ReportWire

Tag: lifespan

  • 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

  • Science Says Optimistic People Live Up to 12 Years Longer. Here’s How You Can Be More Positive, Hopeful, and Confident

    [ad_1]

    Warren Buffett calls it the Methuselah Effect: the financial advantages of a long life, a high rate of return, and as Buffett wrote in his 1965 Buffett Partnership letter, “a combination of both (especially recommended by this author).”

    In business terms, the benefits of living a long life don’t just apply to investing. Starting and building a business that lasts takes time. Time to develop a great team of outstanding employees. Time to make lasting connections, forge lasting partnerships, and build long-term relationships with loyal customers.

    Time matters, if only because we all hope to live as long and healthy a life as possible.

    The problem is, the recommendation bar for living a longer life can seem impossibly high. One study found you need between 150 and 300 minutes of moderate-to-vigorous physical activity to mitigate the risk of death associated with sitting. Another study found you need to jog five days a week for 30 to 40 minutes a pop for your body to have the “age progression” of someone nine years younger.

    But then there’s this. Two studies, one that spanned 10 years and the other 30 years, found that “high optimism” was linked to 11 to 15 percent longer lifespans, even after taking into account factors like health and socioeconomic status. 

    As the researchers write:

    Among psychosocial factors that appear to be potential health assets (e.g., social integration), optimism has some of the strongest and most consistent associations with a wide range of health outcomes, including reduced risk of cardiovascular events, lung function decline, and premature mortality.

    Investigators have speculated that optimism may facilitate healthier bio-behavioral processes, and ultimately longevity, because optimism directly contributes to how goals are translated into behaviors.

    Let’s unpack that. “Social integration” directly correlates with living longer; a clinical review of nearly 150 studies found that people with strong social ties had a 50 percent better chance of survival, regardless of age, sex, health status, and cause of death, than those with weaker ties.

    Make and keep a few close friends, you’ll likely live longer.

    Optimism also directly correlates with living longer, since optimistic people tend to behave differently: While everyone has goals, people who fall on the less optimistic end of the spectrum are much less likely to try to achieve their goals. Why start a journey that feels impossible? 

    On the flip side, “optimism directly contributes to how goals are translated into behaviors.” When the journey seems possible, starting feels much easier.

    All of which is good news for entrepreneurs.

    And for everyone. In his book Bounce, Matthew Syed quotes retired soccer manager Arsene Wenger on how great athletes think:

    To perform to your maximum you have to teach yourself to believe with an intensity that goes way beyond logical justification.

    No top performer has lacked this capacity for irrational optimism; no sports(person) has played to their potential without the ability to remove doubt from their mind.

    The same is true for you. Be smart, be logical, be rational and calculating, and never stop trying to improve your skills.

    But most importantly, be optimistic. Because optimism — and its effect on the way you think and work and persevere — can help you succeed in education, experience, and connectons cannot.

    Still. I know what you’re thinking. “I should be more optimistic. But it’s not like I can just flip a switch.”

    Actually, you can. Research shows that approximately 25 percent of your optimism set-point is genetic. That means 75 percent of your level of optimism can be shaped and learned.  For example, a study published in Journal of Behavior Therapy and Experimental Psychiatry found that participants who spent five minutes a day for two weeks imagining their “best possible self” (in terms of professional, relationship, and personal goals) experienced significant increases in optimism and overall life satisfaction.

    If visualization isn’t your thing (it isn’t mine), try another approach. If, as Jim Rohn says, we are the average of the five people we spend the most time with, just start spending more time with optimistic people. They’re more encouraging. They’re more supportive. Their enthusiasm will naturally rub off on you. 

    If spending time in groups isn’t your thing (it kind of isn’t mine), then take a step back and think about your mindset. Generally speaking, people fall into two camps. Those with a fixed mindset believe intelligence, ability, and skill are inborn and relatively fixed. That we are what we were born with. Someone with a fixed mindset might say, “I didn’t handle that well. I’m not cut out to be a leader.”

    People with a growth mindset believe that intelligence, ability, and skill can be developed through effort. That we are what we work to become. Someone with a growth mindset might say, “I didn’t handle that well, but next time I’ll make sure I’m more prepared.”

    People who embrace a growth mindset believe success is based on effort and application, not innate talent. 

    That makes them more optimistic. 

    And helps them live longer, healthier lives.

    The opinions expressed here by Inc.com columnists are their own, not those of Inc.com.

    [ad_2]

    Jeff Haden

    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

  • Do Fruits and Vegetables Boost Our Mood?  | NutritionFacts.org

    [ad_1]

    A randomized controlled trial investigates diet and psychological well-being.

    “Psychological health can be broadly conceptualized as comprising 2 key components: mental health (i.e., the presence of absence of mental health disorders such as depression) and psychological well-being (i.e., a positive psychological state, which is more than the absence of a mental health disorder,” and that is the focus of an “emerging field of positive psychology [that] focuses on the positive facts of life, including happiness, life satisfaction, personal strengths, and flourishing.” This may translate to physical “benefits of enhanced well-being, including improvements in blood pressure, immune competence, longevity, career success, and satisfaction with personal relationships.”

    What is “The Contribution of Food Consumption to Well-Being,” the title of an article in Annals of Nutrition & Metabolism? Studies have “linked the consumption of fruits and vegetables with enhanced well-being.” A systematic review of research found evidence that fruit and vegetable intake “was associated with increased psychological well-being.” Only an association?

    There is “a famous criticism in this area of research—namely, that deep-down personality or family upbringing might lead people simultaneously to eat in a healthy way and also to have better mental well-being, so that diet is then merely correlated with, but incorrectly gives the appearance of helping to cause, the level of well-being.” However, recent research circumvented this problem by examining if “changes in diet are correlated with changes in mental well-being”—in effect, studying the “Evolution of Well-Being and Happiness After Increases in Consumption of Fruit and Vegetables.” As you can see below and at 1:37 in my video Fruits and Vegetables Put to the Test for Boosting Mood, as individuals began eating more fruits and veggies, there was a straight-line increase in their change in life satisfaction over time.

