ReportWire

Tag: animal products

  • Keeping Better Score of Your Diet | NutritionFacts.org

    [ad_1]

    How can you get a perfect diet score?

    How do you rate the quality of people’s diets? Well, “what could be more nutrient-dense than a vegetarian diet?” Indeed, if you compare the quality of vegetarian diets with non-vegetarian diets, the more plant-based diets do tend to win out, and the higher diet quality in vegetarian diets may help explain greater improvements in health outcomes. However, vegetarians appear to have a higher intake of refined grains, eating more foods like white rice and white bread that have been stripped of much of their nutrition. So, just because you’re eating a vegetarian diet doesn’t mean you’re necessarily eating as healthfully as possible.

    Those familiar with the science know the primary health importance of eating whole plant foods. So, how about a scoring system that simply adds up how many cups of fruits, vegetables, whole grains, beans, chickpeas, split peas, and lentils, and how many ounces of nuts and seeds per 1,000 calories (with or without counting white potatoes)? Looking only at the total intake of whole plant foods doesn’t mean you aren’t also stuffing donuts into your mouth. So, you could imagine proportional intake measures, based on calories or weight, to determine the proportion of your diet that’s whole plant foods. In that case, you’d get docked points if you eat things like animal-derived foods—meat, dairy, or eggs—or added sugars and fats.

    My favorite proportional intake measure is McCarty’s “phytochemical index,” which I’ve profiled previously. I love it because of its sheer simplicity, “defined as the percent of dietary calories derived from foods rich in phytochemicals.” It assigns a score from 0 to 100, based on the percentage of your calories that are derived from foods rich in phytochemicals, which are biologically active substances naturally found in plants that may be contributing to many of the health benefits obtained from eating whole plant foods. “Monitoring phytochemical intake in the clinical setting could have great utility” in helping people optimize their diet for optimal health and disease prevention. However, quantifying phytochemicals in foods or tissue samples is impractical, laborious, and expensive. But this concept of a phytochemical index score could be a simple alternative method to monitor phytochemical intake.

    Theoretically, a whole food, plant-based or vegan diet that excluded refined grains, white potatoes, hard liquors, added oils, and added sugars could achieve a perfect score of 100. Lamentably, most Americans’ diets today might be lucky to score just 20. What’s going on? In 1998, our shopping baskets were filled with about 20% whole plant foods; more recently, that has actually shrunk, as you can see below and at 2:49 in my video Plant-Based Eating Score Put to the Test.

    Wouldn’t it be interesting if researchers used this phytochemical index to try to correlate it with health outcomes? That’s exactly what they did. We know that studies have demonstrated that vegetarian diets have a protective association with weight and body mass index. For instance, a meta-analysis of five dozen studies has shown that vegetarians had significantly lower weight and BMI compared with non-vegetarians. And even more studies show that high intakes of fruits, vegetables, whole grains, and legumes may be protective regardless of meat consumption. So, researchers wanted to use an index that gave points for whole plant foods. They used the phytochemical index and, as you may recall from an earlier video, tracked people’s weight over a few years, using a scale of 0 to 100 to simply reflect what percentage of a person’s diet is whole plant foods. And even though the healthiest-eating tier only averaged a score of about 40, which meant the bulk of their diet was still made up of processed foods and animal products, just making whole plant foods a substantial portion of the diet may help prevent weight gain and decrease body fat. So, it’s not all or nothing. Any steps we can take to increase our whole plant food intake may be beneficial.

    Many more studies have since been performed, with most pointing in the same direction for a variety of health outcomes—indicating, for instance, higher healthy plant intake is associated with about a third of the odds of abdominal obesity and significantly lower odds of high triglycerides. So, the index may be “a useful dietary target for weight loss,” where there is less focus on calorie intake and more on increasing consumption of these high-nutrient, lower-calorie foods over time. Other studies also suggest the same is true for childhood obesity.

    Even at the same weight, with the same amount of belly fat, those eating plant-based diets tend to have higher insulin sensitivity, meaning the insulin they make works better in their body, perhaps thanks to the compounds in plants that alleviate inflammation and quench free radicals. Indeed, the odds of hyperinsulinemia—an indicator of insulin resistance—were progressively lower with greater plant consumption. No wonder researchers found 91% lower odds of prediabetes for people getting more than half their calories from healthy plant foods.

    They also found significantly lower odds of metabolic syndrome and high blood pressure. There were only about half the odds of being diagnosed with hypertension over a three-year period among those eating more healthy plants. Even mental health may be impacted—about 80% less depression, 2/3 less anxiety, and 70% less psychological distress, as you can see below and at 5:15 in my video.

    Is there a link between the dietary phytochemical index and benign breast diseases, such as fibrocystic diseases, fatty necrosis, ductal ectasia, and all sorts of benign tumors? Yes—70% lower odds were observed in those with the highest scores. But what about breast cancer? A higher intake of healthy plant foods was indeed associated with a lower risk of breast cancer, even after controlling for a long list of other factors. And not just by a little bit. Eating twice the proportion of plants compared to the standard American diet was linked to more than 90% lower odds of breast cancer.

    Doctor’s Note

    You can learn more about the phytochemical index in Calculate Your Healthy Eating Score.

    If you’re worried about protein, check out Flashback Friday: Do Vegetarians Get Enough Protein?

    It doesn’t have to be all or nothing, though. Do Flexitarians Live Longer?

    For more on plant-based junk, check out Friday Favorites: Is Vegan Food Always Healthy?.

    [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

  • Is Fasting an Effective Treatment for Diabetes? | NutritionFacts.org

    [ad_1]

    By losing 15% of their body weight, nearly 90% of those who have had type 2 diabetes for less than four years may achieve remission.

    Currently, more than half a billion adults have diabetes, and about a 50% increase is expected in another generation. I’ve got tons of videos on the best diets for diabetes, but what about no diet at all?

    More than a century ago, fasting was said to cure diabetes, quickly halting its progression and eliminating all signs of the disease within days or weeks. Even so, starvation is guaranteed to lead to the complete disappearance of you if kept up long enough. What’s the point of fasting away the pounds if they’re just going to return as soon as you restart the diet that created them in the first place? Might it be useful to kickstart a healthier diet? Let’s see what the science says.

    Type 2 diabetes has long been recognized as a disease of excess, once thought to afflict only “the idle rich…anyone whose environment and self-support does not require of him some sustained vigorous bodily exertion every day, and whose earnings or income permit him, and whose inclination tempts him, to eat regularly more than he needs.” Diabetes is preventable, so might it also be treatable? If we’re dying from overeating, maybe we can be saved by undereating. Remarkably, this idea was proposed about 2,000 years ago in an Ayurvedic text:

    “Poor diabetic people’s medicine
    He should live like a saint (Munni);
    He should walk for 800–900 miles.
    Or he shall dig a pond;
    Or he shall live only on cow dung and cow urine.”

    That reminds me of the Rollo diet for diabetes proposed in 1797, which was composed of rancid meat. That was on top of the ipecac-like drugs he used to induce severe sickness and vomiting. Anything that makes people sick has only “a temporary effect in relieving diabetes” because it reduces the amount of food eaten. His diet plan—which included congealed blood for lunch and spoiled meat for dinner—certainly had that effect.

