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  • From Gastric Balloons to Fake Knee Surgeries: When the Fix Is an Illusion | NutritionFacts.org

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    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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    Michael Greger M.D. FACLM

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  • Wegovy injections vs. pills: Doctors explain the differences

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    Wegovy injections vs. pills: Doctors explain the differences

    When it comes to GLP-1 pills vs. injections, doctors share which form may be best for you.

    Updated: 3:01 PM PST Jan 15, 2026

    Editorial Standards ⓘ

    GLP-1 (glucagon-like peptide-1 receptor agonists) like Ozempic and Wegovy continue to make headlines as more research points to the benefits of taking these medications. Traditionally, patients administer these via injection, but now, one medication in particular is available to take in pill form. So, which works best: Wegovy injection vs. pill? And is the answer the same for all GLP-1s?First, GLP-1s are a class of drugs that mimic the GLP-1 hormone that’s naturally released in your GI tract when you eat, explains Mir Ali, M.D., medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA. These medications help to moderate blood sugar levels, reduce feelings of hunger in the brain, and delay emptying in the stomach, making you feel fuller, longer. As a result, a side effect is weight loss. There are some buzzy GLP-1 medications that have become household names, like Wegovy and Ozempic, but there are also other options you may not have heard about.Ultimately, the best GLP-1 medication is one that you and your healthcare provider agree will best serve your needs. But learning more about the medication you intend to use can’t hurt. Here, find the major differences between GLP-1 injections and pills.There are a lot of medications that fall into the GLP-1 class, including injectable drugs and pills. Some popular ones include Ozempic, Rybelsus, and Wegovy.It’s worth noting that Wegovy (the main active ingredient of which is semaglutide) is the only GLP-1 pill that’s approved for weight loss by the U.S. Food and Drug Administration (FDA). While Rybelsus is sometimes used off-label for weight loss, it’s technically FDA-approved for blood sugar management in people with type 2 diabetes (the same goes for Ozempic). So, keep in mind that the information ahead speaks primarily to Wegovy.Wegovy injection vs. pill: How does each work? GLP-1 injectable medications are usually injected into the belly. “GLP-1 injections deliver the medication into the subcutaneous fat, where it is slowly absorbed,” explains Christoph Buettner, M.D., Ph.D., chief of the division of endocrinology at Rutgers Robert Wood Johnson Medical School. “These drugs have a long half-life, about five to seven days, which is why they only need to be taken once a week.”After they’re injected, the medication steadily enters the bloodstream and activates the GLP-1 receptor, Dr. Buettner explains. Once it’s in your body, the medication signals to your brain to take in less food, says Martin Binks, Ph.D., professor and chair of the Department of Nutrition and Food Studies at George Mason University College of Public Health. “They also help delay stomach emptying, which ultimately improves satiety and reduces hunger,” he says. “The combined influences of these medicines regulate metabolism and appetite.”The GLP-1 pills work similarly, but these contain a higher dose of medication to compensate for absorption into the digestive tract, Dr. Binks says. (The injectable medications have lower doses of medication because they’re slowly released into the bloodstream and bypass the gastrointestinal tract, Dr. Ali explains.)These medications are taken by mouth once a day. They usually need to be taken on an empty stomach, and you can’t eat or take most other medications for up to an hour afterward, Dr. Buettner points out. “These requirements can be inconvenient for many patients,” he says.Which is most effective for weight loss?It depends. There have been a few clinical trials on the impact of GLP-1 injectable medications on weight loss with different results. However, People usually lose about 15% of their body weight while using semaglutide medications like Wegovy.Meanwhile, during clinical trials for the Wegovy oral route, people who took the pill lost about 16.6% of their body weight. (That’s compared to 3% weight loss achieved by people who used a placebo.)While Rybelsus isn’t FDA-approved for weight loss, people typically lose around eight pounds while taking this medication.Which works best?There are a few things to consider. “Both injectables and pill forms can be helpful,” says Dina Hagigeorges, PA.-C., a physician assistant who specializes in weight and wellness at Tufts Medicine Weight + Wellness – Stoneham. “Unfortunately, cost and insurance coverage are a huge deciding factor, as not all insurance plans cover these medications for people.” When paid for out of pocket, injectable GLP-1 medications are usually much more expensive than their oral counterparts.There’s a larger body of research to support injectable medications for weight loss, although the Wegovy pill shows promise, Dr. Ali says. “If someone can tolerate injections, it’s usually the better way to go—they’re taken less frequently,” he says. But these medications aren’t a good fit for people who are scared of needles, and they have to be refrigerated, Dr. Ali points out.“The pills are a good option for people who don’t like injections, and you can easily take them with you when you travel,” Dr. Ali says. “But they have to be taken daily, which is not for everyone.”Side effectsThe side effects are similar for both medications, Dr. Buettner says.These side effects may include:NauseaVomitingDiarrheaConstipationUpset Stomach “The most important thing is choosing a medication that you can use consistently and that aligns with your personal priorities—whether that’s maximum weight loss, convenience, avoiding injections, or simplifying your routine,” he says. “Many patients try one form first and later switch based on their experience.”So, talk to your healthcare provider and keep the line of conversation open. You may find one form of GLP-1 feels like a more natural fit over another.

    GLP-1 (glucagon-like peptide-1 receptor agonists) like Ozempic and Wegovy continue to make headlines as more research points to the benefits of taking these medications. Traditionally, patients administer these via injection, but now, one medication in particular is available to take in pill form. So, which works best: Wegovy injection vs. pill? And is the answer the same for all GLP-1s?

    First, GLP-1s are a class of drugs that mimic the GLP-1 hormone that’s naturally released in your GI tract when you eat, explains Mir Ali, M.D., medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA. These medications help to moderate blood sugar levels, reduce feelings of hunger in the brain, and delay emptying in the stomach, making you feel fuller, longer. As a result, a side effect is weight loss.

    There are some buzzy GLP-1 medications that have become household names, like Wegovy and Ozempic, but there are also other options you may not have heard about.

    Ultimately, the best GLP-1 medication is one that you and your healthcare provider agree will best serve your needs. But learning more about the medication you intend to use can’t hurt. Here, find the major differences between GLP-1 injections and pills.

    There are a lot of medications that fall into the GLP-1 class, including injectable drugs and pills. Some popular ones include Ozempic, Rybelsus, and Wegovy.

    It’s worth noting that Wegovy (the main active ingredient of which is semaglutide) is the only GLP-1 pill that’s approved for weight loss by the U.S. Food and Drug Administration (FDA). While Rybelsus is sometimes used off-label for weight loss, it’s technically FDA-approved for blood sugar management in people with type 2 diabetes (the same goes for Ozempic). So, keep in mind that the information ahead speaks primarily to Wegovy.

    Wegovy injection vs. pill: How does each work?

    GLP-1 injectable medications are usually injected into the belly. “GLP-1 injections deliver the medication into the subcutaneous fat, where it is slowly absorbed,” explains Christoph Buettner, M.D., Ph.D., chief of the division of endocrinology at Rutgers Robert Wood Johnson Medical School. “These drugs have a long half-life, about five to seven days, which is why they only need to be taken once a week.”

    After they’re injected, the medication steadily enters the bloodstream and activates the GLP-1 receptor, Dr. Buettner explains. Once it’s in your body, the medication signals to your brain to take in less food, says Martin Binks, Ph.D., professor and chair of the Department of Nutrition and Food Studies at George Mason University College of Public Health. “They also help delay stomach emptying, which ultimately improves satiety and reduces hunger,” he says. “The combined influences of these medicines regulate metabolism and appetite.”

    The GLP-1 pills work similarly, but these contain a higher dose of medication to compensate for absorption into the digestive tract, Dr. Binks says. (The injectable medications have lower doses of medication because they’re slowly released into the bloodstream and bypass the gastrointestinal tract, Dr. Ali explains.)

    These medications are taken by mouth once a day. They usually need to be taken on an empty stomach, and you can’t eat or take most other medications for up to an hour afterward, Dr. Buettner points out. “These requirements can be inconvenient for many patients,” he says.

    Which is most effective for weight loss?

    It depends. There have been a few clinical trials on the impact of GLP-1 injectable medications on weight loss with different results. However, People usually lose about 15% of their body weight while using semaglutide medications like Wegovy.

    Meanwhile, during clinical trials for the Wegovy oral route, people who took the pill lost about 16.6% of their body weight. (That’s compared to 3% weight loss achieved by people who used a placebo.)

    While Rybelsus isn’t FDA-approved for weight loss, people typically lose around eight pounds while taking this medication.

    Which works best?

    There are a few things to consider. “Both injectables and pill forms can be helpful,” says Dina Hagigeorges, PA.-C., a physician assistant who specializes in weight and wellness at Tufts Medicine Weight + Wellness – Stoneham. “Unfortunately, cost and insurance coverage are a huge deciding factor, as not all insurance plans cover these medications for people.” When paid for out of pocket, injectable GLP-1 medications are usually much more expensive than their oral counterparts.

    There’s a larger body of research to support injectable medications for weight loss, although the Wegovy pill shows promise, Dr. Ali says. “If someone can tolerate injections, it’s usually the better way to go—they’re taken less frequently,” he says. But these medications aren’t a good fit for people who are scared of needles, and they have to be refrigerated, Dr. Ali points out.

    “The pills are a good option for people who don’t like injections, and you can easily take them with you when you travel,” Dr. Ali says. “But they have to be taken daily, which is not for everyone.”

    Side effects

    The side effects are similar for both medications, Dr. Buettner says.

    These side effects may include:

    • Nausea
    • Vomiting
    • Diarrhea
    • Constipation
    • Upset Stomach

    “The most important thing is choosing a medication that you can use consistently and that aligns with your personal priorities—whether that’s maximum weight loss, convenience, avoiding injections, or simplifying your routine,” he says. “Many patients try one form first and later switch based on their experience.”

    So, talk to your healthcare provider and keep the line of conversation open. You may find one form of GLP-1 feels like a more natural fit over another.

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  • Bariatric Surgery: Risks in the OR and Beyond | NutritionFacts.org

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    The extent of risk from bariatric weight-loss surgery may depend on the skill of the surgeon.

    After sleeve gastrectomy and Roux-en-Y gastric bypass, the third most common bariatric procedure is a revision to fix a previous bariatric procedure, as you can see below and at 0:16 in my video The Complications of Bariatric Weight-Loss Surgery.

    Up to 25% of bariatric patients have to go back into the operating room for problems caused by their first bariatric surgery. Reoperations are even riskier, with up to 10 times the mortality rate, and there is “no guarantee of success.” Complications include leaks, fistulas, ulcers, strictures, erosions, obstructions, and severe acid reflux.

    The extent of risk may depend on the skill of the surgeon. In a study published in The New England Journal of Medicine, bariatric surgeons voluntarily submitted videos of themselves performing surgery to a panel of their peers for evaluation. Technical proficiency varied widely and was related to the rates of complications, hospital readmissions, reoperations, and death. Patients operated on by less competent surgeons suffered nearly three times the complications and five times the rate of death.

    “As with musicians or athletes, some surgeons may simply be more talented than others”—but practice may help make them perfect. Gastric bypass is such a complicated procedure that the learning curve may require 500 cases for a surgeon to master the procedure. Risk for complications appears to plateau after about 500 cases, with the lowest risk found among surgeons who had performed more than 600 bypasses. The odds of not making it out alive may be double under the knife of those who had performed less than 75 compared to more than 450, as seen below and at 1:47 in my video.

    So, if you do choose to undergo the operation, I’d recommend asking your surgeon how many procedures they’ve done, as well as choosing an accredited bariatric “Center of Excellence,” where surgical mortality appears to be two to three times lower than non-accredited institutions.

