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Tag: gut flora

  • Which Foods Help a Leaky Gut? | NutritionFacts.org

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    What is the recommended diet for treating leaky gut? Which foods and food components can boost the integrity of our intestinal barrier?

    Our intestinal tract is the largest barrier between us and the environment. More than what we touch or breathe, what we eat is our largest exposure to the outside world. Normally, our entire gastrointestinal tract is impermeable to what’s inside of it, allowing our body to pick and choose what goes in or out. But there are things that may make our gut leaky, and the chief among them is our diet.

    The standard American or Western diet can cause gut dysbiosis, meaning a disruption in our gut microbiome, which can lead to intestinal inflammation and a leaky intestinal barrier. Then, tiny bits of undigested food, microbes, and toxins can slip uninvited through our gut lining into our bloodstream and trigger chronic systemic inflammation.

    “To avoid this dysbiosis and intestinal inflammation, a predominantly vegetarian diet”—in other words, eating plants—“should be preferred.” The gut bacteria of people eating a vegetarian diet are associated with intestinal microbiome balance, high bacterial biodiversity, and integrity of the intestinal barrier. Vegetarians tend to have markedly less uremic toxins, like indole and p-cresol, and because fiber is the primary food for our gut microbiome, the gut bacteria of those eating plant-based diets have been found to produce more of the good stuff—namely short-chain fatty acids that play “a protective and nourishing role” for the cells lining our gut, “ensuring the preservation” of our intestinal barrier. Plant fiber is of “prime importance” to preserving the integrity of our intestinal barrier, but you can’t know for sure until you put it to the test.

    When people with non-alcoholic fatty liver disease were given whole grains, beans, lentils, fruits, vegetables, nuts, and seeds for six months, they had a significant reduction in zonulin levels.

    Zonulin is a protein responsible for the disassembly of the tight junctions between gut-lining cells and is “considered to be the only measurable biomarker that reflects an impairment of the intestinal barrier.” In other words, zonulin is a useful marker of a leaky gut. But since adding all those plants seemed to lower levels, that may “imply that appropriate fiber intake helps to maintain the proper structure and function of the intestinal barrier.” But whole healthy plant foods have a lot more than fiber. How do we know it’s the fiber? And the study didn’t even have a control group. That’s why the researchers said “gut permeability might be improved by dietary fiber” [emphasis added]. To prove cause and effect, it’d be nice to have a randomized, double-blind, crossover study where you compare the effect of the same food with or without fiber.

    Such a study does, in fact, exist! A group of healthy young men was randomized to eat pasta with or without added fiber, and there was a significant drop in zonulin levels in the added-fiber group compared to both pre-intervention levels and those of the control group, as you can see below and at 2:51 in my video How to Heal a Leaky Gut with Diet.

    So, fiber does indeed appear to improve gut leakiness.

    Are there any plant foods in particular that may help? Curcumin, the yellow pigment in the spice turmeric, can help prevent the intestinal damage caused by ibuprofen-type drugs in rats. Similar protection was noted for the broccoli compound sulforaphane in mice. There are no human studies on broccoli yet, but there was a study on three days of the equivalent of about 2 to 3 teaspoons a day of turmeric, which did reduce markers of gastrointestinal barrier damage and inflammation caused by exercise compared to a placebo. Less turmeric may work, too, but no smaller doses have been put to the test.

    If you ask alternative medicine practitioners what treatments they use for a leaky gut, number one on the list—after reducing alcohol consumption—is zinc. You can see the list below and at 3:42 in my video.

    Zinc doesn’t just protect against aspirin-like drug-induced intestinal damage in rats; when put to the test in a randomized trial of healthy adults, the same thing was found. Five days of 250 mg of indomethacin, an NSAID drug, “caused a threefold rise in gut permeability,” as one would expect from that class of drugs. But this rise in permeability did not occur when participants also took zinc, “strongly suggesting a small-intestinal protective effect.” The dose they used was massive, though—75 mg a day, which is nearly twice the tolerable upper daily limit for zinc. What about getting zinc just at regular doses from food?

    A significant improvement in gut leakiness was found even with a dose of just 3 mg of zinc, suggesting that even relatively low zinc supplementation may work. You can get an extra 3 mg of zinc in your daily diet by eating a cup (200g) of cooked lentils.