    “Increased fruit and vegetable consumption was predictive of increased happiness, life satisfaction, and well-being. They were up to 0.24 life-satisfaction points (for an increase of 8 portions a day), which is equal in size to the psychological gain of going from unemployment to employment.” (My Daily Dozen recommendation is for at least nine servings of fruits and veggies a day.)

    That study was done in Australia. It was repeated in the United Kingdom, and researchers found the same results, though Brits may need to bump up their daily minimum consumption of fruits and vegetables to more like 10 or 11 servings a day.

    As researchers asked in the title of their paper, “Does eating fruit and vegetables also reduce the longitudinal risk of depression and anxiety?” Improved well-being is nice, but “governments and medical authorities are often interested in the determinants of major mental ill-health conditions, such as depression and high levels of anxiety, and not solely in a more typical citizen’s level of well-being”—for instance, not just life satisfaction. And, indeed, using the same dataset but instead looking for mental illness, researchers found that “eating fruit and vegetables may help to protect against future risk of clinical depression and anxiety,” as well.

    A systematic review and meta-analysis of dozens of studies found “an inverse linear association between fruit or vegetable intake and risk of depression, such that every 100-gram increased intake of fruit was associated with a 3% reduced risk of depression,” about half an apple. Yet, “less than 10% of most Western populations consume adequate levels of whole fruits and dietary fiber, with typical intake being about half of the recommended levels.” Maybe the problem is we’re just telling people about the long-term benefits of fruit intake for chronic disease prevention, rather than the near-immediate improvements in well-being. Maybe we should be advertising the “happiness’ gains.” Perhaps, but we first need to make sure they’re real.

    We’ve been talking about associations. Yes, “a healthy diet may reduce the risk of future depression or anxiety, but being diagnosed with depression or anxiety today could also lead to lower fruit and vegetable intake in the future.” Now, in these studies, we can indeed show that the increase in fruit and vegetable consumption came first, and not the other way around, but as the great enlightenment philosopher David Hume pointed out, just because the rooster crows before the dawn doesn’t mean the rooster caused the sun to rise.

    To prove cause and effect, we need to put it to the test with an interventional study. Unfortunately, to date, many studies have compared fruit to chocolate and chips, for instance. Indeed, study participants randomized to eat fruit showed significant improvements in anxiety, depression, fatigue, and emotional distress, which is amazing, but that was compared to chocolate and potato chips, as you can see below and at 4:26 in my video. Apples, clementines, and bananas making people feel better than assorted potato chips and chunky chocolate wafers is not exactly a revelation.

    This is the kind of study I’ve been waiting for: a randomized controlled trial in which young adults were randomized to one of three groups—a diet-as-usual group, a group encouraged to eat more fruits and vegetables, or a third group given two servings of fruits and vegetables a day to eat in addition to their regular diet. Those in the third group “showed improvements to their psychological well-being with increases in vitality, flourishing, and motivation” within just two weeks. However, simply educating people to eat their fruits and vegetables may not be enough to reap the full rewards, so perhaps greater emphasis needs to be placed on providing people with fresh produce—for example, offering free fruit for people when they shop. I know that would certainly make me happy!

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • What’s the Best Weight-Loss and Disease-Prevention Diet?  | NutritionFacts.org

    What’s the Best Weight-Loss and Disease-Prevention Diet?  | NutritionFacts.org

    [ad_1]

    The most effective diet for weight loss may also be the most healthful.

    Why are vegetarian diets so effective in preventing and treating diabetes? Maybe it is because of the weight loss. As I discuss in my video The Best Diet for Weight Loss and Disease Prevention, those eating more plant-based tend to be significantly slimmer. That isn’t based on looking at a cross-section of the population either. You can perform an interventional trial and put it to the test in a randomized, controlled community-based trial of a whole food, plant-based diet.

    “The key difference between this trial [of plant-based nutrition] and other approaches to weight loss was that participants were informed to eat the WFPB [whole food, plant-based] diet ad libitum and to focus efforts on diet, rather than increasing exercise.” Ad libitum means they could eat as much as they want; there was no calorie counting or portion control. They just ate. It was about improving the quality of the food rather than restricting the quantity of food. In the study, the researchers had participants focus just on a diet rather than exercising more exercise because they wanted to isolate the effects of eating more healthfully.

    So, what happened? At the start of the study, the participants were, on average, obese at nearly 210 pounds (95 kg) with an average height of about 5’5” (165 cm). Three months into the trial, they were down about 18 pounds (8 kg)—without portion restrictions and eating all the healthy foods they wanted. At six months in, they were closer to 26 pounds (12 kg) lighter. You know how these weight-loss trials usually go, though. However, this wasn’t an institutional study where the participants were locked up and fed. In this trial, no meals were provided. The researchers just informed them about the benefits of plant-based eating and encouraged them to eat that way on their own, with their own families, and in their own homes, in their own communities. What you typically see in these “free-living” studies is weight loss at six months, with the weight creeping back or even getting worse by the end of a year. But, in this study, the participants were able to maintain that weight loss all year, as you can see below and at 1:57 in my video.

    What’s more, their cholesterol got better, too, but the claim to fame is that they “achieved greater weight loss at 6 and 12 months than any other trial that does not limit energy [caloric] intake or mandate regular exercise.” That’s worth repeating. A whole food, plant-based diet achieved the greatest weight loss ever recorded at 6 and 12 months compared to any other such intervention published in the medical literature. Now, obviously, with very low-calorie starvation diets, you can drop down to any weight. “However, medically supervised liquid ‘meal replacements’ are not intended for ongoing use”—obviously, they’re just short-term fixes—“and are associated with ‘high costs, high attrition rates, and a high probability of regaining 50% or more of lost weight in 1 to 2 years.’” In contrast, the whole point of whole food, plant-based nutrition is to maximize long-term health and longevity.