    Similar benefits were seen in people with diabetes during the siege of Paris in the Franco‐Prussian War, leading to the advice to mangez le moins possible, which translates to “eat as little as possible.” This was formalized into the Allen starvation treatment, considered to be “the greatest advance in the treatment of diabetes prior to the discovery of insulin.” Before insulin, there was “The Allen Era.”

    Dr. Allen noted that there are clinical reports of even severe diabetes cases clearing up after the onset of a “wasting condition” like tuberculosis or cancer, so he decided to put it to the test. He found that even in the most severe type of diabetes, he could clear sugar from people’s urine within ten days. Of course, that’s the easy part; it’s harder to maintain once they start eating again. To manage patients’ diabetes, he stuck to two principles: Keep them underweight and restrict the fat in their diet. A person with severe diabetes can be symptom-free for days or weeks, but eating butter or olive oil can make the disease come raging back.

    As I’ve said before, diabetes is a disease of fat toxicity. Infuse fat into people’s veins through an IV, and, by using a high-tech type of MRI scanner, you can show in real time the buildup of fat in muscle cells within hours, accompanied by an increase in insulin resistance. The same thing happens when you put people on a high-fat diet for three days. It can even happen in just one day. Even a single meal can increase insulin resistance within six hours. Acute dietary fat intake rapidly increases insulin resistance. Why do we care? Insulin resistance in our muscles, in the context of too many calories, can lead to a buildup of liver fat, followed by fat accumulation in the pancreas, and eventually full-blown diabetes. “Type 2 diabetes can now be understood as a state of excess fat in the liver and pancreas, and remains reversible for at least 10 years in most individuals.”

    When people are put on a very low-calorie diet—700 calories a day—fat can get pulled out of their muscle cells, accompanied by a corresponding boost in insulin sensitivity, as shown below and at 4:43 in my video Fasting to Reverse Diabetes.

    The fat buildup in the liver has then been shown to decrease substantially, and if the diet is continued, the excess fat in the pancreas also reduces. If caught early enough, reversing type 2 diabetes is possible, which would mean sustained healthy blood sugar levels on a healthy diet.

    With the loss of 15% of body weight, nearly 90% of individuals who have had type 2 diabetes for less than four years can achieve non-diabetic blood sugar levels, whereas it may only be reversible in 50% of those who’ve lived with the disease for longer than eight years. That’s better than bariatric surgery, where those losing even more weight had lower remission rates of 62% and 26%, respectively. Your forks are better than surgeons’ knives. Indeed, most people who have had their type 2 diabetes diagnosis for an average of three years can reverse their disease after losing about 30 pounds, as you can see below and at 5:37 in my video.

    Of course, an extended bout of physician-supervised, water-only fasting could also get you there, but you would have to maintain that weight loss. One of the things that has been said with “certainty” is that if you regain the weight, you regain your diabetes.

    To bring it full circle, “the initial euphoria about ‘medicine’s greatest miracle’”—the discovery of insulin in 1921—“soon gave way to the realisation” that, while it was literally life-saving for people with type 1 diabetes, insulin alone wasn’t enough to prevent such complications as blindness, kidney failure, stroke, and amputations in people with type 2 diabetes. That’s why one of the most renowned pioneers in diabetes care, Elliott Joslin, “argued that self-discipline on diet and exercise, as it was in the days prior to the availability of the drug [insulin], should be central to the management of diabetes….”

    Doctor’s Note

    Check out Diabetes as a Disease of Fat Toxicity for more on the underlying cause of the disease.

    For more on fasting for disease reversal, see:

    Fasting is not the best way to lose weight. To learn more, see related posts below.

    What is the best way to lose weight? See Friday Favorites: The Best Diet for Weight Loss and Disease Prevention.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • How Healthy Are Baruka Nuts? | NutritionFacts.org

    [ad_1]

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

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

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

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

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

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

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

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

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

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

    Doctor’s Note

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

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

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

    [ad_1]

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

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

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

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

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

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

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

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

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

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

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

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

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

    Doctor’s Note

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

    For more on TMAO, check out related posts below. 

    See the microbiome topic page for even more.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Fasting and Plant-Based Diets for Migraines and Traumatic Brain Injuries  | NutritionFacts.org

    [ad_1]

    What effects do fasting and a plant-based diet have on TBI and migraines?

    An uncontrolled and unpublished study purported to show a beneficial effect of fasting on migraine headaches, but fasting may be more likely to trigger a migraine than help it. In fact, “skipped meals are among the most consistently identified dietary triggers” of headaches in general. In a review of hundreds of fasts at the TrueNorth Health Center in California, the incidence of headache was nearly one in three, but TrueNorth also published a remarkable case report on post-traumatic headache.

    The U.S. Centers for Disease Control and Prevention (CDC) estimates that more than a million Americans sustain traumatic brain injuries (TBIs) every year. Chronic pain is a common complication, affecting perhaps three-quarters of those who suffer such an injury. There are drugs, of course, to treat post-traumatic headache. There are always drugs. And if drugs don’t work, there is surgery, cutting the nerves to the head to stop the pain.

    What about fasting and plants? A 52-year-old woman presented with a highly debilitating, difficult-to-manage, unremitting, chronic post-traumatic headache. And when I say chronic, I mean chronic; she experienced pain for 16 years. She then achieved long-term relief after fasting, followed by an exclusively plant-foods diet, free of added sugar, oil, or salt.

    Before then, she had tried drug after drug after drug after drug after drug—with no relief, suffering in constant pain for years. Before the fast, she started out in constant pain. Then, after the fast, the intensity of the pain was cut in half, and though she was still having daily headaches, at least there were some pain-free periods. Six months later, she tried again, and eventually her headaches became mild, lasting less than ten minutes, and infrequent. She continued that way for months and even years, as you can see below and at 1:45 in my video Fasting for Post-Traumatic Brain Injury Headache. 

    Now, of course, it’s hard to disentangle the effects of the fasting from the effects of the whole food, plant-based diet she remained on for those ensuing years. You’ve heard of analgesics (painkillers). Well, there are some foods that may be pro-algesic (pain-promoting), such as foods high in arachidonic acid, including meats, dairy, and eggs. So, the lowering of arachidonic acid—from which our body makes a range of pro-inflammatory compounds—may be accomplished by eating a more plant-based diet. So, maybe that contributed to the benefit in the fasting case, since many plant foods are high in anti-inflammatory components. In terms of migraine headaches, more plant foods and less animal foods may help, but you don’t know until you put it to the test.

    Researchers figured a plant-based diet may offer the best of both worlds, so they designed a randomized, controlled, crossover study where those with recurrent migraines were randomized to eat a strictly plant-based diet or take a placebo pill. Then, the groups switched. During the placebo phase, half of the participants said their pain improved, and the other half said their pain remained the same or got worse. But, during the dietary phase, they almost all got better, as you can see here and at 3:11 in my video.