    Doctor’s Note

    For more on preventing gut dysbiosis and leaky gut, check out Flashback Friday: Gut Dysbiosis: Starving Our Microbial Self and Avoid These Foods to Prevent a Leaky Gut.

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    Michael Greger M.D. FACLM

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

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

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

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

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

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

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

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

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

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

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

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

    Doctor’s Note

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

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

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    Michael Greger M.D. FACLM

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

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

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

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

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

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

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

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

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

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

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

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

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

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

    Doctor’s Note

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

    For more on TMAO, check out related posts below. 

    See the microbiome topic page for even more.

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    Michael Greger M.D. FACLM

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

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    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.

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    Michael Greger M.D. FACLM

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  • Fiber or Low FODMAP for SIBO?  | NutritionFacts.org

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    It may not be the number of bacteria growing in our small intestine, but the type of bacteria, which can be corrected with diet.

    When researchers tested more than a thousand patients suffering for longer than six months from symptoms typical with irritable bowel syndrome (IBS), such as excess gas, bloating, diarrhea, and abdominal pain, but who do not appear to have anything more serious going on, like inflammatory bowel disease, a significant percentage were found to be suffering from lactose intolerance—intolerance to the milk sugar lactose. In infancy, we have an enzyme called lactase in our small intestine that digests milk sugar, but, understandably, most of us lose it after weaning. “Although genetic mutation has led to persistence of lactase in adults, about 75% of the world’s population malabsorbs lactose after age 30” and have lactose intolerance. However, a third of the patients were diagnosed with small intestinal bacterial overgrowth (SIBO).

    “The evidence for SIBO and IBS is shrouded in controversy, predominantly because of the fact that the [breath] tests used in clinical practice to diagnose SIBO are not valid,” as I’ve explored before. As well, the implications of having more versus fewer bacteria growing in the small intestine are unclear since the number doesn’t seem to correlate with the symptoms. It turns out it isn’t the number of bugs growing in the small intestine, but the type of bugs. So, it’s “small intestinal microbial dysbiosis”—not overgrowth in general, but the wrong kind of growth—that appears to underlie symptoms associated with functional gastrointestinal disorders, like IBS.

    How can we prevent this from happening? The symptoms appear to be correlated with a significant drop in the number of Prevotella. Remember them? Prevotella are healthy fiber feeders, “suggestive of a higher fiber intake in healthy individuals,” while the bugs found more in symptomatic patients ate sugar, which “may reflect a higher dietary intake of simple sugars.” However, correlation doesn’t mean causation. To prove cause and effect, we have to put it to the test, which is exactly what researchers did.

    “Switching a group of healthy individuals who habitually ate a high­-fibre diet (>11g per 1,000 calories) to a low­-fibre diet (<10g per day) containing a high concentration of simple sugars for 7 days produced striking results. First, 80% developed de novo [new] gastrointestinal symptoms such as bloating and abdominal pain that resolved on resumption of their habitual high-fibre diet. Second, diet­-related changes in the small intestinal microbiome were predictive of symptoms (such as bloating and abdominal discomfort) and linked to an alteration in duodenal [intestinal] permeability.” In other words, they developed a leaky gut within seven days. And, while some went from SIBO positive to SIBO negative and others from SIBO negative to SIBO positive, it didn’t matter because the number of bacteria growing didn’t correlate with symptoms. It was the type of bacteria growing, as you can see below, and at 3:12 in my video Fiber vs. Low FODMAP for SIBO Symptoms.

    No wonder their guts got leaky. Levels of short-chain fatty acids plummeted. Those are the magical by-products our good gut bugs make from fiber, which “play an important role in epithelial [intestinal] barrier integrity,” meaning they keep our gut from getting leaky.

