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Tag: mortality

  • How Low Can LDL Cholesterol Go on PCSK9 Inhibitors? | NutritionFacts.org

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    People with genetic mutations that leave them with an LDL cholesterol of 30 mg/dL live exceptionally long lives. Can we duplicate that effect with drugs?

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

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

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

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

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

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

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

    Doctor’s Note

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

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

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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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  • Bariatric Surgery: Risks in the OR and Beyond | NutritionFacts.org

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    The extent of risk from bariatric weight-loss surgery may depend on the skill of the surgeon.

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

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

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

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

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

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

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

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

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

    Doctor’s Note

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

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

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

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    Michael Greger M.D. FACLM

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  • Bariatric Weight-Loss Surgery and Mortality | NutritionFacts.org

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    Today, death rates after weight-loss surgery are considered to be “very low,” occurring in perhaps 1 in 300 to 1 in 500 patients on average.

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

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

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

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

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

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

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

    Doctor’s Note

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

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

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

     

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    Michael Greger M.D. FACLM

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  • Is Aflatoxin a Concern? | NutritionFacts.org

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    Is “toxic mold syndrome” a real thing? What do we do about toxic mold contamination of food?

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

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

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

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

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

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

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

    Doctor’s Note

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

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    Michael Greger M.D. FACLM

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  • Are the Effects of Ochratoxin Concerning? | NutritionFacts.org

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    The overall cost-benefit ratio for mycotoxins depends on which food is contaminated.

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

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

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

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

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

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

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

    Doctor’s Note

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

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

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    Michael Greger M.D. FACLM

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  • Prostate Cancer and Mushrooms | NutritionFacts.org

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    What can reishi mushrooms, shiitake mushroom extracts, and whole, powdered white mushrooms do for cancer patients?

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

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

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

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

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

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

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

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

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

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

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

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

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

    Doctor’s Note

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

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

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

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

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    Michael Greger M.D. FACLM

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  • Plant-Based Hospital Menus | NutritionFacts.org

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    The American Medical Association passed a resolution encouraging hospitals to offer healthy plant-based food options.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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    Michael Greger M.D. FACLM

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  • The Hidden Devastation of Hurricanes

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    Parks’s team estimated that, among Medicare patients alone, tropical cyclones are associated with nearly seventeen thousand excess hospitalizations per decade in the United States. “It’s shocking, to be honest,” Parks told me. He sees each hurricane as a profound disruption to affected communities. “Once the water subsides, it becomes a huge, invisible burden,” he said. The hazards extend beyond rain, flooding, or wind. “They’re existential,” he said. “They pull at every element of the fabric of society.”

    A decade ago, two researchers, Edward Rappaport and B. Wayne Blanchard, set out to measure what they called the indirect deaths from storms: “Casualties that, while not directly attributable to one of the physical forces of a tropical cyclone, would not be expected in the absence of the storm.” How many more people are harmed than the official tallies suggest? “To answer those questions, one is faced with others,” the researchers wrote in a 2016 paper. How far in advance of a storm should they search? (During evacuations, a person could die from an untreated emergency or a car crash.) How long after? (Injuries can cause death weeks after they occur.) How far from the storm’s center? Where, and when, and in what way, should they look?

    Rappaport and Blanchard settled on an old-fashioned methodology: scouring reams of death records in the vicinity of fifty-nine storms, dating back to 1963. (To look back at Hurricane Camille, in 1969, they reviewed more than a thousand death-certificate records.) The pair ultimately identified more than fourteen hundred indirect deaths—almost as many as the total number of direct deaths reported from the storms. Many fatalities, such as electrocutions from downed power lines, were accidental. But the largest share reflected Irimpen’s findings from New Orleans. “Heart attacks and other cardiovascular failures are the most pervasive elements in indirect deaths,” the researchers wrote. Most seemed to be triggered by physical exertion—loading sandbags before Hurricane Wilma, for example, or bailing water out of a car owing to Hurricane Floyd. But, during Hurricane Hugo, in 1989, one man reportedly dropped dead after he “saw everything he had, totally demolished.” Their research echoed findings from other studies of disasters. Three years after a 2004 earthquake in Japan, mortality from heart attacks was found to be fourteen per cent higher than pre-quake. In the two weeks after Hurricane Sandy, New Jersey recorded thirty-six more strokes and a hundred and twenty-five more heart attacks than usual. Many were fatal.

    Elena Naumova, a data scientist at Tufts, was part of a team that analyzed around four hundred thousand Medicare hospitalizations after Katrina. They found that hospitalizations for cardiovascular problems increased up to sixfold, and remained elevated for two months. “These are hidden consequences,” Naumova told me. “It’s very hard to connect what happens months later to the hurricane . . . but the risks linger for a long time.” Naumova now thinks of a storm as similar to an outbreak whose effects ripple out in her data. “The health-care system will be constantly bombarded by these cascading effects,” she said. “You see one wave, and another, and another.”

