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Tag: animal studies

  • Prostate Cancer and Mushrooms | NutritionFacts.org

    What can reishi mushrooms, shiitake mushroom extracts, and whole, powdered white mushrooms do for cancer patients?

    “A regular intake of mushrooms can make us healthier, fitter, and happier, and help us live longer,” but what is the evidence for all that? “Mushrooms are widely cited for their medicinal qualities, yet very few human intervention studies have been done using contemporary guidelines.”

    There is a compound called lentinan, extracted from shiitake mushrooms. To get about an ounce, you have to distill around 400 pounds of shiitakes, about 2,000 cups of mushrooms. Researchers injected the compound into cancer patients to see what happens. The pooled response from a dozen small clinical trials found that the objective response rate was significantly improved when lentinan was added to chemotherapy regimens for lung cancer. “Objective response rate” means, for example, tumor shrinkage, but what we really care about is survival and quality of life. Does it actually make cancer patients live any longer or any better? Well, those in the lentinan group suffered less chemo-related toxicity to their gut and bone marrow, so that alone might be reason enough to use it. But what about improving survival?

    I was excited to see that lentinan may significantly improve survival rates for a type of leukemia. Indeed, researchers found that adding lentinan to the standards of care increased average survival, reduced cachexia (cancer-associated muscle wasting), and improved cage-side health. Wait, what? This was improved survival for brown Norwegian rats, so that the so-called clinical benefit only applies if you’re a rat or a veterinarian.

    A compilation of 17 actual human clinical studies did find improvements in one-year survival in advanced cancer patients but no significant difference in the likelihood of living out to two years. Even the compilations of studies that purport that lentinan offers a significant advantage in terms of survival are just talking about statistical significance. As you can see below and at 2:15 in my video White Button Mushrooms for Prostate Cancer, it’s hard to even tell these survival curves apart.

    Lentinan improved survival by an average of 25 days. Now, 25 days is 25 days, but we “should evaluate assertions made by companies about the miraculous properties of medicinal mushrooms very critically.”

    Lentinan has to be injected intravenously. What about mushroom extract supplements you can just take yourself? Researchers have noted that shiitake mushroom extract is available online for the treatment of prostate cancer for approximately $300 a month, so it’s got to be good, right? Men who regularly eat mushrooms do seem to be at lower risk for getting prostate cancer—and apparently not just because they eat less meat or consume more fruits and vegetables in general. So, why not give a shiitake mushroom extract a try? Because it doesn’t work. On its own, it is “ineffective in the treatment of clinical prostate cancer.” Researchers wrote that “the results demonstrate that claims for CAM [complementary and alternative medicine], particularly for herbal and food supplement remedies, can be easily and quickly tested.” Put something to the test? What a concept! Maybe it should be required before individuals spend large amounts of money on unproven treatments, or, in this case, a disproven treatment.

    What about God’s mushroom (also known as the mushroom of life) or reishi mushrooms? “Conclusions: No significant anticancer effects were observed”—not even a single partial response. Are we overthinking it? Plain white button mushroom extracts can kill off prostate cancer cells, at least in a petri dish, but so could the fancy God’s mushroom, but that didn’t end up working in people. You don’t know if plain white button mushrooms work on real people until you put them to the test.

    What I like about this study is that the researchers didn’t use a proprietary extract. They just used regular whole mushrooms, dried and powdered, the equivalent of a half cup to a cup and a half of fresh white button mushrooms a day, in other words, a totally doable amount. The researchers gave them to men with “biochemically recurrent prostate cancer”—the men had already gotten a prostatectomy or radiation in an attempt to cut or burn out all the cancer, but it returned and started growing, as evidenced by a rise in PSA levels, an indicator of prostate cancer progression.

    Of the 26 patients who had gotten the button mushroom powder, 4 appeared to respond, meaning they got a drop in PSA levels by more than 50% after starting the mushrooms, as you can see here and at 4:31 in my video.

    In the next graphic, below and at 4:22, you can see where the four men who responded started out in the months leading up to starting the mushrooms. Patient 2 (“Pt 2”) was my favorite. He had an exponential increase in PSA levels for a year, then he started some plain white mushrooms, and boom! His PSA level dropped to zero and stayed down. A similar response was seen with Patient 1. Patient 4 had a partial response, before his cancer took off again, and Patient 3 appeared to have a delayed partial response.

    Now, in the majority of cases, PSA levels continued to rise, not dipping at all. But even if there is only a 1-in-18 chance you’ll be like Patients 1 and 2, seen below and at 5:12, you may get a prolonged, complete response that continues.

    We aren’t talking about weighing the risks of some toxic chemotherapy for the small chance of benefit, but just eating some inexpensive, easy, tasty plain white mushrooms every day. Yes, the study didn’t have a control group, so it may have just been a coincidence, but rising PSAs in post-prostatectomy patients are almost always indicators of cancer progression. And, what’s the downside of adding white button mushrooms to your diet?

    In these two patients, their PSA levels became undetectable, suggesting that the cancer disappeared altogether. They had already gone through surgery, had gotten their primary tumor removed, along with their entire prostate, and had already gone through radiation to try to clean up any cancer that remained, and yet the cancer appeared to be surging back—until, that is, they started a little plain mushroom powder.

    Doctor’s Note

    If you missed the previous blog, check out Medicinal Mushrooms for Cancer Survival.

    Also check out Friday Favorites: Mushrooms for Prostate Cancer and Cancer Survival.

    For more on mushrooms, see Breast Cancer vs. Mushrooms and Is It Safe to Eat Raw Mushrooms?.

    For more videos on prostate cancer, check the related posts below. 