    During that first phase, the diet group experienced significant improvements in the number of headaches, pain intensity, and days with headaches, as well as a reduction in the amount of painkillers they needed to take. In fact, it worked a little too well. Many individuals were unwilling to return to their previous diets after they completed the diet phase of the trial, thereby refusing to complete the study. Remember, the participants were supposed to go back to their regular diets and take a placebo pill, but they felt so much better on the plant-based diet that they refused. We’ve seen this with other trials, where those trying plant-based diets felt so good, they often refused to abandon them, harming the study. So, plant-based diets can sometimes work a little too well.

    All my videos on fasting are available in a digital download here.  

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Should We Fast for IBS? | NutritionFacts.org

    [ad_1]

    More than half of irritable bowel syndrome (IBS) sufferers appear to have a form of atypical food allergy.

    A chronic gastrointestinal disorder, irritable bowel syndrome affects about one in ten people. You may have heard about low-FODMAP diets, but they don’t appear to work any better than the standard advice to avoid things like coffee or spicy and fatty foods. In fact, you can hardly tell which is which, as shown below and at 0:27 in my video Friday Favorites: Fasting for Irritable Bowel Syndrome.

    Most IBS patients, however, do seem to react to specific foods, such as eggs, wheat, dairy, or soy sauce, but when they’re tested with skin prick tests for typical food allergies, they may come up negative. We want to know what happens inside their gut when they eat those things, though, not what happens on their skin. Enter confocal laser endomicroscopy.

    You can snake a microscope down the throat, into the gut, and watch in real-time as the gut wall becomes inflamed and leaky after foods are dripped in. Isn’t that fascinating? You can actually see cracks forming within minutes, as shown below and at 1:03 in my video. This had never been tested on a large group of IBS patients, though, until now.

    Using this new technology, researchers found that more than half of IBS sufferers have this kind of reaction to various foods—“an atypical food allergy” that flies under the radar of traditional allergy tests. As you can see below and at 1:28 in my video, when you exclude those foods from the diet, there is a significant alleviation of symptoms.

    However, outside a research setting, there’s no way to know which foods are the culprit without trying an exclusion diet, and there’s no greater exclusion diet than excluding everything. A 25-year-old woman had complained of abdominal pain, bloating, and diarrhea for a year, and drugs didn’t seem to help. But, after fasting for ten days, her symptoms improved considerably and appeared to stay that way at least 18 months later. It wasn’t just subjective improvement either. Biopsies were taken that showed the inflammation had gone down, her bowel irritability was measured directly, and expanding balloons and electrodes were inserted in her rectum to measure changes in her sensitivity to pressure and electrical stimulation. Fasting seemed to reboot her gut in a way, but just because it worked for her doesn’t mean it works for others. Case reports are most useful when they inspire researchers to put them to the test.

    “Despite research efforts to develop a cure for IBS, medical treatment for this condition is still unsatisfactory.” We can try to suppress the symptoms with drugs, but what do we do when even that doesn’t work? In a study of 84 IBS patients, 58 of whom failed basic treatment (consisting of pharmacotherapy and brief psychotherapy), 36 of the 58 who were still suffering underwent ten days of fasting, whereas the other 22 stuck with the basic treatment. The findings? Those in the fasting group experienced significant improvements in abdominal pain, bloating, diarrhea, loss of appetite, nausea, anxiety, and interference with life in general, which were significantly better than those of the control group. The researchers concluded that fasting therapy “could be useful for treating moderate to severe patients with IBS.”

    Unfortunately, patient allocation was neither blinded nor randomized in the study, so the comparison to the control group doesn’t mean much. They were also given vitamins B1 and C via IV, which seems typical of Japanese fasting trials, even though one would not expect vitamin-deficiency syndromes—beriberi or scurvy—to present within just ten days of fasting. The study participants were also isolated; might that make the psychotherapy work better? It’s hard to tease out just the fasting effects.

    Psychotherapy alone can provide lasting benefits. Researchers randomized 101 outpatients with irritable bowel syndrome to medical treatment or medical treatment with three months of psychotherapy. After three months, the psychotherapy group did better, and the difference was even more pronounced a year later, a year after the psychotherapy ended. Better at three months, and even better at 15 months, as you can see here and at 3:58 in my video.

    Psychological approaches appear to work about as well as antidepressant drugs for IBS, but the placebo response for IBS is on the order of 40%, whether psychological interventions, drugs, or alternative medicine approaches. So, doing essentially nothing—taking a sugar pill—improves symptoms 40% of the time. In that case, I figure one might as well choose a therapy that’s cheap, safe, simple, and free of side effects, which extended fasting is most certainly not. But, if all else fails, it may be worth exploring fasting under close physician supervision.

    All my fasting videos are available in a digital download here.

    Check the videos on the topic that are already on the site here. 

    For more on IBS, see related posts below. 

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Might Meat Trigger Parkinson’s Disease?  | NutritionFacts.org

    [ad_1]

    What does the gut have to do with developing Parkinson’s disease?

    Parkinson’s disease is an ever-worsening neurodegenerative disorder that results in death and affects about 1 in 50 people as they get older. A small minority of cases are genetic, running in families, but 85% to 90% of cases are sporadic, meaning they seem to pop up out of nowhere. Parkinson’s is caused by the death of a certain kind of nerve cell in the brain. Once about 70% of them are gone, the symptoms start. What kills off those cells? It still isn’t completely clear, but the abnormal clumping of a protein called alpha-synuclein or α-synuclein is thought to be involved. Why? Researchers injected blended Parkinson’s brains into the heads of rats and monkeys, and Parkinson’s pathology and symptoms were induced. It can even happen when injecting just the pure, clumped α-synuclein strands themselves. How, though, do these clumps naturally end up in the brain?

    As I discuss in my video The Role Meat May Play in Triggering Parkinson’s Disease, it all seems to start in the gut. The part of the brain where the pathology often first appears is directly connected to the gut, and we have direct evidence of the spread of Parkinson’s pathology from the gastrointestinal (GI) tract to the brain: α-synuclein from brains of Parkinson’s patients is taken up in the gut wall and creeps up the vagal nerves from the gut into the brain—at least that was the case in rats. If only we could go back and look at people’s colons before they got Parkinson’s. Indeed, we can. Old colon biopsies from people who would later develop Parkinson’s were dredged up, and, years before symptoms arose, you could see the α-synuclein in their gut.

    Research supported by the Michael J. Fox Foundation has found that you can reliably distinguish the colons of patients from controls by the presence of this Parkinson’s protein lodged in the gut wall. But how did it get there in the first place? Are “vertebrate food products…a potential source of prion-like α-synuclein”? Indeed, nearly all the animals with backbones that we consume—cows, chickens, pigs, and fish—express the protein α-synuclein. So, when we eat common meat products, when we eat skeletal muscle, we’re eating nerves, blood cells, and the muscle cells themselves. Every pound of meat contains, on average, half a teaspoon of blood, and that alone could be an α-synuclein source to potentially trigger a clumping cascade of our own α-synuclein in the gut. Though “it may seem intuitive that dietary α-synuclein could seed aggregation in the gut,” this kind of buildup, what evidence do we have that it’s actually happening?

    We have some pretty interesting data. There’s a surgical procedure called a vagotomy, in which the big nerve that goes from our gut to our brain—the vagus nerve—is cut as an old-timey treatment for stomach ulcers. Would cutting communication between the gut and the brain reduce Parkinson’s risk? Apparently so, suggesting that the gut to brain’s vagal nerve may be critically involved in the development of Parkinson’s disease.

