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Tag: Dairy

  • The Link Between Milk and Parkinson’s Disease | NutritionFacts.org

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    Is the brain damage associated with milk consumption due to the banned pesticide heptachlor or the milk sugar galactose?

    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.

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    Michael Greger M.D. FACLM

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  • Could Your Pills and Food Be Causing a Leaky Gut? | NutritionFacts.org

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    Common drugs, foods, and beverages can disrupt the integrity of our intestinal barrier, causing 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).

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    Michael Greger M.D. FACLM

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  • Keeping Better Score of Your Diet | NutritionFacts.org

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    How can you get a perfect diet score?

    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?.

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    Michael Greger M.D. FACLM

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  • How to Beat Heart Disease Before It Starts | NutritionFacts.org

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    Why might healthy lifestyle choices wipe out 90% of our risk for having a heart attack, while drugs may only reduce risk by 20% to 30%?

    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.

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    Michael Greger M.D. FACLM

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  • Can Vegan Fecal Transplants Lower TMAO Levels? | NutritionFacts.org

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    If the microbiome of those eating plant-based diets protects against the toxic effects of TMAO, what about swapping gut flora?

    “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.

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    Michael Greger M.D. FACLM

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  • Fasting and Plant-Based Diets for Migraines and Traumatic Brain Injuries  | NutritionFacts.org

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    What effects do fasting and a plant-based diet have on TBI and migraines?

    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.  

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    Michael Greger M.D. FACLM

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  • Should We Fast for IBS? | NutritionFacts.org

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    More than half of irritable bowel syndrome (IBS) sufferers appear to have a form of atypical food allergy.

    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. 

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    Michael Greger M.D. FACLM

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  • Might Meat Trigger Parkinson’s Disease?  | NutritionFacts.org

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    What does the gut have to do with developing Parkinson’s disease?

    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.

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    Michael Greger M.D. FACLM

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  • My “Maple Crinkle Cake” Is the Dessert That Will Disappear Fast (Everyone Eats Two Slices)

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    You’ve never tried anything like it.
    READ MORE…

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    Patty Catalano

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  • The No-Bake Pumpkin Dessert You Should Make for Every Fall Gathering (I Dream About It All Year!)

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    Kelli FosterCulinary Producer

    I’m a recipe developer, food writer, stylist, and video producer (and The Kitchn’s Dinner Therapist), with more than 10 years professional experience. Since graduating from The French Culinary Institute, I’ve authored 3 cookbooks: Buddha Bowls, Plant-Based Buddha Bowls, and The Probiotic Kitchen.

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    Kelli Foster

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  • Fiber or Low FODMAP for SIBO?  | NutritionFacts.org

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    It may not be the number of bacteria growing in our small intestine, but the type of bacteria, which can be corrected with diet.

    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. 

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    Michael Greger M.D. FACLM

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  • Raw milk debates are turning sour in Florida

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    In the fall of 2024, I predicted that America might be on the brink of having its “raw milk moment” given now Secretary of Health and Human Services Robert F. Kennedy Jr.’s political elevation. Since then, hardly a week has passed without unpasteurized milk making headlines across the country. A recent bacterial outbreak in Florida has now heightened the controversy and further solidified raw milk’s central role in America’s broiling culture wars.

    The Florida Department of Health (DOH) issued a press release in early August detailing a campylobacter and E. coli outbreak in the Sunshine State. Officials alerted that “there have been 21 cases since January 24, 2025, including six children under the age of 10, and seven hospitalizations linked to consumption of raw milk.” The DOH explicitly identified Keely Farms Dairy, a small family farm, as the source of the outbreak.

    Weeks later, a Florida woman, represented by a self-described “national food poisoning law firm,” filed suit against Keely Farms, alleging that its raw milk caused her two-year-old son to contract a bacterial infection and fall ill. The woman further alleges that she fell ill herself and developed sepsis, which eventually led to the loss of her pregnancy.

    The details from the lawsuit are heartbreaking, but the more we learn about the situation surrounding Keely Farms, the more bizarre the story becomes. Despite DOH’s definitive declaration that Keely Farms was the source of the bacterial outbreak, it was later found that the agency had reached this conclusion despite not conducting a single test at the farm, nor alerting the farm that it was under investigation. In a Facebook post, Keely Farms said that the department’s press release “blindsided” them. (The DOH’s press release stated that it would “continue working with Keely Farms Dairy,” insinuating that the relevant parties had been working together throughout.)

