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  • You’re Probably Drinking Enough Water

    You’re Probably Drinking Enough Water

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    As recently as the 1990s, Jodi Stookey, a nutrition consultant based in California, remembers hydration research being a very lonely field. The health chatter was all about fat and carbs; children routinely subsisted on a single pouch of Capri Sun a day. Even athletes were discouraged from sipping on fields and race tracks, lest the excess liquid slow them down. “I can’t tell you how many people told me I was stupid,” Stookey told me, for being one of water’s few advocates.

    But around the turn of the millennium, hydration became an American fixation. Celebrities touted water’s benefits in magazines; branded bottles overran supermarket shelves. Academic research on hydration underwent a mini-boom. After ages of being persistently parched, we were suddenly all drinking, drinking, drinking, because we felt like we should. It was an aquatic about-face—and it didn’t make total scientific sense.

    The importance of hydration, in the abstract, is indisputable. Water keeps our organs chugging and our muscles agile; it helps distribute nutrients through the body and maintains our inner thermostat. Take it away, and cells inevitably die. But the concrete specifics of adequate water intake are still, in large part, a mess. For hydration, “there are no clear numbers, or a threshold you have to maintain,” says Yasuki Sekiguchi, a sports-performance scientist at Texas Tech University. Experts don’t agree on how much water people need, or the best ways to tell when someone should drink; they differ on how to measure hydration, which beverages are adequately hydrating, and how much importance to attribute to thirst. They have yet to reach quorum on what hydration—a process that’s sustained life since its primordial inception—fundamentally is. The murkiness has left the field of hydration research, still relatively young and relatively small, rife with “vicious camps against each other,” says Tamara Hew-Butler, an exercise physiologist at Wayne State University.

    Forget, for instance, one of water’s most persistent myths: the oft-repeated advice to down eight 8-ounce glasses of water each day. No one can say for certain, but one theory is that the idea  sprouted from a misinterpretation of a nutrition document from the 1940s, which stated that 2.5 liters of water a day (that is, approximately 10 8-ounce glasses) was “a suitable allowance for adults” in “most instances.” The guidance also noted, in the very same paragraph, “Most of this quantity is contained in prepared foods.” But the bigger issue is this: Probably no single number for water intake will ever suffice—not for a population of people with varying weights, genetics, diets, and activity levels, living in varying climates. Even within an individual, what’s best will change through a lifetime. The answer to How much water should I be drinking? is invariably Uh, it really depends.


    Today’s hydration zeitgeist seems to hold that no amount of water is too much. The market teems with intake-tracking smartphone apps and time-stamped bottles that cheer drinkers toward hydration goals as high as a gallon a day—a quota astronomical enough to be stressful, even dangerous, should people flood their bodies all at once. But America’s hydration hype machine “has established a narrative that we are all walking around dehydrated, and need to drink more,” Hew-Butler told me. It’s no wonder that some people have reported legitimate anxiety over falling short on water intake.

    No single source sold America on water. But a 2021 episode of the podcast Decoder Ring points to Gatorade as one of the first companies to pitch dehydration as a health problem—while simultaneously offering a cure. The company’s sports drinks were originally billed as thirst-quenchers, designed to stave off performance dips. But by the 1980s, Decoder Ring reported, the Gatorade Sports Science Institute was churning out data that supported the benefits of drinking before the mouth got parched. A decade later, the American College of Sports Medicine was recommending that athletes consume “the maximal amount” of water they could stand to keep down.

    Around the same time, during the fitness craze of the ’70s and ’80s, water was acquiring another identity: the enlightened socialite’s clean drink of choice. When European companies such as Perrier and Evian brought their bottled water to North America, they found a market among those wanting a high-end, calorie- and sweetener-free alternative to sodas, alcohol, and juice. Water “had this healthy, good-for-you halo,” says Michael Bellas, the chair and CEO of the Beverage Marketing Corporation. “There were no negatives.” In 2016, water became the U.S.’s leading bottled beverage, a title it has maintained since.

    As water’s market share grew, so did its mythos. Companies hocked the illusion that their products could make people not just healthier but “sexier and more popular,” Peter Gleick, the author of The Three Ages of Water, told me. Hydration was so clearly vital to life that truth-adjacent ideas about its benefits, many of them pushed by prominent people, were easy to buy. Even concerns over single-use plastic bottles could not slow water’s roll: In response, the world cooked up eco-friendly Yetis, HydroFlasks, and Nalgenes, and made those trendy, too.