    So, while we don’t have sound data to suggest that something like a low FODMAP diet has any benefit for patients with SIBO symptoms, there have been more than a dozen randomized controlled trials that have put fiber to the test. Overall, researchers found there was a significant improvement in symptoms among those randomized to increase their fiber intake. That may help explain why “high-fiber, plant-based diets can prevent many diseases common in industrialized societies.” Such diets have this effect “on the composition and metabolic activity of the colonic microbiota.” Our good gut bugs take plant residues like fiber and produce “health-promoting and cancer-suppressing metabolites” like short-chain fatty acids, which have profound anti-inflammatory properties. “All the evidence points to a physiological need for ~50 g fiber per day, which is the amount contained in the traditional African diet and associated with the prevention of westernized diseases.” That is approximately twice the typical recommendation and three times more than what most people get on a daily basis. Perhaps it should be no surprise that we need so much. Even though we split from chimpanzees millions of years ago, “there is still broad congruency” in the composition of our respective microbiomes to this day. While they’re still eating their 98 to 99 percent plant-based diets to feed their friendly flora with fiber, we’ve largely removed fiber-rich foods from our food supply. 

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    Michael Greger M.D. FACLM

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  • The Validity of SIBO Tests  | NutritionFacts.org

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    Even if we could accurately diagnose small intestinal bacterial overgrowth (SIBO), if there is no difference in symptoms between those testing positive and those testing negative, what’s the point?

    Gastrointestinal symptoms like abdominal pain and bloating account for millions of doctor visits every year. One of the conditions that may be considered for such a “nonspecific presentation” of symptoms is SIBO, a concept that “has gained popularity on the internet in addition to certain clinical and research circles.” SIBO is “broadly defined as excessive bacteria in the small intestine” and typically treated with antibiotics, but “dispensing antibiotics to patients with the nonspecific, common symptoms associated with SIBO is not without risks,” such as the fostering of antibiotic resistance, the emergence of side effects, and the elimination of our good bacteria that could set us up for an invasion of bad bugs like C. diff—all for a condition that may not even be real.

    Even alternative medicine journals admit that SIBO is being overdiagnosed, creating “confusion and fear.” SIBO testing “is overused and overly relied upon. Diagnoses are often handed out quickly and without adequate substantiation. Patients can be indoctrinated into thinking SIBO is a chronic condition that can not be cleared and will require lifelong management. This is simply not true for most and is an example of the damage done by overzealousness.” “The ‘monster’ that we now perceive SIBO to be may be no more than a phantom.”

    The traditional method for a diagnosis was a small bowel aspiration, an invasive test where a long tube is snaked down the throat to take a sample and count the bugs down there, as you can see at 2:10 in my video Are Small Intestinal Bacterial Overgrowth (SIBO) Tests Valid?.

    This method has been almost entirely replaced with breath tests. Normally, a sugar called glucose is almost entirely absorbed in the small intestine, so it never makes it down to the colon. So, the presence of bacterial fermentation of that sugar suggests there are bacteria in the small intestine. Fermentation can be detected because the bacteria produce specific gases that get absorbed in our bloodstream before being exhaled from our lungs, which can then be detected with a breathalyzer-type machine.

    Previously, the sugar lactulose was used, but “lactulose breath tests do not reliably detect the overgrowth of bacteria,” so researchers switched to glucose. However, when glucose was finally put to the test, it didn’t work. The bacterial load in the small intestine was similar for those testing positive or negative, so that wasn’t a useful test either. It turns out that glucose can make it down to the colon after all.

    Researchers labeled the glucose dose with a tracer and found that nearly half of the positive results from glucose breath tests were false positives because individuals were just fermenting it down in their colon, where our bacteria are supposed to be. So, “patients who are incorrectly labeled with SIBO may be prescribed multiple courses of antibiotics” for a condition they don’t even have.

    Why do experts continue to recommend breath testing? Could it be because the “experts” were at a conference supported by a breath testing company, and most had personally received funds from SIBO testing or antibiotic companies?

    Even if we could properly diagnose SIBO, does it matter? For those with digestive symptoms, there is a massive range of positivity for SIBO from approximately 4 percent to 84 percent. Researchers “found there to be no difference in overall symptom scores between those testing positive against those testing negative for SIBO…” So, a positive test result could mean anything. Who cares if some people have bacteria growing in their small intestines if it doesn’t correlate with symptoms?

    Now, antibiotics can make people with irritable bowel-type symptoms who have been diagnosed with SIBO feel better. Does that prove SIBO was the cause? No, because antibiotics can make just as many people feel better who are negative for SIBO. Currently, the antibiotic rifaximin is most often used for SIBO, but it is “not currently FDA-approved for use in this indication, and its cost can be prohibitive.” (The FDA is the U.S. Food and Drug Administration.) In fact, no drug has been approved for SIBO in the United States or Europe, so even with good insurance, it may cost as much as $50 a day in out-of-pocket expenses, and the course is typically two weeks.