    When researchers want to study the collateral consequences of a major event, whether a natural disaster or a pandemic, they often use the concept of excess deaths. Mortality rates don’t capture the full extent of harm; for one thing, they exclude injuries and illnesses that people recover from. But they can capture broad trends that might otherwise escape notice. When Hurricane Maria devastated Puerto Rico, in 2017, the official death toll was sixty-four—a number that seemed low, given the storm’s violence. Then a team of researchers surveyed more than three thousand households, searching for fatalities that could be related to Maria. Based on their results, they estimated that mortality had likely increased more than sixty per cent in the three months after the storm. If all of Puerto Rico experienced a similar uptick, the storm would be responsible for nearly five thousand excess deaths.

    Rachel Young, an environmental economist at the University of California, Berkeley, told me that she had read the Hurricane Maria paper and had an idea: perhaps she’d find a signal if she studied mortality across the entire United States. Young and Solomon Hsiang, a colleague at Stanford, tried to link state-by-state mortality data to five hundred tropical cyclones since 1930. “I ran the analysis, and I thought I must be doing something wrong,” she told me. “We were stunned.” Their results, published last year in Nature, suggested that the average tropical cyclone generated between seven and eleven thousand excess deaths, up to fifteen years after the storm—three hundred times as many as NOAA had tallied. For years, they tried repeatedly to invalidate their findings. “We really wanted to stress-test the result,” Young told me. In the end, they concluded that large storms “reverberate for so much longer than we thought,” she said. “They’re not just disasters of the week.”

    One of the most striking findings in Young and Hsiang’s paper hinted at how storms were causing long-term damage. Infants were impacted more than any other group—and many died at least twenty-one months after the storm in question, meaning that they had not been conceived at the time of landfall. This suggested that “cascades of indirect effects,” not “personal direct exposure,” were proving deadly, Young and Hsiang wrote. Displaced people may lose access to medical care, child care, and support networks; disasters undermine not only physical but also mental health.

    Irimpen’s research at Tulane helps pick apart these cascades. In his initial study, two years post-Katrina, he observed increased unemployment, lack of insurance, smoking, and substance abuse—but not an increase in risk factors traditionally associated with cardiovascular disease, such as diabetes or high blood pressure. Ten years later, however, these illnesses had increased as well. “We think there is a compounding effect,” he explained. Stress and adverse behaviors contribute to chronic diseases, which then further increase the risk of heart attacks. The disaster’s impacts were lasting enough that some of these trends took a decade to detect.

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    Clayton Dalton

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  • Treat the Cause | NutritionFacts.org

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    Treat the underlying cause of chronic lifestyle diseases.

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

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

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

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

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

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

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

    Doctor’s Note

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

    For more on Lifestyle Medicine, see related videos below.

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    Michael Greger M.D. FACLM

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  • A Longer Life on Statins?  | NutritionFacts.org

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    What are the pros and cons of relative risk, absolute risk, number needed to treat, and average postponement of death when taking cholesterol-lowering statin drugs?

    In response to the charge that describing the benefits of statin drugs only in terms of relative risk reduction is a “statistical deception” created to give the appearance that statins are more effective than they really are, it was pointed out that describing things in terms of absolute risk reduction or number needed to treat can depend on the duration of the study.

    For example, let’s say a disease has a 2% chance of killing you every year, but some drug cuts that risk by 50%. That sounds amazing, until you realize that, at the end of a year, your risk will only have fallen from 2% to 1%, so the absolute reduction of risk is only 1%. If a hundred people were treated with the drug, instead of two people dying, one person would die, so a hundred people would have to be treated to save one life, as shown below and at 1:01 in my video How Much Longer Do You Live on Statins?.

    But there’s about a 99% chance that taking the drug all year would have no effect either way. So, to say the drug cuts the risk of dying by 50% seems like an overstatement. But think about it: Benefits accrue over time. If there’s a 2% chance of dying every year, year after year, after a few decades, the majority of those who refused the drug would be dead, whereas the majority who took the drug would be alive. So, yes, perhaps during the first year on the drug, there was only about a 1% chance it would be life-saving, but, eventually, you could end up with a decent chance the drug would save your life after all.

    “This is actually the very reason why the usage of relative risk makes sense…” Absolute risk changes depending on the time frame being discussed, but with relative risk, you know that whatever risk you have, you can cut it in half by taking the drug. On average, statins only cut the risk of a cardiovascular “event” by 25%, but since cardiovascular disease is the number one killer of men and women, if you’re unwilling to change your diet, that’s a powerful argument in favor of taking these kinds of drugs. You can see the same kind of dependency on trial duration, looking at the “postponement of death” by taking a statin. How much longer might you live if you take statins?

