ReportWire

Tag: processed foods

  • Could Your Pills and Food Be Causing a Leaky Gut? | NutritionFacts.org

    [ad_1]

    Common drugs, foods, and beverages can disrupt the integrity of our intestinal barrier, causing a leaky gut.

    Intestinal permeability, the leakiness of our gut, may be a new target for both disease prevention and therapy. With all its tiny folds, our intestinal barrier covers a surface of more than 4,000 square feet—that’s bigger than a tennis court—and requires about 40% of our body’s total energy expenditure to maintain.

    There is growing evidence implicating “the disruption of intestinal barrier integrity” in the development of a number of conditions, including celiac disease and inflammatory bowel disease. Researchers measured intestinal permeability using blue food coloring. It remained in the gut of healthy participants but was detected in the blood of extremely sick patients with sepsis with a damaged gut barrier. You don’t have to end up in the ICU to develop a leaky gut, though. Simply taking some aspirin or ibuprofen can do the trick.

    Indeed, taking two regular aspirin (325 mg tablets) or two extra-strength aspirin (500 mg tablets) just once can increase the leakiness of our gut. These results suggest that even healthy people should be cautious when using aspirin, as it may cause gastrointestinal barrier dysfunction.

    What about buffered aspirin, an aspirin-antacid combination which theoretically “buffers” gastrointestinal irritation? It apparently doesn’t make any difference: Regular aspirin and Bufferin both produced multiple erosions in the inner lining of the stomach and intestine. Researchers put a scope down people’s throats and saw extensive erosions and redness inside 90% of those who took aspirin or Bufferin at their recommended doses. How many hours does it take for the damage to occur? None. It can happen within just five minutes. Acetaminophen, sold as Tylenol in the United States, may not lead to gastrointestinal damage and could be a better choice, unless you have problems with your liver. And rather than making things better, vitamin C supplements appeared to make the aspirin-induced increase in gut leakiness even worse.

    Interestingly, this may be why NSAID drugs like aspirin, ibuprofen, and naproxen “are involved in up to 25% of food-induced anaphylaxis.” In other words, they are associated with over 10-fold higher odds of life-threatening food allergy attacks, presumably because these drugs increase the leakiness of the intestinal barrier, causing tiny food particles to slip into the bloodstream. But can exercise increase risk, too?

    Strenuous exercise—for instance, an hour at 70% maximum capacity—may divert so much blood to the muscles and away from our internal organs that it may cause transient injury to our intestines, causing mild gut leakiness. But this can be aggravated if athletes take ibuprofen or any other NSAID drugs, which is unfortunately all too common.

    Alcohol can also be a risk factor for food allergy attacks for the same reason—increasing gut leakiness. But cut out the alcohol, and our gut might heal up.

    What other dietary components can make a difference? Elevated consumption of saturated fat, which is found in meat, dairy, and junk food, can cause the growth of bad bacteria that make the rotten-egg gas hydrogen sulfide, which can degrade the protective mucus layer. You can see the process below and at 3:21 in my video Avoid These Foods to Prevent a Leaky Gut.

    It is said to be clear that high-fat diets in general have a negative impact on intestinal health by “disrupting the intestinal barrier system through a variety of mechanisms,” but most of the vast array of studies that cited the negative effects were done on lab animals or in a petri dish. Are people affected the same way? You don’t know for sure until you put it to the test.

    Rates of obesity and other cardiometabolic disorders have increased rapidly alongside a transition from traditional lower-fat diets to higher-fat diets. We know a disturbance in our good gut flora has been shown to be associated with a high risk of many of these same diseases, and studies using rodents suggest that a high-fat diet “unbalances” the microbiome while impairing the gut barrier, resulting in disease. To connect all the dots, though, we need a human interventional trial—and we got one: a six-month randomized controlled-feeding trial on the effects of dietary fat on gut microbiota. It found that, indeed, higher fat consumption was associated with unfavorable changes in the gut microbiome and proinflammatory factors in the blood. Note that this wasn’t even primarily saturated fat, such as from meat and dairy. The researchers just replaced refined carbohydrates with refined fats—swapping out white rice and wheat flour for soybean oil. These findings suggest that countries westernizing their diets should advise against increasing dietary fat intake, while countries that have already adopted such diets should consider cutting down.

    Doctor’s Note

    For more on leaky gut, check out The Leaky Gut Theory of Why Animal Products Cause Inflammation and How to Heal a Leaky Gut with Diet.

    I also talked about gut leakiness in my SIBO video: Friday Favorites: Tests, Fiber, and Low FODMAP for Small Intestinal Bacterial Overgrowth (SIBO).

    [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

  • Chlorohydrin 3-MCPD in Bragg’s Liquid Aminos | NutritionFacts.org

    [ad_1]

    Chlorohydrin contaminates hydrolyzed vegetable protein products and refined oils.

    In 1978, chlorohydrins were found in protein hydrolysates. What does that mean? Proteins can be broken down into amino acids using a chemical process called hydrolysis, and free amino acids (like glutamate) can have taste-enhancing qualities. That’s how inexpensive soy sauce and seasonings like Bragg’s Liquid Aminos are made. This process requires high heat, high pressure, and hydrochloric acid to break apart the protein. The problem is that when any residual fat is exposed to these conditions, it can form toxic compounds called chlorohydrins, which are toxic at least to mice and rats.

    Chlorohydrins like 3-MCPD are considered “a worldwide problem of food chemistry,” but no long-term clinical studies on people have been reported to date. The concern is about the detrimental effects on the kidneys and fertility. In fact, there was a time 3-MCPD was considered as a potential male contraceptive because it could so affect sperm production, but research funding was withdrawn after “unacceptable side effects [were] observed in primates.” Researchers found flaccid testes in rats, which is what they were going for, but it caused neurological scars in monkeys.

    What do you do when there are no studies in humans? How do you set some kind of safety factor? It isn’t easy, but you can take the lowest observed adverse effect level (LOAEL) in animal studies, which, in this case, was kidney damage, add in some kind of fudge factor, and then arrive at an estimated tolerable daily intake (TDI). For 3-MCPD, this means that high-level consumers of soy sauce may exceed the limit. This was based on extraordinarily high contamination levels, though. Since that study, Europe introduced a regulatory limit of 20 parts per billion (ppb) of 3-MCPD in hydrolyzed vegetable protein products like liquid aminos and soy sauce. The U.S. standards are much laxer, though, setting a “guidance level” of up to 50 times more, 1,000 parts per billion.

    I called Bragg’s to see where it fell, and the good news is that it is doing an independent, third-party analysis of its liquid aminos for 3-MCPD. The bad news is that, despite my pleas that it be fully transparent, Bragg’s wouldn’t let me share the results with you. I have seen them, though, but I’m only allowed to confirm they comfortably meet the U.S. standards but fail to meet the European standards.

    This is just the start of the 3-MCPD story, though. A study in Italy tested individuals’ urine for 3-MCPD or its metabolites, and 100% of the people turned up positive, confirming that it’s “a widespread food contaminant.” But 100% of people aren’t consuming soy sauce or liquid aminos every day. Remember, the chemical results from a reaction with residual vegetable oil. When vegetable oil itself is refined, when it’s deodorized and bleached, those conditions also lead to the formation of 3-MCPD.

    Indeed, we’ve known for years that various foods are contaminated. In what kinds of foods have these kinds of chemicals been detected? Well, if they’re in oils and fats, then they’re in greasy foods made from them: margarine, baked goods, pastries, deep-fried foods, fatty snacks like potato and corn chips, as well as infant formula.

    The U.S. Food and Drug Administration’s limit for soy sauce is 1,000 ppb, but donuts can have more than 1,200 ppb, salami more than 1,500 ppb, ham nearly 3,000 ppb, and French fries in excess of 6,000 ppb, as seen here and at 4:03 in my video The Side Effects of 3-MCPD in Bragg’s Liquid Aminos.

    Most of us don’t have to worry about this problem, unless we’re consumers of fried food. Someone weighing about 150 pounds, for example, who eats 116 grams of donuts, would exceed the European Food Safety Authority’s TDI, even if those donuts were the person’s only source of exposure. That’s about two donuts, but the same limit-blowing amount of 3-MCPD could be found in only five French fries.

    Doctor’s Note

    Believe me, I pleaded with the Bragg’s folks over and over. It’s curious to me that Bragg’s allowed me to talk about where its level of 3-MCPD fell compared to the standards but not say the number itself. At least it’s doing third-party testing.

    Learn more about this topic in my video 3-MCPD in Refined Cooking Oils.

    You can also check out Friday Favorites: The Side Effects of 3-MCPD in Bragg’s Liquid Aminos and Refined Cooking Oils.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Are Doctors Knowledgeable About Nutrition?  | NutritionFacts.org

    [ad_1]

    Do you know more about basic nutrition than most doctors?

    “A poor diet now outranks smoking as the leading cause of death globally and in the United States, according to the latest data.” The top killer of Americans is the American diet, as you can see below and at 0:23 in my video How Much Do Doctors Actually Know About Nutrition?.

    If diet is humanity’s number one killer, then, obviously, nutrition is the number one subject taught in medical school, right? Sadly, “medical students around the world [are] poorly trained in nutrition.” It isn’t that medical students aren’t interested in learning about it. In fact, “interest in nutrition was ‘uniformly high’ among medical students,” but medical schools just aren’t teaching it. “Without a solid foundation of clinical nutrition knowledge and skills, physicians worldwide are generally not equipped to even begin to have an informed nutrition conversation with their patients….”

