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Tag: cardiovascular disease

  • 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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  • Aiming for a healthier year? A doctor shares the 5 science-backed habits that matter most

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    (CNN) — Was that you I spotted at that New Year’s Day group class at my local YMCA? If not, don’t worry. It’s not too late. The start of a new year is a natural time to think about health and make resolutions for science-backed habits that make a difference over months and years.

    Rather than extreme diets or complicated regimens, decades of research point to a handful of simple behaviors that are consistently tied to better long-term health.

    To start the year right, I wanted you to know the most important things you can focus on this year to improve your current physical and mental well-being and have it pay off for decades to come. And yes, I know how hard it can be to realistically follow through when motivation is low or life gets busy.

    I asked CNN wellness expert Dr. Leana Wen to break down five practical, evidence-based actions that can make a real difference in 2026 and beyond. Wen is an emergency physician and adjunct associate professor at George Washington University. She previously served as Baltimore’s health commissioner.

    CNN: For your first tip, you said to prioritize regular exercise. Why does exercise matter so much for health?

    Dr. Leana Wen: Regular physical activity is one of the most powerful tools we have for preventing chronic disease and improving quality of life. It benefits virtually every organ system in the body. Even short bouts of moderate exercise, such as brisk walking, can lower blood pressure, improve cholesterol levels, boost mood and strengthen the heart.

    For adults, the US Centers for Disease Control and Prevention recommend at least 150 minutes of moderate-intensity activity per week plus muscle-strengthening activities on two or more days. Even if you can’t hit those recommendations, some activity is better than none. If you do not currently exercise, start with a 5- or 10-minute brisk walk once a day; if you already walk regularly, try adding a few extra minutes at a time and increasing your pace.

    CNN: Your second tip is to get checkups at least annually. Why is that so important?

    Wen: Periodic checkups with a clinician are essential because many high-risk conditions develop silently. Hypertension, or high blood pressure, and type 2 diabetes, for example, often have no obvious symptoms until they have already caused significant damage to the heart, kidneys and blood vessels. Detecting and treating these conditions early dramatically lowers the risk of heart attack, stroke, kidney disease and other serious complications.

    A checkup gives you a chance to assess risk factors like cholesterol, glucose levels, body mass index and lifestyle habits. You also can establish monitoring or treatment plans with your provider before problems become severe. Timely treatment through lifestyle changes, medication or both can slow or even reverse disease progression.

    These visits also pose an important opportunity to review vaccinations. Recommendations and public messaging from federal health agencies may change, but your clinician can help you understand which vaccines are appropriate for you based on your age, health conditions and personal risk. Staying up to date on routine vaccines — such as flu, Covid-19 and others recommended for your situation — remains one of the most effective ways to prevent serious illness and protect both individual and community health.

    CNN: Your third tip is to get adequate sleep. Why does sleep matter as much as diet or exercise?

    Wen: Sleep is not optional; it’s a biological necessity that affects nearly every aspect of health we care about. Without adequate sleep, your body has trouble repairing tissues, regulating hormones and managing energy balance.

    Research suggests that chronic insufficient sleep is linked to greater risk of obesity, type 2 diabetes, cardiovascular disease and mood disorders. One reason may involve hormonal regulation: Sleep deprivation increases hunger hormones and decreases satiety hormones, which can promote overeating, especially of high-calorie foods.

    Sleep also affects immune function and cognitive performance, so consistent rest helps us to better respond to stress and supports memory, attention and emotional regulation. Most adults benefit from seven to nine hours of sleep per night, and prioritizing regular sleep schedules can improve quality over time.

    CNN: Your fourth tip centers on diet quality, in particular cutting out ultraprocessed foods. Why is working toward a healthier diet so important, and what steps can people take to improve nutrition?

    Wen: What you eat influences your health in important ways. Ultraprocessed foods have become a dominant part of the American diet, accounting for more than half of total calories in many age groups. These foods, which include sugary drinks, packaged snacks, fast food, ready meals and sweetened cereals, are generally high in added sugars, unhealthy fats and sodium, and low in fiber, vitamins and minerals.

    High consumption of ultraprocessed foods is linked to obesity, type 2 diabetes, cardiovascular disease, and even depression and mental health conditions. Replacing ultraprocessed items with whole or minimally processed foods (vegetables, fruits, whole grains, lean proteins, legumes and nuts) supports both physical and mental health and helps stabilize energy, blood sugar and appetite.

    CNN: Your fifth tip may surprise some people: Consider social connection a core part of staying healthy.

    Wen: Human beings are social creatures, and our relationships have direct implications for our health. Strong social connections with family, friends, colleagues and community groups are associated with lower rates of anxiety and depression, better immune function, and reduced risk of chronic diseases such as hypertension and diabetes. Conversely, social isolation and loneliness have been linked to increased risk of cardiovascular disease, cognitive decline and early mortality.

    Social connection motivates healthier behaviors and provides emotional support during stress, and it encourages engagement in physical activity and other positive habits. Simple acts, such as going for walks with friends, regular catch-up phone calls, shared meals or other group activities, are good for short-term mental health. These interactions also represent a long-term investment in your mental and physical health.

    CNN: What advice do you have for people trying to follow these five tips in real life?

    Wen: The most important thing is to concentrate on consistency. These habits do not need to be done perfectly to have an impact. Small, repeated actions add up. For instance, walking most days is far better than exercising hard once a month. Going to regular checkups is crucial, rather than waiting until something feels wrong. Improving sleep by even 30 to 60 minutes a night can make a meaningful difference.

    It also helps to remember that these five areas are deeply connected. Getting enough sleep makes it easier to exercise and eat well. Regular physical activity improves sleep quality and mood. Social connection supports motivation and resilience, making it more likely that people stick with healthy routines. So instead of treating these as separate goals, think of them as reinforcing one another.

    Finally, give yourself permission to start where you are. Health is not built in January alone, and it is not derailed by a bad week or a missed goal. The aim is consistent progress. Choosing habits that feel realistic and sustainable, and returning to them when life gets busy, is what makes these five tips work over the long run.

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    Katia Hetter and CNN

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

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

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

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

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

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

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

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

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

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

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

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

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

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

    Doctor’s Note

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

    For more on TMAO, check out related posts below. 