    Michael Greger M.D. FACLM

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  • Cancer Survival and Medicinal Mushrooms | NutritionFacts.org

    Did the five randomized controlled trials of reishi mushrooms in cancer patients show benefits in terms of tumor response rate, survival time, or quality of life?

    Can mushrooms be medicinal? Mushroom-based products make up a sizable chunk of the $50 billion supplement market. “This profitable trade provides a powerful incentive for companies to test the credulity of their customers and unsupported assertions have come to define the medical mushroom business.” For example, companies marketing herbal medicines “exploit references to studies on mice in their promotion of mushroom capsules and throat sprays for treating all kinds of ailments”—but we aren’t mice.

    It wouldn’t be surprising if mushrooms had some potent properties. After all, fungi are where we’ve gotten a number of drugs, not the least of which is penicillin, as well as the cholesterol-lowering drug lovastatin and the powerful immunosuppressant drug cyclosporin. Still don’t think a little mushroom can have pharmacological effects? Don’t forget they can produce some of our most powerful poisons, too, like the toxic Carolina false morel that looks rather toadstooly, while others, as you can see here and at 1:15 in my video Medicinal Mushrooms for Cancer Survival, have a more angelic look like the destroying angel—that is its actual name—and as little as a single teaspoon can cause a lingering, painful death.

    We should have respect for the pharmacological potential of mushrooms, but what can they do that’s good for us? Well, consuming shiitake mushrooms each day improves human immunity. Giving people just one or two dried shiitake mushrooms a day (about the weight-equivalent of five to ten fresh ones) for four weeks resulted in an increase in proliferation of gamma-delta T lymphocytes and doubled the proliferation of natural killer cells. Gamma-delta T cells act as a first line of immunological defense, and, even better, natural killer cells kill cancer. Shiitake mushrooms did all this while lowering markers of systemic inflammation.

    Oyster mushroom extracts don’t seem to work as well, but what we care about is whether mushrooms can actually affect cancer outcomes. Shiitakes have yet to show a cancer survival benefit, but what about reishi mushrooms, which have been used as a cancer treatment throughout Asia for centuries?

    What does the science say about reishi mushrooms for cancer treatment? A meta-analysis of five randomized controlled trials showed that patients who had been given reishi mushroom supplements along with chemotherapy and radiation were more likely to respond favorably,  compared to chemotherapy/radiotherapy on its own. Although adding a reishi mushroom extract improved tumor response rates, “the data failed to demonstrate a significant effect on tumour shrinkage when it was used alone,” without chemo and radiation. So, they aren’t recommended as a single treatment, but rather an adjunct treatment for patients with advanced cancer.

    “Response rate” just means the tumor shrinks. Do reishi mushrooms actually improve survival or quality of life? We don’t have convincing data suggesting reishi mushroom products improve survival, but those randomized to reishi were found to have “a relatively better quality of life after treatment than those in the control group.” That’s a win as far as I’m concerned.

    What about other mushrooms? Although whole shiitake mushrooms haven’t been put to the test for cancer yet, researchers have said that lentinan, a compound extracted from shiitakes, “completely inhibits” the growth of a certain kind of sarcoma in mice. But, in actuality, it only worked in one strain of mice and failed in nine others. So, are we more like the 90% of mouse strains in which it didn’t work? We need human trials—and we finally got them. There are data on nearly 10,000 cancer patients who have been treated with the shiitake mushroom extract injected right into their veins. What did the researchers find? We’ll find out next.

    Doctor’s Note

    Stay tuned for White Button Mushrooms for Prostate Cancer.

    Also check out Friday Favorites: Mushrooms for Prostate Cancer and Cancer Survival.

    For more on mushrooms, see Breast Cancer vs. Mushrooms and Is It Safe to Eat Raw Mushrooms?.

    Michael Greger M.D. FACLM

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

    Chlorohydrin contaminates hydrolyzed vegetable protein products and refined oils.

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

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

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

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

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

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

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

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

    Doctor’s Note

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

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

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

    Michael Greger M.D. FACLM

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  • Are Raw Mushrooms Safe to Eat?  | NutritionFacts.org

    Microwaving is probably the most efficient way to reduce agaritine levels in fresh mushrooms.

    There is a toxin in plain white button mushrooms called agaritine, which may be carcinogenic. Plain white button mushrooms grow to be cremini (brown) mushrooms, and cremini mushrooms grow to be portobello mushrooms. They’re all the very same mushroom, similar to how green bell peppers are just unripe red bell peppers. The amount of agaritine in these mushrooms can be reduced through cooking: Frying, microwaving, boiling, and even just freezing and thawing lower the levels. “It is therefore recommended to process/cook Button Mushroom before consumption,” something I noted in a video that’s now more than a decade old.

    However, as shown below and at 0:51 in my video Is It Safe to Eat Raw Mushrooms?, if you look at the various cooking methods, the agaritine in these mushrooms isn’t completely destroyed. Take dry baking, for example: Baking for ten minutes at about 400° Fahrenheit (“a process similar to pizza baking”) only cuts the agaritine levels by about a quarter, so 77 percent still remains.

    Boiling looks better, appearing to wipe out more than half the toxin after just five minutes, but the agaritine isn’t actually eliminated. Instead, it’s just transferred to the cooking water. So, levels within the mushrooms drop by about half at five minutes and by 90 percent after an hour, but that’s mostly because the agartine is leaching into the broth. So, if you’re making soup, for instance, five minutes of boiling is no more effective than dry baking for ten minutes, and, even after an hour, about half still remains.

