When Did Obesity Become a Drug Deficiency?

The tragedy of the GLP-1 era will not be that these drugs failed. The tragedy will be if they succeed so spectacularly that an entire generation of physicians stops asking why we needed them.

BY JOSEPH VARON

View original article at Brownstone.org.

Look at almost any photograph of an American crowd taken 60 years ago. It can be a baseball game, a high school graduation, a beach, an airport terminal, a factory floor, or simply people walking down a city street. Something is immediately noticeable to modern eyes, although almost nobody in the photograph would have considered it remarkable: most people are relatively thin.

They did not have continuous glucose monitors, smartphone applications that counted calories and macronutrients, wearable devices reminding them to stand, boutique fitness studios, bariatric surgery centers, or medications capable of producing 15 or 20 percent reductions in body weight. They were not necessarily more virtuous than we are, and they certainly did not possess superior genes. They lived in a different metabolic environment.

The data backs up what we see in those old photos. In the early 1960s, about 13 percent of American adults were obese. By August 2023, that number had jumped to 40.3 percent, with another 31.7 percent considered overweight and nearly one in ten classified as severely obese.[1] This trend isn’t just in the United States. A huge study of over 220 million people from 200 countries found a dramatic global rise in obesity between 1990 and 2022.[2] Our genes haven’t changed much in that time. Something else has.

We’re now at a turning point in medicine. Faced with one of the biggest and fastest changes in human health, we’re treating the results as a condition that needs lifelong medication. The newest drugs are very effective, and that’s important to recognize. Semaglutide and tirzepatide have led to weight loss that older nonsurgical treatments rarely matched.[3,4] Semaglutide has also reduced the risk of major heart problems in people with overweight or obesity and heart disease who didn’t have diabetes.[5] Tirzepatide has greatly improved sleep apnea in people with obesity.[6] These results are significant, and these drugs are much more than cosmetic weight-loss aids.

That’s why we need to look closely at what’s happening now. The problem isn’t that these drugs don’t work; they clearly do. The real concern is that they might work so well that we stop asking why so many people need them in the first place. We could be seeing a major medical breakthrough, but at the same time, we might be accepting that the effects of an unhealthy environment should just be managed with medication. The real question isn’t whether these “GLP-1” drugs are effective. It’s whether their success is making us stop looking for the root causes of the obesity epidemic.

The Epidemic That Became a Diagnosis

For decades, obesity was framed largely as an individual failure. The explanation was simple: people ate too much, exercised too little, and lacked the discipline necessary to change. That view was scientifically inadequate and often cruel. Body weight is influenced by genetics, neuroendocrine signaling, appetite regulation, insulin sensitivity, adipocyte biology, medications, sleep, psychological factors, socioeconomic conditions, physical activity, and environmental exposures. Contemporary medicine appropriately recognizes obesity as far more complicated than failure of willpower.

Recent international efforts have gone even further, distinguishing excess adiposity from clinical obesity and emphasizing the actual effects of adiposity on organ and tissue function rather than relying exclusively on body mass index.[7]

It was important to stop blaming people for obesity. But now, medicine might be swapping one simple explanation for another. Just because obesity is a real biological condition doesn’t mean it starts inside each person. A disease can be both real and caused by the environment. For example, asthma from air pollution is still asthma, and lead poisoning is still a real illness even if the cause is environmental. If a whole community gets sick after a change in the water supply, doctors treat the patients, but no one thinks the community suddenly developed a genetic problem.

We should be just as curious about obesity. When a condition becomes much more common in just a few generations, our first question should be: what has changed in our environment, habits, or society to cause this? Instead, the focus is quickly shifting to which drug can best fight it. We changed the world around us, saw people’s bodies change in response, and now we’re treating those changes as the main problem.

There is another change that occurred alongside the biological one: our culture gradually changed its definition of what was normal. I have written about this before, using the transformation of Victoria’s Secret as one highly visible example. The famously thin “Angels” who once defined the brand were eventually replaced by models representing a much broader range of body sizes, part of a larger and understandable effort to move away from unrealistic beauty standards and the humiliation of people because of their weight.[8] There was much about that change that was humane and necessary. No person should be shamed, ridiculed, or assigned less dignity because of body size.

