ReportWire

Tag: LDL cholesterol

  • Can Onions Help with Weight Loss, Cholesterol, and PCOS? | NutritionFacts.org

    [ad_1]

    Let’s talk about treating weight loss, cholesterol, and PCOS with diet. What can an eighth of a teaspoon a day of onion powder do for body fat, and what can raw red onion do for cholesterol?

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

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

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

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

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

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

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

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

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

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

    Doctor’s Note

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

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

    [ad_1]

    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. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

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

    [ad_1]

    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.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • How Healthy Are Baruka Nuts? | NutritionFacts.org

    [ad_1]

    How do barukas, also known as baru almonds, compare with other nuts?

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

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

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

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

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

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

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

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

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

    Doctor’s Note

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

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Ideal vs. Normal Cholesterol Levels  | NutritionFacts.org

    [ad_1]

    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.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • A Longer Life on Statins?  | NutritionFacts.org

    [ad_1]

    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.” 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

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

    [ad_1]

    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.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

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

    [ad_1]

    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.”

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Should You Take Statins?  | NutritionFacts.org

    [ad_1]

    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.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Why I Don’t Recommend Moringa Leaf Powder  | NutritionFacts.org

    [ad_1]

    “Clearly, in spite of the widely held ‘belief’ in the health benefits of M. oleifera [moringa], the interest of the international biomedical community in the medicinal potential of this plant has been rather tepid.” In fact, it has been “spectacularly hesitant in exploring its nutritional and medicinal potential. This lukewarm attitude is curious, as other ‘superfoods’ such as garlic and green tea have enjoyed better reception,” but those have more scientific support. There are thousands of human studies on garlic and more than ten thousand on green tea, but only a few hundred on moringa.

    The most promising appears to be moringa’s effects on blood sugar control. Below and at 0:55 in my video The Efficacy and Side Effects of Moringa Leaf Powder, you can see the blood sugar spikes after study participants ate about five control cookies each (top line labeled “a”), compared with cookies containing about two teaspoons of moringa leaf powder into the batter (bottom line labeled “b”). Even with the same amount of sugar and carbohydrates as the control cookies, the moringa-containing cookies resulted in a dampening of the surge in blood sugar.

    Researchers found that drinking just one or two cups of moringa leaf tea before a sugar challenge “suppressed the elevation in blood glucose [sugar] in all cases compared to controls that did not receive the tea initially” and instead drank plain water. As you can see here and at 1:16 in my video, drinking moringa tea with sugar dampened blood sugar spikes after 30 minutes of consumption of the same amount of sugar without moringa tea. It’s no wonder that moringa is used in traditional medicine practice for diabetes, but we don’t really know if it can help until we put it to the test. 
    People with diabetes were given about three-quarters of a teaspoon of moringa leaf powder every day for 12 weeks and had significant improvements in measures of inflammation and long-term blood sugar control. The researchers called it a “quasi-experimental study” because there was no control group. They just took measurements before and after the study participants took moringa powder, and we know that simply being in a dietary study can lead some to eat more healthfully, whether consciously or unconsciously, so we don’t know what effect the moringa itself had. However, even in a moringa study with a control group, it’s not clear if the participants were randomly allocated. The researchers didn’t even specify how much moringa people were given—just that they took “two tablets daily with one tablet each after breakfast and dinner,” but what does “one tablet” mean? There was no significant improvement in this study, but perhaps the participants weren’t given enough moringa. Another study used a tablespoon a day and not only saw a significant drop in fasting blood sugars, but a significant drop in LDL cholesterol as well, as seen below and at 2:27 in my video. 

    Two teaspoons of moringa a day didn’t seem to help, but what about a third, making it a whole tablespoon? Apparently not, since, finally, a randomized, placebo-controlled study using one tablespoon of moringa a day failed to show any benefit on blood sugar control in people with type 2 diabetes.

    So, we’re left with a couple of studies showing potential, but most failing to show benefit. Why not just give moringa a try to see for yourself? That’s a legitimate course of action in the face of conflicting data when we’re talking about safe, simple, side–effect–free solutions, but is moringa safe? Probably not during pregnancy, as “about 80% of women folk” in some areas of the world use it to abort pregnancies, and its effectiveness for that purpose has been confirmed (at least in rats), though breastfeeding women may get a boost of about half a cup in milk production based on six randomized, blinded, placebo-controlled clinical trials.

    Just because moringa has “long been used in traditional medicine” does not in any way prove that the plant is safe to consume. A lot of horribly toxic substances, like mercury and lead, have been used in traditional medical systems the world over, but at least “no major harmful effects of M. oleifera [moringa]…have been reported by the scientific community.” More accurately, “no adverse effects were reported in any of the human studies that have been conducted to date.” In other words, no harmful effects had been reported until now. 

    Stevens-Johnson syndrome (SJS) is probably the most dreaded drug side effect, “a rare but potentially fatal condition characterized by…epidermal detachment and mucous membrane erosions.” In other words, your skin may fall off. Fourteen hours after consuming moringa, a man broke out in a rash. The same thing had happened three months earlier, the last time he had eaten moringa, causing him to suffer “extensive mucocutaneous lesions with blister formation over face, mouth, chest, abdomen, and genitalia.” “This case report suggests that consumption of Moringa leaf is better avoided by individuals who are at risk of developing SJS.” Although it can happen to anyone, HIV is a risk factor.