    Frying for five to ten minutes eliminates a lot of agartine, but microwaving is not only a more healthful way to cook, but it works even better, as you can see here and at 1:39 in my video. Researchers found that just one minute in the microwave “reduced the agaritine content of the mushrooms by 65%,” and only 30 seconds of microwaving eliminated more than 50 percent. So, microwaving is probably the easiest way to reduce agaritine levels in fresh mushrooms. 
    My technique is to add dried mushrooms into the pasta water when I’m making spaghetti. Between the reductions of 20 percent or so from the drying and 60 percent or so from boiling for ten minutes and straining, more than 90 percent of agaritine is eliminated.

    Should we be concerned about the residual agaritine? According to a review funded by the mushroom industry, not at all. “The available evidence to date suggests that agaritine from consumption of…mushrooms poses no known toxicological risk to healthy humans.” The researchers acknowledge agartine is considered a potential carcinogen in mice, but then that data needs to be extrapolated to human health outcomes.

    The Swiss Institute of Technology, for example, estimated that the average mushroom consumption in the country would be expected to cause about two cases of cancer per one hundred thousand people. That is similar to consumption in the United States, as seen below and at 3:00 in my video, so “one could theoretically expect about 20 cancer deaths per 1 x 106 [one million] lives from mushroom consumption.” In comparison, typically, with a new chemical, pesticide, or food additive, we’d like to see the cancer risk lower than one in a million. “By this approach, the average mushroom consumption of Switzerland is 20-fold too high to be acceptable. To remain under the limit”—and keep risk down to one in a million—“‘mushroom lovers’ would have to restrict their consumption of mushrooms to one 50-g serving every 250 days!” That’s about a half-cup serving once in just over eight months. To put that into perspective, even if you were eating a single serving every single day, the resulting additional cancer risk would only be about one in ten thousand. “Put another way, if 10,000 people consumed a mushroom meal daily for 70 years, then in addition to the 3000 cancer cases arising from other factors, one more case could be attributed to consuming mushrooms.” 
    But, again, this is all based “on the presumption that results in such mouse models are equally valid in humans.” Indeed, this is all just extrapolating from mice data. What we need is a huge prospective study to examine the association between mushroom consumption and cancer risk in humans, but there weren’t any such studies—until now.

    Researchers titled their paper: “Mushroom Consumption and Risk of Total and Site-Specific Cancer in Two Large U.S. [Harvard] Prospective Cohorts” and found “no association between mushroom consumption and total and site-specific cancers in U.S. women and men.”

    Eating raw or undercooked shiitake mushrooms can cause something else, though: shiitake mushroom flagellate dermatitis. Flagellate as in flagellation, whipping, flogging. Below and at 4:48 in my video, you can see a rash that makes it look as if you’ve been whipped.

    Here and at 4:58 in my video is another photo of the rash. It’s thought to be caused by a compound in shiitake mushrooms called lentinan, but because heat denatures it, it only seems to be a problem with raw or undercooked mushrooms.

    Now, it is rare. Only about 1 in 50 people are even susceptible, and it goes away on its own in a week or two. Interestingly, it can strike as many as ten days after eating shiitake mushrooms, which is why people may not make the connection. One unfortunate man suffered on and off for 16 years before a diagnosis. Hopefully, a lot of doctors will watch this video, and if they ever see a rash like this, they’ll tell their patients to cook their shiitakes.

    Michael Greger M.D. FACLM

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

    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.

    Michael Greger M.D. FACLM

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

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

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

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

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

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

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

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

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

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

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

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

    Michael Greger M.D. FACLM

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  • Does Marijuana Affect Weight Gain or Bone Density?  | NutritionFacts.org

    Does Marijuana Affect Weight Gain or Bone Density?  | NutritionFacts.org

    Are the apparent adverse effects of heavy cannabis use on the bone just due to users being thinner? 

    It’s been recognized for decades that cigarette smoking can have “a major effect” on bone health, “increasing the lifetime risk of hip fracture by about half.” It also appears to impair bone healing, so much so that surgeons ask if they should discriminate against smokers because their bone and wound-healing complication rates are so high. What about smoking marijuana?

    As I discuss in my video Effects of Marijuana on Weight Gain and Bone Density, “There is accumulating evidence to suggest that cannabinoids [cannabis compounds] and their receptors play important roles in bone metabolism by regulating bone mass, bone loss, and bone cell function.” Okay, but are they “friend or foe?” 

    “Results from research on cannabinoids and bone mineral density in rodent models have been inconsistent. Some studies show increased bone formation, others have demonstrated accelerated bone loss, and yet others have shown no association. This variation in results may be due [in part] to differences in the mouse strain, sex, age…” If you can’t even extrapolate from one mouse to another, how can you extrapolate from mice to human beings?

    What if you just measure cannabis use and bone mineral density in people? Researchers tested thousands of adults and asked them about their cannabis use. There did not appear to be any link between the two, which is a relief. However, in this study, “heavy” cannabis use was defined as just five or more days of use in the previous 30 days. The researchers didn’t ask beyond that, so, theoretically, someone who smoked just five joints in their entire life could be categorized as a “heavy user” if they happened to use it five times in the last four weeks.

    How about cannabis use on 5,000 separate occasions over a lifetime? Now that’s a heavy user—decades of regular use. In that case, heavy use was “associated with low bone mineral density and an increased risk of fractures”—about double the fracture rate presumably due to lower bone density in the hip and spine, although heavy cannabis users were also thinner on average, and thinner people have lighter bones.

    Hip fracture risk goes down as our weight goes up. Nearly half of underweight women have osteoporosis, but less than 1 percent of obese women do, which makes total sense. Being obese forces our body to make our bones stronger to carry around all of that extra weight. That’s why weight-bearing exercise is so important to constantly put stress on our skeleton. When it comes to our bones, it’s use it or lose it. That’s why astronauts can lose a percent of their bone mass every month in “long-duration spaceflight.” Their bodies aren’t stupid. Why waste all that energy making a strong skeleton if you aren’t going to put any weight on it? 