    Of course, “many people regularly consume meat and dairy products, but only a small fraction of the general population will develop PD,” Parkinson’s disease. So, there must be other factors at play that “may provide an opportunity for unwanted dietary α-synuclein to enter the host, and initiate disease.” For example, our gut becomes leakier as we age, so might that play a role? What else makes our gut leaky? “Dietary fiber deprivation has also been shown to degrade the intestinal barrier and enhance pathogen entry.” So, this raises “possibilities for food-based therapies.”

    Parkinson’s patients have significantly less Prevotella in their gut, a friendly fiber-eating flora that bolsters our intestinal barrier function. So, low levels of Prevotella are linked to a leaky gut, which has been linked to intestinal α-synuclein deposition, but fiber-rich foods may bring Prevotella levels back up. “Therefore, it is possible that by adopting a plant-based diet, in addition to the beneficial effects of phytonutrients, increasing overall fiber intake may modify gut microbiota and gut permeability [leakiness] in beneficial ways for people with PD.”

    So, does a vegan diet—one with lots of fiber and no meat—reduce risk for Parkinson’s? Parkinson’s “appears to be rare in quasi-vegan cultures,” with rates that are about five times lower in rural sub-Saharan Africa, for instance. All this time, we were thinking the benefits seen for Parkinson’s from plant-based diets were due to the antioxidants and anti-inflammatory nature of the animal-free diets, but maybe it’s also due to the increased intestinal exposure to fiber and decreased intestinal exposure to ingested nerves, muscles, and blood.

    Wasn’t that fascinating? For more on Parkinson’s, see the related posts below.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Hijacking Our Appetites  | NutritionFacts.org

    [ad_1]

    I debunk the myth of protein as the most satiating macronutrient.

    The importance of satiety is underscored by a rare genetic condition known as Prader-Willi syndrome. Children with the disorder are born with impaired signaling between their digestive system and their brain, so they don’t know when they’re full. “Because no sensation of satiety tells them to stop eating or alerts their body to throw up, they can accidentally consume enough in a single binge to fatally rupture their stomach.” Without satiety, food can be “a death sentence.”

    Protein is often described as the most satiating macronutrient. People tend to report feeling fuller after eating a protein-rich meal, compared to a carbohydrate- or fat-rich one. The question is: Does that feeling of fullness last? From a weight-loss standpoint, satiety ratings only matter if they end up cutting down on subsequent calorie intake, and even a review funded by the meat, dairy, and egg industries acknowledges that this does not seem to be the case for protein. Hours later, protein consumed earlier doesn’t tend to end up cutting calories later on.

    Fiber-rich foods, on the other hand, can suppress appetite and reduce subsequent meal intake more than ten hours after consumption—even the next day—because their site of action is 20 feet down in the lower intestine. Remember the ileal brake from my Evidence-Based Weight Loss lecture? When researchers secretly infused nutrients into the end of the small intestine, study participants spontaneously ate as many as hundreds fewer calories at a meal. Our brain gets the signal that we are full, from head to tail.

    We were built for gluttony. “It is a wonderful instinct, developed over millions of years, for times of scarcity.” Stumbling across a rare bounty, those who could fill themselves the most to build up the greatest reserves would be more likely to pass along their genes. So, we are hard-wired not just to eat until our stomach is full, but until our entire digestive tract is occupied. Only when our brain senses food all the way down at the end does our appetite fully dial down.

    Fiber-depleted foods get rapidly absorbed early on, though, so much of it never makes it down to the lower gut. As such, if our diet is low in fiber, no wonder we’re constantly hungry and overeating; our brain keeps waiting for the food that never arrives. That’s why people who even undergo stomach-stapling surgeries that leave them with a tiny two-tablespoon-sized stomach pouch can still eat enough to regain most of the weight they initially lost. Without sufficient fiber, transporting nutrients down our digestive tract, we may never be fully satiated. But, as I described in my last video, one of the most successful experimental weight-loss interventions ever reported in the medical literature involved no fiber at all, as you can see here and at 2:47 in my video Foods Designed to Hijack Our Appetites.

    At first glance, it might seem obvious that removing the pleasurable aspects of eating would cause people to eat less, but remember, that’s not what happened. The lean participants continued to eat the same amount, taking in thousands of calories a day of the bland goop. Only those who were obese went from eating thousands of calories a day down to hundreds, as shown below and at 3:22 in my video. And, again, this happened inadvertently without them apparently even feeling a difference. Only after eating was disconnected from the reward was the body able to start rapidly reining in the weight.

    We appear to have two separate appetite control systems: “the homeostatic and hedonic pathways.” The homeostatic pathway maintains our calorie balance by making us hungry when energy reserves are low and abolishes our appetite when energy reserves are high. “In contrast, hedonic or reward-based regulation can override the homeostatic pathway” in the face of highly palatable foods. This makes total sense from an evolutionary standpoint. In the rare situations in our ancestral history when we’d stumble across some calorie-dense food, like a cache of unguarded honey, it would make sense for our hedonic drive to jump into the driver’s seat to consume the scarce commodity. Even if we didn’t need the extra calories at the time, our body wouldn’t want us to pass up that rare opportunity. Such opportunities aren’t so rare anymore, though. With sugary, fatty foods around every corner, our hedonic drive may end up in perpetual control, overwhelming the intuitive wisdom of our bodies.

    So, what’s the answer? Never eat really tasty food? No, but it may help to recognize the effects hyperpalatable foods can have on hijacking our appetites and undermining our body’s better judgment.

    Ironically, some researchers have suggested a counterbalancing evolutionary strategy for combating the lure of artificially concentrated calories. Just as pleasure can overrule our appetite regulation, so can pain. “Conditioned food aversions” are when we avoid foods that made us sick in the past. That may just seem like common sense, but it is actually a deep-seated evolutionary drive that can defy rationality. Even if we know for a fact a particular food was not the cause of an episode of nausea and vomiting, our body can inextricably tie the two together. This happens, for example, with cancer patients undergoing chemotherapy. Consoling themselves with a favorite treat before treatment can lead to an aversion to their favorite food if their body tries to connect the dots. That’s why oncologists may advise the “scapegoat strategy” of only eating foods before treatment that you are okay with, never wanting to eat again.

    Researchers have experimented with inducing food aversions by having people taste something before spinning them in a rotating chair to cause motion sickness. Eureka! A group of psychologists suggested: “A possible strategy for encouraging people to eat less unhealthy food is to make them sick of the food, by making them sick from the food.” What about using disgust to promote eating more healthfully? Children as young as two-and-a-half years old will throw out a piece of previously preferred candy scooped out of the bottom of a clean toilet.

    Thankfully, there’s a way to exploit our instinctual drives without resorting to revulsion, aversion, or bland food, which we’ll explore 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

  • Boosting BDNF Levels in Our Brain to Treat Depression  | NutritionFacts.org

    [ad_1]

    We can raise BDNF levels in our brain by fasting and exercising, as well as by eating and avoiding certain foods.