    What about low-carb diets? “Studies on the effects of low-carbohydrate diets have shown higher rates of all-cause mortality”—meaning a shorter lifespan—“decreased peripheral flow-mediated dilation [artery function], worsening of coronary artery disease, and increased rates of constipation, headache, halitosis [bad breath], muscle cramps, general weakness, and rash.”

    The point of weight loss is not to fit into a smaller casket. A whole food, plant-based diet is more effective than low-carb diets for weight loss and has the bonus of having all good side effects, such as decreasing the risk of diabetes beyond just weight loss.

    “The lower risk of type 2 diabetes among vegetarians may be explained in part by improved weight status (i.e., lower BMI). However, the lower risk also may be explained by higher amounts of ingested dietary fiber and plant protein, the absence of meat- and egg-derived protein and heme iron, and a lower intake of saturated fat. Most studies report the lowest risk of type 2 diabetes among individuals who adhere to vegan diets. This may be explained by the fact that vegans, in contrast to ovo- and lacto-ovo-vegetarians, do not ingest eggs. Two separate meta-analyses linked egg consumption with a higher risk of type 2 diabetes.”

    Maybe it’s eating lower on the food chain, thereby avoiding the highest levels of persistent organic pollutants, like dioxins, PCBs, and DDT in animal products. Those have been implicated as a diabetes risk factor. Or maybe it has to do with the gut microbiome. With all that fiber in a plant-based diet, it’s no surprise there would be fewer disease-causing bugs and more protective gut flora, which can lead to less inflammation throughout the body that “may be the key feature linking the vegan gut microbiota with protective health effects”—including the metabolic dysfunction you can see in type 2 diabetes.

    The multiplicity of benefits from eating plant-based can help with compliance and family buy-in. “Whereas a household that includes people who do not have diabetes may be unlikely to enthusiastically follow a ‘diabetic diet,’ a low-fat plant-based approach is not disease-specific and has been shown to improve other chronic conditions. While the patient [with diabetes] will likely see improvement in A1C [blood sugar control], a spouse suffering from constipation or high blood pressure may also see improvements, as may children with weight issues,” if you make healthy eating a family affair.

    This is just a taste of my New York Times best-selling book, How Not to Diet. (As with all of my books, all proceeds I received went to charity.) Watch the book trailer. You may also be interested in its companion, The How Not to Diet Cookbook.

    Check out my hour-long Evidence-Based Weight Loss lecture for more. 

    [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

  • 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

  • Lose Weight by Eating More in the Morning  | NutritionFacts.org

    Lose Weight by Eating More in the Morning  | NutritionFacts.org

    [ad_1]

    A calorie is not a calorie. It isn’t only what you eat, but when you eat.

    Mice are nocturnal creatures. They eat during the night and sleep during the day. However, if you only feed mice during the day, they gain more weight than if they were fed a similar amount of calories at night. Same food and about the same amount of food, but different weight outcomes, as you can see in the graph below and at 0:18 in my video Eat More Calories in the Morning to Lose Weight, suggesting that eating at the “wrong” time may lead to disproportionate weight gain. In humans, the wrong time would presumably mean eating at night. 

    Recommendations for weight management often include advice to limit nighttime food consumption, but this was largely anecdotal until it was first studied experimentally in 2013. Researchers instructed a group of young men not to eat after 7:00 pm for two weeks. Compared to a control period during which they continued their regular habits, they ended up about two pounds lighter after the night-eating restriction. This is not surprising, given that dietary records show the study participants inadvertently ate fewer calories during that time. To see if timing has metabolic effects beyond just foreclosing eating opportunities, you’d have to force people to eat the same amount of the same food, but at different times of the day. The U.S. Army stepped forward to carry out just such an investigation.

    In their first set of experiments, Army researchers had people eat a single meal a day either as breakfast or dinner. The results clearly showed the breakfast group lost more weight, as you can see in the graph below and at 1:35 in my video. When study participants ate only once a day at dinner, their weight didn’t change much, but when they ate once a day at breakfast, they lost about two pounds a week. 

    Similar to the night-eating restriction study, this is to be expected, given that people tend to be hungrier in the evening. Think about it. If you went nine hours without eating during the day, you’d be famished, but people go nine hours without eating overnight all the time and don’t wake up ravenous. There is a natural circadian rhythm to hunger that peaks around 8:00 pm and drops to its lowest level around 8:00 am, as you can see in the graph below and at 2:09 in my video. That may be why breakfast is typically the smallest meal of the day. 

    The circadian rhythm of our appetite isn’t just behavioral, but biological, too. It’s not just that we’re hungrier in the evening because we’ve been running around all day. If you stayed up all night and slept all day, you’d still be hungriest when you woke up that evening. To untangle the factors, scientists used what’s called a “forced desynchrony” protocol. Study participants stayed in a room without windows in constant, unchanging, dim light and slept in staggered 20-hour cycles to totally scramble them up. This went on for more than a week, so the subjects ended up eating and sleeping at different times throughout all phases of the day. Then, the researchers could see if cyclical phenomena are truly based on internal clocks or just a consequence of what you happen to be doing at the time.  

    For instance, there is a daily swing in our core body temperature, blood pressure, hormone production, digestion, immune activity, and almost everything else, but let’s use temperature as an example. As you can see in the graph below and at 3:21 in my video, our body temperature usually bottoms out around 4:00 am, dropping from 98.6°F (37°C) down to more like 97.6°F (36.4°C). Is this just because our body cools down as we sleep? No. By keeping people awake and busy for 24 hours straight, it can be shown experimentally that it happens at about the same time no matter what. It’s part of our circadian rhythm, just like our appetite. It makes sense, then, if you are only eating one meal per day and want to lose weight, you’d want to eat in the morning when your hunger hormones are at their lowest level. 

    Sounds reasonable, but it starts to get weird.

