Category: Nutrition

  • What Does Personalized Nutrition Actually Deliver?

    What Does Personalized Nutrition Actually Deliver?

    There’s a lot of focus on personalized nutrition, but maybe we should focus on taking personal responsibility for our health.

    “Personalized nutrition (PN) is rooted in the concept that one size does not fit all,” and who doesn’t want to think they’re special? The idea of personalized nutrition is inherently appealing to our ego; that’s why simple messages recognizing individuality deeply resonate with us and why such messages are popular in marketing and sales. This focus on uniqueness has spurred the creation of personalized foods, along with the suggestion that “3D Food Printing seems to be a good candidate for food customization.”

    Now, there certainly are some legitimate differences between people. Some have a peanut allergy and keel over if they eat a peanut, others have celiac disease and need to avoid gluten, and some are genetically lactose-intolerant. There’s an enzyme mutation common in some parts of Asia that protects against alcoholism because people with the altered enzyme don’t metabolize alcohol as efficiently, so toxic metabolites build up. I published a fascinating video about fast versus slow caffeine metabolizers and the difference in health benefits that actually extends to athletic performance. Caffeine is ergogenic—performance-enhancing—but only in fast metabolizers, shaving more than a minute off 10 kilometers (about 6 miles) of cycling, whereas slower metabolizers either got no benefit or the caffeine actually slowed them down, adding two minutes to their cycling time, depending on which kinds of genes they have that code the enzyme that breaks it down. You can see these results below and at 1:24 in my video How Useful Is Personalized Nutrition?.

    But for most people, in most situations, we are more similar than different.

    While there is a specific minority of people who need a more personalized approach to nutrition, there is currently insufficient evidence to support truly personalized nutrition for most people. Yet a surprising number of direct-to-consumer genetic testing companies have proliferated, offering personalized nutrition advice. For example, there are supplement-hawking companies that claim to help consumers optimize micronutrient status based on a handful of genetic variants, even though most variants explain just a few percent of the difference in levels between people.

    Personalized nutrition is part of a broader push towards personalized medicine, also known as precision medicine. There is a “massive cultural allure” of personal control over diagnosis, treatment of disease, and prevention, spurring demand and intense commercialization. But unlike monogenetic diseases—which are rare genetic diseases caused by a single malfunctioning gene, like hemophilia or sickle cell anemia—most diseases are caused by a complex interaction between multiple genes and environmental factors, which pose a “major challenge for the realization of personalized medicine.”

    Take something like adult stature, for example. Researchers have found at least 40 locations on our chromosomes that have been associated with human height, which is strongly inherited. The genes from parents account for about 80% of the difference in height between people, yet those dozens of identified genes explain only about 5% of height variation between individuals.

    Researchers find those genetic links by using genome-wide association studies, in which all the chromosomes are scanned to look for statistical associations between diseases and any particular stretches of DNA. That’s interesting, but companies marketing genetic susceptibility tests are reinterpreting these data as if they predict individual risks. But all you’re really getting are modest genetic associations with a slight increase in disease risk and with little predictive power when compared to more significant contributions of things we already know, like lifestyle behaviors. Currently, the practice of using a person’s DNA to predict disease “has been judged to provide little to no useful information.”

    For example, let’s say a person’s genetic analysis says they’re at slightly greater risk for some grave condition compared to others in their ancestral group. This person was advised to exercise, keep their weight down, not drink too much alcohol, and eat fruits, vegetables, and whole grains. It’s sound advice, but we should be living this way regardless of our genetic risk. And we know—at least we should know—these simple, basic strategies to reduce risks of common chronic diseases. “The problem, of course, is that very few individuals live this way. Actually, to be more precise, almost nobody lives this way.” That’s not just hyperbole—nationwide surveys show that nearly everyone in the United States consumes a diet that’s not on par with even the wimpy recommendations of the Dietary Guidelines.

    Indeed, almost “no one in the United States is eating a healthy diet.” Findings like that remind us that when it comes to public health, “worrying about personalizing our preventive strategies based on genetic risk information borders on the absurd.”

    Doctor’s Note

    Here’s the video I mentioned about fast versus slow caffeine metabolizers and the difference in health benefits extending to athletic performance: Friday Favorites: Do the Health Benefits of Coffee Apply to Everyone?.

    For more about lifestyle approaches, check out related posts below.