    So, maybe the reason heavy cannabis users have frailer bones is because they tend to be about 15 pounds lighter. Wait a second. Marijuana users are slimmer? What about the munchies? “The lower BMI that was observed in heavy cannabis users at first sight seems counterintuitive,” given marijuana’s appetite stimulation, but this isn’t the first time this has been noted. 

    “Popular culture commonly depicts marijuana users as a sluggish, lethargic, and unproductive subculture of compulsive snackers,” and marijuana has indeed been found to increase food intake. A single hit can increase appetite, so you’d expect obesity rates to rise in states that legalized it. But, if anything, the rise in obesity appeared to slow after medical marijuana laws were passed, whereas it appeared to just keep rising in other states, as you can see in the graph below and at 3:45 in my video. 

    The reason pot smokers may be slimmer is because of the effect of smoked marijuana on metabolism. We’ve known for more than nearly 40 years that within 15 minutes of lighting up, our metabolic rate goes up by about 25 percent and stays there for at least an hour, as you can see below and at 4:04 in my video. So, that may be playing a role. 

    Is that why heavy cannabis use is associated with lower bone mineral density and increased risk of fractures? Because users just aren’t as overweight? No. Even when taking BMI into account, heavy cannabis use appears to be “an independent predictor” of weaker bones.

    I originally released a series of marijuana videos in a webinar and downloadable digital DVD. There are still a few videos coming out over the next year, but if you missed any of the already published ones, see the related posts below. 

    For more on bone health, check out the related posts below. 

    Michael Greger M.D. FACLM

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  • Fighting Cancer and the Common Cold with Garlic  | NutritionFacts.org

    Fighting Cancer and the Common Cold with Garlic  | NutritionFacts.org

    Raw garlic is compared to roasted, stir-fried, simmered, and jarred garlic.

    Garlic lowers blood pressure, regulates cholesterol, and stimulates immunity. I’ve talked before about its effect on heart disease risk factors, but what about immunity? Eating garlic appears to offer the best of both worlds, dampening the overreactive face of the immune system by suppressing inflammation while boosting protective immunity—for example, the activity of our natural killer cells, which our body uses to purge cells that have been stricken by viruses or cancer. “In World War II garlic was called ‘Russian Penicillin’ because, after running out of antibiotics, the soviet government turned to these ancient treatments for its soldiers,” but does it work? You don’t know until you put it to the test.

    How about preventing the common cold? As I discuss in my video Benefits of Garlic for Fighting Cancer and the Common Cold, it is perhaps “the world’s most widespread viral infection, with most people suffering approximately two to five colds per year.” In the first study “to use a double-blind, placebo-controlled design to investigate prevention of viral disease with a garlic supplement,” those randomized to the garlic suffered 60 percent fewer colds and were affected 70 percent fewer days. So, those on garlic not only had fewer colds, but they also recovered faster, suffering only one and a half days instead of five. Accelerated relief, reduced symptom severity, and faster recovery to full fitness. Interesting, but that study was done about two decades ago. What about all of the other randomized controlled trials? There aren’t any. There’s only that one trial to date. Still, the best available balance of evidence suggests that, indeed, “garlic may prevent occurrences of the common cold.”

    What about cancer? Is garlic “a stake through the heart of cancer?” As you can see below and at 2:05 in my video, various garlic supplements have been tested on cells in a petri dish or lab animals, but there weren’t any human studies to see if garlic could affect gene expression until now. 

    Researchers found that if you eat one big clove’s worth of crushed raw garlic, you get an alteration of the expression of your genes related to anti-cancer immunity within hours. You can see a big boost in the production of cancer-suppressing proteins like oncostatin when you drip garlic directly on cells in a petri dish, as shown in the graph below and at 2:25 in my video.   

    What’s more, you can also see boosted gene expression directly in your bloodstream within three hours of eating it, as seen below and at 2:34 in my video. Does this then translate into lower cancer risk?

    As you can see in the graph below and at 2:44 in my video, after putting together ten population studies, researchers found that those reporting higher consumption of garlic only had half the risk of stomach cancer.

    How do you define “high” garlic consumption? Each study was different, from a few times a month to every day. Regardless, those who ate more garlic appeared to have lower cancer rates than those who ate less, suggesting a protective effect. Stomach cancer is a leading cause of cancer-related death around the world, and garlic “is relatively cheap; the product is freely available and easy to incorporate into a daily diet in a palatable manner”—and safely, too, so why not? And, perhaps, the more, the better. 

    The only way to prove garlic can prevent cancer is to put it to the test. Thousands of individuals were randomized to receive seven years of a garlic supplement or a placebo. Those getting garlic did tend to get less cancer and die from less cancer, as you can see below and at 3:35 in my video, but the findings were not statistically significant, meaning that could have just happened by chance. 

    Why didn’t we see a more definitive result, given that garlic eaters appear to have much lower cancer rates? Well, the researchers didn’t give them garlic; they gave them garlic extract and oil pills. It’s possible that some of the purported active components weren’t preserved in supplement form. Indeed, one study of garlic supplements, for example, found that it might take up to 27 capsules to obtain the same amount of garlic goodness found in just half a clove of crushed raw garlic.  

    What happens if you cook garlic? If you compare raw chopped garlic to garlic simmered for 15 minutes, boiled for 6 minutes, or stir-fried for just 1 minute, you can get a three-fold drop in one of the purported active ingredients called allicin when you boil it, even more of a loss if you simmer it too long, and seemingly total elimination by even a single minute of stir-frying, as seen below and at 4:21 in my video. What about roasted garlic? Surprisingly, even though roasting is hotter than boiling, that cooking method preserved about twice as much. Raw garlic has the most, but it may be easier for some folks to eat two to three cloves of cooked garlic than even half a clove of raw. 