    It’s not always the surgeon’s fault, though. In a report entitled “The Dangers of Broccoli,” a surgeon described a case in which a woman went to an all-you-can-eat buffet three months after a gastric bypass operation. She chose really healthy foods—good for her!—but evidently forgot to chew. Her staples ruptured, and she ended up in the emergency room, then the operating room. They opened her up and found “full chunks of broccoli, whole lima beans, and other green leafy vegetables” inside her abdominal cavity. A cautionary tale to be sure, but perhaps one that’s less about chewing food better after surgery than about chewing better foods before surgery—to keep all your internal organs intact in the first place.

    Even if the surgical procedure goes perfectly, lifelong nutritional replacement and monitoring are required to avoid vitamin and mineral deficits. We’re talking about more than anemia, osteoporosis, or hair loss. Such deficits can cause full-blown cases of life-threatening deficiencies, such as beriberi, pellagra, kwashiorkor, and nerve damage that can manifest as vision loss years or even decades after surgery in the case of copper deficiency. Tragically, in reported cases of severe deficiency of a B vitamin called thiamine, nearly one in three patients progressed to permanent brain damage before the condition was caught.

    The malabsorption of nutrients is intentional for procedures like gastric bypass. By cutting out segments of the intestines, you can successfully impair the absorption of calories—at the expense of impairing the absorption of necessary nutrition. Even people who just undergo restrictive procedures like stomach stapling can be at risk for life-threatening nutrient deficiencies because of persistent vomiting. Vomiting is reported by up to 60% of patients after bariatric surgery due to “inappropriate eating behaviors.” (In other words, trying to eat normally.) The vomiting helps with weight loss, similar to the way a drug for alcoholics called Antabuse can be used to make them so violently ill after a drink that they eventually learn their lesson.

    “Dumping syndrome” can work the same way. A large percentage of gastric bypass patients can suffer from abdominal pain, diarrhea, nausea, bloating, fatigue, or palpitations after eating calorie-rich foods, as they bypass your stomach and dump straight into your intestines. As surgeons describe it, this is a feature, not a bug: “Dumping syndrome is an expected and desired part of the behavior modification caused by gastric bypass surgery; it can deter patients from consuming energy-dense food.

    Doctor’s Note

    This is the second in a four-part series on bariatric surgery. If you missed the first one, see The Mortality Rate of Bariatric Weight-Loss Surgery.

    Up next: Bariatric Surgery vs. Diet to Reverse Diabetes and How Sustainable Is the Weight Loss After Bariatric Surgery?.

    My book How Not to Diet is focused exclusively on sustainable weight loss. Check it out from your local library, or pick it up from wherever you get your books. (All proceeds from my books are donated to charity.)

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    Michael Greger M.D. FACLM

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  • A Longer Life on Statins?  | NutritionFacts.org

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    What are the pros and cons of relative risk, absolute risk, number needed to treat, and average postponement of death when taking cholesterol-lowering statin drugs?

    In response to the charge that describing the benefits of statin drugs only in terms of relative risk reduction is a “statistical deception” created to give the appearance that statins are more effective than they really are, it was pointed out that describing things in terms of absolute risk reduction or number needed to treat can depend on the duration of the study.

    For example, let’s say a disease has a 2% chance of killing you every year, but some drug cuts that risk by 50%. That sounds amazing, until you realize that, at the end of a year, your risk will only have fallen from 2% to 1%, so the absolute reduction of risk is only 1%. If a hundred people were treated with the drug, instead of two people dying, one person would die, so a hundred people would have to be treated to save one life, as shown below and at 1:01 in my video How Much Longer Do You Live on Statins?.

    But there’s about a 99% chance that taking the drug all year would have no effect either way. So, to say the drug cuts the risk of dying by 50% seems like an overstatement. But think about it: Benefits accrue over time. If there’s a 2% chance of dying every year, year after year, after a few decades, the majority of those who refused the drug would be dead, whereas the majority who took the drug would be alive. So, yes, perhaps during the first year on the drug, there was only about a 1% chance it would be life-saving, but, eventually, you could end up with a decent chance the drug would save your life after all.

    “This is actually the very reason why the usage of relative risk makes sense…” Absolute risk changes depending on the time frame being discussed, but with relative risk, you know that whatever risk you have, you can cut it in half by taking the drug. On average, statins only cut the risk of a cardiovascular “event” by 25%, but since cardiovascular disease is the number one killer of men and women, if you’re unwilling to change your diet, that’s a powerful argument in favor of taking these kinds of drugs. You can see the same kind of dependency on trial duration, looking at the “postponement of death” by taking a statin. How much longer might you live if you take statins?

    The average postponement of death has some advantages over other statistics because it may offer “a better intuitive understanding among lay persons,” whereas a stat like a number needed to treat has more of a win-or-lose “lottery-like” quality. So, when a statin drug prevents, say, one heart attack out of a hundred people treated over five years, it’s not as though the other 99 completely lost out. Their cholesterol also dropped, and their heart disease progression presumably slowed down, too, just not enough to catch a heart attack within that narrow time frame.

    So, what’s the effect of statins on average survival? According to an early estimate, if you put all the randomized trials together, the average postponement of death was calculated at maybe three or four days. Three or four days? Who would take a drug every day for years just to live a few more days? Well, let’s try to put that into context. Three or four days is comparable to the gains in life expectancy from other medical interventions. For example, it’s nearly identical to what you’d get from “highly effective childhood vaccines.” Because vaccines have been so effective in wiping out infectious diseases, these days, they only add an average of three extra days to a child’s life. But, of course, “those whose deaths are averted gain virtually their whole lifetimes.” That’s why we vaccinate. It just seems like such a small average benefit because it gets distributed over the many millions of kids who get the vaccine. Is that the same with statins?

    An updated estimate was published in 2019, which explained that the prior estimate of three or four days was plagued by “important weaknesses,” and the actual average postponement of death was actually ten days. Headline writers went giddy from these data, but what they didn’t understand was that this was only for the duration of the trial. So, if your life expectancy is only five years, then, yes, statins may increase your lifespan by only ten days, but statins are meant to be taken a lot longer than five years. What you want to know is how much longer you might get to live if you stick with the drugs your whole life.

    In that case, it isn’t an extra ten days, but living up to ten extra years. Taking statins can enable you to live years longer. That’s because, for every millimole per liter you lower your bad LDL cholesterol, you may live three years longer and maybe even six more years, depending on which study you’re reading. A millimole in U.S. units is 39 points. Drop your LDL cholesterol by about 39 points, and you could live years longer. Exercise your whole life, and you may only increase your lifespan by six months, and stopping smoking may net you nine months. But if you drop your LDL cholesterol by about 39 points, you could live years longer. You can accomplish that by taking drugs, or you can achieve that within just two weeks of eating a diet packed with fruits, vegetables, and nuts, as seen here and at 5:30 in my video. 

    Want to know what’s better than drugs? “Something important and fundamental has been lost in the controversy around this broad expansion of statin therapy.…It is imperative that physicians (and drug labels) inform patients that not only their lipid [cholesterol] levels but also their cardiovascular risk can be reduced substantially by adoption of a plant-based dietary pattern, and without drugs. Dietary modifications for cardiovascular risk reduction, including plant-based diets, have been shown to improve not only lipid status, but also obesity, hypertension, systemic inflammation, insulin sensitivity, oxidative stress, endothelial function, thrombosis, and cardiovascular event risk…The importance of this [plant-based] approach is magnified when one considers that, in contrast to statins, the ‘side effects’ of plant-based diets—weight loss, more energy, and improved quality of life—are beneficial.” 

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    Michael Greger M.D. FACLM

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  • The Real Benefits of Statins and Their Side Effects  | NutritionFacts.org

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    A Mayo Clinic visualization tool can help you decide if cholesterol-lowering statin drugs are right for you.

    “Physicians have a duty to inform their patients about the risks and benefits of the interventions available to them. However, physicians rarely communicate with methods that convey absolute information, such as numbers needed to treat, numbers needed to harm, or prolongation of life, despite patients wanting this information.” That is, for example, how many people are actually helped by a particular drug, how many are actually hurt by it, or how much longer the drug will enable you to live, respectively.

    If doctors inform patients only about the relative risk reduction—for example, telling them a pill will cut their risk of heart attacks by 34 percent—nine out of ten agree to take it. However, give them the same information framed as absolute risk reduction—“1.4% fewer patients had heart attacks”—then those agreeing to take the drug drops to only four out of ten. And, if they use the number needed to treat, only three in ten patients would agree to take the pill. So, if you’re a doctor and you really want your patient to take the drug, which statistic are you going to use?

    The use of relative risk stats to inflate the benefits and absolute risk stats to downplay any side effects has been referred to as “statistical deception.” To see how one might spin a study to accomplish this, let’s look at an example. As you can see below and at 1:49 in my video, The True Benefits vs. Side Effects of Statins, there is a significantly lower risk of the incidence of heart attack over five years in study participants randomized to a placebo compared to those getting the drug. If you wanted statins to sound good, you’d use the relative risk reduction (24 percent lower risk). If you wanted statins to sound bad, you’d use the absolute risk reduction (3 percent fewer heart attacks).

    Then you could flip it for side effects. For example, the researchers found that 0.3 percent (1 out of 290 women in the placebo group) got breast cancer over five years, compared to 4.1 percent (12 out of 286) in the statin group. So, a pro-statin spin might be a 24 percent drop in heart attack risk and only 3.8 percent more breast cancers, whereas an anti-statin spin might be only 3 percent fewer heart attacks compared to a 1,267 percent higher risk of breast cancer. Both portrayals are technically true, but you can see how easily you could manipulate people if you picked and chose how you were presenting the risks and benefits. So, ideally, you’d use both the relative risk reduction stat and the absolute risk reduction stat.

    In terms of benefits, when you compile many statin trials, it looks like the relative risk reduction is 25 percent. So, if your ten-year risk of a heart attack or stroke is 5 percent, then taking a statin could lower that from 5 percent to 3.75 percent, for an absolute risk reduction of 1.25 percent, or a number needed to treat of 80, meaning there’s about a 1 in 80 chance that you’d avoid a heart attack or stroke by taking the drug for the next ten years. As you can see, as your baseline risk gets higher and higher, even though you have that same 25 percent risk reduction, your absolute risk reduction gets bigger and bigger. And, with a 20 percent baseline risk, that means you have a 1 in 20 chance of avoiding a heart attack or stroke over the subsequent decade if you take the drug, as seen below and at 3:31 in my video.

    So, those are the benefits. In terms of risk, that breast cancer finding appears to be a fluke. Put together all the studies, and “there was no association between use of statins and the risk of cancer.” In terms of muscle problems, estimates of risk range from approximately 1 in 1,000 to closer to 1 in 50.

    If all those numbers just blur together, the Mayo Clinic developed a great visualization tool, seen below and at 4:39 in my video.

    For those at average risk, 10 people out of 100 who do not take a statin may have a heart attack over the next ten years. If, however, all 100 people took a statin every day for those ten years, 8 would still have a heart attack, but 2 would be spared, so there’s about a 1 in 50 chance that taking the drug would help avert a heart attack over the next decade. What are the downsides? The cost and inconvenience of taking a pill every day, which can cause some gastrointestinal side effects, muscle aching, and stiffness in about 5 percent, reversible liver inflammation in 2 percent, and more serious damage in perhaps 1 in 20,000 patients.

    Note that the two happy faces in the bottom left row of the YES STATIN chart represent heart attacks averted, not lives saved. The chance that a few years of statins will actually save your life if you have no known heart disease is about 1 in 250.

    If you want a more personalized approach, the Mayo Clinic has an interactive tool that lets you calculate your ten-year risk. You can get there directly by going to bit.ly/statindecision.