    My take on moringa is that the evidence of benefit isn’t compelling enough to justify shopping online for something special when you can get healthy vegetables in your local market, like broccoli, which has yet to be implicated in any genital blistering. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Does Black Cumin Seed (Nigella Sativa) Help with Weight Loss?  | NutritionFacts.org

    [ad_1]

    For three cents a day, black cumin may improve our cholesterol and triglyceride levels, blood pressure, and blood sugar control, as well as accelerate the loss of body fat.

    Black cumin, also known as Nigella sativa or simply “black seed,” is not related to cumin; it’s a member of the buttercup family rather than the carrot family. Black cumin, with its peppery flavor, is a spice commonly used in Indian and Middle Eastern cuisines, but it’s also been prized for its purported medicinal benefits. Described as “a miracle herb,” with mentions going back to the Old Testament, it was found cached in King Tut’s tomb, and it’s been reported that the “Islamic prophet Muhammad once stated that the black seed can heal every disease except death.” Only in the last 50 years or so has it been put to the test, though, culminating in more than a thousand papers published in the medical literature.

    Typical doses used in studies are one or two grams a day, which is only about a quarter teaspoon. This enables researchers to perform randomized, double-blind, placebo-controlled trials by putting the whole-food spice powder into capsules rather than studying a component or extract.

    A systematic review and meta-analysis of randomized, placebo-controlled trials found that daily black cumin consumption significantly improves cholesterol and triglycerides. Researchers also found that it not only improves blood pressure, but it also improves blood sugar control. Some of the results are quite extraordinary. For example, one study found that postmenopausal women randomized to a gram a day (less than a quarter teaspoon) of black cumin powder reduced their LDL cholesterol by 27 percent within two months, significantly better than placebo. Those are the kinds of results we’d expect from a statin drug, yet it was achieved with just a sprinkle’s worth of a simple spice. Black cumin may also help with menopausal symptoms.

    Now, it doesn’t appear to cure anything—a month after stopping the spice, cholesterol levels began to creep back up, for instance, as you can see below and at 2:00 in my video Benefits of Black Cumin Seed (Nigella Sativa) for Weight Loss—but it does appear to be a cheap, safe, effective, and delicious (if you like spice) treatment for some of our deadliest risk factors. And its side effects include loss of appetite and weight loss! 

    The latest systematic review and meta-analysis of randomized controlled weight-loss trials found that about a quarter teaspoon of black cumin powder a day does appear to cause weight loss within a span of a few months. If it really can benefit so many facets of health, why don’t we hear more about it? Why wasn’t I taught about it in medical school? Maybe because there’s little profit motive. Black cumin is just a common, natural spice. The daily dose used in most of these studies would cost about three cents a day. Stockholders won’t be thrilled to sell something that can’t be patented and costs only three pennies a day. Black cumin has become a staple in my family’s daily diet. I keep a pepper mill filled with it right on the kitchen table and grind it onto foods just as I would black pepper—easy and delicious.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Treating Hashimoto’s Disease (Hypothyroidism) Naturally with Diet  | NutritionFacts.org

    [ad_1]

    What were the results of a randomized, double-blind, placebo-controlled trial of a daily half teaspoon of powdered black cumin in Hashimoto’s patients?

    “Autoimmune thyroiditis, also known as Hashimoto’s thyroiditis, is an organ-specific autoimmune disorder,” where our body attacks our own thyroid gland, often leading to hypothyroidism due to destruction and scarring of the gland itself. We know there’s a genetic component, since identical twins are more likely to share the disease than fraternal twins. “However, even with identical twins, the concordance rate was only about 50%, emphasizing that important factors such as the environment play a role in disease pathogenesis.” Indeed, even if your identical twin, who has basically your exact same DNA, has the disease, there’s only like a flip of a coin’s chance you’ll get it. Genes load the gun, but the environment may pull the trigger.

    More than 90 synthetic chemicals were noted to show disruption of hormonal balance or thyroid dysfunction.” However, only a few such ‘pollutants show evidence that they contribute to autoimmune thyroid disease.” These include polyaromatic hydrocarbons. Smokers get a lot of them from cigarettes, but in nonsmokers, exposure comes almost entirely from food, as you can see below and at 1:18 in my video Diet for Hypothyroidism: A Natural Treatment for Hashimoto’s Disease. 

    Polycyclic aromatic hydrocarbons are primarily formed when muscle meats, such as beef, pork, fish, or chicken, are cooked using high-temperature methods, such as grilling. PBBs, polybrominated biphenols, are a type of flame-retardant chemical no longer manufactured in the United States, but are still found in the aquatic food chain. PCBs, polychlorinated biphenols, are used in a number of industrial processes and end up in people’s bodies, again, largely through the consumption of fish, but also eggs and other meats, as seen here and at 1:41 in my video.

    So, one might suspect those eating plant-based diets would have lower rates of hypothyroidism, and, indeed, despite their lower iodine intake, vegan diets tended to be protective. But they’ve never been put to the test in an interventional trial. A modification of the Paleolithic diet has been tried in Hashimoto’s patients, but it didn’t appear to improve thyroid function. What did, though, is Nigella Sativa. That name should sound familiar to anyone who’s read my book How Not to Diet or watched my live Evidence-Based Weight Loss presentation. Nigella Sativa is the scientific name for black cumin, which is just a simple spice that’s also used for a variety of medicinal purposes.

