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Tag: saturated fat

  • 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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  • 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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  • 3-MCPD in Refined Cooking Oils | NutritionFacts.org

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    There is another reason to avoid palm oil and question the authenticity of extra-virgin olive oil.

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

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

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

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

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

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

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

    Doctor’s Note

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

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

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    Michael Greger M.D. FACLM

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  • Boosting BDNF Levels in Our Brain to Treat Depression  | NutritionFacts.org

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    We can raise BDNF levels in our brain by fasting and exercising, as well as by eating and avoiding certain foods.

    There is accumulating evidence that brain-derived neurotrophic factor (BDNF) may be playing a role in human depression. BDNF controls the growth of new nerve cells. “So, low levels of this peptide could lead to an atrophy of specific brain areas such as the amygdala and the hippocampus, as it has been observed among depressed patients.” That may be one of the reasons that exercise is so good for our brains. Start an hour-a-day exercise regimen, and, within three months, there can be a quadrupling of BDNF release from our brain, as seen below and at 0:35 in my video How to Boost Brain BDNF Levels for Depression Treatment.

    This makes sense. Any time we were desperate to catch prey (or desperate not to become prey ourselves), we needed to be cognitively sharp. So, when we’re fasting, exercising, or in a negative calorie balance, our brain starts churning out BDNF to make sure we’re firing on all cylinders. Of course, Big Pharma is eager to create drugs to mimic this effect, but is there any way to boost BDNF naturally? Yes, I just said it: fasting and exercising. Is there anything we can add to our diet to boost BDNF?

    Higher intakes of dietary flavonoids appear to be protectively associated with symptoms of depression. The Harvard Nurses’ Health Study followed tens of thousands of women for years and found that those who were consuming the most flavonoids appeared to reduce their risk of becoming depressed. Flavonoids occur naturally in plants, so there’s a substantial amount in a variety of healthy foods. But how do we know the benefits are from the flavonoids and not just from eating more healthfully in general? We put it to the test.

    Some fruits and vegetables have more flavonoids than others. As shown below and at 1:51 in my video, apples have more than apricots, plums more than peaches, red cabbage more than white, and kale more than cucumbers. Researchers randomized people into one of three groups: more high-flavonoid fruits and vegetables, more low-flavonoid fruits and vegetables, or no extra fruits and vegetables at all. After 18 weeks, only the high-flavonoid group got a significant boost in BDNF levels, which corresponded with an improvement in cognitive performance. The BDNF boost may help explain why each additional daily serving of fruits or vegetables is associated with a 3 percent decrease in the risk of depression. 

    What’s more, as seen here and at 2:27 in my video, a teaspoon a day of the spice turmeric may boost BNDF levels by more than 50 percent within a month. This is consistent with the other randomized controlled trials that have so far been done. 

    Nuts may help, too. In the PREDIMED study, where people were randomized to receive weekly batches of nuts or extra-virgin olive oil, the nut group lowered their risk of having low BDNF levels by 78 percent, as shown below and at 2:46.

    And BDNF is not implicated only in depression, but schizophrenia. When individuals with schizophrenia underwent a 12-week exercise program, they got a significant boost in their BDNF levels, which led the researchers to “suggest that exercise-induced modulation of BDNF may play an important role in developing non-pharmacological treatment for chronic schizophrenic patients.”

    What about schizophrenia symptoms? Thirty individuals with schizophrenia were randomized to ramp up to 40 minutes of aerobic exercise three times a week or not, and there did appear to be an improvement in psychiatric symptoms, such as hallucinations, as well as an increase in their quality of life, with exercise. In fact, researchers could actually visualize what happened in their brains. Loss of brain volume in a certain region appears to be a feature of schizophrenia, but 30 minutes of exercise, three times a week, resulted in an increase of up to 20 percent in the size of that region within three months, as seen here and at 3:46 in my video. 

    Caloric restriction may also increase BDNF levels in people with schizophrenia. So, researchers didn’t just have study participants eat less, but more healthfully, too—less saturated fat and sugar, and more fruits and veggies. The study was like the Soviet fasting trials for schizophrenia that reported truly unbelievable results, supposedly restoring people to function, and described fasting as “an unparalleled achievement in the treatment of schizophrenia”—but part of the problem is that the diagnostic system the Soviets used is completely different than ours, making any results hard to interpret. There was a subgroup that seemed to correspond to the Western definition, but they still reported 40 to 60 percent improvement rates from fasting, but fasting wasn’t all they did. After the participants fasted for up to a month, they were put on a meat- and egg-free diet. So, when the researchers reported these remarkable effects even years later, they were for those individuals who stuck with the meat- and egg-free diet. Evidently, the closer the diet was followed, the better the effect, and those who broke the diet relapsed. The researchers noted: “Not all patients can remain vegetarian, but they must not take meat for at least six months, and then in very small portions.” We know from randomized controlled trials that simply eschewing meat and eggs can improve mental states within just two weeks, so it’s hard to know what role fasting itself played in the reported improvements.

    A single high-fat meal can drop BDNF levels within hours of consumption, and we can prove it’s the fat itself by seeing the same result after injecting fat straight into our veins. Perhaps that helps explain why increased consumption of saturated fats in a high-fat diet may contribute to brain dysfunction—that is, neurodegenerative diseases, long-term memory loss, and cognitive impairment. It may also help explain why the standard American diet has been linked to a higher risk of depression, as dietary factors modulate the levels of brain-derived neurotrophic factor.

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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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  • What About Saturated Fat and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    What About Saturated Fat and Vegetarians’ Stroke Risk?  | NutritionFacts.org

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    How can we explain the drop in stroke risk as the Japanese diet became westernized with more meat and dairy?

    As Japan westernized, the country’s stroke rate plummeted, as you can see in the graph below and at 0:15 in my video Vegetarians and Stroke Risk Factors: Saturated Fat?. 

    Stroke had been a leading cause of death in Japan, but the mortality rate decreased sharply as they moved away from their traditional diets and started eating more like those in the West. Did the consumption of all that extra meat and dairy have a protective effect? After all, their intake of animal fat and animal protein was going up at the same time their stroke rates were going down, as shown below and at 0:35 in my video. 

    Commented a noted Loma Linda cardiology professor, “Protection from stroke by eating animal foods? Surely not!…Many vegetarians, like myself, have almost come to expect the data to indicate that they have an advantage, whatever the disease that is being considered. Thus, it is disquieting to find evidence in a quite different direction for at least one subtype of stroke.” 

    Can dietary saturated fat, like that found in meat and dairy, be beneficial in preventing stroke risk? There appeared to be a protective association—but only in East Asian populations, as you can see below and at 1:11 in my video. 

    High dietary saturated fat was found to be associated with a lower risk of stroke in Japanese but not in non-Japanese. So, what was it about the traditional Japanese diet that the westernization of their eating habits made things better when it came to stroke risk? Well, at the same time, their meat and dairy intake was going up, and their salt intake was going down, as you can see below and at 1:40. 

    The traditional Japanese diet was packed with salt. They had some of the highest salt intakes in the world, about a dozen spoonsful of salt a day. Before refrigeration became widely available, they ate all sorts of salted, pickled, and fermented foods from soy sauce to salted fish. In the areas with twice the salt intake, they had twice the stroke mortality, but when the salt intake dropped, so did the stroke death rates, because when the salt consumption went down, their blood pressure went down, too. High blood pressure is perhaps “the single most important potentially modifiable risk factor for stroke,” so it’s no big mystery why the westernization of the Japanese diet led to a drop in stroke risk.  