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    Michael Greger M.D. FACLM

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  • Are We Being Misled About the Benefits and Risks of Statins?  | NutritionFacts.org

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    What is the dirty little secret of drugs for lifestyle diseases?

    Drug companies go out of their way—in direct-to-consumer ads, for example—to “present pharmaceutical drugs as a preferred solution to cholesterol management while downplaying lifestyle change.” You see this echoed in the medical literature, as in this editorial in the Journal of the American Medical Association: “Despite decades of exhortation for improvement, the high prevalence of poor lifestyle behaviors leading to elevated cardiovascular disease risk factors persists, with myocardial infarction [heart attack] and stroke remaining the leading causes of death in the United States. Clearly, many more adults could benefit from…statins for primary prevention.” Do we really need to put more people on drugs? A reply was published in the British Medical Journal: “Once again, doctors are implored to ‘get real’—stop hoping that efforts to help their patients and communities adopt healthy lifestyle habits will succeed, and start prescribing more statins. This is a self-fulfilling prophecy. Note that the author of these comments [the pro-statin editorial] disclosed receipt of funding from 11 drug companies, at least four of which produce or are developing new classes of cholesterol-lowering agents,” which make billions of dollars a year in annual sales.

    Every time the cholesterol guidelines expand the number of people eligible for statins, they’re decried as a “big kiss to big pharma.” This is understandable, since the majority of guideline panel members “had industry ties,” financial conflicts of interest. But these days, all the major statins are off-patent, so there are inexpensive generic versions. For example, the safest, most effective statin is generic Lipitor, sold as atorvastatin for as little as a few dollars a month. So, nowadays, the cholesterol guidelines are not necessarily “part of an industry plot.”

    “The US way of life is the problem, not the guidelines…” The reason so many people are candidates for cholesterol- and blood-pressure-lowering medications is that so many people are taking such terrible care of themselves. The bottom line is that “individuals must take more responsibility for their own health behaviors.” What if you are unwilling or unable to improve your diet and make lifestyle changes to bring down that risk? If your ten-year risk of having a heart attack is 7.5 percent or more and going to stay that way, then the benefits of taking a statin drug likely outweigh the risk. That’s really for you to decide, though. It’s your body, your choice.

    “Whether or not the overall benefit-harm balance justifies the use of a medication for an individual patient cannot be determined by a guidelines committee, a health care system, or even the attending physician. Instead, it is the individual patient who has a fundamental right to decide whether or not taking a drug is worthwhile.” This was recognized by some of medicine’s “historical luminaries such as Hippocrates,” but “only in recent decades has the medical profession begun to shift from a paternalistic ‘doctor knows best’ stance towards one explicitly endorsing patient-centered, evidence-based, shared decision-making.” One of the problems with communicating statin evidence to support this shared decision-making is that most doctors “have a poor understanding of concepts of risk and probability and…increasing exposure to statistics in undergraduate and postgraduate education hasn’t made much difference.” But that understanding is critical for preventive medicine. When doctors offer a cholesterol-lowering drug, “they’re doing something quite different from treating a patient who has sought help because she is sick. They’re not so much doctors as life insurance salespeople, peddling deferred benefits in exchange for a small (but certainly not negligible) ongoing inconvenience and cost. In this new kind of medicine, not understanding risk is the equivalent of not knowing about the circulation of the blood or basic anatomy. So, let’s dive in and see exactly what’s at stake.

    Below and at 3:55 in my video Are Doctors Misleading Patients About Statin Risks and Benefits? is an ad for Lipitor. When drug companies say a statin reduces the risk of a heart attack by 36 percent, that’s the relative risk.

    If you follow the asterisk I’ve circled after the “36%” in the ad, you can see how they came up with that. I’ve included it here and at 3:56 in my video. In a large clinical study, 3 percent of patients not taking the statin had a heart attack within a certain amount of time, compared to 2 percent of patients who did take the drug. So, the drug dropped heart attack risk from 3 percent to 2 percent; that’s about a one-third drop, hence the 36 percent reduced relative risk statistic. But another way to look at going from 3 percent to 2 percent is that the absolute risk only dropped by 1 percent. So, in effect, “your chance to avoid a nonfatal heart attack during the next 2 years is about 97% without treatment, but you can increase it to about 98% by taking a Crestor [a statin] every day.” Another way to say that is that you’d have to treat 100 people with the drug to prevent a single heart attack. That statistic may shock a lot of people.

    If you ask patients what they’ve been led to believe, they don’t think the chance of avoiding a heart attack within a few years on statins is 1 in 100, but 1 in 2. “On average, it was believed that most patients (53.1%) using statins would avoid a heart attack after statin treatment for 5 years.” Most patients, not just 1 percent of patients. And this “disparity between actual and expected effect could be viewed as a dilemma. On the one hand, it is not ethically acceptable for caregivers to deliberately support and maintain illusive treatment expectations by patients.” We cannot mislead people into thinking a drug works better than it really does, but on the other hand, how else are we going to get people to take their pills?

    When asked, people want an absolute risk reduction of at least about 30 percent to take a cholesterol-lowering drug every day, whereas the actual absolute risk reduction is only about 1 percent. So, the dirty little secret is that, if patients knew the truth about how little these drugs actually worked, almost no one would agree to take them. Doctors are either not educating their patients or actively misinforming them. Given that the majority of patients expect a much larger benefit from statins than they’d get, “there is a tension between the patient’s right to know about benefiting from a preventive drug and the likely reduction in uptake [willingness to take the drugs] if they are so informed,” and learn the truth. This sounds terribly paternalistic, but hundreds of thousands of lives may be at stake.

    If patients were fully informed, people would die. About 20 million Americans are on statins. Even if the drugs saved 1 in 100, that could mean hundreds of thousands of lives lost if everyone stopped taking their statins. “It is ironic that informing patients about statins would increase the very outcomes they were designed to prevent.”

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    Michael Greger M.D. FACLM

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  • Should You Take Statins?  | NutritionFacts.org

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    How can you calculate your own personal heart disease risk to help you determine if you should start on a cholesterol-lowering statin drug?

    The muscle-related side effects from cholesterol-lowering statins “are often severe enough for patients to stop taking the drug. Of course, these side effects could be coincidental or psychosomatic and have nothing to do with the drug,” given that many clinical trials show such side effects are rare. “It is also possible that previous clinical trials”—funded by the drug companies themselves—“under-recorded the side effects of statins.” The bottom line is that there’s an urgent need to establish the true incidence of statin side effects.

    “What proportion of symptomatic side effects in patients taking statins are genuinely caused by the drug?” That’s the title of a journal article that reports that, even in trials funded by Big Pharma, “only a small minority of symptoms reported on statins are genuinely due to the statins,” and those taking statins are significantly more likely to develop type 2 diabetes than those randomized to placebo sugar pills. Why? We’re still not exactly sure, but statins may have the double-whammy effect of impairing insulin secretion from the pancreas while also diminishing insulin’s effectiveness by increasing insulin resistance.

    Even short-term use of statins may “approximately double the odds of developing diabetes and diabetic complications.” As shown below and at 1:49 in my video Who Should Take Statins?, fewer people develop diabetes and diabetic complications off statins over a period of about five years than those who do develop diabetes while on statins. “Of more concern, this increased risk persisted for at least 5 years after statin use stopped.”

    “In view of the overwhelming benefit of statins in the reduction of cardiovascular events,” the number one killer of men and women, any increase in risk of diabetes, our seventh leading cause of death, would be outweighed by any cardiovascular benefits, right? That’s a false dichotomy. We don’t have to choose between heart disease and diabetes. We can treat the cause of both with the same diet and lifestyle changes. The diet that can not only stop heart disease, but also reverse it, is the same one that can reverse type 2 diabetes. But what if, for whatever reason, you refuse to change your diet and lifestyle? In that case, what are the risks and benefits of starting statins? Don’t expect to get the full scoop from your doctor, as most seemed clueless about statins’ causal link with diabetes, so only a small fraction even bring it up with their patients.

    “Overall, in patients for whom statin treatment is recommended by current guidelines, the benefits greatly outweigh the risks.” But that’s for you to decide. Before we quantify exactly what the risks and benefits are, what exactly are the recommendations of current guidelines?

    How should you decide if a statin is right for you? “If you have a history of heart disease or stroke, taking a statin medication is recommended, without considering your cholesterol levels.” Period. Full stop. No discussion needed. “If you do not yet have any known cardiovascular disease,” then the decision should be based on calculating your own personal risk. If you know your cholesterol and blood pressure numbers, it’s easy to do that online with the American College of Cardiology risk estimator or the Framingham risk profiler.

    My favorite is the American College of Cardiology’s estimator because it gives you your current ten-year risk and also your lifetime risk. So, for a person with a 5.8 percent risk of having a heart attack or stroke within the next decade, if they don’t clean up their act, that lifetime risk jumps to 46 percent, nearly a flip of the coin. If they improved their cholesterol and blood pressure, though, they could reduce that risk by more than tenfold, down to 3.9 percent, as shown below and at 4:11 in my video.

    Since the statin decision is based on your ten-year risk, what do you do with that number? As you can see here and at 4:48 in my video, under the current guidelines, if your ten-year risk is under 5 percent, then, unless there are extenuating circumstances, you should just stick to diet, exercise, and smoking cessation to bring down your numbers. In contrast, if your ten-year risk hits 20 percent, then the recommendation is to add a statin drug on top of making lifestyle modifications. Unless there are risk-enhancing factors, the tendency is to stick with lifestyle changes if risk is less than 7.5 percent and to move towards adding drugs if above 7.5 percent.

    Risk-enhancing factors that your doctor should take into account when helping you make the decision include a bad family history, really high LDL cholesterol, metabolic syndrome, chronic kidney or inflammatory conditions, or persistently high triglycerides, C-reactive protein, or LP(a). You can see the whole list here and at 4:54 in my video.

    If you’re still uncertain, guidelines suggest you consider getting a coronary artery calcium (CAC) score, but even though the radiation exposure from that test is relatively low these days, the U.S. Preventive Services Task Force has explicitly concluded that the current evidence is insufficient to conclude that the benefits outweigh the harms.

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    Michael Greger M.D. FACLM

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  • Hepatitis B vaccine Q&A: Why do babies need the shot?

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    The people at highest risk for contracting hepatitis B include health care workers, IV drug users and people having sex.

    So why do babies get vaccinated for hepatitis B as soon as they are born? It’s a fair question, and health care providers have compelling answers. 

    Hepatitis B is a virus that can do serious, sometimes fatal, liver damage. Although groups that are more exposed to swapping bodily fluids are at greater risk, anyone can get infected.

    Getting infected with hepatitis B as a baby is extra dangerous. Infected infants have a 90% chance of developing the disease’s more dangerous chronic form. And a quarter of those babies will go on to die prematurely from the disease when they become adults, according to the American Academy of Pediatrics. 

    When the vaccine was invented in the 1980s, doctors initially vaccinated only the highest risk individuals. Cases didn’t meaningfully decline. 

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    In 1991, the Centers for Disease Control and Prevention began recommending vaccinations for everyone at birth. 

    The protocol produced results: New infections dropped significantly, especially among children and adolescents.

    “Now it’s a very uncommon disease in young children because of that vaccine,” Dr. Paul Offit, Children’s Hospital of Philadelphia pediatrician and infectious disease expert, said. “It was a remarkable, remarkable achievement.”

    Today, infants get their first dose within 24 hours of birth and receive two to three more doses by the time they are 6 months old. 

    But the CDC’s independent vaccine panel is scheduled to reevaluate the vaccine schedule at its Sept. 18 meeting. KFF Health News reported that the panel is expected to vote on whether to delay the vaccine until children are 4. 