    What about pickled garlic or those jars of minced garlic packed in water or oil? Fancy, fermented black garlic? Though jarred garlic may be more convenient, they have comparatively less garlicky goodness, especially pickled garlic, and the black garlic falls far behind, as you can see in the graph below and at 5:12 in my video. 

    Can you eat too much? The garlic meta-analysis suggests there are no real safety concerns with side effects or overdosing, though that’s with internal use. You should not stick crushed garlic on your skin. It can cause irritation and, if left on long enough, can actually burn you. Wrap your knees with a garlic paste bandage or stick some on your back overnight, and you can end up burned, as seen below, and at 5:42 and 5:44 in my video.  

    Definitely don’t rub garlic on babies, even if you see an online article saying that topical garlic is good for respiratory disorders and your little one is congested. Below and at 5:57 in my video, you can see the blisters she got. The poor pumpkin! “It is crucial…to explain to patients that ‘natural’ does not equal ‘safe’…” 

    Don’t put it on your toes, don’t use it as a face mask, and don’t use it to try to get out of military service either.  

    If you just eat it like you’re supposed to, there shouldn’t be a problem. Some people can get an upset stomach if they eat too much, though, and you can’t really say there aren’t any side effects, given the “body odor and bad breath.”

    The other video I mentioned is Friday Favorites: Benefits of Garlic Powder for Heart Disease. What else can garlic do? See related posts below.

    And, for more on specific foods for fighting colds and cancer, check out related posts below. 

    Michael Greger M.D. FACLM

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  • What the Science Says About Time-Restricted Eating  | NutritionFacts.org

    What the Science Says About Time-Restricted Eating  | NutritionFacts.org

    Are there benefits to giving yourself a bigger daily break from eating? 
     
    The reason many blood tests are taken after an overnight fast is that meals can tip our system out of balance, bumping up certain biomarkers for disease, such as blood sugars, insulin, cholesterol, and triglycerides. Yet, as you can see in the graph below and at 0:20 in my video Time-Restricted Eating Put to the Test, fewer than one in ten Americans may even make it 12 hours without eating. As evolutionarily unnatural as getting three meals a day is, most of us are eating even more than that. One study used a smartphone app to record more than 25,000 eating events and found that people tended to eat about every three hours over an average span of about 15 hours a day. Might it be beneficial to give our bodies a bigger break? 

    Time-restricted feeding is “defined as fasting for periods of at least 12 hours but less than 24 hours,” and this involves trying to confine caloric intake to a set window of time, typically ranging from 3 to 4 hours, 7 to 9 hours, or 10 to 12 hours a day, which results in a daily fast lasting 12 to 21 hours. When mice are restricted to a daily feeding window, they gain less weight even when fed the same amount as mice “with ad-lib access.” Rodents have such high metabolisms, though, that a single day of fasting can starve away as much as 15 percent of their lean body mass. This makes it difficult to extrapolate from mouse models. You don’t know what happens in humans until you put it to the test. 
     
    The drop-out rates in time-restricted feeding trials certainly appear lower than most prolonged forms of intermittent fasting, suggesting it’s more easily tolerable, but does it work? Researchers found that when people stopped eating from 7:00 p.m. to 6:00 a.m. for two weeks, they lost about a pound each week compared to no time restriction. Note that “there were no additional instructions or recommendations on the amount or type of food consumed,” and no gadgets, calorie counting, or record-keeping either. The study participants were just told to limit their food intake to the hours of 6:00 a.m. and 7:00 p.m., a simple intervention that’s easy to understand and put into practice. 
     
    The next logical step? Put it to the test for months instead of just weeks. Obese men and women were asked to restrict eating to the eight-hour window between 10:00 a.m. and 6:00 p.m. Twelve weeks later, they had lost nearly seven pounds, as you can see in the graph below and at 2:18 in my video. This deceptively simple intervention may be operating from several different angles. People not only tend to eat more food later in the day, but eat higher fat foods later in the day. By eliminating eating in the late-evening hours, one removes prime-time snacking on the couch, a high-risk time for overeating. And, indeed, during the no-eating-after-7:00-p.m. study, the subjects were inadvertently eating about 250 fewer calories a day. Then, there are also the chronobiological benefits of avoiding late-night eating. 

    I did a whole series of videos about the role our circadian rhythms have in the obesity epidemic, how the timing of meals can be critical, and how we can match meal timing to our body clocks. Just to give you a taste: Did you know that calories eaten at dinner are significantly more fattening than the same number of calories eaten at breakfast? See the table below and at 3:08 in my video. 

    Calories consumed in the morning cause less weight gain than the same calories eaten in the evening. A diet with a bigger breakfast causes more weight loss than the same exact diet with a bigger dinner, as you can see in the graph below and at 3:21 in my video, and nighttime snacks are more fattening than the same snacks if eaten in the daytime. Thanks to our circadian rhythms, metabolic slowing, hunger, carbohydrate intolerance, triglycerides, and a propensity for weight gain are all things that go bump in the night.  


    What about the fasting component of time-restricted feeding? There’s already the double benefit of getting fewer calories and avoiding night-time eating. Does the fact that you’re fasting for 11 or 16 hours a day play any role, considering the average person may only make it about 9 hours a day without eating? How would you design an experiment to test that? What if you randomized people into two groups and had both groups eat the same number of calories a day and also eat late into the evening, but one group fasted even longer, for 20 hours? That’s exactly what researchers at the USDA and National Institute of Aging did. 
     