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  • The Link Between Milk and Parkinson’s Disease

    The Link Between Milk and Parkinson’s Disease

    Is the brain damage associated with milk consumption due to the banned pesticide heptachlor or the milk sugar galactose?

    Parkinson’s disease is a neurodegenerative brain disorder that affects millions of people. What causes it? Well, if you look at lifestyle factors associated with Parkinson’s disease, dairy consumption is the strongest dietary factor associated with an increased risk of Parkinson’s disease. In fact, dairy products are the only food group consistently linked with a high risk of developing Parkinson’s. Five large prospective studies have confirmed the link. This includes the two Harvard cohorts, the Nurses’ Health Study and the Health Professionals Follow-up Study, which followed more than 100,000 people combined for decades in “the largest analysis of dairy and PD [Parkinson’s disease] to date,” analyzing more than 1,000 newly diagnosed cases. All the studies found a link between dairy and Parkinson’s, with most finding a significant link—about a 50% increase in risk overall in those drinking the most milk compared to those drinking the least, at a p-value below 0.00001, meaning there’s less than a 1 in 100,000 chance you’d randomly get a finding that extreme. You can see this in the chart below and at 1:13 in my video, The Role Milk May Play in Triggering Parkinson’s Disease.

    Okay, but why is there a link at all? “Despite clear-cut associations between milk intake and” incidence of Parkinson’s, “there is no rational explanation,” concluded one review. A year later, though, we got a clue: “Midlife milk consumption and substantia nigra neuron density at death.” What does that mean? Parkinson’s is caused primarily by the loss of a certain type of nerve cells in a critical part of the brain, with symptoms first appearing once most of these neurons have died. So one study looked at how much milk people drank when they were in their 40s, 50s, and 60s, and then examined their brains at autopsy and counted how many of those critical neurons they had left. In every single quadrant, neuron density was highest “in those who consumed no milk and lowest in those who consumed the most milk.” Even after removing the Parkinson’s cases, those drinking two cups (473 mL) of milk a day had up to 40% fewer nerve cells in most quadrants of that critical brain region. What’s in milk that could be wiping out brain cells? Among the people who drank the most milk, residues of the pesticide “heptachlor epoxide were found in 9 out of 10 brains.” So, maybe the finding of pesticide residues more commonly in the brains of those who drank the most milk could explain how milk could be cause-and-effect related to Parkinson’s disease risk.

    Now, that’s not the only potential explanation. In one of my videos, I talked about how meat contains that clumpy neurotoxic protein alpha-synuclein. Well, dairy products may contain trace amounts as well, but we don’t have confirmation of that. Could the milk sugar “galactose be the missing link?” Galactose is what the lactose in milk breaks down into once it’s in the body. It’s also what’s used to induce aging—to experimentally cause aging—in the brain. When you drink it, the galactose is picked up by your brain within a few hours, and for doses above 100 mg/kg, it appears that galactose can cause pathological alterations in brain cells, similar to those observed in Parkinson’s disease. This amount “can be reached and surpassed” by simply drinking two glasses (473 mL) of milk (the main dietary source of galactose) each day. And of all your brain cells, those dopaminergic neurons—the ones that you need to retain to prevent Parkinson’s—may be more vulnerable to galactose-induced damage because they are more vulnerable to oxidative stress.

    Galactose may also explain the findings linking milk drinking with higher death rates. You may be thinking, “Well, duh—the saturated butterfat is just cutting people’s lives short,” but higher mortality with high milk consumption has been observed regardless of the milk fat content. Skim milk might be fat-free, but it’s not lactose-free.

    Can’t you just drink lactose-free milk, like Lactaid? That has the lactase enzyme added to make lactose-free milk. But it just breaks down lactose into galactose in the carton rather than in your gut, so you’re still ingesting the same amount of galactose. Perhaps it’s no wonder that more milk intake at midlife may be linked to a greater rate of cognitive decline. Remember, researchers use galactose to create brain aging in the laboratory. D-galactose, a metabolic derivative of lactose, has been extensively used in animal models “to mimic cognitive aging” through oxidative stress. Compared to those who said they “almost never” drink milk, those drinking more than one glass (237 mL) a day appear more likely to suffer a decline in global cognitive function.

    Doctor’s Note

    Here’s the meat video I mentioned: The Role Meat May Play in Triggering Parkinson’s Disease.

    You may remember that I’ve explored this before in Could Lactose Explain the Milk and Parkinson’s Disease Link?. Uric acid may also be a contender—see Parkinson’s Disease and the Uric Acid Sweet Spot.

