starts churning out BDNF to make sure we’re firing on all cylinders. Of course, Big Pharma is eager to create drugs to mimic this effect, but is there any way to boost BDNF naturally? Yes, I just said it: fasting and exercising. Is there anything we can add to our diet to boost BDNF?

Higher intakes of dietary flavonoids appear to be protectively associated with symptoms of depression. The Harvard Nurses’ Health Study followed tens of thousands of women for years and found that those who were consuming the most flavonoids appeared to reduce their risk of becoming depressed. Flavonoids occur naturally in plants, so there’s a substantial amount in a variety of healthy foods. But how do we know the benefits are from the flavonoids and not just from eating more healthfully in general? We put it to the test.

Some fruits and vegetables have more flavonoids than others. As shown below and at 1:51 in my video, apples have more than apricots, plums more than peaches, red cabbage more than white, and kale more than cucumbers. Researchers randomized people into one of three groups: more high-flavonoid fruits and vegetables, more low-flavonoid fruits and vegetables, or no extra fruits and vegetables at all. After 18 weeks, only the high-flavonoid group got a significant boost in BDNF levels, which corresponded with an improvement in cognitive performance. The BDNF boost may help explain why each additional daily serving of fruits or vegetables is associated with a 3 percent decrease in the risk of depression. 

What’s more, as seen here and at 2:27 in my video, a teaspoon a day of the spice turmeric may boost BNDF levels by more than 50 percent within a month. This is consistent with the other randomized controlled trials that have so far been done. 

Nuts may help, too. In the PREDIMED study, where people were randomized to receive weekly batches of nuts or extra-virgin olive oil, the nut group lowered their risk of having low BDNF levels by 78 percent, as shown below and at 2:46.

And BDNF is not implicated only in depression, but schizophrenia. When individuals with schizophrenia underwent a 12-week exercise program, they got a significant boost in their BDNF levels, which led the researchers to “suggest that exercise-induced modulation of BDNF may play an important role in developing non-pharmacological treatment for chronic schizophrenic patients.”

What about schizophrenia symptoms? Thirty individuals with schizophrenia were randomized to ramp up to 40 minutes of aerobic exercise three times a week or not, and there did appear to be an improvement in psychiatric symptoms, such as hallucinations, as well as an increase in their quality of life, with exercise. In fact, researchers could actually visualize what happened in their brains. Loss of brain volume in a certain region appears to be a feature of schizophrenia, but 30 minutes of exercise, three times a week, resulted in an increase of up to 20 percent in the size of that region within three months, as seen here and at 3:46 in my video. 

Caloric restriction may also increase BDNF levels in people with schizophrenia. So, researchers didn’t just have study participants eat less, but more healthfully, too—less saturated fat and sugar, and more fruits and veggies. The study was like the Soviet fasting trials for schizophrenia that reported truly unbelievable results, supposedly restoring people to function, and described fasting as “an unparalleled achievement in the treatment of schizophrenia”—but part of the problem is that the diagnostic system the Soviets used is completely different than ours, making any results hard to interpret. There was a subgroup that seemed to correspond to the Western definition, but they still reported 40 to 60 percent improvement rates from fasting, but fasting wasn’t all they did. After the participants fasted for up to a month, they were put on a meat- and egg-free diet. So, when the researchers reported these remarkable effects even years later, they were for those individuals who stuck with the meat- and egg-free diet. Evidently, the closer the diet was followed, the better the effect, and those who broke the diet relapsed. The researchers noted: “Not all patients can remain vegetarian, but they must not take meat for at least six months, and then in very small portions.” We know from randomized controlled trials that simply eschewing meat and eggs can improve mental states within just two weeks, so it’s hard to know what role fasting itself played in the reported improvements.

A single high-fat meal can drop BDNF levels within hours of consumption, and we can prove it’s the fat itself by seeing the same result after injecting fat straight into our veins. Perhaps that helps explain why increased consumption of saturated fats in a high-fat diet may contribute to brain dysfunction—that is, neurodegenerative diseases, long-term memory loss, and cognitive impairment. It may also help explain why the standard American diet has been linked to a higher risk of depression, as dietary factors modulate the levels of brain-derived neurotrophic factor.

For more than a century, fasting has been espoused as a treatment of supposed “great utility in the preservation of health,” especially rejuvenating the body and, above all, the mind. When people fast for even 18 hours, though, they may get hungry and irritable. After one or two days, positive mood goes down and negative mood goes up, and after three days, fasters can increasingly feel sad, self-blame, and suffer a loss of libido. Then, something strange starts to happen: People experience a “fasting-induced mood enhancement…reflected by decreased anxiety, depression, fatigue, and improved vigor.” Studies tend to show this across the board. Once you get over the hump, fasters frequently experience “an increased level of vigilance and a mood improvement, a subjective feeling of well-being, and sometimes of euphoria.” And, no wonder, as, by then, endorphin levels may rise by nearly 50 percent, as seen here and at 1:06 in my video Friday Favorites: Fasting to Treat Depression. 

This enhancement of mood, alertness, and calm makes a certain amount of evolutionary sense. Our body wants us to feel poorly initially so we continue to eat, day to day, when food is available, but if we go a couple of days without food, our body realizes we can’t just mope in our cave; we need to get motivated to go out and find some calories.

So, can fasting be used for mood disorders, like depression? It’s great that people can feel better after a few days of fasting, but the critical question revolves around the “persistence of mood improvement over time” once fasting ends and eating resumes. The little published evidence we have comes out of Japan and the former Soviet Union, and some of it is just ridiculous, like this study that included women with a variety of symptoms, which the researchers blame mostly on marital conflict, as you can see below and at 2:08 in my video. Husband not treating you right? How about some “electroshock therapy”? That didn’t seem to help much, so what about “hunger therapy”? Of course, starving the women made them hungry, but that’s what Thorazine is for. If they keep getting injected with an antipsychotic to calm them down, they can sail right through. So, what happened in the study? What would we even do with those results? 

Another study, however, skipped the Thorazine. The participants fasted for ten days, but they were also kept in bed all day on “absolute bed rest,” completely isolated and “prohibited from seeing other people except the attending doctor and nurse…also denied access to television, radio, newspapers or any other forms of information.” So, if people got better or worse, it would be impossible to tease out the effects of the fasting component on its own. But researchers found that they apparently did get better, with efficacy reportedly demonstrated in 31 out of 36 patients suffering from depression, as seen here and at 2:56 in my video.

The researchers concluded that fasting therapy may provide an alternative to the use of antidepressant drugs, “thinking the fasting therapy may be a kind of shock therapy.” People are so relieved to be eating again, to get out of solitary confinement, and to even just get out of bed that they report feeling better. That was at the time of discharge, though. How did they feel the next day, the next week, the next month? Fasting is, by definition, unsustainable, so what we want to ideally see are some kind of longer-lasting effects.

Researchers did a follow-up with a few hundred patients, not just a few months later, but after a few years. Of the 69 who were evidently suffering from depression, 90 percent reported feeling good or excellent results at the end of the ten-day fast, and, remarkably, years later, 87 percent of the 62 individuals who replied claimed that they were still doing well. Now, there was no control group, so we don’t know if they would have done just as well or even better without the fast, and it was all self-reporting, so there may have been a response bias where participants tried to please the researchers. Who knows? Maybe they were afraid they’d get sent back to solitary if they didn’t respond affirmatively. We have no idea, but we do have good evidence for the short-term mood benefits.

Why would fasting improve feelings of depression? In addition to the endorphins and the surge in serotonin, the so-called happiness hormone, when we fast, there is a bump in brain-derived neurotrophic factor (BDNF), which is considered to play a crucial role in mood disorders. Researchers have perked up rodents with it, but we aren’t rats or mice. What about us? Humans with major depression have lower levels of BDNF circulating in their bloodstream. Autopsy studies of suicide victims show only about half the BDNF in certain key brain regions, compared to controls, suggesting it may play an important role in suicidal behavior, as seen here and at 4:38 in my video. 

We can boost BDNF with antidepressant drugs and electroshock; we can also boost it with caloric restriction. We can get a 70 percent boost in levels after three months of cutting 25 percent of calories out of our daily diet, as shown below and at 4:51.

Is there anything we can add to our diets to boost BNDF levels so we can get the benefits without the hunger? We’ll find out next.

As this study asks, “Medical Marijuana: A Panacea or Scourge?” For 5,000 years, cannabis “has been used throughout the world medically, recreationally, and spiritually.” It was even prescribed by American physicians “for a plethora of indications” from the mid-19th century to the 1930s, a fact that’s often used by medical marijuana proponents as evidence justifying the modern medical applications.” But the field of old-timey medicine is “fraught with potions and herbal remedies,” not to mention bloodletting and other questionable and harmful remedies.

Skeptics criticize the medical marijuana movement as the “‘medical excuse marijuana’ movement,” insinuating that children with epilepsy and the terminally ill are being “used as a ‘Trojan horse’ for the legalization of recreational cannabis use” or to peddle “outlandish claims” about “miracle cancer cures,” frustrating researchers in the field who just want to get at the science.

For example, what about the therapeutic use of cannabis for inflammatory bowel diseases like Crohn’s disease and ulcerative colitis? Conventional therapies work mainly by suppressing the immune system to try to tamp down inflammation. “Given the limited therapy options and known adverse side effects with chronic use” from these drugs, people suffering from these diseases often need to have inflamed sections of their bowels removed surgically, so it’s clear why there’s so much interest in alternative approaches.

About one in six IBD patients who use marijuana say it helps with their symptoms, so researchers decided to put it to the test. Thirteen patients with IBD were given a third of a pound of marijuana to smoke at their leisure over a period of three months, and they reported feeling significantly better with “reported improvement in general health perception, social functioning, ability to work, physical pain, and depression.” There wasn’t a control group, so it’s unknown if they would have improved anyway or what role the placebo effect may have played. It’s like some of the studies of cannabis used for pediatric epilepsy that had response rates exceeding 30 percent and a frequency cut in half in a third of the kids. Amazing results until you realize you can sometimes get similarly amazing responses from giving kids nothing but a sugar pill placebo, as seen below and at 2:21 in my video Friday Favorites: Cannabis for Inflammatory Bowel Disease (IBD). That’s why it’s critical to do randomized, double-blind, placebo-controlled trials, but there weren’t any on cannabis and IBD until 2013. 

For 21 patients with Crohn’s disease, nothing seemed to help. So researchers randomized them to either smoke two joints a day of marijuana or a look-alike placebo. The results? Ninety percent of those in the cannabis group got better, compared to only 40 percent in the placebo group. Shown below and at 3:11 in my video is a graph of their symptom scores. As you can see, there was no big change in the placebo group over the two-month study, but the cannabis group cut their symptoms by about half. 

The researchers acknowledge that long-term cannabis use is not without risks, but it may be a cakewalk compared to the potential adverse—and even life-threatening—side effects of some of the more powerful conventional therapies, so the study was heralded in a paper entitled “High Hope for Medical Marijuana in Digestive Disorders.”