    See the microbiome topic page for even more.

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    Michael Greger M.D. FACLM

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  • 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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  • 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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  • Ideal vs. Normal Cholesterol Levels  | NutritionFacts.org

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    Having a “normal” cholesterol level in a society where it’s normal to die from a heart attack isn’t necessarily a good thing.

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

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

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

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

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

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

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

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

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

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

    For more on cholesterol, see the related posts below.

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    Michael Greger M.D. FACLM

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  • Skinny Is the New Fat: Plenty of People Have ‘Normal’ BMI but Hidden Obesity, Study Finds

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    Your number on the bathroom scale could be misleading. New research finds that a substantial portion of people with “normal” weight still have obesity—and the higher risk of other health problems that goes along with it.

    A large, international team of scientists examined survey data from the World Health Organization. They found that roughly one in five people worldwide with a healthy body mass index (BMI) show clear signs of abdominal obesity, or excess body fat. These skinny-fat individuals were also more likely to have conditions like high blood pressure. Doctors could be missing important health issues if they only focus on their patients’ BMI, the researchers say.

    “Relying solely on BMI may be insufficient to identify these high-risk individuals and provide timely interventions,” they wrote in their paper, published this month in JAMA Network Open.

    “Normal” but obese

    BMI is calculated using a person’s weight and height, with obesity traditionally defined as having a BMI of 30 and over. In recent years, however, some doctors and patients have pushed for an expansion of what should be considered obese.

    In January, a large group of obesity experts, backed by organizations like the American Heart Association, released alternative criteria for diagnosing obesity. This criterion asks doctors to either use BMI alongside one other measurement of excess body fat or to rely on these other measurements entirely. One such measurement is waist circumference.

    In this new study, the researchers analyzed data from the WHO STEPS survey, a long-running project monitored by the WHO that allows countries to keep track of their residents’ risk factors for noncommunicable diseases, particularly those related to their lifestyle. In total, they looked at nearly a half million participants across 91 countries between 2000 and 2020.

    All in all, 21% of respondents met the threshold for “normal-weight abdominal obesity,” meaning they had a healthy BMI but a large enough waistline to be categorized as obese. Compared to people with a normal BMI and healthy waistline, this group also had a higher prevalence of hypertension, high cholesterol, and diabetes, the researchers found.

    Not just BMI

    Other recent research has highlighted the importance of moving past BMI alone.

    A study earlier this month, for instance, found that nearly 70% of Americans today meet the newer definition of obesity; this included 25% of Americans who had a normal BMI but other measures of excess body fat, such as waist circumference. This study also found that people with skinny obesity had a higher overall risk of health problems than nonobese people. That said, the authors of the latest study say theirs is the first to examine how common this form of hidden obesity is across the globe.

    Rather than wholly abandon BMI altogether, the study researchers argue that doctors should use it in combination with these other measurements to truly get a better sense of their patients’ overall cardiovascular and metabolic health.

    “Our findings suggest the need to use both BMI and waist circumference together, rather than in isolation, to provide a more complete and accurate assessment of cardiometabolic risk across diverse populations,” they wrote.

    These results should also motivate the average person to get a thorough checkup at their next physical, one that doesn’t just stop at BMI.

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    Ed Cara

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  • Semaglutide Helps Your Heart Even If the Scale Doesn’t Budge, Study Shows

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    The benefits of semaglutide, the active ingredient in popular drugs Ozempic and Wegovy, aren’t just limited to treating obesity. New research shows that semaglutide can protect people’s hearts regardless of how many pounds they lose while taking it.

    Scientists examined data from a large-scale clinical trial of people with obesity and pre-existing cardiovascular disease. Compared to people on placebo, they found, those on semaglutide were less likely to develop heart attacks and other cardiovascular problems—even when people hadn’t lost much weight at all. The results indicate that semaglutide can improve heart health in more than one way, the researchers and outside experts say.

    The findings “highlight that the cardioprotective effects of semaglutide may be independent of adiposity and weight loss,” Laurence Sperling, a preventive cardiologist at Emory University not affiliated with the study, told Gizmodo.

    Good for the heart

    Semaglutide and other GLP-1 drugs have heralded a new era of obesity (and diabetes) treatment. But for a time, it was unclear if these drugs would also improve people’s cardiovascular health, and to what extent.

    Novo Nordisk (the makers of Ozempic and Wegovy) funded a large, randomized, controlled, and double-blinded study designed to answer that open question—the SELECT trial. It involved roughly 17,000 people with obesity and a history of cardiovascular disease, who were followed for up to five years. The primary results from the SELECT trial, published almost two years ago, showed that high-dose semaglutide (the version approved as Wegovy for treating obesity) reduced people’s risk of heart attacks and other major cardiovascular events by 20% during the study period. Based on these findings, the Food and Drug Administration expanded its approval of Wegovy to also cover the prevention of cardiovascular disease in high-risk groups.

    Since obesity is known to increase the risk of heart disease, it’s easy to assume that semaglutide’s heart benefits are mostly tied to helping people lose weight. But some evidence has already suggested it’s more complicated than that. In this new research, some of the researchers who conducted the SELECT trial took a closer look at their data.

    They ultimately found no clear relationship between how much weight someone had lost early into the study (20 weeks in) and their reduced risk of cardiovascular disease. The heart-protective benefits of semaglutide were also largely the same across different baseline weight groups. In other words, someone who was overweight (a body mass index between 27 and 30) at the start of the study tended to see a similar reduction in heart disease risk as compared to someone with the highest level of obesity (a BMI over 40).

    “This gives us important information that maybe we should be looking at the indication for these drugs beyond just whether your BMI is more than 27,” Howard Weintraub, preventive cardiologist and clinical director at the Center for the Prevention of Cardiovascular Disease at NYU Langone Heart, told Gizmodo. Weintraub was one of the lead researchers of the original SELECT trial but wasn’t involved in the new research.

    The study did see an association between someone’s waist circumference throughout the study and heart disease risk. The more a person’s waist shrunk, for instance, the greater reduction in risk they had. Waist circumference is another measure of excess body fat. So semaglutide’s slimming of body fat does seem to help explain why it prevents heart disease—but only partly. The researchers estimated that just a third of semaglutide’s effect on lowering cardiovascular disease could be accounted for by a trimming waistline.