    How bad is it? One study, “Assessing the clinical nutrition knowledge of medical doctors,” found the majority of participants got 70 percent of the questions wrong—and they were multiple choice questions, so they should have gotten about a fifth of them right just by chance. “Wrong answers in the…knowledge test were not limited to difficult or demanding questions” either. For example, less than half of the doctors were able to guess how many calories are in fat, carbohydrates, and protein; only one in ten knew the recommended protein intake; and only about one in three knew what a healthy body mass index (BMI) was. We’re talking about really basic nutrition knowledge.

    Even worse, not only did the majority of medical doctors get a failing grade, but 30 percent of those who failed had “a high self-perception of their CN [clinical nutrition] expertise.” They weren’t only clueless about nutrition; they were clueless that they were clueless about nutrition, a particularly bad combination given that doctors are “trusted and influential sources” of healthy eating advice. “For those consumers who get information from their personal healthcare professional, 78% indicate making a change in their eating habits as a result of those conversations.” So, if the doctor got everything they know from some article in a magazine while waiting in the grocery store checkout aisle, that’s what the patients will be following.

    Of doctors surveyed, “only 25% correctly identified the American Heart Association recommended number of fruit and vegetable servings per day, and fewer still (20%) were aware of the recommended daily added sugar limit for adults.” So how are they going to counsel their patients? And get ready for this: Of the doctors who perceived themselves as having high nutrition knowledge, 93 percent couldn’t answer those two basic multiple-choice questions, as seen here and at 2:39 in my video.

    “Physicians with no genuine expertise in, say, neurosurgery [brain surgery] are neither likely to broadcast detailed opinions on that topic nor to have their ‘expert’ opinions solicited by the media. Most topical domains in medicine enjoy such respect: we defer expert opinion and commentary to actual experts. Not so nutrition, where the common knowledge that physicians are generally ill-trained in this area is conjoined to routine invitations to physicians for their expert opinions on the matter. All too many are willing to provide theirs, absent any basis for actual expertise…” Or worse, they’re “often made on the basis of native bias and personal preference, at times directly tethered to personal gain—such as diet book sales—and so arises yet another ethical challenge.” That’s one of the reasons all the proceeds I receive from my books are donated directly to charity. I don’t want even the appearance of any conflicts of interest.

    “In a culture that routinely fails to distinguish expertise from mere opinion or personal anecdote, we physicians should be doing all we can to establish relevant barriers to entry for expert opinion in this [diet and nutrition], as in all other matters of genuine medical significance.” I mean, we aren’t talking celebrity gossip. Lives are at stake. “Entire industries are devoted to marketing messages that may conspire directly against well-informed medical advice in this area.”

    “Medical education must be brought up to date. For physicians to be ill-trained in the very area most impactful on the rate of premature death at the population level is an absurd anachronism….The mission of medicine is to protect, defend, and advance the human condition. That mission cannot be fulfilled if the diet is neglected.”

    A possible starting place? “Physicians and health care organizations can collectively begin to emphasize their seriousness about nutrition in health care by practicing what they (theoretically) preach. Is it appropriate to serve pizza and soft drinks at a resident conference while bemoaning the high prevalence of obesity and encouraging patients to eat healthier? A similarly poor example exists in medical conferences, including national meetings, where some morning sessions are accompanied by foods such as donuts and sausage.”

    [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

  • Dietary Diversity and Overeating  | NutritionFacts.org

    [ad_1]

    Big Food uses our hard-wired drive for dietary diversity against us.

    How did we evolve to solve the daunting task of selecting a diet that supplies all the essential nutrients? Dietary diversity. By eating a variety of foods, we increase our chances of hitting all the bases. If we only ate for pleasure, we might just stick with our favorite food to the exclusion of all others, but we have an innate tendency to switch things up.

    Researchers found that study participants ended up eating more calories when provided with three different yogurt flavors than just one, even if that one is the chosen favorite. So, variation can trump sensation. They don’t call it the spice of life for nothing.

    It appears to be something we’re born with. Studies on newly weaned infants dating back nearly a century show that babies naturally choose a variety of foods even over their preferred food. This tendency seems to be driven by a phenomenon known as sensory-specific satiety.

    Researchers found that, “within 2 minutes after eating the test meal, the pleasantness of the taste, smell, texture, and appearance of the eaten food decreased significantly more than for the uneaten foods.” Think about how the first bite of chocolate tastes better than the last bite. Our body tires of the same sensations and seeks out novelty by rekindling our appetite every time we’re presented with new foods. This helps explain the “dessert effect,” where we can be stuffed to the gills but gain a second wind when dessert arrives. What was adaptive for our ancient ancestors to maintain nutritional adequacy may be maladaptive in the age of obesity.

    When study participants ate a “varied four-course meal,” they consumed 60 percent more calories than those given the same food for each course. It’s not only that we get bored; our body has a different physiological reaction.

    As you can see below and at 2:13 in my video How Variation Can Trump Sensation and Lead to Overeating, researchers gave people a squirt of lemon juice, and their salivary glands responded with a squirt of saliva. But when they were given lemon juice ten times in a row, they salivated less and less each time. When they got the same amount of lime juice, though, their salivation jumped right back up. We’re hard-wired to respond differently to new foods. 
    Whether foods are on the same plate, are at the same meal, or are even eaten on subsequent days, the greater the variety, the more we tend to eat. When kids had the same mac and cheese dinner five days in a row, they ended up eating hundreds fewer calories by the fifth day, compared to kids who got a variety of different meals, as you can see below and at 2:35 in my video.

    Even just switching the shape of food can lead to overeating. When kids had a second bowl of mac and cheese, they ate significantly more when the noodles were changed from elbow macaroni to spirals. People allegedly eat up to 77 percent more M&Ms if they’re presented with ten different colors instead of seven, even though all the colors taste the same. “Thus, it is clear that the greater the differences between foods, the greater the enhancement of intake,” the greater the effect. Alternating between sweet and savory foods can have a particularly appetite-stimulating effect. Do you see how, in this way, adding a diet soda, for instance, to a fast-food meal can lead to overconsumption?

    The staggering array of modern food choices may be one of the factors conspiring to undermine our appetite control. There are now tens of thousands of different foods being sold.

    The so-called supermarket diet is one of the most successful ways to make rats fat. Researchers tried high-calorie food pellets, but the rats just ate less to compensate. So, they “therefore used a more extreme diet…[and] fed rats an assortment of palatable foods purchased at a nearby supermarket,” including such fare as cookies, candy, bacon, and cheese, and the animals ballooned. The human equivalent to maximize experimental weight gain has been dubbed the cafeteria diet.

    It’s kind of the opposite of the original food dispensing device I’ve talked about before. Instead of all-you-can-eat bland liquid, researchers offered free all-you-can-eat access to elaborate vending machines stocked with 40 trays with a dizzying array of foods, like pastries and French fries. Participants found it impossible to maintain energy balance, consistently consuming more than 120 percent of their calorie requirements.

    Our understanding of sensory-specific satiety can be used to help people gain weight, but how can we use it to our advantage? For example, would limiting the variety of unhealthy snacks help people lose weight? Two randomized controlled trials made the attempt and failed to show significantly more weight loss in the reduced variety diet, but they also failed to get people to make much of a dent in their diets. Just cutting down on one or two snack types seems insufficient to make much of a difference, as seen below and at 4:44 in my video. A more drastic change may be needed, which we’ll cover next.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Are Carboxymethylcellulose, Polysorbate 80, and Other Emulsifiers Safe?  | NutritionFacts.org

    [ad_1]

    Emulsifiers are the most widely used food additives. What are they doing to our gut microbiome?

    When grocery shopping these days, unless you’re sticking to the produce aisle, “it is nearly impossible to avoid processed foods, particularly in the consumption of a typical Western diet,” which is characterized by insufficient plant foods, too much meat, dairy, and eggs, and a lot of processed junk, “along with increased exposure to additives due to their use in processed foods.”

    The artificial sweetener sucralose, for example, which is sold as Splenda, “irrefutably disrupts the gut microbiome at doses relevant to human use” and “induces glucose intolerance.” In other words, it can make our blood sugars worse instead of better. It’s relatively easy to avoid artificial sweeteners, but “it may be much more difficult to avoid ingestion of emulsifiers…because they are commonly added to a wide variety of foods within the modern Western diet.” In fact, “emulsifiers are the most widely used additives,” and “most processed foods contain one or more emulsifiers that allow such foods to maintain desired textures and avoid separation into distinct parts (e.g, oil and water layers).” We now consume emulsifiers by the megaton every year, thanks to a multibillion-dollar industry, as you can see below and at 1:03 in my video Are Emulsifiers Like Carboxymethylcellulose and Polysorbate 80 Safe?.

    Emulsifiers are commonly found in fatty dressings, breads and other baked goods, mayonnaise and other fatty spreads, candy, and beverages. “Like all authorized food additives, emulsifiers have been evaluated by risk assessors, who consider them safe. However, there are growing concerns among scientists about their possible harmful effects on our intestinal barriers and microbiota,” in terms of causing a leaky gut. As well, they could possibly “increase the absorption of several environmental toxins, including endocrine disruptors and carcinogens” present in the food.

    We know that the consumption of ultra-processed foods may contribute to weight gain. Healthier, longer-lived populations not only have low meat intake and high plant intake, but they also eat minimally processed foods and “have far less chronic diseases, obesity rates, and live longer disease-free.” Based on a number of preclinical studies, it may be that the emulsifiers found in processed foods are playing a role, but who cares if “emulsifiers make rats gain weight”? When we read that “emulsifiers can cause striking changes in the microbiota,” they aren’t talking about the microbiota of humans.