The study was funded by a medical marijuana advocacy organization, the main supplier in the country, in fact. So, expectations may have been placed on the participants about how much better they would feel—in other words, they may have been primed for the placebo effect. But the researchers controlled for that, right? Those getting the real cannabis did significantly better than those randomized to get the placebo. But the point of a placebo is that it is indistinguishable from the real thing, so the participants don’t know which group they’re in—the control group or the treatment group. How can that be accomplished with a psychoactive drug? It can’t, which is the problem. The researchers tried to hide which group participants were in by only recruiting patients who had never tried cannabis before in the hopes that they wouldn’t notice placebo pot, but, unsurprisingly, most of them did. So, we’re basically left with another unblinded study. The researchers asked a bunch of subjective questions, like “How are you feeling?” and those who pretty much knew they were taking the drug said they were feeling better.

There were no significant changes in objective lab values, like CRP, a sign of inflammation, so perhaps the “cannabis may simply be masking symptoms without affecting intestinal inflammation.” Another indicator that it may not be affecting the course of the disease itself is how quickly the symptoms rebound. Two weeks after the study ended, those in the cannabis group were right back to where they started, as shown here (see week 10) and at 5:05 in my video. 

So, “there was no difference in objective inflammatory markers to indicate disease modification. Given the rapid rebound…to pretreatment levels after the 2-week washout period, it seems more plausible that cannabis ameliorated the symptoms of Crohn’s disease, rather than actually modulating the disease.” That may be, but the symptoms are terrible. A reduction in pain is a reduction in pain. Indeed, “from the point of view of the patients, a marked symptomatic improvement and ability to resume normal life is not trivial, even if inflammation persists.” Of course, what if cannabis somehow makes the disease worse in the long run?

A survey study published the following year found that cannabis provided the same immediate symptomatic relief but was associated with a worse disease prognosis over time. Patients with IBD reported that cannabis improved their pain, cramping, and diarrhea, but use for more than six months by Crohn’s patients appeared to be a strong predictor of them ending up in surgery; they had five times the odds of going under the knife. There are two possible explanations for this: It’s quite possible that the increased disease severity led to the cannabis use and not the other way around. The alternative explanation: “Cannabis use may worsen the prognosis of IBD, leading to greater surgeries and hospitalizations.”

This is why we need prospective clinical trials where people are followed over time to see which came first. Until then, perhaps we should consider cannabis use for IBD as “potentially harmful.” Not just to err on the side of caution, but because there was a study on hepatitis C patients that found that daily cannabis use was associated with nearly seven times the odds of worse liver fibrosis, which is like scar tissue. If cannabis really does make fibrosis worse, that may explain why cannabis users with IBD may be more likely to require surgery. 

Both the Women’s Intervention Nutrition Study and the Women’s Health Initiative study showed that women randomized to a lower-fat diet enjoyed improved breast cancer survival. However, in the Women’s Healthy Eating and Living Study, women with breast cancer were also randomized to drop their fat intake down to 15 to 20 percent of calories, yet there was no difference in breast cancer relapse or death after seven years.

Any time there’s an unexpected result, you must question whether the participants actually followed through with study instructions. For instance, if you randomized people to stop smoking and they ended up with the same lung cancer rates as those in the group who weren’t instructed to quit, one likely explanation is that the group told to stop smoking didn’t actually stop. In the Women’s Healthy Eating and Living Study, both the dietary intervention group and the control group started out at about 30 percent of calories from fat. Then, the diet group was told to lower their fat intake to 15 to 20 percent of calories. By the end of the study, they had in fact gone from 28.5 percent fat to 28.9 percent fat, as you can see below and at 1:16 in my video The Food That Can Downregulate a Metastatic Cancer Gene. They didn’t even reduce their fat intake. No wonder they didn’t experience any breast cancer benefit. 

When you put together all the trials on the effect of lower-fat diets on breast cancer survival, even including that flawed study, you see a reduced risk of breast cancer relapse and a reduced risk of death. In conclusion, going on a low-fat diet after a breast cancer diagnosis “can improve breast cancer survival by reducing the risk of recurrence.” We may now know why: by targeting metastasis-initiating cancer cells through the fat receptor CD36.

We know that the cancer-spreading receptor is upregulated by saturated fat. Is there anything in our diet that can downregulate it? Broccoli.

Broccoli appears to decrease CD36 expression by as much as 35 percent (in mice). Of all fruits and vegetables, cruciferous vegetables like broccoli were the only ones associated with significantly less total risk of cancer and not just getting cancer in the first place, as you can see here and at 2:19 in my video.

Those with bladder cancer who eat broccoli also appear to live longer than those who don’t, and those with lung cancer who eat more cruciferous veggies appear to survive longer, too.

For example, as you can see below and at 2:45 in my video, one year out, about 75 percent of lung cancer patients eating more than one serving of cruciferous vegetables a day were still alive (the top line in red), whereas, by then, most who had been getting less than half a serving a day had already died from their cancer (the bottom line in green).

Ovarian cancer, too. Intake of cruciferous vegetables “significantly favored survival,” whereas “a survival disadvantage was shown for meats.” Milk also appeared to double the risk of dying. Below and at 3:21 in my video are the survival graphs. Eight years out, about 40 percent of ovarian cancer patients who averaged meat or milk every day were deceased (the boldest line, on the bottom), compared to only about 20 percent who had meat or milk only a few times a week at most (the faintest line, on the top). 

Now, it could be that the fat and cholesterol in meat increased circulating estrogen levels, or it could be because of meat’s growth hormones or all its carcinogens. And galactose, the sugar naturally found in milk, may be directly toxic to the ovary. Dairy has all its hormones, too. However, the lowering of risk with broccoli and the increasing of risk with meat and dairy are also consistent with the CD36 mechanism of cancer spread.

Researchers put it to the test in patients with advanced pancreatic cancer who were given pulverized broccoli sprouts or a placebo. The average death rate was lower in the broccoli sprout group compared to the placebo group. After a month, 18 percent of the placebo group had died, but none in the broccoli group. By three months, another 25 percent of the placebo group had died, but still not a single death in the broccoli group. And by six months, 43 percent of the remaining patients in the placebo group were deceased, along with the first 25 percent of the broccoli group. Unfortunately, even though the capsules for both groups looked the same, “true blinding was not possible,” and the patients knew which group they were in “because the pulverized broccoli sprouts could be easily distinguished from the methylcellulose [placebo] through their characteristic smell and taste.” So, we can’t discount the placebo effect. What’s more, the study participants weren’t properly randomized “because many of the patients refused to participate unless they were placed into the [active] treatment group.” That’s understandable, but it makes for a less rigorous result. A little broccoli can’t hurt, though, and it may help. It’s the lack of downsides of broccoli consumption that leads to “Advising Women Undergoing Treatment for Breast Cancer” to include the “liberal culinary use of cruciferous vegetables,” for example.

It’s the same for reducing saturated fat. The title of an editorial in a journal of the National Cancer Institute asked: “Is It Time to Give Breast Cancer Patients a Prescription for a Low-Fat Diet?” “Although counseling women to consume a healthy diet after breast cancer diagnosis is certainly warranted for general health, the existing data still fall a bit short of proving this will help reduce the risk of breast cancer recurrence and mortality.” But what do we have to lose? After all, it’s still certainly warranted for general health.

The leading cause of cancer-related death is metastasis. Cancer kills because cancer spreads. The five-year survival rate for women with localized breast cancer is nearly 99 percent, for example, but that falls to only 27 percent in women with metastasized cancer. Yet, “our ability to effectively treat metastatic disease has not changed significantly in the past few decades…” The desperation is evident when there are such papers as “Targeting Metastasis with Snake Toxins: Molecular Mechanisms.”

We have built-in defenses, natural killer cells that roam the body, killing off budding tumors. But, as I’ve discussed, there’s a fat receptor called CD36 that appears to be essential for cancer cells to spread, and these cancer cells respond to dietary fat intake, but not all fat.

CD36 is upregulated by palmitic acid, as much as a 50-fold increase within 12 hours of consumption, as shown below and at 1:13 in my video How to Help Control Cancer Metastasis with Diet.

Palmitic acid is a saturated fat made from palm oil that can be found in junk food, but it is most concentrated in meat and dairy. This may explain why, when looking at breast cancer mortality and dietary fat, “there was no difference in risk of breast-cancer-specific death…for women in the highest versus the lowest category of total fat intake,” but there’s about a 50 percent greater likelihood of dying of breast cancer with higher intake of saturated fat. Researchers conclude: “These meta-analyses have shown that saturated fat intake negatively impacts breast cancer survival.”

This may also explain why “intake of high-fat dairy, but not low-fat dairy, was related to a higher risk of mortality after breast cancer diagnosis.” If a protein in dairy, like casein, was the problem, skim milk might be even worse, but that wasn’t the case. It’s the saturated butterfat, perhaps because it triggered that cancer-spreading mechanism induced by CD36. Women who consumed one or more daily servings of high-fat dairy had about a 50 percent higher risk of dying from breast cancer.

We see the same with dairy and its relationship to prostate cancer survival. Researchers found that “drinking high-fat milk increased the risk of dying from prostate cancer by as much as 600% in patients with localized prostate cancer. Low-fat milk was not associated with such an increase in risk.” So, it seems to be the animal fat, rather than the animal protein, and these findings are consistent with analyses from the Health Professionals Follow-up Study (HPFS) and the Physicians’ Health Study (PHS), conducted by Harvard researchers.

There is even more evidence that the fat receptor CD36 is involved. The “risk of colorectal cancer for meat consumption” increased from a doubling to an octupling—that is, the odds of getting cancer multiplied eightfold for those who carry a specific type of CD36 gene. So, “Is It Time to Give Breast Cancer Patients a Prescription for a Low-Fat Diet?” A cancer diagnosis is often referred to as a ‘teachable moment’ when patients are motivated to make changes to their lifestyle, and so provision of evidence-based guidelines is essential.”

In a randomized, prospective, multicenter clinical trial, researchers set out “to test the effect of a dietary intervention designed to reduce fat intake in women with resected, early-stage breast cancer,” meaning the women had had their breast cancer surgically removed. As shown below and at 4:02 in my video, the study participants in the dietary intervention group dropped their fat intake from about 30 percent of calories down to 20 percent, reduced their saturated fat intake by about 40 percent, and maintained it for five years. “After approximately 5 years of follow-up, women in the dietary intervention group had a 24% lower risk of relapse”—a 24-percent lower risk of the cancer coming back—“than those in the control group.” 

That was the WINS study, the Women’s Intervention Nutrition Study. Then there was the Women’s Health Initiative study, where, again, women were randomized to lower their fat intake down to 20 percent of calories, and, again, “those randomized to a low-fat dietary pattern had increased breast cancer overall survival. Meaning: A dietary change may be able to influence breast cancer outcome.” What’s more, not only was their breast cancer survival significantly greater, but the women also experienced a reduction in heart disease and a reduction in diabetes.