    For more on Parkinson’s disease, check out related posts below.



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  • Can Onions Help with Weight Loss, Cholesterol, and PCOS?

    Can Onions Help with Weight Loss, Cholesterol, and PCOS?

    Let’s talk about treating weight loss, cholesterol, and PCOS with diet. What can an eighth of a teaspoon a day of onion powder do for body fat, and what can raw red onion do for cholesterol?

    In one of my previous videos about onions, I talked about the data supporting—or not supporting—the role of onions in boosting testosterone in men, protecting bone health, controlling allergies, and dealing with the side effects of chemotherapy. What about weight loss? Enter the “Effect of Steamed Onion (ONIRO) Consumption on Body Fat and Metabolic Profiles in Overweight Subjects.” Researchers used steamed onions, which aren’t as spicy and have a weaker smell, so they could better disguise them as a placebo. They dried them into onion powder and gave people a minuscule amount—about an eighth of a teaspoon (300 mg) a day. Surely, a little daily dusting of onion powder wouldn’t affect people’s weight. But check out the results reported in the abstract: Measurements using a DEXA scan showed a significant reduction in body fat mass, and a CT scan revealed a significant decrease in whole, visceral, and subcutaneous fat areas.

    Hold on. If a little onion powder is so effective for weight loss, why wasn’t it featured in my book How Not to Diet? Because, as so often happens in studies, the spin in the abstract doesn’t accurately represent the actual data. The DEXA scan results measured no significant change of fat in the group that got the placebo capsules. They only appeared to lose about a spoonful (7 g) of fat, whereas the group unknowingly taking an eighth of a teaspoon of onion powder stuffed into capsules lost nearly one and a half pounds (0.64 kg) of body fat—a significant drop from baseline, but not a statistically significant drop compared to the placebo group, meaning the loss could have just been due to chance. Same thing with the CT scan results: 5 times more loss of overall fat and over 30 times more loss of the dangerous visceral fat, but the results did not reach statistical significance compared to placebo.

    A more recent study tried four teaspoons (9 g) of onion powder a day and similarly failed to accelerate the loss of visceral, total, or subcutaneous fat compared to placebo—but the placebo was also four teaspoons (9 g) of onion powder a day. They used yellow onions versus white onions, and it seems they both may have caused a loss of abdominal body fat, without a significant difference between them. Either way, you might look at these two studies and think, sure, but what are the downsides? It’s only an eighth of a teaspoon of onion powder a day, so why not give it a try? It can’t hurt, but we just don’t have enough evidence to be confident it will actually help.

    Let’s talk about polycystic ovary syndrome, also known as PCOS. It’s one of the most common hormone disorders, affecting 5% to 10% of reproductive-aged women. In addition to causing symptoms like irregular periods, “PCOS is a pre-diabetic state, with decreased insulin sensitivity.” PCOS treatment is challenging due to medication side effects. So, are there dietary options? How about a randomized controlled clinical trial of raw red onion intake?

    Why onions? Well, onion extracts can evidently improve blood sugar and insulin sensitivity in rats with diabetes and, more importantly, were found to reduce blood sugar levels in humans with diabetes, but evidently not in non-diabetic humans. People with PCOS are kind of pre-diabetic, so would it work for them? First, let’s look at those other two studies. To study the “Metabolic Effects of Onion and Green Beans,” people with diabetes spent a week eating either a small onion (60 g) each day or the same diet with about six cups (600 g) of green beans instead—and both approaches worked. The onion lowered people’s blood sugar levels by about 10% compared to a non-onion control diet, while the green beans lowered them by roughly 15% compared to the control.

    Here’s the study that supposedly shows no blood sugar benefits for people without diabetes. It’s true—onions don’t seem to lower normal blood sugar levels, which is a good thing, but check out what happens when you feed people sugar. Have people consume about two and a half tablespoons (50 g) of corn syrup, and their blood sugar levels shoot up over the next two hours before their body can tamp it back down. But give people the exact same amount of sugar along with more and more onion extract, and the blood sugar spike is significantly dampened, almost as much as if you had instead given them an antidiabetic drug, as you can see below and at 4:00 in my video Onions Put to the Test for Weight Loss, Cholesterol, and PCOS Treatment.

    We see the same blunting effect on blood sugar when people get a shot of adrenaline and eat onion extract, compared to receiving adrenaline without the onion extract, as you can see below and at 4:11 in my video.

