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  • Eating Fast Is Bad for You—Right?

    Eating Fast Is Bad for You—Right?

    For as long as I have been feeding myself—which, for the record, is several decades now—I have been feeding myself fast. I bite big, in rapid succession; my chews are hasty and few. In the time it takes others to get through a third of their meal, mine is already gone. You could reasonably call my approach to eating pneumatic, reminiscent of a suction-feeding fish or a Roomba run amok.

    Where my vacuuming mouth goes, advice to constrain it follows. Internet writers have declared slowness akin to slimness; self-described “foodies” lament that there’s “nothing worse” than watching a guest inhale a painstakingly prepared meal. There are even children’s songs that warn against the perils of eating too fast. My family and friends—most of whom have long since learned to avoid “splitting” entrees with me—often comment on my speed. “Slow down,” one of my aunts fretted at a recent meal. “Don’t you know that eating fast is bad for you?”

    I do, or at least I have heard. Over the decades, a multitude of studies have found that people who eat faster are more likely to consume more calories and carry more weight; they’re also more likely to have high blood pressure and diabetes. “The data are very robust,” says Kathleen Melanson of the University of Rhode Island; the evidence holds up when researchers look across geographies, genders, and age. The findings have even prompted researchers to conduct eating-speed interventions, and design devices—vibrating forks and wearable tech—that they hope will slow diners down.

    But the widespread mantra of go slower probably isn’t as definitive or universal as it at first seems. Fast eaters like me aren’t necessarily doomed to metabolic misfortune; many of us can probably safely and happily keep hoovering our meals. Most studies examining eating speed rely on population-level observations taken at single points in time, rather than extended clinical trials that track people assigned to eat fast or slow; they can speak to associations between pace and certain aspects of health, but not to cause and effect. And not all of them actually agree on whether protracted eating boosts satisfaction or leads people to eat less. Even among experts, “there is no consensus about the benefits of eating slow,” says Tany E. Garcidueñas-Fimbres, a nutrition researcher at Universitat Rovira i Virgili, in Spain, who has studied eating rates.

    The idea that eating too fast could raise certain health risks absolutely does make sense. The key, experts told me, is the potential mismatch between the rate at which we consume nutrients and the rate at which we perceive and process them. Our brain doesn’t register fullness until it’s received a series of cues from the digestive tract: chewing in the mouth, swallowing down the throat; distension in the stomach, transit into the small intestine. Flood the gastrointestinal tract with a ton of food at once, and those signals might struggle to keep pace—making it easier to wolf down more food than the gut is asking for. Fast eating may also inundate the blood with sugar, risking insulin resistance—a common precursor to diabetes, says Michio Shimabukuro, a metabolism researcher at Fukushima Medical University, in Japan.

    The big asterisk here is that a lot of these ideas are still theoretical, says Janine Higgins, a pediatric endocrinologist at the University of Colorado Anschutz Medical Campus, who’s studied eating pace. Research that merely demonstrates an association between fast eating and higher food intake cannot prove which observation led to the other, if there’s a causal link at all. Some other factor—stress, an underlying medical condition, even diet composition—could be driving both. “The good science is just completely lacking,” says Susan Roberts, a nutrition researcher at Tufts University.

    Scientists don’t even have universal definitions of what “slow” or “fast” eating is, or how to measure it. Studies over the years have used total meal time, chew speed, and other metrics—but all have their drawbacks. Articles sometimes point to a cutoff of 20 minutes per meal, claiming that’s how long the body takes to feel full. But Matthew Hayes, a nutritional neuroscientist at the University of Pennsylvania, criticized that as an oversimplification: Satisfaction signals start trickling into the brain almost immediately when we eat, and fullness thresholds vary among people and circumstances. Studies that ask volunteers to rate their own speeds have issues too: People often compare themselves with friends and family, who won’t represent the population at large. Eating rate can also fluctuate over a lifetime or even a day, depending on hunger, stress, time constraints, the pace of present company, even the tempo of background music.