But compassion and normalization are not the same thing. As obesity became progressively more common, society did more than become more accepting of people with obesity; it also became increasingly reluctant to acknowledge obesity itself as abnormal. The distinction matters because one can respect every human body while still recognizing that excess adiposity carries important medical consequences.

In a remarkably short period, we changed the food environment, changed the physical environment, watched the population become heavier, and then changed the cultural image of what a normal body looked like. Now we are entering the next stage of that progression: pharmacologically treating the metabolic consequences.

What Changed Was Almost Everything

Today, people live in a very different world than past generations. Food is everywhere, all the time. Much of it is designed to be convenient, tasty, long-lasting, quick to eat, and easy to buy again. Foods that once took time to prepare can now be eaten in seconds. Drinks can add a lot of calories without making us feel full. Portion sizes have grown, people move less, jobs are more sedentary, transportation often means less walking, and entertainment usually means sitting. No single food or habit explains obesity, but the environment that shapes our eating and activity has changed a lot.

A key experiment by Hall and his team at the National Institutes of Health showed this clearly. In a controlled study, people ate either ultra-processed or unprocessed diets, matched for calories, nutrients, sugar, salt, and fiber. They could eat as much or as little as they wanted. On an ultra-processed diet, people ate about 500 more calories a day and gained weight. On the unprocessed diet, they lost weight.[9] No one told them to eat more or took away their willpower. Just changing the food environment changed how much they ate.

Physical activity has also dropped a lot. A large study of over 5 million people found that not getting enough exercise became more common worldwide from 2000 to 2022, and by 2022, almost a third of adults weren’t active enough.[10] Sleep is important too, even though it’s often overlooked. Research shows that not getting enough sleep raises the risk of obesity.[11] All these factors, along with stress, income, medications, food access, work hours, city design, and more, combine in ways that can’t be fixed by simply telling people to eat less and move more.

Scientists are also looking at environmental chemicals that might affect metabolism and hormones. The idea of “obesogens” is still new and shouldn’t be seen as the only reason for the obesity epidemic. Still, studies suggest that some environmental exposures could affect how our bodies store fat, use energy, or regulate appetite in ways that make weight gain more likely.[12] The right approach is to keep studying these possibilities, especially since the rise in obesity is so widespread.

The most defensible conclusion is therefore also the least sensational: obesity probably does not have one cause. Food changed. Physical activity changed. Sleep changed. Work changed. Transportation changed. Stress changed. Medications changed. Chemical exposures changed. Marketing changed. Portion sizes changed. The economics of food changed. The built environment changed. Human beings then responded biologically to those changes.

The mystery is not that metabolism responded to a dramatically altered environment. The mystery is why medicine became so comfortable treating that response without demonstrating comparable urgency about the environment that produced it.

Then Came the Drugs That Actually Worked

Obesity medicine has a long and sometimes uncomfortable pharmacological history. Earlier drugs frequently produced modest weight loss, troublesome adverse effects, or both. Several were eventually withdrawn because their risks became unacceptable. Against that background, modern incretin-based therapies represented a genuine therapeutic breakthrough. In the STEP 1 trial, adults with overweight or obesity who received once-weekly semaglutide 2.4 mg lost an average of 14.9 percent of their baseline body weight over 68 weeks, compared with 2.4 percent among those receiving placebo, with both groups receiving lifestyle intervention.[3] For nonsurgical obesity treatment, this was an extraordinary result.

Tirzepatide moved the numbers even further. In SURMOUNT-1, 2,539 adults with obesity or overweight and at least one weight-related complication, but without diabetes, were randomized to tirzepatide or placebo. At 72 weeks, average weight reductions were 15.0 percent, 19.5 percent, and 20.9 percent with the 5 mg, 10 mg, and 15 mg doses, respectively, compared with 3.1 percent with placebo.[4] Weight reductions exceeding 20 percent begin to approach territory historically associated with bariatric procedures rather than medication. For patients who have struggled unsuccessfully with obesity for years, it is easy to understand why these drugs can feel revolutionary.

More importantly, the story extends beyond the scale. In SELECT, more than 17,000 adults with preexisting cardiovascular disease and overweight or obesity, but without diabetes, were randomized to semaglutide or placebo. Major cardiovascular events occurred in 6.5 percent of patients receiving semaglutide and 8.0 percent receiving placebo, corresponding to a hazard ratio of 0.80.[5] Subsequent analysis also demonstrated a lower incidence of a prespecified composite kidney endpoint among patients receiving semaglutide.[13] Tirzepatide has produced substantial reductions in apnea-hypopnea index among patients with obesity and moderate-to-severe obstructive sleep apnea.[6] These findings make it impossible to dismiss the GLP-1 era as mere pharmaceutical vanity medicine.