    The average postponement of death has some advantages over other statistics because it may offer “a better intuitive understanding among lay persons,” whereas a stat like a number needed to treat has more of a win-or-lose “lottery-like” quality. So, when a statin drug prevents, say, one heart attack out of a hundred people treated over five years, it’s not as though the other 99 completely lost out. Their cholesterol also dropped, and their heart disease progression presumably slowed down, too, just not enough to catch a heart attack within that narrow time frame.

    So, what’s the effect of statins on average survival? According to an early estimate, if you put all the randomized trials together, the average postponement of death was calculated at maybe three or four days. Three or four days? Who would take a drug every day for years just to live a few more days? Well, let’s try to put that into context. Three or four days is comparable to the gains in life expectancy from other medical interventions. For example, it’s nearly identical to what you’d get from “highly effective childhood vaccines.” Because vaccines have been so effective in wiping out infectious diseases, these days, they only add an average of three extra days to a child’s life. But, of course, “those whose deaths are averted gain virtually their whole lifetimes.” That’s why we vaccinate. It just seems like such a small average benefit because it gets distributed over the many millions of kids who get the vaccine. Is that the same with statins?

    An updated estimate was published in 2019, which explained that the prior estimate of three or four days was plagued by “important weaknesses,” and the actual average postponement of death was actually ten days. Headline writers went giddy from these data, but what they didn’t understand was that this was only for the duration of the trial. So, if your life expectancy is only five years, then, yes, statins may increase your lifespan by only ten days, but statins are meant to be taken a lot longer than five years. What you want to know is how much longer you might get to live if you stick with the drugs your whole life.

    In that case, it isn’t an extra ten days, but living up to ten extra years. Taking statins can enable you to live years longer. That’s because, for every millimole per liter you lower your bad LDL cholesterol, you may live three years longer and maybe even six more years, depending on which study you’re reading. A millimole in U.S. units is 39 points. Drop your LDL cholesterol by about 39 points, and you could live years longer. Exercise your whole life, and you may only increase your lifespan by six months, and stopping smoking may net you nine months. But if you drop your LDL cholesterol by about 39 points, you could live years longer. You can accomplish that by taking drugs, or you can achieve that within just two weeks of eating a diet packed with fruits, vegetables, and nuts, as seen here and at 5:30 in my video. 

    Want to know what’s better than drugs? “Something important and fundamental has been lost in the controversy around this broad expansion of statin therapy.…It is imperative that physicians (and drug labels) inform patients that not only their lipid [cholesterol] levels but also their cardiovascular risk can be reduced substantially by adoption of a plant-based dietary pattern, and without drugs. Dietary modifications for cardiovascular risk reduction, including plant-based diets, have been shown to improve not only lipid status, but also obesity, hypertension, systemic inflammation, insulin sensitivity, oxidative stress, endothelial function, thrombosis, and cardiovascular event risk…The importance of this [plant-based] approach is magnified when one considers that, in contrast to statins, the ‘side effects’ of plant-based diets—weight loss, more energy, and improved quality of life—are beneficial.” 

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    Michael Greger M.D. FACLM

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  • The Real Benefits of Statins and Their Side Effects  | NutritionFacts.org

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    A Mayo Clinic visualization tool can help you decide if cholesterol-lowering statin drugs are right for you.

    “Physicians have a duty to inform their patients about the risks and benefits of the interventions available to them. However, physicians rarely communicate with methods that convey absolute information, such as numbers needed to treat, numbers needed to harm, or prolongation of life, despite patients wanting this information.” That is, for example, how many people are actually helped by a particular drug, how many are actually hurt by it, or how much longer the drug will enable you to live, respectively.

    If doctors inform patients only about the relative risk reduction—for example, telling them a pill will cut their risk of heart attacks by 34 percent—nine out of ten agree to take it. However, give them the same information framed as absolute risk reduction—“1.4% fewer patients had heart attacks”—then those agreeing to take the drug drops to only four out of ten. And, if they use the number needed to treat, only three in ten patients would agree to take the pill. So, if you’re a doctor and you really want your patient to take the drug, which statistic are you going to use?

    The use of relative risk stats to inflate the benefits and absolute risk stats to downplay any side effects has been referred to as “statistical deception.” To see how one might spin a study to accomplish this, let’s look at an example. As you can see below and at 1:49 in my video, The True Benefits vs. Side Effects of Statins, there is a significantly lower risk of the incidence of heart attack over five years in study participants randomized to a placebo compared to those getting the drug. If you wanted statins to sound good, you’d use the relative risk reduction (24 percent lower risk). If you wanted statins to sound bad, you’d use the absolute risk reduction (3 percent fewer heart attacks).

    Then you could flip it for side effects. For example, the researchers found that 0.3 percent (1 out of 290 women in the placebo group) got breast cancer over five years, compared to 4.1 percent (12 out of 286) in the statin group. So, a pro-statin spin might be a 24 percent drop in heart attack risk and only 3.8 percent more breast cancers, whereas an anti-statin spin might be only 3 percent fewer heart attacks compared to a 1,267 percent higher risk of breast cancer. Both portrayals are technically true, but you can see how easily you could manipulate people if you picked and chose how you were presenting the risks and benefits. So, ideally, you’d use both the relative risk reduction stat and the absolute risk reduction stat.