    In an evolutionary sense, all of us humans eat absurdly fast. We eat “orders of magnitude quicker” than our primate relatives, just over one hour a day compared with their almost 12, says Adam van Casteren, a feeding ecologist at the University of Manchester, in England. That’s thanks largely to how we treat our food: Fire, tools such as knives, and, more recently, chemical processing have softened nature’s raw ingredients, liberating us from “the prison of mastication,” as van Casteren puts it. Modern Western diets have taken that pattern to an extreme. They’re chock-full of ultra-processed foods, so soft and sugar- and fat-laden that they can be gulped down with nary a chew—which could be one of the factors that drive faster eating and chronic metabolic ills.

    In plenty of circumstances, slowing down will come with perks, not least because it could curb the risk of choking or excess gas. It could also temper blood-sugar spikes in people with diets heavy in processed foods—which whiz through the digestive tract, Roberts told me, though the healthier move would probably be eating fewer of those foods to begin with. And some studies focused on people with high BMI, including Melanson’s, have shown that eating slower can aid weight loss. But, she cautioned, those results won’t necessarily apply to everyone.

    The main impact of leisurely eating may not even be about chewing rates or bite size per se, but about helping people eat more mindfully. “A lot of us are distracted when we eat,” says Fatima Cody Stanford, an obesity-medicine physician at Massachusetts General Hospital. “And so we are missing our hunger and satiety cues.” In countries such as the United States, people also have to wrestle with the immense pressure “to be done with lunch really fast,” Herman Pontzer, an anthropologist at Duke University, told me. Couple that with the fast foods we tend to reach for, and maybe it’s no shock that people don’t feel satisfied as they scarf down their meals.

    The point here isn’t to demonize slow eating; in the grand scheme of things, it seems a pretty healthful thing to do. At the same time, that doesn’t mean that “eat slow” should be a blanket command. For people already eating a lot of high-fiber foods—which the body naturally processes ploddingly—Roberts doesn’t think sluggish chewing has much to add. The extolling of slow eating is, at best, “a half truth,” Hayes told me, that’s become easy to exploit.

    I do feel self-conscious when I’m the first person at the table to finish by a mile, and I don’t enjoy the stares and the comments about my “big appetite.” Certain super-slow eaters might get teased for making others wait, but they’re generally not getting chastised for ruining their health. When I asked experts if it was harmful to eat too slowly, several of them told me they’d never even considered it—and that the answer was probably no.

    Still, for the most part, I’m happy to be the Usain Bolt of chewing. My hot foods stay hot, and my cold foods stay cold. I’ve intermittently tried slow eating over the years, deploying some of the usual tricks: smaller utensils, tinier bites, crunchier foods. I even, once, tried to count my chews. The biggest difference I felt, though, wasn’t fullness or more satisfaction; I just kind of hated the way that my mushy food lingered in my mouth.

    Maybe if I’d stuck with slow eating, I would have lost some gassiness, choking risk, or weight—but also, I think, some joy. There’s something to speed-eating that can be plain old fun, akin to the rush of zooming down an empty highway in a red sports car. If I have just an hour-ish (or, knowing me, less) of eating each day, I’d prefer to relish every brisk, indecorous bite.

    Katherine J. Wu

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  • We’ve Had a Cheaper, More Potent Ozempic Alternative for Decades

    We’ve Had a Cheaper, More Potent Ozempic Alternative for Decades

    The Ozempic craze shows no signs of slowing. Demand for the drug, popularly used for weight loss, is so monumental that it is already changing the diet industry and spurring a “marketing bonanza” among the dozens of telehealth start-ups that now prescribe it. A highly public ad campaign from one start-up, Ro, banks on the drug’s simple premise: “A weekly shot to lose weight.”

    Never before has a weight-loss treatment been hyped this way and been able to deliver on its promise. Ozempic itself is technically a diabetes drug, but its active ingredient, semaglutide, has been approved by the FDA for weight loss under the brand name Wegovy, and can reduce a person’s body weight by up to 20 percent through a weekly injection. An even more powerful drug, known as tirzepatide, or Mounjaro, may soon be approved for weight loss, and a host of new medications are coming down the pipeline. All signs suggest that America is on the verge of a weight-loss revolution.