    It’s not that water isn’t healthy. There’s just no evidence to show that guzzling tons of water can fix all our ailments. For people prone to kidney stones and UTIs, drinking more has been shown to cut down on risks; as a swap for sugary beverages, it can also help with weight loss. But for a variety of other issues—such as heart disease, metabolic issues, and cancer—the data is often “really mixed,” Hew-Butler told me. Although researchers have sometimes found evidence that dehydration may raise certain conditions’ risks, that doesn’t automatically imply the inverse—that extra water intake then lowers risk from a typical baseline. At very rare extremes, overdoing it on water can kill us, too.

    The connections between hydration and health are shaky enough that health authorities have been reluctant to push a strict recommended daily allowance, like the ones that exist for various vitamins. Instead, the National Academy of Medicine proposes a tentative “adequate intake”: 3.7 liters of total water intake for men, and 2.7 for women (both including hydration from food). Recently, Abigail Colburn, a physiology researcher at Yale, and her colleagues ran an analysis that concluded those figures were sound. Still, the numbers came from population surveys, published in the early aughts, of the amounts that Americans were already drinking—a reflection of how things were, but not necessarily how they should be. And they represent medians within a huge range. Over the years, multiple studies have documented people living, by all appearances healthfully, on daily water budgets that span less than a liter to four, five, or six—sometimes more.

    If researchers don’t agree on how much water is good, they also differ on how little water is bad: the point at which dehydration starts to become a problem—or how long people can linger at that threshold without raising long-term health risks.

    A bit of water loss should be completely fine. Fluid status is, by design, “a constantly changing state,” Colburn told me. When the body doesn’t take in enough water to recoup the liquid it’s lost—as it naturally does throughout the day, via sweat, urine, and breath—the brain releases a hormone called vasopressin that prompts the kidneys to hold onto fluid. The urine gets darker and less voluminous; eventually, blood-salt levels rise, and the mouth and throat ache with thirst. The goal is to get the body to excrete less water out and take more in so we don’t wring our vital tissues dry. Life forms have evolved to tread carefully down this cascade of steps, and the flexibility is built in—much like a rubber band that snaps back after being stretched and released.

    But some researchers have started to worry about repeatedly asking the body to compensate for less than optimal hydration—stretching the band over and over again. The issue isn’t chronic dehydration, Colburn told me, but a subtler precursor state called underhydration, which occurs after a lack of water intake has prompted the body to conserve but before the appearance of signals such as thirst. It’s not clear how worrying teetering on that precipice is. In the same way a rubber band is “designed to stretch,” our fluid balance is built to bounce back, says Evan Johnson, a hydration expert at the University of Wyoming. Over time, though, wear and tear could add up, and resilience could drop.

    Tracking those outcomes gets even more complicated when researchers try to quantify how dehydrated individual people are—another thing that experts can’t agree on. “We really don’t have a gold standard for measuring the all-encompassing term of hydration,” Johnson told me, especially one that’s both simple and cheap, and can account for body water’s constant flux. Which leaves scientists with imperfect proxies. Broadly speaking, there’s a urine camp and a blood camp, Stookey told me. Those in the pee camp tend to be hydration conservatives. A change in urine color or volume, they argue, is an early sign—well in advance of thirst—of impending dehydration. The blood-camp crew is more laissez-faire. Diet, medications, and supplements can all alter the shade of urine, making it a fickle clue; Hew-Butler for instance, defines true dehydration as what happens when the plasma’s gotten saltier than usual, to the point where cells have started to shrink—a sign that retaining water is no longer sufficient, and that the body needs to drink.


    Which camp researchers fall into influences how bad they think America’s hydration problem is. “When you draw blood, most people are within a normal range if they’re not thirsty,” Hew-Butler told me. But Stookey, who’s firmly in the pee camp, contends that a majority of Americans are “walking around dehydrated” and should be drinking far more. Colburn, too, would rather err on the side of heeding urine’s warning signs. By the time thirst kicks in, “you’re already in a dangerous zone,” she told me.

    There can be a middle ground. Sekiguchi, of Texas Tech, told me that for most young, healthy people who are spending plenty of time in the air-conditioned indoors—as so many Americans do—it’s probably fine to just drink when thirsty. (That advice works less well for older people, because the sensation of thirst tends to dull with age.) When specific circumstances shift—a stint of heavy exercise, a week of toasty days—people can take notice, and adjust accordingly.

