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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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  • My Easy & Delicious Hawaiian Roll Sliders Are the Star of Every Game Day Gathering

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    Rachel PerlmutterCulinary Producer

    I’m a recipe developer, food stylist, and content producer. I’ve spent the past seven years at meal kit companies like Marley Spoon and Dinnerly, teaching at food nonprofits, and doing a little farming. Originally from Houston, I live with my partner, dog, cat, and rabbit. We all love local, seasonal produce.

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    Rachel Perlmutter

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  • Keeping Better Score of Your Diet | NutritionFacts.org

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    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?.

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    Michael Greger M.D. FACLM

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

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    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.

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    Michael Greger M.D. FACLM

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

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    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.

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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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  • RANCHERS NUMBERS DECLINING: Bailout for farmers doesn’t include ranchers yet

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    TAHLEQUAH – The president announced on Dec. 8, that the U.S. Department of Agriculture will make $12 billion available to farmers in a one-time bridge payment to farmers, to be released by Feb. 28, 2026.

    President Donald J. Trump, along with U.S. Secretary of Agriculture Brooke L. Rollins, announced the payments in response to temporary trade market disruptions and increased production costs.

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  • RANCHERS NUMBERS DECLINING: Bailout for farmers doesn’t include ranchers yet

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    TAHLEQUAH – The president announced on Dec. 8, that the U.S. Department of Agriculture will make $12 billion available to farmers in a one-time bridge payment to farmers, to be released by Feb. 28, 2026.

    President Donald J. Trump, along with U.S. Secretary of Agriculture Brooke L. Rollins, announced the payments in response to temporary trade market disruptions and increased production costs.

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    kAm#682C5:?8 =236=:?8 2D &]$] 3667[ 96 D2:5 E96 5:776C6?E G6?F6D =:<6 8C@46CJ DE@C6D[ C6DE2FC2?ED[ 7C@K6? >62=D 2?5 E96 >62E 42D6[ >2<6 :E 5:77:4F=E E@ =236=]k^Am

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    By Lee Guthrie | lguthrie@tahlequahdailypress.com

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  • RANCHERS NUMBERS DECLINING: Bailout for farmers doesn’t include ranchers yet

    [ad_1]

    TAHLEQUAH – The president announced on Dec. 8, that the U.S. Department of Agriculture will make $12 billion available to farmers in a one-time bridge payment to farmers, to be released by Feb. 28, 2026.

    President Donald J. Trump, along with U.S. Secretary of Agriculture Brooke L. Rollins, announced the payments in response to temporary trade market disruptions and increased production costs.

    This page requires Javascript.

    Javascript is required for you to be able to read premium content. Please enable it in your browser settings.

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    By Lee Guthrie | lguthrie@tahlequahdailypress.com

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  • New Jersey man is first to die of red meat allergy linked to lone star ticks

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    A 47-year-old New Jersey man is the first known person to die from an allergy to red meat caused by alpha-gal syndrome, a disease transmitted by various ticks. 

    A study published Wednesday in the Journal of Allergy and Clinical Immunology documented the man’s death and the increasing population of lone star ticks in the Northeast. The species is the most common carrier of alpha-gal syndrome, though deer ticks — the carriers of Lyme disease — also can carry it. 

    MORE: Nurse who beat hard-to-treat cancer says she stayed strong by thinking of herself as a ‘survivor’

    These developments warrant a “major need” for public education about alpha-gal syndrome, including its cause and symptoms, researchers wrote.

    Here’s what to know about lone star ticks and alpha-gal syndrome, including how the allergy is treated and prevented.

    What is alpha-gal syndrome?

    Alpha-gal syndrome, or AGS, also is known as the red meat allergy or the tick bite meat allergy. It is caused by alpha gal, a sugar molecule found in the tissues of most mammals. The molecule is not naturally found in humans, but it can be passed to them through the tick’s saliva. 