    In terms of benefits, when you compile many statin trials, it looks like the relative risk reduction is 25 percent. So, if your ten-year risk of a heart attack or stroke is 5 percent, then taking a statin could lower that from 5 percent to 3.75 percent, for an absolute risk reduction of 1.25 percent, or a number needed to treat of 80, meaning there’s about a 1 in 80 chance that you’d avoid a heart attack or stroke by taking the drug for the next ten years. As you can see, as your baseline risk gets higher and higher, even though you have that same 25 percent risk reduction, your absolute risk reduction gets bigger and bigger. And, with a 20 percent baseline risk, that means you have a 1 in 20 chance of avoiding a heart attack or stroke over the subsequent decade if you take the drug, as seen below and at 3:31 in my video.

    So, those are the benefits. In terms of risk, that breast cancer finding appears to be a fluke. Put together all the studies, and “there was no association between use of statins and the risk of cancer.” In terms of muscle problems, estimates of risk range from approximately 1 in 1,000 to closer to 1 in 50.

    If all those numbers just blur together, the Mayo Clinic developed a great visualization tool, seen below and at 4:39 in my video.

    For those at average risk, 10 people out of 100 who do not take a statin may have a heart attack over the next ten years. If, however, all 100 people took a statin every day for those ten years, 8 would still have a heart attack, but 2 would be spared, so there’s about a 1 in 50 chance that taking the drug would help avert a heart attack over the next decade. What are the downsides? The cost and inconvenience of taking a pill every day, which can cause some gastrointestinal side effects, muscle aching, and stiffness in about 5 percent, reversible liver inflammation in 2 percent, and more serious damage in perhaps 1 in 20,000 patients.

    Note that the two happy faces in the bottom left row of the YES STATIN chart represent heart attacks averted, not lives saved. The chance that a few years of statins will actually save your life if you have no known heart disease is about 1 in 250.

    If you want a more personalized approach, the Mayo Clinic has an interactive tool that lets you calculate your ten-year risk. You can get there directly by going to bit.ly/statindecision.

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    Michael Greger M.D. FACLM

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  • Being Underweight Might Be Deadlier Than Being Overweight

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    If asked whether one would prefer to be too skinny or fat, chances are most people would reply that they’d rather be too skinny. Distorted standards of beauty and their propagation on social media are certainly to blame for this, in addition to the knowledge that being overweight typically brings along a host of health risks. A new study, however, suggests that being too thin can actually be deadlier.

    Researchers used health data to investigate the relationship between body mass index (BMI) and mortality in 85,761 individuals, revealing that people can be “fat but fit.” They presented their results at the annual meeting of the European Association for the Study of Diabetes (EASD), which started today.

    BMI measures fat based on height and weight and classifies individuals as underweight (less than 18.5), normal (18.5 to less than 25), overweight (25 to less than 30), obese (30 to less than 40), or severely obese (40 and over). In the research, scientists divided the normal range into lower normal (18.5 to <20), middle normal (20.0 to <22.5), and upper normal (22.5 to <25.0). 81.4% of the studied participants were female, and the median age was 66.4 years. Researchers accounted for sex, comorbidity level, and education level.

    What BMI range has higher mortality?

    “There are conflicting findings about the BMI range linked to lowest mortality,” Sigrid Bjerge Gribsholt, lead author of the research and a researcher at Aarhus University’s department of clinical medicine, said in a European Association for the Study of Diabetes statement. “It was once thought to be 20 to 25 but it may be shifting upward over time owing to medical advances and improvements in general health.”

    7,555 (8%) of the participants died during the team’s five years of follow-up, and researchers compared the likelihood of mortality in different BMI ranges to that of people with a BMI in the upper normal level. Their results indicate that underweight individuals were 2.73 times more likely to die than upper-normal individuals. Lower-normal individuals were two times more likely to die, and middle-normal individuals were 27% more likely to die than upper-normal individuals. Interestingly, overweight individuals as well as individuals in the lower part of the obese range (30.0 to <35.0) were just as likely to die as upper-normal individuals.

    Researchers sometimes call this being metabolically healthy or “fat but fit.” Individuals with a BMI between 35 and less than 40, however, were 23% more likely to die. Severely obese people (BMI of 40 and over) were 2.1 times more likely to die than upper-normal individuals. In other words, a high BMI was not linked to higher mortality until a score of 35, and even scores between 35 and <40 only had a slightly higher risk of death. The team found similar patterns of mortality in the relationship between BMI and obesity in different ages, sexes, and levels of education.