    When they abandoned their more traditional diets, their obesity rates went up and so did their diabetes and coronary artery disease, but, as they gave up the insanely high salt intake, their insanely high stroke rates correspondingly fell. 

    Stomach cancer is closely associated with excess salt intake. When you look at their stomach cancer rates, they came down beautifully as they westernized their diets away from salt-preserved foods, as you can see in the graph below and at 2:50 in my video. 

    But, of course, as they started eating more animal foods like dairy, their rates of fatal prostate cancer, for example, shot through the roof. Compared to Japan, the United States has 7 times more deaths from prostate cancer, 5 times more deadly breast cancer, 3 times more colon cancer and lymphoma mortality, and 6 to 12 times the death rate from heart disease, as you can see in the graph below and at 3:15 in my video. Yes, Japanese stroke and stomach cancer rates were higher, but they were also eating up to a quarter cup of salt a day. 

    That would seem to be the most likely explanation, rather than some protective role of animal fat. And, indeed, it was eventually acknowledged in the official Japanese guidelines for the prevention of cardiovascular disease: “Refrain from the consumption of large amounts of fatty meat, animal fat, eggs, and processed foods…”

    Now, one of the Harvard cohorts found a protective association between hemorrhagic strokes and both saturated fat and trans fat, prompting a “sigh of relief…heard throughout the cattle-producing Midwestern states,” even though the researchers concluded that, of course, we all have to cut down on animal fat and trans fat for the heart disease benefit. Looking at another major Harvard cohort, however, they found no such protective association for any kind of stroke, and when they put all the studies together, zero protection was found across the board, as you can see below and at 4:07 in my video. 

    Observational studies have found that higher LDL cholesterol seems to be associated with a lower risk of hemorrhagic stroke, raising the possibility that cholesterol may be “a double-edged sword,” by decreasing the risk of ischemic stroke but increasing the risk of hemorrhagic stroke. But low cholesterol levels in the aged “may be a surrogate for nutritional deficiencies…or a sign of debilitating diseases,” or perhaps the individuals were on a combination of cholesterol-lowering drugs and blood thinners, and that’s why we tend to see more brain bleeds in those with low cholesterol. You don’t know until you put it to the test.

    Researchers put together about two dozen randomized controlled trials and found that the lower your cholesterol, the better when it comes to overall stroke risk, with “no significant increase in hemorrhagic stroke risk with lower achieved low-density lipoprotein [LDL] cholesterol levels.”

    The genetic data appear mixed, with some suggesting a lifetime of elevated LDL would give you a higher hemorrhagic stroke risk, while other data suggest more of that double-edged sword effect. However, with lower cholesterol, “any possible excess of hemorrhagic [bleeding] stroke is greatly outweighed by the protective effect against ischaemic stroke,” the much more common clotting type of stroke, not to mention heart disease. It may be on the order of 18 fewer clotting strokes for every 1 extra bleeding stroke with cholesterol-lowering. 

    Does this explain the increased stroke risk found among vegetarians? Hemorrhagic stroke is the type of stroke that appeared higher in vegetarians, but the cholesterol levels in vegans were even lower, and, if anything, vegans trended towards a higher clotting stroke risk, so it doesn’t make sense. If there is some protective factor in animal foods, it is to be hoped that a diet can be found that still protects against the killer number one, heart disease, without increasing the risk of the killer number five, stroke. But, first, we have to figure out what that factor is, and the hunt continues. 

    Aren’t there studies suggesting that saturated fat isn’t as bad as we used to think? Check out: 

    Just like the traditional Japanese diet had a lot going for it despite having high sodium as the fatal flaw, what might be the Achilles’ heel of plant-based diets when it comes to stroke risk? 

    This is the seventh video in this stroke series. See the related posts below for the others.

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  • The Stroke Risk of Vegetarians  | NutritionFacts.org

    The Stroke Risk of Vegetarians  | NutritionFacts.org

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    The first study in history on the incidence of stroke in vegetarians and vegans suggests they may be at higher risk.

    “When ranked in order of importance, among the interventions available to prevent stroke, the three most important are probably diet, smoking cessation, and blood pressure control.” Most of us these days are doing pretty good about not smoking, but less than half of us exercise enough. And, according to the American Heart Association, only 1 in 1,000 Americans is eating a healthy diet and less than 1 in 10 is even eating a moderately healthy diet, as you can see in the graph below and at 0:41 in my video Do Vegetarians Really Have Higher Stroke Risk?. Why does it matter? It matters because “diet is an important part of stroke prevention. Reducing sodium intake, avoiding egg yolks, limiting the intake of animal flesh (particularly red meat), and increasing the intake of whole grains, fruits, vegetables, and lentils….Like the sugar industry, the meat and egg industries spend hundreds of millions of dollars on propaganda, unfortunately with great success.” 

    The paper goes on to say, “Box 1 provides links to information about the issue.” I was excited to click on the hyperlink for “Box 1” and was so honored to see four links to my videos on egg industry propaganda, as you can see below and at 1:08 in my video. 

    The strongest evidence for stroke protection lies in increasing fruit and vegetable intake, with more uncertainty regarding “the role of whole grains, animal products, and dietary patterns,” such as vegetarian diets. One would expect meat-free diets would do great. Meta-analyses have found that vegetarian diets lower cholesterol and blood pressure, as well as enhance weight loss and blood sugar control, and vegan diets may work even better. All the key biomarkers are going in the right direction. Given this, you may be surprised to learn that there hadn’t been any studies on the incidence of stroke in vegetarians and vegans until now. And if you think that is surprising, wait until you hear the results. 

    “Risks of Ischaemic Heart Disease and Stroke in Meat Eaters, Fish Eaters, and Vegetarians Over 18 Years of Follow-Up: Results from the Prospective EPIC-Oxford Study”: There was less heart disease among vegetarians (by which the researchers meant vegetarians and vegans combined). No surprise. Been there, done that. But there was more stroke, as you can see below, and at 2:14 in my video. 

    An understandable knee-jerk reaction might be: Wait a second, who did this study? Was there a conflict of interest? This is EPIC-Oxford, world-class researchers whose conflicts of interest may be more likely to read: “I am a member of the Vegan Society.”

    What about overadjustment? When the numbers over ten years were crunched, the researchers found 15 strokes for every 1,000 meat eaters, compared to only 9 strokes for every 1,000 vegetarians and vegans, as you can see below and at 2:41 in my video. In that case, how can they say there were more strokes in the vegetarians? This was after adjusting for a variety of factors. The vegetarians were less likely to smoke, for example, so you’d want to cancel that out by adjusting for smoking to effectively compare the stroke risk of nonsmoking vegetarians to nonsmoking meat eaters. If you want to know how a vegetarian diet itself affects stroke rates, you want to cancel out these non-diet-related factors. Sometimes, though, you can overadjust. 

    The sugar industry does this all the time. This is how it works: Imagine you just got a grant from the soda industry to study the effect of soda on the childhood obesity epidemic. What could you possibly do after putting all the studies together to conclude that there was a “near zero” effect of sugary beverage consumption on body weight? Well, since you know that drinking liquid candy can lead to excess calories that can lead to obesity, if you control for calories, if you control for a factor that’s in the causal chain, effectively only comparing soda drinkers who take in the same number of calories as non-soda-drinkers, then you could undermine the soda-to-obesity effect, and that’s exactly what they did. That introduces “over adjustment bias.” Instead of just controlling for some unrelated factor, you control for an intermediate variable on the cause-and-effect pathway between exposure and outcome.