    In one study, Hashimoto’s patients received a half teaspoon of powdered black cumin every day for eight weeks in a randomized, double-blind, placebo-controlled trial. Not only was there a significant reduction in body weight, which is why I profiled it in my book, but the black cumin also significantly reduced the thyroid-stimulating hormone, a sign that thyroid function was improving. It even lowered the level of autoimmune anti-thyroid antibodies, as well as increased blood levels of thyroid hormone T3 in these Hashimoto’s patients. In addition, there was a significant drop in Interleukin 23, a proinflammatory cell signal thought to help promote the autoimmune inflammation of the thyroid, which “further confirms the anti-inflammatory nature of the plant.” And what were the side effects? There was a 17 percent drop in “bad” LDL cholesterol, as shown below and at 3:19 in my video.

    Given the fact that patients with Hashimoto’s may be at particularly high risk of developing heart disease, this is exactly the kind of side effects we’d want. “Considering these health-promoting effects of N. Sativa [black cumin], it can be considered as a therapeutic approach in the management of Hashimoto-related metabolic abnormalities.”

    A similar trial failed to find a benefit, though. Same dose, same time frame, but no significant changes in thyroid function. In contrast with the previous study, though, the study participants were not all Hashimoto’s patients, but rather hypothyroid for any reason, and that may have diluted the results. And it’s possible that telling patients to take the black cumin doses with their thyroid hormone replacement therapy may have interfered with its absorption, which is an issue similar to other foods and drugs, and why patients are normally told to take it on an empty stomach. Since there are no downsides—it’s just a simple spice—I figure, why not give it a try? The worst that can happen is you’ll have tastier food.

    Doctor’s Note:

    I get a lot of questions about thyroid function, and I am glad to have been able to do this series. If you missed any of the other videos, see the related posts below.

    For more on black cumin, see my book How Not to Diet and my presentation Evidence-Based Weight Loss. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Statins and Muscle Pain Side Effects  | NutritionFacts.org

    [ad_1]

    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.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

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

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

    [ad_1]

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • The 411 on Statins | NutritionFacts.org

    The 411 on Statins | NutritionFacts.org

    [ad_1]

    The cholesterol-lowering statin drug Lipitor has become the best-selling drug of all time, generating more than $140 billion in global sales. This class of drugs garnered so much enthusiasm in the medical community that some U.S. health authorities facetiously proposed they be added to the public water supply like fluoride is. One cardiology journal even offered the tongue-in-cheek suggestion for fast-food restaurants to offer “MacStatin” [sic] condiments along with ketchup packets to help neutralize the effects of unhealthy dietary choices.

    What Are Statins and How Do They Work?

    Statins are drugs that can lower cholesterol. They work by blocking a substance that our body requires to make cholesterol.

    Are Statins Bad for You?

    Although statins may be effective at lowering cholesterol and potentially helping to reduce the risk of heart disease and even stroke, they come with a host of possible side effects that may do much more harm than good.

    What Possible Side Effects?

    As I discuss in the video Who Should Take Statins?, muscle-related side effects from cholesterol-lowering statin drugs “are often severe enough [to make] patients stop taking [them]. Of course, these side effects could be coincidental or psychosomatic and nothing to do with the drug,” given that many clinical trials show such side effects are rare. Of course, it is also possible that studies funded by the drug companies themselves may under-report side effects. The bottom line is that there’s an urgent need to establish the true incidence of statin side effects.

    Researchers have found that 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, as well as diminishing insulin’s effectiveness by increasing insulin resistance.

    Even short-term statin use may approximately “double the odds of developing diabetes and diabetic complications,” and increased risks may persist for years after stopping statins.

    Who Should Take Statins?

    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.” Period. Full stop. No discussion needed. However, if you don’t have any known cardiovascular disease, then the decision should be based on calculating your own personal risk, which you can easily do online if you know your cholesterol and blood pressure numbers, with the American College of Cardiology risk estimator or the Framingham risk profiler. (My favorite is the ACC estimator because it gives your current ten-year risk, as well as your lifetime risk.)

    Under the current guidelines, if your ten-year risk is below 5 percent, unless there are extenuating circumstances, you should stick to diet, exercise, and smoking cessation to bring down your numbers. In contrast, if your ten-year risk hits or exceeds 20 percent, then the recommendation is to add a statin drug on top of making lifestyle modifications. Under 7.5 percent, the tendency is to stick with lifestyle changes unless there are risk-enhancing factors; above 7.5 percent, move towards adding drugs. What are the risk-enhancing factors to take into account when making the decision? A bad family history, really high LDL, metabolic syndrome, chronic kidney or inflammatory conditions, and persistently high triglycerides, C-reactive protein, or LP(a).

    Relative Risk vs. Absolute Risk

    One of the problems with communicating statin evidence to support shared decision-making is that most doctors have a poor understanding of concepts of risk, probability, and statistics, but that understanding is critical for preventive medicine. As discussed in my video Are Doctors Misleading Patients About Statin Risks and Benefits?, when doctors offer a cholesterol-lowering drug, they’re doing something quite different from treating a patient who is sick.

    When drug companies say a statin reduces the risk of a heart attack by 36 percent, that’s the relative risk. In a large clinical study, 3 percent of patients not taking the statin drug had a heart attack within a certain amount of time, compared to 2 percent taking the drug. So, the drug dropped heart attack risk from about 3 percent to 2 percent, which is about a one-third drop—hence, the 36 percent reduced relative risk statistic. Another way to look at the change from 3 percent to 2 percent is that the absolute risk only dropped 1 percent. So, in effect, one’s chance of avoiding a heart attack over the next few years may be about 97 percent without treatment, but it can be increased to about 98 percent by taking daily statin drug. Yet another way to look at it: A hundred people would need to take the drug to prevent a single heart attack.