    Men and women were randomized to eat three meals a day or fit all of those same calories into a four-hour window between 5:00 p.m. and 9:00 p.m., then fast the rest of the day. If the weight-loss benefits from the other two time-restricted feeding studies were due to the passive calorie restriction or avoidance of late-night eating, then, presumably, both of these groups should end up the same because they’re both eating the same amount and they’re both eating late. That’s not what happened, though. As you can see below and at 4:49 in my video, after eight weeks, the time-restricted feeding group ended up with less body fat, nearly five pounds less. They got about the same number of calories, but they lost more weight. 

    As seen below and at 5:00 in my video, a similar study with an eight-hour eating window resulted in three more pounds of fat loss. So, there does seem to be something to giving your body daily breaks from eating around the clock.


    Because that four-hour eating window in the study was at night, though, the participants suffered the chronobiological consequences—significant elevations in blood pressure and cholesterol levels—despite the weight loss, as you can see below and at 5:13 in my video. The best of both worlds was demonstrated in 2018: early time-restricted feeding, eating with a narrow window earlier in the day, which I covered in my video The Benefits of Early Time-Restricted Eating. 


    Isn’t that mind-blowing about the circadian rhythm business? Calories in the morning count less and are healthier than calories in the evening. So, if you’re going to skip a meal to widen your daily fasting window, skip dinner instead of breakfast. 

    If you missed any of the other videos in this fasting series, check out the related videos below. 

    Michael Greger M.D. FACLM

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  • ‘Gut Health’ Has a Fatal Flaw

    ‘Gut Health’ Has a Fatal Flaw

    In my childhood home, an often-repeated phrase was “All disease begins in the gut.” My dad, a health nut, used this mantra to justify his insistence that our family eat rice-heavy meals, at the exact same time every day, to promote regularity and thus overall health. I would roll my eyes, dubious that his enthusiasm for this practice was anything more than fussiness.

    Now, to my chagrin, his obsession has become mainstream. Social-media testimonials claim that improving your “gut health” not only helps with stomach issues such as bloating and pain but also leads to benefits beyond the gastrointestinal system (easing problems including, but not limited to, itching, puffy face, slow-growing hair, low energy, acne, weight gain, and anxiety). You can now find a staggering range of products claiming to support digestive health: Joining traditionally gut-friendly fermented foods such as yogurt and sauerkraut are “probiotic” or “prebiotic” teas, cookies, gummies, supplements, powders, and even sodas.

    The reality is less straightforward. Maintaining the health of the gastrointestinal tract, like the health of any body part, is always a good idea. But expecting certain foods and products to overhaul gut health is unrealistic, as is believing that they will guarantee greater overall well-being. Those claims are “a little bit premature,” Karen Corbin, an investigator at the Translational Research Institute of Metabolism and Diabetes, told me. Obsessing over it just isn’t worth the trouble, and can even do more harm than good. “Gut health” cookies, after all, are still cookies.

    In my dad’s defense, your gut does matter for your health. A massive microbial civilization lives mostly along the large intestine, helping the body get the most out of food. Broadly, a healthy gut is one where the different segments of this population—numerous species of bacteria, fungi, and viruses—live in harmony. An unhealthy one implies a disturbance of the peace: One group may grow too powerful, or an invading microbe may throw things off-balance, leading to problems including gastroenteritis and a compromised immune system.

    Diet in particular has a profound impact on the gut—and how it subsequently makes you feel. “Food can have effects on the microbiome, which can then secondarily affect the host,” Purna Kashyap, a gastroenterologist at the Mayo Clinic, told me. The effects of food on a person and their microbes, he added, are generally congruent; fast food, for example, is “bad for both of us.” Neglect to feed your microbiome and the balance of microbes could tip into disarray, resulting in an imbalanced gut and corresponding bloating, stomach pain, and problems with bowel movements.

    Fermented foods such as yogurt and kimchi, long considered good for digestive health, are known as “probiotics” because they contain live bacteria that take up residence in your gut. Other foods are considered “prebiotic” because they feed the microbes already in your gut—mostly fiber, because it isn’t digested in the stomach. Getting more fiber improves regularity and supports a more normal GI system, Corbin said.

    But the fundamental problem with the gut-health obsession is that “there’s no clear definition of a healthy gut microbiome,” Corbin said. The makeup and balance of people’s microbiomes vary based on numerous factors, including genes, diet, environment, and even pets. This means that a treatment that works to rebalance one gut might not work for another. It also means that a product promoting a healthy gut doesn’t mean anything concrete. The idea that achieving gut health, however it’s defined, can solve stomach-related issues is misguided; many diseases can cause abdominal distress.

    Less certain is how much gut health is responsible for benefits beyond the gastrointestinal tract. No doubt the microbiome is connected to other parts of the body; recent research has suggested that it has a role in weight gain, depression, and even cancer, supporting the idea that having a healthy gut could lead to other benefits. But the mechanisms underpinning them are largely unknown. Which microbes are involved? What are they doing? There are “a lot of tall claims based on animal studies that the microbiome influences diabetes or obesity or whatever,” and the translatability of those studies to humans is “really unlikely,” Daniel Freedberg, a gastroenterologist at Columbia University, told me. Until scientists can show definitively that microbe X leads to outcome Y, Corbin said, any relationships between the gut and overall health are “just correlations.”