    When a tick carrying this sugar molecule bites a person, it may be transferred into the bloodstream. This triggers an immune response, because the immune system recognizes it as a foreign substance and perceives it as a threat. When the person then consumes red meat or animal products containing the sugar molecules, the immune system may go into overdrive two or more hours afterward. 

    Symptoms of this allergic reaction may include hives, swelling, abdominal pain and nausea. Some people may go into anaphylactic shock. 

    The allergy’s severity can increase with additional tick bites or exposure to foods with the sugar molecule. Not everyone who is bitten by a lone star tick will develop AGS or have consistent reactions. 

    How did the New Jersey man die? 

    The man, whose name and hometown were not disclosed in the study, became ill after a family camping trip last summer. After eating a dinner of beef steak, he awoke in the middle of the night and experienced severe abdominal pain, diarrhea and vomiting. 

    The pain was so severe that the man told his son he thought he would die from it, but his condition gradually improved. Two weeks later, he ate a hamburger at a barbecue with his wife. Hours afterward, the man’s son found him unconscious on the bathroom floor and surrounded by vomit. He was pronounced dead that night, with the autopsy ruling the cause as a “sudden unexplained death.” 

    But the man’s wife pressed for answers, and a postmortem blood sample showed more than 2,000 nanograms per milliliter of tryptase, an enzyme that is released during an allergic reaction. She informed a medical team that her husband had had 12 or 13 chigger bites, which researchers said likely were the larvae of lone star ticks. 

    The man’s death is the first documented anaphylactic death tied to AGS in which symptoms started several hours after meat was consumed. 

    How common is AGS?

    There were 110,000 suspected cases of alpha-gal syndrome identified in the United States between 2010 and 2022, the Centers for Disease Control and Prevention reported in 2023. But as many as 450,000 people may have been impacted by AGS. 

    That’s because many people may not seek testing due to the ambiguity of the syndrome’s symptoms, and many medical professionals are unfamiliar with AGS or do not know how to diagnose it, the CDC found. 

    Some people may have AGS without realizing it, the Mayo Clinic says.

    How is AGS diagnosed and treated? 

    To be diagnosed with AGS, people must undergo a physical examination and discuss their symptoms and medical history with a medical provider. A blood test may be ordered to confirm the presence of alpha-gal antibodies in the blood, but the Mayo Clinic notes that it’s possible to have the antibodies without developing AGS.

    The only way to treat alpha-gal syndrome is to avoid eating red meat and other animal products that may trigger reactions, the Mayo Clinic says. Some studies have indicated that AGS reactions wane as people avoid additional tick bites and make dietary changes. 

    Allergy medications may help calm mild allergic reactions, the Mayo Clinic says. An anaphylactic response may require epinephrine and treatment in an emergency department. 

    How can AGS be prevented?

    Preventing tick bites is the easiest way to avoid AGS. 

    Ticks typically thrive in grassy, wooded areas and often on animals. When outdoors, avoid densely wooded areas, and walk in the center of trails. Treating clothes and boots with permethrin also can help.

    Conduct tick checks after being outdoors. Look for them on your body, clothes and pets. Showering shortly after coming inside can wash off unattached ticks.

    At home, treat outdoor areas with pesticides and remove leaf litter. Clear away tall grasses and brush, and mow the yard frequently. 

    What are lone star ticks?

    Lone star ticks are native to the southeast, but they have been spreading north and west over the last two decades. They were first observed in Pennsylvania in 2017, and now are widely distributed across the Northeast, South and Midwest. 

    The increased prevalence of ticks, including deer ticks, has been partially attributed to rising deer populations, which are common hosts for ticks. Ticks are commonly found in forests but also live in yards and urban parks.

    Lone star ticks are larger and have longer limbs than deer ticks, also known as black-legged ticks. They are comparable in size to dog ticks, but have shorter limbs. Female lone star ticks have a white spot on their backs, which gives the species its name. But both male and females can transmit alpha-gal syndrome. 

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    Molly McVety

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  • Stovetop Stuffing Meat Loaf

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    Stovetop Stuffing Meat Loaf  |  Kitchen Nostalgia

















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