    The team’s findings were published Tuesday in The Lancet.

    Beyond weight loss

    The authors say these findings could have far-reaching implications for how semaglutide and similar GLP-1 drugs should be used. If its heart benefits are largely independent of weight loss, then it wouldn’t be helpful to limit the prescribing of these drugs based solely on BMI. People taking semaglutide who lose enough weight to no longer qualify as obese might still benefit from continuing the drug for its heart-protective effects—just as those who don’t lose much weight may, too.

    It’s even possible that GLP-1 therapy could one day be reframed as a standalone treatment for heart disease, regardless of BMI. Richard Kovacs, the interim chief of cardiovascular medicine at Indiana University’s School of Medicine, who is not involved with the study, notes that these findings could shape future guidelines in how doctors manage cardiovascular disease.

    “This is a potential guideline changer because of its robust effect here. This is a well-run, large trial that we’re all familiar with. It’s an important analysis of it,” Kovacs, who is also the chief medical officer for the American College of Cardiology, told Gizmodo. At the same time, he adds, it would probably still take more data from at least one other large randomized trial for such a change to happen easily.

    One important question left to answer is exactly how these drugs can improve our heart health. The researchers argue that some of the drug’s protection likely stems from its anti-inflammatory effects, both on excess body fat and elsewhere. But the drug’s influence on blood sugar control or our blood vessels could also be playing a part.

    Yet another question is whether these heart-bolstering effects can be seen in people who aren’t overweight or obese—something that Kovacs suspects will be put to the test soon enough. And it’s still important to study whether similar benefits are apparent with other GLP-1 medications, including newer drugs that are combining GLP-1s with other compounds.

    For now, this research is continuing to demonstrate that there’s still so much left to learn about these already game-changing drugs.

    “I don’t think we know everything that the GLP-1 agonists do yet,” Weintraub said. “So doctors will need to look at this beyond the prism of a TikTok video, where kids are looking to lose a couple of pounds to look better. That may certainly happen, but I think the cosmetic issues and the role of weight loss are just a small part of it. And as a cardiologist, I’m more motivated by the sort of findings we’re seeing here in reducing cardiovascular disease.”

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    Ed Cara

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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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  • Are We Being Misled About the Benefits and Risks of Statins?  | NutritionFacts.org

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    What is the dirty little secret of drugs for lifestyle diseases?

    Drug companies go out of their way—in direct-to-consumer ads, for example—to “present pharmaceutical drugs as a preferred solution to cholesterol management while downplaying lifestyle change.” You see this echoed in the medical literature, as in this editorial in the Journal of the American Medical Association: “Despite decades of exhortation for improvement, the high prevalence of poor lifestyle behaviors leading to elevated cardiovascular disease risk factors persists, with myocardial infarction [heart attack] and stroke remaining the leading causes of death in the United States. Clearly, many more adults could benefit from…statins for primary prevention.” Do we really need to put more people on drugs? A reply was published in the British Medical Journal: “Once again, doctors are implored to ‘get real’—stop hoping that efforts to help their patients and communities adopt healthy lifestyle habits will succeed, and start prescribing more statins. This is a self-fulfilling prophecy. Note that the author of these comments [the pro-statin editorial] disclosed receipt of funding from 11 drug companies, at least four of which produce or are developing new classes of cholesterol-lowering agents,” which make billions of dollars a year in annual sales.

    Every time the cholesterol guidelines expand the number of people eligible for statins, they’re decried as a “big kiss to big pharma.” This is understandable, since the majority of guideline panel members “had industry ties,” financial conflicts of interest. But these days, all the major statins are off-patent, so there are inexpensive generic versions. For example, the safest, most effective statin is generic Lipitor, sold as atorvastatin for as little as a few dollars a month. So, nowadays, the cholesterol guidelines are not necessarily “part of an industry plot.”

    “The US way of life is the problem, not the guidelines…” The reason so many people are candidates for cholesterol- and blood-pressure-lowering medications is that so many people are taking such terrible care of themselves. The bottom line is that “individuals must take more responsibility for their own health behaviors.” What if you are unwilling or unable to improve your diet and make lifestyle changes to bring down that risk? If your ten-year risk of having a heart attack is 7.5 percent or more and going to stay that way, then the benefits of taking a statin drug likely outweigh the risk. That’s really for you to decide, though. It’s your body, your choice.

    “Whether or not the overall benefit-harm balance justifies the use of a medication for an individual patient cannot be determined by a guidelines committee, a health care system, or even the attending physician. Instead, it is the individual patient who has a fundamental right to decide whether or not taking a drug is worthwhile.” This was recognized by some of medicine’s “historical luminaries such as Hippocrates,” but “only in recent decades has the medical profession begun to shift from a paternalistic ‘doctor knows best’ stance towards one explicitly endorsing patient-centered, evidence-based, shared decision-making.” One of the problems with communicating statin evidence to support this shared decision-making is that most doctors “have a poor understanding of concepts of risk and probability and…increasing exposure to statistics in undergraduate and postgraduate education hasn’t made much difference.” But that understanding is critical for preventive medicine. When doctors offer a cholesterol-lowering drug, “they’re doing something quite different from treating a patient who has sought help because she is sick. They’re not so much doctors as life insurance salespeople, peddling deferred benefits in exchange for a small (but certainly not negligible) ongoing inconvenience and cost. In this new kind of medicine, not understanding risk is the equivalent of not knowing about the circulation of the blood or basic anatomy. So, let’s dive in and see exactly what’s at stake.

    Below and at 3:55 in my video Are Doctors Misleading Patients About Statin Risks and Benefits? is an ad for Lipitor. When drug companies say a statin reduces the risk of a heart attack by 36 percent, that’s the relative risk.