    None of this is to say that paying more attention to your digestive health is a bad idea. Especially for people diagnosed with gastrointestinal problems like IBS or Crohn’s disease, it can be essential. For everyone else, pursuing a healthy gut with food and supplements can be a nonspecific process with poorly defined goals. The food industry has capitalized on interest in probiotics and prebiotics—as well as lesser-known postbiotics and synbiotics—making products such as “insanely probiotic” yogurt, probiotic-fortified chocolate and spaghetti, and prebiotic sodas. Particularly with probiotics, the specifics are lacking. Which bacteria, and how many of them, actually make it past the stomach into the colon isn’t well understood. “A lot of probiotics are unlikely to contain viable bacteria, and probably very few of them are really making it through to the colon,” Freedberg said.

    Prebiotics are generally more important, although the source matters. Prebiotic fiber is “one of the most important things that determines what bacteria are there,” Freedberg told me, but getting small amounts from fiber-fortified products isn’t going to make a huge difference. The soda brands Poppi and Olipop largely contain inulin, a type of fiber that’s common in food manufacturing for its slightly sweet taste, Freedberg explained, though it probably doesn’t contain a lot, otherwise it would become “sludgy.” Olipop contains about nine grams of fiber per can, roughly the same amount as one cup of cooked lima beans.

    Of course, any product that is inherently unhealthy won’t magically become good for you the moment fiber or live bacteria are added to it. With desserts and salty snacks, no amount of fiber “is going to overcome the issue” that they are full of sugar or salt, Corbin said. Concerns about medium aside, though, gut-health products elicited a shrug from her: Buying foods containing additional prebiotic fiber is a “reasonable approach,” so long as they’re healthy to begin with. If probiotics make a patient feel “fantastic,” Freedberg said, “I’m not going to rock the boat.” Prebiotic and probiotic products may help to a degree, but don’t expect them to overhaul an unhealthy gut one soda at a time. All of the experts I spoke with said that people concerned about their gut health should eat a lot of fruits, vegetables, whole grains, and legumes, and cut out junk that won’t feed their microbiome. In other words, a basic healthy diet is more than enough to achieve good gut health.

    My dad’s gut-health mantra was apparently borrowed from Hippocrates, suggesting that people have been obsessing over the digestive system for thousands of years with the belief that it is the key to overall health. The draw of this idea is its simplicity: Proposing that the body’s many ills can be collapsed into a single mega-ailment makes treatment seem refreshingly uncomplicated compared with the medical interventions needed to address individual problems. That the proposed treatments are easy and self-administrable—sipping fibrous soda, popping bacteria-packed pills—adds to the appeal.

    But perhaps what is most compelling about the idea is that there is some truth to it. Lately, research on the microbiome has seen some promising advances. A large study published in 2022 showed significantly elevated levels of certain bacteria in people with depressive symptoms. Another study, co-authored by Corbin in 2023, was one of the first to show, in a human clinical trial, that a high-fiber diet shifts the microbiome in a way that could promote weight loss. This moment is especially confusing because we are finally beginning to understand the gut’s connections to the rest of the body, and how eating certain foods can soothe it. Much more is known about the gut than in the days of Hippocrates, but still far less than the gut influencers on social media would have you believe.

    Yasmin Tayag

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

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


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

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

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

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


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

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

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

    For more on longevity, see related videos below.





    Michael Greger M.D. FACLM

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  • Putting Alternate-Day Intermittent Fasting to the Test  | NutritionFacts.org

    Putting Alternate-Day Intermittent Fasting to the Test  | NutritionFacts.org


    Does eating every other day prevent the metabolic slowing that accompanies weight loss, or does it improve compliance over constant, day-to-day caloric restriction? 

    Rather than cutting calories day in and day out, what if you instead ate as much as you wanted every other day or for only a few hours a day? Or, what if you fasted two days a week or five days a month? These are all examples of intermittent fasting regimens, as you can see below and at 0:10 in my video Alternate-Day Intermittent Fasting Put to the Test, and that may even be how we were built. Three meals a day may be a relatively novel behavior for our species. For millennia, “our ancestors could not eat three meals every day. They consumed meals much less frequently, and often consumed one large meal per day or went for several days without food.” 

    Intermittent fasting is often presented as a means of stressing your body—in a good way. There is a concept in biology called hormesis, which can be thought of as the “that which doesn’t kill you makes you stronger” principle. Exercise is the classic example: You put stress on your heart and muscles, and as long as there is sufficient recovery time, you are all the healthier for it. Is that the case with intermittent fasting? Mark Twain thought so: “A little starvation can really do more for the average sick man than can the best medicines and the best doctors. I do not mean a restricted diet, I mean total abstention from food for one or two days.” 
     
    But, Twain also said, “Many a small thing has been made large by the right kind of advertising.” Is the craze over intermittent fasting just hype? Many diet fads have their roots “in legitimate science,” but over time, facts can get distorted, benefits exaggerated, and risks downplayed. In other words, “science takes a back seat to marketing.” At the same time, you don’t want to lose out on any potential benefit by dismissing something out of hand based on the absurdist claims of overzealous promoters. You don’t want to throw the baby out with the baby fat. 
     
    Religious fasting is the most studied form of intermittent fasting, specifically Ramadan, a month-long period in which “Muslims abstain from food and drink from sunrise until sunset.” The effects are complicated by a change in sleeping patterns and also thirst. The same dehydration issue arises with Yom Kippur when observant Jews stop eating and drinking for about 25 hours. The most studied form of intermittent fasting that deals only with food restriction is alternate-day fasting, which involves eating every other day, alternating with days consuming little or no calories. 
     
    At rest, we burn about a 50:50 mix of carbohydrates and fat, but we usually run out of glycogen—our carbohydrate stores—within 12 to 36 hours of stopping eating. At that point, our body has to shift to rely more on our fat stores. This metabolic switch may help explain why the greatest rate of breakdown and burning of fat over a three-day fast happens between hours 18 and 24 of the 72 hours. The hope is to reap some of the benefits of taking a break from eating without the risks of prolonged fasting. 
     