    But guidelines for typical water intake, under typical conditions, are quickly going out the window as heat waves get more frequent and intense. When temperatures skyrocket and humidity makes otherwise-cooling sweat stick stubbornly on skin, our bodies need more water to keep cool and functional, beyond what thirst alone might dictate. Part of the problem is that thirst vanishes more quickly than the body rehydrates, Sekiguchi told me, which means that people who drink until they think they’re sated tend to replace only a fraction of the fluids that they’ve lost.

    “We’re never going to be able to tell people an exact number,” Colburn told me, for how much to drink. But in reality, many of the healthy people most worried about fine-tuning their hydration to a perfect level are probably among those that least need to fret. The dangers of water tend to happen not in those middle grounds, but at its extremes—especially when failing infrastructure hampers access to water, or contamination makes it undrinkable. Many of the populations that are most vulnerable to dehydration’s effects also happen to be the same groups that probably aren’t getting enough to drink, Johnson told me. While bottled-water markets boom, plenty of pockets of the U.S. still lack consistent access to safe, reliable water from the tap. And the situation is even worse in many places abroad. Perhaps nothing reminds us of water’s power like dramatic deficit: Water, simply, is what keeps us alive.


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    Katherine J. Wu

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  • Long COVID Has Forced a Reckoning for One of Medicine’s Most Neglected Diseases

    Long COVID Has Forced a Reckoning for One of Medicine’s Most Neglected Diseases

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    Kira Stoops lives in Bozeman, Montana—a beautiful mountain town where it sometimes feels like everyone regularly goes on 50-mile runs. Stoops, however, can’t walk around her own block on most days. To stand for more than a few minutes, she needs a wheeled walker. She reacts so badly to most foods that her diet consists of just 12 ingredients. Her “brain fog” usually lifts for a mere two hours in the morning, during which she can sometimes work or, more rarely, see friends. Stoops has myalgic encephalomyelitis, or chronic fatigue syndrome (ME/CFS). “I’m considered a moderate patient on the mild side,” she told me.

    ME/CFS involves a panoply of debilitating symptoms that affect many organ systems and that get worse with exertion. The Institute of Medicine estimates that it affects 836,000 to 2.5 million people in the U.S. alone, but is so misunderstood and stigmatized that about 90 percent of people who have it have never been diagnosed. At best, most medical professionals know nothing about ME/CFS; at worst, they tell patients that their symptoms are psychosomatic, anxiety-induced, or simply signs of laziness. While ME/CFS patients, their caregivers, and the few doctors who treat them have spent years fighting for medical legitimacy, the coronavirus pandemic has now forced the issue.

    A wide variety of infections can cause ME/CFS, and SARS-CoV-2, the coronavirus that causes COVID-19, is no different: Many cases of long COVID are effectively ME/CFS by another name. The exact number is hard to define, but past studies have shown that 5 to 27 percent of people infected by various pathogens, including Epstein-Barr virus and the original SARS, develop ME/CFS. Even if that proportion is 10 times lower for SARS-CoV-2, the number of Americans with ME/CFS would still have doubled in the past three years. “We’re adding an immense volume of patients to an already dysfunctional and overburdened system,” Beth Pollack, a scientist at MIT who studies complex chronic illnesses, told me.

    The U.S. has so few doctors who truly understand the disease and know how to treat it that when they convened in 2018 to create a formal coalition, there were only about a dozen, and the youngest was 60. Currently, the coalition’s website lists just 21 names, of whom at least three have retired and one is dead, Linda Tannenbaum, the CEO and president of the Open Medicine Foundation, told me. These specialists are concentrated on the coasts; none work in the Midwest. American ME/CFS patients may outnumber the population of 15 individual states, but ME/CFS specialists couldn’t fill a Major League Baseball roster. Stoops, who is 39, was formally diagnosed with ME/CFS only four years ago, and began receiving proper care from two of those specialists—Lucinda Bateman of the Bateman Horne Center and David Kaufman from the Center for Complex Diseases. Bateman told me that even before the pandemic, she could see fewer than 10 percent of the patients who asked for a consultation. “When I got into those practices, it was like I got into Harvard,” Stoops told me.