    If you follow the asterisk I’ve circled after the “36%” in the ad, you can see how they came up with that. I’ve included it here and at 3:56 in my video. In a large clinical study, 3 percent of patients not taking the statin had a heart attack within a certain amount of time, compared to 2 percent of patients who did take the drug. So, the drug dropped heart attack risk from 3 percent to 2 percent; that’s about a one-third drop, hence the 36 percent reduced relative risk statistic. But another way to look at going from 3 percent to 2 percent is that the absolute risk only dropped by 1 percent. So, in effect, “your chance to avoid a nonfatal heart attack during the next 2 years is about 97% without treatment, but you can increase it to about 98% by taking a Crestor [a statin] every day.” Another way to say that is that you’d have to treat 100 people with the drug to prevent a single heart attack. That statistic may shock a lot of people.

    If you ask patients what they’ve been led to believe, they don’t think the chance of avoiding a heart attack within a few years on statins is 1 in 100, but 1 in 2. “On average, it was believed that most patients (53.1%) using statins would avoid a heart attack after statin treatment for 5 years.” Most patients, not just 1 percent of patients. And this “disparity between actual and expected effect could be viewed as a dilemma. On the one hand, it is not ethically acceptable for caregivers to deliberately support and maintain illusive treatment expectations by patients.” We cannot mislead people into thinking a drug works better than it really does, but on the other hand, how else are we going to get people to take their pills?

    When asked, people want an absolute risk reduction of at least about 30 percent to take a cholesterol-lowering drug every day, whereas the actual absolute risk reduction is only about 1 percent. So, the dirty little secret is that, if patients knew the truth about how little these drugs actually worked, almost no one would agree to take them. Doctors are either not educating their patients or actively misinforming them. Given that the majority of patients expect a much larger benefit from statins than they’d get, “there is a tension between the patient’s right to know about benefiting from a preventive drug and the likely reduction in uptake [willingness to take the drugs] if they are so informed,” and learn the truth. This sounds terribly paternalistic, but hundreds of thousands of lives may be at stake.

    If patients were fully informed, people would die. About 20 million Americans are on statins. Even if the drugs saved 1 in 100, that could mean hundreds of thousands of lives lost if everyone stopped taking their statins. “It is ironic that informing patients about statins would increase the very outcomes they were designed to prevent.”

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  • Should You Take Statins?  | NutritionFacts.org

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    How can you calculate your own personal heart disease risk to help you determine if you should start on a cholesterol-lowering statin drug?

    The muscle-related side effects from cholesterol-lowering statins “are often severe enough for patients to stop taking the drug. Of course, these side effects could be coincidental or psychosomatic and have nothing to do with the drug,” given that many clinical trials show such side effects are rare. “It is also possible that previous clinical trials”—funded by the drug companies themselves—“under-recorded the side effects of statins.” The bottom line is that there’s an urgent need to establish the true incidence of statin side effects.

    “What proportion of symptomatic side effects in patients taking statins are genuinely caused by the drug?” That’s the title of a journal article that reports that, even in trials funded by Big Pharma, “only a small minority of symptoms reported on statins are genuinely due to the statins,” and those taking statins are significantly more likely to develop type 2 diabetes than those randomized to placebo sugar pills. Why? We’re still not exactly sure, but statins may have the double-whammy effect of impairing insulin secretion from the pancreas while also diminishing insulin’s effectiveness by increasing insulin resistance.

    Even short-term use of statins may “approximately double the odds of developing diabetes and diabetic complications.” As shown below and at 1:49 in my video Who Should Take Statins?, fewer people develop diabetes and diabetic complications off statins over a period of about five years than those who do develop diabetes while on statins. “Of more concern, this increased risk persisted for at least 5 years after statin use stopped.”

    “In view of the overwhelming benefit of statins in the reduction of cardiovascular events,” the number one killer of men and women, any increase in risk of diabetes, our seventh leading cause of death, would be outweighed by any cardiovascular benefits, right? That’s a false dichotomy. We don’t have to choose between heart disease and diabetes. We can treat the cause of both with the same diet and lifestyle changes. The diet that can not only stop heart disease, but also reverse it, is the same one that can reverse type 2 diabetes. But what if, for whatever reason, you refuse to change your diet and lifestyle? In that case, what are the risks and benefits of starting statins? Don’t expect to get the full scoop from your doctor, as most seemed clueless about statins’ causal link with diabetes, so only a small fraction even bring it up with their patients.

    “Overall, in patients for whom statin treatment is recommended by current guidelines, the benefits greatly outweigh the risks.” But that’s for you to decide. Before we quantify exactly what the risks and benefits are, what exactly are the recommendations of current guidelines?

    How should you decide if a statin is right for you? “If you have a history of heart disease or stroke, taking a statin medication is recommended, without considering your cholesterol levels.” Period. Full stop. No discussion needed. “If you do not yet have any known cardiovascular disease,” then the decision should be based on calculating your own personal risk. If you know your cholesterol and blood pressure numbers, it’s easy to do that online with the American College of Cardiology risk estimator or the Framingham risk profiler.

    My favorite is the American College of Cardiology’s estimator because it gives you your current ten-year risk and also your lifetime risk. So, for a person with a 5.8 percent risk of having a heart attack or stroke within the next decade, if they don’t clean up their act, that lifetime risk jumps to 46 percent, nearly a flip of the coin. If they improved their cholesterol and blood pressure, though, they could reduce that risk by more than tenfold, down to 3.9 percent, as shown below and at 4:11 in my video.

    Since the statin decision is based on your ten-year risk, what do you do with that number? As you can see here and at 4:48 in my video, under the current guidelines, if your ten-year risk is under 5 percent, then, unless there are extenuating circumstances, you should just stick to diet, exercise, and smoking cessation to bring down your numbers. In contrast, if your ten-year risk hits 20 percent, then the recommendation is to add a statin drug on top of making lifestyle modifications. Unless there are risk-enhancing factors, the tendency is to stick with lifestyle changes if risk is less than 7.5 percent and to move towards adding drugs if above 7.5 percent.

    Risk-enhancing factors that your doctor should take into account when helping you make the decision include a bad family history, really high LDL cholesterol, metabolic syndrome, chronic kidney or inflammatory conditions, or persistently high triglycerides, C-reactive protein, or LP(a). You can see the whole list here and at 4:54 in my video.