    Here’s what you should know about hepatitis B and what is behind the CDC’s longstanding “at birth” hepatitis B vaccine recommendation.

    What is hepatitis B? 

    The hepatitis B virus attacks the liver. Some people become very sick upon initial infection. Others have only mild symptoms or none at all. Acute cases can resolve on their own, but sometimes they develop into chronic infections. 

    Long-lasting infections can be asymptomatic, and dangerous. They develop more slowly and symptoms may not show up until much later in life, sometimes decades after the first exposure. 

    “It’s a stealth infection,” said Dr. William Schaffner, Vanderbilt University School of Medicine professor and infectious disease expert. “After you get over the acute infection, you can have this smoldering infection and be contagious to others and feel perfectly normal.”

    Untreated, chronic hepatitis B infections can cause cirrhosis and death. It is also one of the leading causes of liver cancer. Patients can seek treatments to reduce the virus’ worst effects. But there is no cure. 

    The CDC estimates about 640,000 adults have chronic hepatitis B, but because of its asymptomatic nature, about half of people with the virus do not know they are infected and contagious.

    Who gets hepatitis B and how? 

    Anyone can get it. 

    Hepatitis B is transmitted through bodily fluids like blood, semen and vaginal fluids. It is usually transmitted through sexual activity, direct contact with blood, or from mother to child during delivery due to contact with bodily fluids.

    Because hepatitis B is an especially tough virus, it can live outside the body on surfaces for up to seven days. Even a small amount can be infectious.

    That means that although you can get it through sexual contact or health care work, mundane contact can also result in transmission. Small amounts of dried blood on innocuous household items like nail clippers, razors or toothbrushes could be enough.

    Many hepatitis B patients are never sure how they contracted it.

    “Those environmental routes of transmission of hepatitis B undoubtedly play a small but notable role,” Schaffner said. 

    Because so many people are unaware they are infected, preventing transmission was much more difficult — until the vaccine. 

    How do babies get hepatitis B?

    The fact that so many infected people have no idea they have it makes it nearly impossible to guarantee a child will never come into contact with a hepatitis B-positive individual.

    Babies can get infected from their mothers during childbirth. Testing for hepatitis B during pregnancy is recommended, and patients who receive regular prenatal care are highly likely to be tested at some point. But not all expecting mothers receive regular medical care. In some cases, those at highest risk for contracting hepatitis B are also less likely to access prenatal care, Schaffner said.

    The vaccine works well to prevent infection in babies born to mothers with hepatitis B. 

    But even if a mom tests negative, the child’s risk of contracting hepatitis is not zero. The reasons are varied: The test produces some false negatives. Pregnant patients can contract hepatitis B after being tested. Children may become infected simply by being in contact with the world at large.

    Offit said that prior to the vaccine being recommended for all infants, around half of children under 10 were infected from their mother during birth. The other half contracted it somewhere else. 

    How does the vaccine work and has it been effective at reducing cases? 

    The hepatitis B vaccine was first introduced in 1981; the version in use today was put in place in 1986. 

    It uses proteins from the surface of the hepatitis B virus to provoke an immune response that gives the body a defense against future infection. It is not a live virus, and the vaccine can’t infect someone with hepatitis B. 

    Doctors expect the vaccine may provide lifelong protection, but they are still monitoring results of the 39-year-old vaccine.

    Prior to the vaccine, around 200,000 to 300,000 people were infected with hepatitis B each year, including approximately 20,000 children, older CDC reports show. 

    Since hepatitis B vaccines began being universally administered to babies, overall cases are down to around 14,000 annually. The change is especially dramatic among young people. In 2022, the CDC reported 252 new chronic hepatitis B infections among people up to age 19, or 0.4 out of every 100,000 kids. 

    Dr. James Campbell, a University of Maryland pediatric infectious disease doctor, said the low rate is directly related to the recommended hepatitis B vaccine schedule: “Because we’ve been vaccinating nearly the entire population since 1991 those people are now 30 something years old.” New infections are largely among older Americans. 

    All the doctors we spoke with, the CDC and the American Academy of Pediatrics describe the vaccine as safe and effective. 

    But why not delay the vaccine until a child is a little older?

    When it comes to hepatitis B, that first year of life is critical.

    Whereas the Department of Health and Human Services reports that 90% of infants who become infected go on to develop a chronic hepatitis B infection, that rate is 2% to 6% for adults. And with research showing that 25% of infected infants die prematurely from the disease, public health officials have long held that early delivery is crucial. 

    “Think about it,” Campbell said. “We used to have 18,000 or 20,000 kids a year being born with this, a quarter of them going on to have liver cancer. We now have almost none.”

    Delaying administration by even a few months increases a baby’s risk should they come into contact with the virus, Offit said. And Schaffner said delaying a vaccine can easily lead to never getting it: An unvaccinated child can become an unprotected adolescent or young adult with sexual partners, “and boom, then they get infected,” he said.  

    What are the hepatitis B vaccine’s safety risks?

    The most common side effects are mild and short term including pain or soreness where the shot is given, headache, fatigue or fever, according to the CDC. Very rarely, some people have a severe allergic reaction to the shot called anaphylaxis, which can be treated. 

    The vaccine contains small amounts of aluminium, an additive used to enhance the body’s immune response. Although large amounts of aluminum can be harmful, the vaccine contains less aluminum than infants get from their natural surroundings. 

    According to the Children’s Hospital of Philadelphia, babies get about 4.4mg of aluminum from vaccines in their first six months; they get around 7mg from breastmilk and around 38 mg from formula in the same time. 

    I heard that the risk of a baby dying from hepatitis B is 1 in 7 million. Is that wrong?

    Health and Human Services Secretary Robert F. Kennedy used that statistic during recent Senate testimony. “That means you need to give 7 million hepatitis B vaccines to prevent one death,” he said.

    The vaccine is not administered to prevent babies from dying as babies. It aims to prevent them from developing the more harmful chronic hepatitis B, which can be fatal when they get older. It also prevents severe illness. 

    Kennedy’s statistic for babies who will eventually die from hepatitis B is still missing a lot of context.  

    It’s based on a 2020 research paper that tried to quantify how many people would have died of hepatitis B in 2014 had there never been mass vaccination. 

    The study estimated that 1,740 children ages 10 or younger would have contracted a deadly case of hepatitis B in a single year, 2014. 

    But to make his “1 in 7 million” calculation, Kennedy left out 99% of those deadly cases — any considered to be due to “elevated risk” of exposure, including among children born to infected mothers, children living with infected individuals, or those in communities with large numbers of infected people. 

    Since many people do not know they are infected, it can be hard to know if you are at elevated risk or reside in a community with infected individuals. 

    Vaccines given at birth “protect not only infants and children in their infancy and childhood, but throughout their lives,” Schaffner said. “It’s a larger series of issues that we’re trying to address. We’re trying to protect not only babies, but the transmission of the virus to the next generation.”

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  • The Validity of SIBO Tests  | NutritionFacts.org

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

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

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

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

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

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

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

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

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

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

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

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    Michael Greger M.D. FACLM

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  • Why I Don’t Recommend Moringa Leaf Powder  | NutritionFacts.org

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    “Clearly, in spite of the widely held ‘belief’ in the health benefits of M. oleifera [moringa], the interest of the international biomedical community in the medicinal potential of this plant has been rather tepid.” In fact, it has been “spectacularly hesitant in exploring its nutritional and medicinal potential. This lukewarm attitude is curious, as other ‘superfoods’ such as garlic and green tea have enjoyed better reception,” but those have more scientific support. There are thousands of human studies on garlic and more than ten thousand on green tea, but only a few hundred on moringa.

    The most promising appears to be moringa’s effects on blood sugar control. Below and at 0:55 in my video The Efficacy and Side Effects of Moringa Leaf Powder, you can see the blood sugar spikes after study participants ate about five control cookies each (top line labeled “a”), compared with cookies containing about two teaspoons of moringa leaf powder into the batter (bottom line labeled “b”). Even with the same amount of sugar and carbohydrates as the control cookies, the moringa-containing cookies resulted in a dampening of the surge in blood sugar.

    Researchers found that drinking just one or two cups of moringa leaf tea before a sugar challenge “suppressed the elevation in blood glucose [sugar] in all cases compared to controls that did not receive the tea initially” and instead drank plain water. As you can see here and at 1:16 in my video, drinking moringa tea with sugar dampened blood sugar spikes after 30 minutes of consumption of the same amount of sugar without moringa tea. It’s no wonder that moringa is used in traditional medicine practice for diabetes, but we don’t really know if it can help until we put it to the test. 
    People with diabetes were given about three-quarters of a teaspoon of moringa leaf powder every day for 12 weeks and had significant improvements in measures of inflammation and long-term blood sugar control. The researchers called it a “quasi-experimental study” because there was no control group. They just took measurements before and after the study participants took moringa powder, and we know that simply being in a dietary study can lead some to eat more healthfully, whether consciously or unconsciously, so we don’t know what effect the moringa itself had. However, even in a moringa study with a control group, it’s not clear if the participants were randomly allocated. The researchers didn’t even specify how much moringa people were given—just that they took “two tablets daily with one tablet each after breakfast and dinner,” but what does “one tablet” mean? There was no significant improvement in this study, but perhaps the participants weren’t given enough moringa. Another study used a tablespoon a day and not only saw a significant drop in fasting blood sugars, but a significant drop in LDL cholesterol as well, as seen below and at 2:27 in my video. 

    Two teaspoons of moringa a day didn’t seem to help, but what about a third, making it a whole tablespoon? Apparently not, since, finally, a randomized, placebo-controlled study using one tablespoon of moringa a day failed to show any benefit on blood sugar control in people with type 2 diabetes.

    So, we’re left with a couple of studies showing potential, but most failing to show benefit. Why not just give moringa a try to see for yourself? That’s a legitimate course of action in the face of conflicting data when we’re talking about safe, simple, side–effect–free solutions, but is moringa safe? Probably not during pregnancy, as “about 80% of women folk” in some areas of the world use it to abort pregnancies, and its effectiveness for that purpose has been confirmed (at least in rats), though breastfeeding women may get a boost of about half a cup in milk production based on six randomized, blinded, placebo-controlled clinical trials.

    Just because moringa has “long been used in traditional medicine” does not in any way prove that the plant is safe to consume. A lot of horribly toxic substances, like mercury and lead, have been used in traditional medical systems the world over, but at least “no major harmful effects of M. oleifera [moringa]…have been reported by the scientific community.” More accurately, “no adverse effects were reported in any of the human studies that have been conducted to date.” In other words, no harmful effects had been reported until now. 

    Stevens-Johnson syndrome (SJS) is probably the most dreaded drug side effect, “a rare but potentially fatal condition characterized by…epidermal detachment and mucous membrane erosions.” In other words, your skin may fall off. Fourteen hours after consuming moringa, a man broke out in a rash. The same thing had happened three months earlier, the last time he had eaten moringa, causing him to suffer “extensive mucocutaneous lesions with blister formation over face, mouth, chest, abdomen, and genitalia.” “This case report suggests that consumption of Moringa leaf is better avoided by individuals who are at risk of developing SJS.” Although it can happen to anyone, HIV is a risk factor.

    My take on moringa is that the evidence of benefit isn’t compelling enough to justify shopping online for something special when you can get healthy vegetables in your local market, like broccoli, which has yet to be implicated in any genital blistering. 

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    Michael Greger M.D. FACLM

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  • Statins and Muscle Pain Side Effects  | NutritionFacts.org

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    Why is the incidence of side effects from statins so low in clinical trials while appearing to be so high in the real world?