    The Myth vs. the Reality

    If you ask patients what they were led to believe, they think the chance of avoiding a heart attack within a few years on statins is 1 in 2, when it’s really 1 in a 100. And, if you ask, they want an absolute risk reduction of at least 30 percent or so 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. So, doctors are either not educating their patients or they’re actively misinforming them.

    Weighing the Risks and Benefits of Statins

    If all those numbers are blurring together, the Mayo Clinic developed a great visualization tool. For individuals at average risk who do not take a daily statin, 10 out of 100 may have a heart attack over the next ten years. However, if all 100 people took a statin every day for those ten years, 8 would have a heart attack and 2 would be spared. That’s about a 1 in 50 chance that taking the drug would help you avert a heart attack over the next decade. What if you have no known heart disease and you take statins for a few years? The chance statins will actually save your life is about 1 in 250.

    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 maybe 5 percent, reversible liver inflammation in 2 percent, and more serious damage in perhaps 1 in 20,000 patients.

    Mayo Clinic's visualization tool for the benefits and risks of statins

    If you want a more personalized approach, calculate your ten-year risk. I cover this in more detail in my video The True Benefits vs. Side Effects of Statins.

    Alternatives to Statins?

    As I discuss in my video How Much Longer Do You Live on Statins?, taking statins can enable you to live years longer because, for every millimole per liter you drop your bad LDL cholesterol, you may live three or even six years longer, depending on which study you’re reading. A millimole in U.S. units (mg/dL) is 39 points. Drop your LDL cholesterol about 39 mg/dL or 1 mmol/L, and you could live years longer. Exercise your whole life, and you may only increase your lifespan by six months, whereas stopping smoking may net you nine months. So, how can you drop your LDL cholesterol by about 39 points? You can accomplish that by taking drugs every day, or you can achieve that within just two weeks of eating a diet packed with fruits, vegetables, and nuts.

    table showing the effects of a vegetable diet on cholesterol levels

    A plant-based diet has been shown to substantially reduce cholesterol levels and cardiovascular risk, as well as obesity, hypertension, and systemic inflammation—without negative side effects.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Eating to Lower Lp(a)  | NutritionFacts.org

    Eating to Lower Lp(a)  | NutritionFacts.org

    [ad_1]

    What should we eat—and not eat—to lower the cardiovascular disease risk factor lipoprotein(a)?

    Lipoprotein A, also known as Lp(a), is an independent, genetic, and causal factor for cardiovascular disease and heart attacks. At any level of LDL cholesterol, our risk of heart attack and stroke is two- to three-fold higher when our Lp(a) is elevated. With a high enough Lp(a) level, atherosclerosis continues to progress even if we get our LDL cholesterol way down, which may help explain why so many people continue to have heart attacks and strokes even under treatment for high cholesterol. It’s been suggested that “it would be worthwhile to check Lp(a) levels in a patient who has suffered an event but has no traditional risk factors to explain it.” What’s the point of checking it, though, if there isn’t much we can do about it? “To date, no drug to reduce circulating Lp(a) levels has been approved for clinical use.”

    Some researchers blame our lack of knowledge on the fact that Lp(a) is not found in typical lab animals, like rats and mice. It’s only found in two places in nature: primates and hedgehogs. Hedgehogs? How strange is that? No wonder Lp(a) is “an enigmatic protein that has mystified medical scientists ever since” it was first discovered more than half a century ago. But who needs mice when you have men? The level in our bloodstream is “primarily determined” by genetics. For the longest time, Lp(a) was not thought to be significantly influenced by factors such as diet. Given its similarity to LDL, though, one might assume lifestyle changes, “such as increased physical activity or the adoption of a healthy diet,” would help. “However, the effects of these interventions on Lp(a) concentrations are so far either only marginal or lacking in evidence,” but might that be because they have not tried a plant-based diet yet?

    As I discuss in my video How to Lower Lp(a) with Diet, when it comes to raising LDL cholesterol, we’ve known for years that the trans fats found in meat and dairy are just as bad as the industrially produced trans fats found in partially hydrogenated oil and junk food. But, when it comes to Lp(a), as you can see below and at 2:05 in my video, trans fats from meat and dairy appear to be even worse. 

    Just cutting out meat and following a lacto-ovo vegetarian diet did not appear to help, but, as you can see below and at 2:19 in my video, when study participants were put on a whole food, plant-based diet packed with a dozen servings of fruits and vegetables a day, their Lp(a) levels dropped by 16 percent within four weeks. 

    Of course, in those 30 days, the study subjects also lost about 15 pounds, as you can see below and at 2:28, but weight loss does not appear to affect Lp(a) levels, so you figure that it must have been due to the diet. 

    If you’re already eating a healthy plant-based diet and your Lp(a) levels are still too high, are there any particular foods that can help? As with cholesterol, even if the average total cholesterol of those eating strictly plant-based may be right on target at less than 150, with an LDL under 70, there’s a bell curve with plus or minus 30 points that fall on either side, as you can see below and at 2:45 in my video. 

    Enter the “Portfolio Diet,” which is not only plant-based, but also adds specific cholesterol-lowing foods—so, think nuts, beans, oatmeal, and berries to drag cholesterol down even further. The infographic is below and at 3:11 in my video.  