    The Army scientists repeated the experiment, but this time, they had the participants eat exactly 2,000 calories either as breakfast or as dinner, taking appetite out of the picture. The subjects weren’t allowed to exercise either. Same number of calories, so the same change in weight, right? No. As you can see in the graph below and at 4:18 in my video, the breakfast-only group still lost about two pounds a week compared to the dinner-only group. Two pounds of weight loss eating the same number of calories. That’s why this concept of chronobiology, meal timing—when to eat—is so important. 

    Isn’t that wild? Two pounds of weight loss a week eating the same number of calories! That was a pretty extreme study, though. What about just shifting a greater percentage of calories to earlier in the day? That’s the subject of my next video: Breakfast Like a King, Lunch Like a Prince, Dinner Like a Pauper. First, let’s take a break from chronobiology to look at the Benefits of Garlic for Fighting Cancer and the Common Cold. Then, we’ll resume checking other videos in the related posts below.

    If you missed the first three videos in this extended series, also check out related posts below. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • The Pros of Early Time-Restricted Eating  | NutritionFacts.org

    The Pros of Early Time-Restricted Eating  | NutritionFacts.org

    [ad_1]

    Calories eaten in the morning count less than calories eaten in the evening, and they’re healthier, too.
     
    Time-restricted feeding, where you limit the same amount of eating to a narrow evening window, has benefits compared to eating in the evening and earlier in the day, but it also has adverse effects because you’re eating so much, so late, as you can see below and at 0:12 my video The Benefits of Early Time-Restricted Eating. 

    The best of both worlds was demonstrated in 2018 when researchers put time-restricted feeding into a narrow window earlier in the day. As you can see below and at 0:28 in my video, individuals who were randomized to eat the same food, but only during an 8:00 a.m. to 3:00 p.m. eating window, experienced a drop in blood pressure, oxidative stress, and insulin resistance, even when all of the study subjects were maintained at the same weight. Same food, same weight, but with different results. The drops in blood pressure were extraordinary, from 123/82 down to 112/72 in five weeks, and that is comparable to the effectiveness of potent blood-pressure drugs.


    The longest study to date on time-restricted feeding only lasted for 16 weeks. It was a pilot study without a control group that involved only eight people, but the results are still worth noting. Overweight individuals, who, like most of us, had been eating for more than 14 hours a day, were instructed to stick to a consistent 10- to 12-hour feeding window of their own choosing, as you can see below and at 1:17 in my video. On average, they were able to successfully reduce their daily eating duration by about four and a half hours and had lost seven pounds within 16 weeks. 

    They also reported feeling more energetic and sleeping better, as seen in the graph below and at 1:32 in my video. This may help explain why “all participants voluntarily expressed an interest in continuing unsupervised with the 10-11 hr time-restricted eating regimen after the conclusion of the 16-week supervised intervention.” You don’t often see that after weight-loss studies. 

    Even more remarkably, eight months later and even one year post-study, they had retained their improved energy and sleep (see in the graph below and 1:55 in my video), as well as retained their weight loss (see in the graph below and 1:58 in my video)—all from one of the simplest of interventions: sticking to a consistent 10- to 12-hour feeding window of their own choosing. 
    How did it work? Even though the study “participants were not overtly asked to change nutrition quality or quantity,” they appeared to unintentionally eat hundreds of fewer calories a day. With self-selected time frames for eating, you wouldn’t necessarily think to expect circadian benefits, but because they had been asked to keep the eating window consistent throughout the week, “metabolic jet lag could be minimized.” The thinking is that because people tend to start their days later on weekends, they disrupt their own circadian rhythm. And, indeed, it is as if they had flown a few time zones west on Friday evening, then flew back east on Monday morning, as you can see in the graph below and at 2:40 in my video. So, some of the metabolic advantages may have been due to maintaining a more regular eating schedule. 


    Early or mid-day time-restricted feeding may have other benefits as well. Prolonged nightly fasting with reduced evening food intake has been associated with lower levels of inflammation and has also been linked to better blood sugar control, both of which might be expected to lower the risk of diseases, such as breast cancer. So, data were collected on thousands of breast cancer survivors to see if nightly fasting duration made a difference. Those who couldn’t go more than 13 hours every night without eating had a 36 percent higher risk of cancer recurrence. These findings have led to the suggestion that efforts to “avoid eating after 8 pm and fast for 13 h or more overnight may be a beneficial consideration for those patients looking to decrease cancer risk and recurrence,” though we would need a randomized controlled trial to know for sure. 
     
    Early time-restricted feeding may even play a role in the health of perhaps the longest-living population in the world, the Seventh-day Adventist Blue Zone in California. As you can see in the graph below and at 3:55 in my video, slim, vegetarian, nut-eating, exercising, non-smoking Adventists live about a decade longer than the general population. 

    Their greater life expectancy has been ascribed to these healthy lifestyle behaviors, but there’s one lesser-known component that may also be playing a role. Historically, eating two large meals a day, breakfast and lunch, with a prolonged overnight fast, was a part of Adventist teachings. Today, only about one in ten Adventists surveyed were eating just two meals a day. However, most of them, more than 60 percent of them, reported that breakfast or lunch was their largest meal of the day, as you can see below and at 4:26 in my video. Though this has yet to be studied concerning longevity, frontloading one’s calories earlier in the day with a prolonged nightly fast has been associated with significant weight loss over time. This led the researchers to conclude: “Eating breakfast and lunch 5–6 h apart and making the overnight fast last 18–19 h may be a useful practical strategy” for weight control. The weight may be worth the wait. 


    For more on fasting, click here. 
     
    My big takeaway from all of the intermittent fasting research I looked at is, whenever possible, eat earlier in the day. At the very least, avoid late-night eating whenever you can. Eating breakfast like a king and lunch like a prince, with or without an early dinner for a pauper, would probably be best. 
     
    For more on fasting, fasting for disease reversal, and fasting and cancer, check the related videos below.  

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • A Look at the 5:2 Diet and the Fasting-Mimicking Diet  | NutritionFacts.org

    A Look at the 5:2 Diet and the Fasting-Mimicking Diet  | NutritionFacts.org

    [ad_1]

    What are the effects of eating only five days a week or following a fasting-mimicking diet five days a month? 
     