The leading cause of death in cancer patients is metastasis formation. That’s how most people die of cancer—not from the primary tumor, but the cancer spreading through the body. “It is estimated that metastasis is responsible for ~90% of cancer deaths,” and little progress has been made in stopping the spread, despite our modern medical armamentarium. In fact, we can sometimes make matters worse. In an editorial entitled “Therapy-Induced Metastasis,” its authors “provide evidence that all the common therapies, including radiotherapy, chemotherapy, fine needle biopsies, surgical procedures and anaesthesia, have the potential to contribute to tumour progression.” You can imagine how cutting around a tumor and severing blood vessels might lead to the “migration of residual tumour cells,” but why chemotherapy? How might chemo exacerbate metastases? “Despite reducing the size of primary tumors, chemotherapy changes the tumor microenvironment”—its surrounding tissues—“resulting in an increased escape of cancer cells into the blood stream.” Sometimes, chemo, surgery, and radiation are entirely justified, but, again, other times, these treatments can make matters worse. If only we had a way to treat the cause of the cancer’s spreading.

The development of antimetastatic therapies has been hampered by the fact that the cells that initiate metastasis remain unidentified. Then, a landmark study was published: “Targeting Metastasis-Initiating Cells Through the Fatty Acid Receptor CD36.” Researchers found a subpopulation of human cancer cells “unique in their ability to initiate metastasis”; they all express high levels of a fat receptor known as CD36, dubbed “the fat controller.” It turns out that palmitic acid or a high-fat diet specifically boosts the metastatic potential of these cancer cells. Where is palmitic acid found? Although it was originally discovered in palm oil, palmitic acid is most concentrated in meat and dairy. “Emerging evidence shows that palmitic acid (PA), a common fatty acid in the human diet, serves as a signaling molecule regulating the progression and development of many diseases at the molecular level.” It is the saturated fat that is recognized by CD36 receptors on cancer cells, and we know it is to blame, because if the CD36 receptor is blocked, so are metastases.

The study was of a human cancer, but it was a human cancer implanted into mice. However, clinically (meaning in cancer patients themselves), the presence of these CD36-studded metastasis-initiating cells does indeed correlate with a poor prognosis. CD36 appears to drive the progression of brain tumors, for example. As seen in the survival curves shown below and at 3:21 in my video What Causes Cancer to Metastasize?, those with tumors with less CD36 expression lived significantly longer. It is the same with breast cancer mortality: “In this study, we correlated the mortality of breast cancer patients to tumor CD36 expression levels.” That isn’t a surprise, since “CD36 plays a critical role in proliferation, migration and…growth of…breast cancer cells.” If we inhibit CD36, we can inhibit “the migration and invasion of the breast cancer cells.” 

Below and at 3:46 in my video, you can see breast cancer cell migration and invasion, before and after CD36 inhibition. (The top lines with circles are before CD36 inhibition, and the bottom lines with squares are after.)

This isn’t only in “human melanoma- and breast cancer–derived tumours” either. Now we suspect that “CD36 expression drives ovarian cancer progression and metastasis,” too, since we can inhibit ovarian cancer cell invasion and migration, as well as block both lymph node and blood-borne metastasis, by blocking CD36. We also see the same kind of effect with prostate cancer; suppress the uptake of fat by prostate cancer cells and suppress the tumor. This was all studied with receptor-blocking drugs and antibodies in a laboratory setting, though. If these “metastasis-initiating cancer cells particularly rely on dietary lipids [fat] to promote metastasis,” the spread of cancer, why not just block the dietary fat in the first place?

“Lipid metabolism fuels cancer’s spread.” Cancer cells love fat and cholesterol. The reason is that so much energy is stored in fat. “Hence, CD36+ metastatic cells might take advantage of this feature to obtain the high amount of energy that is likely to be required for them to anchor and survive at sites distant from the primary tumour”—to set up shop throughout the body.

“The time when glucose [sugar] was considered as the major, if not only, fuel to support cancer cell proliferation is over.” There appears to be “a fatter way to metastasize.” No wonder high-fat diets (HFD) may “play a crucial role in increasing the risk of different cancer types, and a number of clinical studies have linked HFD with several advanced cancers.”

If dietary fat may be “greasing the wheels of the cancer machine,” might there be “specific dietary regimens” we could use to starve cancers of dietary fat? You don’t know until you put it to the test, which we’ll look at next.

Dairy milk supplies between a quarter and a half of the daily iodine requirement in the United States, though milk itself has “little native iodine.” The iodine content in cow’s milk is mainly determined by factors like “the application of iodine-containing teat disinfectants,” and the “iodine residues in milk originate mainly from the contamination of the teat surface…” Indeed, the teats of dairy cows are typically sprayed or dipped with betadine-type disinfectants, and the iodine just kind of leaches into their milk, as you can see at 0:35 in my video Friday Favorites: The Healthiest Natural Source of Iodine. 

Too bad most of the plant-based milks on the market aren’t enriched with iodine, too. Fortified soy milk is probably the healthiest of the plant milks, but even if it were enriched with iodine, what about the effects soy may have on thyroid function? When I searched the medical literature on soy and thyroid, this study popped up: “A Cost-Effective, Easily Available Tofu Model for Training Residents in Ultrasound-Guided Fine Needle Thyroid Nodule Targeting Punctures”—an economical way to train residents to do thyroid biopsies by sticking the ultrasound probe right on top a block of tofu and get to business, as you can see below and at 1:10 in my video. It turns out that our thyroid gland looks a lot like tofu on ultrasound.

Anyway, “the idea that soya may influence thyroid function originated over eight decades ago when marked thyroid enlargement was seen in rats fed raw soybeans.” (People living in Asian countries have consumed soy foods for centuries, though, “with no perceptible thyrotoxic effects,” which certainly suggests their safety.) The bottom line is that there does not seem to be a problem for people who have normal thyroid function. However, soy foods may inhibit the oral absorption of Synthroid and other thyroid hormone replacement drugs, but so do all foods. That’s why we tell patients to take it on an empty stomach. But you also have to be getting enough iodine, so it may be particularly “important for soy food consumers to make sure their intake of iodine is adequate.”

What’s the best way to get iodine? For those who use table salt, make sure it’s iodized. “Currently, only 53% of salt sold for use in homes contains iodine, and salt used in processed foods typically is not iodized.” Ideally, we shouldn’t add any salt at all, of course, since it is “a public health hazard.” A paper was titled: “Salt, the Neglected Silent Killer.” Think it’s a little over the top? Dietary salt is the number one dietary risk factor for death on planet Earth, wiping out more than three million people a year, twice as bad as not eating your vegetables, as you can see here and at 2:38 in my video. 

In that case, what’s the best source of iodine then? Sea vegetables, as you can see below and at 2:50. We can get a little iodine here and there from a whole variety of foods, but the most concentrated source by far is seaweed. We can get up to nearly 2,000 percent of our daily allowance in just a single gram, about the weight of a paperclip. 

“Given that iodine is extensively stored in the thyroid, it can safely be consumed intermittently,” meaning we don’t have to get it every day, “which makes seaweed use in a range of foods attractive and occasional seaweed intake enough to ensure iodine sufficiency.” However, some seaweed has overly high iodine content, like kelp, and should be used with caution. Too much iodine can cause hyperthyroidism, a hyperactive thyroid gland. A woman presented with a racing heartbeat, insomnia, anxiety, and weight loss, thanks to taking just two tablets containing kelp a day.

In my last video, I noted how the average urinary iodine level of vegans was less than the ideal levels, but there was one kelp-eating vegan with a urinary concentration over 9,000 mcg/liter. Adequate intake is when you’re peeing out 100 to 199 mcg/liter, and excessive iodine intake is when you break 300 mcg/liter. Clearly, 9,437 mcg/liter is way too much. 
 
As you can see below and at 3:57 in my video, the recommended average daily intake is 150 mcg per day for non-pregnant, non-breastfeeding adults, and we may want to stay below 600 mcg a day on a day-to-day basis, but a tablespoon of kelp may contain about 2,000 mcg. So, I’d stay away from kelp because it has too much iodine, and I’d also stay away from hijiki because it contains too much arsenic. 

This can give you an approximate daily allowance of iodine from some common seaweed preparations: two nori sheets, which you can just nibble on them as snacks like I do; one teaspoon of dulse flakes, which you can just sprinkle on anything; one teaspoon of dried arame, which is great to add to soups; or one tablespoon of seaweed salad.

If iodine is concentrated in marine foods, “this raises the question of how early hominins living in continental areas could have met their iodine requirements.” What do bonobos do? They’re perhaps our closest relatives. During swamp visits, they all forage for aquatic herbs.  

Doctor’s Note:

This is the second in a four-video series on thyroid function. If you missed the previous one, check out Are Vegans at Risk for Iodine Deficiency?.

Coming up are The Best Diet for Hypothyroidism and Hyperthyroidism and Diet for Hypothyroidism: A Natural Treatment for Hashimoto’s Disease.

What else can seaweed do? See the related posts below.

“Adequate dietary iodine is required for normal thyroid function.” In fact, the two thyroid hormones are named after how many iodine atoms they contain: T3 and T4. “Given that iodine is extensively stored in the thyroid gland itself, it can safely be consumed intermittently,” so we don’t need to consume it every day. However, our overall diet does need a good source of it. Unfortunately, the common sources aren’t particularly health-promoting: iodized salt and dairy foods. (Iodine-based cleansers like betadine are used on cows “to sanitize the udders, resulting in leaching of iodine in the milk.”) Iodine may also be added to cattle feed, and some commercially produced breads contain food additives with iodine.

If you put people on a paleo-type diet and cut out their dairy and table salt, they can develop an iodine deficiency, even though they double their intake of seafood, which can also be a source of iodine. What about those switching to diets centered around whole plant foods? They also cut down on ice cream and Wonder Bread, and if they aren’t eating anything from the sea, like seaweed or other sea vegetables, they can run into the same problem.

A three-year-old’s parents reported striving to feed her only the healthiest foods, and her diet included only plant-based, unsalted, and unseasoned foods. She got no unprocessed foods, but she also got no vitamin supplementation, which could be deadly. Without vitamin B12, those on strictly plant-based diets can develop irreversible nerve damage, but in this case, a goiter arose first, due to inadequate iodine intake.

In another case of “veganism as a cause of iodine-deficient hypothyroidism,” a toddler became ill after weaning. Before weaning, he was fine because his mother kept taking her prenatal vitamins, which fortunately contained iodine.