    What about Lp(a)? Nuts have been put to the test. Two and a half ounces of almonds every day dropped levels, but only by about 8 percent. That is better than another nut study, though, that found no effect at all, as you can see below and at 3:29 in my video. An additional study found “no significant changes,” and researchers reported that subjects in their study “did not experience a change in Lp(a).” Ah, nuts.  

    There is one plant that appears to drop Lp(a) levels by 20 percent, which is enough to take people exceeding the U.S. cut-off down to a more optimum level. And that plant is a fruit: Emblica officinalis, otherwise known as amla or Indian gooseberry. A randomized, double-blind, placebo-controlled study asked smokers before and after the trial about their “mouth hygiene, cough with expectoration, shortness of breath on exertion, loss of appetite, feelings of impending doom, palpitation, sleep deprivation, irritability, heartburn and tiredness,” as well as such objective measurements as their blood count, cholesterol, DNA damage, antioxidant status, and lung function. The amla extract used “showed a significant improvement compared to the placebo group in all the subjective and objective parameters tested with no reports of adverse events.” No side effects at all. That’s unbelievable! No, that’s unbelievable. And indeed, it’s completely not true.  

    Yes, subjective complaints got better in the amla group, but they got better in the placebo group, too, with arbitrary scoring systems and no statistical analysis whatsoever. And, of the two dozen objective measures, only half could be said to reach any kind of before-and-after statistical significance and only three were significant enough to account for the fact that if you measure two dozen things, a few might pop up as positive if only by chance. Any time you see this kind of spin in the abstract, which is sometimes the only part of a study people read, you should suspect some kind of conflict of interest. However, no conflicts of interest were declared by the researchers, but that’s bullsh*t, as the study was funded by the very company selling those amla supplements! Sigh.

    Anyway, one of those three significant findings was the Lp(a), so it might be worth a try in the context of a plant-based diet, which, in addition to helping with weight loss, can dramatically improve blood pressure (even after cutting down on blood pressure medications) and contribute to a 25-point drop in LDL cholesterol. Also, it may contribute to a 30 percent drop in C-reactive protein and significant reductions in other inflammatory markers for “a systemic, cardio-protective effect”—all thanks to this single dietary approach.

    You may be interested in my video on Trans Fat in Meat and Dairy. Did you know that animal products are exempted from the ban? See Banning Trans Fat in Processed Foods but Not Animal Fat.

    For more on amla and what else it can do, check out the related posts below.

    If you missed my previous video on Lp(a), watch Treating High Lp(a)—A Risk Factor for Atherosclerosis. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • How to Treat High Lp(a), an Atherosclerosis Risk Factor  | NutritionFacts.org

    How to Treat High Lp(a), an Atherosclerosis Risk Factor  | NutritionFacts.org

    [ad_1]

    What could help explain severe coronary disease in someone with a healthy lifestyle who is considered to be at low cardiovascular disease risk? A young man ended up in the ER after a heart attack and was ultimately found to have severe coronary artery disease. Given his age, blood pressure, and cholesterol, his ten-year risk of a heart attack should have only been about 2 percent, but he had a high lipoprotein(a), also known as Lp(a). In fact, it was markedly high at 80 mg/dL, which may help explain it. You can see the same in women: a 27-year-old with a heart attack with a high Lp(a). What is Lp(a), and what can we do about it? 

    As I discuss in my video Treating High Lp(a): A Risk Factor for Atherosclerosis, Lp(a) is an “underestimated cardiovascular risk factor.” It causes coronary artery disease, heart attacks, strokes, peripheral arterial disease, calcified aortic valve disease, and heart failure. And these can occur in people who don’t even have high cholesterol—because Lp(a) is cholesterol, as you can see below and at 1:15 in my video. It’s an LDL cholesterol molecule linked to another protein, which, like LDL, transfers cholesterol into the lining of our arteries, contributing to the inflammation in atherosclerotic plaques. But “this increased risk caused by Lp(a) has not yet gained recognition by practicing physicians.” 

    “The main reason for the limited clinical use of Lp(a) is the lack of effective and specific therapies to lower Lp(a) plasma levels.” Because “Lp(a) concentrations are approximately 90% genetically determined,” the conventional thinking has been you’re just kind of born with higher or lower levels and there isn’t much you can do about it. Even if that were the case, though, you might still want to know about it. If it were high, for instance, that would be all the more reason to make sure all the other risk factors that you do have more control over are as good as possible. It may help you quit smoking, for example, and motivate you to do everything you can to lower your LDL cholesterol as much as possible.  

    Lp(a) levels in the blood can vary a thousand-fold between individuals, “from less than 0.1 mg/dL to as high as 387 mg/dL.” You can see a graph of the odds of heart disease at different levels in the graph below and at 2:20 in my video. Less than 20 mg/dL is probably optimal, with greater than 30 to 50 mg/dL considered to be elevated. Even when the more conservative threshold of greater than 50 mg/dL is used, that describes about 10 to 30 percent of the global population, an estimated 1.4 billion people. So, if we’re in the one in five people with elevated levels, what can we do about it? 