    But for people with obesity, semaglutide isn’t even the most effective weight-loss treatment around—not even close. Bariatric surgery, which has existed for many decades, is still significantly more potent. This class of procedures, which, broadly speaking, reconfigure the digestive system so people feel less hungry and more full, is considered to be the “gold standard” for treating obesity, Holly Lofton, an obesity-medicine physician at NYU, told me. Most people experience weight loss of 50 percent and, with one procedure, up to 80 percent, according to the Cleveland Clinic.

    Despite the impressive abilities of the new crop of weight-loss drugs—and bold assertions that such drugs could someday replace surgery outright—several doctors told me that surgery will likely continue to be the top-line treatment for obesity, even as the medications improve. People may seek out treatment with the new drugs because they’re so popular, but “long term, there will be an increase in surgery,” Shauna Levy, a professor specializing in bariatric surgery at Tulane University School of Medicine, told me. The new drugs, however potent, may be less a revolutionary fix for obesity and more a powerful tool for treating it—one of many that already exist.


    Unlike semaglutide, bariatric surgery, first introduced in the 1950s, took several decades to become accepted by the medical community. Initial attempts made people so sick that, at times, the surgery had to be reversed. The term bariatric surgery refers to several different procedures that reshape the gastrointestinal tract so that it absorbs fewer nutrients, holds less food, or both. These days, the most commonly performed surgery is called a Roux-en-Y, which shrinks the stomach to the size of a walnut—so people need less food to feel satisfied—and then reconnects it to the small intestine in a Y shape, rather than linearly. This gastric bypass lets food circumvent most of the stomach, leaving fewer opportunities for the body to harvest nutrients. In another common procedure, surgeons sculpt the stomach into a banana-size “sleeve” and toss the rest; another common type involves rerouting the intestines in a way that minimizes the area where calories can be absorbed.

    But bariatric surgery does more than shrink gastrointestinal real estate. It exerts a less visible but equally powerful effect on the many different hormones that control hunger. Some procedures remove the part of the gut that produces the “hunger hormone,” ghrelin, while the rerouting of food through a Roux-en-Y ramps up the release of “incretin” hormones that create the feeling of fullness after eating.

    In a sense, the new weight-loss drugs are essentially trying to re-create the effects of bariatric surgery: The success of these drugs is due to their ability to mimic the incretin hormones and get people to feel satisfied with less food. Semaglutide masquerades as the hormone GLP-1, whereas Mounjaro poses as both GLP-1 and GIP. But these are just two hormones; bariatric surgery “touches on multiple different hormones and different pathways” and, as such, is “more comprehensive,” Levy said. In one study, Mounjaro, considered the most powerful of the current crop of medications, led to 20 percent or more weight loss in 57 percent of people who took the highest dose—an impressive feat, but still a far cry from what is possible with surgery. Similarly, Ozempic and Mounjaro, both technically diabetes drugs, have powerful effects on blood-sugar levels over time, but many surgery patients “leave the hospital already in remission from their diabetes,” Levy said.

    In addition to sheer potency, surgery is also much more affordable than these weight-loss drugs. Unlike the drugs, bariatric surgery is covered by Medicare if the patient meets certain criteria, including having a BMI equal to or greater than 35 and at least one comorbidity related to obesity. Many private insurers cover it too, albeit to varying degrees. Out of pocket, surgery costs $15,000 to $25,000—not cheap, but still cheaper than shelling out more than $1,000 a month indefinitely. “The patient must understand that they have to continue taking medication forever,” Lofton said. People who stop taking semaglutide generally regain the weight they lost. Lofton told me about one patient who had to forgo rent just to pay for the drugs: Factoring in insurance, “you can pay for three months of medicine and then have surgery at the same price.”

    Neither treatment, of course, is without its potential downsides. Semaglutide can cause temporary but nasty side effects such as nausea, vomiting, and diarrhea—and though it is considered safe for treating obesity, long-term data on this usage span just two years. Because many surgeries are done laparoscopically—using only tiny incisions—mortality is vanishingly low, and many patients go home after two or three days; full recovery usually takes four to six weeks. In the long term, complications such as hernias, gallstones, and low blood sugar can develop.