    So, are there blood sugar benefits for both people with and without diabetes? No difference was found in blood sugar levels or other markers of insulin resistance between the high-onion and low-onion groups of PCOS patients, nor were there any differences in a marker of inflammation between the two groups. But women with PCOS aren’t just at higher risk for diabetes and inflammation—they are also at higher risk for high cholesterol.

    Women with PCOS are over seven times more likely to have a heart attack and develop heart disease, the number one killer of women. But consuming raw red onion appears to be effective in lowering cholesterol, though the group that ate more onions only dropped their LDL cholesterol about 5 points (5 mg/dL), which was not significantly different than the group that ate fewer onions.

    I did find this study from 50 years ago where researchers fed people nearly an entire stick (100 g) of butter, and their cholesterol shot up about 30 points within hours of consumption but by only 9 points or 3 points when combined with about a third of a cup (50 g) of raw or boiled onion. The moral of the story: Don’t eat a stick of butter.

    Doctor’s Note

    Check out the previous video I mentioned: Friday Favorites: Are Onions Beneficial for Testosterone, Osteoporosis, Allergies, and Cancer?.



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  • Weight-Loss Devices to the Extreme

    Weight-Loss Devices to the Extreme

    Let’s discuss the safety and efficacy of various weight-loss methods, ranging from Botox and corsets to siphons and tapeworms.

    A moderately obese person doing moderately intense physical activity, like biking or brisk walking, would burn off approximately 350 calories an hour, but most drinks, snacks, and other processed junk are consumed at a rate of about 70 calories (293 kJ) per minute. Therefore, it only takes five minutes to wipe out a whole hour of exercise.

    Enter the AspireAssist siphon assembly.

    It’s a percutaneous gastrostomy device, meaning surgeons cut a hole in a person’s stomach and tunnel a fistula out through the abdominal wall. So, after each meal, the person can attach a suction gadget to the hole and directly drain out their stomach contents, as you can see below and at 0:47 in my video Extreme Weight-Loss Devices.

    This means you could gorge on donuts, spew them out through the hole in your stomach, then gorge on more donuts. Have your cake, and eat it, too…and two, three, and four times!

    It seems to be the quintessential American invention, straight from the land that brought us Jell-O salads, spray cheese, and deep-fried Snickers bars. Patients do lose weight, perhaps in part because the fistula may interfere with the relaxation of the stomach wall during a meal. The process also requires drinking lots of water and thoroughly chewing food, both of which may help with weight loss by increasing hydration and slowing the eating rate. Patients also started making healthier choices to avoid the unpleasant sight of gastric aspirate from unhealthy foods. (The tubing is clear, and, evidently, fried foods look particularly gross as they are pumped out.)

    All patients need to take supplemental potassium, since it’s sucked out in stomach juices. Otherwise, they risk becoming potassium-deficient (a common complication in bulimia), but most side effects are just minor wound complications. Serious adverse effects, like abdominal abscesses, are rare. The big selling point is that the siphon device doesn’t change the gastrointestinal tract’s anatomy. That seems like a low bar, but in today’s Wild West world of weight-loss procedures, you can’t take anything for granted. Take the duodenal-jejunal bypass liner, for example.

    Gastric bypass surgery works in part by cutting out a portion of the small intestine so it’s no longer in the flow of food, thereby helping to prevent the absorption of calories. Instead of major surgery, how about just dropping down a couple of feet of plastic tubing to line the intestinal walls? The problem with the EndoBarrier is that it has to be anchored in the digestive tract. This is accomplished with 10 barbed hooks that cause lacerations, accounting for the majority of the 891 adverse effects reported in 1,056 patients—nearly 9 out of 10 people. Severe penetrating trauma, resulting in esophageal perforation or liver abscesses, is rarer (occurring in only about 1 in 27 patients).

    Concern has been raised about the “palatability” of the AspireAssist stomach pump, but the most cringeworthy endoscopic procedure I discovered in my research was intestinal “resurfacing.” Why cover the inside of your intestines with plastic to prevent absorption when you can just “thermally ablate the superficial duodenal mucosa”? In other words, have your intestinal lining burned off—or rather, “resurfaced.”

    Surgeons have tried injecting Botox into the stomach walls of obese individuals, hoping it would partially paralyze their gastric muscles, slow stomach emptying, make people feel fuller longer, and lose weight. It didn’t work.