    The way we know that Lp(a) causes atherosclerosis is that we can put it to the ultimate test. There is something called apheresis, which is essentially like a dialysis machine where they can take out your blood, wash out some of the Lp(a), and give your blood back to you. And when you do that, you can reverse the progression of the disease. As you can see in the graph below and at 3:06 in my video, atherosclerosis continues to get worse in the control group, but it gets better in the apheresis group. This is great for proving the role of Lp(a), but it has limited clinical application, given the “cost, limited access to centers, and the time commitment required for biweekly sessions of 2 to 4 h each.” 

    It causes a big drop in blood levels, but they quickly creep back up, so you have to keep going in, as you can see in the graph below and at 3:26 in my video, costing more than $50,000 a year. 

    There has to be a better way. We’ll explore the role diet can play, next.  

    I’ve been wanting to do videos about Lp(a), but there just wasn’t much we could do about it until now. So, how do we lower Lp(a) with diet? Stay tuned for the exciting conclusion in my next video.

    What can we do to minimize heart disease risk? My video How Not to Die from Heart Disease is a good starting point. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Irregular Meals, Night Shifts, and Metabolic Harms  | NutritionFacts.org

    Irregular Meals, Night Shifts, and Metabolic Harms  | NutritionFacts.org

    [ad_1]

    What can shift workers do to moderate the adverse effects of circadian rhythm disruption?

    Shift workers may have higher rates of death from heart disease, stroke, diabetes, dementia, and cardiovascular disease, as well as higher rates of death from cancer. Graveyard shift, indeed! But, is it just because they’re eating out of vending machines or not getting enough sleep? Highly controlled studies have recently attempted to tease out these other factors by putting people on the same diets with the same sleep—but at the wrong time of day. Redistributing eating to the nighttime resulted in elevated cholesterol and increases in blood pressure and inflammation. No wonder shift workers are at higher risk. Shifting meals to the night in a simulated night-shift protocol effectively turned about one-third of the subjects prediabetic in just ten days. Our bodies just weren’t designed to handle food at night, as I discuss in my video The Metabolic Harms of Night Shifts and Irregular Meals.

    Just as avoiding bright light at night can prevent circadian misalignment, so can avoiding night eating. We may have no control over the lighting at our workplace, but we can try to minimize overnight food intake, which has been shown to help limit the negative metabolic consequences of shift work. When we finally do get home in the morning, though, we may disproportionately crave unhealthy foods. In one experiment, 81 percent of participants in a night-shift scenario chose high-fat foods, such as croissants, out of a breakfast buffet, compared to just 43 percent of the same subjects during a control period on a normal schedule.

    Shiftwork may also leave people too fatigued to exercise. But, even at the same physical activity levels, chronodisruption can affect energy expenditure. Researchers found that we burn 12 to 16 percent fewer calories while sleeping during the daytime compared to nighttime. Just a single improperly-timed snack can affect how much fat we burn every day. Study subjects eating a specified snack at 10:00 am burned about 6 more grams of fat from their body than on the days they ate the same snack at 11:00 pm. That’s only about a pat and a half of butter’s worth of fat, but it was the identical snack, just given at a different time. The late snack group also suffered about a 9 percent bump in their LDL cholesterol within just two weeks.

    Even just sleeping in on the weekends may mess up our metabolism. “Social jetlag is a measure of the discrepancy in sleep timing between our work days and free days.” From a circadian rhythm standpoint, if we go to bed late and sleep in on the weekends, it’s as if we flew a few time zones west on Friday evening, then flew back Monday morning. Travel-induced jet lag goes away in a few days, but what might the consequences be of constantly shifting our sleep schedule every week over our entire working career? Interventional studies have yet put it to the test, but population studies suggest that those who have at least an hour of social jet lag a week (which may describe more than two-thirds of people) have twice the odds of being overweight. 

    If sleep regularity is important, what about meal regularity? “The importance of eating regularly was highlighted early by Hippocrates (460–377 BC) and later by Florence Nightingale,” but it wasn’t put to the test until the 21st century. A few population studies had suggested that those eating meals irregularly were at a metabolic disadvantage, but the first interventional studies weren’t published until 2004. Subjects were randomized to eat their regular diets divided into six regular eating occasions a day or three to nine daily occasions in an irregular manner. Researchers found that an irregular eating pattern can cause a drop in insulin sensitivity and a rise in cholesterol levels, as well as reduce the calorie burn immediately after meals in both lean and obese individuals. The study participants ended up eating more, though, on the irregular meals, so it’s difficult to disentangle the circadian effects. The fact that overweight individuals may overeat on an irregular pattern may be telling in and of itself, but it would be nice to see such a study repeated using identical diets to see if irregularity itself has metabolic effects.

    Just such a study was published in 2016: During two periods, people were randomized to eat identical foods in a regular or irregular meal pattern. As you can see in the graph below and at 4:47 in my video, during the irregular period, people had impaired glucose tolerance, meaning higher blood sugar responses to the same food.

    They also had lower diet-induced thermogenesis, meaning the burning of fewer calories to process each meal, as seen in the graph below and at 4:55 in my video.

    The difference in thermogenesis only came out to be about ten calories per meal, though, and there was no difference in weight changes over the two-week periods. However, diet-induced thermogenesis can act as “a satiety signal.” The extra work put into processing a meal can help slake one’s appetite. And, indeed, “lower hunger and higher fullness ratings” during the regular meal period could potentially translate into better weight control over the long term. 

    The series on chronobiology is winding down with just two videos left in this series: Shedding Light on Shedding Weight and Friday Favorites: Why People Gain Weight in the Fall.

    If you missed any of the other videos, see the related posts below. 
     