    Overadjustment is how meat and dairy industry-funded researchers have been accused of “obscuring true associations” between saturated fat and cardiovascular disease. We know that saturated fat increases cholesterol, which increases heart disease risk. Therefore, if you control for cholesterol, effectively only comparing saturated fat eaters with the same cholesterol levels as non-saturated-fat eaters, that could undermine the saturated fat-to-heart disease effect.

    Let’s get back to the EPIC-Oxford study. Since vegetarian eating lowers blood pressure and a lowered blood pressure leads to less stroke, controlling for blood pressure would be an overadjustment, effectively only comparing vegetarians to meat eaters with the same low blood pressure. That’s not fair, since lower blood pressure is one of the benefits of vegetarian eating, not some unrelated factor like smoking. So, that would undermine the afforded protection. Did the researchers do that? No. They only adjusted for unrelated factors, like education, socioeconomic class, smoking, exercise, and alcohol. That’s what you want. You want to tease out the effects of a vegetarian diet on stroke risk. You want to try to equalize everything else to tease out the effects of just the dietary choice. And, since the meat eaters in the study were an average of ten years older than the vegetarians, you can see how vegetarians could come out worse after adjusting for that. Since stroke risk can increase exponentially with age, you can see how 9 strokes among 1,000 vegetarians in their 40s could be worse than 15 strokes among 1,000 meat-eaters in their 50s. 

    The fact that vegetarians had greater stroke risk despite their lower blood pressure suggests there’s something about meat-free diets that so increases stroke risk it’s enough to cancel out the blood pressure benefits. But, even if that’s true, you would still want to eat that way. As you can see in the graph below and at 6:16 in my video, stroke is our fifth leading cause of death, whereas heart disease is number one. 

    So, yes, in the study, there were more cases of stroke in vegetarians, but there were fewer cases of heart disease, as you can see below and at 6:29. If there is something increasing stroke risk in vegetarians, it would be nice to know what it is in hopes of figuring out how to get the best of both worlds. This is the question we will turn to next. 

    I called it 21 years ago. There’s an old video of me on YouTube where I air my concerns about stroke risk in vegetarians and vegans. (You can tell it’s from 2003 by my cutting-edge use of advanced whiteboard technology and the fact that I still had hair.) The good news is that I think there’s an easy fix.

    This is the third in a 12-video series on stroke risk. Links to the others are in the related posts below.

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    Michael Greger M.D. FACLM

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  • Corporate Influence and Our Epidemic of Obesity  | NutritionFacts.org

    Corporate Influence and Our Epidemic of Obesity  | NutritionFacts.org

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    Like the tobacco industry adding extra nicotine to cigarettes, the food industry employs taste engineers to accomplish a similar goal of maximizing the irresistibility of its products. 

    The plague of tobacco deaths wasn’t due just to the mass manufacturing and marketing of cheap cigarettes. Tobacco companies actively sought to make their products even more crave-able by spraying sheets of tobacco with nicotine and additives like ammonia to provide “a bigger nicotine ‘kick.’” Similarly, taste engineers are hired by the food industry to maximize product irresistibility.

    Taste is the leading factor in food choice. “Sugar, fat, and salt have been called the three points of the compass” to produce “superstimulating” and “hyper palatability” to tempt people into impulsive buys and compulsive consumption. Foods are intentionally designed to hook into our evolutionary triggers and breach whatever biological barriers help “keep consumption within reasonable limits.”

    Big Food is big business. The processed food industry alone brings in more than $2 trillion a year. That affords them the economic might to manipulate not only taste profiles, but public policy and scientific inquiry, too. The food, alcohol, and tobacco industries have all used similar unsavory tactics: blocking health regulations, co-opting professional organizations, creating front groups, and distorting the science. The common “corporate playbook” shouldn’t be surprising, given the common corporate threads. At one time, for example, tobacco giant Philip Morris owned both Kraft and Miller Brewing.

    As you can see below and at 1:45 in my video The Role of Corporate Influence in the Obesity Epidemic, in a single year, the food industry spent more than $50 million to hire hundreds of lobbyists to influence legislation. Most of these lobbyists were “revolvers,” former federal employees in the revolving door between industry and its regulators, who could push corporate interests from the inside, only to be rewarded with cushy lobbying jobs after their “public service.” In the following year, the industry acquired a new weapon—a stick to go along with all those carrots. On January 21, 2010, the Supreme Court’s five-to-four Citizen’s United ruling permitted corporations to spend unlimited amounts of money on campaign ads to trash anyone who dared stand against them. No wonder our elected officials have so thoroughly shrunk from the fight, leaving us largely with a government of Big Food, by Big Food, and for Big Food. 

    Globally, a similar dynamic exists. Weak tea calls from the public health community for voluntary standards are met not only with vicious fights against meaningful change but also massive transnational trade and foreign investment deals that “cement the protection of their [food industry] profits” into the laws of the lands.

    The corrupting commercial influence extends to medical associations. Reminiscent of the “just what the doctor ordered” cigarette ads of yesteryear, as you can see below and at 3:05 in my video, the American Academy of Family Physicians accepted millions from The Coca-Cola Company to “develop consumer education content on beverages and sweeteners.” 

    On the front line, fake grassroots “Astroturf” groups are used to mask the corporate message. RJ Reynolds created Get Government Off Our Back (memorably acronymed GGOOB), “a front group created by the tobacco industry to fight regulation,” for instance. Americans Against Food Taxes may as just as well be called “Food Industry Against Food Taxes.” The power of front group formation is enough to bind bitter corporate rivals; the Sugar Association and the Corn Refiners Association linked arms with the National Confectioners Association to partner with Americans for Food and Beverage Choice.

    Using another tried-and-true tobacco tactic, research front groups can be used to subvert the scientific process by shaping or suppressing the science that deviates from the corporate agenda. Take the trans fat story. Food manufacturers have not only “long denied that trans fats were associated with disease,” but actively “worked to limit research on trans fats” and “discredit potentially damaging findings.”

    At what cost? The global death toll from foods high in trans fat, saturated fat, salt, and sugar is at 14 million lost lives every year. The inability of countries around the world to turn the tide on obesity “is not a failure of individual will-power. This is a failure of political will to take on big business,” said the Director-General of the World Health Organization. “It is a failure of political will to take on the powerful food and soda industries.” She ended her keynote address before the National Academy of Medicine entitled “Obesity and Diabetes: The Slow-Motion Disaster” with these words: “The interests of the public must be prioritized over those of corporations.”

    Are you mad yet? To sum up my answer to the question underlying my What Triggered the Obesity Epidemic? webinar, it’s the food. I close next with my wrap-up video: The Role of the Toxic Food Environment in the Obesity Epidemic. 

    This was part of an 11-part series. See the related posts below.

    If the political angle interests you, check out: 

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    Michael Greger M.D. FACLM

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  • What Is the Role of Our Genes in the Obesity Epidemic?  | NutritionFacts.org

    What Is the Role of Our Genes in the Obesity Epidemic?  | NutritionFacts.org

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    The “fat gene” accounts for less than 1 percent of the differences in size between people.

    To date, about a hundred genetic markers have been linked to obesity, but when you put them all together, overall, they account for less than 3 percent of the difference in body mass index (BMI) between people. You may have heard about the “fat gene,” called FTO, short for FaT mass and Obesity-associated). It’s the gene most strongly linked to obesity, but it explains less than 1 percent of the difference in BMI between people, a mere 0.34 percent. 