    Often, mice are used to study the impact on the microbiome, but “only a few percent of the bacterial genes are shared between mice and humans.” Even the gut flora of different strains of mice can be considerably different from each other, so if we can’t even extrapolate from one type of mouse to another, how are we supposed to translate results from mice to humans? “Remarkably, there has been little study of the potential harmful effects of ingested…emulsifiers in humans.”

    Take lecithin, for example, which is “perhaps best known as a key component of egg yolks.” Lecithin was found to be worse than polysorbate 80 in terms of allowing bacteria to leak through the gut wall into the bloodstream. However, it’s yet to be determined whether lecithin consumption in humans causes the same problem. “There is certainly a paucity in the data of human trials with the effects of emulsifiers in processed foods,” but we at least have data on human tissue, cells, and gut flora.

    A study was titled: “Dietary emulsifiers directly alter the human microbiota composition and gene expression ex vivo potentiating intestinal inflammation.” Ex vivo means outside the body. Researchers inoculated an artificial gut with fresh human feces until a stable culture was established, then added carboxymethylcellulose (CMC) or polysorbate 80 (P80), resulting in boosts in proinflammatory potential starting within one day with the carboxymethylcellulose and within the first week with polysorbate 80, as you can see below and at 3:39 in my video.

    “This approach revealed that both P80 and CMC acted directly upon human microbiota to increase its proinflammatory potential…” When researchers then tested the effect of these emulsifiers on the protective mucus layer in petri dish cultures of human gut lining cells, they found that they can partially disrupt the protective layer. As you can see below and at 4:00 in my video, the green staining is the mucus. Both emulsifiers cut down the levels.

    However, this study and the last both used emulsifier concentrations that were far in excess of what people might typically get day-to-day. 

    “Translocation of Crohn’s disease Escherichia coli across M-cells: contrasting effects of soluble plant fibres and emulsifiers” is probably the study that raised the greatest potential concern. The researchers surgically obtained cells, as well as actual intestinal wall tissue, and found that polysorbate 80 could double the invasion of E. coli through the intestinal lining tissue, as shown here and at 4:27 in my video.

    In contrast, adding fiber—in this case, fiber from plantains—could seal up the gut wall tissue twice as tightly, as seen below and at 4:33.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Eating to Treat Crohn’s Disease  | NutritionFacts.org

    [ad_1]

    Switching to a plant-based diet has been shown to achieve far better outcomes than those reported on conventional treatments for both active and quiescent stages of Crohn’s disease (CD) and ulcerative colitis.

    Important to our understanding and the prevention of the global increase of inflammatory bowel disease (IBD), we know that “dietary fiber reduces risk, whereas dietary fat, animal protein, and sugar increase it.” “Despite the recognition of westernization of lifestyle as a major driver of the growing incidence of IBD, no countermeasures against such lifestyle changes have been recommended, except that patients with Crohn’s disease should not smoke.”

    We know that “consuming whole, plant-based foods is synonymous with an anti-inflammatory diet.” Lists of foods with inflammatory effects and anti-inflammatory effects are shown here and at 0:50 in my video, The Best Diet for Crohn’s Disease.

    How about putting a plant-based diet to the test?

    Cutting down on red and processed meats didn’t work, but what about cutting down on all meat? A 25-year-old man “with newly diagnosed CD…failed to enter clinical remission despite standard medical therapy. After switching to a diet based exclusively on grains, legumes [beans, split peas, chickpeas, and lentils], vegetables, and fruits, he entered clinical remission without need for medication and showed no signs of CD on follow-up colonoscopy.”

    It’s worth delving into some of the details. The conventional treatment he was started on is infliximab, sold as REMICADE®, which can cause a stroke and may increase our chances of getting lymphoma or other cancers. (It also costs $35,000 a year.) It may not even work in 35 to 40 percent of patients, and that seemed to be the case with the 25-year-old man. So, his dose was increased after 37 weeks, but he was still suffering after two years on the drug. Then he completely eliminated animal products and processed foods from his diet and finally experienced a complete resolution of his symptoms.

    “Prior to this, his diet had been the typical American diet, consisting of meat, dairy products, refined grains, processed foods, and modest amounts of vegetables and fruits. Having experienced complete clinical remission for the first time since his Crohn’s disease diagnosis, the patient decided to switch to a whole food, plant-based diet permanently, severely reducing his intake of processed foods and limiting animal products to one serving, or less, per week.” Whenever his diet slipped, his symptoms started coming back, but he could always eliminate them by eating healthier again. After six months adhering to these diet and lifestyle changes, including stress relief and exercise, a follow-up “demonstrated complete mucosal healing [of the gut lining] with no visible evidence of Crohn’s disease.”

    We know that “a diet consisting of whole grains, legumes, fruits, and vegetables has been shown to be helpful in the prevention and treatment of heart disease, obesity, diabetes, hypertension, gallbladder disease, rheumatoid arthritis, and many cancers. Although further research is required, this case report suggests that Crohn’s disease might be added to this list of conditions.” That further research has already been done! About 20 patients with Crohn’s disease were placed on a semi-vegetarian diet—no more than half a serving of fish once a week and half a serving of meat once every two weeks—and they achieved a 100 percent remission rate at one year and 90 percent at two years.

    Some strayed from the diet, though. What happened to them? As you can see below and at 3:32 in my video, after one year, half had relapsed, and, at year two, only 20 percent had remained in remission. But those who stuck with the semi-veg diet had remarkable success. It was a small study with no formal control group, but it represents the best-reported result in Crohn’s relapse prevention published in the medical literature to date. 

    Nowadays, Crohn’s patients are often treated with so-called biologic drugs, expensive injected antibodies that suppress the immune system. They have effectively induced and maintained remission in Crohn’s disease, but not in everybody. The current remission rate in Crohn’s with early use of REMICADE® is 64 percent. So, 30 to 40 percent of patients “are likely to experience a disabling disease course even after their first treatment.” What about adding a plant-based diet? Remission rates jumped up to 100 percent for those who didn’t have to drop out due to drug side effects. Even after excluding milder cases, researchers found that 100 percent of those with serious, even “severe/fulminant disease, achieved remission.”

    If we look at gold standard systematic reviews, they conclude that the effects of dietary interventions on inflammatory bowel diseases—Crohn’s disease and ulcerative colitis—are uncertain. However, this is because only randomized controlled trials were considered. That’s totally understandable, as that is the most rigorous study design. “Nevertheless, people with IBD deserve advice based on the ‘best available evidence’ rather than no advice at all…” And switching to a plant-based diet has been shown to achieve “far better outcomes” than those reported on conventional treatments in both active and quiescent stages in Crohn’s disease and ulcerative colitis. For example, below and at 5:37 in my video, you can see one-year remission rates in Crohn’s disease (100 percent) compared to budesonide, an immunosuppressant corticosteroid drug (30 to 40 percent), a half elemental diet, such as at-home tube feedings (64 percent), the $35,000-a-year drug REMICADE® (46 percent), or the $75,000-a-year drug Humira (57 percent). 

    Safer, cheaper, and more effective. That’s why some researchers have made the “recommendation of plant-based diets for inflammatory bowel disease.”

    It would seem clear that treatment based on addressing the cause of the disease is optimal. Spreading the word about healthier diets could help halt the scourge of inflammatory bowel disease, but how will people hear about this amazing research without some kind of public education campaign? That’s what NutritionFacts.org is all about.

    Doctor’s Note:

    This is the third in a series on inflammatory bowel disease. If you missed the first two, see Preventing Inflammatory Bowel Disease with Diet and The Best Diet for Ulcerative Colitis Treatment.

    My previous Crohn’s videos include Preventing Crohn’s Disease with Diet and Does Nutritional Yeast Trigger Crohn’s Disease?. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Can We Safely Use Aluminum Foil, Bottles, and Pots?  | NutritionFacts.org

    Can We Safely Use Aluminum Foil, Bottles, and Pots?  | NutritionFacts.org

    [ad_1]

    DNA damage is assessed in users of aluminum cookware.

    “Over the last decades, the toxicity of aluminum for humans has been heavily discussed and is still not completely clarified.” Those occupationally exposed to aluminum—for instance, in smelter plants—suffer from oxidative stress and free radicals that can damage their DNA. What about just using aluminum cookware? Articles like “Metal Exposures from Aluminum Cookware: An Unrecognized Public Health Risk in Developing Countries,” suggesting an “unrecognized public health risk,” were limited to the developing world where “cookware is made in informal shops by casting liquid aluminum melted from a collection of scrap metal,” including the likes of vehicle radiators, lead batteries, and computer parts, which is how you can get so much lead leaching into people’s food. 

    Then “The Relationship Between Plasma Aluminum Content, Lymphocyte DNA Damage, and Oxidative Status in Persons Using Aluminum Containers and Utensils Daily” was published, suggesting that aluminum itself may be harmful. Most of our aluminum exposure comes from processed junk food containing aluminum additives, “including those within some processed cheeses, baking powders, cake mixes, frozen dough, and pancake mixes.” However, about 20 percent of the daily intake of aluminum may come from aluminum cooking utensils, such as “pans, pots, kettles, and trays.” 

    Might this cause a problem? Researchers took blood from consumers who used aluminum cookware versus those who did not and found that not only did the aluminum users have twice the level of aluminum in their blood, as you can see below and at 1:33 in my video Are Aluminum Pots, Bottles, and Foil Safe?, but they had more free radical damage of their body fats and proteins. What’s more, the total antioxidant capacity of the bloodstream of those using aluminum cookware was compromised, so they suffered significantly more DNA damage. 