    Researchers in Sweden tried randomizing people to wear corsets for 12 to 16 hours a day, seven days a week, for nine months. And it didn’t work. The study participants just didn’t wear the corsets—they were “perceived as uncomfortable.” Duh.

    “Sanitized tapeworms” have evidently been widely advertised as a weight-loss remedy since back in the early 1900s. The fact that living tapeworms have been discovered during bariatric surgery operations suggests that infesting yourself with parasites may not be particularly effective either.

    Speaking of disgusting strategies, how about disgust itself? A study entitled “Harnessing the Power of Disgust: A Randomized Trial to Reduce High-Calorie Food Appeal Through Implicit Priming” tried using subliminal messages to ruin people’s appetite. Just before showing images of healthy foods, researchers briefly flashed happy images—such as a group of kittens—for 20 milliseconds. That’s too quick to consciously register, but the hope was to plant a positive imprint on the brain. Before showing images of high-calorie foods like ice cream, they flashed negative scenes, like a cockroach on a pizza slice, vomit in a dirty bathroom, and a burn wound. Apparently, it worked! Subjects subsequently reported a reduced desire to eat high-calorie foods, though this wasn’t tested directly. The researchers concluded that subliminal revulsion might be “a successful tactic to combat the onslaught of food cues that promote unhealthy eating….”

    The rest of the world looks on, bemused by American machinations, penning commentaries like “Don’t Let Them Eat Cake! A View from Across the Pond.” A paper in the journal Obesity Surgery entitled “What Are the Yanks Doing?” reviewed “The U.S. Experience with Implantable Gastric Stimulation,” inserting electrodes into the muscular layer of the stomach wall. When that didn’t work, colon electrical stimulation was tried.

    Even more shocking were studies like “Repetitive electric brain stimulation reduces food intake in humans.” Though placing deep-brain electrodes is considered a complication-prone operation, scientists have long pondered whether “placing an electrode somewhere in the brain could make people eat less.” Holes were drilled through the skulls of five obese individuals, and wires were pushed into their brains for “electrostimulatory exploration.” Once the researchers poked around and found spots where they were able to elicit convincing hunger responses, they sent in enough juice to fry out electro-coagulatory lesions. It seemed to work in cats and monkeys, but the researchers found that burning holes in people’s brains did not result in weight loss in obese humans. Thankfully, as I explained in my book How Not to Diet, healthy, sustainable weight loss isn’t brain surgery.

    Doctor’s Note

    Check out Is Gastric Balloon Surgery Safe and Effective for Weight Loss?.

    What about drugs? See Are Weight Loss Pills Safe? and Are Weight Loss Pills Effective?.

    So, what’s the best way to lose weight? I wrote a whole book about it! How Not to Diet is focused exclusively on sustainable weight loss. Borrow it from your local library or pick up a copy from your favorite bookseller. (All proceeds from my books are donated to charity.) To whet your appetite, take a peek: Trailer for How Not to Diet: Dr. Greger’s Guide to Weight Loss.

    For more on this topic, check out related posts below.



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  • When the Fix Is an Illusion

    When the Fix Is an Illusion

    Sham surgery trials have shown that some of our most popular surgeries are themselves shams.

    Intragastric balloons “arrived with much fanfare in the 1980s,” since they could be implanted into the stomach and inflated with air or water to fill much of the space. Unfortunately, surgical devices are often brought to the market before there is adequate evidence of effectiveness and safety, and the balloons were no exception.

    The “gastric bubble” had its bubble burst when a study at the Mayo Clinic found that 8 out of 10 balloons “spontaneously deflated,” which is potentially dangerous because they could pass into the intestines and cause an obstruction, as you can see below and at 0:40 in my video Is Gastric Balloon Surgery Safe and Effective for Weight Loss?.

    Before balloons deflated, however, they apparently caused gastric erosions in half the patients, damaging their stomach lining. The kicker is that, in terms of inducing weight loss, they didn’t even work when compared to diet and other behavior modification strategies. Eventually, intragastric balloons were pulled from the market. But now, balloons are back.

    After a 33-year hiatus, the U.S. Food and Drug Administration started approving a new slew of intragastric balloons in 2015, which immediately resulted in the placement of more than 5,000 devices. By then, the Sunshine Act had passed. It forced drug companies and the surgical and medical device industry to disclose any payments made to physicians, shining a disinfecting light on industry enticements. By now, most people know about the overly cozy financial relationships doctors can have with Big Pharma, but fewer may realize that surgeons can also get payments from the companies for the devices they use. The 100 top physician recipients of industry payments received an unbelievable $12 million from device companies in a single year. Yet outrageously, when they published papers, only a minority disclosed the blatant conflict of interest.