    There is accumulating evidence that brain-derived neurotrophic factor (BDNF) may be playing a role in human depression. BDNF controls the growth of new nerve cells. “So, low levels of this peptide could lead to an atrophy of specific brain areas such as the amygdala and the hippocampus, as it has been observed among depressed patients.” That may be one of the reasons that exercise is so good for our brains. Start an hour-a-day exercise regimen, and, within three months, there can be a quadrupling of BDNF release from our brain, as seen below and at 0:35 in my video How to Boost Brain BDNF Levels for Depression Treatment.

    This makes sense. Any time we were desperate to catch prey (or desperate not to become prey ourselves), we needed to be cognitively sharp. So, when we’re fasting, exercising, or in a negative calorie balance, our brain starts churning out BDNF to make sure we’re firing on all cylinders. Of course, Big Pharma is eager to create drugs to mimic this effect, but is there any way to boost BDNF naturally? Yes, I just said it: fasting and exercising. Is there anything we can add to our diet to boost BDNF?

    Higher intakes of dietary flavonoids appear to be protectively associated with symptoms of depression. The Harvard Nurses’ Health Study followed tens of thousands of women for years and found that those who were consuming the most flavonoids appeared to reduce their risk of becoming depressed. Flavonoids occur naturally in plants, so there’s a substantial amount in a variety of healthy foods. But how do we know the benefits are from the flavonoids and not just from eating more healthfully in general? We put it to the test.

    Some fruits and vegetables have more flavonoids than others. As shown below and at 1:51 in my video, apples have more than apricots, plums more than peaches, red cabbage more than white, and kale more than cucumbers. Researchers randomized people into one of three groups: more high-flavonoid fruits and vegetables, more low-flavonoid fruits and vegetables, or no extra fruits and vegetables at all. After 18 weeks, only the high-flavonoid group got a significant boost in BDNF levels, which corresponded with an improvement in cognitive performance. The BDNF boost may help explain why each additional daily serving of fruits or vegetables is associated with a 3 percent decrease in the risk of depression. 

    What’s more, as seen here and at 2:27 in my video, a teaspoon a day of the spice turmeric may boost BNDF levels by more than 50 percent within a month. This is consistent with the other randomized controlled trials that have so far been done. 

    Nuts may help, too. In the PREDIMED study, where people were randomized to receive weekly batches of nuts or extra-virgin olive oil, the nut group lowered their risk of having low BDNF levels by 78 percent, as shown below and at 2:46.

    And BDNF is not implicated only in depression, but schizophrenia. When individuals with schizophrenia underwent a 12-week exercise program, they got a significant boost in their BDNF levels, which led the researchers to “suggest that exercise-induced modulation of BDNF may play an important role in developing non-pharmacological treatment for chronic schizophrenic patients.”

    What about schizophrenia symptoms? Thirty individuals with schizophrenia were randomized to ramp up to 40 minutes of aerobic exercise three times a week or not, and there did appear to be an improvement in psychiatric symptoms, such as hallucinations, as well as an increase in their quality of life, with exercise. In fact, researchers could actually visualize what happened in their brains. Loss of brain volume in a certain region appears to be a feature of schizophrenia, but 30 minutes of exercise, three times a week, resulted in an increase of up to 20 percent in the size of that region within three months, as seen here and at 3:46 in my video. 

    Caloric restriction may also increase BDNF levels in people with schizophrenia. So, researchers didn’t just have study participants eat less, but more healthfully, too—less saturated fat and sugar, and more fruits and veggies. The study was like the Soviet fasting trials for schizophrenia that reported truly unbelievable results, supposedly restoring people to function, and described fasting as “an unparalleled achievement in the treatment of schizophrenia”—but part of the problem is that the diagnostic system the Soviets used is completely different than ours, making any results hard to interpret. There was a subgroup that seemed to correspond to the Western definition, but they still reported 40 to 60 percent improvement rates from fasting, but fasting wasn’t all they did. After the participants fasted for up to a month, they were put on a meat- and egg-free diet. So, when the researchers reported these remarkable effects even years later, they were for those individuals who stuck with the meat- and egg-free diet. Evidently, the closer the diet was followed, the better the effect, and those who broke the diet relapsed. The researchers noted: “Not all patients can remain vegetarian, but they must not take meat for at least six months, and then in very small portions.” We know from randomized controlled trials that simply eschewing meat and eggs can improve mental states within just two weeks, so it’s hard to know what role fasting itself played in the reported improvements.

    A single high-fat meal can drop BDNF levels within hours of consumption, and we can prove it’s the fat itself by seeing the same result after injecting fat straight into our veins. Perhaps that helps explain why increased consumption of saturated fats in a high-fat diet may contribute to brain dysfunction—that is, neurodegenerative diseases, long-term memory loss, and cognitive impairment. It may also help explain why the standard American diet has been linked to a higher risk of depression, as dietary factors modulate the levels of brain-derived neurotrophic factor.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Eating to Downregulate a Gene for Metastatic Cancer  | NutritionFacts.org

    [ad_1]

    Women with breast cancer should include the “liberal culinary use of cruciferous vegetables.”

    Both the Women’s Intervention Nutrition Study and the Women’s Health Initiative study showed that women randomized to a lower-fat diet enjoyed improved breast cancer survival. However, in the Women’s Healthy Eating and Living Study, women with breast cancer were also randomized to drop their fat intake down to 15 to 20 percent of calories, yet there was no difference in breast cancer relapse or death after seven years.

    Any time there’s an unexpected result, you must question whether the participants actually followed through with study instructions. For instance, if you randomized people to stop smoking and they ended up with the same lung cancer rates as those in the group who weren’t instructed to quit, one likely explanation is that the group told to stop smoking didn’t actually stop. In the Women’s Healthy Eating and Living Study, both the dietary intervention group and the control group started out at about 30 percent of calories from fat. Then, the diet group was told to lower their fat intake to 15 to 20 percent of calories. By the end of the study, they had in fact gone from 28.5 percent fat to 28.9 percent fat, as you can see below and at 1:16 in my video The Food That Can Downregulate a Metastatic Cancer Gene. They didn’t even reduce their fat intake. No wonder they didn’t experience any breast cancer benefit. 

    When you put together all the trials on the effect of lower-fat diets on breast cancer survival, even including that flawed study, you see a reduced risk of breast cancer relapse and a reduced risk of death. In conclusion, going on a low-fat diet after a breast cancer diagnosis “can improve breast cancer survival by reducing the risk of recurrence.” We may now know why: by targeting metastasis-initiating cancer cells through the fat receptor CD36.

    We know that the cancer-spreading receptor is upregulated by saturated fat. Is there anything in our diet that can downregulate it? Broccoli.

    Broccoli appears to decrease CD36 expression by as much as 35 percent (in mice). Of all fruits and vegetables, cruciferous vegetables like broccoli were the only ones associated with significantly less total risk of cancer and not just getting cancer in the first place, as you can see here and at 2:19 in my video.

    Those with bladder cancer who eat broccoli also appear to live longer than those who don’t, and those with lung cancer who eat more cruciferous veggies appear to survive longer, too.

    For example, as you can see below and at 2:45 in my video, one year out, about 75 percent of lung cancer patients eating more than one serving of cruciferous vegetables a day were still alive (the top line in red), whereas, by then, most who had been getting less than half a serving a day had already died from their cancer (the bottom line in green).