    One of the potential benefits of alternate-day fasting over chronic calorie restriction is that you get regular breaks from feeling constant hunger. But might people become so famished on their fasting day that they turn the next into a feasting day? After your fasting day, if you ate more than twice as much as you normally would, that presumably would defeat the whole point of alternate-day fasting. Mice fed every other day don’t lose weight. They just eat roughly twice as much food in one day as non-fasted mice would regularly eat in two days. That is not, however, what happens in people. 
     
    Study participants were randomized to fast for a day and a half—from 8:00 p.m. to 8:00 a.m. the second morning after beginning. Fasting for 36 hours only led to people eating an average of 20 percent more the day after they broke the fast, compared to a control group who didn’t fast at all. That would leave the fasters with a large calorie deficit, equivalent to a daily caloric restriction of nearly a thousand calories a day. This particular study involved lean men and women, but similar results have been found amongst overweight or obese subjects. Researchers typically found only about a 10 to 25 percent compensatory increase in calorie intake over baseline on non-fasting days, and this seems to be the case whether the fasting day was a true zero-calorie fast or a modified fast day of a few hundred calories, which may lead to better compliance. 
     
    Some studies have found that participants appeared to eat no more, or even eat less, on days after a day-long mini-fast. Even within studies, great variability is reported. In a 24-hour fasting study where individuals ate an early dinner and then had a late dinner the next day after skipping breakfast and lunch, the degree of compensation at the second dinner ranged from 7 percent to 110 percent, as you can see in the graph below and at 4:40 in my video. This means that some of the participants got so hungry by the time supper rolled around that they ate more than 24 hours’ worth of calories in a single meal. The researchers suggested that perhaps people first try “test fasts” to see how much their hunger and subsequent intake ramp up before considering an intermittent fasting regimen. Hunger levels can change over time, though, dissipating as your body habituates to the new normal. 


    In an eight-week study in which obese subjects were restricted to about 500 calories every other day, after approximately two weeks, they reportedly started feeling very little hunger on their slashed calorie days. This no doubt helped them lose about a dozen pounds on average over the duration of the study, but there was no control group with whom to compare. A similar study that did have a control group found a similar amount of weight loss—about ten pounds—over 12 weeks in a group of “normal weight” individuals, which means overweight on average. For these modified regimens where people are prescribed 500 calories on their “fasting” days, researchers found that, from a weight-loss perspective, it did not appear to matter whether those calories are divided up throughout the day or eaten in a single meal. 
     
    Instead of prescribing a set number of calories on “fasting” days, which many people find difficult to calculate outside of a study setting, a pair of Iranian researchers came upon a brilliant idea of unlimited above-ground vegetables. Starchy root vegetables are relatively calorie-dense compared to other vegetables. Veggies that grow above the ground include stem vegetables (like celery and rhubarb), flowering vegetables (like cauliflower), leafy vegetables (like, well, leafy vegetables), and all of the fruits we tend to think of as vegetables (like tomatoes, peppers, okra, eggplant, string beans, summer squash, and zucchini). So, instead of prescribing a certain number of calories for “fasting” days, researchers had subjects alternate between their regular diet and helping themselves to an all-you-can-eat, above-ground vegetable feast (along with naturally non-caloric beverages, like green tea or black coffee) every other day. After eight weeks, the subjects lost an average of 13 pounds and two inches off their waist, as you can see below and at 6:59 in my video. 


    The same variability discovered for calorie compensation has also been found for weight loss, as seen in the graph below and at 7:10 in my video. In a 12-month trial in which subjects were instructed to eat only one-quarter of their caloric needs every other day, weight changes varied from a loss of about 37 pounds to a gain of about 8 pounds. The biggest factor differentiating the low-weight-loss group from the high-weight-loss group appeared to be not how much they feasted on their regular diet days, but how much they were able to comply with the calorie restriction on their fast days. 

     
    Overall, ten out of ten alternate-day fasting studies showed significant reductions in body fat. Small short-term studies show about a 4 to 8 percent drop in body weight after 3 to 12 weeks. How does that compare with continuous calorie restriction? Researchers compared zero-calorie, alternate-day fasting head-to-head to a daily 400-calorie restriction for eight weeks. Both groups lost the same amount of weight, about 17 pounds, and, in the follow-up check-in six months later after the trial had ended, both groups had maintained a similar degree of weight loss; both were still down about a dozen pounds, as you can see below and at 8:10 in my video. 


    The hope that intermittent fasting would somehow avoid the metabolic adaptations that slow weight loss or improve compliance doesn’t seem to have materialized. The same compensatory reactions in terms of increased appetite and a slower metabolism plague both continuous and intermittent caloric restriction. The longest trial of alternate-day fasting found that “alternate-day fasting may be less sustainable” than more traditional approaches. By the end of the year, the drop-out rate of the alternate-day fasting group was 38 percent, compared to 29 percent in the continuous calorie-restriction group.  

    Although alternate-day fasting regimens haven’t been shown to produce superior weight loss to date, for individuals who may prefer this pattern of calorie restriction, are there any downsides? Find out in my video Is Alternate-Day Intermittent Fasting Safe?. 
     
    I packed a lot into this one. Bottom line: Fasting doesn’t appear to provide an edge over traditional calorie cutting, but if you prefer it, why not give fasting a try? Before you do, first check out Is Alternate-Day Intermittent Fasting Safe?.  

    What about total fasting? For that and even more, check out the related videos below.

    I have a whole chapter on intermittent fasting in my book How Not to Diet—order now! (All proceeds I receive from my books are donated to charity.) 





    Michael Greger M.D. FACLM

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