    But there’s a reason bariatric surgery has not led to a weight-loss revolution of the kind that now gets associated with semaglutide. Despite its dramatic effects, and obesity’s prevalence across America, only 1 percent of people eligible for surgery actually get it. People hesitate for many reasons, medical and otherwise, but the most pervasive issue is a lack of awareness that surgery is even a safe or realistic option for weight loss. Bariatric surgery is plagued by stigma even within the medical community: In the 1990s, it was dismissed as a “barbaric” way to address an issue that, many believed, could be treated with diet and exercise. “There are a lot of primary-care doctors who are not talking enough about surgery” because they were trained with that old mindset, Levy said. ​​It doesn’t help that bariatric surgery hasn’t exactly been a media sensation, with few high-profile patient advocates beyond Al Roker and Mariah Carey. In contrast, stories of celebrities on weight-loss drugs abound. Unlike surgery, semaglutide has the potential to be taken recreationally.


    The advantages that surgery has over weight-loss drugs may change as the drugs become more potent and eventually cheaper. But for now, semaglutide won’t dramatically shift the way obesity is treated, doctors told me—in fact, these new drugs may act as a conduit to surgery itself. Levy predicts that their sheer popularity will trigger a brief dip in the bariatric-surgery rate, but as price remains an issue, and people with obesity are unable to reach their weight-loss goals on the drugs alone, “they may start opening their mind to surgery.”

    Certainly, in some patients, weight-loss drugs alone could lead to lasting weight loss. And they can benefit those who are overweight but don’t qualify for surgery. But more widely, these drugs will likely be used in tandem with bariatric surgery to produce more dramatic, longer-lasting results, experts told me. “I don’t see this as an either/or,” Fatima Cody Stanford, an obesity-medicine physician at Massachusetts General Hospital and Harvard Medical School, told me. “I see it as surgery plus medicine.”

    Drugs can help fill in any gaps that surgery leaves behind. Weight can rebound after a procedure, because the body has a way of rebalancing itself; hormones that were tamped down due to bariatric surgery, Stanford said, can “start to reemerge with a vengeance.” About a fifth of people, and perhaps even more, regain a significant amount of weight—15 percent or more—two to five years after surgery. All of the doctors I spoke with said that medication could be a powerful tool to prevent post-surgery weight rebounds—though to keep that weight off, the medication would still have to be taken in perpetuity. Stanford estimated that more than 90 percent of her patients are on weight-loss drugs after surgery—and not necessarily semaglutide; older medications often suffice. Drugs could also be used to help people prepare for surgery, Lofton said. Some doctors encourage patients to lose weight beforehand to decrease the risk of complications such as blood clots, heart attack, and infection.

    Despite the hype, weight-loss drugs were never a perfect treatment for obesity. Neither is bariatric surgery, for that matter. “It is not a cure,” Lofton told me. A cure, she explained, would ensure that hunger doesn’t return and that fat cells don’t get bigger, a hallmark of obesity: “We have nothing that does that”—not even more potent next-gen drugs will provide a permanent fix. But the effect of combining surgery and medication could come close, she said.

    That no cure for obesity exists is evidence of its complexity. All of the experts I spoke with pointed out that obesity has long been misunderstood as a failure of personal will, as laziness or gluttony. That misunderstanding has led to inadequate care: Many people who regain weight after a bariatric procedure are made to feel by their doctors like they “wasted the surgery,” even if human biology is to blame, Stanford said. Ozempic and other weight-loss medications frame obesity as a condition that can be treated with drugs—in other words, a disease. Patients on those medications may realize, “Hey, maybe it’s not just me being lazy this whole time—maybe there is science to it and an actual disease here,” said Levy. Collectively understanding obesity as an illness that exists alongside heart disease and cancer—diseases routinely treated with medication and surgery—instead of as a matter of personal inadequacy will have far more profound impacts on people with obesity than any drug alone.

    Yasmin Tayag

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