    ME/CFS specialists, already overwhelmed with demand for their services, now have to decide how to best use and spread their knowledge, at a time when more patients and doctors than ever could benefit from it. Kaufman recently discharged many of the more stable ME/CFS patients in his care—Stoops among them—so that he could start seeing COVID long-haulers who “were just making the circuit of doctors and getting nowhere,” he told me. “I can’t clone myself, and this was the only other way to” make room for new patients.

    Bateman, meanwhile, is feverishly focused on educating other clinicians. The hallmark symptom of ME/CFS—post-exertional malaise, or PEM—means even light physical or mental exertion can trigger major crashes that exacerbate every other symptom. Doctors who are unfamiliar with PEM, including many now running long-COVID clinics, can unwittingly hurt their patients by encouraging them to exercise. Bateman is racing to spread that message, and better ways of treating patients, but that means she’ll have to reduce her clinic hours.

    These agonizing decisions mean that many existing ME/CFS patients are losing access to the best care they had found so far—what for Stoops meant “the difference between being stuck at home, miserable and in pain, and actually going out once or twice a day, seeing other humans, and breathing fresh air,” she told me. But painful trade-offs might be necessary to finally drag American medicine to a place where it can treat these kinds of complex, oft-neglected conditions. Kaufman is 75 and Bateman is 64. Although both of them told me they’re not retiring anytime soon, they also won’t be practicing forever. To make full use of their expertise and create more doctors like them, the medical profession must face up to decades spent dismissing illnesses such as ME/CFS—an overdue reckoning incited by long COVID. “It’s a disaster possibly wrapped up in a blessing,” Stoops told me. “The system is cracking and needs to crack.”


    Many ME/CFS specialists have a deep knowledge of the disease because they’ve experienced it firsthand. Jennifer Curtin, one of the youngest doctors in the field, has two family members with the disease, and had it herself for nine years. She improved enough to make it through medical school and residency training, which showed her that ME/CFS “just isn’t taught,” she told me. Most curricula don’t include it; most textbooks don’t mention it.

    Even if doctors learn about ME/CFS, America’s health-care system makes it almost impossible for them to actually help patients. The insurance model pushes physicians toward shorter visits; 15 minutes might feel luxurious. “My average visit length is an hour, which doesn’t include the time I spend going over the patient’s 500 to 1,700 pages of records beforehand,” Curtin said. “It’s not a very scalable kind of care.” (She works with Kaufman at the Center for Complex Diseases, which bills patients directly.) This also explains why the cohort of ME/CFS clinicians is aging out, with little young blood to refresh them. “Hospital systems want physicians to see lots of patients and they want them to follow the rules,” Kaufman said. “There’s less motivation for moving into areas of medicine that are more unknown and challenging.”

    ME/CFS is certainly challenging, not least because it’s just “one face of a many-sided problem,” Jaime Seltzer, the director of scientific and medical outreach at the advocacy group MEAction, told me. The condition’s root causes can also lead to several distinct but interlocking illnesses, including mast cell activation syndrome, Ehlers-Danlos syndrome, fibromyalgia, dysautonomia (usually manifesting as POTS), and several autoimmune and gastrointestinal disorders. “I’m still amazed at how often patients come in with Complaint No. 1, and then I find five to seven of the other things,” Kaufman said. These syndromes collectively afflict many organ systems, which can baffle doctors who’ve specialized in just one. Many of them disproportionately affect women, and are subject to medicine’s long-standing tendency to minimize or psychologize women’s pain, Pollack told me: An average woman with Ehlers-Danlos syndrome typically spends 16 years getting a diagnosis, while a man needs only four.

    People with long COVID might have many of these conditions and not know about any—because their doctors don’t either. Like ME/CFS, they rarely feature in medical training, and it’s hard to “teach someone about all of them when they’ve never heard of any of them,” Seltzer said. Specialists like Bateman and Kaufman matter because they understand not just ME/CFS but also the connected puzzle pieces. They can look at a patient’s full array of symptoms and prioritize the ones that are most urgent or foundational. They know how to test for conditions that can be invisible to standard medical techniques: “None of my tests came back abnormal until I saw an ME/CFS doctor, and then all my tests came back abnormal,” said Hannah Davis of the Patient-Led Research Collaborative, who has had long COVID since March 2020.