    Indeed, as you can see below and at 1:52 in my video, those with the highest levels of aluminum in their blood tended to suffer significantly more damage to their DNA. No surprise, since “aluminum is considered to be a pro-oxidant agent.”

    These folks weren’t just casually using aluminum pots, though. Specifically, they use them every day to cook and store acidic foods, like yogurt and tomato sauce, which can leach out more aluminum. But, even using “camping dishes,” which tend to be aluminum since it’s so light, for just one week, could greatly exceed the tolerable weekly intake guidelines, especially for children, if you incorporated something acidic, like marinating a fresh catch in lemon juice. Once in a while won’t make much difference, but these findings suggest that you may not want to cook in aluminum day in and day out. 

    What about aluminum drinking bottles? They’re nice and light, but children drinking two cups a day of tea or juice from them could exceed the tolerable aluminum exposure limit. So, out of an abundance of caution, safety authorities like the German Federal Institute for Risk Assessment “recommend that consumers avoid the use of aluminum pots or dishes for acidic or salted foodstuffs such as apple sauce, rhubarb, tomato puree, or salt herring…thus prophylactically avoiding the ‘unnecessary ingestion’ of aluminum.” 

    What about aluminum foil? Wrapping and baking food in aluminum foil is a common culinary practice. The concern is that this could represent “a potentially hazardous source of aluminum in the human diet.” When put to the test, there was leakage of aluminum from the foil to the food, but the amount was so small that it would be more of an issue for small children or those suffering from diminished kidney function. 

    What about just wrapping food in foil to store it in the refrigerator? Only marginal increases in aluminum are seen—except when the food is in contact with the foil and, at the same time, certain other types of metal, such as stainless steel, which is largely iron. That sets up a battery and “can lead to tremendous food aluminum concentrations.” For example, as you can see below and at 4:34 in my video, the aluminum levels in a ham before and after a day coveredin foil are negligible; there’s hardly a bump in the foil-covered ham. But, if that same foil-wrapped ham sits on top of a steel tray or serving plate for a day, the aluminum levels in the ham shoot up.

    Finally, you know how aluminum foil is often glossy on one side and dull on the other? Which would be worse? Fish fillets were baked and grilled both ways, wrapped with the glossy side out versus the dull side out, and no significant difference was found.

    This is the first in a series of three videos on cookware. Stay tuned for Stainless Steel or Cast Iron: Which Cookware Is Best? Is Teflon Safe? and Are Melamine Dishes and Polyamide Plastic Utensils Safe?.

    I’ve discussed aluminum in antiperspirants, food, medications, and tea. Check out the related posts.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • What About Animal Protein and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    What About Animal Protein and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    [ad_1]

    Might animal protein-induced increases in the cancer-promoting growth hormone IGF-1 help promote brain artery integrity? 

    In 2014, a study on stroke risk and dietary protein found that greater intake was associated with lower stroke risk and, further, that the animal protein appeared particularly protective. Might that help explain why, as shown in the graph below and at 0:31 in my video Vegetarians and Stroke Risk Factors: Animal Protein?, vegetarians were recently found to have a higher stroke rate than meat eaters?

    Animal protein consumption increases the levels of a cancer-promoting growth hormone in the body known as IGF-1, insulin-like growth factor 1, which “accelerates the progression of precancerous changes to invasive lesions.” High blood concentrations are associated with increased risks of breast, colorectal, lung, and prostate cancers, potentially explaining the association between dairy milk intake and prostate cancer risk, for example. However, there are also IGF-1 receptors on blood vessels, so perhaps IGF-1 promotes cancer and brain artery integrity.

    People who have strokes appear to have lower blood levels of IGF-1, but it could just be a consequence of the stroke rather than the cause. There weren’t any prospective studies over time until 2017 when researchers found that, indeed, higher IGF-1 levels were linked to a lower risk of stroke—but is it cause and effect? In mice, the answer seems to be yes, and in a petri dish, IGF-1 appears to boost the production of elastin, a stretchy protein that helps keep our arteries elastic. As you can see in the graph below and at 1:41 in my video, higher IGF-1 levels are associated with less artery stiffness, but people with acromegaly, like Andre the Giant, those with excessive levels of growth hormones like IGF-1, do not appear to have lower stroke rates, and a more recent study of dietary protein intake and risk of stroke that looked at a dozen studies of more than half a million people (compared to only seven studies with a quarter million in the previous analysis), found no association between dietary protein intake and the risk of stroke. If anything, dietary plant protein intake may decrease the risk of stroke. 

    However, those with high blood pressure who have low IGF-1 levels do appear to be at increased risk of developing atherosclerosis, which is the thickening of the artery walls leading up to the brain, but no such association was found in people with normal blood pressure. So, there may be “a cautionary lesson for vegans” here. Yes, a whole food, plant-based diet “can down-regulate IGF-1 activity” and may slow the human aging process, not to mention reduce the risk of some of the common cancers that plague the Western world. But, “perhaps the ‘take-home’ lesson should be that people who undertake to down-regulate IGF-1 activity [by cutting down on animal protein intake] as a pro-longevity measure should take particular care to control their blood pressure and preserve their cerebrovascular health [the health of the arteries in their brain] – in particular, they should keep salt intake relatively low while insuring an ample intake of potassium” to keep their blood pressures down. So, that means avoiding processed foods and avoiding added salt, and, in terms of potassium-rich foods, eating beans, sweet potatoes, and dark-green leafy vegetables. 

    Might this explain the higher stroke risk found among vegetarians? No—because dairy and egg whites are animal proteins, too. Only vegans have lower IGF-1 levels in both men and women, so low levels of IGF-1 can’t explain why higher rates of stroke were found in vegetarians. Then what is it? I think the best explanation for the mystery is something called homocysteine, which I cover next. 

    If you aren’t familiar with IGF-1, my videos Flashback Friday: Animal Protein Compared to Cigarette Smoking and How Not to Die from Cancer are good primers. 

    Beyond eating a plant-based diet, how else can we lower our blood pressure? Check out the chapter of hypertension in my book How Not to Die at your local public library. 

    This is the eighth video in a 12-part series on vegetarians’ stroke risk. If you missed any of the previous ones, check out the related posts below.

    Coming up, we turn to what I think is actually going on:

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • What About Vegan Junk Food and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    What About Vegan Junk Food and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    [ad_1]

    Just because you’re eating a vegetarian or vegan diet doesn’t mean you’re eating healthfully.

    “Plant-Based Diets Are Associated with a Lower Risk of Incident Cardiovascular Disease, Cardiovascular Disease Mortality, and All-Cause Mortality in a General Population of Middle-Aged Adults”: This study of a diverse sample of 12,000 Americans found that “progressively increasing the intake of plant foods by reducing the intake of animal foods is associated with benefits on cardiovascular health and mortality.” Still, regarding plant-based diets for cardiovascular disease prevention, “all plant foods are not created equal.” As you can see in the graph below and at 0:40 in my video Vegetarians and Stroke Risk Factors: Vegan Junk Food?, a British study found higher stroke risk in vegetarians. Were they just eating a lot of vegan junk food? 

    “Any diet devoid of animal food sources can be claimed to be a vegetarian [or vegan] diet; thus, it is important to determine” what is being eaten. One of the first things I look at when I’m trying to see how serious a population is about healthy eating is something that is undeniably, uncontroversially bad: soda, aka liquid candy. Anyone drinking straight sugar water doesn’t have health on top of mind.

    A large study was conducted of plant-based eaters in the United States, where people tend to cut down on meat for health reasons far more than for ethics, as you can see in the graph below and at 1:20 in my video.

    Researchers found that flexitarians drink fewer sugary beverages than regular meat eaters, as do pescatarians, vegetarians, and vegans, as you can see below and at 1:30.

    However, in the study from the United Kingdom where the increased stroke risk in vegetarians was found and where people are more likely to go veg or vegan for ethical reasons, researchers found that pescatarians drink less soda, but the vegetarians and vegans drink more, as shown in the graph below and at 1:44. 

    I’m not saying that’s why they had more strokes; it might just give us an idea of how healthfully they were eating. In the UK study, the vegetarian and vegan men and women ate about the same amounts of desserts, cookies, and chocolate, as you can see in the graph below and at 1:53. 

    They also consumed about the same total sugar, as shown below and at 2:02. 

    In the U.S. study, the average non-vegetarian is nearly obese, the vegetarians are a little overweight, and the vegans were the only ideal weight group. In this analysis of the UK study, however, everyone was about the same weight. The meat eaters were lighter than the vegans, as you can see below, and at 2:19 in my video. The EPIC-Oxford study seems to have attracted a particularly “health-conscious” group of meat eaters weighing substantially less than the general population. 

    Let’s look at some specific stroke-related nutrients. Dietary fiber appears to be beneficial for the prevention of cardiovascular disease, including stroke, and it seems the more, the better, as you can see in the graph below and at 2:43 in my video. 

    Based on studies of nearly half a million men and women, there doesn’t seem to be any upper threshold of benefit—so, again, “the more, the better.” At more than 25 grams of soluble fiber and 47 grams of insoluble dietary fiber, you can start seeing a significant drop in associated stroke risk. So, one could consider these values “as the minimal recommendable daily intake of soluble and insoluble fiber…to prevent stroke at a population level.” That’s what you see in people eating diets centered around minimally processed plant foods. Dean Ornish, M.D., got up around there with his whole food, plant-based diet. It might not be as much as we were designed to eat, based on the analyses of fossilized feces, but that’s about where we might expect significantly lower stroke risk, as shown below and at 3:25 in my video. 