    As I discuss in my video The Role of Genes in the Obesity Epidemic, FTO codes for a brain protein that appears to affect our appetite. Are you one of the billion people who carry the FTO susceptibility genes? It doesn’t matter because it only appears to result in a difference in intake of a few hundred extra calories a year. The energy imbalance that led to the obesity epidemic is on the order of hundreds of calories a day, and that’s the gene known so far to have the most effect. The chances of accurately predicting obesity risk based on FTO status is “only slightly better than tossing a coin.” In other words, no, those genes don’t make you look fat.

    When it comes to obesity, the power of our genes is nothing compared to the power of our fork. Even the small influence the FTO gene does have appears to be weaker among those who are physically active and may be abolished completely in those eating healthier diets. FTO only appears to affect those eating diets higher in saturated fat, which is predominantly found in meat, dairy, and junk food. Those eating more healthfully appear to be at no greater risk of weight gain, even if they inherited the “fat gene” from both of their parents.

    Physiologically, FTO gene status does not appear to affect our ability to lose weight. Psychologically, knowing we’re at increased genetic risk for obesity may motivate some people to eat and live more healthfully, but it may cause others to fatalistically throw their hands up in the air and resign themselves to thinking that it just runs in their family, as you can see in the graph below and at 2:11 in my video. Obesity does tend to run in families, but so do lousy diets. 

    Comparing the weight of biological versus adopted children can help tease out the contributions of lifestyles versus genetics. Children growing up with two overweight biological parents were found to be 27 percent more likely to be overweight themselves, whereas adopted children placed in a home with two overweight parents were 21 percent more likely to be overweight. So, genetics do play a role, but this suggests that it’s more the children’s environment than their DNA.

    One of the most dramatic examples of the power of diet over DNA comes from the Pima Indians of Arizona. As you can see in the graph below and at 3:05 in my video, they not only have among the highest rates of obesity, but they also have the highest rates of diabetes in the world. This has been ascribed to their relatively fuel-efficient genetic makeup. Their propensity to store calories may have served them well in times of scarcity when they were living off of corn, beans, and squash, but when the area became “settled,” their source of water, the Gila River, was diverted upstream. Those who survived the ensuing famine had to abandon their traditional diet to live off of government food programs and chronic disease rates skyrocketed. Same genes, but different diet, different result. 

    In fact, a natural experiment was set up. The Pima living over the border in Mexico come from the same genetic pool but were able to maintain more of their traditional lifestyle, sticking with their main staples of beans, wheat flour tortillas, and potatoes. Same genes, but seven times less obesity and about four times less diabetes. You can see those graphs below and at 3:58 and 4:02 in my video. Genes may load the gun, but diet pulls the trigger.

    Of course, it’s not our genes! Our genes didn’t suddenly change 40 years ago. At the same time, though, in a certain sense, it could be thought of as all in our genes. That’s the topic of my next video The Thrifty Gene Theory: Survival of the Fattest.

    This is the second in an 11-video series on the obesity epidemic. If you missed the first one, check out The Role of Diet vs. Exercise in the Obesity Epidemic. 

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    Michael Greger M.D. FACLM

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  • Headache and Migraine Relief from Foods  | NutritionFacts.org

    Headache and Migraine Relief from Foods  | NutritionFacts.org

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    Plant-based diets are put to the test for treating migraine headaches.

    Headaches are one of the top five reasons people end up in emergency rooms and one of the leading reasons people see their doctors in general. One way to try to prevent them is to identify their triggers and avoid them. Common triggers for migraines include stress, smoking, hunger, sleep issues, certain foods (like chocolate, cheese, and alcohol), your menstrual cycle, or certain weather patterns (like high humidity).

    In terms of dietary treatments, the so-called Father of Modern Medicine, William Osler suggested trying a “strict vegetable diet.” After all, the nerve inflammation associated with migraines “may be reduced by a vegan diet as many plant foods are high in anti-inflammatory compounds and antioxidants, and likewise, meat products have been reported to have inflammatory properties.” It wasn’t put to the test, though, for another 117 years.

    As I discuss in my video Friday Favorites: Foods That Help Headache and Migraine Relief, among study participants given a placebo supplement, half said they got better, while the other half said they didn’t. But, when put on a strictly plant-based diet, they did much better, experiencing a significant drop in the severity of their pain, as you can see in the graph below and at 1:08 in my video. 

    Now, “it is possible that the pain-reducing effects of the vegan diet may be, at least in part, due to weight reduction.” The study participants lost about nine more pounds when they were on the plant-based diet for a month, as shown below, and at 1:22. 

    Even just lowering the fat content of the diet may help. Those placed on a month of consuming less than 30 daily grams of fat (for instance, less than two tablespoons of oil all day), experienced “statistically significant decreases in headache frequency, intensity, duration, and medication intake”—a six-fold decrease in the frequency and intensity, as you can see below and at 1:44 in my video. They went from three migraine attacks every two weeks down to just one a month. And, by “low fat,” the researchers didn’t mean SnackWell’s; they meant more fruits, vegetables, and beans. Before the food industry co-opted and corrupted the term, eating “low fat” meant eating an apple, for example, not Kellogg’s Apple Jacks.  

    Now, they were on a low-fat diet—about 10 percent fat for someone eating 2,500 calories a day. What about just less than 20 percent fat compared to a more normal diet that’s still relatively lower fat than average? As you can see below and at 2:22 in my video, the researchers saw the same significant drops in headache frequency and severity, including a five-fold drop in attacks of severe pain. Since the intervention involved at least a halving of intake of saturated fat, which is mostly found in meat, dairy, and junk, the researchers concluded that reduced consumption of saturated fat may help control migraine attacks—but it isn’t necessarily something they’re getting less of. There are compounds “present in Live green real veggies” that might bind to a migraine-triggering peptide known as calcitonin gene-related peptide, CGRP. 

    Drug companies have been trying to come up with something that binds to CGRP, but the drugs have failed to be effective. They’re also toxic, which is a problem we don’t have with cabbage, as you can see below and at 3:01 in my video. 

    Green vegetables also have magnesium. Found throughout the food supply but most concentrated in green leafy vegetables, beans, nuts, seeds, and whole grains, magnesium is the central atom to chlorophyll, as shown below and at 3:15. So, you can see how much magnesium foods have in the produce aisle by the intensity of their green color. Although magnesium supplements do not appear to decrease migraine severity, they may reduce the number of attacks you get in the first place. You can ask your doctor about starting 600 mg of magnesium dicitrate every day, but note that magnesium supplements can cause adverse effects, such as diarrhea, so I recommend getting it the way nature intended—in the form of real food, not supplements.  

    Any foods that may be particularly helpful? You may recall that I’ve talked about ground ginger. What about caffeine? Indeed, combining caffeine with over-the-counter painkillers, like Tylenol, aspirin, or ibuprofen, may boost their efficacy, at doses of about 130 mg for tension-type headaches and 100 mg for migraines. That’s about what you might expect to get in three cups of tea, as you can see below, and at 4:00 in my video. (I believe it is just a coincidence that the principal investigator of this study was named Lipton.) 

    Please note that you can overdo it. If you take kids and teens with headaches who were drinking 1.5 liters of cola a day and cut the soda, you can cure 90 percent of them. However, this may be a cola effect rather than a caffeine effect. 

    And, finally, one plant food that may not be the best idea is the Carolina Reaper, the hottest chili pepper in the world. It’s so mind-numbingly hot it can clamp off the arteries in your brain, as seen below and at 4:41 in my video, and you can end up with a “thunderclap headache,” like the 34-year-old man who ate the world’s hottest pepper and ended up in the emergency room. Why am I not surprised it was a man? 