    If you’re still uncertain, guidelines suggest you consider getting a coronary artery calcium (CAC) score, but even though the radiation exposure from that test is relatively low these days, the U.S. Preventive Services Task Force has explicitly concluded that the current evidence is insufficient to conclude that the benefits outweigh the harms.

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    Michael Greger M.D. FACLM

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  • Mental Illness Linked to Higher Heart Disease Risk and Shorter Lives

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    A sweeping review published in The Lancet Regional Health—Europe has drawn a direct line between mental health disorders and cardiovascular disease (CVD), showing that individuals living with psychiatric conditions face not only a higher risk of heart problems but also a shorter life expectancy. The paper, authored by researchers from Emory University, the University of Copenhagen, the University of Leeds, and others, concludes that people with depression, schizophrenia, bipolar disorder, post-traumatic stress disorder (PTSD), and anxiety live 10 to 20 years less on average, mainly due to heart disease.

    A Bidirectional Threat

    The analysis shows that the connection between mental health and cardiovascular disease is not one-directional. The stress of a heart attack or stroke can trigger psychiatric disorders, while psychiatric conditions themselves set the stage for heart disease. The risks are striking as depression raises cardiovascular risk by 72 percent, schizophrenia by 95 percent, bipolar disorder by 57 percent, PTSD by 61 percent, and anxiety disorders by 41 percent. “It is important to understand that stress, anxiety, and depression can affect your heart, just like other physical factors,” the paper noted, offering guidance for how doctors might begin crucial conversations with patients.

    A Widespread Burden

    One in four people will experience a mental health disorder in their lifetime, yet many go untreated and often receive poor cardiovascular care. “Despite having more interactions with the healthcare system, they undergo fewer physical checkups and screenings and receive fewer diagnoses and treatments for CVD and its risk factors,” the authors reported. According to 2023 U.S. survey data cited in the study, more than half of those who met the criteria for a mental health disorder had not received any treatment, with even lower rates among non-White populations.

    Shared Risk Factors

    Researchers identified a cluster of overlapping drivers—poverty, trauma, social disadvantage, substance use, and poor access to health care—that amplify the dual risks of mental illness and cardiovascular disease. Lifestyle behaviors such as smoking, poor diet, physical inactivity, and disrupted sleep patterns are also more common among people with psychiatric conditions. The biological picture is equally troubling. Dysregulation of the stress response system, inflammation, and autonomic nervous system dysfunction are all pathways through which psychiatric disorders may accelerate cardiovascular decline.

    Breaking the Cycle

    The study calls for a fundamental shift in medical practice. “For the best care, an integrated approach is needed to address the complex needs of this vulnerable population,” the authors wrote. “Such approach should offer enhanced support and interdisciplinary care encompassing mental, cardiovascular, and behavioral health, as well as consideration of the social needs and barriers to care.” Among the interventions reviewed, exercise emerged as one of the most effective treatments, improving both mood and heart health. Evidence shows that physical activity can deliver improvements on par with or greater than medication or psychotherapy for depression. Mind-body practices like yoga and mindfulness, while requiring more evaluation, also show promise for improving outcomes across both mental and cardiovascular health.

    A Call to Integrate Care

    The authors stressed that progress depends on healthcare systems breaking down the wall between physical and mental health. For decades, treatment has been siloed, with psychiatrists focusing on the mind and cardiologists on the body. That separation, the study finds, has left millions vulnerable. The authors argue for expanded insurance coverage, investment in housing and employment stability, and the inclusion of psychiatric patients in cardiovascular research. Above all, they call for integrated care models that recognize the tight link between mental and cardiovascular health.

    Global Health Priority

    The stakes are enormous. The World Health Organization has set a 2025 target to reduce the global burden of cardiovascular disease. The paper argues that this goal cannot be reached without directly addressing the disparities faced by those with psychiatric disorders.

    “Closing the disparity gap for individuals with mental health disorders would be consistent with the World Health Organization 2025 targets of reducing the global burden of CVD,” the researchers concluded. “Reducing these disparities would also uphold the rights of people with mental health disorders to achieve the highest possible level of health and to fully participate in society and the workforce.”

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    Stacy M. Brown, NNPA Newswire Senior National Correspondent and NNPA

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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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  • Cleaning Products, Air Fresheners, and Lung Function  | NutritionFacts.org

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    There is a reason the U.S. Centers for Disease Control and Prevention prohibits not only smoking but also scented or fragranced products in its buildings.

    In a recent review entitled “Damaging Effects of Household Cleaning Products on the Lungs,” researchers noted: “Adverse respiratory effects of cleaning products were first observed in populations experiencing high levels of exposure at the workplace, such as cleaners and health-care workers, with a primary focus on asthma.” Occupational use of disinfectants has also been linked to a higher risk of developing chronic obstructive pulmonary disease, such as emphysema.

    As I discuss in my video Friday Favorites: The Effects of Cleaning Products and Air Fresheners on Lung Function, we now know that, in addition to workplace exposures, “exposure to household cleaning products has also emerged as a risk factor for respiratory disorders in childhood,” as well potentially being “an important risk factor for adult asthma.” Common household cleaning spray use accounts for as many as one in seven adult asthma cases. The thought is that inhaling chemical irritants may cause injury to the airways, leading to oxidative stress and inflammation. What can we do about it?

    Well, it may be limited to sprays. Researchers found that cleaning products that were not sprayed were not associated with asthma. It’s also possible that environmentally friendly cleaning products “may represent a safer alternative,” though they may still present some risk.

    Ideally, safer cleaning products should be available. Unfortunately, the research suggesting harm has “seldom been heeded by manufacturers, vendors, and commercial cleaning companies.” I wonder how much of that is because “most of the workers exposed to cleaning products are women”—both occupationally and, perhaps, domestically.

    One of the problems may be the fragrance chemicals. One in three Americans surveyed “reported health problems, such as migraine headaches and respiratory difficulties, when exposed to fragranced products.” And, for about half of them, the problems were so bad they actually lost work over it, either “workdays or a job due to fragranced product exposure in the workplace.”

    “Results from this study reveal that over one-third of Americans suffer adverse health effects, such as respiratory difficulties and migraine headaches, from exposure to fragranced products. Of those individuals, half reported that the effects can be disabling. Yet over 99% of Americans are exposed to fragranced products at least once a week, from their own or others’ use.”