    Instead of eating every other day, what if you ate five days a week and fasted for the other two? As I discuss in my video The 5:2 Diet and the Fasting-Mimicking Diet Put to the Test, the available data are similar to that of alternate-day fasting: About a dozen pounds of weight loss was reported in overweight men and also reported in overweight women over six months, with no difference found between participants on the 5:2 intermittent fasting regimen and those on a continuous 500-calories-a-day restriction. The largest trial to date found an 18-pound weight loss within six months in the 5:2 group, which isn’t significantly different from the 20 pounds lost in the continuous calorie restriction group. Weight maintenance over the subsequent six months was also found to be no different.
     
    Though feelings of hunger may be more pronounced on the 5:2 pattern than on an equivalent level of daily calorie cutting, it does not seem to lead to overeating on non-fasting days. One might expect going two days without food may negatively impact mood, but no such adverse impact was noted for those fully fasting on zero calories or sticking to just two packets of oatmeal on each of the “fasting” days. (The oatmeal provides about 500 calories a day.) Like alternate-day fasting, the 5:2 fasting pattern appeared to have inconsistent effects on cognition and on preserving lean mass, and it also failed to live up to the “popular notion” that intermittent fasting would be “easier” to adhere to than daily calorie restriction. 
     
    Compared to those in the continuous-restriction control group, fewer subjects in the 5:2 pattern group expressed interest in continuing their diet after the study was over. This was attributed to quality-of-life issues, with 5:2 fasting participants citing headaches, lack of energy, and difficulty fitting the fasting days into their weekly routine. However, as you can see below and at 1:53 in my video, there has yet to be a single 5:2 diet study showing elevated LDL cholesterol compared with continuous calorie restriction at six months. Nor has it been shown for a year. This offers a potential advantage over alternate-day regimens. 

    Instead of 5:2, what about 25:5, spending five consecutive days a month on a “fasting-mimicking diet” (FMD)? Longevity researcher Valter Longo designed a five-day meal plan to try to simulate the metabolic effects of fasting by being low in protein, sugars, and calories with zero animal protein and zero animal fat. By making the diet plant-based, he hoped to lower the level of the cancer-promoting growth hormone IGF-1. He indeed accomplished this goal, along with a drop in markers of inflammation, after three cycles of his five-days-a-month program, as you can see below and at 2:33 in my video. 

    One hundred men and women were randomized to consume his fasting-mimicking diet for five consecutive days per month or maintain their regular diet the whole time. As you can see in the graph below and at 2:47 in my video, after three months, the FMD group was down about six pounds compared to the control group, with significant drops in body fat and waist circumference, accompanied by a drop in blood pressure. 

    Those who were the worst off accrued the most dramatic benefits, as seen in the graph below and at 3:04 in my video. What’s even wilder is that three further months after completion, some of the benefits appeared to persist, suggesting the effects “may last for several months.” It’s unclear, though, if those randomized to the FMD group used it as an opportunity to make positive lifestyle changes that helped maintain some of the weight loss. 


    Dr. Longo created a company to market his meal plan commercially, but, to his credit, says “he does not receive a salary or a consulting fee from the company…and will donate 100% of his shares to charity.” The whole diet appears to be mostly dehydrated soup mixes, herbal teas like hibiscus and chamomile, kale chips, nut-based energy bars, an algae-based DHA supplement, and a multivitamin dusted with vegetable powder. Why spend 50 dollars a day on a few processed snacks when you could instead eat a few hundred calories a day of real vegetables? 
     
    How interesting was that? All-you-can-eat above-ground vegetables for five days would have the same low amount of protein, sugars, and calories with zero animal protein or animal fat. But we’ll probably never know if it works as well, better, or worse because it’s hard to imagine such a study ever getting done without the financial incentive. 

    To learn more about IGF-1, see my video Flashback Friday: Animal Protein Compared to Cigarette Smoking.
     
    In this series on fasting, I’ve covered several topics, including the basics of calories and weight loss, water-only fasting, and the types of alternate-day fasting, see them all in the related videos below. 
     
    I close out the series with videos on time-restricted eating: Time-Restricted Eating Put to the Test and The Benefits of Early Time-Restricted Eating. 
     
    If you want all of the videos in one place, I’ve done three webinars on fasting—Intermittent Fasting, Fasting for Disease Reversal, and Fasting and Cancer—and they’re all available for download now. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Is Our Life Expectancy Extended by Intermittent Fasting?  | NutritionFacts.org

    Is Our Life Expectancy Extended by Intermittent Fasting?  | NutritionFacts.org

    [ad_1]

    Alternate-day modified fasting is put to the test for lifespan extension. 

    Is it true that alternate-day calorie restriction prolongs life? Doctors have anecdotally attributed improvements in a variety of disease states to alternate-day fasting, including asthma; seasonal allergies; autoimmune diseases, such as rheumatoid arthritis and osteoarthritis; infectious diseases, such as toenail fungus, periodontal disease, and viral upper respiratory tract infections; neurological conditions, such as Tourette’s syndrome and Meniere’s disease; atrial fibrillation; and menopause-related hot flashes. The actual effect on chronic disease, however, remains unclear, as I discuss in my video Does Intermittent Fasting Increase Human Life Expectancy?. 
     
    Alternate-day fasting has been put to the test for asthma in overweight adults, and researchers found that asthma-related symptoms and control significantly improved, as did the patients’ quality of life, including objective measurements of lung function and inflammation. As you can see in the graphs below and at 0:56 in my video, there were significant improvements in peak airflow, mood, and energy. Their weight also improved—about a 19-pound drop in eight weeks—so it’s hard to tease out the effects specific to the fasting beyond the benefits we might expect from weight loss by any means. 