    I’ve previously covered ginger and topical lavender for migraines. Saffron may help relieve PMS symptoms, including headaches. A more exotic way a plant-based diet can prevent headaches is by helping to keep tapeworms out of your brain.

    Though hot peppers can indeed trigger headaches, they may also be used to treat them. Check out my video on relieving cluster headaches with hot sauce. 

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    Michael Greger M.D. FACLM

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  • How Much Added Sugar Is Okay?  | NutritionFacts.org

    How Much Added Sugar Is Okay?  | NutritionFacts.org

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    Public health authorities continue to lower the upper tolerable limit of daily added sugar intake.

    Dating back to the original “Dietary Goals for the United States” in 1977, also known as the so-called McGovern Report, leading nutrition scientists didn’t only call for a reduction in meat and other sources of saturated fat and cholesterol, such as dairy and eggs, but also sugar. The goal was to reduce America’s sugar intake to no more than 10 percent of our daily diet.

    “The conclusions would hang sugar,” reported the president of the Sugar Association. “The McGovern Report has to be neutralized.” The National Cattlemen’s Association was on its side and, just like Big Sugar, appealed to the Senate Select Committee to withdraw the report.

    “The Sugar Industry Empire Strikes Back”—and it appeared to work. When the official U.S. Dietary Guidelines were released in 1980 and again in 1985, it was without a specific limit, like 10 percent. It “said, simply, and in just four words, ‘Avoid too much sugar.’” (Whatever that means.) “In 1990, it went to five words, ‘Use sugars only in moderation,’ and in 1995 to six: ‘Choose a diet moderate in sugars.’” In 2000, it at least went back to limiting intake—specifically, “‘Choose beverages and foods to limit your intake of sugars’ (ten words), but even that was too strong. Under pressure from sugar lobbyists, the government agencies substituted the word ‘moderate’ for ‘limit’ so it read ‘Choose beverages and foods to moderate your intake of sugars.’” Then, the 2005 guidelines committee dropped the s-word completely, encouraging Americans to “Choose carbohydrates wisely…” Again, what does that mean? If only there were a dietary guidelines committee that could guide us….

    The Sugar Association expressed optimism about that 2005 Committee. In its Sugar E-News, it wrote that Sugar Association Incorporated (SAI) “is committed to the protection and promotion of sucrose [table sugar] consumption. Any disparagement of sugar will be met with forceful, strategic public comments”—and it wasn’t kidding. “In 2003, [the World Health Organization] WHO released a joint report with the Food and Agriculture Organization entitled Diet, nutrition and the prevention of chronic diseases which, for the first time [since the McGovern Report], called for a reduction in sugar intake to under 10% of total dietary energy [caloric] consumption.” The Sugar Association responded by threatening to get the United States to withdraw all funding from the WHO. You can see it yourself in black and white at 2:22 in my video Friday Favorites: The Recommended Daily Added Sugar Intake. The Sugar Association threatened to pressure Congress to withdraw funding from the World Health Organization—polio vaccinations and AIDS medications be damned! Don’t mess with the candy man. The threat was described as “tantamount to blackmail and worse than any pressure exerted by the tobacco lobby.” 

    Fifteen years later and 40 years after the first proposed McGovern Report, the 2015 to 2020 Dietary Guidelines for Americans lays out the 10 percent limit as a key recommendation: “Consume less than 10 percent of calories per day from added sugars.” This is currently exceeded by every age bracket in the United States starting at age one, as you can see in the graph below and at 2:58 in my video, with adolescents averaging 87 grams of sugar a day. That means the average teen is effectively eating 29 sugar packets a day. 

    The Sugar Association describes the 10 percent limit as “extremely low.” Well, I mean, it is only up to about a dozen spoonsful a day. Of course, there is no dietary requirement for added sugar at all, and every single calorie we get from added sugar is a wasted opportunity to get calories from sources that provide nutrition. To the American Heart Association’s credit, it went further by trying to push added sugar intake down to about 6 percent of calories, for which a single can of soda could send you over the limit. That’s an added sugar limit exceeded by 90 percent of Americans.

    In 2017, the American Heart Association (AHA) released its guidelines for children, recommending they get no more than about six teaspoons per day. In that case, a single serving of nearly a hundred cereals on the U.S. market would exceed the entire recommended daily limit. The AHA recommends no added sugars at all for children under the age of two, a recommendation that’s violated in up to 80 percent of toddlers, as you can see below and at 4:20 in my video. 

    In the United States, “at least 65 countries have implemented dietary guidelines or public health policies to curb sugar consumption to encourage maintenance of healthy body weight.” In the United Kingdom, the Scientific Advisory Committee on Nutrition made new recommendations to reduce added sugars down to 5 percent, which is also the direction the World Health Organization is headed. The WHO always seems to be ahead of the curve. Why? Because its policy-making process is at least partially protected “against industry influence.” Unlike governments, which may have competing interests in commerce and trade, “WHO is exclusively concerned with health.”

    I spoke at a hearing of the 2020 Dietary Guidelines Committee. Watch the highlights and my speech here: Highlights from the 2020 Dietary Guidelines Hearing.

    The sugar industry keeps pretty busy, as you’ll see from my recent videos, Friday Favorites: Are Fortified Kids’ Breakfast Cereals Healthy or Just Candy? and Flashback Friday: Sugar Industry Attempts to Manipulate the Science.

    Check the related posts below for my other popular videos and blogs on sugar.

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  • How Safe Is Alternate-Day Intermittent Fasting?  | NutritionFacts.org

    How Safe Is Alternate-Day Intermittent Fasting?  | NutritionFacts.org

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    Eating every other day can raise your cholesterol. 
     
    Are there any downsides to fasting every other day? For example, might go all day without eating impair your ability to think clearly? Surprisingly, as I discuss in my video Is Alternate-Day Intermittent Fasting Safe?, the results appear to be “equivocal.” Some studies show no measurable effects and the ones that do fail to agree on which cognitive domains are affected. Might the cycles of fasting and feasting cause eating disorder–type behaviors, like bingeing? So far, no harmful psychological effects have been found. In fact, there may be some benefit. However, the studies that have put it to the test specifically excluded those with a documented history of eating disorders, for whom the effects may differ. 
     
    What about bone health? No change in bone mineral density was noted after six months of alternate-day fasting despite about 16 pounds of weight loss, which would typically result in a dip in bone mass. However, the researchers did not note any skeletal changes in the control group either, and they lost a similar amount of weight using continuous caloric restriction. They suggested this is because both groups tended to be “more physically active than the average obese American,” getting about 1,000 to 2,000 more steps a day. 
     
    Proponents of intermittent fasting suggest it can better protect lean body mass, but most of the intermittent trials have employed less accurate methods of body composition analysis, whereas the majority of continuous caloric restriction trials used “vastly more accurate techniques.” So, to date, it is not clear if there’s a difference in lean mass preservation. 
     
    Improvements in blood pressure and triglycerides have been noted on intermittent fasting regimens, though this is presumed to be due to the reduction in body fat since the effect appears to be “dependent on the amount of weight lost.” Alternate-day fasting can improve artery function, too, as you can see in the graph below and at 1:55 in my video, though it does depend on what you’re eating on the non-fasting day. For study participants randomized to an alternate-day diet high in saturated fat, their artery function worsened despite a ten-pound weight loss, whereas it improved, as expected, in the lower-fat group. The decline in artery function was presumed to be because of the pro-inflammatory nature of saturated fat. 