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Syncing Your Brain and Body Clocks  | NutritionFacts.org

    Syncing Your Brain and Body Clocks  | NutritionFacts.org

    [ad_1]

    Exposure to bright light synchronizes the central circadian clock in our brain, whereas proper meal timing helps sync the timing of different clock genes throughout the rest of our body. 
     
    One of the most important breakthroughs in recent years has been the discovery of “peripheral clocks.” We’ve known for decades about the central clock—the so-called suprachiasmatic nucleus. It sits in the middle of our brain right above the place where our optic nerves cross, allowing it to respond to day and night. Now we also know there are semi-autonomous clocks in nearly every organ of our body. Our heart runs on a clock, our lungs run on one, and so do our kidneys, for instance. In fact, up to 80 percent of the genes in our liver are expressed in a circadian rhythm.

    Our entire digestive tract is, too. The rate at which our stomach empties, the secretion of digestive enzymes, and the expression of transporters in our intestinal lining for absorbing sugar and fat all cycle around the clock. So, too, does the ability of our body fat to sop up extra calories. The way we know these cycles are driven by local clocks, rather than being controlled by our brain, is that you can take surgical biopsies of fat, put them in a petri dish, and watch them continue to rhythm away.

    All of this clock talk is not just biological curiosity. Our health may depend on keeping all of them in sync. “Imagine a child playing on a swing.” Picture yourself pushing, but you become distracted by what’s going on around you in the playground and stop paying attention to the timing of the push. So, you forget to push or you push too early or too late. What happens? Out of sync, the swinging becomes erratic, slows, or even stops. That is what happens when we travel across multiple time zones or have to work the night shift.

    The “pusher” in this case is the light cues falling onto our eyes. Our circadian rhythm is meant to get a “push” from bright light every morning at dawn, but if the sun rises at a different time or we’re exposed to bright light in the middle of the night, this can push our cycle out of sync and leave us feeling out of sorts. That’s an example of a mismatch between the external environment and our central clock. Problems can also arise from a misalignment between the central clock in our brain and all the other organ clocks throughout our body. An extreme illustration of this is a remarkable set of experiments suggesting that even our poop can get jet lag.

    As you can see below and at 2:31 in my video How to Sync Your Central Circadian Clock to Your Peripheral Clocks, our microbiome seems to have its own circadian rhythm.

    Even though the bacteria are down where the sun doesn’t shine, there’s a daily oscillation in both bacterial abundance and activity in our colon, as you can see in the graph below and at 2:43 in my video. Interesting, but who cares? We all should. 

    Check this out: If you put people on a plane and fly them halfway around the world, then feed their poop to mice, those mice grow fatter than mice fed preflight feces. The researchers suggest the fattening flora was a consequence of “circadian misalignment.” Indeed, several lines of evidence now implicate “chronodisruption”—the state in which our central and peripheral clocks diverge out of sync—as playing a role in conditions such as premature aging and cancer, as well as ranging to others like mood disorders and obesity.

    Exposure to bright light is the synchronizing swing pusher for our central clock. What drives our internal organ clocks that aren’t exposed to daylight? Food intake. That’s why the timing of our meals may be so important. Researchers removed all external timing cues by keeping study participants under constant dim light and found that you could effectively decouple central rhythms from peripheral ones just by shifting meal times. They took blood draws every hour and biopsies of the subjects’ fat every six hours to demonstrate the resulting metabolic disarray.

    Just as morning light can help sync the central clock in our brain, morning meals can help sync our peripheral clocks throughout the rest of our body. Skipping breakfast disrupts the normal expression and rhythm of these clock genes themselves, which coincides with adverse metabolic effects. Thankfully, they can be reversed. Take a group of habitual breakfast-skippers and have them eat three meals at 8:00 am, 1:00 pm, and 6:00 pm, and their cholesterol and triglycerides improve, compared to taking meals five hours later at 1:00 pm, 6:00 pm, and 11:00 pm. There is a circadian rhythm to cholesterol synthesis in the body, too, which is also “strongly influenced by food intake.” This is evidenced by the 95 percent drop in cholesterol production in response to a single day of fasting. That’s why a shift in meal timing of just a few hours can result in a 20-point drop in LDL cholesterol, thanks to eating earlier meals, as you can see below and at 5:00 in my video. 

    If light exposure and meal timing help keep everything synced, what happens when our circumstances prevent us from sticking to a normal daytime cycle? We’ll find out in The Metabolic Harms of Night Shifts and Irregular Meals. If you’re just coming into the series, be sure to check out the related posts below.  

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Circadian Rhythms and Our Blood Sugar Levels  | NutritionFacts.org

    Circadian Rhythms and Our Blood Sugar Levels  | NutritionFacts.org

    [ad_1]

    The same meal eaten at the wrong time of day can double blood sugar. 

    We’ve known for more than half a century that our glucose tolerance—the ability of our body to keep our blood sugars under control—declines as the day goes on. As you can see in the graph below and at 0:25 in my video How Circadian Rhythms Affect Blood Sugar Levels, if you hook yourself up to an IV and drip sugar water into your vein at a steady pace throughout the day, your blood sugars will start to go up at about 8:00 pm, even though you haven’t eaten anything and the infusion rate didn’t change.