Most vegetarians and vegans are apparently unaware of the importance of iodine intake during pregnancy, “for the neurodevelopment of the unborn child, similar to their omnivorous counterparts.” The American Thyroid Association and the American Academy of Pediatrics have recommended that women, even just planning on getting pregnant, should take a daily supplement containing 150 micrograms (mcg) of iodine, yet only 60 percent of prenatal vitamins marketed in the United States contain this essential mineral. So, despite the recommendations, about 40 percent of prenatal vitamins don’t contain it. “Therefore, it is extremely important that women, especially when pregnant, breastfeeding, or planning a pregnancy, read the labels of their multivitamin supplements to ensure that they are receiving an adequate amount of iodine.”

Women of reproductive age have an average iodine level of 110 mcg/liter, which is fine for nonpregnant individuals, but we’d really like women to get at least 150 mcg/liter during pregnancy. (It’s basically a 24-hour urine test, in which iodine sufficiency is defined as 100 mcg/liter of urine in nonpregnant adults; the average vegan failed to reach this in the largest study done to date, one out of Boston.)

The recommended average daily intake is 150 mcg per day for most people, which we can get in about a cup and a half of cow’s milk. Regrettably, plant-based milks aren’t typically fortified with iodine and average only about 3 mcg per cup. Although many plant-based milks are fortified with calcium, researchers found in the largest systematic study to date that only 3 out of 47 were fortified with iodine. Those that were fortified had as much as cow’s milk, but those that weren’t fell short, as you can see at 3:30 in my video Are Vegans at Risk for Iodine Deficiency?. 

Plant-based milk companies brag about enriching their milks with calcium and often vitamins B12, D, and A, but only rarely are attempts made to match iodine content. The only reason cow’s milk has so much is that producers enrich the animals’ feed or it comes dripping off their udders. So, why don’t plant-milk companies add iodine, too? I was told by a food scientist at Silk that my carrageenan video played a role in the company switching to another thickener. Hopefully, Silk will see this video, too, and consider adding iodine, or maybe another company will snatch the opportunity for a market advantage.  

The researchers conclude that individuals who consume plant-based milks not fortified with iodine may be at risk for iodine deficiency, unless they consume alternative dietary iodine sources, the healthiest of which are sea vegetables, which we’ll cover next.

Doctor’s Note:

This is the first in a four-video series on thyroid function. The next three are: 

• Friday Favorites: The Healthiest Natural Source of Iodine
• The Best Diet for Hypothyroidism and Hyperthyroidism
• Diet for Hypothyroidism: A Natural Treatment for Hashimoto’s Disease

For more on iodine, see the related posts below.

The U.S. Centers for Disease Control and Prevention (CDC) recommends that everyone over the age of six months get a routine flu shot every year, unless you have some sort of contraindication, such as an allergy to any of the vaccine’s components. CDC recommends getting vaccinated by the end of October, but it may even be beneficial when received in December or later. How effective are flu vaccines? It depends on the year, but, as you can see below and at 0:33 in my video Friday Favorites: Elderberry Benefits and Side Effects: Does It Help with Colds and the Flu?, the flu vaccine typically reduces the risk of getting the flu by about 40 to 50 percent.

So, in healthy adults, we can say with moderate certainty that we can decrease our risk of influenza from about 2 percent each year down to just under 1 percent. Older adults may get a similar relative risk reduction, but the baseline risk is higher and the consequences greater, so the absolute benefits are greater, too. In kids, flu vaccines shine; there’s a high certainty of evidence of a substantial drop in risk. But even in this kind of best-case scenario, there’s still a risk with vaccination, so what else can we do?

In the United States alone, each year, Americans experience millions of cases of influenza and hundreds of millions of colds. What about elderberry supplements? In a test tube, elderberry extracts can inhibit pathogens, including the flu virus. In a petri dish, it can rev up the production of flu-fighting molecules from human immune system cells, like tumor necrosis factor, as much as nearly 45-fold. Elderberry juice can help mice fight off the flu. But what about actual people?

The first clinical trial was published back in the 1990s: a double-blind, randomized, placebo-controlled trial to treat flu-like symptoms. Researchers found that the odds for improvement before the fifth day in those in the treated group were more than 20 times the odds of the participants in the control group (p < 0.001). Two subsequent double-blind, randomized, placebo-controlled trials showed similar accelerated healing in the elderberry groups, as you can see here and at 1:54 in my video. 

I was excited to see this study—“Elderberry Supplementation Reduces Cold Duration and Symptoms in Air-Travelers”—given a 200-city book tour I was embarking on. It was a randomized, double-blind, placebo-controlled clinical trial of 312 economy class passengers. While taking elderberry didn’t seem to prevent people from coming down with cold symptoms, the duration and severity of symptoms in those who did get a cold seemed to have been lessened, and they suffered an average of about five days instead of seven.

A similar study using the herb echinacea found a lessening of symptom scores, but it was of only borderline statistical significance. Nevertheless, even though most of the individual trials didn’t find statistically significant improvements, when all such studies were compiled, it seems there may be about a 20 percent decrease incidence of colds, as seen below and at 2:50 in my video.

Note, though, that there is a concern about publication bias and selective reporting. A number of findings and some entire studies seem to be MIA, suggesting that negative studies may have been quietly shelved. So, we aren’t really sure about echinacea, but all the elderberry studies seem to have positive results, suggesting elderberry supplementation “provides an effective treatment option when advanced or more invasive care [more serious treatment] is not warranted.” This conclusion came from someone with apparent conflicts of interest, though. In fact, each of the four elderberry studies was funded by the elderberry product companies themselves.

Any other berries that might be helpful? A randomized, placebo-controlled, interventional study—funded, predictably, by Ocean Spray—found that the gamma-delta-T-cells of those drinking a low-calorie cranberry juice beverage for ten weeks appeared to be proliferating at nearly fivefold the rate. These immune cells “serve as a first line of defense.” Though the study participants didn’t get fewer colds, they did seem to suffer less, but not enough to prevent days missed from work or an impairment of their activities, as shown here and at 3:56 in my video. 

At least cranberries have never been reported to cause pancreatitis. A man taking an elderberry extract not only suffered an attack of acute pancreatitis, a sudden painful inflammation of the pancreas, but it went away when he stopped it, then reappeared again years later when he tried taking it again, which suggests cause-and-effect. Why take elderberry extracts when you can just eat the elderberries themselves? Well, cooked are fine, but “consuming uncooked blue or black elderberries can cause nausea and vomiting.”

I found out the hard way, as I explained in an answer to the question, “What was the worst day of your life?” in my London Real interview on my How Not to Die book tour. It turns out elderberry fruits form cyanide, such that eight people had to be medevacked out after someone brought freshly squeezed elderberry juice to a gathering.

Doctor’s Note:

Here’s the London Real interview I mentioned.

What else can we do for the common cold? See the related posts below.

And, speaking of cranberries, Can Cranberry Juice Treat Bladder Infections?. Watch the video to find out. 

Our bodies are meant to have a certain balance of sodium and potassium intake, yet many people, including the majority in the United States, get vastly more sodium and far less potassium than the recommended amounts. Indeed, sodium and potassium goals are currently met by less than 0.015 percent of the U.S. population—close to 99.99 percent noncompliance, with only 1 in 6,000 Americans hitting the recommended guidelines.

What’s So Bad About Salt?

Of all the terrible things about our diets, high dietary sodium intake—that is, high salt intake—is the leading risk, estimated to be causing millions of deaths every year mainly through adverse effects on blood pressure and increased risks of stroke, heart attack, and kidney damage. Hypertension, known commonly as high blood pressure, is called the “silent and invisible killer” because it rarely causes symptoms but is one of the most powerful independent predictors of some of our leading causes of death. I discuss this in my video Are Potassium Chloride Salt Substitutes Effective?.

How Much Sodium Is Healthy in a Day?

Our bodies evolved to handle only about 750 milligrams of sodium a day. Nevertheless, the American Heart Association calls for us to stay under 1,500 milligrams, twice that amount. However, we’re consuming more than four times what’s natural, and it’s only getting worse, having increased over the last couple of decades. An eye-opening 98.8 percent of Americans exceed even that elevated 1,500 milligrams threshold.

Daily Potassium Intake

While many of us are consuming too much sodium, we may also be getting too little potassium, a mineral that lowers blood pressure. Less than 2 percent of U.S. adults, for instance, consume the recommended daily minimum intake of potassium based on chronic disease prevention. So, more than 98 percent of Americans may eat potassium-deficient diets. 

This deficiency is even more striking when comparing our current intake with that of our ancestors, who consumed large amounts of dietary potassium. We evolved probably getting more than 10,000 milligrams of potassium a day. The recommendation was to get about half that amount, yet most of us don’t come anywhere close.

Why Are So Many of Us Lacking in Potassium?

We evolved consuming a diet very rich in potassium and low in sodium, but, today, this pattern has been reversed. The flip reflects a shift away from traditional plant-based diets high in potassium and low in sodium towards the standard American diet. I’m talking about a shift away from fruits, greens, roots, and tubers to an eating pattern filled with salty, processed foods stripped of potassium.

Why Do We Need Potassium?

Low potassium intake has been implicated in high blood pressure and cardiovascular disease, and several meta-analyses have confirmed that high potassium intake appears to reduce the risk of stroke. It follows that potassium is now considered a “nutrient of public health concern” because most Americans don’t reach the recommended minimum daily intake.

What Is the Best Substitute for Salt?

Potassium chloride, which is often found in zero-sodium salt substitutes. We know from randomized controlled trials that sodium reduction leads to blood pressure reduction and increasing potassium intake can also lower blood pressure. So should we be “salting” our food with potassium chloride instead of sodium chloride?

What Is Potassium Chloride? Is It a Viable (and Tasty) Salt Substitute?

Potassium chloride is a naturally occurring mineral salt, which is obtained the same way we get regular sodium salt. Since we get too much sodium and not enough potassium, this would seem to make potassium chloride a win-win solution. Consider these examples:

• In a randomized controlled trial, households had just 25 percent of the sodium chloride salt replaced with potassium chloride. At that level, most people either can’t tell the difference or even prefer the salt with the potassium mixed in. The findings? The use of the salt substitute with one-quarter potassium chloride was associated with cutting the risk of developing hypertension in half.
• In another study, five kitchens in a veterans’ retirement home were randomized into two groups for about two and a half years. They either salted their meals with regular salt or, unbeknownst to the cooks and the diners alike, a 50/50 blend of potassium chloride. Those in the half-potassium group cut their risk of dying from cardiovascular disease by about 40 percent and lived up to nearly one year longer. The life expectancy difference at age 70 was equivalent to that which would have naturally occurred in 14 years––meaning that just switching to half potassium salt appeared to effectively make people more than a decade younger when it came to risk of death.

Side Effects of Potassium Chloride?