    What’s more, while antibiotics may help in the short term, they may make matters worse in the long term. Those “who are given a course of antibiotics are more than three times as likely to report more bowel symptoms 4 months later than controls.” So, what can we do for these kinds of symptoms? That’s exactly what I’m going to turn to next.

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    Michael Greger M.D. FACLM

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

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    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.

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    Michael Greger M.D. FACLM

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

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    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?. 

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    Michael Greger M.D. FACLM

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

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    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.

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    Michael Greger M.D. FACLM

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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    Michael Greger M.D. FACLM

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  • Syncing Your Brain and Body Clocks  | NutritionFacts.org

    Syncing Your Brain and Body Clocks  | NutritionFacts.org

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

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

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

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

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

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

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

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

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

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

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    Michael Greger M.D. FACLM

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  • Pre-Cut Vegetables and Endotoxins  | NutritionFacts.org

    Pre-Cut Vegetables and Endotoxins  | NutritionFacts.org

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    Endotoxins can build up on pre-cut vegetables and undermine some of their benefits.

    You may remember when I introduced the endotoxin theory literature in my video The Exogenous Endotoxin Theory, which sought to explain how a single Sausage and Egg McMuffin meal could cripple artery function within hours of consumption. Maybe it’s because such a meal causes inflammation within hours of consumption by inducing low-grade endotoxemia, endotoxins in the bloodstream, as I previously discussed in my video Dead Meat Bacteria Endotoxemia. Endotoxins are structural components of gram-negative bacteria like E. coli, as you can see below and at 0:35 in my video Are Pre-Cut Vegetables Just as Healthy?. Certain foods, like ground meat, have high bacterial loads, so the thought was that the endotoxins in the food were triggering the inflammation.

    Critics of the theory argued that because we already have so many bacteria living in our colon, so many endotoxins just sitting down in our large intestine, a few more endotoxins in our food wouldn’t matter much in terms of causing systemic inflammation. After all, we have about two pounds of pure bacteria down there where the sun don’t shine, so there could be about a whole ounce of endotoxin. The lethal dose of intravenously injected endotoxin can be just a few millionths of a gram, so we could have a million lethal doses down there. However, the apparent paradox is explained by compartmentalization. It’s location, location, location.

    Poop is harmless when it’s in your colon, but it shouldn’t be injected into your bloodstream or eaten for that matter, particularly with fat, as that can promote the absorption of endotoxins in the small intestine. That goes for well-cooked poop, too.

    As you can see in the graph below and at 1:44 in my video, you can boil endotoxins for two hours straight with no detriment in their ability to induce inflammation. You could easily kill off any bacteria if you boiled your poop soup long enough, but you can’t kill off the endotoxins they make, just like you can’t cook the crap out of the meat. The consumption of meat contaminated with feces doesn’t just cause food poisoning. It can spill out onto the animal’s skin during the evisceration process when the digestive tract is ruptured. 

    Even when slaughterhouse workers trim off “visible fecal contamination,” the trimming itself can, ironically, sometimes lead to an increase in certain fecal bacteria, thought to be caused by “cross-contamination resulting from the handling to removal fecal contamination” from one carcass to the next. Then, even when properly stored in the fridge, endotoxins start accumulating along with the bacterial growth, as you can see in the graph below and at 2:30 in my video. 

    What about other foods? The highest levels of endotoxins were found in meat and dairy, and the lowest levels in fresh fruits and vegetables. That was testing whole fruits and vegetables, though. “Most spoilage organisms cannot penetrate the plant’s surface barrier and spoil the inner tissues.” That’s why fruits and veggies can sit out in the fields all day in the sun. But, once you cut them open, bacteria can gain access to the inner tissues, and, within a matter of days, your veggies can start to spoil. So, what does that mean for all those convenient pre-cut veggies these days?