    “In line with earlier research, we found that people who are in the underweight range face a much higher risk of death,” Gribsholt said. A possible explanation could be that some people lose weight from illness. “In those cases, it is the illness, not the low weight itself, that increases the risk of death, which can make it look like having a higher BMI is protective,” she admitted. However, “it is also possible that people with higher BMI who live longer—most of the people we studied were elderly—may have certain protective traits that influence the results.”

    BMI doesn’t reveal everything

    What’s more, fat distribution plays an important role in an individual’s health, said Jens Meldgaard Bruun, a co-author of the study and also a researcher at Aarhus University’s department of clinical medicine. “Visceral fat—fat that is very metabolically active and stored deep within the abdomen, wrapped around the organs—secretes compounds that adversely affect metabolic health,” he explained. As such, people with a BMI of 35 who are apple-shaped (with fat around their abdomen) may have adverse health conditions that don’t affect others also with a BMI of 35 but who have fat on their hips, backside, and thighs.

    “It is clear that the treatment of obesity should be personalized to take into account factors such as fat distribution and the presence of conditions such as type 2 diabetes when setting a target weight,” Bruun concluded.

    In a world ruled by social media and advertising-driven unrealistic body expectations, the study joins previous research trying to set the record straight on healthy body weight. What’s more, it highlights—again—that BMI scores alone don’t necessarily provide the full picture, though the scale seems to be accurate regarding American obesity.

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    Margherita Bassi

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  • Two Years After Maui Burned, Researchers Reveal the Wildfire’s True Death Toll

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    In August 2023, downed power lines on Maui, Hawaii, sparked a wildfire that quickly exploded into multiple, fast-moving blazes fanned by high winds. Over several days, the fires reduced much of the town of Lāhainā to ashes, displacing thousands and killing more than 100 people.

    New research published Thursday, August 22, in the journal Frontiers in Climate suggests this disaster also caused a population-wide increase in mortality beyond what the official death count captured. By calculating the all-cause excess fatality rate—how many more deaths took place over a given period than expected—scientists found a 67% increase in the local mortality rate for August 2023. During the deadliest week of the blaze, the local death rate was 367% higher than expected. These findings underscore a need for improved disaster preparedness that incorporates Native Hawaiian ecological knowledge, the researchers concluded.

    What excess death rate reveals

    Looking at the excess death rate offered a fuller picture of the fire’s impact, co-first author Michelle Nakatsuka, a medical student and researcher at New York University’s Grossman School of Medicine, told Gizmodo in an email. “The official numbers mostly count direct causes, like burns or smoke inhalation, but excess deaths capture [the] true toll better by telling us how many more people died than would have otherwise been expected in the month of the Lāhainā fires,” she explained.

    Disasters like wildfires often cause deaths in indirect ways that affect communities over time. When clinics shut down and roads are blocked off, people can’t refill their prescriptions or get dialysis treatments, Nakatsuka explained. Stress and displacement can worsen chronic conditions, and power or communication failures can delay emergency responses. “These impacts are amplified in under-resourced settings and [are] disproportionately suffered by vulnerable groups, like the elderly or people of color,” she said.

    The tragic toll of the Maui fires

    Even with this knowledge, Nakatsuka and her colleagues were surprised by the increase in excess mortality during the month of August 2023. Their analysis included all causes of death except covid-19. “While we anticipated an increase in excess deaths, seeing more than 80 additional deaths in the month of the Lāhainā fires was striking,” Nakatsuka said. “It was also surprising to see that the proportion of those deaths occurring outside of medical settings was larger than expected,” she added.

    Indeed, the number of deaths that didn’t take place in a medical context—such as the emergency room—rose from 68% in previous months to 80% in August 2023. These people died in homes or public locations, suggesting that many were unable to reach medical care because of the fires.

    A path to resilience

    While all-cause excess mortality is useful for correlating increased fatalities with natural disasters, it offers little insight into the details of these deaths, Nakatsuka clarified. “The main limitation here is that we can’t say exactly which deaths were caused by the fires or look into Lāhainā-specific excess mortality; we can only measure the overall increase in deaths,” she said, adding that future research should analyze death records alongside medical and toxicology reports to identify causes of death.

    Still, these findings reveal a need to improve Maui’s disaster preparedness and invest in wildfire mitigation strategies rooted in Indigenous knowledge, Nakatsuka said. “Native Hawaiian practices center around caring for the land (mālama ʻāina) in ways that naturally reduce fire risk, like restoring native plants, maintaining diverse ecosystems, and managing water resources,” she said. “Bringing Indigenous knowledge together with modern climate prediction tools will minimize risk of future climate crises and center the community’s voice at the heart of disaster prevention and recovery efforts.”

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    Ellyn Lapointe

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  • True Health Intiative: Scientific Consensus on a Healthy Diet  | NutritionFacts.org

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    The leading risk factor for death in the United States is the American diet.