As I discuss in my video Potassium Chloride Salt Substitute Side Effects, potassium chloride is “generally regarded as safe” by the U.S. Food and Drug Administration. Healthy individuals don’t have to worry about getting too much potassium because their kidneys excrete any excess in urine, but that’s with potassium in food. What about supplements? No adverse effects have been shown for long-term intakes of potassium supplements as high as 3,000 milligrams a day, and blood levels of potassium are maintained in the normal range by healthy kidneys, even when potassium intake is increased to approximately 15,000 milligrams a day. This isn’t surprising, given that we evolved eating so many healthy plant foods, so many fruits and vegetables, rich in potassium.

The normal range for potassium levels in the blood is between 3.5 and 5.0. There are a small number of individuals who may run into problems, primarily those with severely impaired kidney function. That’s why there’s been such a reluctance to push potassium‐based salt substitutes on a population level. Serious issues may arise if your kidneys can’t regulate your potassium. There may be concern if you have known kidney disease, diabetes (diabetes can lead to kidney damage), severe heart failure, or adrenal insufficiency, or if you’re an older adult or on medications that impair potassium excretion. If you aren’t sure if you’re at risk, ask your doctor about getting your kidney function tested.

Conclusion

National and international health organizations have called for warning labels on salt packets and salt shakers, with messages like “too much sodium in the diet causes high blood pressure and increases risk of stomach cancer, stroke, heart disease, and kidney disease. Limit your use.” So, pass (on) the salt shaker and try some potassium chloride instead.

By cultivating muscle meat directly, without associated organs like intestines, the incidence of foodborne diseases “could be significantly reduced,” as could exposure to antibiotics, “pesticides, arsenic, dioxins, and hormones associated with conventional meat.” Currently, the U.S. Food and Drug Administration has approved seven hormone drugs to bulk up the production of milk and meat. “In the European Union, there exists a total ban on such use,” however. Even without injected hormones, though, animal products naturally have hormones because they come from animals. “Eggs, example given, contribute more to the dietary intake of estradiol [estrogens] than beef, whether the animal is legally treated with hormones or not.” After all, eggs come straight from a hen’s ovaries, so, of course, they’re swimming with hormones. But if you’re directly growing just muscle meat or egg white protein, you don’t need to include reproductive organs, adrenal glands, or any of the associated hormones.

“Chemical safety is another concern for meat produced under current production systems.” There are chemical toxicants and industrial pollutants that build up in the food chain, such as pesticides, PCBs, heavy metals, and flame retardants, but there is no food chain with cultivated meat. We could produce all the tuna we wanted, with zero mercury.

When the World Health Organization determined that processed meat was a known human carcinogen and unprocessed meat a probable human carcinogen, it wasn’t even talking about the carcinogenic environmental pollutants. When researchers tested retail meat for the presence of “33 chemicals with calculated carcinogenic potential,” like polycyclic aromatic hydrocarbons (PAHs), organochlorine pesticides like DDT, and dioxin-like PCBs, they concluded that, in order to reduce the risk of cancer, we should limit beef, pork, or chicken consumption to a maximum of five servings a month.

Why cultivate meat at all when you can just buy organic? Surprisingly, “consumption of organic meat does not diminish the carcinogenic potential associated with the intake of persistent organic pollutants (POPs).” A number of studies have recently compared the presence of environmental contaminants in organic meat versus conventional meat, and the researchers found, surprisingly, that organic meat was sometimes more contaminated. Not only organic beef either. Higher levels were also found in pork and poultry.

If you look at the micropollutants and chemical residues in both organic and conventional meat, several environmental contaminants, including dioxins, PCBs, lead, and arsenic, were measured at significantly higher levels in the organic samples. As you can see below and at 2:56 in my video, The Human Health Effects of Cultivated Meat: Chemical Safety, the green is organic meat, and the blue is conventional. 

Cooking helps to draw off some of the fat where the PCBs are concentrated, as shown here and at 3:01.

Seafood seems to be an exception. Steaming, for example, generally increases contaminant levels, increasing contaminant exposure and concentrating mercury levels as much as 47 percent, as you can see here and at 3:15 in my video. Better not to have toxic buildup in the first place.

More than 95 percent of human exposure to industrial pollutants like dioxins and PCBs comes from foods like meat, including fatty fish, and dairy, but the pollutants don’t appear magically. The only way the chicken, fish, and other meat lead to human exposure is because the animals themselves built up a lifetime of exposure in our polluted world, from incinerators, power plants, sewer sludge, and on and on, as you can see here and at 3:40 in my video.

Unlike conventional meat production, a slaughter-free harvest would not only mean no more infected animals, but no more contaminated animals either. In terms of pollutants, it would be like taking a time machine back before the Industrial Revolution.

Doctor’s Note:

Cultivated meat means less contamination with fecal residues, toxic pollutants, antibiotics, and hormones; up to 99 percent less environmental impact; and zero pandemic risk. Cultivated meat allows people to have their meat and eat it, too, without affecting the rest of us.

This is the final video in this cultivated meat series. If you missed the first two, check out the videos on Food Safety and Antibiotic Resistance.

I previously did a video series on plant-based meats; see the related posts below.

All videos in the plant-based meat series are also available in a digital download from a webinar I did. SeeThe Human Health Implications of Plant-Based and Cultivated Meat for Pandemic Prevention and Climate Mitigation.

Cultivating muscle meat directly from cells instead of raising and slaughtering animals would reduce the risk of foodborne illnesses “due to fecal contamination during slaughtering and evisceration of carcasses” because there would be no feces, no slaughter, and no carcasses to eviscerate. In addition, cultivating meat would also reduce the threat from antibiotic resistance.

To compensate for overcrowded, stressful, and unhygienic conditions on factory farms, animals are typically dosed en masse with antibiotics. A lot of antibiotics. About 20 million pounds of medically important antibiotics a year, as you can see here and at 0:57 in my video, The Human Health Effects of Cultivated Meat: Antibiotic Resistance. 

In the United States, for example, farm animals are given about 2 million pounds of penicillin drugs and 15 million pounds of tetracyclines annually. This is madness. 

Antibiotic drugs important to human medicine go right into the feed and water of animals like cows, pigs, and chickens, by the ton and by the thousands of tons, as shown below and at 1:02 in my video. And that is all without a prescription.

Ninety-seven percent of the tens of millions of pounds of antibiotics given to farm animals in the United States are bought over the counter—without a prescription or even an order from a veterinarian, as seen here and a 1:24. To get even a few milligrams of penicillin, we need a doctor’s prescription, because these are miracle wonder drugs that can’t be squandered. Meanwhile, farmers can just back their trucks up to the feedstore. 

Now, half the Salmonella in retail meat—chicken, turkey, beef, and pork—is resistant to tetracycline, as shown below and at 1:50 in my video. About a quarter of the bugs are now resistant to three or more entire classes of antibiotics, including some resistant to “cephalosporins such as ceftriaxone [which] are critically important drugs we use to treat severe Salmonella infections, especially in children.” 

Such agricultural applications for antimicrobials are now considered an “urgent threat to human health.” “The link between antibiotic use in animals and antibiotic resistance in humans is unequivocal.”

As shown here and at 2:20 in my video, it all starts with the poop. 

Antibiotic-resistant bugs are selected for and then can spread via meat or produce contaminated by poop or they can spread through the wind, the air, or the water, or be carried by insects. There are many pathways by which resistant superbugs can escape. So, even if you don’t eat meat, you can be “put at risk by the pathogens released from stressed, immunocompromised, contaminant-filled livestock” dosed with antibiotics. That’s one of the reasons the American Public Health Association called for a moratorium on factory farms, due in part to all the pollution from concentrated animal feed operations (CAFOs) to the surrounding communities. 

Every year, more than five tons of animal manure are produced for every man, woman, and child in the United States. Again, it all starts with the poop. But cultivated meat means no guts, no poop, no fecal infections, and no antibiotics necessary. It also means no fecal or antibiotic residues left in “foodstuffs such as milk, egg, and meat” that can potentially cause a variety of side effects beyond just the transfer of antibiotic-resistant bacteria to humans.

And, as you can see here and at 3:30 in my video, things are getting worse, not better. U.S. animal agriculture is using more antibiotics now than ever.

This isn’t only because more animals are being raised for food, either. Antibiotic sales in the United States are outpacing meat production. Yes, meat production is going up, but there is a serious rise in antibiotic sales for meat production, as shown below and at 3:46.

With the combined might of Big Ag and Big Pharma (who profit from selling all the drugs), it’s hard to imagine anything changing on the political side. The only hope may be a change in the production side.

“The unstoppable rise of super-resistant strains of bacteria is a serious worldwide problem, resulting in 700 000 deaths every year,” and the projections for global antibiotic use in the production of farm animals are “ominous,” estimated to exceed 100,000 tons of antibiotics pumped into animals raised for food by 2030. Quite simply, we may be “on the path to untreatable infections” by using even some of our “last resort antibiotics,” like carbapenems, just to shave a few cents off a pound of meat.

And it’s not just foodborne bacteria. Mad cow disease, swine flu, and bird flu have the potential to kill millions of people. Skeptical? I’ve got a book for you to read, whose author’s “superb storytelling ability makes every page of the book interesting and fascinating for both specialist and layperson.” (Thanks, Virology Journal, for the wonderful book review and calling my book “a must read.”)

Given the threat of the chickens coming home to roost, an editorial in the American Journal of Public Health thought that “it is curious, therefore, that changing the way humans treat animals—most basically, ceasing to eat them or, at the very least, radically limiting the quantity of them that are eaten—is largely off the radar as a significant preventative measure. Such a change, if sufficiently adopted or imposed, could still reduce the chances of the much-feared influenza epidemic…Yet humanity does not consider this option.”

That may be moot, though, because we could cultivate all the chicken we want, without guts or lungs.

It’s hard to stress the importance of that American Journal of Public Health editorial. As devastating as COVID-19 has been, it may just be a dress rehearsal for an even greater threat waiting in the wings—the wings of chickens.

According to the Centers for Disease Control and Prevention, the leading candidate for the next pandemic is a bird flu virus known as H7N9, which is a hundred times deadlier than COVID-19. Instead of 1 in 250 patients dying, H7N9 has killed 40 percent of the people it infects.

The last time a bird flu virus jumped directly to humans and caused a pandemic, it triggered the deadliest plague in human history—the 1918 pandemic that killed 50 million people. That had a 2 percent death rate. What if we had a pandemic infecting billions where death was closer to a flip of a coin?

The good news is that there is something we can do about it. Just as eliminating the exotic animal trade and live animal markets may go a long way toward preventing the next coronavirus pandemic, reforming the way we raise domestic animals for food may help forestall the next killer flu. The bottom line is that it’s not worth risking the lives of millions of people for the sake of cheaper chicken.

If you missed the previous video, see The Human Health Effects of Cultivated Meat: Food Safety. Up next is The Human Health Effects of Cultivated Meat: Chemical Safety. 

We had the pleasure of talking with Remy Morimoto Park about food, culture, and AAPI Month. We hope you enjoy this interview and her recipes for Crunchy Pad Thai Inspired Salad and Miso Soup.