    The same amount of sugar is going into your system every minute, but your ability to handle it deteriorates in the evening before bouncing right back in the morning. A meal eaten at 8:00 pm can cause twice the blood sugar response as an identical meal eaten at 8:00 am, as shown in the graph below and at 0:51 in my video. It’s as if you ate twice as much. Your body just isn’t expecting you to be eating when it’s dark outside. Our species may have only discovered how to use fire about a quarter million years ago. We just weren’t built for 24-hour diners. 

    One of the tests for diabetes is called the glucose tolerance test, which sees how fast our body can clear sugar from our bloodstream. You swig down a cup of water with about four and a half tablespoons of regular corn syrup mixed in, then have your blood sugar measured two hours later. By that point, your blood sugar should be under 140 mg/dL. Between 140 and 199 is considered to be a sign of prediabetes, and 200 and up is a sign of full-blown diabetes, as you can see in the graph below and at 1:37 in my video. 

    The circadian rhythm of glucose tolerance is so powerful that a person can test normal in the morning but as a prediabetic later in the day. Prediabetics who average 163 mg/dL at 7:00 am may test out as frank diabetics at over 200 mg/dL at 7:00 pm, as you can see in the graph below and at 1:53 in my video. 

    Choosing lower glycemic foods may help promote weight loss, but timing is critical. Due to this circadian pattern in glucose tolerance, a low-glycemic food at night can cause a higher blood sugar spike than a high-glycemic food eaten in the morning, as you can see below and at 2:05 in my video.

    We’re so metabolically crippled at night that researchers found that eating a bowl of All Bran cereal at 8:00 pm caused as high a blood sugar spike as eating Rice Krispies at 8:00 am, as you can see in the graph below and at 2:23 in my video.

    High glycemic foods at night would seem to represent the worst of both worlds. So, if you’re going to eat refined grains and sugary junk, it might be less detrimental in the morning, as you can see in the graph below and at 2:32 in my video.  

    The drop in glucose tolerance over the day could therefore help explain the weight-loss benefits of frontloading calories towards the beginning of the day. Even just taking lunch earlier versus later may make a difference, as you can see in the graph below and at 2:48 in my video.

    People randomized to eat a large lunch at 4:30 pm suffered a 46 percent greater blood sugar response compared to an identical meal eaten just a few hours earlier at 1:00 pm. A meal at 7:00 am can cause 37 percent lower blood sugars than an identical meal at 1:00 pm, as you can see below, and at 3:04 in my video.

    Now, there doesn’t seem to be any difference between a meal at 8:00 pm and the same meal at midnight; they both seem to be too late, as you can see below, and at 3:15 in my video.

    But, eating that late, at midnight or even 11:00 pm, can so disrupt your circadian rhythm that it can mess up your metabolism the next morning, resulting in significantly higher blood sugars after breakfast, compared to eating the same dinner at 6:00 pm the evening before, as shown in the graph below and at 3:32 in my video.

    So, these revelations of chronobiology bring the breakfast debate full circle. Skipping breakfast not only generally fails to cause weight loss, but it worsens overall daily blood sugar control in both diabetic individuals and people who are not diabetic, as you can see in the graph below and at 3:44 in my video.

    Below and at 3:53, you can see a graph showing how the breakfast skippers have higher blood sugars even while they’re sleeping 20 hours later. This may help explain why those who skip breakfast appear to be at higher risk of developing type 2 diabetes in the first place. 

    Breakfast skippers also tend to have higher rates of heart disease, as well as having higher rates of atherosclerosis, in general. Is this just because “skipping breakfast tends to cluster with other unhealthy choices, including smoking” and sicklier eating habits overall? The link between skipping breakfast and heart disease—even premature death in general—seems to survive attempts to control for these confounding factors, but you don’t really know until you put it to the test.

    Does skipping breakfast lead to higher cholesterol, for example? Yes, researchers found a significant rise in LDL (bad) cholesterol in study participants randomized to skip breakfast; they were about 10 points higher within just two weeks, as you can see below and at 4:45 in my video.

    The Israeli study with the caloric distribution of 700 calories for breakfast, 500 for lunch, and 200 for dinner that I’ve discussed previously found that the triglycerides of the king-prince-pauper group (those eating more at breakfast versus dinner) got significantly better—a 60-point drop—while those of the pauper-prince-king group got significantly worse (a 26-point rise). So, consuming more calories in the morning relative to the evening may actually have a triple benefit: more weight loss, better blood sugar control, and lower heart disease risk, as you can see below and at 5:18 in my video. 

    If you’re going to skip any meal, whether you’re practicing intermittent fasting or time-restricted feeding (where you try to fit all of your food intake into a certain time window each day), it may be safer and more effective to skip dinner rather than breakfast.

    I’m back with the next installment of the chronobiology series! I previously explored eating breakfast for weight loss (Is Breakfast the Most Important Meal for Weight Loss? and Is Skipping Breakfast Better for Weight Loss?), introduced chronobiology (How Circadian Rhythms Can Control Your Health and Weight), and looked at the science on eating more in the mornings than the evenings (Eat More Calories in the Morning to Lose Weight, Breakfast Like a King, Lunch Like a Prince, Dinner Like a Pauper, and Eat More Calories in the Morning Than the Evening).

    Next, you’ll see How to Sync Your Central Circadian Clock to Your Peripheral Clocks.

    The series will wrap up in the next couple of weeks. See videos and blogs in related posts below.

    Note: The Israeli 700/500/200 study that I mentioned is detailed in the Breakfast Like a King, Lunch Like a Prince, Dinner Like a Pauper video if you want to know more. Also, check the corresponding blog in related posts. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link