    About a decade ago, the American Heart Association (AHA) expressed concern that its “2020 target of improving cardiovascular health by 20% by 2020 will not be reached if current trends continue.” By 2006, most people were already not smoking and had nearly achieved their goal for exercise. But when it came to healthy diet score, only about 1 percent got a 4 or 5 out of its diet quality score of 0 to 5, as you can see below and at 0:35 in my video, Friday Favorites: The Scientific Consensus on a Healthy Diet. And that’s with such “ideal” criteria as drinking less than four and a half cups of soda a week.

    In the last decade, the AHA saw a bump in the prevalence of the ideal healthy diet score to about 1 percent of Americans reaching those kinds of basic criteria, but, given its “aggressive” goal of reaching a “20% target” by 2020, it hoped to turn that 1 percent into about 1.2 percent. (Really, as you can see here and at 1:01 in my video.)

    So, how’d we do? According to the 2019 update, it seems we’ve slipped down to as low as one in a thousand, and American teens scored a big fat zero. No wonder, perhaps, that “for all mortality-based metrics, the US rank declined…to 27th or 28th among 34 OECD [industrialized] countries. Citizens living in countries with a substantially lower gross domestic product and health expenditure per capita…have lower mortality rates than those in the United States.” Slovenia, for example, beat the United States, ranking 24th in life expectancy. More recently, the United States’s life expectancy slipped further, down to 43rd in the world, although the United States spent the most ($3.0 trillion) on health care…”

    What is the leading risk factor for death in the United States? As seen below and at 2:04 in my video, it is the standard American diet. Those trillions in health care spending aren’t addressing the root cause of disease, disability, and death. 

    Here are some of the lung cancer death curves, below and at 2:08 in my video:

    It took decades to finally turn the corner, but it’s so nice to finally see those drops. When will we see the same with diet?

    “Approximately 80% of chronic disease and premature death could be prevented by not smoking, being physically active, and adhering to a healthful dietary pattern.” What exactly is meant by “healthy diet”? “Unfortunately, media messages surrounding nutrition are often inconsistent, confusing, and do not enable the public to make positive changes in health behaviors….Certainly, there is pressure within today’s competitive journalism market for sensationalism. There may even be a disincentive to present the facts in the context of the total body of information consumers need to act on dietary recommendations.” And there’s an incentive to sell more magazines and newspapers. The paper I’m quoting was written in 1997, before the lure of clickbait headlines. In fact, about three-quarters of a century ago, it was noted: “It is unfortunate that the subject of nutrition seems to have a special appeal to the credulous, the social zealot and, in the commercial field, the unscrupulous….The combination is one calculated to strike despair in the hearts of the sober, objective scientist.”

    Indeed, the most important health care problem we face may be “our poor lifestyle choices based on misinformation.” It is like the climate change deniers: “Analogous to outspoken cynics denying climate change and influencing public opinion, healthy lifestyle and dietary advice are overshadowed by critics, diet books, the food industry, and misguided information in the media.” Maybe we need an entity like the Intergovernmental Panel on Climate Change (IPCC)—but for nutrition.

    These days, “no single expert, regardless of academic stature or reputation, has the prominence to overcome the obstacles created by confusing media messages and deliver the fundamental principles of healthy living effectively to the public.”

    What if there were “a global coalition consisting of a variety of nutrition experts, who collectively represent the views held by the majority of scientists, physicians, and health practitioners” that could “serve as the guiding resource of sound nutrition information for improved health and prevention of disease”?

    Enter the True Health Initiative, which “was conceived for that very purpose.” A nonprofit coalition of hundreds of experts from dozens of countries has agreed to a consensus statement on the fundamentals of healthy living. See www.truehealthinitiative.org.

    Spoiler alert: The healthiest diet is one generally comprised mostly of minimally processed plants.

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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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  • Statins and Muscle Pain Side Effects  | NutritionFacts.org

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    Why is the incidence of side effects from statins so low in clinical trials while appearing to be so high in the real world?

    “There is now overwhelming evidence to support reducing LDL-C (low-density lipoprotein cholesterol)”—so-called bad cholesterol—to reduce atherosclerotic cardiovascular disease (CVD),” the number one killer of men and women. So, why is adherence to cholesterol-lowering statin drug therapy such “a major challenge worldwide”? Researchers found “that the majority of studies reported that at least 40%, and as much as 80%, of patients did not comply fully with statin treatment recommendations.” Three-quarters of patients may flat out stop taking them, and almost 90 percent may discontinue treatment altogether.

    When asked why they stopped taking the pills, most “former statin users or discontinuers…cited muscle pain, a side effect, as the primary reason…” “SAMSs”—statin-associated muscle symptoms—“are by far the most prevalent and important adverse event, with up to 72% of all statin adverse events being muscle-related.” Taking coenzyme Q10 supplements as a treatment for statin-associated muscle symptoms was a good idea in theory, but they don’t appear to help. Normally, side-effect symptoms go away when you stop the drug but can sometimes linger for a year or more. There is “growing evidence that statin intolerance is predominantly psychosocial, not pharmacological.” Really? It may be mostly just in people’s heads?