Please tell us a little bit about yourself and your work. 

I am a vegan cookbook author and health and wellness content creator. I started Veggiekins blog while I was in college as a means for sharing recipes and spreading the vegan lifestyle, and it has since turned into my full-time job, which has been absolutely incredible. I’m also the founder of a matcha brand, Frauth. Outside of work, I split my time between New York and Los Angeles, and you can usually find me at a farmers market!

In your experience, how have you found food to tell a story and shape culture? 

I think that when you come from any type of culture, food is so important because it’s one way culture is passed down from generation to generation. I think that’s why sharing recipes and passing them down is so crucial for preserving culture. In my Asian cultures––Japanese, Korean, and Taiwanese––I think food is really important because it’s also how we communicate with each other and share love. In our cultures, it’s not quite as common to express verbally that you love someone. We really don’t talk too much about feelings, but we always gather around the table to share a meal as a family and many of our holidays and family gatherings revolve around food. There’s a joke that your Asian parents might not apologize or say they love you, but they will always put food on the table for you or cut up a fruit plate for you to communicate that. So, with that in mind, I think that food is a pivotal part of Asian culture. For me personally, a lot of my memories from childhood revolve around a specific meal or have a specific dish tied to it. Food evokes a lot of really powerful memories, and I think it’s a really great vehicle for storytelling in that way. 

How do you educate people about the intersection of food, health, community, and culture?

When it comes to most Asian cuisines, there really isn’t very much dairy, which I think is incredible. It also makes them such great foundations for lots of vegan-friendly options. As well, in my three cultures, there are different types of existing plant-based diets followed by religious groups, for example. I think there is a lot to explore, and the same can be said about most cultures. For example, in Korea, there are monks who eat temple food, which is primarily-plant based; in Japan, the Shojin cuisine is also primarily plant-based; and in China, a lot of Buddhists don’t eat any meat or animal products at all. Additionally, my grandparents always told me that, when they were younger, they primarily ate plant-based––mostly grains and vegetables––because meat and animal products were so expensive and reserved more for the higher classes in society. Nowadays, I think people associate meat with Asian cuisine (e.g., Korean BBQ), though, in reality, a lot of Asian cuisine historically revolved around grains and plants.

What are some plant-based ingredients and vegan dishes you would like to highlight as traditional to your cultures and/or other Asian cultures? What are your favorites to cook with?

A plant-based ingredient that I think is essential to Asian culture is tofu, of course! No Asian person is unfamiliar with tofu, and I think that’s incredible because it’s such a great source of plant protein. Rice and other grains are also commonly used throughout Asian cuisines, and some of my personal favourites include tempeh and some of the more unique Asian veggies you wouldn’t typically find at a conventional grocery store (e.g., bean sprouts, bok choy, morning glory, and pea shoots). There’s a great diversity of veggies to choose from in Asian cuisine.

As a plant-based chef, what do you envision as the way forward to encourage people to include more fruits and vegetables into their diets? 

One of the things I like to stress the most is that vegetables can be treated with as much care, if not more care, than meat and other animal products. I think a lot of people put in the minimum effort when preparing veggies or may even just eat them raw. When we marinate, smoke, sous vide, roast, or slow cook them, the result is so different. 

Nowadays, people have developed this hunger for more global cuisines and are more interested in trying dishes from other cultures, which is a great way to encourage individuals to incorporate more fruits and veggies into their diets. When you start to explore beyond just the United States, for instance, and see what the world has to offer, you find that there are so many different types of fruits and vegetables that you can enjoy. Additionally, there are so many more flavor profiles and spice blends to work with to season your vegetables. Keeping it interesting for the palate is so important! 

What significance does AAPI Month have for you, and how do you celebrate your heritage? 

AAPI month means a lot to me because I’m not just Asian, but Asian American. I was born in the United States to parents who had already immigrated here and speak primarily English in the house. I don’t feel 100% Asian and, of course, don’t feel 100% American either, so I think that the distinction is really nuanced and makes me feel seen. It’s an incredible sign that people are really embracing others and diversity, which is so important. It’s helped to introduce other cultures to other people and encourage curiosity and hunger for knowledge about others.

I really celebrate my heritage through food and sharing recipes that feel are authentic to my culture and my Asian-American family. It’s such a treat to be able to share that with others and especially to do that plant-based!

Please tell us a little bit about your cookbook, Sesame, Soy, Spice, and what inspired you to write it.

My cookbook was really inspired by my family and my upbringing. “Asian American” is truly the best way to describe my family and the food we eat because we are Asian (and three types of Asian at that), but we are also very much American. Growing up, the food on our table looked like a combination of both western and American foods, as well as the Asian dishes I grew up eating. For example, one thing I love is popcorn, but with Japanese furikake seasoning on top. Sometimes we might sub out chili paste or hot sauce with gochujang, a Korean fermented red pepper paste.

Throughout my cookbook, I really wanted to emphasize that eating vegan does not mean you have to give up your culture and that it can actually be so much fun reconnecting with your culture through trying to recreate those favorite recipes as vegan. It not only makes living a vegan lifestyle more exciting and inclusive, but also more sustainable because there’s more variety in the foods you eat. When I first became vegan, I thought I could only eat foods like salad bowls, grain bowls, and smoothie bowls. Then I realized that it’s not really a diet but a way of life and that almost any cuisine can be vegan-friendly if you get creative in the kitchen.

Through the short stories in my cookbook, I also document my journey to becoming vegan and making peace with my relationship with food. I share the story of how becoming vegan taught me compassion and aided in that journey. The process of writing the cookbook was very meaningful to my family because we really got to connect more than ever through food. I would chat with them about recipes from childhood that I wanted to try to recreate, and we would speak on the phone while we were both in the kitchen, trying to work out a recipe. It was a very nostalgic time for me because, often, we’d end up reminiscing about memories from my childhood while cooking.

Crunchy Pad Thai Inspired Salad 

1 to 2 servings, 10 minutes prep

For the Pad Thai Inspired Dressing ½ fresh lime, juiced 2 tbsps Umami Sauce  2 tsps tamarind purée 1 clove garlic, finely minced 1 tbsp rice wine vinegar 2 tbsp cashew butter (optional, for creaminess) For the Salad 2 cups shredded purple cabbage 3-4 mini cucumbers, julienned 1 large carrot, juliennned ½ cup chiffonaded radicchio  Handful thinly sliced breakfast radishes  1 cup shredded green papaya (optional) Optional Fresh Thai chili peppers Crushed peanuts to garnish Dried chili flakes to garnish Green onions to garnish

Instructions

1. In a large bowl, add all the dressing ingredients, then whisk them together. Adjust to taste. If using cashew butter, you may choose to thin it with 1 to 2 tablespoons of water.
2. Add all of the salad ingredients to the bowl, then toss, using your hands or tongs to coat the veggies.
3. Garnish with peanuts, chili flakes, and green onion, if desired.

Miso Soup

8 servings, 30 minutes prep, 15 minutes cook time, 30 minutes soaking time 

For the Dashi Broth 10 cups filtered water 5-6 dried shiitake mushrooms 3 kombu pieces (roughly 3 x 3-inches) 1 leek stem, sliced diagonally 1 carrot, sliced diagonally 3 scallions (white parts), halved ½ yellow onion, halved 12 oz firm silken tofu ¼ cup dried wakame Other Ingredients 5 tbsps red miso paste 5 tbsps white miso paste For Garnish  Scallions (green tops), thinly sliced Ichimi togarashi, to taste Cooked mushrooms (optional)

Instructions

Prepare Dashi Broth 

1. To your cooking pot, add the water, dried mushrooms, and kombu. Let soak for about 15 to 30 minutes. (The longer you soak, the more flavor will be released).
2. Bring to a boil, then lower the heat to a simmer. Let simmer for 10 minutes.
3. Add the leek, carrots, scallions, and onion, and cook for another 10 minutes.
4. Add the tofu, then remove the pot from the heat.

Re-Hydrate Wakame

1. In a small bowl, add the dried wakame with enough hot water to cover. Let soak until the wakame is soft to the touch, then drain and set aside.

Add Miso Paste

1. In a small jar or bowl, add the red and white miso with a little water. You want to add just enough water so the misos turn into a thin paste. Use a whisk or chopsticks to break down the paste so it’s pourable. 
2. Add the wakame and the whisked miso to the pot, and gently stir to combine. Adjust to taste.
3. Garnish with green scallion tops, ichimi togarashi, and cooked mushrooms, if desired.

For more about Remy, check out her blog, Instagram, TikTok, and YouTube. 

Black cumin, also known as Nigella sativa or simply “black seed,” is not related to cumin; it’s a member of the buttercup family rather than the carrot family. Black cumin, with its peppery flavor, is a spice commonly used in Indian and Middle Eastern cuisines, but it’s also been prized for its purported medicinal benefits. Described as “a miracle herb,” with mentions going back to the Old Testament, it was found cached in King Tut’s tomb, and it’s been reported that the “Islamic prophet Muhammad once stated that the black seed can heal every disease except death.” Only in the last 50 years or so has it been put to the test, though, culminating in more than a thousand papers published in the medical literature.

Typical doses used in studies are one or two grams a day, which is only about a quarter teaspoon. This enables researchers to perform randomized, double-blind, placebo-controlled trials by putting the whole-food spice powder into capsules rather than studying a component or extract.

A systematic review and meta-analysis of randomized, placebo-controlled trials found that daily black cumin consumption significantly improves cholesterol and triglycerides. Researchers also found that it not only improves blood pressure, but it also improves blood sugar control. Some of the results are quite extraordinary. For example, one study found that postmenopausal women randomized to a gram a day (less than a quarter teaspoon) of black cumin powder reduced their LDL cholesterol by 27 percent within two months, significantly better than placebo. Those are the kinds of results we’d expect from a statin drug, yet it was achieved with just a sprinkle’s worth of a simple spice. Black cumin may also help with menopausal symptoms.

Now, it doesn’t appear to cure anything—a month after stopping the spice, cholesterol levels began to creep back up, for instance, as you can see below and at 2:00 in my video Benefits of Black Cumin Seed (Nigella Sativa) for Weight Loss—but it does appear to be a cheap, safe, effective, and delicious (if you like spice) treatment for some of our deadliest risk factors. And its side effects include loss of appetite and weight loss! 

The latest systematic review and meta-analysis of randomized controlled weight-loss trials found that about a quarter teaspoon of black cumin powder a day does appear to cause weight loss within a span of a few months. If it really can benefit so many facets of health, why don’t we hear more about it? Why wasn’t I taught about it in medical school? Maybe because there’s little profit motive. Black cumin is just a common, natural spice. The daily dose used in most of these studies would cost about three cents a day. Stockholders won’t be thrilled to sell something that can’t be patented and costs only three pennies a day. Black cumin has become a staple in my family’s daily diet. I keep a pepper mill filled with it right on the kitchen table and grind it onto foods just as I would black pepper—easy and delicious.