    “There is now overwhelming evidence to support reducing LDL-C (low-density lipoprotein cholesterol)”—so-called bad cholesterol—to reduce atherosclerotic cardiovascular disease (CVD),” the number one killer of men and women. So, why is adherence to cholesterol-lowering statin drug therapy such “a major challenge worldwide”? Researchers found “that the majority of studies reported that at least 40%, and as much as 80%, of patients did not comply fully with statin treatment recommendations.” Three-quarters of patients may flat out stop taking them, and almost 90 percent may discontinue treatment altogether.

    When asked why they stopped taking the pills, most “former statin users or discontinuers…cited muscle pain, a side effect, as the primary reason…” “SAMSs”—statin-associated muscle symptoms—“are by far the most prevalent and important adverse event, with up to 72% of all statin adverse events being muscle-related.” Taking coenzyme Q10 supplements as a treatment for statin-associated muscle symptoms was a good idea in theory, but they don’t appear to help. Normally, side-effect symptoms go away when you stop the drug but can sometimes linger for a year or more. There is “growing evidence that statin intolerance is predominantly psychosocial, not pharmacological.” Really? It may be mostly just in people’s heads?

    “Statins have developed a bad reputation with the public, a phenomenon driven largely by proliferation on the Internet of bizarre and unscientific but seemingly persuasive criticism of these drugs.” “Does Googling lead to statin intolerance?” But people have stopped taking statins for decades before there even was an Internet. What kinds of data have doctors suggested that patients are falsely “misattribut[ing] normal aches and pains to be statin side effects”?

    Well, if you take people who claim to have statin-related muscle pain and randomize them back and forth between statins and an identical-looking placebo in three-week blocks, they can’t tell whether they’re getting the real drug or the sugar pill. The problem with that study, though, is that it may take months not only to develop statin-induced muscle pain, but months before it goes away, so no wonder three weeks on and three weeks off may not be long enough for the participants to discern which is which.

    However, these data are more convincing: Ten thousand people were randomized to a statin or a sugar pill for a few years, but so many more people were dying in the sugar pill group that the study had to be stopped prematurely. So then everyone was offered the statin, and the researchers noted that there was “no excess of reports of muscle-related AEs” (adverse effects) among patients assigned to the statin over those assigned to the placebo. But when the placebo phase was over and the people knew they were on a statin, they went on to report more muscle side effects than those who knew they weren’t taking the statin. “These analyses illustrate the so-called nocebo effect,” which is akin to the opposite of the placebo effect.

    Placebo effects are positive consequences falsely attributed to a treatment, whereas nocebo effects are negative consequences falsely attributed to a treatment, as was evidently seen here. There was an excess rate of muscle-related adverse effects reported only when patients and their doctors were aware that statin therapy was being used, and not when its use was concealed. The researchers hope “these results will help assure both physicians and patients that most AEs associated with statins are not causally related to use of the drug and should help counter…exaggerated claims about statin-related side effects.”

    These are the kinds of results from “placebo-controlled randomised trials [that] have shown definitively that almost all of the symptomatic adverse events that are attributed to statin therapy in routine practice are not actually caused by it (ie, they represent misattribution.)” Now, “only a few patients will believe that their SAMS are of psychogenic origin” and just in their head, but their denial may have “deadly consequences.” Indeed, “discontinuing statin treatment may be a life-threatening mistake.”

    Below and at 4:46 in my video How Common Are Muscle Side Effects from Statins?, you can see the mortality of those who stopped their statins after having a possible adverse reaction compared to those who stuck with them. This translates into about “1 excess death for every 83 patients who discontinued treatment” within a four-year period. So, when there are media reports about statin side effects and people stop taking them, this could “result in thousands of fatal and disabling heart attacks and strokes, which would otherwise have been avoided. Seldom in the history of modern therapeutics have the substantial proven benefits of a treatment been compromised to such an extent by serious misrepresentations of the evidence for its safety.” But is it a misrepresentation to suggest “that statin therapy causes side-effects in up to one fifth of patients”? That is what is seen in clinical practice; between 10 to 25 percent of patients placed on statins complain of muscle problems. However, because we don’t see anywhere near those kinds of numbers in controlled trials, patients are accused of being confused. Why is the incidence of side effects from statins so low in clinical trials while appearing to be so high in the real world? 

    Take this meta-analysis of clinical trials, for example: It found muscle problems not in 1 in 5 patients, but only 1 in 2,000. Should everyone over a certain age be on statins? Not surprisingly, every one of those trials was funded by statin manufacturers themselves. So, for example, “how could the statin RCTs [randomized controlled trials] miss detecting mild statin-related muscle adverse side effects such as myalgia [muscle pain]? By not asking. A review of 44 statin RCTs reveals that only 1 directly asked about muscle-related adverse effects.” So, are the vast majority of side effects just being missed in all these trials, or are the vast majority of side effects seen in clinical practice just a figment of patients’ imagination? The bottom line is we don’t know, but there is certainly an urgent need to figure it out.

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    Michael Greger M.D. FACLM

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

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    Switching to a plant-based diet has been shown to achieve far better outcomes than those reported on conventional treatments for both active and quiescent stages of Crohn’s disease (CD) and ulcerative colitis.

    Important to our understanding and the prevention of the global increase of inflammatory bowel disease (IBD), we know that “dietary fiber reduces risk, whereas dietary fat, animal protein, and sugar increase it.” “Despite the recognition of westernization of lifestyle as a major driver of the growing incidence of IBD, no countermeasures against such lifestyle changes have been recommended, except that patients with Crohn’s disease should not smoke.”

    We know that “consuming whole, plant-based foods is synonymous with an anti-inflammatory diet.” Lists of foods with inflammatory effects and anti-inflammatory effects are shown here and at 0:50 in my video, The Best Diet for Crohn’s Disease.

    How about putting a plant-based diet to the test?

    Cutting down on red and processed meats didn’t work, but what about cutting down on all meat? A 25-year-old man “with newly diagnosed CD…failed to enter clinical remission despite standard medical therapy. After switching to a diet based exclusively on grains, legumes [beans, split peas, chickpeas, and lentils], vegetables, and fruits, he entered clinical remission without need for medication and showed no signs of CD on follow-up colonoscopy.”

    It’s worth delving into some of the details. The conventional treatment he was started on is infliximab, sold as REMICADE®, which can cause a stroke and may increase our chances of getting lymphoma or other cancers. (It also costs $35,000 a year.) It may not even work in 35 to 40 percent of patients, and that seemed to be the case with the 25-year-old man. So, his dose was increased after 37 weeks, but he was still suffering after two years on the drug. Then he completely eliminated animal products and processed foods from his diet and finally experienced a complete resolution of his symptoms.

    “Prior to this, his diet had been the typical American diet, consisting of meat, dairy products, refined grains, processed foods, and modest amounts of vegetables and fruits. Having experienced complete clinical remission for the first time since his Crohn’s disease diagnosis, the patient decided to switch to a whole food, plant-based diet permanently, severely reducing his intake of processed foods and limiting animal products to one serving, or less, per week.” Whenever his diet slipped, his symptoms started coming back, but he could always eliminate them by eating healthier again. After six months adhering to these diet and lifestyle changes, including stress relief and exercise, a follow-up “demonstrated complete mucosal healing [of the gut lining] with no visible evidence of Crohn’s disease.”

    We know that “a diet consisting of whole grains, legumes, fruits, and vegetables has been shown to be helpful in the prevention and treatment of heart disease, obesity, diabetes, hypertension, gallbladder disease, rheumatoid arthritis, and many cancers. Although further research is required, this case report suggests that Crohn’s disease might be added to this list of conditions.” That further research has already been done! About 20 patients with Crohn’s disease were placed on a semi-vegetarian diet—no more than half a serving of fish once a week and half a serving of meat once every two weeks—and they achieved a 100 percent remission rate at one year and 90 percent at two years.

    Some strayed from the diet, though. What happened to them? As you can see below and at 3:32 in my video, after one year, half had relapsed, and, at year two, only 20 percent had remained in remission. But those who stuck with the semi-veg diet had remarkable success. It was a small study with no formal control group, but it represents the best-reported result in Crohn’s relapse prevention published in the medical literature to date. 

    Nowadays, Crohn’s patients are often treated with so-called biologic drugs, expensive injected antibodies that suppress the immune system. They have effectively induced and maintained remission in Crohn’s disease, but not in everybody. The current remission rate in Crohn’s with early use of REMICADE® is 64 percent. So, 30 to 40 percent of patients “are likely to experience a disabling disease course even after their first treatment.” What about adding a plant-based diet? Remission rates jumped up to 100 percent for those who didn’t have to drop out due to drug side effects. Even after excluding milder cases, researchers found that 100 percent of those with serious, even “severe/fulminant disease, achieved remission.”

    If we look at gold standard systematic reviews, they conclude that the effects of dietary interventions on inflammatory bowel diseases—Crohn’s disease and ulcerative colitis—are uncertain. However, this is because only randomized controlled trials were considered. That’s totally understandable, as that is the most rigorous study design. “Nevertheless, people with IBD deserve advice based on the ‘best available evidence’ rather than no advice at all…” And switching to a plant-based diet has been shown to achieve “far better outcomes” than those reported on conventional treatments in both active and quiescent stages in Crohn’s disease and ulcerative colitis. For example, below and at 5:37 in my video, you can see one-year remission rates in Crohn’s disease (100 percent) compared to budesonide, an immunosuppressant corticosteroid drug (30 to 40 percent), a half elemental diet, such as at-home tube feedings (64 percent), the $35,000-a-year drug REMICADE® (46 percent), or the $75,000-a-year drug Humira (57 percent). 

    Safer, cheaper, and more effective. That’s why some researchers have made the “recommendation of plant-based diets for inflammatory bowel disease.”

    It would seem clear that treatment based on addressing the cause of the disease is optimal. Spreading the word about healthier diets could help halt the scourge of inflammatory bowel disease, but how will people hear about this amazing research without some kind of public education campaign? That’s what NutritionFacts.org is all about.

    Doctor’s Note:

    This is the third in a series on inflammatory bowel disease. If you missed the first two, see Preventing Inflammatory Bowel Disease with Diet and The Best Diet for Ulcerative Colitis Treatment.

    My previous Crohn’s videos include Preventing Crohn’s Disease with Diet and Does Nutritional Yeast Trigger Crohn’s Disease?. 

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    Michael Greger M.D. FACLM

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

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

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

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

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

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

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

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

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

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

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

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

    Doctor’s Note:

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

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    Michael Greger M.D. FACLM

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  • The Efficacy of Weight-Loss Supplements  | NutritionFacts.org

    The Efficacy of Weight-Loss Supplements  | NutritionFacts.org

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    Are there any safe and effective dietary supplements for weight loss?

    In a previous discussion, I noted that an investigation found that four out of five bottles of commercial herbal supplements bought at major U.S. retailers—GNC, Walgreens, Target, and Walmart—didn’t contain any of the herbs listed on their labels, instead “often containing little more than cheap fillers like powdered rice, asparagus and houseplants…”

    You might hope your supplement just contains houseplants. Weight-loss supplements are infamous for being “adulterated with prescription and over-the-counter” drugs. In a sampling of 160 weight-loss supplements that “were claimed as 100% natural,” more than half were tainted with drugs and active pharmacological ingredients, ranging from antidepressants like Prozac to erectile dysfunction medications like Viagra. Diuretic drugs are frequent contaminants, which makes sense. In my previous videos on ketogenic diets, I talk about rapid water loss being “the $33-billion diet gimmick” that has sold low-carb diets for more than a century. But why the Viagra?

    At least the spiked Viagra and Prozac are legal drugs. Researchers in Denver tested every weight-loss supplement they could find within a ten-mile radius. Alarmingly, they found that a third were adulterated with banned ingredients. The most common illegal adulterant of weight-loss supplements is sibutramine, which was sold as Meridia before it was yanked off the market back in 2010 for heart attack and stroke risk. Now, it is also blamed for cases of slimming supplement–induced psychosis.