    Ovarian cancer, too. Intake of cruciferous vegetables “significantly favored survival,” whereas “a survival disadvantage was shown for meats.” Milk also appeared to double the risk of dying. Below and at 3:21 in my video are the survival graphs. Eight years out, about 40 percent of ovarian cancer patients who averaged meat or milk every day were deceased (the boldest line, on the bottom), compared to only about 20 percent who had meat or milk only a few times a week at most (the faintest line, on the top). 

    Now, it could be that the fat and cholesterol in meat increased circulating estrogen levels, or it could be because of meat’s growth hormones or all its carcinogens. And galactose, the sugar naturally found in milk, may be directly toxic to the ovary. Dairy has all its hormones, too. However, the lowering of risk with broccoli and the increasing of risk with meat and dairy are also consistent with the CD36 mechanism of cancer spread.

    Researchers put it to the test in patients with advanced pancreatic cancer who were given pulverized broccoli sprouts or a placebo. The average death rate was lower in the broccoli sprout group compared to the placebo group. After a month, 18 percent of the placebo group had died, but none in the broccoli group. By three months, another 25 percent of the placebo group had died, but still not a single death in the broccoli group. And by six months, 43 percent of the remaining patients in the placebo group were deceased, along with the first 25 percent of the broccoli group. Unfortunately, even though the capsules for both groups looked the same, “true blinding was not possible,” and the patients knew which group they were in “because the pulverized broccoli sprouts could be easily distinguished from the methylcellulose [placebo] through their characteristic smell and taste.” So, we can’t discount the placebo effect. What’s more, the study participants weren’t properly randomized “because many of the patients refused to participate unless they were placed into the [active] treatment group.” That’s understandable, but it makes for a less rigorous result. A little broccoli can’t hurt, though, and it may help. It’s the lack of downsides of broccoli consumption that leads to “Advising Women Undergoing Treatment for Breast Cancer” to include the “liberal culinary use of cruciferous vegetables,” for example.

    It’s the same for reducing saturated fat. The title of an editorial in a journal of the National Cancer Institute asked: “Is It Time to Give Breast Cancer Patients a Prescription for a Low-Fat Diet?” “Although counseling women to consume a healthy diet after breast cancer diagnosis is certainly warranted for general health, the existing data still fall a bit short of proving this will help reduce the risk of breast cancer recurrence and mortality.” But what do we have to lose? After all, it’s still certainly warranted for general health.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Eating to Help Control Cancer Metastasis  | NutritionFacts.org

    [ad_1]

    Randomized controlled trials show that lowering saturated fat intake can lead to improved breast cancer survival.

    The leading cause of cancer-related death is metastasis. Cancer kills because cancer spreads. The five-year survival rate for women with localized breast cancer is nearly 99 percent, for example, but that falls to only 27 percent in women with metastasized cancer. Yet, “our ability to effectively treat metastatic disease has not changed significantly in the past few decades…” The desperation is evident when there are such papers as “Targeting Metastasis with Snake Toxins: Molecular Mechanisms.”

    We have built-in defenses, natural killer cells that roam the body, killing off budding tumors. But, as I’ve discussed, there’s a fat receptor called CD36 that appears to be essential for cancer cells to spread, and these cancer cells respond to dietary fat intake, but not all fat.

    CD36 is upregulated by palmitic acid, as much as a 50-fold increase within 12 hours of consumption, as shown below and at 1:13 in my video How to Help Control Cancer Metastasis with Diet.

    Palmitic acid is a saturated fat made from palm oil that can be found in junk food, but it is most concentrated in meat and dairy. This may explain why, when looking at breast cancer mortality and dietary fat, “there was no difference in risk of breast-cancer-specific death…for women in the highest versus the lowest category of total fat intake,” but there’s about a 50 percent greater likelihood of dying of breast cancer with higher intake of saturated fat. Researchers conclude: “These meta-analyses have shown that saturated fat intake negatively impacts breast cancer survival.”

    This may also explain why “intake of high-fat dairy, but not low-fat dairy, was related to a higher risk of mortality after breast cancer diagnosis.” If a protein in dairy, like casein, was the problem, skim milk might be even worse, but that wasn’t the case. It’s the saturated butterfat, perhaps because it triggered that cancer-spreading mechanism induced by CD36. Women who consumed one or more daily servings of high-fat dairy had about a 50 percent higher risk of dying from breast cancer.

    We see the same with dairy and its relationship to prostate cancer survival. Researchers found that “drinking high-fat milk increased the risk of dying from prostate cancer by as much as 600% in patients with localized prostate cancer. Low-fat milk was not associated with such an increase in risk.” So, it seems to be the animal fat, rather than the animal protein, and these findings are consistent with analyses from the Health Professionals Follow-up Study (HPFS) and the Physicians’ Health Study (PHS), conducted by Harvard researchers.

    There is even more evidence that the fat receptor CD36 is involved. The “risk of colorectal cancer for meat consumption” increased from a doubling to an octupling—that is, the odds of getting cancer multiplied eightfold for those who carry a specific type of CD36 gene. So, “Is It Time to Give Breast Cancer Patients a Prescription for a Low-Fat Diet?” A cancer diagnosis is often referred to as a ‘teachable moment’ when patients are motivated to make changes to their lifestyle, and so provision of evidence-based guidelines is essential.”

    In a randomized, prospective, multicenter clinical trial, researchers set out “to test the effect of a dietary intervention designed to reduce fat intake in women with resected, early-stage breast cancer,” meaning the women had had their breast cancer surgically removed. As shown below and at 4:02 in my video, the study participants in the dietary intervention group dropped their fat intake from about 30 percent of calories down to 20 percent, reduced their saturated fat intake by about 40 percent, and maintained it for five years. “After approximately 5 years of follow-up, women in the dietary intervention group had a 24% lower risk of relapse”—a 24-percent lower risk of the cancer coming back—“than those in the control group.” 

    That was the WINS study, the Women’s Intervention Nutrition Study. Then there was the Women’s Health Initiative study, where, again, women were randomized to lower their fat intake down to 20 percent of calories, and, again, “those randomized to a low-fat dietary pattern had increased breast cancer overall survival. Meaning: A dietary change may be able to influence breast cancer outcome.” What’s more, not only was their breast cancer survival significantly greater, but the women also experienced a reduction in heart disease and a reduction in diabetes.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Dietary Components That May Cause Cancer to Metastasize  | NutritionFacts.org

    [ad_1]

    Palmitic acid, a saturated fat concentrated in meat and dairy, can boost the metastatic potential of cancer cells through the fat receptor CD36.

    The leading cause of death in cancer patients is metastasis formation. That’s how most people die of cancer—not from the primary tumor, but the cancer spreading through the body. “It is estimated that metastasis is responsible for ~90% of cancer deaths,” and little progress has been made in stopping the spread, despite our modern medical armamentarium. In fact, we can sometimes make matters worse. In an editorial entitled “Therapy-Induced Metastasis,” its authors “provide evidence that all the common therapies, including radiotherapy, chemotherapy, fine needle biopsies, surgical procedures and anaesthesia, have the potential to contribute to tumour progression.” You can imagine how cutting around a tumor and severing blood vessels might lead to the “migration of residual tumour cells,” but why chemotherapy? How might chemo exacerbate metastases? “Despite reducing the size of primary tumors, chemotherapy changes the tumor microenvironment”—its surrounding tissues—“resulting in an increased escape of cancer cells into the blood stream.” Sometimes, chemo, surgery, and radiation are entirely justified, but, again, other times, these treatments can make matters worse. If only we had a way to treat the cause of the cancer’s spreading.