Is Kombucha Tea Good for You? is one of my first videos. It was featured in a blog entry entitled “NutritionFacts.org: the first month,” where I marveled the video had reached nearly 100,000 people. You can see it below and at 0:20 in my video Kombucha’s Side Effects: Is It Bad for You?. I’m honored to say that we now reach more than 100,000 people a day.

In that first kombucha video, I profiled a report published in the Journal of Intensive Care Medicine of “a case of kombucha tea toxicity” in which a young man ended up in an acidotic coma. The authors concluded, “While Kombucha tea is considered a healthy elixir, the limited evidence currently available raises considerable concern that it may pose serious health risks. Consumption of this tea should be discouraged, as it may be associated with life-threatening lactic acidosis.” And this was just one of several case reports of “serious, and sometimes fatal, hepatic [liver] dysfunction and lactic acidosis within close proximity of ingestion.”

For example, there were two cases in Iowa of severe metabolic acidosis, including one death. There was also a triggering of a life-threatening autoimmune muscle disease that required emergency surgery and was “probably related to the consumption of a fermented Kombucha beverage.” Another patient presented with shortness of breath, shaking, and a movement disorder “after consumption of tea and no other medications,” and a middle-aged woman complained of xerostomia, dizziness, nausea, vomiting, headache, and neck pain,” and her symptoms recurred on reingestion of the tea. There was another case of severe metabolic lactic acidosis, as well as a case of hepatotoxicity (liver toxicity) that resolved after stopping kombucha.

Why these sporadic cases? Maybe some unusual toxins developed in a particular batch. I mean, it is a fermented product, so it’s possible there was just some contamination by a bad bug, like the time people smeared kombucha on their skin because they were told it had “magical healing power.” What it had instead was anthrax. So, even though such reports were rare, I concluded ten years ago that we should probably stick to foods that haven’t put people in a coma. But what about its risks versus benefits? Maybe kombucha is worth it. After all, it’s “reputed to cure cancer,” “eliminate wrinkles,” “and even restore gray hair to its original color”—as “marketed by alternative and naturopathic healers throughout the United States.”

“Currently, kombucha is alternately praised as ‘the ultimate health drink’ or damned as ‘unsafe medicinal tea.’” It’s been “claimed to be a universal wonderful drug…a potion which improves awareness and concentration, slimming, also purifying, regenerating and life extending.” Which is it? Is it “potion or poison?

Back in the 1920s, 1930s, and 1940s, there were several medical studies conducted by recognized physicians confirming all sorts of beneficial effects, as you can see below and at 2:55 in my video. 

I couldn’t wait to read them. Dufrense and Farnworth were cited, and when I went to that paper, I saw the same claim, citing Allen 1998. When I went to that source, I saw the citation is for a random kombucha website, as shown below, and at 3:10 in my video. And guess what? That website’s been defunct since 2001, and “much of the Kombucha information” posted came from comments on some mailing list.

Finally, in 2003, a systematic review of the clinical evidence that had been published was conducted. “The main result of this systematic review, it seems, is the total lack of efficacy data…No clinical studies were found relating to the efficacy of this remedy.” We just have these cautionary tales, these case reports. So, based on these data, it was concluded that the largely undetermined benefits do not outweigh the documented risks of kombucha. It can therefore not be recommended for therapeutic use.” That was back in 2003, though. How about a 2019 systematic review of the empirical evidence of human health benefit?

“The nonhuman subjects literature claims numerous health benefits of kombucha,” with “nonhuman” meaning mice and rats. We need human clinical trials, yet there is still not a single controlled human study. (I did find one uncontrolled study purporting to show a significant reduction in fasting and after-meal blood sugars among individuals with type 2 diabetes, though, as seen below and at 4:19 in my video.)

“Nonetheless,” despite no controlled trials, “significant commercial shelf space is now dedicated to kombucha products, and there is widespread belief that the products promote health.” So, we are left with this extreme disparity between science and belief: “There is no convincingly positive clinical evidence at all; the [health] claims for it are as far-reaching as they are implausible; the potential for harm seems considerable. In such extreme cases, healthcare professionals should discourage consumers from using (and paying for) remedies that only seem to benefit those who sell them.”

Doctor’s Note:

Friday Favorites: What Are the Best Beverages? Watch the video to find out. 

“Autoimmune thyroiditis, also known as Hashimoto’s thyroiditis, is an organ-specific autoimmune disorder,” where our body attacks our own thyroid gland, often leading to hypothyroidism due to destruction and scarring of the gland itself. We know there’s a genetic component, since identical twins are more likely to share the disease than fraternal twins. “However, even with identical twins, the concordance rate was only about 50%, emphasizing that important factors such as the environment play a role in disease pathogenesis.” Indeed, even if your identical twin, who has basically your exact same DNA, has the disease, there’s only like a flip of a coin’s chance you’ll get it. Genes load the gun, but the environment may pull the trigger.

More than 90 synthetic chemicals were noted to show disruption of hormonal balance or thyroid dysfunction.” However, only a few such ‘pollutants show evidence that they contribute to autoimmune thyroid disease.” These include polyaromatic hydrocarbons. Smokers get a lot of them from cigarettes, but in nonsmokers, exposure comes almost entirely from food, as you can see below and at 1:18 in my video Diet for Hypothyroidism: A Natural Treatment for Hashimoto’s Disease. 

Polycyclic aromatic hydrocarbons are primarily formed when muscle meats, such as beef, pork, fish, or chicken, are cooked using high-temperature methods, such as grilling. PBBs, polybrominated biphenols, are a type of flame-retardant chemical no longer manufactured in the United States, but are still found in the aquatic food chain. PCBs, polychlorinated biphenols, are used in a number of industrial processes and end up in people’s bodies, again, largely through the consumption of fish, but also eggs and other meats, as seen here and at 1:41 in my video.

So, one might suspect those eating plant-based diets would have lower rates of hypothyroidism, and, indeed, despite their lower iodine intake, vegan diets tended to be protective. But they’ve never been put to the test in an interventional trial. A modification of the Paleolithic diet has been tried in Hashimoto’s patients, but it didn’t appear to improve thyroid function. What did, though, is Nigella Sativa. That name should sound familiar to anyone who’s read my book How Not to Diet or watched my live Evidence-Based Weight Loss presentation. Nigella Sativa is the scientific name for black cumin, which is just a simple spice that’s also used for a variety of medicinal purposes.

In one study, Hashimoto’s patients received a half teaspoon of powdered black cumin every day for eight weeks in a randomized, double-blind, placebo-controlled trial. Not only was there a significant reduction in body weight, which is why I profiled it in my book, but the black cumin also significantly reduced the thyroid-stimulating hormone, a sign that thyroid function was improving. It even lowered the level of autoimmune anti-thyroid antibodies, as well as increased blood levels of thyroid hormone T3 in these Hashimoto’s patients. In addition, there was a significant drop in Interleukin 23, a proinflammatory cell signal thought to help promote the autoimmune inflammation of the thyroid, which “further confirms the anti-inflammatory nature of the plant.” And what were the side effects? There was a 17 percent drop in “bad” LDL cholesterol, as shown below and at 3:19 in my video.

Given the fact that patients with Hashimoto’s may be at particularly high risk of developing heart disease, this is exactly the kind of side effects we’d want. “Considering these health-promoting effects of N. Sativa [black cumin], it can be considered as a therapeutic approach in the management of Hashimoto-related metabolic abnormalities.”

A similar trial failed to find a benefit, though. Same dose, same time frame, but no significant changes in thyroid function. In contrast with the previous study, though, the study participants were not all Hashimoto’s patients, but rather hypothyroid for any reason, and that may have diluted the results. And it’s possible that telling patients to take the black cumin doses with their thyroid hormone replacement therapy may have interfered with its absorption, which is an issue similar to other foods and drugs, and why patients are normally told to take it on an empty stomach. Since there are no downsides—it’s just a simple spice—I figure, why not give it a try? The worst that can happen is you’ll have tastier food.

Doctor’s Note:

I get a lot of questions about thyroid function, and I am glad to have been able to do this series. If you missed any of the other videos, see the related posts below.

For more on black cumin, see my book How Not to Diet and my presentation Evidence-Based Weight Loss. 

Several autoimmune diseases affect the thyroid gland, and Graves’ disease and Hashimoto’s thyroiditis are the most common. Graves’ disease results in hyperthyroidism, an overactive thyroid gland. Though slaughter plants are supposed to remove animals’ thyroid glands as they “shall not be used for human food,” should some neck meat slip in, you can suffer a similar syndrome called Hamburger thyrotoxicosis. That isn’t from your body making too much thyroid hormone, though. Rather, it’s from your body eating too much thyroid hormone. Graves’ disease is much more common, and meat-free diets may be able to help with both diseases, as plant-based diets may be associated with a low prevalence of autoimmune disease in general, as observed, for example, in rural sub-Saharan Africa. Maybe it’s because plants are packed with “high amounts of antioxidants, possible protective factors against autoimmune disease,” or because they’re packed with anti-inflammatory compounds. After all, “consuming whole, plant-based foods is synonymous with an anti-inflammatory diet.” But you don’t know until you put it to the test.

It turns out that the “exclusion of all animal foods was associated with half the prevalence of hyperthyroidism compared with omnivorous diets. Lacto-ovo [dairy-and-egg] and pesco [fish] vegetarian diets were associated with intermediate protection.” But, for those eating strictly plant-based, there is a 52 percent lower odds of hyperthyroidism.

As I discuss in my video The Best Diet for Hypothyroidism and Hyperthyroidism, this apparent protection “may be due to the exclusion of animal foods, the [beneficial] effects of plant foods, or both. Animal foods like meat, eggs, and dairy products may contain high oestrogen concentrations, which have been linked to autoimmunity in cell and animal studies.” Or it could be because the decrease in animal protein by excluding animal foods may downregulate IGF-1, which is not just a cancer-promoting growth hormone, but may play a role in autoimmune diseases. The protection could also come from the goodness in plants that may “protect cells against autoimmune processes,” like the polyphenol phytochemicals, such as flavonoids found in plant foods. Maybe it’s because environmental toxins build up in the food chain. For example, fish contaminated with industrial pollutants, like PCBs, are associated with an increased frequency of thyroid disorders.

But what about the other autoimmune thyroid disease, Hashimoto’s thyroiditis, which, assuming you’re getting enough iodine, is the primary cause of hypothyroidism, an underactive thyroid gland? Graves’ disease wasn’t the only autoimmune disorder that was rare or virtually unknown among those living in rural sub-Saharan Africa, eating near-vegan diets. They also appeared to have less Hashimoto’s.