    ME/CFS specialists also know how to help, in ways that are directly applicable to cases of long COVID with overlapping symptoms. ME/CFS has no cure but can be managed, often through “simple, inexpensive interventions that can be done through primary care,” Bateman told me. Over-the-counter antihistamines can help patients with inflammatory problems such as mast cell activation syndrome. Low doses of naltrexone, commonly used for addiction disorders, can help those with intense pain. A simple but rarely administered test can show if patients have orthostatic intolerance—a blood-flow problem that worsens other symptoms when people stand or sit upright. Most important, teaching patients about pacing—carefully sensing and managing your energy levels—can prevent debilitating crashes. “We don’t go to an ME/CFS clinic and walk out in remission,” Stoops told me. “You go to become stabilized. The ship has 1,000 holes, and doctors can patch one before the next explodes, keeping the whole thing afloat.”

    That’s why the prospect of losing specialists is so galling. Stoops understands why her doctors might choose to focus on education or newly diagnosed COVID long-haulers, but ME/CFS patients are “just so lost already, and to lose what little we have is a really big deal,” she said. Kaufman has offered to refer her to generalist physicians or talk to primary-care doctors on her behalf. But it won’t be the same: “Having one appointment with him is like six to eight appointments with other practitioners,” she said. He educates her about ME/CFS; with other doctors, it’s often the other way round. “I’m going to have to work much harder to receive a similar level of care.”

    At least, she will for now. The ME/CFS specialists who are shifting their focus are hoping that they can use this moment of crisis to create more resources for everyone with these diseases. In a few years, Bateman hopes, “there will be 100 times more clinicians who are prepared to manage patients, and many more people with ME/CFS who have access to care.”


    For someone who is diagnosed with ME/CFS today, the landscape already looks very different than it did just a decade ago. In 2015, the Institute of Medicine published a landmark report redefining the diagnostic criteria for the disease. In 2017, the CDC stopped recommending exercise therapy as a treatment. In 2021, Bateman and 20 other clinicians published a comprehensive guide to the condition in the journal of the Mayo Clinic. For any mainstream disease, such events—a report, a guideline revision, a review article—would be mundane. For ME/CFS, they felt momentous. And yet, “the current state of things is simply intolerable,” Julie Rehmeyer, a journalist with ME/CFS, told me. Solving the gargantuan challenge posed by complex chronic diseases demands seismic shifts in research funding, medical training, and public attitudes. “Achieving shifts like that takes something big,” Rehmeyer said. “Long COVID is big.”

    COVID long-haulers have proved beyond any reasonable doubt that acute viral infections can leave people chronically ill. Many health-care workers, political-decision makers, and influencers either know someone with long COVID or have it themselves. Even if they still don’t know about ME/CFS, their heightened awareness of post-viral illnesses is already making a difference. Mary Dimmock’s son developed ME/CFS in 2011, and before the pandemic, one doctor in 10 might take him seriously. “Now it’s the flip: Only one doctor out of 10 will be a real jerk,” Dimmock told me. “I attribute that to long COVID.”

    But being believed is the very least that ME/CFS patients deserve. They need therapeutics that target the root causes of the disease, which will require a clear understanding of those causes, which will require coordinated, well-funded research—three things ME/CFS has historically lacked. But here, too, “long COVID is going to be a catalyst,” Amy Proal, the president of the Polybio Research Foundation, told me. She is leading the Long Covid Research Initiative—a group of scientists, including ME/CFS researchers, that will use state-of-the-art techniques to see exactly how the new coronavirus causes long COVID, and rapidly push potential treatments through clinical trials. The National Institutes of Health has also committed $1.15 billion to long-COVID research, and while some advocates are concerned about how that money will be spent, Rehmeyer notes that the amount is still almost 80 times greater than the paltry $15 million spent on ME/CFS every year—less than any other disease in the NIH’s portfolio, relative to its societal burden. “Even if 90 percent is wasted, we’d be doing a lot better,” she said.

    While they wait for better treatments, patients also need the medical community to heed the lessons that they and their clinicians have learned. For example, the American Academy for Family Physicians website still wrongly recommends exercise therapy and links ME/CFS to childhood abuse. “That group of doctors is very important to these patients,” Dimmock said, “so what does that say to them about what this disease is all about?”