    The benefit of balloons over most types of bariatric surgery is that they’re reversible, but that doesn’t mean they’re benign. The FDA has released a series of advisories about the risks, which include death. But how could someone suffer a stomach perforation with a smooth, rounded object? By that smooth, rounded object causing the patient to vomit so much that they rupture their stomach and die. Nausea and vomiting are unsurprisingly “very common side effects,” affecting the majority of those who have balloons placed inside of them. Persistent vomiting likely also explains cases of life-threatening nutrient deficiencies after balloon implantation.

    Some complications, such as bowel obstruction, are due to the balloons deflating, but others, oddly enough, are due to the balloons suddenly overinflating, causing pain, vomiting, and abdominal distention, as you can see below and at 2:45 in my video.

    This issue was first noticed in breast implants, as documented in reports such as “The Phenomenon of the Spontaneously Autoinflating Breast Implant.” Out of nowhere, the implants can just start growing, increasing breast volume by an average of more than 50%. “It remains an underreported and poorly understood phenomenon,” one review noted. (Interestingly, breast implants were actually used as some of the first failed experimental intragastric balloons.)

    As with any medical decision, though, it’s all about risks versus benefits. Industry-funded trials display “notable weight loss,” but it’s hard to tease out the effect of the balloon on its own from the accompanying “supervised diet and lifestyle changes” prescribed in the studies. In drug trials, you can randomize study participants to sugar pills, but how do you eliminate the placebo effect of undergoing a procedure? Perform sham surgery.

    In 2002, a courageous study was published in The New England Journal of Medicine. The most common orthopedic surgery—arthroscopic surgery of the knee—was put to the test. Billions of dollars are spent on sticking scopes into knee joints and cutting away damaged tissue in osteoarthritis and knee injuries, but does that actually work? People suffering from knee pain were randomized to get the actual surgery versus a sham surgery, in which surgeons sliced into people’s knees and pretended to perform the procedure—even splashing saline—without actually treating the joint.

    The trial caused an uproar. How could anyone randomize people to get cut open for fake surgery? Professional medical associations questioned the ethics of the surgeons as well as “the sanity” of the patients who agreed to be part of the trial. Guess what happened? The surgical patients got better, but so did the placebo patients, as you can see below and at 4:42 in my video.

    The surgeries had no actual effect. Currently, rotator cuff shoulder surgery is facing the same crisis of confidence.

    When intragastric balloons were put to the test, sham-controlled trials showed that both older and newer devices sometimes fail to offer any weight-loss benefit. Even when they do work, the weight loss may be temporary because balloons are only allowed to stay in for six months (at which point the deflation risk gets too great). Why can’t you keep putting new ones in? That’s been tried; it failed to improve long-term weight outcomes. A sham-controlled trial showed that any effects of the balloon on appetite and satiety may vanish with time, perhaps as your body gets used to the new normal.

    What sham surgery trials have shown us is that some of our most popular surgeries are themselves shams. Doctors like to pride themselves on being men and women of science. For example, we rightly rail against the anti-vaccination movement. Many of us in medicine have been troubled by the political trend in which people “choose their own facts.” But when I read that some of these still-popular surgeries are not only useless but may actually make matters worse (for example, increasing the risk of progression to a total knee replacement), I can’t help but think we are hardly immune to our own versions of fake news and alternative facts.

    Doctor’s Note

    Next in this two-part series is Extreme Weight-Loss Devices.

    For more on bariatric surgery, check out related posts below.

    My book How Not to Diet is focused exclusively on sustainable weight loss. Borrow it from your local library or pick up a copy from your favorite bookseller. (All proceeds from my books are donated to charity.)



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  • Nuts, Sperm, and Sex: The Surprising Connection

    Nuts, Sperm, and Sex: The Surprising Connection

    Walnuts, almonds, and hazelnuts are put to the test for erectile and sexual function, sperm count, and semen quality.

    In 2013, I posted a video based on a study that found that men with erectile dysfunction who ate 100 grams of pistachios (a little more than three handsful) a day for three weeks had “a significant improvement in erectile function.” It’s always nice to see a whole-food intervention have clinical effects, and I was curious to revisit the topic and see what’s been published since.