    For the most remarkable study on alternate-day fasting, you have to go back more than a half-century. Though the 2017 cholesterol findings were the most concerning data I could find on alternate-day fasting, the most enticing was published in Spain in 1956. The title of the study translates as “The Hunger Diet on Alternate Days in the Nutrition of the Aged.” Inspired by the data being published on life extension with caloric restriction on lab rats, researchers split 120 residents of a nursing home in Madrid into two groups. Sixty residents continued to eat their regular diet, and the other half were put on an alternate-day modified fast. On the odd days of the month, they ate a regular 2,300-calorie diet; on the even days, they were given only a pound of fresh fruits and a liter of milk, estimated to add up to about 900 calories. This continued for three years. So, what happened? 
     
    As you can see below and at 2:16 in my video, throughout the study, 13 participants died in the control group, compared to only 6 in the intermittent fasting group, but those numbers were too small to be statistically significant. 

    What was highly significant, though, was the number of days spent hospitalized: Residents in the control group spent a total of 219 days in the infirmary, whereas the alternate-day fasting group only chalked up 123 days, as you can see below and at 2:38 in my video. 


    This is held up as solid evidence that alternate-day fasting may improve one’s healthspan and potentially even one’s lifespan, but a few caveats must be considered. It’s not clear how the residents were allocated to their respective groups. If, instead of being randomized, healthier individuals were inadvertently placed in the intermittent fasting group, that could skew the results in their favor. As well, it appears the director of the study was also in charge of medical decisions at the nursing home. In that role, he could have unconsciously been biased toward hospitalizing more folks in the control group. Given the progress that has been made in regulating human experimentation, it’s hard to imagine such a trial being run today, so we may never know if such impressive findings can be replicated. 

    Well, that was interesting! I had never even heard of that study until I started digging into the topic.  

    Check out my fasting series and popular videos on the subject here.  

    For more on longevity, see related videos below.



    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Flavonoid Benefits from Apple Peels  | NutritionFacts.org

    Flavonoid Benefits from Apple Peels  | NutritionFacts.org

    [ad_1]

    Peeled apples are pitted head-to-head against unpeeled apples (and spinach) in a test of artery function. 

    Regularly eating apples may contribute to a lower risk of dying prematurely. “Moderate apple consumption,” meaning one or two apples a week, “was associated with a 20% lower risk of all-cause mortality”—that is, dying from all causes put together—“whereas those who ate an apple a day had a 35% lower risk of all-cause mortality compared with women with low apple consumption.” 
     
    You’ll often hear me talking about a lower or higher risk of mortality, but what does that mean? Isn’t the risk of dying 100 percent for everyone, eventually? As you can see in my graph below and at 0:40 in my video Friday Favorites: For Flavonoid Benefits, Don’t Peel Apples, I present some survival curves to help you visualize these concepts. For example, if you follow thousands of older women over time, nearly half succumb over a period of 15 years, but that half includes those who rarely, if ever, ate apples—less than 20 apples a year. Instead, those averaging more like half a small apple a day lived longer; over the same time period, closer to 40 percent or so of them died. And, those who ate one small apple or about a quarter of a large apple a day survived even longer. 

    Why is that the case? It seems to be less the apple of one’s eye than the apple of one’s arteries. Even a fraction of an apple a day is associated with 24 percent lower odds of having severe major artery calcifications, a marker of vascular disease. You may think that’s an obvious benefit since apples are fruits and fruits are healthy, but the effect was not found for pears, oranges, or bananas. 
     
    Both of these studies were done on women, but a similar effect (with apples and onions) was found for men. We think it’s because of the flavonoids, naturally occurring phytonutrients concentrated in apples. As you can see below and at 2:02 in my video, they’re thought to improve artery function and lower blood pressure, leading to improvements in blood flow throughout the body and brain, thereby decreasing the risk of heart disease and strokes. You don’t know, though, until you put it to the test.


    When I first saw a paper on testing flavonoid-rich apples, I assumed they had selectively bred or genetically engineered a special apple. But, no. The high-flavonoid apple was just an apple with its peel, compared to the low-flavonoid apple, which was the exact same apple with its peel removed. After eating the apples, flavonoid levels in the bloodstream shot up over the next three hours in the unpeeled apple group, compared to the peeled group, as you can see below, and at 2:36 in my video. This coincided with significantly improved artery function in the unpeeled apple group compared to the peeled one. The researchers concluded that “the lower risk of CVD [cardiovascular disease] with higher apple consumption is most likely due to the high concentration of flavonoids in the skin which improve endothelial [arterial] function”—though, it could be anything in the peel. All we know is that apple peels are particularly good for us, improving artery function and lowering blood pressure. 
    Even compared to spinach? As you can see in the graph below and at 3:14 in my video, if you give someone about three-quarters of a cup of cooked spinach, their blood pressure drops within two to three hours. If you instead eat an apple with some extra peel thrown in, you get a similar effect. The researchers concluded that apples and spinach almost immediately improve artery function and lower blood pressure. 
    What’s nice about these results is that we’re talking about whole foods, not some supplement or extract. So, easily, “this could be translated into a natural and low-cost method of reducing the cardiovascular risk profile of the general population.” 

    For more about apples, see the topic page and check out the related videos below. 

    What about dried apples? See Dried Apples vs. Cholesterol. What about apple cider vinegar? Check out Flashback Friday: Does Apple Cider Vinegar Help with Weight Loss?. And what about apples going head-to-head with açai berries? See The Antioxidant Effects of Açai vs. Apples.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Restricting Calories for Longevity?  | NutritionFacts.org

    Restricting Calories for Longevity?  | NutritionFacts.org

    [ad_1]

    Though a bane for dieters, a slower metabolism may actually be a good thing.

    We’ve known for more than a century that calorie restriction can increase the lifespan of animals, and metabolic slowdown may be the mechanism. That could be why the tortoise lives ten times longer than the hare. Rabbits can live for 10 to 20 years, whereas “Harriet,” a tortoise “allegedly collected from the Galapagos Islands by Charles Darwin, was estimated to be about 176 years old when she died in 2006.” Slow and steady may win the race. 
     