    How much were the UK vegetarians getting? 22.1 grams. Now, in the UK, they measure fiber a little differently, so it may be closer to 30 grams, but that’s still not the optimal level for stroke prevention. It’s so little fiber that the vegetarians and vegans only beat out the meat eaters by about one or two bowel movements a week, as you can see below and at 3:48 in my video, suggesting the non-meat eaters were eating lots of processed foods. 

    The vegetarians were only eating about half a serving more of fruits and vegetables. Intake is thought to reduce stroke risk in part because of their potassium content, but the UK vegetarians at higher stroke risk were eating so few greens and beans that they couldn’t even match the meat eaters. The vegetarians (and the meat eaters) weren’t even reaching the recommended minimum daily potassium intake of 4,700 mg a day.

    What about sodium? “The vast majority of the available evidence indicates that elevated salt intake is associated with higher stroke risk…” There is practically a straight-line increase in the risk of dying from a stroke, the more salt you eat, as you can see in the graph below and at 4:29 in my video. 

    Even just lowering sodium intake by a tiny fraction every year could prevent tens of thousands of fatal strokes. “Reducing Sodium Intake to Prevent Stroke: Time for Action, Not Hesitation” was the title of the paper, but the UK vegetarians and vegans appeared to be hesitating, as did the other dietary groups. “All groups exceeded the advised less than 2400 mg daily sodium intake”—and that didn’t even account for salt added to the table! The American Heart Association recommends less than 1,500 mg a day. So, they were all eating a lot of processed foods. It’s no wonder the vegetarians’ blood pressures were only one or two points lower. High blood pressure is perhaps “the single most important potentially modifiable risk factor for stroke.” 

    What evidence do I have that the vegetarians’ and vegans’ stroke risk would go down if they ate more healthfully? Well, in rural Africa, where they were able to nail the fiber intake that our bodies were designed to get by eating so many whole, healthy plant foods—including fruits, vegetables, grains, greens, beans, and protein almost entirely from plant sources—not only was heart disease, our number one killer, “almost non-existent,” but so was stroke. It only surged up from nowhere “with the introduction of salt and refined foods” to their diet. 

    “It is notable that stroke and senile dementia appear to be virtually absent in Kitava, an Oceanic culture [near Australia] whose quasi-vegan traditional diet is very low in salt and very rich in potassium.” They ate fish a few times a week, but the other 95 percent or so of their diet was made up of vegetables, fruits, corn, and beans. They had an apparent absence of stroke, even despite their ridiculously high rates of smoking, 76 percent of men and 80 percent of women. We evolved by eating as little as less than an eighth of a teaspoon of salt a day, and our daily potassium consumption is thought to have been as high as 10,000 mg or so. We went from an unsalted, whole-food diet to eating salty, processed foods depleted of potassium whether we eat meat or not. 

    Caldwell Esselstyn at the Cleveland Clinic tried putting about 200 patients with established cardiovascular disease on a whole food, plant-based diet. Of the 177 who stuck with the diet, only a single patient went on to have a stroke in the subsequent few years, compared to a hundred-fold greater rate of adverse events, including multiple strokes and deaths in those who strayed from the diet. “This is not vegetarianism,” Esselstyn explains. Vegetarians can eat a lot of less-than-ideal foods, “such as milk, cream, butter, cheese, ice cream, and eggs. This new paradigm is exclusively plant-based nutrition.” 

    This entire train of thought—that the reason typical vegetarians don’t have better stroke statistics is because they’re not eating particularly stellar diets—may explain why they don’t have significantly lower stroke rates. However, it still doesn’t explain why they may have higher stroke rates. Even if they’re eating similarly crappy, salty, processed diets, at least they aren’t eating meat, which we know increases stroke risk. There must be something about vegetarian diets that so increases stroke risk that it offsets their inherent advantages. We’ll continue our hunt for the answer next. 

    From a medical standpoint, labels like vegan and vegetarian just tell me what you don’t eat. It’s like identifying yourself as a “No-Twinkie-tarian.” You don’t eat Twinkies? Great, but what’s the rest of your diet like? 

    What are the healthiest foods? Check out my Daily Dozen.

    To catch up on the rest of this series, see related posts below. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • What About Omega-3s and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    What About Omega-3s and Vegetarians’ Stroke Risk?  | NutritionFacts.org

    [ad_1]

    Does eating fish or taking fish oil supplements reduce stroke risk? 

    In my last video, we started to explore what might explain the higher stroke risk in vegetarians found in the EPIC-Oxford study. As you can see below and at 0:25 in my video Vegetarians and Stroke Risk Factors: Omega-3s?, vegetarians have a lower risk of heart disease and cardiovascular disease overall, but a higher risk of stroke. We looked into vitamin D levels as a potential mechanism, but that didn’t seem to be the reason. What about long-chain omega-3s, the fish fats like EPA and DHA? 

    Not surprisingly, their levels are found to be “markedly lower in vegetarians and particularly in vegans than in meat-eaters.” They’re about 30 percent lower in vegetarians and more than half as low in vegans, as you can see below and at 0:45 in my video. 

    According to “the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date,” combining 28 randomized controlled trials, stroke has no benefit. There is evidence that taking fish oil “does not reduce heart disease, stroke or death,” or overall mortality, either. This may be because, on the one hand, the omega-3s may be helping, but the mercury in fish may be making things worse. “Balancing the benefits with the contaminant risks of fish consumption has represented a challenge for regulatory agencies and public health professionals.”  

    For example, dietary exposure to polychlorinated biphenyls (PCBs) may be associated with an increased risk of stroke. In one study, for instance, “neither fish nor intake of PCBs was related to stroke risk. However, with adjustment for fish intake,” that is, at the same fish intake, “dietary PCBs were associated with an increased risk of total stroke,” so the PCB pollutants may be masking the fish benefit. If we had a time machine and could go back before the Industrial Revolution and find fish in an unpolluted state, we might find that it is protective against stroke. Still, looking at the EPIC-Oxford study data, if fish were protective, then we might expect that the pescatarians (those who eat fish but no other meat) would have lower numbers of strokes since they would have the fish benefit without the risk from other meat. But, no. That isn’t the reality. So, it doesn’t seem to be the omega-3s either.

    Let’s take a closer look at what the vegetarians are eating.

    When it comes to plant-based diets for cardiovascular disease prevention, all plant foods are not created equal. There are two types of vegetarians—those who do it for their health, and those who do it for ethical reasons, like global warming or animals—and the latter tend to eat different diets. Health vegans tend to eat more fruits and fewer sweets, for instance, and you don’t tend to see them chomping down on vegan donuts, as shown below and at 2:41 in my video. 

    “Concerns about health and costs were primary motivations for [meat] reduction” in the United States. A middle-class American family is four times more likely to reduce meat for health reasons compared to environmental or animal welfare concerns, as you can see in the graph below and at 2:55 in my video. 

    But in the United Kingdom, where the EPIC-Oxford stroke study was done, ethics was the number one reason given for becoming vegetarian or vegan, as you can see in below and at 3:05 in my video.

    We know that “plant-based diets, diets that emphasize higher intakes of plant foods and lower intakes of animal foods, are associated with a lower risk of incident cardiovascular disease, cardiovascular disease mortality, and all-cause mortality”—a lower risk of dying from all causes put together—“in a general US adult population.” But, that’s only for healthy plant foods. Eating a lot of Wonder Bread, soda, and apple pie isn’t going to do you any favors. “For all types of plant-based diets, however, it is crucial that the choice of plant foods is given careful consideration.” We should choose whole fruits and whole grains over refined grains and avoid trans fats and added sugars. Could it be that the veggie Brits were just eating more chips? We’ll find out next. 

    Another strikeout trying to explain the increased risk. Could it be that the vegetarians were eating particularly unhealthy diets? Labels like vegetarian or vegan just tell me what is not being eaten. You can be vegetarian and consume a lot of unhealthy fare, like french fries, potato chips, and soda. That’s why, as a physician, I prefer the term whole food, plant-based nutrition. That tells me what you do eat. You eat vegetables and follow a diet centered around the healthiest foods out there.

    If you missed the first four videos in this series, see:

     Surprised about the fishy oil findings? Learn more: Is Fish Oil Just Snake Oil? and Omega-3s and the Eskimo Fish Tale. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

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

    Eating to Lower Lp(a)  | NutritionFacts.org

    [ad_1]

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Obesity and a Toxic Food Environment  | NutritionFacts.org

    Obesity and a Toxic Food Environment  | NutritionFacts.org

    [ad_1]

    Implausible explanations for the obesity epidemic serve the needs of food manufacturers and marketers more than public health and an interest in truth. 

    When it comes to uncovering the root causes of the obesity epidemic, there appears to be manufactured confusion, “with major studies reasserting that the causes of obesity are ‘extremely complex’ and ‘fiendishly hard to untangle,’” but having just reviewed the literature, it doesn’t seem like much of a mystery to me.

    It’s the food.

    Attempts at obfuscation—rolling out hosts of “implausible explanations,” like sedentary lifestyles or lack of self-discipline—cater to food manufacturers and marketers more than the public’s health and our interest in the truth. “When asked about the role of restaurants in contributing to the obesity problem, Steven Anderson, president of the National Restaurant Association stated, “Just because we have electricity doesn’t mean you have to electrocute yourself.” Yes, but Big Food is effectively attaching electrodes to shock and awe the reward centers in our brains to undermine our self-control.