    Despite all evidence to the contrary, many clinicians and researchers still don’t see ME/CFS as a legitimate illness and are quick to dismiss any connection between it and long COVID. To ensure that both groups of patients get the best possible treatments, instead of advice that might harm them, ME/CFS specialists are working to disseminate their hard-won knowledge. Bateman and her colleagues have been creating educational resources for clinicians and patients, continuing-medical-education courses, and an online lecture series. Jennifer Curtin has spent two years mapping all the decisions she makes when seeing a new patient, and is converting those into a tool that other clinicians can use. As part of her new start-up, called RTHM, she’s also trying to develop better ways of testing for ME/CFS and its related syndromes, of visualizing the hefty electronic health records that chronically ill patients accumulate, and of tracking the treatments they try and their effects. “There are a lot of things that need to be fixed for this kind of care to be scalable,” Curtin told me.

    Had such shifts already occurred, the medical profession might have had more to offer COVID long-haulers beyond bewilderment and dismissal. But if the profession starts listening to the ME/CFS community now, it will stand the best chance of helping people being disabled by COVID, and of steeling itself against future epidemics. Pathogens have been chronically disabling people for the longest time, and more pandemics are inevitable. The current one could and should be the last whose long-haulers are greeted with disbelief.

    New centers that cater to ME/CFS patients are already emerging. RTHM is currently focused on COVID long-haulers but will take on some of David Kaufman’s former patients in November, and will open its waiting list to the broader ME/CFS community in December. (It is currently licensed to practice in just five states but expects to expand soon.) David Putrino, who leads a long-COVID rehabilitation clinic in Mount Sinai, is trying to raise funds for a new clinic that will treat both long COVID and ME/CFS. He credits ME/CFS patients with opening his eyes to the connection between long COVID and their condition.

    Every ME/CFS patient I’ve talked with predicted long COVID’s arrival well before most doctors or even epidemiologists started catching up. They know more about complex chronic illnesses than many of the people now treating long COVID do. Despite having a condition that saps their energy, many have spent the past few years helping long-haulers navigate what for them was well-trodden terrain: “I did barely anything but work in 2020,” Seltzer told me. Against the odds, they’ve survived. But the pandemic has created a catalytic opportunity for the odds to finally be tilted in their favor, “so that neither patients nor doctors of any complex chronic illness have to be heroes anymore,” Rehmeyer said.

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    Ed Yong

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  • Lowering the Cost of Insulin Could Be Deadly

    Lowering the Cost of Insulin Could Be Deadly

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    When I heard that my patient was back in the ICU, my heart sank. But I wasn’t surprised. Her paycheck usually runs short at the end of the month, so her insulin does too. As she stretches her supply, her blood sugar climbs. Soon the insatiable thirst and constant urination follow. And once her keto acids build up, her stomach pains and vomiting start. She always manages to make it to the hospital before the damage reaches her brain and heart. But we both worry that someday, she won’t.

    The Inflation Reduction Act, passed last month, aims to help people like her by lowering the cost of insulin across America. Although efforts to expand protections to privately insured Americans were blocked in the Senate, Democrats succeeded in capping expenses for the drug among Americans on Medicare at $35 a month, offering meaningful savings for our seniors, some of whom will save hundreds of dollars a month thanks to the measure. In theory, the policy (and similar ones at the state level) will help the estimated 25 percent of Americans on insulin who have been forced to ration the drug because of cost, and will prevent some of the 600 annual American deaths from diabetic ketoacidosis, the fate from which I’m trying to save my patient.

    Indeed, laws capping co-payments for insulin are welcome news both financially and medically to patients who depend on the drug for survival. However, in their current version, such laws might backfire, leading to even more diabetes-related deaths overall.

    How could that be true? Thanks to the development of new drugs, insulin’s role in diabetes treatment has been declining over the past decade. It remains essential to the small percent of patients with type 1 diabetes, including my patient. But for the 90 percent of Americans with diabetes who have type 2, it should not routinely be the first-, second-, or even third-line treatment. The reasons for this are many: Of all diabetes medications, insulin carries the highest risk of causing dangerously low blood sugar. The medication most commonly comes in injectable form, so administering it usually means painful needle jabs. All of this effort is rewarded with (usually unwanted) weight gain. Foremost and finally, although insulin is excellent at tamping down high blood sugar—the hallmark of diabetes and the driver of some of its complications—it is not as impressive as other medications at mitigating the most deadly and debilitating consequences of the disease: heart attacks, kidney disease, and heart failure.