    The effect on asthmatics may be even worse, affecting closer to two-thirds of Americans. One compound that may be of particular concern is called 1,4-dichlorobenzene, also known as para-dichlorobenzene, which is found in many air fresheners, toilet bowl deodorants, and mothballs. It breaks down in the body into a compound called 2,5-dichlorophenol, which we pee out, giving researchers a reliable measure of our dichlorobenzene exposure. Not only may it make respiratory problems worse for those already suffering from compromised airways, but exposure to dichlorobenzene “at [blood] levels found in the U.S. general population, may result in reduced pulmonary [lung] function” in people who start out with normal breathing. What’s worse, higher exposures “were associated with greater prevalence of CVD [cardiovascular disease] and all cancers combined,” another reason to avoid it. We’d better read labels, right?

    Surprisingly, “no law in the US requires the disclosure of all ingredients in fragranced consumer products.” In fact, for laundry supplies, cleaning products, and air fresheners, manufacturers “do not need to list the presence of a ‘fragrance’ on either the label or MSDS,” the material safety data sheet. We won’t know until we smell it.

    I support the U.S. Centers for Disease Control and Prevention’s ban. Not only is “the use of tobacco products (including cigarettes, cigars, pipes, smokeless tobacco, or other tobacco products)…prohibited at all times,” but “scented or fragranced products are prohibited at all times in all interior space owned, rented, or leased by CDC.” I wish rideshare services like Uber and Lyft would have a similar policy. I’d even be happy with just a fragrance-free option. About one in five of more than a thousand Americans surveyed said they “would enter a business but then leave as quickly as possible if they smelled air fresheners or some fragranced product,” so it’s in the best interest of businesses, too. “Over 50% of the population would prefer that workplaces, health care facilities and professionals, hotels, and airplanes were fragrance-free.”

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    Michael Greger M.D. FACLM

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  • Eating with Hypothyroidism and Hyperthyroidism  | NutritionFacts.org

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

    Several autoimmune diseases affect the thyroid gland, and Graves’ disease and Hashimoto’s thyroiditis are the most common. Graves’ disease results in hyperthyroidism, an overactive thyroid gland. Though slaughter plants are supposed to remove animals’ thyroid glands as they “shall not be used for human food,” should some neck meat slip in, you can suffer a similar syndrome called Hamburger thyrotoxicosis. That isn’t from your body making too much thyroid hormone, though. Rather, it’s from your body eating too much thyroid hormone. Graves’ disease is much more common, and meat-free diets may be able to help with both diseases, as plant-based diets may be associated with a low prevalence of autoimmune disease in general, as observed, for example, in rural sub-Saharan Africa. Maybe it’s because plants are packed with “high amounts of antioxidants, possible protective factors against autoimmune disease,” or because they’re packed with anti-inflammatory compounds. After all, “consuming whole, plant-based foods is synonymous with an anti-inflammatory diet.” But you don’t know until you put it to the test.

    It turns out that the “exclusion of all animal foods was associated with half the prevalence of hyperthyroidism compared with omnivorous diets. Lacto-ovo [dairy-and-egg] and pesco [fish] vegetarian diets were associated with intermediate protection.” But, for those eating strictly plant-based, there is a 52 percent lower odds of hyperthyroidism.

    As I discuss in my video The Best Diet for Hypothyroidism and Hyperthyroidism, this apparent protection “may be due to the exclusion of animal foods, the [beneficial] effects of plant foods, or both. Animal foods like meat, eggs, and dairy products may contain high oestrogen concentrations, which have been linked to autoimmunity in cell and animal studies.” Or it could be because the decrease in animal protein by excluding animal foods may downregulate IGF-1, which is not just a cancer-promoting growth hormone, but may play a role in autoimmune diseases. The protection could also come from the goodness in plants that may “protect cells against autoimmune processes,” like the polyphenol phytochemicals, such as flavonoids found in plant foods. Maybe it’s because environmental toxins build up in the food chain. For example, fish contaminated with industrial pollutants, like PCBs, are associated with an increased frequency of thyroid disorders.

    But what about the other autoimmune thyroid disease, Hashimoto’s thyroiditis, which, assuming you’re getting enough iodine, is the primary cause of hypothyroidism, an underactive thyroid gland? Graves’ disease wasn’t the only autoimmune disorder that was rare or virtually unknown among those living in rural sub-Saharan Africa, eating near-vegan diets. They also appeared to have less Hashimoto’s.

    There is evidence that those with Hashimoto’s have compromised antioxidant status, but we don’t know if it’s cause or effect. But if you look at the dietary factors associated with blood levels of autoimmune anti-thyroid antibodies, animal fats seem to be associated with higher levels, whereas vegetables and other plant foods are associated with lower levels. So, again, anti-inflammatory diets may be useful. It’s no surprise, as Hashimoto’s is an inflammatory disease—that’s what thyroiditis means: inflammation of the thyroid gland.

    Another possibility is the reduction in intake of methionine, an amino acid concentrated in animal protein, thought to be one reason why “regular consumption of whole-food vegan diets is likely to have a favourable influence on longevity through decreasing the risk of cancer, coronary [heart] disease, and diabetes.” Methionine restriction improves thyroid function in mice, but it has yet to be put to the test for Hashimoto’s in humans.

    If you compare the poop of patients with Hashimoto’s to controls, the condition appears to be related to a clear reduction in the concentration of Prevotella species. Prevotella are good fiber-eating bugs known to enhance anti-inflammatory activities. Decreased Prevotella levels are also something you see in other autoimmune conditions, such as multiple sclerosis and type 1 diabetes. How do you get more Prevotella? Eat more plants. If a vegetarian goes on a diet of meat, eggs, and dairy, within as few as four days, their levels can drop. So, one would expect those eating plant-based diets to have less Hashimoto’s, but in a previous video, I expressed concern about insufficient iodine intake, which could also lead to hypothyroidism. So, which is it? Let’s find out.