    “Statins have developed a bad reputation with the public, a phenomenon driven largely by proliferation on the Internet of bizarre and unscientific but seemingly persuasive criticism of these drugs.” “Does Googling lead to statin intolerance?” But people have stopped taking statins for decades before there even was an Internet. What kinds of data have doctors suggested that patients are falsely “misattribut[ing] normal aches and pains to be statin side effects”?

    Well, if you take people who claim to have statin-related muscle pain and randomize them back and forth between statins and an identical-looking placebo in three-week blocks, they can’t tell whether they’re getting the real drug or the sugar pill. The problem with that study, though, is that it may take months not only to develop statin-induced muscle pain, but months before it goes away, so no wonder three weeks on and three weeks off may not be long enough for the participants to discern which is which.

    However, these data are more convincing: Ten thousand people were randomized to a statin or a sugar pill for a few years, but so many more people were dying in the sugar pill group that the study had to be stopped prematurely. So then everyone was offered the statin, and the researchers noted that there was “no excess of reports of muscle-related AEs” (adverse effects) among patients assigned to the statin over those assigned to the placebo. But when the placebo phase was over and the people knew they were on a statin, they went on to report more muscle side effects than those who knew they weren’t taking the statin. “These analyses illustrate the so-called nocebo effect,” which is akin to the opposite of the placebo effect.

    Placebo effects are positive consequences falsely attributed to a treatment, whereas nocebo effects are negative consequences falsely attributed to a treatment, as was evidently seen here. There was an excess rate of muscle-related adverse effects reported only when patients and their doctors were aware that statin therapy was being used, and not when its use was concealed. The researchers hope “these results will help assure both physicians and patients that most AEs associated with statins are not causally related to use of the drug and should help counter…exaggerated claims about statin-related side effects.”

    These are the kinds of results from “placebo-controlled randomised trials [that] have shown definitively that almost all of the symptomatic adverse events that are attributed to statin therapy in routine practice are not actually caused by it (ie, they represent misattribution.)” Now, “only a few patients will believe that their SAMS are of psychogenic origin” and just in their head, but their denial may have “deadly consequences.” Indeed, “discontinuing statin treatment may be a life-threatening mistake.”

    Below and at 4:46 in my video How Common Are Muscle Side Effects from Statins?, you can see the mortality of those who stopped their statins after having a possible adverse reaction compared to those who stuck with them. This translates into about “1 excess death for every 83 patients who discontinued treatment” within a four-year period. So, when there are media reports about statin side effects and people stop taking them, this could “result in thousands of fatal and disabling heart attacks and strokes, which would otherwise have been avoided. Seldom in the history of modern therapeutics have the substantial proven benefits of a treatment been compromised to such an extent by serious misrepresentations of the evidence for its safety.” But is it a misrepresentation to suggest “that statin therapy causes side-effects in up to one fifth of patients”? That is what is seen in clinical practice; between 10 to 25 percent of patients placed on statins complain of muscle problems. However, because we don’t see anywhere near those kinds of numbers in controlled trials, patients are accused of being confused. Why is the incidence of side effects from statins so low in clinical trials while appearing to be so high in the real world? 

    Take this meta-analysis of clinical trials, for example: It found muscle problems not in 1 in 5 patients, but only 1 in 2,000. Should everyone over a certain age be on statins? Not surprisingly, every one of those trials was funded by statin manufacturers themselves. So, for example, “how could the statin RCTs [randomized controlled trials] miss detecting mild statin-related muscle adverse side effects such as myalgia [muscle pain]? By not asking. A review of 44 statin RCTs reveals that only 1 directly asked about muscle-related adverse effects.” So, are the vast majority of side effects just being missed in all these trials, or are the vast majority of side effects seen in clinical practice just a figment of patients’ imagination? The bottom line is we don’t know, but there is certainly an urgent need to figure it out.

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    Michael Greger M.D. FACLM

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  • Eating to Keep Ulcerative Colitis in Remission  | NutritionFacts.org

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    Plant-based diets can be 98 percent effective in keeping ulcerative colitis patients in remission, far exceeding the efficacy of other treatments.

    “One of the most common questions physicians treating patients with IBD [inflammatory bowel disease] are asked is whether changing diet could positively affect the course of their disease.” Traditionally, we had to respond that we didn’t know. That may now be changing, given the “evidence in the literature that hydrogen sulfide may play a role in UC,” ulcerative colitis. And, since the sulfur-containing amino acids concentrated in meat cause an increase in colonic levels of this rotten egg gas, perhaps we should “take off the meat.” Indeed, animal protein isn’t associated only with an increased risk of getting inflammatory bowel disease in the first place, but also IBD relapses once you have the disease.