There is evidence that those with Hashimoto’s have compromised antioxidant status, but we don’t know if it’s cause or effect. But if you look at the dietary factors associated with blood levels of autoimmune anti-thyroid antibodies, animal fats seem to be associated with higher levels, whereas vegetables and other plant foods are associated with lower levels. So, again, anti-inflammatory diets may be useful. It’s no surprise, as Hashimoto’s is an inflammatory disease—that’s what thyroiditis means: inflammation of the thyroid gland.

Another possibility is the reduction in intake of methionine, an amino acid concentrated in animal protein, thought to be one reason why “regular consumption of whole-food vegan diets is likely to have a favourable influence on longevity through decreasing the risk of cancer, coronary [heart] disease, and diabetes.” Methionine restriction improves thyroid function in mice, but it has yet to be put to the test for Hashimoto’s in humans.

If you compare the poop of patients with Hashimoto’s to controls, the condition appears to be related to a clear reduction in the concentration of Prevotella species. Prevotella are good fiber-eating bugs known to enhance anti-inflammatory activities. Decreased Prevotella levels are also something you see in other autoimmune conditions, such as multiple sclerosis and type 1 diabetes. How do you get more Prevotella? Eat more plants. If a vegetarian goes on a diet of meat, eggs, and dairy, within as few as four days, their levels can drop. So, one would expect those eating plant-based diets to have less Hashimoto’s, but in a previous video, I expressed concern about insufficient iodine intake, which could also lead to hypothyroidism. So, which is it? Let’s find out.

“In conclusion, a vegan diet tended to be associated with lower, not higher, risk of hypothyroid disease.” Why “tended”? The associated protection against hypothyroidism incidence and prevalence studies did not reach statistical significance. It wasn’t just because they were slimmer either. The lower risk existed even after controlling for body weight. So, researchers think it might be because animal products may induce inflammation. The question I have is: If someone who already has Hashimoto’s, what happens if they change their diet? That’s exactly what I’ll explore next.

This is the third in a four-video series on thyroid function. The first two were Are Vegans at Risk for Iodine Deficiency? and Friday Favorites: The Healthiest Natural Source of Iodine.

Stay tuned for the final video: Diet for Hypothyroidism: A Natural Treatment for Hashimoto’s Disease. 

In a 1932 article in Popular Mechanics entitled “Fifty Years Hence,” Winston Churchill predicted that we would one day “escape the absurdity of growing a whole chicken in order to eat the breast or wing, by growing these parts separately under a suitable medium.” Indeed, growing meat straight from muscle cells could reduce greenhouse gas emissions by as much as 96 percent, lower water usage by as much as 96 percent, and lower land usage by 99 percent.

If we are to avoid dangerous climate change by the middle of the century, global meat consumption simply cannot continue to rise at the current rate. And there have certainly been initiatives like Meatless Mondays to try to get people to cut down, but so far, “they do not appear to be contributing in any significant way to the translation of the idea of eating less meat into the mainstream.” So, “in the light of people’s continued desire to eat meat, it seems the problems associated with consumption are unlikely to be fully resolved by attitude change. Instead, they must be addressed from an alternate perspective: changing the product.”

From an environmental standpoint, it seems like a slam dunk. From an animal welfare standpoint, it could get rid of factory farms and slaughter plants for good, and I wouldn’t have to stumble across articles like this in the scientific literature: “Discerning Pig Screams in Production Environments.” I mean, what more do we need to know about modern animal agriculture than the fact that, “in recent years, a number of so-called…‘ag-gag’ laws have been proposed and passed…across the USA,” banning undercover photographing or videotaping inside such operations to keep us all in the dark.

What about the human health implications of cultivated meat? I get the animal welfare, environment, and food security benefits, but what about “the potential for cultured meat to have health/safety benefits to individual consumers”? Nutritionally, the most important advantage is being able to swap out the type the fat. Right now, producers are growing straight muscle tissue, so it could be marbled with something less harmful than animal fat, though, of course, there’s still animal protein.

When it comes to health, the biggest, clearest advantage is food safety, reducing the risk of foodborne pathogens. There has been a sixfold increase in food poisoning over the last few decades, with tens of millions “sickened annually by infected food in the United States alone,” including hundreds of thousands of hospitalizations and thousands of annual deaths. Contaminated meats and other animal products are the most common cause.

When the cultivated meat industry calls its products clean meat, that’s not just a nod to clean energy. Food-poisoning pathogens like E. coli, Campylobacter, and Salmonella are fecal bacteria. They are a result of fecal contamination. They’re intestinal bugs, so we don’t have to worry about them if we’re making meat without the intestines.

Yes, there are all sorts of “methods to remove visible fecal contamination” in slaughter plants these days and even experimental imaging technologies designed to detect more “diluted fecal contaminations,” but we are still left at the retail level with about 10 percent of chicken contaminated with Salmonella and 40 percent of retail chicken contaminated with Campylobacter. What’s more, most poultry and about half of retail ground beef and pork chops are contaminated with E. coli, an indicator of fecal residue, as shown here and at 3:47 in my video The Human Health Effects of Cultivated Meat: Food Safety. We don’t have to cook the crap out of cultivated meat, though, because there isn’t any crap to begin with.

Doctor’s Note:

This is the first in a three-video series on cultivated meat. Stay tuned for The Human Health Effects of Cultivated Meat: Antibiotic Resistance and The Human Health Effects of Cultivated Meat: Chemical Safety.

I previously did a video series on plant-based meats. Check them in the related posts below.

The videos are also all available in a digital download from a webinar I did: The Human Health Implications of Plant-Based and Cultivated Meat for Pandemic Prevention and Climate Mitigation.

“There is now overwhelming evidence to support reducing LDL-C (low-density lipoprotein cholesterol)”—so-called bad cholesterol—to reduce atherosclerotic cardiovascular disease (CVD),” the number one killer of men and women. So, why is adherence to cholesterol-lowering statin drug therapy such “a major challenge worldwide”? Researchers found “that the majority of studies reported that at least 40%, and as much as 80%, of patients did not comply fully with statin treatment recommendations.” Three-quarters of patients may flat out stop taking them, and almost 90 percent may discontinue treatment altogether.

When asked why they stopped taking the pills, most “former statin users or discontinuers…cited muscle pain, a side effect, as the primary reason…” “SAMSs”—statin-associated muscle symptoms—“are by far the most prevalent and important adverse event, with up to 72% of all statin adverse events being muscle-related.” Taking coenzyme Q10 supplements as a treatment for statin-associated muscle symptoms was a good idea in theory, but they don’t appear to help. Normally, side-effect symptoms go away when you stop the drug but can sometimes linger for a year or more. There is “growing evidence that statin intolerance is predominantly psychosocial, not pharmacological.” Really? It may be mostly just in people’s heads?

“Statins have developed a bad reputation with the public, a phenomenon driven largely by proliferation on the Internet of bizarre and unscientific but seemingly persuasive criticism of these drugs.” “Does Googling lead to statin intolerance?” But people have stopped taking statins for decades before there even was an Internet. What kinds of data have doctors suggested that patients are falsely “misattribut[ing] normal aches and pains to be statin side effects”?

Well, if you take people who claim to have statin-related muscle pain and randomize them back and forth between statins and an identical-looking placebo in three-week blocks, they can’t tell whether they’re getting the real drug or the sugar pill. The problem with that study, though, is that it may take months not only to develop statin-induced muscle pain, but months before it goes away, so no wonder three weeks on and three weeks off may not be long enough for the participants to discern which is which.

However, these data are more convincing: Ten thousand people were randomized to a statin or a sugar pill for a few years, but so many more people were dying in the sugar pill group that the study had to be stopped prematurely. So then everyone was offered the statin, and the researchers noted that there was “no excess of reports of muscle-related AEs” (adverse effects) among patients assigned to the statin over those assigned to the placebo. But when the placebo phase was over and the people knew they were on a statin, they went on to report more muscle side effects than those who knew they weren’t taking the statin. “These analyses illustrate the so-called nocebo effect,” which is akin to the opposite of the placebo effect.

Placebo effects are positive consequences falsely attributed to a treatment, whereas nocebo effects are negative consequences falsely attributed to a treatment, as was evidently seen here. There was an excess rate of muscle-related adverse effects reported only when patients and their doctors were aware that statin therapy was being used, and not when its use was concealed. The researchers hope “these results will help assure both physicians and patients that most AEs associated with statins are not causally related to use of the drug and should help counter…exaggerated claims about statin-related side effects.”

These are the kinds of results from “placebo-controlled randomised trials [that] have shown definitively that almost all of the symptomatic adverse events that are attributed to statin therapy in routine practice are not actually caused by it (ie, they represent misattribution.)” Now, “only a few patients will believe that their SAMS are of psychogenic origin” and just in their head, but their denial may have “deadly consequences.” Indeed, “discontinuing statin treatment may be a life-threatening mistake.”

Below and at 4:46 in my video How Common Are Muscle Side Effects from Statins?, you can see the mortality of those who stopped their statins after having a possible adverse reaction compared to those who stuck with them. This translates into about “1 excess death for every 83 patients who discontinued treatment” within a four-year period. So, when there are media reports about statin side effects and people stop taking them, this could “result in thousands of fatal and disabling heart attacks and strokes, which would otherwise have been avoided. Seldom in the history of modern therapeutics have the substantial proven benefits of a treatment been compromised to such an extent by serious misrepresentations of the evidence for its safety.” But is it a misrepresentation to suggest “that statin therapy causes side-effects in up to one fifth of patients”? That is what is seen in clinical practice; between 10 to 25 percent of patients placed on statins complain of muscle problems. However, because we don’t see anywhere near those kinds of numbers in controlled trials, patients are accused of being confused. Why is the incidence of side effects from statins so low in clinical trials while appearing to be so high in the real world? 

Take this meta-analysis of clinical trials, for example: It found muscle problems not in 1 in 5 patients, but only 1 in 2,000. Should everyone over a certain age be on statins? Not surprisingly, every one of those trials was funded by statin manufacturers themselves. So, for example, “how could the statin RCTs [randomized controlled trials] miss detecting mild statin-related muscle adverse side effects such as myalgia [muscle pain]? By not asking. A review of 44 statin RCTs reveals that only 1 directly asked about muscle-related adverse effects.” So, are the vast majority of side effects just being missed in all these trials, or are the vast majority of side effects seen in clinical practice just a figment of patients’ imagination? The bottom line is we don’t know, but there is certainly an urgent need to figure it out.

Important to our understanding and the prevention of the global increase of inflammatory bowel disease (IBD), we know that “dietary fiber reduces risk, whereas dietary fat, animal protein, and sugar increase it.” “Despite the recognition of westernization of lifestyle as a major driver of the growing incidence of IBD, no countermeasures against such lifestyle changes have been recommended, except that patients with Crohn’s disease should not smoke.”

We know that “consuming whole, plant-based foods is synonymous with an anti-inflammatory diet.” Lists of foods with inflammatory effects and anti-inflammatory effects are shown here and at 0:50 in my video, The Best Diet for Crohn’s Disease.