    Confusing things further, Keely Farms was recently inspected by the Florida Department of Agriculture. “We passed, as always,” Keely Farms posted.

    Selling raw milk for human consumption is illegal in Florida. As a result, milk that has not been pasteurized—the process of heating the liquid to a specific temperature for five to 30 seconds to kill harmful bacteria—can only be sold for livestock feed. Keely Farms’ raw milk was appropriately labeled as “not for human consumption,” meaning that the 21 Floridians who allegedly drank the farm’s milk (and those who also gave it to their children) chose to do so despite this warning.

    It’s unclear how the current litigation involving Keely Farms will ultimately play out, although it’s likely that more follow-on suits will be filed, using the DOH’s press release as evidentiary fodder. 

    Politico recently noted that raw milk has gone from “the darling of the organic liberals, deserving of sympathetic coverage…to the conservative culture war signal that is a sweetheart of deep-red state legislatures.” This is on display in Florida. Despite the DOH targeting Keely Farms for its raw milk, Florida’s Surgeon General Joseph A. Ladapo—an appointee of Republican Gov. Ron DeSantis and the head of the DOH—recently expressed support for human consumption of raw milk in a social media post. 

    On the other hand, Florida’s agriculture commissioner, who was endorsed by President Donald Trump, has encouraged Floridians to only drink pasteurized milk, citing the dangers of raw milk. This means that the head of the Florida agency that targeted Keely Farms’ raw milk products is unexpectedly pro-raw milk, while the head of the state agency that inspected and greenlighted Keely Farms’ operations is against raw milk.

    This confusion highlights how raw milk has become a political flashpoint. The state health agency blamed Keely Farms while skipping basic investigative steps, the agriculture department cleared the farm, and their leaders publicly contradicted their own agencies.

    When policy decisions are filtered through the lens of culture wars, the result is not clarity or safety but a muddle of mixed signals. Floridians are left unsure whether raw milk is a health risk, a personal freedom, or just another pawn in America’s endless red vs. blue standoff.

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    C. Jarrett Dieterle

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  • Hijacking Our Appetites  | NutritionFacts.org

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    I debunk the myth of protein as the most satiating macronutrient.

    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.

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    Michael Greger M.D. FACLM

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  • Are Carboxymethylcellulose, Polysorbate 80, and Other Emulsifiers Safe?  | NutritionFacts.org

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    Emulsifiers are the most widely used food additives. What are they doing to our gut microbiome?

    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.

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    Michael Greger M.D. FACLM

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  • Eating to Downregulate a Gene for Metastatic Cancer  | NutritionFacts.org

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    Women with breast cancer should include the “liberal culinary use of cruciferous vegetables.”

    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.

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    Michael Greger M.D. FACLM

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  • Eating to Help Control Cancer Metastasis  | NutritionFacts.org

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    Randomized controlled trials show that lowering saturated fat intake can lead to improved breast cancer survival.

    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.

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    Michael Greger M.D. FACLM

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  • Dietary Components That May Cause Cancer to Metastasize  | NutritionFacts.org

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    Palmitic acid, a saturated fat concentrated in meat and dairy, can boost the metastatic potential of cancer cells through the fat receptor CD36.

    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.

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    Michael Greger M.D. FACLM

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  • Eating with Hypothyroidism and Hyperthyroidism  | NutritionFacts.org

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    Is the apparent protection of plant-based diets for thyroid health due to the exclusion of animal foods, the benefits of plant foods, or both?

    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. 

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    Michael Greger M.D. FACLM

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  • A Healthy, Natural Source of Iodine?  | NutritionFacts.org

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    How much nori, dulse, or arame approximates the recommended daily allowance for iodine?

    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.

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    Michael Greger M.D. FACLM

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  • Vegans and Iodine Deficiency Risk  | NutritionFacts.org

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    Most plant-based milks are not fortified with iodine.

    “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: 

    For more on iodine, see the related posts below.

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    Michael Greger M.D. FACLM

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