    The development of antimetastatic therapies has been hampered by the fact that the cells that initiate metastasis remain unidentified. Then, a landmark study was published: “Targeting Metastasis-Initiating Cells Through the Fatty Acid Receptor CD36.” Researchers found a subpopulation of human cancer cells “unique in their ability to initiate metastasis”; they all express high levels of a fat receptor known as CD36, dubbed “the fat controller.” It turns out that palmitic acid or a high-fat diet specifically boosts the metastatic potential of these cancer cells. Where is palmitic acid found? Although it was originally discovered in palm oil, palmitic acid is most concentrated in meat and dairy. “Emerging evidence shows that palmitic acid (PA), a common fatty acid in the human diet, serves as a signaling molecule regulating the progression and development of many diseases at the molecular level.” It is the saturated fat that is recognized by CD36 receptors on cancer cells, and we know it is to blame, because if the CD36 receptor is blocked, so are metastases.

    The study was of a human cancer, but it was a human cancer implanted into mice. However, clinically (meaning in cancer patients themselves), the presence of these CD36-studded metastasis-initiating cells does indeed correlate with a poor prognosis. CD36 appears to drive the progression of brain tumors, for example. As seen in the survival curves shown below and at 3:21 in my video What Causes Cancer to Metastasize?, those with tumors with less CD36 expression lived significantly longer. It is the same with breast cancer mortality: “In this study, we correlated the mortality of breast cancer patients to tumor CD36 expression levels.” That isn’t a surprise, since “CD36 plays a critical role in proliferation, migration and…growth of…breast cancer cells.” If we inhibit CD36, we can inhibit “the migration and invasion of the breast cancer cells.” 

    Below and at 3:46 in my video, you can see breast cancer cell migration and invasion, before and after CD36 inhibition. (The top lines with circles are before CD36 inhibition, and the bottom lines with squares are after.)

    This isn’t only in “human melanoma- and breast cancer–derived tumours” either. Now we suspect that “CD36 expression drives ovarian cancer progression and metastasis,” too, since we can inhibit ovarian cancer cell invasion and migration, as well as block both lymph node and blood-borne metastasis, by blocking CD36. We also see the same kind of effect with prostate cancer; suppress the uptake of fat by prostate cancer cells and suppress the tumor. This was all studied with receptor-blocking drugs and antibodies in a laboratory setting, though. If these “metastasis-initiating cancer cells particularly rely on dietary lipids [fat] to promote metastasis,” the spread of cancer, why not just block the dietary fat in the first place?

    “Lipid metabolism fuels cancer’s spread.” Cancer cells love fat and cholesterol. The reason is that so much energy is stored in fat. “Hence, CD36+ metastatic cells might take advantage of this feature to obtain the high amount of energy that is likely to be required for them to anchor and survive at sites distant from the primary tumour”—to set up shop throughout the body.

    “The time when glucose [sugar] was considered as the major, if not only, fuel to support cancer cell proliferation is over.” There appears to be “a fatter way to metastasize.” No wonder high-fat diets (HFD) may “play a crucial role in increasing the risk of different cancer types, and a number of clinical studies have linked HFD with several advanced cancers.”

    If dietary fat may be “greasing the wheels of the cancer machine,” might there be “specific dietary regimens” we could use to starve cancers of dietary fat? You don’t know until you put it to the test, which we’ll look at next.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

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

    [ad_1]

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

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

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

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

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

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

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

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

    Doctor’s Note:

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

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Eating with Hypothyroidism and Hyperthyroidism  | NutritionFacts.org

    [ad_1]

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

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

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

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

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

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

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

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

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

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

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Chemical Safety, Cultivated Meat, and Our Health  | NutritionFacts.org

    [ad_1]

    More than 95 percent of human exposure to industrial pollutants like dioxins and PCBs comes from fish, other meat, and dairy.

    By cultivating muscle meat directly, without associated organs like intestines, the incidence of foodborne diseases “could be significantly reduced,” as could exposure to antibiotics, “pesticides, arsenic, dioxins, and hormones associated with conventional meat.” Currently, the U.S. Food and Drug Administration has approved seven hormone drugs to bulk up the production of milk and meat. “In the European Union, there exists a total ban on such use,” however. Even without injected hormones, though, animal products naturally have hormones because they come from animals. “Eggs, example given, contribute more to the dietary intake of estradiol [estrogens] than beef, whether the animal is legally treated with hormones or not.” After all, eggs come straight from a hen’s ovaries, so, of course, they’re swimming with hormones. But if you’re directly growing just muscle meat or egg white protein, you don’t need to include reproductive organs, adrenal glands, or any of the associated hormones.

    “Chemical safety is another concern for meat produced under current production systems.” There are chemical toxicants and industrial pollutants that build up in the food chain, such as pesticides, PCBs, heavy metals, and flame retardants, but there is no food chain with cultivated meat. We could produce all the tuna we wanted, with zero mercury.

    When the World Health Organization determined that processed meat was a known human carcinogen and unprocessed meat a probable human carcinogen, it wasn’t even talking about the carcinogenic environmental pollutants. When researchers tested retail meat for the presence of “33 chemicals with calculated carcinogenic potential,” like polycyclic aromatic hydrocarbons (PAHs), organochlorine pesticides like DDT, and dioxin-like PCBs, they concluded that, in order to reduce the risk of cancer, we should limit beef, pork, or chicken consumption to a maximum of five servings a month.

    Why cultivate meat at all when you can just buy organic? Surprisingly, “consumption of organic meat does not diminish the carcinogenic potential associated with the intake of persistent organic pollutants (POPs).” A number of studies have recently compared the presence of environmental contaminants in organic meat versus conventional meat, and the researchers found, surprisingly, that organic meat was sometimes more contaminated. Not only organic beef either. Higher levels were also found in pork and poultry.

    If you look at the micropollutants and chemical residues in both organic and conventional meat, several environmental contaminants, including dioxins, PCBs, lead, and arsenic, were measured at significantly higher levels in the organic samples. As you can see below and at 2:56 in my video, The Human Health Effects of Cultivated Meat: Chemical Safety, the green is organic meat, and the blue is conventional. 

    Cooking helps to draw off some of the fat where the PCBs are concentrated, as shown here and at 3:01.

    Seafood seems to be an exception. Steaming, for example, generally increases contaminant levels, increasing contaminant exposure and concentrating mercury levels as much as 47 percent, as you can see here and at 3:15 in my video. Better not to have toxic buildup in the first place.

    More than 95 percent of human exposure to industrial pollutants like dioxins and PCBs comes from foods like meat, including fatty fish, and dairy, but the pollutants don’t appear magically. The only way the chicken, fish, and other meat lead to human exposure is because the animals themselves built up a lifetime of exposure in our polluted world, from incinerators, power plants, sewer sludge, and on and on, as you can see here and at 3:40 in my video.