    An analysis of weight-loss supplements bought off the internet that were advertised with claims like “purely natural products,” “harmless,” or “traditional herbal” found that a third of them contained high doses of the banned drug sibutramine and the rest had caffeine. Wouldn’t you be able to tell if caffeine was added to a supplement? Perhaps not, if it also had temazepam, a controlled substance (benzodiazepine) “downer” sedative found in half of the caffeine-tainted supplements.

    Doesn’t the FDA demand recalls of adulterated supplements? Yes, but they often just pop back up on store shelves. Twenty-seven supplements were purchased at least six months after recalls were released, and two-thirds still contained banned substances. That’s 17 out of 27 with the same pharmaceutical adulterant found originally, and 6 containing one or more additional banned ingredients. Aren’t the manufacturers penalized for noncompliance? Yes, but “the fines for violations are small compared to the profits.”

    One of the ways supplement makers can skirt the law is by labeling them as “not intended for human consumption because it shifts the responsibility from the seller to the user”—for example, labeling the fatal fat-burner DNP as “an industrial- or research chemical.” This is how designer street drugs can be sold openly at gas stations and convenience stores as “bath salts.” Another way is to claim synthetic stimulants added to slimming supplements are actually natural food constituents, like listing the designer drug dimethylamylamine (DMAA) as “geranium oil extract.” The FDA banned it in 2012 after it was determined that DMAA “was not found in geraniums.” Who eats geraniums anyway? Despite being tentatively tied to cases of sudden death and associated with hemorrhagic stroke, DMAA has continued to be found in weight-loss supplements with innocuous names like Simply Skinny Pollen made by Bee Fit with Trish.

    There is little doubt that certain banned supplements, like ephedra, could help people lose weight. “There’s only one problem, and it’s a big one: This supplement may kill you,” wrote a founding member of the American Board of Integrative Medicine.

    Are there any safe and effective dietary supplements for weight loss? As I discuss in my video Friday Favorites: Are Weight-Loss Supplements Safe and Effective?, when popular slimming supplements were put to the test in a randomized placebo-controlled trial, not a single one could beat out placebo sugar pills. “A systematic review of systematic reviews” of diet pills came to a similar conclusion: None appears to generate appreciable impacts “on body weight without undue risks.” That was the conclusion reached in a similar review out of the Weight Management Center at Johns Hopkins, which ended with: “In closing, it is fitting to highlight that perhaps the most general and safest alternative/herbal approach to weight control is to substitute low-energy density [low-calorie] foods for high-energy density and processed foods, thereby reducing total energy intake.” In other words, eat more whole plant foods and fewer animal foods and junk. “By taking advantage of the low-energy density [low-calorie] and health-promoting effects of plant-based foods, one may be able to achieve weight loss, or at least assist weight maintenance without cutting” down on the volume of food consumed or compromising its nutrient value.

    Learn more about the risks of supplements in my video Are Weight Loss Supplements Safe?.

    I referred to a keto diet video I did, check out the related posts below the links to other videos and blogs in that series.

    Learn more about optimal weight loss in my book, How Not to Diet. 

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    Michael Greger M.D. FACLM

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  • The Safety of Weight-Loss Supplements  | NutritionFacts.org

    The Safety of Weight-Loss Supplements  | NutritionFacts.org

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    Only 2 out of 12 supplement companies were found to have weight-loss products that were even accurately labeled.

    According to a national survey, one-third of adults who have made serious attempts at weight loss have tried using dietary supplements, for which Americans spend billions of dollars every year. Most people mistakenly thought that over-the-counter appetite suppressants, herbal products, and weight-loss supplements had to be approved for safety by a governmental agency, like the U.S. Food and Drug Administration (FDA), before being sold to the public or at least include some kind of warning on the label about potential side effects. Nearly half even thought they had to demonstrate some sort of effectiveness. None of that is true.

    As I discuss in my video Friday Favorites: Are Weight Loss Supplements Safe and Effective?, the “FDA has estimated that dietary supplements cause 50,000 adverse events annually,” most commonly liver and kidney damage. Of course, prescription drugs don’t just have adverse effects; they kill more than 100,000 Americans every year. But, you at least notionally have the opportunity to parse out the risks versus benefits of prescription drugs, thanks to testing and monitoring requirements typically involving thousands of individuals.

    When the manufacturer of Metabolife 356, a supplement containing ephedrine, had it tested on 35 people, only minor side effects were found, such as dry mouth, headache, and insomnia. However, once unleashed on a broad population, nearly 15,000 adverse effects were reported, including heart attacks, strokes, seizures, and deaths, before it was pulled from the market.

    Given the lack of government oversight, there is no guarantee that what’s on the label is even in the bottle, as you can see in the graph below and at 1:55 in my video. FDA inspectors have found that 70 percent of supplement manufacturers violated so-called Good Manufacturing Practices, which are considered the minimum quality standards. This includes things like basic sanitation and ingredient identification. Not 7 percent in violation, but 70 percent.

    DNA testing of herbal supplements across North America found that most could not be authenticated. In a significant percentage of the supplements tested, the main labeled ingredient was missing completely and substituted with something else. For example, a so-called St. John’s wort supplement contained nothing but senna, a laxative that can cause anal blistering. Only 2 out of 12 supplement companies had products that were accurately labeled.

    This problem isn’t limited to fly-by-night phonies in some dark corner of the internet either. The New York State Attorney General commissioned DNA testing of 78 bottles of commercial herbal supplements sold by Walgreens, Walmart, Target, and GNC “and found that four out of five…did not contain any of the herbs on their labels.” Instead, the capsules “often contained little more than cheap fillers like powdered rice, asparagus and houseplants…”

    What about weight-loss medications? See Are Weight Loss Pills Safe? and Are Weight Loss Pills Effective?. Also, see related posts below.

    Take a deep dive into the best way to lose weight with my book How Not to Diet. 

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    Michael Greger M.D. FACLM

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  • The Mothers Who Aren’t Waiting to Give Their Children Cystic-Fibrosis Drugs

    The Mothers Who Aren’t Waiting to Give Their Children Cystic-Fibrosis Drugs

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    At six months pregnant, Sonja Lee Finnegan flew from Switzerland to France to buy $20,000 worth of drugs from a person she had never met. The drug she was after, Trikafta, is legal in Switzerland and approved for cystic fibrosis, a rare genetic disease that fills the lungs with thick mucus. Finnegan could not get it from a doctor, because she herself does not have cystic fibrosis. But the baby she was carrying inside her does, and she wanted to start him on the Trikafta as early as possible—before he was even born.

    She felt so strongly because Trikafta is, without exaggeration, a miracle drug. As I wrote in the latest issue of this magazine, the daily pills have in the past five years transformed cystic fibrosis from a fatal disease into one where most patients can live an essentially normal life. Trikafta, a combination of three drugs, is not a cure, and it does not entirely reverse organ damage already caused by CF, but patients who grew up believing they would die young are instead saving for retirement. And children born with CF today can expect to live to a ripe old age, as long as they start the drugs early.

    How early is best? The drugs are officially approved for CF patients as young as 2, but a handful of enterprising mothers in the United States have gotten it prescribed off-label, to treat children diagnosed in the womb. Where doctors are more cautious, mothers are still pushing the limits of when to start the drugs. A mom in Canada sent her husband across the border to get Trikafta from someone in the United States. And Finnegan flew to France to meet a patient willing to sell their excess supply.

    Getting hold of Trikafta is in fact the hardest part. Parents told me of both insurance plans and obstetricians skeptical of a powerful new medication never tested in pregnant women—and not without reason. Trikafta has side effects, and it is new enough that not all of its ramifications are fully understood. But Finnegan pored over all the research she could find and decided that Trikafta was worth it. For $20,000, she bought a five-months supply—a relative bargain compared with Trikafta’s list price of $300,000-plus a year in the United States.

    To her, it was worth $20,000 for her son to avoid CF complications that can require major surgery at birth. It was worth $20,000 to prevent permanent damage to his organs that begins even in utero. She felt lucky she could afford it at all. Trikafta in pregnancy is not currently standard practice, but a miracle drug was out there. For her son, she would figure out a way to get it.

    The very first expecting moms on Trikafta were women with CF taking the drugs for themselves. Not long after the medication became available, in the fall of 2019, doctors noticed a baby boom in the CF community. Trikafta, it turns out, affects more than the lungs; it can also reverse the infertility common in women with CF, thought to be caused by unusually thick cervical mucus. (Most men with CF are born infertile, because the vas deferens, which carries sperm, never develops.)

    Experts worried at first about what Trikafta could do to developing fetuses. “People were like, ‘Don’t do this. We don’t know if it’s a teratogen’”—a substance that causes birth defects, says Ted Liou, the director of the adult-CF center at the University of Utah. (The CF doctors quoted in this article have all conducted clinical trials for or received speaking or consulting fees from Vertex, the manufacturer of Trikafta and several other drugs for CF.) That fear turned out to be unfounded: Hundreds of babies later, there has been, at least anecdotally, no uptick in severe birth defects.

    Read: The cystic-fibrosis breakthrough that changed everything

    Doctors started to see hints that Trikafta in utero could help babies with CF too. Of the hundreds of children born to mothers on Trikafta, only a few of the babies had CF themselves. This is because cystic fibrosis is a recessive disorder, meaning a mother with CF could have a child with CF only if the father also passed on a CF mutation. But the first documented case came to the attention of Christopher Fortner, the director of the CF center and pediatric-CF program at SUNY Upstate, who published a case report in 2021. Trikafta, he told me, made a clear difference for this baby girl.

    Cystic fibrosis is caused by an imbalance of salt and water in the body, and this affects developing organs even before birth. One in five infants with CF are born with an intestinal blockage caused by meconium—the normally sticky black stool of newborns—that has turned too thick and hard to pass. This is called meconium ileus, and in the worst cases, the intestines can rupture. Emergency surgery is necessary. Elsewhere in the body, the pancreas never forms properly with CF. “By the time they’re born, their pancreas is really not a functional organ,” Fortner said. Adults on Trikafta still have to take pancreatic enzymes with every meal, but there is some evidence that young children can gain pancreatic function if they begin the CF drugs early enough.

    When this baby girl was born, though, her meconium and her pancreas levels were normal from the very start; the standard newborn screening for CF would have never caught her. Fortner started her on enzymes as a precaution, but he stopped them after a week. She is 3 years old now and in preschool. Unlike generations of CF kids before her, she will never have to see the school nurse for enzymes every time she wants to eat. And she may never suffer the recurring lung infections that once made CF ultimately fatal. “The life she’s living,” Fortner said, “that was a whole lot like a cure to me.”

    Moms who do not have CF themselves have a much harder time getting their unborn children on Trikafta. In 2021, Yolanda Huffhines’s second child was diagnosed with CF prenatally, after a genetic test was recommended because Huffhines’s first child had cystic fibrosis. The diagnosis did not come as a shock this time, but she began to worry when the baby showed signs of meconium ileus while still in utero.

    After coming across a study in ferrets, Huffhines brought the idea of Trikafta to her doctors, who were not all enthused. Her obstetrician in particular was against it. But she found that CF doctors were more willing to weigh the well-known risks of cystic fibrosis—especially meconium ileus—against the less well-known risks of Trikafta. She asked Patrick Flume, who directs the adult-CF center at the Medical University of South Carolina, what he would do if it were his wife and child. He told her he would get Trikafta, and he agreed to help.