    Large clinical trials have shown that two newer classes of diabetes medicines, SGLT2 inhibitors and GLP-1 receptor agonists, outperform alternatives (including insulin) in reducing the risk of these disabling or deadly outcomes. Giving patients these drugs instead of older options over a period of three years prevents, on average, one death for about every 100 treated. And SGLT2 inhibitors and GLP-1 receptor agonists pose less risk of causing dangerously low blood sugar, generally do not require frequent injections, and help patients lose weight. Based on these data, the American Diabetes Association now recommends SGLT2 inhibitors and GLP-1 receptor agonists be used before insulin for most patients with type 2 diabetes.

    When a young person dies from diabetic ketoacidosis because they rationed insulin, the culprit is clear. But when a patient with diabetes dies of a heart attack, the absence of an SGLT2 inhibitor or GLP-1 receptor agonist doesn’t get blamed, because other explanations abound: their uncontrolled blood pressure, the cholesterol medication they didn’t take, the cigarettes they continued to smoke, bad genes, bad luck. But every year, more than 1,000 times more Americans die of heart disease than DKA, and of those 700,000 deaths, a good chunk are diabetes-related. (The exact number remains murky.) Diabetes is a major reason that more than half a million Americans depend on dialysis to manage their end-stage kidney disease, and that about 6 million live with congestive heart failure. The data are clear—SGLT2 inhibitors and GLP-1 receptor agonists could help reduce these numbers.

    Still, uptake of these lifesaving drugs is sluggish. Only about one in 10 people with type 2 diabetes is taking them (fewer still among patients who are not wealthy or white). The main cause is simple and stupid: American laws prioritize profits and patents over patients. Because SGLT2 inhibitors and GLP-1 receptor agonists remain under patent protections, drug companies can charge exorbitant rates for them: hundreds if not thousands of dollars a month, sometimes even more than insulin. Doctors spend hours completing arduous paperwork in the hopes of persuading insurers to help our patients, but we’re frequently denied anyway. And even when we do succeed, many patients are left with painful co-payments and deductibles. The most maddening part is that despite their substantial up-front expense, these medications are quite cost-effective in the long run because they prevent pricey complications down the road.

    This is where addressing the cost of insulin—and only insulin—becomes problematic. Doctors are forced daily to decide between the best medication for our patients and the medication that our patients can afford. Katie Shaw, a primary-care physician with a bustling practice at Johns Hopkins, where I’m a senior resident, told me that plenty of her patients can’t afford SGLT2 inhibitors and GLP-1 receptor agonists. In such instances, Shaw is forced to use older oral alternatives and occasionally insulin. “They’re better than nothing at all,” she said.

    If the cost of insulin is capped on its own, insulin will be more likely to jump in front of SGLT2 inhibitors and GLP-1 receptor agonists in treatment plans. That will mean more disease, more disability, and more death from diabetes.

    Medicare patients might avoid some of these effects thanks to provisions in the IRA allowing Medicare to negotiate drug prices and capping out-of-pocket spending on prescriptions at $2,000 a year. The law also guarantees price negotiations for a handful of medications, but SGLT2 inhibitors and GLP-1 receptor agonists won’t necessarily be on the list. And most Americans are not on Medicare. Already, Shaw said, the patients in her practice who tend to be least able to afford SGLT2 inhibitors and GLP-1 receptor agonists are working-class people with private insurance. Some health centers, including the one Shaw and I work at, enjoy access to a federal drug-discount program that can make patent-protected medications, including SGLT2 inhibitors and GLP-1 receptor agonists, more affordable for the uninsured. But most Americans without insurance aren’t so lucky.

    It would be cruel to choose between a world in which more people with type 2 diabetes are nudged toward a drug that won’t stave off the most dangerous complications, and one in which those with type 1 diabetes are priced out of life. In place of capping the out-of-pocket cost of just insulin, lawmakers should cap the out-of-pocket cost of all diabetes medications. This will both protect Americans dependent on insulin and smooth SGLT2 inhibitors’ and GLP-1 receptor agonists’ path to their revolutionary public-health potential.

    The argument for lowering the cost of these drugs for patients is the same as the argument for insulin affordability: that it is both foolish and inhumane to make lifesaving diabetes medications unaffordable when their use prevents costly and deadly downstream complications.

    Patients like mine need affordable access to insulin. But even more need access to SGLT2 inhibitors and GLP-1 receptor agonists. If the laws stop at insulin, many Americans could die unnecessarily—not from inadequate access to insulin, but from preferential access to it.

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    Michael Rose

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