    Unlike conventional meat production, a slaughter-free harvest would not only mean no more infected animals, but no more contaminated animals either. In terms of pollutants, it would be like taking a time machine back before the Industrial Revolution.

    Doctor’s Note:

    Cultivated meat means less contamination with fecal residues, toxic pollutants, antibiotics, and hormones; up to 99 percent less environmental impact; and zero pandemic risk. Cultivated meat allows people to have their meat and eat it, too, without affecting the rest of us.

    This is the final video in this cultivated meat series. If you missed the first two, check out the videos on Food Safety and Antibiotic Resistance.

    I previously did a video series on plant-based meats; see the related posts below.

    All videos in the plant-based meat series are also available in a digital download from a webinar I did. SeeThe Human Health Implications of Plant-Based and Cultivated Meat for Pandemic Prevention and Climate Mitigation.

    [ad_2]

    Michael Greger M.D. FACLM

    Source link

  • Antibiotic Resistance, Cultivated Meat, and Our Health  | NutritionFacts.org

    [ad_1]

    Medically important antibiotics are being squandered by animal agriculture to compensate for typical factory farming practices.

    Cultivating muscle meat directly from cells instead of raising and slaughtering animals would reduce the risk of foodborne illnesses “due to fecal contamination during slaughtering and evisceration of carcasses” because there would be no feces, no slaughter, and no carcasses to eviscerate. In addition, cultivating meat would also reduce the threat from antibiotic resistance.

    To compensate for overcrowded, stressful, and unhygienic conditions on factory farms, animals are typically dosed en masse with antibiotics. A lot of antibiotics. About 20 million pounds of medically important antibiotics a year, as you can see here and at 0:57 in my video, The Human Health Effects of Cultivated Meat: Antibiotic Resistance. 

    In the United States, for example, farm animals are given about 2 million pounds of penicillin drugs and 15 million pounds of tetracyclines annually. This is madness. 

    Antibiotic drugs important to human medicine go right into the feed and water of animals like cows, pigs, and chickens, by the ton and by the thousands of tons, as shown below and at 1:02 in my video. And that is all without a prescription.

    Ninety-seven percent of the tens of millions of pounds of antibiotics given to farm animals in the United States are bought over the counter—without a prescription or even an order from a veterinarian, as seen here and a 1:24. To get even a few milligrams of penicillin, we need a doctor’s prescription, because these are miracle wonder drugs that can’t be squandered. Meanwhile, farmers can just back their trucks up to the feedstore. 

    Now, half the Salmonella in retail meat—chicken, turkey, beef, and pork—is resistant to tetracycline, as shown below and at 1:50 in my video. About a quarter of the bugs are now resistant to three or more entire classes of antibiotics, including some resistant to “cephalosporins such as ceftriaxone [which] are critically important drugs we use to treat severe Salmonella infections, especially in children.” 

    Such agricultural applications for antimicrobials are now considered an “urgent threat to human health.” “The link between antibiotic use in animals and antibiotic resistance in humans is unequivocal.”

    As shown here and at 2:20 in my video, it all starts with the poop. 

    Antibiotic-resistant bugs are selected for and then can spread via meat or produce contaminated by poop or they can spread through the wind, the air, or the water, or be carried by insects. There are many pathways by which resistant superbugs can escape. So, even if you don’t eat meat, you can be “put at risk by the pathogens released from stressed, immunocompromised, contaminant-filled livestock” dosed with antibiotics. That’s one of the reasons the American Public Health Association called for a moratorium on factory farms, due in part to all the pollution from concentrated animal feed operations (CAFOs) to the surrounding communities. 

    Every year, more than five tons of animal manure are produced for every man, woman, and child in the United States. Again, it all starts with the poop. But cultivated meat means no guts, no poop, no fecal infections, and no antibiotics necessary. It also means no fecal or antibiotic residues left in “foodstuffs such as milk, egg, and meat” that can potentially cause a variety of side effects beyond just the transfer of antibiotic-resistant bacteria to humans.

    And, as you can see here and at 3:30 in my video, things are getting worse, not better. U.S. animal agriculture is using more antibiotics now than ever.

    This isn’t only because more animals are being raised for food, either. Antibiotic sales in the United States are outpacing meat production. Yes, meat production is going up, but there is a serious rise in antibiotic sales for meat production, as shown below and at 3:46.

    With the combined might of Big Ag and Big Pharma (who profit from selling all the drugs), it’s hard to imagine anything changing on the political side. The only hope may be a change in the production side.

    “The unstoppable rise of super-resistant strains of bacteria is a serious worldwide problem, resulting in 700 000 deaths every year,” and the projections for global antibiotic use in the production of farm animals are “ominous,” estimated to exceed 100,000 tons of antibiotics pumped into animals raised for food by 2030. Quite simply, we may be “on the path to untreatable infections” by using even some of our “last resort antibiotics,” like carbapenems, just to shave a few cents off a pound of meat.

    And it’s not just foodborne bacteria. Mad cow disease, swine flu, and bird flu have the potential to kill millions of people. Skeptical? I’ve got a book for you to read, whose author’s “superb storytelling ability makes every page of the book interesting and fascinating for both specialist and layperson.” (Thanks, Virology Journal, for the wonderful book review and calling my book “a must read.”)

    Given the threat of the chickens coming home to roost, an editorial in the American Journal of Public Health thought that “it is curious, therefore, that changing the way humans treat animals—most basically, ceasing to eat them or, at the very least, radically limiting the quantity of them that are eaten—is largely off the radar as a significant preventative measure. Such a change, if sufficiently adopted or imposed, could still reduce the chances of the much-feared influenza epidemic…Yet humanity does not consider this option.”

    That may be moot, though, because we could cultivate all the chicken we want, without guts or lungs.

    It’s hard to stress the importance of that American Journal of Public Health editorial. As devastating as COVID-19 has been, it may just be a dress rehearsal for an even greater threat waiting in the wings—the wings of chickens.

    According to the Centers for Disease Control and Prevention, the leading candidate for the next pandemic is a bird flu virus known as H7N9, which is a hundred times deadlier than COVID-19. Instead of 1 in 250 patients dying, H7N9 has killed 40 percent of the people it infects.

    The last time a bird flu virus jumped directly to humans and caused a pandemic, it triggered the deadliest plague in human history—the 1918 pandemic that killed 50 million people. That had a 2 percent death rate. What if we had a pandemic infecting billions where death was closer to a flip of a coin?

    The good news is that there is something we can do about it. Just as eliminating the exotic animal trade and live animal markets may go a long way toward preventing the next coronavirus pandemic, reforming the way we raise domestic animals for food may help forestall the next killer flu. The bottom line is that it’s not worth risking the lives of millions of people for the sake of cheaper chicken.

    If you missed the previous video, see The Human Health Effects of Cultivated Meat: Food Safety. Up next is The Human Health Effects of Cultivated Meat: Chemical Safety. 

    [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

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

    [ad_1]

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

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

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

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

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

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

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

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

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

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

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

    Doctor’s Note:

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

    [ad_2]

    Michael Greger M.D. FACLM

    Source link