    “In conclusion, a vegan diet tended to be associated with lower, not higher, risk of hypothyroid disease.” Why “tended”? The associated protection against hypothyroidism incidence and prevalence studies did not reach statistical significance. It wasn’t just because they were slimmer either. The lower risk existed even after controlling for body weight. So, researchers think it might be because animal products may induce inflammation. The question I have is: If someone who already has Hashimoto’s, what happens if they change their diet? That’s exactly what I’ll explore next.

    This is the third in a four-video series on thyroid function. The first two were Are Vegans at Risk for Iodine Deficiency? and Friday Favorites: The Healthiest Natural Source of Iodine.

    Stay tuned for the final video: Diet for Hypothyroidism: A Natural Treatment for Hashimoto’s Disease. 

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    Michael Greger M.D. FACLM

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  • 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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  • Is Creatine Safe and Efficient for High Homocysteine?  | NutritionFacts.org

    Is Creatine Safe and Efficient for High Homocysteine?  | NutritionFacts.org

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    Those on a healthy plant-based diet who have elevated homocysteine levels despite taking sufficient vitamin B12 may want to consider taking a gram a day of contaminant-free creatine.

    The average blood levels of homocysteine in men are about 1.5 points higher than in women, which may be one of the reasons men tend to be at higher risk for cardiovascular disease. Women don’t need to make as much creatine as men since they tend to have less muscle mass. That may help explain “the ‘gender gap’ in homocysteine levels.” If you remember from my previous video and as seen below and at 0:36 in The Efficacy and Safety of Creatine for High Homocysteine, in the process of making creatine, our body produces homocysteine as a by-product. So, for people with stubbornly high homocysteine levels that don’t respond sufficiently to B vitamins, “creatine supplementation may represent a practical strategy for decreasing plasma homocysteine levels”—that is, lowering the level of homocysteine into the normal range. 

    It seemed to work in rats. What about humans? Well, it worked in one study, but it didn’t seem to work in another. It didn’t work in yet another either. And, in another study, homocysteine levels were even driven up. So, this suggestion that taking creatine supplements would lower homocysteine was called into question. 

    However, all those studies were done with non-vegetarians, so they were already effectively supplementing with creatine every day in the form of muscle meat. In that way, researchers were testing higher versus lower supplementation. Those eating strictly plant-based make all their creatine from scratch, so they may be more sensitive to an added creatine source. There weren’t any studies on creatine supplementation in vegans to lower homocysteine until now. 

    Researchers took vegans who were not supplementing their diets with vitamin B12, so some of their homocysteine levels were through the roof. A few were as high as 50 when the ideal is more like under 10, for example. After taking some creatine for a few weeks, all of their homocysteine levels normalized. You can see the before and after in the graph below and at 2:04 in my video. 

    Now, they didn’t normalize, as that would have been a level under 10, but that’s presumably because they weren’t taking any B12. Give vegetarians and vegans vitamin B12 supplements, either dosing daily or once a week, and their levels normalize in a matter of months, as you can see below and at 2:20 in my video. However, the fact that you could bring down homocysteine levels with creatine alone, even without any B12, suggests—to me at least—that if your homocysteine is elevated (above 10) on a plant-based diet despite taking B12 supplements and eating greens and beans to get enough folate, it might be worth experimenting with supplementing with a gram of creatine a day for a few weeks to see if your homocysteine comes down. 

    Why just a single gram? That’s approximately how much non-vegetarians do not have to make themselves; it’s the amount that erased vegetarian discrepancies in blood and muscle, as you can see in the graph below and at 3:01 in my video, and how much has been shown to be safe in the longer term. 

    How safe is it? We can take a bit of comfort in the fact that it’s “one of the world’s best-selling dietary supplements,” with literally billions of servings taken, and the only consistently reported side effect has been weight gain, presumed to be from water retention. The only serious side effects appear to be among those with pre-existing kidney diseases taking whopping doses closer to 20 grams a day. A concern was raised that creatine could potentially form a carcinogen known as N-nitrososarcosine when it hit the acid bath of the stomach, but, when it actually put to the test, researchers found this does not appear to be a problem. 

    Bottom line: Doses of supplemental creatine up to 3 grams a day are “unlikely to pose any risk,” provided “high purity creatine” is used. However, as we all know, dietary supplements in the United States “are not regulated by the US Food and Drug Administration and may contain contaminants or variable quantities of the desired supplement” and may not even contain what’s on the label. We’re talking about “contaminants…that may be generated during the industrial production.” When researchers looked at 33 samples of creatine supplements made in the United States and Europe, they found that they all actually contained creatine, which is nice, but about half exceeded the maximum level recommended by food safety authorities for at least one contaminant. The researchers recommend that “consumers give their preference to products obtained by producers that ensure the highest quality control and certify the maximum amount of contaminants present in their products.” Easier said than done.

    Because of the potential risks, I don’t think people should take creatine supplements willy-nilly, but the potential benefits may exceed the potential risks if, again, you’re on a healthy plant-based diet and taking B12, and your homocysteine levels are still not under 10. In that case, I would suggest giving a gram a day of creatine a trying to see if it brings it down.

    The reason I did this whole video series goes back to “Risks of Ischaemic Heart Disease and Stroke in Meat Eaters, Fish Eaters, and Vegetarians Over 18 Years of Follow-Up: Results from the Prospective EPIC-Oxford Study,” which found that, although the overall cardiovascular risk is lower in vegetarians and vegans combined, they appeared to be at slightly higher stroke risk, as you can see in the graph below and at 5:06 in my video. 

    I went through a list of potential causes, as you can see at 5:11 and below, and arrived at elevated homocysteine. What’s the solution? A regular, reliable source of vitamin B12. The cheapest, easiest method that I personally use is one 2,500 mcg chewable tablet of cyanocobalamin, the most stable source of B12, once a week. (In fact, you can just use 2,000 mcg once a week.) And, again, a backup plan for those doing that but still having elevated homocysteine is an empirical trial of a single gram a day of creatine supplementation, which was shown to improve at least capillary blood flow in those who started out with high homocysteine levels. 