    While endotoxins were not detectable in the majority of unprocessed vegetables, once you damage the protective outer layers of vegetables, you diminish their resistance to microbial growth. So, while freshly cut carrots and onions start with undetectable levels, day after day after they’ve been chopped, you start to get the growth of bacteria and, along with them, endotoxin buildup—even if they’ve been kept chilled in the fridge. Not as much as meat, but not insignificant either, as you can see in the graph below and at 3:27 in my video. Enough to make a difference, though? You don’t know until you put it to the test.

    What would happen if you switched people between foods expected to have a lower endotoxin load to foods containing more endotoxins? For instance, going from intact meat, such as a steak, and whole fruits and vegetables, to more like ground beef, pre-cut veggies, and more ready-made meals, as shown below and at 3:39 in my video. After just one week on the lower-endotoxin diet, people’s white blood cell count, which is an indicator of total body inflammation, dropped by 12 percent, then bumped back up by 14 percent after just four days on the higher-endotoxin diet. They also lost a pound and a half on the lower-endotoxin diet and slimmed their waists a bit. 

    They weren’t eating otherwise identical diets, though. It looks like they were eating more meat and cheese on the higher-endotoxin diet and perhaps getting more food additives in the ready-made meals. So, how do we know endotoxins had anything to do with it? That’s where the onion study comes in. Another study was designed based on two meals that differed in their content of bacterial products but were otherwise nutritionally identical. So, researchers compared freshly chopped onion to prechopped onion that had been refrigerated for a few days. The pre-chopped onion wasn’t spoiled; it was still before the “best before” date. So, would it make any difference?

    Within three hours of consumption, the fresh onion meal caused significant reductions in several markers of inflammation. That’s what fruits and vegetables do—they reduce inflammation—but these effects were not observed after eating the pre-chopped onions. For example, three hours after eating freshly chopped onions, researchers saw a significant drop in inflammatory status, but there was no significant change three hours after eating the same amount of pre-chopped onions, as you can see in the graph below and at 5:06 in my video. So, it’s not like the pre-chopped onions caused more inflammation, like in the meat, eggs, and dairy studies, but it did appear that some of the onion’s anti-inflammatory effects were extinguished. “In conclusion, the modern trend towards eating minimally processed vegetables”—pre-cut vegetables—“rather than whole [intact] foods is likely to be associated with increased oral endotoxin exposure.” It’s still better to eat pre-cut veggies than no veggies, but cutting your own might be the healthiest.

     For some other practical veggie videos and blogs check out the related posts below. 

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    Michael Greger M.D. FACLM

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  • Fighting Inflammation with Flaxseeds  | NutritionFacts.org

    Fighting Inflammation with Flaxseeds  | NutritionFacts.org

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    Elevated levels of pro-inflammatory, aging-associated oxylipins can be normalized by eating ground flaxseed. 

    I previously explored the “Potent Antihypertensive Effect of Dietary Flaxseed in Hypertensive Patients” study in my video Flaxseeds for Hypertension. That was a double-blind, randomized, placebo-controlled trial where researchers disguised ground flaxseed in baked goods versus flax-free placebo muffins and saw an extraordinary drop in high blood pressure. As you can imagine, the flaxseed industry was overjoyed, praising the “impressive” findings, as was I. After all, high blood pressure is “the single largest risk factor” for death in the world. Yes, we give people medications, lots and lots of medications, but most people don’t take them. Nine out of ten people take less than 80 percent of their prescribed blood pressure pills. 
     
    It’s not difficult to understand why. “Patients are asked to follow an inconvenient and potentially costly regimen, which will likely have a detrimental effect on health-related quality of life, to treat a mostly asymptomatic condition that commonly does not cause problems for many years.” So, they may feel worse instead of better, due to the side effects. Then, some think the answer is to give them even more drugs to counteract the effects of the first drugs, like giving men Viagra to counteract the erectile dysfunction caused by their blood pressure pills. 
     
    How about using a dietary strategy instead, especially if it can be just as effective? And, indeed, the drop in blood pressure the researchers saw in the flaxseed study “was greater than the average decrease observed with the standard dose of anti-hypertensive medications.” Flaxseeds are cheaper, too, compared to even single medications, and most patients are on multiple drugs. Plus, flaxseeds have good side effects beyond their anti-hypertensive actions. Taking tablespoons of flaxseed a day is a lot of fiber for people living off of cheeseburgers and milkshakes their whole lives, and your gut bacteria may need a little time to adjust to the new bounty. So, those who start with low-fiber diets may want to take it a little slow with the flaxseeds at first. 
     