    Even if you ignore all the lab animal studies on hazelnuts improving the function of rat testicles—really, there’s a study titled “Hazelnut Consumption Improves Testicular Antioxidant Function and Semen Quality in Young and Old Male Rats”—you still never know what you’ll find searching the medical literature for nuts and sexual function. I found “a case of penile strangulation with a metal hex nut” in which someone put one on his penis “for sexual pleasure” but couldn’t remove it. (I guess some kinds of nuts can sometimes make things worse.) They tried the Dundee technique, which involves creating 20 puncture holes to relieve the pressure, but that didn’t work, so then they tried a diamond disk cutter. It slipped a few times, but the hex nut was successfully removed. All’s well that ends well.

    That got me curious. Evidently, penile entrapment is so common that there is an entire grading system that emergency room doctors can use, as you can see here and at 1:21 in my video Mixed Nuts Put to the Test for Erectile Dysfunction. If a drill isn’t available, the surgeons advised, “a hammer and chisel may be used to remove nuts.”

    A drill? Oh, they mean a dental drill. Doctors describing one case bragged about the “precisely cut edges,” but it looks pretty jagged to me. You can see for yourself below and at 1:38 in my video.

    To “preserve the penis from fatal outcomes” (that’s a strange way to put it), urologists should be aware of all the available tools and approaches, and if you don’t know how to operate the saw, you can always call in the local blacksmith—but only if “special consent [is] taken from the patient”!

    But how are you going to remove an iron barbell or steel sledgehammer head? “With a heavy-duty air grinder provided by the fire department,” requiring six hours of cutting and fire coats to protect the patient from the sparks. Use whatever it takes—hack saw, “cement eater.” You can even use the silk winding method pioneered by Dong et al.

    Back to the task at hand! Consuming “at least one serving of vegetables a day and more than two servings of nuts a week was associated with a more than 50% decrease in the probability of ED” [erectile dysfunction] in a snapshot-in-time cross-sectional study. But such observational studies can’t prove cause and effect. It’s like finding that men who eat healthier have better sperm motility. Maybe men who eat nuts are just health nuts, and the improvement is due to some other factor, like exercise. What we need is an interventional trial.

    And there is one: a randomized controlled trial studied the “effect of nut consumption on semen quality and functionality.” Healthy men were fed the standard American diet with or without a mixture of nuts—a handful (30 grams) of walnuts and half a handful (15 grams) each of almonds and hazelnuts. Individuals in the nut group experienced significant improvements in their total sperm count, vitality, motility, and shape, perhaps because those “in the nut group showed a significant reduction in SDF”—sperm DNA fragmentation. The nuts appeared to protect their sperm DNA. It’s too bad that the researchers didn’t measure the men’s erectile and sexual dysfunction while they were at it. Oh, but they did!

    What is the effect of nut consumption on erectile and sexual function from that same study? The researchers report that those in the nut group saw a significant increase in orgasmic function and sexual desire, but what about erectile function? Any time you see this kind of selective glass-half-full reporting, you suspect some kind of industry funding, and, indeed, that was the case here; the study was partially funded by the International Nut and Dried Fruit Council. Yes, there was a marginal increase in orgasmic function and sexual desire of questionable clinical significance, but there was no improvement in erectile function, intercourse satisfaction, or overall satisfaction. As with so many comparisons, even the so-called significant findings may not even be statistically significant.

    But why did the pistachios I talked about back in 2013 work, while these other nuts didn’t? Well, the original study was done on men mostly in their 40s and 50s who already had chronic erectile dysfunction for at least one year, whereas the average age of participants in the newer study was 24. So, the individuals in the later study may have started out with near-maximum circulation, not leaving much room for the nuts to work any magic.

    Doctor’s Note

    Sorry for that crazy tangent! I just wanted to give people a taste of what it can be like when you dive deep into the medical literature.

    The 2013 video I mentioned is Pistachio Nuts for Erectile Dysfunction.

    What about walnuts for arterial blood flow? See Walnuts and Artery Function.

    More on fertility and sexual function in the related posts below.

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  • Which Foods Help a Leaky Gut?

    Which Foods Help a Leaky Gut?

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

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

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

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

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

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

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

    So, fiber does indeed appear to improve gut leakiness.

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

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

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

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

    Doctor’s Note

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



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  • Could Your Pills and Food Be Causing a Leaky Gut?