    Even with a sympathetic doctor, getting Trikafta wasn’t easy. First, Flume tried giving her a stash from a patient who no longer needed it, which was vetoed because his hospital couldn’t ensure that it had been properly stored. Then he asked the manufacturer, Vertex, which also said no. (The company told me it couldn’t provide Trikafta to anyone outside the drug’s official indications.) Finally, Flume told me, he decided to write a prescription as if the mother were his patient. When the insurance company asked if she had at least one copy of a specific CF mutation that Trikafta was developed for, he answered yes, truthfully. Because Huffhines is a carrier, she does have one copy. She started Trikafta at 32 weeks, and by the time her daughter was born, the meconium ileus had disappeared.

    Huffhines’s experience on Trikafta was not entirely smooth, though. The drugs come with some well-documented side effects, such as cataracts and liver damage, that have to be monitored, Flume told me, as with any new drug. Although Trikafta during pregnancy went fine for Huffhines, she started to experience unusual symptoms when she continued the medication so her daughter could get it through breast milk. Her usual migraines started going “through the roof,” and her scheduled blood work revealed that her liver enzymes had gone haywire—a sign of liver damage. She had to stop.

    Quitting Trikafta cold turkey could be harmful for newborns, though, which Huffines knew from studying the ferret research. (Suddenly withdrawing, Fortner told me, may cause pancreatitis.) She wondered: Was it possible to give a baby Trikafta directly? The pills would be too big, obviously, but her husband had scales for gunpowder that could weigh down to the milligram. She got a new one overnighted, and she began crushing the pills to give to her daughter—a technique that has since been taught to other moms. Her daughter did well. Huffhines’s doctors ended up publishing a case report in 2022—the first documenting a carrier of CF taking Trikafta.

    The long-term impacts of being on Trikafta in utero still need to be studied. The oldest child is still only 3. In adults, a small minority who have started Trikafta have reported sudden and severe anxiety, insomnia, depression, or other neuropsychiatric symptoms. The link is not fully proven or understood in adults, and it’s completely unexplored for fetal brain development. Elena Schneider-Futschik, a pharmacologist at the University of Melbourne, told me she is collaborating with researchers in the United Kingdom to get long-term developmental data on children exposed to Trikafta before birth. For now, she said, “we don’t know.”

    Fortner, who has heard from several pregnant mothers since his first case report, said he does not deter parents already set on getting Trikafta, but he does not, in all cases, push them toward it, either. Given the unknowns, he’s not sure that the benefits outweigh the risks. The clearest exceptions are cases of meconium ileus, in which doing nothing comes with its own costs. Flume told me about a recent patient whose baby was showing signs of an intestinal blockage and whose insurance initially denied Trikafta. The medication was eventually approved—but the mom went into labor the day she was due to start. Her baby needed emergency surgery. “This is something that did not need to happen,” he said.

    By the time Finnegan, in Switzerland, went looking for Trikafta last year, she had the earlier cases as models. Her baby wasn’t showing signs of meconium ileus, but she didn’t want to wait until he did, if he was going to end up down that path. Although her doctors were supportive, they could not get her Trikafta. That’s why she had to take unorthodox measures.

    She took her first pill in August, and her son was born in October with a working pancreas and no intestinal blockage. He is far too young for this to matter, but she hopes that the Trikafta allowed his vas deferens to develop normally too. Someday, he might want children of his own, and the impacts of getting Trikafta in utero might carry over into the next generation.

    Finnegan has been documenting her experience on social media, where she says her posts have inspired other pregnants moms to get on Trikafta for their unborn children. She knows of about 20 now, and after she got in touch with Schneider-Futschik, the researcher decided to survey these moms too. Meanwhile, Finnegan is sharing the stories of other moms as well, making note of details such as how long the mom was on Trikafta, what side effects she experienced, whether meconium ileus was resolved, and if insurance covered the drugs—a case series, of sorts, presented on Instagram. They are still few enough that every case is notable. In the future, though, all of this might become the utterly unremarkable standard of care.

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    Sarah Zhang

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  • Fighting Inflammation with Flaxseeds  | NutritionFacts.org

    Fighting Inflammation with Flaxseeds  | NutritionFacts.org

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

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

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

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

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

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

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

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

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

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    Michael Greger M.D. FACLM

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  • Ozempic Can Turn Into No-zempic

    Ozempic Can Turn Into No-zempic

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    No medication in the history of modern weight loss has inspired as much awe as the latest class of obesity drugs. Wegovy and Zepbound are so effective that they are often likened to “magic” and “miracles.” Indeed, the weekly injections, which belong to a broader class known as GLP-1s, can lead to weight loss of 20 percent or more, fueling hype about a future in which many more millions of Americans take them. Major food companies including Nestlé and Conagra are considering tailoring their products to suit GLP-1 users. Underlying all this excitement is a huge assumption: They work for everyone.

    But for a lot of people, they just don’t. Anita, who lives in Arizona, told me she “took it for granted” that she would lose weight on a GLP-1 drug because “the people around me who were on it were just dropping weight like mad.” Instead, she didn’t shed any pounds. Likewise, Kathryn, from Florida, hasn’t lost any weight since starting the medication in October. “I was really hoping this was something that would be a game changer for me, but it feels like it was just a lot of wasted money,” she told me. (I’m identifying both Anita and Kathryn by their first name only to allow them to speak openly about their health issues.)

    Some people can’t tolerate the side effects of the drugs and have to stop taking them. Others simply don’t respond. For some, the strength of the dose, or length of the treatment, does not seem to make a difference. Appetites might remain robust; the “food chatter” in the brain may stay noisy. Together, both groups of less successful GLP-1 users account for a not-insignificant share of patients on these drugs—potentially up to a third. “We don’t really know why it happens, [but] we know it does happen,” Louis Aronne, an obesity-medicine specialist at Weill Cornell Medical College, told me. Despite the promise of a so-called Ozempic revolution, lots of “No-zempics” have been left behind.

    Of the two biggest reasons some people don’t lose weight on GLP-1 drugs—side effects and nonresponse—the former is much more straightforward. The GLP-1 drugs Wegovy and Zepbound (which contain the active ingredients semaglutide and tirzepatide, respectively), are known for causing potentially gnarly gastrointestinal symptoms, such as nausea and vomiting, although most people’s reactions are mild and temporary. Yet some have it far worse. Severe, albeit uncommon, side effects include pancreatitis, severe gastrointestinal distress, low blood sugar, and even hair loss, which “can push people off” the drugs, Steven Heymsfield, a professor who studies obesity at Louisiana State University, told me. In one of the biggest studies of semaglutide, encompassing more than 17,000 people over about five years, nearly 17 percent of patients discontinued the medication because of side effects.

    Far more mysterious are the people who tolerate the drugs but respond weakly to them—or sometimes not at all. Researchers have known this might happen since these drugs were in early clinical trials. About 14 percent of people who took semaglutide for obesity saw minimal impacts of less than 5 percent weight loss in one study, as did 9 to 15 percent of people who took tirzepatide in a similar one. In her own experience working with patients, “somewhere between a quarter and a third” are nonresponders, Fatima Cody Stanford, an obesity-medicine specialist at Harvard, told me, adding that it can take up to three months to determine whether the drug is working or not. That the same medication at the same dosage can lead to dramatic weight loss in one person and hardly any in another “remains confounding,” Aronne told me.

    The broad explanation is that it has something to do with genetics. The drugs work by masquerading as the appetite-suppressing hormone GLP-1 and binding to its receptor, like a key fitting into a lock. Although the lock’s overall shape is generally consistent from person to person, its nooks and crannies can vary because of genetic differences. “For some people, that key just won’t fit right,” Eduardo Grunvald, an obesity-medicine doctor at UC San Diego Health, told me. In other cases, genes may limit the effects of these drugs after they bind to GLP-1 receptors. One possibility is that people metabolize the drugs differently: Some patients may break them down too quickly for them to take effect; others may process them too slowly, potentially building up such high levels of the medications that they become toxic, Heymsfield said.

    For No-zempic patients, perhaps the most consequential impact of individual variation is on the propensity for obesity itself. “We are all very different from a genetic standpoint, in terms of our risk of weight gain,” Grunvald said. Numerous factors can drive obesity, including diet, environment, stress, and—most pertinent to GLP-1 drugs—altered brain function.

    GLP-1 drugs target a pathway that regulates appetite and insulin levels. Some cases of obesity can be caused by a disruption in that particular mechanism, in which case GLP-1s can indeed be wondrous. But “not everyone has dysfunction in this particular pathway,” Stanford said. When that is the case, the drugs won’t be very effective. A different pathway, for example, controls the absorption of fat from food; another increases energy expenditure. In these people, GLP-1s might tamp down appetite to a degree, maybe leading to some weight loss, but a different drug may be required to treat obesity at its root. “It is not all about food intake,” Stanford said.

    That’s not to say that No-zempics are out of options. They might have better success switching from one GLP-1 to the other, or even stacking them, Heymsfield said. Some patients who don’t respond to GLP-1s at all can get better results with older drugs that work on different obesity pathways, Aronne said. One, called Qysmia, a combination of the decades-old drugs phentermine and topiramate, can lead to an average weight loss of 14 percent body weight at its highest dose. If medications don’t work, bariatric surgery remains a powerful option, one that may even be growing in popularity. Last year, the number of bariatric surgeries performed in the U.S. grew despite the boom in GLP-1 usage, a trend that some expect to continue, because so many people don’t tolerate the drugs.

    The intense hype around the game-changing nature of GLP-1s makes it easy to forget that they are, in fact, just drugs. “Every drug that’s ever been made” works in some people and not in others, Heymsfield said; there’s no reason to think GLP-1s would be any different. Remembering that they are in an early stage of development has a sobering effect. Eventually, obesity drugs may leave fewer people behind. The category is expanding rapidly: By one count, more than 90 new drug candidates are in development.

    They are evolving to attack obesity from multiple fronts, which, at least in theory, widens their net of potential users. In an early study on an experimental candidate named retatrutide—called a triple agonist because it acts on GLP-1 as well as two other targets involved in obesity, GIP and glucagon receptors—100 percent of people on the highest dose lost 5 percent or more of their body weight. New candidates are also expected to have fewer side effects. They have to, Heymsfield said, because the competition is so steep that any new drug has to be “as good with less side effects, or better.”

    But no matter how good these drugs get, it’s unrealistic to think that they’ll become a one-size-fits-all treatment for everyone with obesity. The disease is simply too complex, with too many drivers, for a single type of medication to treat it. More than 200 different drugs exist for treating high blood pressure alone; in comparison, Aronne said, regulating weight is “far more complicated.” The future, rife with options, holds promise that No-zempics may find a way forward. Yet considering all the unknowns about obesity and what causes it, that may not be enough to guarantee that they will see the results they want.

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    Yasmin Tayag

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  • Are You Sure You Want an Ozempic Pill?

    Are You Sure You Want an Ozempic Pill?

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    Within the first five seconds of a recent Ozempic commercial, a sky-blue injector pen tumbles toward the viewer, encircled by a big red O. Obesity drugs have become so closely associated with injections that the two are virtually synonymous. Like Ozempic, whose name is now a catchall term for obesity drugs, Wegovy and Zepbound come packaged in Sharpie-like injection pens that patients self-administer once a week. Patients “don’t come in asking for Wegovy,” Laura Davisson, a professor of medical weight management at West Virginia University, told me. “They come in asking for one of ‘those injectables.’”

    Needles are the present, but supposedly not the future. Nobody really likes injections, and taking a pill would be far easier. In the frenzy over obesity drugs, a class known as GLP-1 agonists, drugmakers have raced to create them in pill form, and Wall Street investors are hungry at the prospect. Earlier this year, Pfizer’s CEO, Albert Bourla, estimated that obesity pills could be worth $30 billion, or a third of the total obesity-drug market. Because people have a “preference” for pills, he said at a conference, they will be what ultimately “unlocks the market” for obesity medications. By one count, at least 32 oral GLP-1 drugs, from many different companies, are in the works.