    A concern has been raised about the effects of alternate-day fasting on cholesterol. After 24 hours without food, LDL cholesterol may temporarily bump up, but this is presumably because so much fat is being released into the system by the fast. As you can see in the graph below and at 2:33 in my video, an immediate negative effect on carbohydrate tolerance may stem from the same phenomenon—the repeated elevations of free fat floating around in the bloodstream. After a few weeks, though, LDL levels start to drop as the weight comes off. However, results from the largest and longest trial of alternate-day fasting have given me pause. 


    A hundred obese men and women were randomized into one of three groups: alternate-day modified fasting (25 percent of their baseline calories on fasting days and 125 percent calories on eating days), continuous, daily caloric restriction (75 percent of baseline), or a control group instructed to maintain their regular diet. So, for those going into the trial eating 2,000 calories a day, they would continue to eat 2,000 calories a day in the control group. The calorie-restriction group would get 1,500 calories every day, and the intermittent-restriction group would alternate between 500 calories a day and 2,500 calories the next. 
     
    As you can see in the graph below and at 3:32 in my video, with the same overall, average, prescribed calorie cutting in the two weight-loss groups, they both lost about the same amount of weight, but, surprisingly, the cholesterol effects were different. In the continuous calorie-restriction group, the LDL levels dropped as expected compared to the control group as the pounds came off. 

    But, in the alternate-day modified fasting group, they didn’t, as you can see below, and at 3:55 in my video. At the end of the year, the LDL cholesterol in the intermittent fasting group ended up being 10 percent higher than in the constant calorie-restriction group—despite the same loss of body fat. Given that LDL cholesterol is a prime causal risk factor for heart disease, our number one killer—or is even the prime risk factor—this strikes a significant blow against alternate-day fasting. If you want to try it anyway, I would advise you to have your cholesterol monitored to make sure it comes down with your weight. 


    If you’re diabetic, you must talk with your physician about medication adjustment for any changes in diet, including fasting of any duration. Even with proactive medication reduction, advice to immediately break the fast should sugars drop too low, and weekly medical supervision, people with type 2 diabetes who fasted for even just two days a week were twice as likely to suffer from hypoglycemic episodes compared to an unfasted control group. We still don’t know the best way to tweak blood sugar medications to prevent blood sugar from dropping too low on fasting days. 
     
    Even fasting for just one day can significantly slow the clearance of some drugs (like the blood-thinning drug Coumadin) or increase the clearance of others (like caffeine). Fasting for 36 hours can cut your caffeine buzz by 20 percent. So, consultation with your medical professional before fasting is an especially good idea for anyone on any kind of medication. 

    If you missed it, check out Alternate-Day Intermittent Fasting Put to the Test. 
     
    So, with ambiguous cognitive, lean mass, and bone effects, plus these cholesterol findings, I wouldn’t suggest alternate-day fasting for weight loss, but dropping pounds isn’t the only thing this way of eating is purported to do. Check out Does Intermittent Fasting Increase Human Life Expectancy?. 
     
    For other types of intermittent fasting, total fasting, and more on fasting, check out the related videos below. 



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  • Keto Diets and Diabetes  | NutritionFacts.org

    Keto Diets and Diabetes  | NutritionFacts.org

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    Ketogenic diets are put to the test for diabetes reversal. 
     
    As you can see at the start of my video Does a Ketogenic Diet Help Diabetes or Make It Worse?, ketogenic diets can lower blood sugars better than conventional diets. So much so, in fact, that there is a keto product company that claims ketogenic diets can “reverse” diabetes. However, they are confusing the symptom (high blood sugars) with the disease (carbohydrate intolerance). People with diabetes can’t properly handle carbohydrates, and this manifests as high blood sugars. Clearly, if you stick to eating mostly fat, your blood sugars will stay low, but you may be actually making the underlying disease worse at the same time. 
     
    We’ve known for nearly a century that if you put people on a ketogenic diet, their carbohydrate intolerance can skyrocket within just two days. Below and at 0:46 in my video, you can see a graph from the study showing the blood sugar response two days after eating sugar. On a high-carb diet, blood sugar response is about 90 mg/dL. But, the blood sugar response to the same amount of sugar after a high-fat diet is about 190 mg/dL, nearly double. The intolerance to carbohydrates skyrocketed on a high-fat diet. 

    After one week on an 80 percent fat diet, you can quintuple your blood sugar spike in reaction to the same carb load compared to a week on a low-fat diet, as you can see in the graph below and at 1:12 in my video. 

    Even a single day of excessive dietary fat intake can do it, as you can see in the graph below and at 1:26 in my video. If you’re going in for a diabetes test, having a fatty dinner the night before can adversely affect your results. Just one meal high in saturated fat can make carbohydrate intolerance, the cause of diabetes, worse within four hours. 


    Given enough weight loss by any means, whether from cholera or bariatric surgery, type 2 diabetes can be reversed, but a keto diet for diabetes may not just be papering over the cracks, but actively throwing fuel on the fire. 
     
    I’ve been trying to think of a good metaphor. It’s easy to come up with things that just treat the symptoms without helping the underlying disease, like giving someone with pneumonia aspirin for their fever instead of antibiotics. However, a keto diet for diabetes is worse than that because it may treat the symptoms while actively worsening the disease. It may be more like curing the fever by throwing that pneumonia patient out into a snow bank or “curing” your amputated finger by amputating your hand. One of the co-founders of masteringdiabetes.org suggested it’s like a CEO who makes their bad bottom line look better by borrowing tons of cash. The outward numbers look better, but on the inside, the company is just digging itself into a bigger hole. 
     
    Do you remember The Club, that popular car anti-theft device that attaches to the steering wheel and locks it in place so the steering column can only turn a few inches? Imagine you’re in a car at the top of a hill with the steering wheel locked. Then, the car starts rolling down the hill. What do you do? Imagine there’s also something stuck under your brake pedal. The keto-diet equivalent response to this situation is who cares if you’re barreling down into traffic with a locked steering wheel and no brakes—just stick to really straight deserted roads without any stop signs or traffic lights. If you do that, problem solved! The longer you go, the more speed you’ll pick up. If you should hit a dietary bump in the road or start to veer off the path, the consequences could get more and more disastrous over time. However, if you stick to the keto straight and narrow, you’ll be a-okay! In contrast, the non-keto response would be to just unlock the steering wheel and dislodge whatever’s under your brake. In other words, fix the underlying problem instead of just whistling past—and then into—the graveyard. 
     
    The reason keto proponents claim they can “reverse” diabetes is they can successfully wean type 2 diabetics off their insulin. That’s like faith-healing someone out of the need for a wheelchair by making them stay in bed the rest of their life. No need for a wheelchair if you never move. Their carbohydrate intolerance isn’t gone. Their diabetes isn’t gone. In fact, it could be just as bad or even worse. Type 2 diabetes is reversed when you are weaned off insulin while eating a normal diet like everyone else. Then and only then do you not have diabetes anymore. A true diabetes reversal diet, as you can see below and at 4:58 in my video, is practically the opposite of a ketogenic diet: getting diabetics off their insulin within a matter of weeks by eating more than 300 grams of carbs a day! 
    The irony doesn’t stop there. One of the reasons people with diabetes suffer such nerve and artery damage is due to an inflammatory metabolic toxin known as methylglyoxal, which forms at high blood sugar levels. Methylglyoxal is the most potent creator of advanced glycation end products (AGEs), which are implicated in degenerative diseases—from Alzheimer’s and cataracts to kidney disease and strokes, as you can see below and at 5:31 in my video. 