    It is hard to eat healthfully against the headwind of such strong evolutionary forces. No matter what our level of nutrition knowledge, in the face of pepperoni pizza, “our genes scream, ‘Eat it now!’” Anyone who doubts the power of basic biological drives should see how long they can go without blinking or breathing. Any conscious decision to hold your breath is soon overcome by the compulsion to breathe. In medicine, shortness of breath is sometimes even referred to as “air hunger.” The battle of the bulge is a battle against biology, so obesity is not some moral failing. It’s not gluttony or sloth. It is a natural, “normal response, by normal people, to an abnormal situation”—the unnatural ubiquity of calorie-dense, sugary, and fatty foods.

    The sea of excess calories we are now floating in (and some of us are drowning in) has been referred to as a “toxic food environment.” This helps direct focus away from the individual and towards the societal forces at work, such as the fact that the average child is blasted with 10,000 commercials for food a year. Or maybe I should say ads for pseudo food, as 95 percent are for “candy, fast food, soft drinks [aka liquid candy], and sugared cereals [aka breakfast candy].”

    Wait a second, though. If weight gain is just a natural reaction to the easy availability of mountains of cheap, yummy calories, then why isn’t everyone fat? As you can see below and at 2:41 in my video The Role of the Toxic Food Environment in the Obesity Epidemic, in a certain sense, most everyone is. It’s been estimated that more than 90 percent of American adults are “overfat,” defined as having “excess body fat sufficient to impair health.” This can occur even “in those who are normal-weight and non-obese, often due to excess abdominal fat.

    However, even if you look just at the numbers on the scale, being overweight is the norm. If you look at the bell curve and input the latest data, more than 70 percent of us are overweight. A little less than one-third of us is normal weight, on one side of the curve, and more than a third is on the other side, so overweight that we’re obese. You can see in the graph below and at 3:20 in my video.

    If the food is to blame, though, why doesn’t everyone get fat? That’s like asking if cigarettes are really to blame, why don’t all smokers get lung cancer? This is where genetic predispositions and other exposures can weigh in to tip the scales. Different people are born with a different susceptibility to cancer, but that doesn’t mean smoking doesn’t play a critical role in exploding whatever inherent risk you have. It’s the same with obesity and our toxic food environment. It’s like the firearm analogy: Genes may load the gun, but diet pulls the trigger. We can try to switch the safety back on with smoking cessation and a healthier diet.

    What happened when two dozen study participants were given the same number of excess calories? They all gained weight, but some gained more than others. Overfeeding the same 1,000 calories a day, 6 days a week for 100 days, caused weight gains ranging from about 9 pounds up to 29 pounds. The same 84,000 extra calories caused different amounts of weight gain. Some people are just more genetically susceptible. The reason we suspect genetics is that the 24 people in the study were 12 sets of identical twins, and the variation in weight gain between each of them was about a third less. As you can see in the graph below and at 4:41 in my video, a similar study with weight loss from exercise found a similar result. So, yes, genetics play a role, but that just means some people have to work harder than others. Ideally, inheriting a predisposition for extra weight gain shouldn’t give a reason for resignation, but rather motivation to put in the extra effort to unseal your fate. 

    Advances in processing and packaging, combined with government policies and food subsidy handouts that fostered cheap inputs for the “food industrial complex,” led to a glut of ready-to-eat, ready-to-heat, ready-to-drink hyperpalatable, hyperprofitable products. To help assuage impatient investors, marketing became even more pervasive and persuasive. All these factors conspired to create unfettered access to copious, convenient, low-cost, high-calorie foods often willfully engineered with chemical additives to make them hyperstimulatingly sweet or savory, yet only weakly satiating. 

    As we all sink deeper into a quicksand of calories, more and more mental energy is required to swim upstream against the constant “bombardment of advertising” and 24/7 panopticons of tempting treats. There’s so much food flooding the market now that much of it ends up in the trash. Food waste has progressively increased by about 50 percent since the 1970s. Perhaps better in the landfills, though, than filling up our stomachs. Too many of these cheap, fattening foods prioritize shelf life over human life.

    But dead people don’t eat. Don’t food companies have a vested interest in keeping their consumers healthy? Such naiveté reveals a fundamental misunderstanding of the system. A public company’s primary responsibility is to reap returns for its investors. “How else could we have tobacco companies, who are consummate marketers, continuing to produce products that kill one in two of their most loyal customers?” It’s not about customer satisfaction, but shareholder satisfaction. The customer always comes second.

    Just as weight gain may be a perfectly natural reaction to an obesogenic food environment, governments and businesses are simply responding normally to the political and economic realities of our system. Can you think of a single major industry that would benefit from people eating more healthfully? “Certainly not the agriculture, food product, grocery, restaurant, diet, or drug industries,” wrote emeritus professor Marion Nestle in a Science editorial when she was chair of nutrition at New York University. “All flourish when people eat more, and all employ armies of lobbyists to discourage governments from doing anything to inhibit overeating.”

    If part of the problem is cheap tasty convenience, is hard-to-find food that’s gross and expensive the solution? Or might there be a way to get the best of all worlds—easy, healthy, delicious, satisfying meals that help you lose weight? That’s the central question of my book How Not to Diet. Check it out for free at your local library.

    This is it—the final video in this 11-part series. If you missed any of the others, see the related posts below. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

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

    Corporate Influence and Our Epidemic of Obesity  | NutritionFacts.org

    [ad_1]

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

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

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

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

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

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

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

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

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

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

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

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

    If the political angle interests you, check out: 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Should We Take Any Responsibility for the Obesity Epidemic?  | NutritionFacts.org

    Should We Take Any Responsibility for the Obesity Epidemic?  | NutritionFacts.org

    [ad_1]

    The power of the “eat more” food environment can overcome our conscious controls.

    Food and beverage companies frame body weight as “a matter of personal choice.” Even when we aren’t distracted, the power of the “eat more” food environment may sometimes overcome our conscious controls of overeating. One look around the room at a dietician convention can tell you that even nutrition professionals are vulnerable to the aggressively marketed ubiquity of tasty, cheap, convenient calories. This suggests there are aspects of our eating behaviors “that defy personal insight or are below individual awareness,” flying below the radar of conscious awareness. Appetite physiologists call the result of these subconscious actions “passive overconsumption.”

    Remember that brain scan study where the thought of a milkshake lit up the same reward pathways in the brain as substance abuse? That was triggered just by a picture of a milkshake. Dopamine gets released, cravings get activated, and we’re motivated to eat. Intellectually, we know it’s just an image, but our lizard brain sees survival. It’s just a reflexive response over which we have little control, which is why marketers ensure there are pictures of milkshakes and their equivalents everywhere.

    As I discuss in my video The Role of Personal Responsibility in the Obesity Epidemic, maintaining a balance between calories in and calories out feels like a series of voluntary acts under conscious control, but it may be more akin to bodily functions, such as blinking, breathing, coughing, swallowing, or sleeping. You can try to will yourself power over any of these, but by and large, they just happen automatically, driven by ancient scripts.

    Not only are food ads ubiquitous, but so is the food. The types of establishments selling food products expanded dramatically in the 1970s and 1980s. Now, you can find candy and snacks at the checkout counters of “gasoline stations, building material outlets, auto parts stores, drug stores, and home furnishing stores” and more. The largest food retailer in the United States is Wal-Mart. You can get that jolt of “dopamine and the associated artificially induced feelings of hunger in modern society” around every turn. Every day, we run the gauntlet.

    It’s also become “socially acceptable to eat food at any time of day and anywhere—in cars, in your hand, on the street—places where eating had never been acceptable.” We’ve become a snacking society. Vending machines are everywhere. Daily eating episodes seem to have gone up by about a quarter since the late 1970s, increasing from about four to five occasions a day, potentially accounting for twice the calorie increase attributed to increasing portion sizes. Snacks and beverages alone could account for the bulk of the calorie surplus implicated in the obesity epidemic.

    And think of the children. Here we are trying to do the best for our kids, role-modeling healthy habits and feeding them healthy foods, but then they venture out into a veritable tornado of junky food and manipulative messages. A commentary in The New England Journal of Medicine asked: “But why should Mr. and Ms. G.’s efforts to protect their children from life-threatening illness be undermined by massive marketing campaigns from the manufacturers of junk food?” Pediatricians are now encouraged to have the “French Fry Discussion” with parents at the 12-month well-child visit instead of waiting until their kids are two—though even that may be too late. As you can see below and at 3:35 in my video, two-thirds of infants are being fed junk food by their first birthday. 

    Dr. David Katz may have said it best in the Harvard Health Policy Review: “Those who contend that parental or personal responsibility should carry the day despite these environmental temptations might consider the implications of generalizing the principle. Perhaps children should be encouraged, but not required, to attend school and tempted each morning by alternatives, such as buses to the circus, zoo, or beach.” 

    It may be helpful to take a step back and think of what’s at stake here. We aren’t just talking about being manipulated into buying a different brand of toothpaste. The obesity pandemic has resulted in millions of deaths and untold suffering. If you aren’t mad yet, brace yourself for my next video: The Role of Corporate Influence in the Obesity Epidemic.

    This is the ninth video in my 11-part series. If you missed any of the previous ones, see the related posts below.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Are Food Ads Making Us Obese?  | NutritionFacts.org

    Are Food Ads Making Us Obese?  | NutritionFacts.org

    [ad_1]

    We all like to think we make important life decisions, like what to eat, consciously and rationally, but if that were the case, we wouldn’t be in the midst of an obesity epidemic.