    Not all studies have shown significant blood pressure–lowering effects, though. There have been more than a dozen trials by now, involving more than a thousand subjects. And, yes, when you put them all together, overall, there were “significant reductions in both SBP and DBP”—systolic blood pressure (the upper number) and diastolic blood pressure (the lower number)—“following supplementation with various flaxseed products.” But none was as dramatic as what the researchers had found in that six-month trial. The longer trials tended to show better results, and some of the trials just used flaxseed oil or some kind of flaxseed extract. We think this is because the whole is greater than the sum of its parts. “Each of the components of interest within flaxseed, ALA, lignans, fiber, and peptides”—the omega-3s, the cancer-fighting lignans, all the soluble fiber, and the plant proteins, for instance—“all contribute towards BP reduction.” Okay, but how? Why? What is the mechanism? 
     
    Some common blood-pressure medications like Norvasc or Procardia work in part by reducing the ability of the heart to contract or by slowing down the heart. So, might it be that’s how flaxseeds work, too? But, no. In my video Benefits of Flaxseeds for Inflammation, I profile the “Dietary Flaxseed Reduces Central Aortic Blood Pressure Without Cardiac Involvement but Through Changes in Plasma Oxylipins” study. What are oxylipins? 
     
    “Oxylipins are a group of fatty acid metabolites” involved in inflammation and, as a result, have been implicated in many pro-inflammatory conditions, including aging and cardiovascular disease. “The best-characterized oxylipins about cardiovascular disease are derived from the w-6 fatty acid arachidonic acid,” a long-chain omega-6 fatty acid. These are found preformed in animal products, particularly chicken and eggs, and can be made inside the body from junky oils rich in omega-6, such as cottonseed oil, as noted below and at 3:49 in my video. But, as this study is titled, “Elevated levels of pro-inflammatory oxylipins in older subjects are normalized by flaxseed consumption.” 

    That’s how we think flaxseed consumption reduces blood pressure in patients with hypertension: by inhibiting the enzyme that makes these pro-inflammatory oxylipins. I’ll spare you from acronym overload, but eating flaxseeds inhibits the activity of the enzyme that makes these pro-inflammatory oxylipins, called leukotoxin diols, which in turn may lower blood pressure. “Identifying the biological mechanism adds confidence to the antihypertensive actions of dietary flaxseed,” but that’s not all oxylipins do. Oxylipins may also play a role in the aging process. However, we may be able to “beneficially disrupt these biological changes associated with inflammation and aging” with a nutritional intervention like flaxseed. Older adults around age 50 have higher levels of this arachidonic acid–derived oxylipin compared to younger adults around age 20, as you can see in the graph below and at 4:56 in my video. “These elevated concentrations of pro-inflammatory oxylipins in the older age group…may…explain the higher levels of inflammation in older versus younger individuals.” As we get older, we’re more likely to be stricken with inflammatory conditions like arthritis. So, this “elevation of pro-inflammatory oxylipins…may predispose individuals to chronic disease conditions.”

    What if you took those older adults and gave them muffins, like the ones with ground flaxseed? That’s just what a group of researchers did. Four weeks later, the subjects’ levels dropped down to like 20-year-olds’ levels, as seen in the graph below and at 5:32 in my video, “demonstrating that a potential therapeutic strategy to correct the deleterious pro-inflammatory oxylipin profile is via a dietary supplementation with flaxseed.”

    What about flax and cancer? See the related posts below. 

    I also have a video on diabetes: Flaxseeds vs. Diabetes. 

    If you’re interested in weight loss, see Benefits of Flaxseed Meal for Weight Loss. 

    What about the cyanide content of flax? I answered that in Friday Favorites: How Well Does Cooking Destroy the Cyanide in Flaxseeds and Should We Be Concerned About It?.

    What else can help fight inflammation? Check out in related posts below.

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    Michael Greger M.D. FACLM

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  • The Safety of Keto Diets  | NutritionFacts.org

    The Safety of Keto Diets  | NutritionFacts.org

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

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

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


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

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

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

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

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    Michael Greger M.D. FACLM

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