    You get AGEs in your body from two sources: You can eat them preformed in your diet or make them internally from methylglyoxal if you have high blood sugar levels. On a keto diet, one would expect high exposure to preformed AGEs, since they’re found concentrated in animal-derived foods high in fat and protein, but we would expect less internal, new formation due to presumably low levels of methylglyoxal, given lower blood sugars from not eating carbs. Dartmouth researchers were surprised to find more methylglyoxal! As shown in the graph below and at 6:11 in my video, a few weeks on the Atkins diet led to a significant increase in methylglyoxal levels. Those in active ketosis did even worse, doubling the level of this glycotoxin in their bloodstream. 

    It turns out that high sugars may not be the only way to create this toxin, as you can see below and at 6:24 in my video. One of the ketones you make on a ketogenic diet is acetone (known for its starring role in nail polish remover). Acetone does more than just make keto dieters fail breathalyzer tests, “feel queasy and light-headed, and develop what’s been described as ‘rotten apple breath.’” Acetone can oxidize in the blood to form acetol, which may be a precursor for methylglyoxal.

    That may be why keto dieters can end up with levels of this glycotoxin as high as those with out-of-control diabetes, which can cause the nerve damage and blood vessel damage you see in diabetics. That’s another way keto dieters can end up with a heart attack. The irony of treating diabetes with a ketogenic diet may extend beyond just making the underlying diabetes worse, but by mimicking some of the disease’s dire consequences. 

    This is part of a seven-video series on keto, which you can find in related videos below.

    I also recently tackled diabetes.

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    Michael Greger M.D. FACLM

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  • The Safety of Keto Diets  | NutritionFacts.org

    The Safety of Keto Diets  | NutritionFacts.org

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    What are the effects of ketogenic diets on nutrient sufficiency, gut flora, and heart disease risk? 

    Given the decades of experience using ketogenic diets to treat certain cases of pediatric epilepsy, a body of safety data has accumulated. Nutrient deficiencies would seem to be the obvious issue. Inadequate intake of 17 micronutrients, vitamins, and minerals has been documented in those on strict ketogenic diets, as you can see in the graph below and at 0:14 in my video Are Keto Diets Safe?. 

    Dieting is a particularly important time to make sure you’re meeting all of your essential nutrient requirements, since you may be taking in less food. Ketogenic diets tend to be so nutritionally vacuous that one assessment estimated that you’d have to eat more than 37,000 calories a day to get a sufficient daily intake of all essential vitamins and minerals, as you can see in the graph below and at 0:39 in my video. 


    That is one of the advantages of more plant-based approaches. As the editor-in-chief of the Journal of the American Dietetic Association put it, “What could be more nutrient-dense than a vegetarian diet?” Choosing a healthy diet may be easier than eating more than 37,000 daily calories, which is like putting 50 sticks of butter in your morning coffee. 
     
    We aren’t just talking about not reaching your daily allowances either. Children have gotten scurvy on ketogenic diets, and some have even died from selenium deficiency, which can cause sudden cardiac death. The vitamin and mineral deficiencies can be solved with supplements, but what about the paucity of prebiotics, the dozens of types of fiber, and resistant starches found concentrated in whole grains and beans that you’d miss out on? 
     
    Not surprisingly, constipation is very common on keto diets. As I’ve reviewed before, starving our microbial self of prebiotics can have a whole array of negative consequences. Ketogenic diets have been shown to “reduce the species richness and diversity of intestinal microbiota,” our gut flora. Microbiome changes can be detected within 24 hours of switching to a high-fat, low-fiber diet. A lack of fiber starves our good gut bacteria. We used to think that dietary fat itself was nearly all absorbed in the small intestine, but based on studies using radioactive tracers, we now know that about 7 percent of the saturated fat in a fat-rich meal can make it down to the colon. This may result in “detrimental changes” in our gut microbiome, as well as weight gain, increased leaky gut, and pro-inflammatory changes. For example, there may be a drop in beneficial Bifidobacteria and a decrease in overall short-chain fatty acid production, both of which would be expected to increase the risk of gastrointestinal disorders. 
     
    Striking at the heart of the matter, what might all of that saturated fat be doing to our heart? If you look at low-carbohydrate diets and all-cause mortality, those who eat lower-carb diets suffer “a significantly higher risk of all-cause mortality,” meaning they live, on average, significantly shorter lives. However, from a heart-disease perspective, it matters if it’s animal fat or plant fat. Based on the famous Harvard cohorts, eating more of an animal-based, low-carb diet was associated with higher death rates from cardiovascular disease and a 50 percent higher risk of dying from a heart attack or stroke, but no such association was found for lower-carb diets based on plant sources.  
     
    And it wasn’t just Harvard. Other researchers have also found that “low-carbohydrate dietary patterns favoring animal-derived protein and fat sources, from sources such as lamb, beef, pork, and chicken, were associated with higher mortality, whereas those that favored plant-derived protein and fat intake, from sources such as vegetables, nuts, peanut butter, and whole-grain bread, were associated with lower mortality…” 
     
    Cholesterol production in the body is directly correlated to body weight, as you can see in the graph below and at 3:50 in my video. 

    Every pound of weight loss by nearly any means is associated with about a one-point drop in cholesterol levels in the blood. But if we put people on very-low-carb ketogenic diets, the beneficial effect on LDL bad cholesterol is blunted or even completely neutralized. Counterbalancing changes in LDL or HDL (what we used to think of as good cholesterol) are not considered sufficient to offset this risk. You don’t have to wait until cholesterol builds up in your arteries to have adverse effects either; within three hours of eating a meal high in saturated fat, you can see a significant impairment of artery function. Even with a dozen pounds of weight loss, artery function worsens on a ketogenic diet instead of getting better, which appears to be the case with low-carb diets in general.  

    For more on keto diets, check out my video series here. 

    And, to learn more about your microbiome, see the related videos below.

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    Michael Greger M.D. FACLM

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  • Keto Diet to Effectively Fight Cancer?  | NutritionFacts.org

    Keto Diet to Effectively Fight Cancer?  | NutritionFacts.org

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    What does the science say about the clinical use of ketogenic diets for epilepsy and cancer? 

    Blood sugar, also known as blood glucose, is the universal go-to fuel for the cells throughout our bodies. Our brain burns through a quarter pound of sugar a day because “glucose is the preferred metabolic fuel.” We can break down proteins and make glucose from scratch, but most comes from our diet in the form of sugars and starches. If we stop eating carbohydrates (or stop eating altogether), most of our cells switch over to burning fat. Fat has difficulty getting through the blood-brain barrier, though, and our brain has a constant, massive need for fuel. Just that one organ accounts for up to half of our energy needs. Without it, the lights go out…permanently. 

    To make that much sugar from scratch, our body would need to break down about half a pound of protein a day. That means we’d cannibalize ourselves to death within two weeks, but people can fast for months. What’s going on? The answer to the puzzle was discovered in 1967. Harvard researchers famously stuck catheters into the brains of obese subjects who had been fasting for more than a month and discovered that ketones had replaced glucose as the preferred fuel for the brain. Our liver can turn fat into ketones, which can then breach the blood-brain barrier and sustain our brain if we aren’t getting enough carbohydrates. Switching fuels has such an effect on brain activity that it has been used to treat epilepsy since antiquity. 