    In sum, plant-based diets appear to “markedly reduce risk” for multiple leading killer diseases—heart disease, type 2 diabetes, and many common types of cancer—but “an increased risk for stroke may represent an ‘Achilles heel.’ Nonetheless, vegans have the potential to achieve a truly exceptional ‘healthspan’ if they face this problem forthrightly by restricting salt intake and taking other practical measures that promote cerebrovascular [brain artery] health…Nonetheless, these considerations do not justify nutritional nihilism. On balance, low-fat vegan diets offer such versatile protection for long-term health that they remain highly recommendable. Most likely, the optimal strategy is to adopt such a [plant-based] diet, along with additional measures—appropriate food choices, exercising training, judicious supplementation [of vitamin B12]—that will mitigate the associated stroke risk.” And try not to huff whipped cream charging canister gas. Leave the “whippets” alone.

    This concludes my series on stroke risk. If you missed any of the other videos, see the related posts below.

    I’m assuming that nearly everyone taking their B12 will have normal homocysteine levels, so these last two videos are just for the rare person who doesn’t. However, those on a healthy plant-based diet with elevated homocysteine levels despite taking sufficient vitamin B12 should consider taking a gram a day of contaminant-free creatine, which should be about a quarter teaspoon.

    Where do you get contaminant-free creatine? Since regulations are so lax, you can’t rely on supplement manufacturers no matter what they say, so I would recommend going directly to the chemical suppliers that sell it to laboratories and guarantee a certain purity. Here are some examples (in alphabetical order) of some of the largest companies where you can get unadulterated creatine: Alfa Aesar, Fisher Scientific, Sigma-Aldrich, and TCI America.

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    Michael Greger M.D. FACLM

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  • Creatinine to Normalize Homocysteine in Vegetarians?  | NutritionFacts.org

    Creatinine to Normalize Homocysteine in Vegetarians?  | NutritionFacts.org

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    What are the consequences of having to make your creatine rather than relying on dietary sources?

    “Almost universally, research findings show a poor vitamin B12 status among vegetarians” because they aren’t taking vitamin B12 supplements like they should, which results in an elevation in homocysteine levels. This may explain why vegetarians were recently found to have higher rates of stroke, as you can see in the graph below and at 0:30 in my video Should Vegetarians Take Creatine to Normalize Homocysteine?.

    Of course, plant-based eating is just one of many ways to become deficient in vitamin B12. Even nitrous oxide (laughing gas) can do it in as little as two days, thanks to the recreational use of whipped cream canister gas. (I just learned about “whippits”!)

    When researchers gave vegetarians and vegans as little as 50 daily micrograms of cyanocobalamin, which is the recommended and most stable form of vitamin B12 supplement, their homocysteine levels, which had started up in the elevated zone, normalized right down into the safe zone under 10 mmol/L within only one to two months. Just 2,000 micrograms of cyanocobalamin once a week gave the same beautiful result, as you can see in the graph below and at 1:15 in my video. 

    Not always, though. In another study, even 500 daily micrograms, taken as either a sublingual chewable or swallowable regular B12 supplement, didn’t normalize homocysteine within a month, as shown below and at 1:24. Now, presumably, if the participants had kept it up, their levels would have continued to fall as they did in the 50-daily-microgram study.

    If you’re plant-based and have been taking your B12, but your homocysteine level is still too high (above 10 mmol/L), is there anything else you can do? Well, inadequate folate intake can also increase homocysteine, but folate comes from the same root as foliage. It’s found in beans and leaves, concentrated in greens. If you’re eating beans and greens, taking your B12, and your homocysteine level is still too high, I’d suggest taking 1 gram of creatine a day as an experiment, then getting your homocysteine levels retested in a month to see if it helped.

    Creatine is a compound formed naturally in the human body that is primarily involved with energy production in our muscles and brain. It’s also formed naturally in the bodies of many other animals. So, when we eat their muscles, we can also take in some of the creatine in their bodies through our diet. We only need about 2 grams of creatine a day, so those who eat meat may get about 1 gram from their diet and their body makes the rest from scratch. There are rare birth defects where you’re born without the ability to make it, in which case, you have to get it from your diet. Otherwise, our bodies can make as much as we need to maintain normal concentrations in our muscles.

    As you can see in the graph below and at 2:54 in my video, when you cut out meat, the amount of creatine floating around in your bloodstream goes down.

    However, the amount in your brain remains the same, as shown in the graph below and at 2:57. This shows that dietary creatinine doesn’t influence the levels of brain creatine, because our brain makes all the creatine we need. The level in vegetarian muscles is lower, but that doesn’t seem to affect exercise performance, as both vegetarians and meat eaters respond to creatine supplementation with similar increases in muscle power output. If vegetarian muscle creatine were insufficient, then presumably an even bigger boost would be seen. So, all that seems to happen when we eat meat is that our body doesn’t have to make as much. What does all of this have to do with homocysteine?

    As you can see below and at 3:36 in my video, in the process of making creatine, our body produces homocysteine as a waste product. Now, normally this isn’t a problem because our body has two ways to detoxify it: by using vitamin B6 or a combination of vitamin B12 and folate. Vitamin B6 is found in both plant and animal foods, and it’s rare to be deficient. But, vitamin B12 is mainly found in animal foods, so its level can be too low in those eating plant-based who don’t also supplement or eat B12-fortified foods. And, as I mentioned, folate is concentrated in plant foods, so it can be low in those who don’t regularly eat greens, beans, or folic-acid-fortified grains. Without that escape valve, homocysteine levels can get too high. However, if you’re eating a healthy plant-based diet and taking your B12 supplement, your homocysteine levels should be fine. 

    What if they aren’t? We might predict that if we started taking creatine supplements, our level of homocysteine might go down since we won’t have to make so much of it from scratch, producing homocysteine as a by-product, but you don’t know until you put it to the test. I’ll cover that next. 

    This is the eleventh in a 12-video series exploring stroke risk. If you missed the last two, see Vegetarians and Stroke Risk Factors: Vitamin B12 and Homocysteine? and How to Test for Functional Vitamin B12 Deficiency.

    This whole creatine angle was new to me. I had long worried about homocysteine levels being too high among those getting inadequate B12 intake, but I didn’t realize there was another potential mechanism for bringing it down other than with vitamin B. Let’s see if it pans out in my final video of the series: The Efficacy and Safety of Creatine for High Homocysteine. 

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    Michael Greger M.D. FACLM

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