    This is a recent development. “Because the concept of IBD as a lifestyle disease mediated mainly by a westernized diet is not widely appreciated, an analysis of diet in the follow-up period [after diagnosis] in relation to a relapse of IBD has been ignored”—but no longer. Ulcerative colitis patients in remission and their diets were followed for a year to see which foods were linked to the return of their bloody diarrhea. Researchers found that the “strongest relationship between a dietary factor and an increased risk of relapse observed in this study was for a high intake of meat,” as I discuss in my video The Best Diet for Ulcerative Colitis Treatment.

    What if people lower their intake of sulfur-containing amino acids by decreasing their consumption of animal products? Researchers tried this on four ulcerative colitis patients, and without any change in their medications, the patients experienced about a fourfold improvement in their loose stools. In fact, they felt so much better that the researchers didn’t think it was ethical to try switching the patients back to their typical diets. “Sulfur-containing amino acids are the primary source of dietary sulfur,” so a “low-sulfur” diet essentially means “a shift from a more traditional western diet (high in animal protein and fat, and low in fiber) to more of a plant-based diet (high in fiber, lower in animal protein and fat).” “Altogether, westernized diets are pro-inflammatory, and PBD [plant-based diets] are anti-inflammatory.”

    What can treatment with a plant-based diet do after the onset of ulcerative colitis during a low-carbohydrate weight-loss diet? A 36-year-old man lost 13 pounds on a low-carb diet, but he also lost his health; he was diagnosed with ulcerative colitis. When he was put on a diet centered around whole plant foods, his symptoms resolved without medication. He achieved remission. That was just one case, though. Case reports are akin to glorified anecdotes. The value of case reports lies in their ability to inspire researchers to put them to the test, and that’s exactly what they did.

    Until then, there had never been a study published that focused on using plant-based diets for treating ulcerative colitis. Wrote the researchers, a group of Japanese gastroenterologists, “We consider that the lack of a suitable diet is the biggest issue faced in the current treatment of IBD. We regard IBD as a lifestyle disease caused mainly by our omnivorous (Western) diet. We have been providing a plant-based diet (PBD) to all patients with IBD” for more than a decade and have published extraordinary results, far better than have been reported elsewhere in the medical literature to date. (I profiled some of their early work in one of the first videos that went up on NutritionFacts.org.) The researchers found a plant-based diet to be “effective in the maintenance of remission” in Crohn’s disease by 100 percent at one year and 90 percent at two years. What about a plant-based diet for relapse prevention in ulcerative colitis?

    “Educational hospitalization” involved bringing patients into the hospital to control their diet and educate them about the benefits of plant-based eating (so they’d be more motivated to continue it at home). “Most patients (77%) experienced some improvement, such as disappearance or decrease of bloody stool during hospitalization.” Fantastic!

    Here’s the really exciting part. The researchers then followed the patients for five years, and 81 percent of them remained in remission for the entire five years, and 98 percent kept the disease at bay for at least one year. That blows away other treatments. Those relapse rates are far lower than those reported with medication. Under conventional treatment, other studies found that about half of the individuals relapse, compared to only 2 percent of those taught to eat healthier.

    “A PBD was previously shown to be effective in both the active and quiescent stages of Crohn’s disease. The current study showed that a PBD is effective in both the active and quiescent stages of UC as well.” So, the researchers did another study on even more severely affected cases with active disease and found the same results, with plant-based eating beating conventional drug therapy by far. People felt so much better that they were still eating more plant-based food even six years later. The researchers conclude that a plant-based diet is effective for treating ulcerative colitis to prevent a relapse.

    Why? Well, plant-based diets are rich in fiber, which feeds our good gut bugs. “This observation might partly explain why a PBD prevents a variety of chronic diseases. Indeed, the same explanation applies to IBD, indicating that replacing an omnivorous diet with a PBD in IBD is the right approach.” 
     
    It’s like using plant-based diets to treat the cause of heart disease, our number one killer. Plant-based eating isn’t only safer and cheaper, but it also works better with no noted adverse side effects. Let’s compare that to the laundry list of side effects of immunosuppressants used for ulcerative colitis, like cyclosporine, which you can see below and at 5:40 in my video. 

    We now have even fancier drugs costing about $60,000 a year, about $5,000 a month, and they don’t even work very well; clinical remission at one year is only about 17 to 34 percent. And, instead of no adverse side effects, the drugs can give us a stroke, give us heart failure, and can even give us cancer, including a rare type of cancer that often results in death. Also, a serious brain disease known as progressive multifocal leukoencephalopathy, which can kill us, and for which there is no known treatment or cure. One drug lists an “increased risk of death” but touts that it’s just “a small pill” in an “easy-to-open bottle.” I’d skip the pills (and their potential side effects) and stick with plant-based eating.

    Doctor’s Note:

    If you missed the previous video, see Preventing Inflammatory Bowel Disease with Diet and stay tuned for The Best Diet for Crohn’s Disease Treatment, coming up next. 
     
    Check the related posts below for some older videos on IBD that may be of interest to you.

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    Michael Greger M.D. FACLM

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