    In fact, the prescription of fasting for the treatment of epileptic seizures dates back to Hippocrates. In the Bible, even Jesus seems to have concurred. To this day, it’s unclear why switching from blood sugar to ketones as a primary fuel source has such a dampening effect on brain overactivity. How long can one fast? To prolong the fasting therapy, in 1921, a distinguished physician scientist at the Mayo Clinic suggested trying what he called “ketogenic diets,” high-fat diets designed to be so deficient in carbohydrates that they could effectively mimic the fasting state. “Remarkable improvement” was noted the first time it was put to the test, efficacy that was later confirmed in randomized, controlled trials. Ketogenic diets started to fall out of favor in 1938 with the discovery of the anti-seizure drug that would become known as Dilantin, but they’re still being used today as a third- or fourth-line treatment for drug-refractory epilepsy in children. 

    Oddly, the success of ketogenic diets against pediatric epilepsy seems to get conflated by “keto diet” proponents into suggesting a ketogenic diet is beneficial for everyone. Know what else sometimes works for intractable epilepsy? Brain surgery, but I don’t hear people clamoring to get their skulls sawed open. Since when do medical therapies translate into healthy lifestyle choices? Scrambling brain activity with electroshock therapy can be helpful in some cases of major depression, so should we get out the electrodes? Ketogenic diets are also being tested to see if they can slow the growth of certain brain tumors. Even if they work, you know what else can help slow cancer growth? Chemotherapy. So why go keto when you can just go chemo? 

    Promoters of ketogenic diets for cancer are paid by so-called ketone technology companies that offer to send you salted caramel bone broth powder for a hundred bucks a pound or companies that market ketogenic meals and report “extraordinary” anecdotal responses in some cancer patients. But more concrete evidence is simply lacking, and even the theoretical underpinnings may be questionable. A common refrain is that “cancer feeds on sugar.” But all cells feed on sugar. Advocating ketogenic diets for cancer is like saying Hitler breathed air so we should boycott oxygen. 

    Cancer can feed on ketones, too. Ketones have been found to fuel human breast cancer growth and drive metastases in an experimental model, more than doubling tumor growth. Some have even speculated that this may be why breast cancer often metastasizes to the liver, the main site of ketone production. As you can see below and at 4:59 in my video Is Keto an Effective Cancer-Fighting Diet?, if you drip ketones directly onto breast cancer cells in a petri dish, the genes that get turned on and off make for much more aggressive cancer, associated with significantly lower five-year survival in breast cancer patients, as you can see in the following graph and at 5:05 in my video. Researchers are even considering designing ketone-blocking drugs to prevent further cancer growth by halting ketone production.  

    Let’s also think about what eating a ketogenic diet might entail. High animal fat intake may increase the mortality risk among breast cancer survivors and potentially play a role in the development of breast cancer in the first place through oxidative stress, hormone disruption, or inflammation. This applies to men, too. “A strong association” has been found “between saturated fat intake and prostate cancer progression and survival.” Those in the top third of consumption of these kinds of fat-rich animal foods appeared to triple their risk of dying from prostate cancer. This isn’t necessarily fat in general either. No difference has been found in breast cancer death rates based on total fat intake. However saturated fat intake specifically may negatively impact breast cancer survival, increasing the risk of dying from it by 50 percent. There’s a reason the official American Cancer Society and American Society of Clinical Oncology Breast Cancer Survivorship Care Guideline recommend a dietary pattern for breast cancer patients that’s essentially the opposite of a ketogenic diet. It calls for a diet that’s “high in vegetables, fruits, whole grains, and legumes [beans, split peas, chickpeas, and lentils]; low in saturated fats; and limited in alcohol consumption.” 

    “To date, not a single clinical study has shown a measurable benefit from a ketogenic diet in any human cancer.” There are currently at least a dozen trials underway, however, and the hope is that at least some cancer types will respond. Still, even then, that wouldn’t serve as a basis for recommending ketogenic diets for the general population any more than recommending everyone get radiation, surgery, and chemo just for kicks. 

    “Keto” has been the most-searched keyword on NutritionFacts.org for months, and I didn’t have much specific to offer…until now. Check out my other videos on the topic in related videos below. 

     For an overview of my cancer work, watch How Not to Die from Cancer. 

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  • 7 Cereals Can No Longer Claim ‘Healthy’ Label Under FDA Rule

    7 Cereals Can No Longer Claim ‘Healthy’ Label Under FDA Rule

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    Oct. 13, 2022 — Generations of Americans grew up being told that breakfast cereals like Corn Flakes and Raisin Bran were healthy ways to start their days.

    But now, under new federal guidelines, those cereals and other mainstays of the breakfast table can no longer make that claim.

    The guidance was proposed after the White House Conference on Hunger, Nutrition, and Health, “as well as the release of the related national strategy, which aims to end hunger, improve nutrition and physical activity, reduce diet-related diseases and close disparity gaps by 2030,” the FDA wrote in a press release.

    To be considered “healthy,” foods must meet certain criteria. The FDA used cereal as an example to illustrate how the guidelines affect how food will be presented to consumers.

    For that “healthy” label, cereals need three-fourth ounces of whole grains and no more than 1 gram of saturated fat, 230 milligrams of sodium, and 2.5 grams of added sugars, CNBC reported.

    Here are seven common American brands that don’t meet the “healthy” label standards:

    • Raisin Bran (9 grams of added sugars)
    • Honey Nut Cheerios (12 grams of added sugars)
    • Corn Flakes (300 milligrams of sodium; 4 grams of added sugars)
    • Honey Bunches of Oats, Honey Roasted (8 grams of added sugars)
    • Frosted Mini Wheats (12 grams of added sugars)
    • Life (8 grams of added sugars)
    • Special K (270 milligrams of sodium; 4 grams of added sugars)

    “Nutrition is key to improving our nation’s health,” said Xavier Becerra, Health and Human Services secretary. “Healthy food can lower our risk for chronic disease. But too many people may not know what constitutes healthy food. FDA’s move will help educate more Americans to improve health outcomes, tackle health disparities and save lives.”

     

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  • These 7 Cereals Can No Longer Claim ‘Healthy’ Label Under FDA Rule

    These 7 Cereals Can No Longer Claim ‘Healthy’ Label Under FDA Rule

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    Oct. 13, 2022 — Generations of Americans grew up being told that breakfast cereals like Corn Flakes and Raisin Bran were healthy ways to start their days.

    But now, under new federal guidelines, those cereals and other mainstays of the breakfast table can no longer make that claim.

    The guidance was proposed after the White House Conference on Hunger, Nutrition, and Health, “as well as the release of the related national strategy, which aims to end hunger, improve nutrition and physical activity, reduce diet-related diseases and close disparity gaps by 2030,” the FDA wrote in a press release.

    To be considered “healthy,” foods must meet certain criteria. The FDA used cereal as an example to illustrate how the guidelines affect how food will be presented to consumers.

    For that “healthy” label, cereals need three-fourth ounces of whole grains and no more than 1 gram of saturated fat, 230 milligrams of sodium, and 2.5 grams of added sugars, CNBC reported.

    Here are seven common American brands that don’t meet the “healthy” label standards:

    • Raisin Bran (9 grams of added sugars)
    • Honey Nut Cheerios (12 grams of added sugars)
    • Corn Flakes (300 milligrams of sodium; 4 grams of added sugars)
    • Honey Bunches of Oats, Honey Roasted (8 grams of added sugars)
    • Frosted Mini Wheats (12 grams of added sugars)
    • Life (8 grams of added sugars)
    • Special K (270 milligrams of sodium; 4 grams of added sugars)

    “Nutrition is key to improving our nation’s health,” said Xavier Becerra, Health and Human Services secretary. “Healthy food can lower our risk for chronic disease. But too many people may not know what constitutes healthy food. FDA’s move will help educate more Americans to improve health outcomes, tackle health disparities and save lives.”

     

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