    The opening words of the Institute of Medicine’s report on the potential threat posed by food ads were: “Marketing works.” Certainly, there is a “large number of well-conducted randomized experiments” I could go through with you that “have shown that exposure to marketing—especially, but not only, advertising—changes people’s eating behavior. Marketing causes people to choose to eat more.” But, what do you need to know beyond the fact that the industry spends tens of billions of dollars a year on it? To get people to drink its brown sugar water, do you think Coca-Cola would spend a penny more than it thought it had to? It’s like when my medical colleagues accept “drug lunches” from pharmaceutical representatives and take offense that I would suggest it might affect their prescribing practices. Do they really think drug companies are in the business of giving away free money for nothing? They wouldn’t do it if it didn’t work. 

    To give you a sense of marketing’s insidious nature, let me share an interesting piece of research published in the world’s leading scientific journal: “In-Store Music Affects Product Choice” documented an experiment in which French accordion music or German Bierkeller music was played on alternate days in the wine section of a grocery store. As you can see below and at 1:27 in my video The Role of Food Advertisements in the Obesity Epidemic, on the days the French music played in the background, people were three times more likely to buy French wine, and on German music days, shoppers were about three times more likely to buy German wine. And it wasn’t a difference of just a few percent; it was a complete three-fold reversal. Despite the dramatic effect, when shoppers were approached afterward, the vast majority of them denied the music had influence on their choice. 

    Most of our day-to-day behavior does not appear to be dictated by careful, considered deliberations, even if we’d like to think that were the case. Rather, we tend to make more automatic, impulsive decisions triggered by unconscious cues or habitual patterns, especially when we are “under stress, tired, or preoccupied. This unconscious part of our brain is estimated to function and guide our behaviors at least 95% of the time.” This is the arena where marketing manipulations do most of their dirty work. 

    The part of our brain that governs conscious awareness may only be able to process about 50 bits of information per second, which is roughly equivalent to a short tweet. Our entire cognitive capacity, on the other hand, is estimated to process more than 10 million bits per second. Because we’re only able to purposefully process a limited amount of information at a time, if we’re distracted or otherwise unable to concentrate, our decisions can become even more impulsive. An elegant illustration of this “cognitive overload” effect was provided from an experiment involving fruit salad and chocolate cake.

    Before calls could be made at the touch of a button or the sound of our voice, the seven-digit span of phone numbers in the United States was based in part on the longest sequence most people can recall on the fly. We only seem to be able to hold about seven chunks of information (plus or minus two) in our immediate short-term memory. The study’s setup: Randomize people to memorize either a seven-digit number or a two-digit number to be recalled in another room down the hall. On the way, offer them the choice of a fruit salad or a piece of chocolate cake. Memorizing a two-digit number is easy and presumably takes few cognitive resources. As you can see in the graph below and at 3:52 in my video, under the two-digit condition, most study participants chose fruit salad. Faced with the same decision, most of those trying to keep seven digits in their heads just went for the cake. 

    This can play out in the real world by potentiating the effect of advertising. Have people watch a TV show with commercials for unhealthy snacks, and, no surprise, they eat more unhealthy snacks compared to those exposed to non-food ads. Or maybe that is a surprise. We all like to think we’re in control and not so easily manipulated. The kicker, though, is that we may be even more susceptible the less we pay attention. Randomize people to the same two-digit or seven-digit memorization task during the TV show, and the snack-attack effect was magnified among those who were more preoccupied. How many of us have the TV on in the background or multi-task during commercial breaks? Research suggests that may make us even more impressionable to the subversion of our better judgment. 

    There’s an irony in all of this. Calls for restrictions on marketing are often resisted by invoking the banner of freedom. What does that even mean in this context, when research shows how easily our free choices can be influenced without our conscious control? A senior policy researcher at the RAND Corporation even went as far as to suggest that, given the dire health consequences of our unhealthy eating habits, “the marketing techniques of which we are unaware should be considered in the same light as the invisible carcinogens and toxins in the air and water that can poison us without our awareness.”

    Given the role marketing can play even when we least suspect it, what is the role of personal responsibility in the obesity epidemic? That’s the subject of my next video.

    We are winding down this series on obesity, with three videos remaining: 

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Do Taxpayer Subsidies Play a Role in the Obesity Epidemic?  | NutritionFacts.org

    Do Taxpayer Subsidies Play a Role in the Obesity Epidemic?  | NutritionFacts.org

    [ad_1]

    Why are U.S. taxpayers giving billions of dollars to support the likes of the sugar and meat industries?

    The rise in calorie surplus sufficient to explain the obesity epidemic was less a change in food quantity than in food quality. Access to cheap, high-calorie, low-quality convenience foods exploded, and the federal government very much played a role in making this happen. U.S. taxpayers give billions of dollars in subsidies to prop up the likes of the sugar industry, the corn industry and its high-fructose syrup, and the production of soybeans, about half of which is processed into vegetable oil and the other half is used as cheap feed to help make dollar-menu meat. You can see a table of subsidy recipients below and at 0:49 in my video The Role of Taxpayer Subsidies in the Obesity Epidemic. Why do taxpayers give nearly a quarter of a billion dollars a year to the sorghum industry? When was the last time you sat down to some sorghum? It’s almost all fed to cattle and other livestock. “We have created a food price structure that favors relatively animal source foods, sweets, and fats”—animal products, sugars, and oils.

    The Farm Bill started out as an emergency measure during the Great Depression of the 1930s to protect small farmers but was weaponized by Big Ag into a cash cow with pork barrel politics—including said producers of beef and pork. From 1970 to 1994, global beef prices dropped by more than 60 percent. And, if it weren’t for taxpayers “sweetening the pot” with billions of dollars a year, high-fructose corn syrup would cost the soda industry about 12 percent more. Then we hand Big Soda billions more through the Supplemental Nutrition Assistance Program (SNAP), formerly known as the Food Stamps Program, to give sugary drinks to low-income individuals. Why is chicken so cheap? After one Farm Bill, corn and soy were subsidized below the cost of production for cheap animal fodder. We effectively handed the poultry and pork industries about $10 billion each. That’s not chicken feed—or rather, it is! 

    This is changing what we eat. 

    As you can see below and at 2:03 in my video, thanks in part to subsidies, dairy, meats, sweets, eggs, oils, and soda were all getting relatively cheaper compared to the overall consumer food price index as the obesity epidemic took off, whereas the relative cost of fresh fruits and vegetables doubled. This may help explain why, during about the same period, the percentage of Americans getting five servings of fruits and vegetables a day dropped from 42 percent to 26 percent. Why not just subsidize produce instead? Because that’s not where the money is. 

    “To understand what is shaping our foodscape today, it is important to understand the significance of differential profit.” Whole foods or minimally processed foods, such as canned beans or tomato paste, are what the food business refers to as “commodities.” They have such slim profit margins that “some are typically sold at or below cost, as ‘loss leaders,’ to attract customers to the store” in the hopes that they’ll also buy the “value-added” products. Some of the most profitable products for producers and vendors alike are the ultra-processed, fatty, sugary, and salty concoctions of artificially flavored, artificially colored, and artificially cheap ingredients—thanks to taxpayer subsidies. 

    Different foods reap different returns. Measured in “profit per square foot of selling space” in the supermarket, confectionaries like candy bars consistently rank among the most lucrative. The markups are the only healthy thing about them. Fried snacks like potato chips and corn chips are also highly profitable. PepsiCo’s subsidiary Frito-Lay brags that while its products represented only about 1 percent of total supermarket sales, they may account for more than 10 percent of operating profits for supermarkets and 40 percent of profit growth. 

    It’s no surprise, then, that the entire system is geared towards garbage. The rise in the calorie supply wasn’t just more food but a different kind of food. There’s a dumb dichotomy about the drivers of the obesity epidemic: Is it the sugar or the fat? They’re both highly subsidized, and they both took off. As you can see below and at 4:29 and 4:35 in my video, along with a significant rise in refined grain products that is difficult to quantify, the rise in obesity was accompanied by about a 20 percent increase in per capita pounds of added sugars and a 38 percent increase in added fats. 

     

    More than half of all calories consumed by most adults in the United States were found to originate from these subsidized foods, and they appear to be worse off for it. Those eating the most had significantly higher levels of chronic disease risk factors, including elevated cholesterol, inflammation, and body weight. 

    If it really were a government of, by, and for the people, we’d be subsidizing healthy foods, if anything, to make fruits and vegetables cheap or even free. Instead, our tax dollars are shoveled to the likes of the sugar industry or to livestock feed to make cheap, fast-food meat. 

    Speaking of sorghum, I had never had it before and it’s delicious! In fact, I wish I had discovered it before How Not to Diet was published. I now add sorghum and finger millet to my BROL bowl which used to just include purple barley groats, rye groats, oat groats, and black lentils, so the acronym has become an unpronounceable BROLMS. Anyway, sorghum is a great rice substitute for those who saw my rice and arsenic video series and were as convinced as I am that we need to diversify our grains. 

    We now turn to marketing. After all of the taxpayer-subsidized glut of calories in the market, the food industry had to find a way to get it into people’s mouths. So, next: The Role of Marketing in the Obesity Epidemic. 

    We’re about halfway through this series on the obesity epidemic. If you missed any so far, check out the related videos below.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Processed Foods and Obesity  | NutritionFacts.org

    Processed Foods and Obesity  | NutritionFacts.org

    [ad_1]

    The rise in the U.S. calorie supply responsible for the obesity epidemic wasn’t just about more food, but a different kind of food.

    The rise in the number of calories provided by the food supply since the 1970s “is more than sufficient to explain the US epidemic of obesity.” Similar spikes in calorie surplus were noted in developed countries around the world in parallel with and presumed to be primarily responsible for, the expanding waistlines of their populations. After taking exports into account, by the year 2000, the United States was producing 3,900 calories for every man, woman, and child—nearly twice as much as many people need. 