    But a future dominated by obesity pills is hardly certain. So far, the only oral GLP-1 that exists is a pill for diabetes called Rybelsus. Like Ozempic and Wegovy, its active ingredient is a compound called semaglutide, but the shots come in far more powerful doses, making it possible to lose even more weight. Developing oral obesity drugs that are as tolerable and effective as their injectable counterparts has so far been a challenge. Earlier this month, Pfizer stopped testing one of its pill candidates, citing concerns about side effects and patient adherence. Even when pills do come to market, doctors told me, there’s no guarantee that people will flock to them.

    That drugmakers view the injectable nature of GLP-1s as one of their biggest flaws is no surprise. Getting a shot is a broadly despised experience, something people generally tolerate rather than choose. Children get stickers for enduring immunizations; adults who get vaccinated do so only because they must (and they are often rewarded with stickers too). The CDC estimates that one in four adults, and two out of three children, have strong fears about needles. “Some people hate needles, plain and simple,” Ted Kyle, an obesity-policy expert, told me.

    But not all needles are made equal. Wegovy and Zepbound are injected subcutaneously, or just under the skin. Relative to COVID or flu shots, which are jabbed into muscle, they don’t cause much discomfort. “I’ve been really surprised at how receptive my patients have been to using injectable medications,” Davisson said. Other doctors I spoke with agreed. “More patients than you would expect really don’t mind injectables,” because they’re easy and relatively painless to administer, Katherine Saunders, a clinical-medicine professor at Weill Cornell Medicine, told me.

    The unobtrusive dosing schedule of the injectables adds to their appeal. Wegovy and Zepbound are administered once weekly, unlike many of the pills in development, which are meant to be taken once or more daily. That can be a hassle, especially if they have to be taken at the same time every day, or if they come with restrictions on eating or drinking. “For some people, it’s easier to take an injection and forget about it for a week” than to remember to take a pill every day, Eduardo Grunvald, an obesity-medicine physician at UC San Diego Health, told me. Assuming pills are preferable to shots is a “knee-jerk reaction,” he added.

    Despite the unexpected upsides of the shots, they’re far from perfect. Making injectable pens is generally more expensive than pills and requires a lot of hardware, including the pen casing, cap, and needle cover. On top of that, the injectable obesity drugs must be refrigerated before they are first used, adding to storage and production costs. Pills are generally shelf-stable and don’t require much packaging beyond a child-proof bottle. Saunders predicts they would be less expensive and less prone to shortages that have plagued Wegovy.

    Still, creating an obesity pill isn’t as simple as packaging the same drugs in capsule form. Drugmakers have already run into a number of issues. Absorption is a big one: Because pills pass through the stomach before entering the bloodstream, they must be able to withstand a large degree of degradation. One way to get these drugs to lead to greater weight loss is to increase the dose. While the highest dose of Wegovy is 2.4 milligrams, Rybelsus maxes out at 14 milligrams.

    Hiking up the dose seems to work, though doing so could have consequences beyond weight loss. All GLP-1 drugs come with a range of unpleasant side effects involving the gastrointestinal system, and patients report nausea at similar rates in Rybelsus and Ozempic, according to the FDA. But this may differ in practice, as other doctors have noted. Saunders said that her patients on oral semaglutide report more nausea than those using injectables. Regardless, newer oral medications may have even more distinct differences, as drugmakers race to create more potent pills. In Pfizer’s discontinued trial of danuglipron, nausea rates reached up to 73 percent.

    Drugmakers also skirt the issue of degradation by pursuing sturdier drugs. The problem with semaglutide is that it’s a peptide—essentially a small protein—precisely the kind of molecule that the stomach excels at digesting. Some new drugs in the pipeline are so-called non-peptide small molecules, which are sturdier but still have the same biological effect. Orforglipron, a pill that Eli Lilly is testing, falls into this category, as does danuglipron, the drug responsible for Pfizer’s recent setbacks. Small-molecule drugs have the added benefit of being cheaper to produce at scale than peptides, Kyle, the obesity-policy expert, added.

    Another pesky problem with oral drugs is that they tend to come with strict dosing requirements. People on Rybelsus, for example, are instructed to take it 30 minutes before eating or drinking anything and can drink only four ounces of plain water along with it, because otherwise absorption could be compromised. “It can be a nuisance,” Grunvald said. Similarly bothersome instructions likely played a part in the drop-out rates reaching more than 50 percent in Pfizer’s recently discontinued trial: Danuglipron had to be taken twice daily. “A lot of people found it not worth the trouble,” Kyle said, noting that Pfizer is still pursuing a once-daily version of the same drug. A recent review of GLP-1 drugs showed that, compared with the injectable form, oral semaglutide is associated with lower rates of side-effect reporting but higher discontinuation rates, potentially reflecting its bothersome dosage requirements.

    Despite these hurdles, it seems inevitable that obesity-drug pills will eventually become available. Novo Nordisk is expected to file for FDA approval for its high-dose semaglutide obesity pill this year; Pfizer is forging ahead with a once-daily version of danuglipron, with more data expected “in the first half of 2024,” a spokesperson told me. A report from BMO Equity Research published in September predicted that oral formulations could be approved “by the late 2020s.” The biggest upside to pills may not be that they are pills but that they will, eventually, be cheaper than injectables—and cost is among the biggest impediments to more people taking obesity drugs.

    Whether they’ll replace injectables outright is far from certain. “It will come down to patient preference,” Grunvald said. Most likely, pills and injections will coexist to meet different needs, and perhaps even be used together to treat individual patients. In the so-called phased approach, obesity treatment could start with more expensive and powerful injectable drugs, then transition to less potent but cheaper orals for the long term. Eli Lilly, for one, sees its oral candidate, orforglipron, as a potential weight-loss-maintenance drug.

    There is so much competition in the obesity-drug space that future medications may take more unexpected forms. Amgen is studying a once-monthly injection; Novo Nordisk is developing a hydrogel form of semaglutide that would need to be taken only three times a year. If the future of obesity drugs will come down to what patients prefer, then the more options, the better.

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    Yasmin Tayag

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  • Does Using Weed Cause Vasodilation

    Does Using Weed Cause Vasodilation

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    At some point, you must have experienced a bloated face,  red and puffy eyes, as well as dehydrated skin after smoking. Have you ever stopped to think and ask yourself why this happens whenever you smoke? Does using weed cause vasodilation.  The answer is maybe.

    Photo by Jeff W via Unsplash

    What is Vasodilation?

    Vasodilation is a mechanism to enhance blood flow to areas of the body that are lacking oxygen and/or nutrients. The vasodilation causes a decrease in systemic vascular resistance (SVR) and an increase in blood flow, resulting in a reduction of blood pressure.

    The word “vasodilation” is used to describe the opening up of the body’s blood vessels.

    It is the opposite of “vasoconstriction” where the blood vessels close up within the body. It is a temporary situation. It occurs naturally in your body in response to triggers such as low oxygen levels, a decrease in available nutrients, and increases in temperature. It causes the widening of your blood vessels, which in turn increases blood flow and lowers blood pressure.

    Consuming marijuana could bring about vasodilation. When using cannabis, blood flow to some parts of the body is restricted or reduced. Oxygen transportation is also slowed down and not quickly delivered as promptly.  While not dangerous, vasodilation can occur.

    Epidemiological and experimental studies have demonstrated that the ingestion of alcohol is associated with an immediate decreasing of blood pressure (an effect typical of vasodilators), which is followed by a rebounding elevation of blood pressure.

    The easiest way to know this is happening is by the obvious reddening of the eyes, as well as the puffy/bloated face of the user. Unfortunately, many are not aware of this physiological mechanism, so they pin it on smoke irritation.

    Some medical practitioners prescribe cannabis-based medications to patients suffering from glaucoma, high blood pressure, etc. This is because of the vasodilating response that would be induced by these drugs to help lower the blood pressure.

    Smoking Marijuana
    Photo by Skitterphoto via Pixabay

    Vasodilation and Cannabis

    While researchers have been able to find useful medical applications for cannabis in the human body, they have still not discovered the full extent of the effects of cannabis consumption on other organs in the body. And the risks involved are most times underestimated. The vasodilating effects of cannabis are one of the physiological responses of the body that have been investigated.

    What Makes Cannabis a Vasodilator?

    THC (Tetrahydrocannabinol) is the main psychoactive element present in cannabis. It is the agent that causes a noticeable increase in the heart rate, as well as a lowered blood pressure.

    Another vasodilating effect is dizziness. This is because THC reacts with cannabinoid receptors present around the body, most especially the eyes to induce these effects.

    RELATED: This Is What Happens When You’re Allergic To Marijuana

    Although THC is not the only cannabinoid responsible for all these, it is responsible for the bulk of these reactions. The amount of THC present in the cannabis strain ingested determines the extent of vasodilation in the user’s body.

    For example, consuming a cannabis strain with less than 15% THC might result in little or no noticeable reddening of the eyes, compared to consuming over 30% THC cannabis strain. It also depends on the user’s tolerance, because everyone’s body anatomy is unique.

    What Causes Reddening Of the Eyes?

    The main reason your eyes get red — or bloodshot and bloated — when you use marijuana is due to vasodilation being set off by THC and other cannabinoids present in cannabis. When your eyes redden and get puffy, it indicates that there is an increased blood flow to your eyeball due to the dilation of blood vessels and capillaries around the eye area.

    After the effects of the drugs begin to wear off, the capillaries and blood vessels gradually begin to close off and constrict. Till everything is back to normal.

    Can Vasodilation Be Halted?

    Vasodilation is a subconscious response, hence it cannot be prevented from occurring. Neither can it be halted when it has started. It only stops when the last effects of cannabis wear off in the body. You have zero control over the workings of vasodilation, nor vasoconstriction.

    However, you can put in the effort to mask/cover up the effects of using cannabis by hiding your bloated face and puffy eyes.

    Masking Vasodilation

    Like I mentioned above vasodilation can’t be stopped, however with a few techniques you can effectively mask the signs. Here are some ways you can hide your puffy reds eyes effectively.

    RELATED: Why Smoking Weed Makes Your Eyes Red

    Eye drops—Allergy and Artificial: Allergy drops help with bloodshot eyes. It effectively reduces discomfort and redness. If it is itchy, it also helps soothe the eyes. Artificial teardrops can also help, although it is not as efficient as allergy eye drops, which is not surprising.

    Both drops contain Tetryzoline, which acts as a constricting agent for the blood vessels. And both drops are easy to get at the nearest pharmacy over the counter.

    Why Does Smoking Weed Make Your Eyes Red?
    Photo by Elizabeth Fernandez/Getty Images

    Using Sunglasses: This is a perfect way to hide the use of marijuana, especially when in a public gathering with people you do not stare at your bloodshot eyes.

    For example, you can use it for a lecture in college. It’s simple, less expensive, and fast to just pick your glasses, put them on and go about basking in your high. The only downside to this is that you cannot wear sunglasses at night, so as not to damage your eyesight.

    Doing away with caffeinated drink: Coffee is also like cannabis, they are both vasodilators. Stay hydrated. Take a very cold bath if you can or put ice bags over your eyes.

    Calmly wait for symptoms to subside: The redness will even be reduced and everything will go back to normal. The duration may vary from 1-12 hours depending on your body’s tolerance, weight, metabolism. And the strain and dose of cannabis ingested. Choose strains of cannabis with low THC.

    Vasodilation is a temporary issue which can be partially mitigated with some simple steps. There isn’t a long term danger.

     

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    Anthony Washington

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