    As I discuss in my video The Benefits of Calorie Restriction for Longevity, one of the ways our body lowers our resting metabolic rate is by creating cleaner-burning, more efficient mitochondria, the power plants that fuel our cells. It’s like our body passes its own fuel-efficiency standards. These new mitochondria create the same energy with less oxygen and produce less free radical “exhaust.” After all, when our body is afraid famine is afoot, it tries to conserve as much energy as it can. 
     
    Indeed, the largest caloric restriction trial to date found metabolic slowing and a reduction in free radical-induced oxidative stress, both of which may slow the rate of aging. The flame that burns twice as bright burns half as long. But, whether this results in greater human longevity is an unanswered question. Caloric restriction is often said “to extend lifespan in every species studied,” but that isn’t even true of all strains within a single species. Two authors of one article, for instance, don’t even share the same view: One doesn’t think calorie restriction will improve human longevity at all, while the other suggests that a 20 percent calorie restriction starting at age 25 and sustained for 52 years could add five years onto your life. Either way, the reduced oxidative stress would be expected to improve our healthspan. 
     
    Members of the Calorie Restriction Society, self-styled CRONies (for Calorie-Restricted Optimal Nutrition), appear to be in excellent health, but they’re a rather unique, self-selected group of individuals. You don’t really know until you put it to the test. Enter the CALERIE study, the Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy, the first clinical trial to test the effects of caloric restriction. 
     
    Hundreds of non-obese men and women were randomized to two years of 25 percent calorie restriction. They only ended up achieving half that, yet they still lost about 18 pounds and three inches off their waists, wiping out more than half of their visceral abdominal fat, as you can see in the graph below and at 2:47 in my video. 

    That translated into significant improvements in cholesterol levels, triglycerides, insulin sensitivity, and blood pressure, which you can see in the graph below and at 2:52 in my video. Eighty percent of those who were overweight when they started were normal-weight by the end of the trial, “compared with a 27% increase in those who became overweight in the control group.” 

    In the famous Minnesota Starvation Study that used conscientious objectors as guinea pigs during World War II, the study subjects suffered both physically and psychologically, experiencing depression, irritability, and loss of libido, among other symptoms. The participants started out lean, though, and had their calorie intake cut in half. The CALERIE study ended up being four times less restrictive, only about 12 percent below baseline calorie intake, and enrolled normal-weight individuals, which in the United States these days means overweight on average. As such, the CALERIE trial subjects experienced nothing but positive quality-of-life benefits, with significant improvements in mood, general health, sex drive, and sleep. They only ended up eating about 300 fewer calories a day than they had eaten at baseline. So, they got all of these benefits—the physiological benefits and the psychological benefits—just from cutting about a small bag of chips’ worth of calories from their daily diets. 
     
    What happened at the end of the trial, though? As researchers saw in the Minnesota Starvation Study and in calorie deprivation experiments done on Army Rangers, as soon as the subjects were released from restriction, they tended to rapidly regain the weight and sometimes even more, as you can see below and at 4:18 in my video. 

    The leaner they started out, the more their bodies seemed to drive them to overeat to pack back on the extra body fat, as seen in the graph below and at 4:27 in my video. In contrast, after the completion of the CALERIE study, even though their metabolism was slowed, the participants retained about 50 percent of the weight loss two years later. They must have acquired new eating attitudes and behaviors that allowed them to keep their weight down. After extended calorie restriction, for example, cravings for sugary, fatty, and junky foods may actually go down. 
    This is part of my series on calorie restriction, intermittent fasting, and time-restricted eating. See related videos below.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • WTF Fun Fact 13663 – Dog Longevity Drug

    WTF Fun Fact 13663 – Dog Longevity Drug

    [ad_1]

    For dog lovers, the prospect of a dog longevity drug sounds fantastic. Who doesn’t want their furry friends to live longer, healthier lives?

    Recent developments from a San Francisco-based biotech company, Loyal, bring this dream closer to reality. They’ve announced an anti-aging drug for dogs that has cleared its first hurdle for FDA approval. This marks a pivotal moment in veterinary medicine, as it’s the first time the FDA has shown openness to endorsing longevity drugs for pets.

    Dog Longevity Drug Holds Promise of Longer Lives for Man’s Best Friend

    Loyal’s groundbreaking drug, LOY-001, targets a growth and metabolism hormone called IGF-1. This hormone, linked with size, appears in higher levels in larger dogs and lower in smaller ones. Studies on other species suggest inhibiting IGF-1 can increase lifespans. LOY-001 is aimed at healthy dogs over seven years old and weighing more than 40 pounds. Administered every three to six months by a vet, it holds the potential to slow down the aging process in dogs.

    Parallel to this, Loyal is developing LOY-003, a daily pill form of the treatment. CEO Celine Halioua emphasizes that they’re not creating immortal dogs. The goal is to slow their rate of aging, thus maintaining a healthier state for a longer period.

    As promising as these developments are, they raise significant ethical questions, particularly concerning the quality of extended life for these animals. Veterinarian Kate Creevy, involved in a similar trial for an anti-aging drug called rapamycin, stresses the importance of ensuring that any extended lifespan is accompanied by good health and quality of life.

    Moreover, the human manipulation of dogs through selective breeding, which may have contributed to accelerated aging in larger breeds, underlines the ethical complexities in altering canine aging processes.

    Trials and the Future of Canine Health

    Loyal plans to start a large clinical trial for LOY-001 with around 1,000 large and giant dogs by either 2024 or 2025. The ultimate aim is to have a market-ready product by 2026. This trial not only represents a major step in veterinary medicine but also opens doors to understanding aging in more complex organisms like humans.

    The success of Loyal’s drug could potentially revolutionize how we approach canine health and aging. It offers a glimpse into a future where our canine companions can enjoy longer, healthier lives alongside us. However, it’s crucial to balance this scientific advancement with ethical considerations to ensure the well-being of these beloved animals.