    It wasn’t always this way. The number of calories in the food supply actually declined over the first half of the twentieth century and only started its upward climb to unprecedented heights in the 1970s. The drop in the first half of the century was attributed to the reduction in hard manual labor. The population had decreased energy needs, so they ate decreased energy diets. They didn’t need all the extra calories. But then the “energy balance flipping point” occurred, when the “move less, stay lean phase” that existed throughout most of the century turned into the “eat more, gain weight phase” that plagues us to this day. So, what changed?

    As I discuss in my video The Role of Processed Foods in the Obesity Epidemic, what happened in the 1970s was a revolution in the food industry. In the 1960s, most food was prepared and cooked in the home. The typical “married female, not working” spent hours a day cooking and cleaning up after meals. (The “married male, non-working spouse” averaged nine minutes, as you can see below and at 1:34 in my video.) But then a mixed-blessing transformation took place. Technological advances in food preservation and packaging enabled manufacturers to mass prepare and distribute food for ready consumption. The metamorphosis has been compared to what happened a century before with the mass production and supply of manufactured goods during the Industrial Revolution. But this time, they were just mass-producing food. Using new preservatives, artificial flavors, and techniques, such as deep freezing and vacuum packaging, food corporations could take advantage of economies of scale to mass produce “very durable, palatable, and ready-to-consume” edibles that offer “an enormous commercial advantage over fresh and perishable whole or minimally processed foods.” 

    Think ye of the Twinkie. With enough time and effort, “ambitious cooks” could create a cream-filled cake, but now they are available around every corner for less than a dollar. If every time someone wanted a Twinkie, they had to bake it themselves, they’d probably eat a lot fewer Twinkies. The packaged food sector is now a multitrillion-dollar industry.

    Consider the humble potato. We’ve long been a nation of potato eaters, but we usually baked or boiled them. Anyone who’s made fries from scratch knows what a pain it is, with all the peeling, cutting, and splattering of oil. But with sophisticated machinations of mechanization, production became centralized and fries could be shipped at -40°F to any fast-food deep-fat fryer or frozen food section in the country to become “America’s favorite vegetable.” Nearly all the increase in potato consumption in recent decades has been in the form of french fries and potato chips. 

    Cigarette production offers a compelling parallel. Up until automated rolling machines were invented, cigarettes had to be rolled by hand. It took 50 workers to produce the same number of cigarettes a machine could make in a minute. The price plunged and production leapt into the billions. Cigarette smoking went from being “relatively uncommon” to being almost everywhere. In the 20th century, the average per capita cigarette consumption rose from 54 cigarettes a year to 4,345 cigarettes “just before the first landmark Surgeon General’s Report” in 1964. The average American went from smoking about one cigarette a week to half a pack a day.

    Tobacco itself was just as addictive before and after mass marketing. What changed was cheap, easy access. French fries have always been tasty, but they went from being rare, even in restaurants, to being accessible around each and every corner (likely next to the gas station where you can get your Twinkies and cigarettes).

    The first Twinkie dates back to 1930, though, and Ore-Ida started selling frozen french fries in the 1950s. There has to be more to the story than just technological innovation, and we’ll explore that next.

    This explosion of processed junk was aided and abetted by Big Government at the behest of Big Food, which I explore in my video The Role of Taxpayer Subsidies in the Obesity Epidemic.

    This is the fifth video in an 11-part series. Here are the first four: 

    Videos still to come are listed in the related videos below.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Cutting the Calorie-Rich-And-Processed Foods  | NutritionFacts.org

    Cutting the Calorie-Rich-And-Processed Foods  | NutritionFacts.org

    [ad_1]

    We have an uncanny ability to pick out the subtle distinctions in calorie density of foods, but only within the natural range.

    The traditional medical view on obesity, as summed up nearly a century ago: “All obese persons are, alike in one fundamental respect,—they literally overeat.” While this may be true in a technical sense, it is in reference to overeating calories, not food. Our primitive urge to overindulge is selective. People don’t tend to lust for lettuce. We have a natural inborn preference for sweet, starchy, or fatty foods because that’s where the calories are concentrated.

    Think about hunting and gathering efficiency. We used to have to work hard for our food. Prehistorically, it didn’t make sense to spend all day collecting types of food that on average don’t provide at least a day’s worth of calories. You would have been better off staying back at the cave. So, we evolved to crave foods with the biggest caloric bang for their buck.

    If you were able to steadily forage a pound of food an hour and it had 250 calories per pound, it might take you ten hours just to break even on your calories for the day. But if you were gathering something with 500 calories a pound, you could be done in five hours and spend the next five working on your cave paintings. So, the greater the energy density—that is, the more calories per pound—the more efficient the foraging. We developed an acute ability to discriminate foods based on calorie density and to instinctively desire the densest.

    If you study the fruit and vegetable preferences of four-year-old children, what they like correlates with calorie density. As you can see in the graph below and at 1:52 in my video Friday Favorites: Cut the Calorie-Rich-And-Processed Foods, they prefer bananas over berries and carrots over cucumbers. Isn’t that just a preference for sweetness? No, they also prefer potatoes over peaches and green beans over melon, just like monkeys prefer avocados over bananas. We appear to have an inborn drive to maximize calories per mouthful. 

    All the foods the researchers tested in the study with four-year-old kids naturally had less than 500 calories per pound. (Bananas topped the chart at about 400.) Something funny happens when you start going above that: We lose our ability to differentiate. Over the natural range of calorie densities, we have an uncanny aptitude to pick out the subtle distinctions. However, once you start heading towards bacon, cheese, and chocolate territory, which can reach thousands of calories per pound, our perceptions become relatively numb to the differences. It’s no wonder since these foods were unknown to our prehistoric brains. It’s like the dodo bird failing to evolve a fear response because they had no natural predators—and we all know how that turned out—or sea turtle hatchlings crawling in the wrong direction towards artificial light rather than the moon. It is aberrant behavior explained by an “evolutionary mismatch.”

    The food industry exploits our innate biological vulnerabilities by stripping crops down into almost pure calories—straight sugar, oil (which is pretty much pure fat), and white flour (which is mostly refined starch). It also removes the fiber, because that effectively has zero calories. Run brown rice through a mill to make white rice, and you lose about two-thirds of the fiber. Turn whole-wheat flour into white flour, and lose 75 percent. Or you can run crops through animals (to make meat, dairy, and eggs) and remove 100 percent of the fiber. What you’re left with is CRAP—an acronym used by one of my favorite dieticians, Jeff Novick, for Calorie-Rich And Processed food.

    Calories are condensed in the same way plants are turned into addictive drugs like opiates and cocaine: “distillation, crystallization, concentration, and extraction.” They even appear to activate the same reward pathways in the brain. Put people with “food addiction” in an MRI scanner and show them a picture of a chocolate milkshake, and the areas that light up in their brains (as you can see below and at 4:15 in my video) are the same as when cocaine addicts are shown a video of crack smoking. (See those images below and at 4:18 in my video.) 

    “Food addiction” is a misnomer. People don’t suffer out-of-control eating behaviors to food in general. We don’t tend to compulsively crave carrots. Milkshakes are packed with sugar and fat, two of the signals to our brain of calorie density. When people are asked to rate different foods in terms of cravings and loss of control, most incriminated was a load of CRAP—highly processed foods like donuts, along with cheese and meat. Those least related to problematic eating behaviors? Fruits and vegetables. Calorie density may be the reason people don’t get up in the middle of the night and binge on broccoli.

    Animals don’t tend to get fat when they are eating the foods they were designed to eat. There is a confirmed report of free-living primates becoming obese, but that was a troop of baboons who stumbled across the garbage dump at a tourist lodge. The garbage-feeding animals weighed 50 percent more than their wild-feeding counterparts. Sadly, we can suffer the same mismatched fate and become obese by eating garbage, too. For millions of years, before we learned how to hunt, our biology evolved largely on “leaves, roots, fruits, and nuts.” Maybe it would help if we went back to our roots and cut out the CRAP. 

    A key insight I want to emphasize here is the concept of animal products as the ultimate processed food. Basically, all nutrition grows from the ground: seeds, sunlight, and soil. That’s where all our vitamins come from, all our minerals, all the protein, all the essential amino acids. The only reason there are essential amino acids in a steak is because the cow ate them all from plants. Those amino acids are essential—no animals can make them, including us. We have to eat plants to get them. But we can cut out the middlemoo and get nutrition directly from the Earth, and, in doing so, get all the phytonutrients and fiber that are lost when plants are processed through animals. Even ultraprocessed junk foods may have a tiny bit of fiber remaining, but all is lost when plants are ultra-ultraprocessed through animals.

    Having said that, there was also a big jump in what one would traditionally think of as processed foods, and that’s the video we turn to next: The Role of Processed Foods in the Obesity Epidemic.

    We’re making our way through a series on the cause of the obesity epidemic. So far, we’ve looked at exercise (The Role of Diet vs. Exercise in the Obesity Epidemic) and genes (The Role of Genes in the Obesity Epidemic and The Thrifty Gene Theory: Survival of the Fattest), but, really, it’s the food.

    If you’re familiar with my work, you know that I recommend eating a variety of whole plant foods, as close as possible to the way nature intended. I capture this in my Daily Dozen, which you can download for free here or get the free app (iTunes and Android). On the app, you’ll see that there’s also an option for those looking to lose weight: my 21 Tweaks. But before you go checking them off, be sure to read about the science behind the checklist in my book How Not to Diet. Get it for free at your local public library. If you choose to buy a copy, note that all proceeds from all of my books go to charity. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link