    Could Your Pills and Food Be Causing a Leaky Gut?

    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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  • Keeping Better Score of Your Diet

    Keeping Better Score of Your Diet

    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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  • How Low Can LDL Cholesterol Go on PCSK9 Inhibitors?

    How Low Can LDL Cholesterol Go on PCSK9 Inhibitors?

    People with genetic mutations that leave them with an LDL cholesterol of 30 mg/dL live exceptionally long lives. Can we duplicate that effect with drugs?

    Data extrapolated from large cholesterol-lowering trials using statin drugs suggest that the incidence of cardiovascular events like heart attacks would approach zero if LDL cholesterol could be forced down below 60 mg/dL for first-time prevention and around 30 mg/dL for those trying to prevent another one. But is lower actually better? And is it even safe to have LDL cholesterol levels that low?

    We didn’t know until PCSK9 inhibitors were invented. Are PCSK9 Inhibitors for LDL Cholesterol Safe and Effective? I explore that issue in my video of the same name. PCSK9 is a gene that mutated to give people such low LDL cholesterol, and that’s how Big Pharma thought of trying to cripple PCSK9 with drugs. After a heart attack, intensive lowering of an individual’s LDL cholesterol beyond a target of 70 mg/dL does seem to work better than more moderate lowering. There were fewer cardiovascular deaths, heart attacks, or strokes at an LDL less than 30 mg/dL compared with 70 mg/dL or higher, and even compared to less than 70 mg/dL. There is a consistent risk reduction even when starting as low as an average of 63 mg/dL, and pushing LDL down to 21 mg/dL, remarkably, showed “no observed offsetting” of adverse side effects.

    Maybe that shouldn’t be so surprising, since that’s about the level at which we start life. And there’s another type of genetic mutation that leaves people with LDL levels of about 30 mg/dL their whole lives, and they are known to have an exceptionally long life expectancy. So, where did we get this idea that cholesterol could fall too low?

    The common claim that lowering cholesterol can be dangerous due to depletion of cell cholesterol is unsupported by evidence and does not consider the exquisite balancing mechanisms our body uses. After all, that’s how we evolved. Until recently, most of us used to have LDL levels around 50 mg/dL, so that’s pretty normal for the human species. The absence of evidence that low or lowered cholesterol levels are somehow bad for us contrasts with the overwhelming evidence that cholesterol reduction decreases risk for coronary artery disease, our number one killer.

    What about hormone production, though? Since the body needs cholesterol for the synthesis of steroid hormones—like adrenal hormones and sex hormones—there’s a concern that there wouldn’t be enough. You don’t know, though, until you put it to the test. For decades, we’ve known that women on cholesterol-lowering drugs don’t have a problem with estrogen production and that lowering cholesterol doesn’t affect adrenal gland function. As well, it doesn’t impair testicular function in terms of causing testosterone levels to fall below normal. If anything, statin drugs can improve erectile function in men, which is what you’d expect from lowering cholesterol. But you’ll notice these studies only looked at lowering LDL to 70 mg/dL or below. What about really low LDL?

    On PCSK9 inhibitors, you can get most people under an LDL of 40 mg/dL and some under 15 mg/dL! And there is no evidence that adrenal, ovarian, or testicular hormone production is impaired, even in patients with LDL levels below 15 mg/dL. The risk of heart attacks falls in a straight line as LDL gets lower and lower, even below 10 mg/dL, for example, without apparent safety concerns, but that’s over the duration of exposure to these drugs. The longest follow-up to date of those whose LDL, by way of using multiple medications, was kept less than 30 mg/dL is six years.

    Now, we can take comfort in the fact that those with extreme PCSK9 mutations, leading to a lifelong reduction in levels of LDL to under 20 mg/dL their whole lives, remain healthy and have healthy kids. Cholesterol-affecting mutations are what cause the so-called “longevity syndromes,” but that doesn’t necessarily mean the drugs are safe. The bottom line is we should try to get our LDL cholesterol down as low as we can, but much longer follow-up data are necessary anytime a new class of drugs is introduced. So far, so good, but we’ve only been following the data for about 10 years. For example, we didn’t know statins increased diabetes risk until decades after they were approved and millions had been exposed. Also worth noting: PCSK9 inhibitors cost about $14,000 a year.

    Doctor’s Note

    How can we decrease cholesterol with diet? See Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

    For more on statin drugs, see the related posts below. 



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