    — WTF fun facts

    Source: “A New Drug That Could Extend Dogs’ Lives Inches Closer to Approval” — Smithsonian Magazine

    [ad_2]

    WTF

    Source link

  • Muscle Shrinkage and Bone Loss on Keto Diets?  | NutritionFacts.org

    Muscle Shrinkage and Bone Loss on Keto Diets?  | NutritionFacts.org

    [ad_1]

    Ketogenic diets have been found to undermine exercise efforts and lead to muscle shrinkage and bone loss. 
     
    An official International Society of Sports Nutrition position paper covering keto diets notes the “ergolytic effect” of keto diets on both high- and low-intensity workouts. Ergolytic is the opposite of ergogenic. Ergogenic means performance-boosting, whereas ergolytic means performance-impairing. 
     
    For nonathletes, ketosis may also undermine exercise efforts. Ketosis was correlated with increased feelings of “perceived exercise effort” and “also significantly correlated to feelings of ‘fatigue’ and to ‘total mood disturbance,’” during physical activity. “Together, these data suggest that the ability and desire to maintain sustained exercise might be adversely impacted in individuals adhering to ketogenic diets for weight loss.” 
     
    You may recall that I’ve previously discussed that shrinkage of measured muscle mass among CrossFit trainees has been reported. So, a ketogenic diet may not just blunt the performance of endurance athletes, but their strength training as well. As I discuss in my video Keto Diets: Muscle Growth and Bone Density, study participants performed eight weeks of the battery of standard upper and lower body training protocols, like bench presses, pull-ups, squats, and deadlifts, and there was no surprise. You boost muscle mass—unless you’re on a keto diet, in which case there was no significant change in muscle mass after all that effort. Those randomized to a non-ketogenic diet added about three pounds of muscle mass, whereas the same amount of weight lifting on the keto diet tended to subtract muscle mass by about 3.5 ounces on average. How else could you do eight weeks of weight training and not gain a single ounce of muscle on a ketogenic diet? Even keto diet advocates call bodybuilding on a ketogenic diet an “oxymoron.” 
     
    What about bone loss? Sadly, bone fractures are one of the side effects that disproportionately plague children placed on ketogenic diets, along with slowed growth and kidney stones. Ketogenic diets may cause a steady rate of bone loss as measured in the spine, presumed to be because ketones are acidic, so keto diets can put people in what’s called a “chronic acidotic state.” 
     
    Some of the case reports of children on keto diets are truly heart-wrenching. One nine-year-old girl seemed to get it all, including osteoporosis, bone fractures, and kidney stones, then she got pancreatitis and died. Pancreatitis can be triggered by having too much fat in your blood. As you can see in the graph below and at 2:48 in my video, a single high-fat meal can cause a quintupling of the spike in triglycerides in your bloodstream within hours of consumption, which can put you at risk for inflammation of the pancreas.  

    The young girl had a rare genetic disorder called glucose transporter deficiency syndrome. She was born with a defect in ferrying blood sugar into her brain. That can result in daily seizures starting in infancy, but a ketogenic diet can be used as a way to sneak fuel into the brain, which makes a keto diet a godsend for the 1 in 90,000 families stricken with this disorder.

    As with anything in medicine, it’s all about risks versus benefits. As many as 30 percent of patients with epilepsy don’t respond to anti-seizure drugs. Unfortunately, the alternatives aren’t pretty and can include brain surgery that implants deep electrodes through the skull or even removes a lobe of your brain. This can obviously lead to serious side effects, but so can having seizures every day. If a ketogenic diet can help with seizures, the pros can far outweigh the cons. For those just choosing a diet to lose weight, though, the cost-benefit analysis would really seem to go the other way. Thankfully, you don’t need to mortgage your long-term health for short-term weight loss. We can get the best of both worlds by choosing a healthy diet, as I discussed in my video Flashback Friday: The Weight Loss Program That Got Better with Time.
     
    Remember the study that showed the weight loss was nearly identical in those who had been told to eat the low-carb Atkins diet for a year and those told to eat the low-fat Ornish diet, as seen below and at 4:18 in my video? The authors concluded, “This supports the practice of recommending any diet that a patient will adhere to in order to lose weight.” That seems like terrible advice. 

    There are regimens out there like “The Last Chance Diet which consisted of a low-calorie liquid formula made from leftover byproducts from a slaughterhouse [that] was linked to approximately 60 deaths from cardiovascular-related events.” An ensuing failed lawsuit from one widower laid the precedent for the First Amendment protection for those who produce deadly diet books. 

    It’s possible to construct a healthy low-carb diet or an unhealthy low-fat one—a diet of cotton candy would be zero fat—but the health effects of a typical low-carb ketogenic diet like Atkins are vastly different from a low-fat plant-based diet like Ornish’s. As you can see in the graph below and at 5:26 in my video, they would have diametrically opposed effects on cardiovascular risk factors in theory, based on the fiber, saturated fat, and cholesterol contents of their representative meal plans. 

    And when actually put to the test, low-carb diets were found to impair artery function. Over time, blood flow to the heart muscle itself is improved on an Ornish-style diet and diminished on a low-carb one, as shown below and at 5:44 in my video. Heart disease tends to progress on typical weight-loss diets and actively worsens on low-carb diets, but it may be reversed by an Ornish-style diet. Given that heart disease is the number one killer of men and women, “recommending any diet that a patient will adhere to in order to lose weight” seems irresponsible. Why not tell people to smoke? Cigarettes can cause weight loss, too, as can tuberculosis and a meth habit. The goal of weight loss is not to lighten the load for your pallbearers. 

     
    For more on keto diets, see my videos on the topic. Interested in enhancing athletic performance? Check out the related videos below. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • The Safety of Keto Diets  | NutritionFacts.org

    The Safety of Keto Diets  | NutritionFacts.org

    [ad_1]

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

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

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


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

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

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

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

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

    Keto Diet to Effectively Fight Cancer?  | NutritionFacts.org

    [ad_1]

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

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

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

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

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

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

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

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

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

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

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link