Physicians should welcome effective therapies. A patient with severe obesity, cardiovascular disease, diabetes, sleep apnea, impaired mobility, or other obesity-related complications should not be denied a beneficial treatment because society has failed to solve the larger causes of obesity. We treat the patient who exists today, not the healthier society we wish existed. The mistake would be turning that entirely reasonable clinical principle into permission to stop asking the larger question.

What Happens When the Injection Stops?

Perhaps the most revealing aspect of GLP-1 therapy appears when treatment ends. In the STEP 1 extension, participants who discontinued semaglutide regained approximately two-thirds of their previous weight loss during the following year, while many cardiometabolic improvements moved back toward baseline.[14] SURMOUNT-4 demonstrated a similar phenomenon with tirzepatide. After an initial 36-week period during which participants lost an average of 20.9 percent of their body weight, those randomized to discontinue tirzepatide and receive placebo regained substantial weight, whereas those who continued therapy maintained and further increased their weight reduction.[15]

The conventional interpretation is straightforward: obesity is a chronic relapsing disease, and chronic diseases frequently require chronic treatment. This argument has considerable logic. Blood pressure often rises when antihypertensive medications are stopped. LDL cholesterol generally rises after discontinuation of lipid-lowering therapy. Nobody claims that the recurrence of hypertension proves that antihypertensive drugs failed.

The 2026 American Diabetes Association Standards of Care therefore recommend continuing obesity pharmacotherapy beyond achievement of weight-loss goals when indicated for chronic therapy, noting that discontinuation often results in recurrent weight gain and reemergence of cardiometabolic risk factors.[16] The World Health Organization likewise now states that GLP-1 therapies may be used as long-term treatment for adults living with obesity. However, its recommendation is conditional and recognizes the need for comprehensive behavioral and lifestyle intervention.[17]

Yet, obesity differs from many chronic diseases in one important respect: its prevalence changed dramatically within a remarkably short historical period. That should make us cautious about letting “chronic disease” end the discussion. If the environment continually pushes human metabolism toward excess adiposity, and a drug successfully counteracts that pressure only while it is administered, lifelong pharmacotherapy may be entirely appropriate for some patients. But it should simultaneously intensify our interest in the pressure itself. Otherwise, we risk defining successful medicine as the indefinite pharmacological adaptation of human beings to an unhealthy environment.

Losing Weight Is Not the Same As Losing Fat

Another part of this conversation deserves more attention, particularly as these medications expand into older populations. Large reductions in body weight do not consist exclusively of adipose tissue. During weight loss, some lean tissue is generally lost as well, regardless of whether weight reduction occurs through caloric restriction, surgery, or pharmacotherapy. The relevant question is not whether lean mass changes, but how much is lost, in whom, and what the functional consequences may be.

A DXA substudy of SURMOUNT-1 found that participants receiving tirzepatide experienced a 21.3 percent reduction in body weight, accompanied by a 33.9 percent reduction in fat mass and a 10.9 percent reduction in lean mass. Approximately three-quarters of the lost weight was fat, and one-quarter was lean mass.[18] That is a far more nuanced finding than the popular claim that GLP-1 drugs “destroy muscle.”

They do not. Body composition generally improves because more fat than lean tissue is lost proportionally. Nevertheless, lean tissue is biologically important, and its loss should not be treated as irrelevant simply because the scale is moving in the desired direction.

This is especially important in older patients, in whom sarcopenia, frailty, falls, osteoporosis, and loss of functional independence already represent major clinical concerns. Skeletal muscle is not decorative tissue. It is central to glucose disposal, mobility, balance, strength, metabolic reserve, and resilience during acute illness.

A 35-year-old with severe obesity losing some lean mass during substantial fat reduction is not clinically equivalent to a frail 78-year-old doing the same. Responsible obesity medicine therefore cannot consist simply of prescribing an injection and celebrating weight loss. Nutrition, adequate protein intake, resistance exercise, physical function, and muscle preservation should become integral parts of treatment. The goal is not to make patients lighter. The goal is to make them healthier.

The Economics of Treating the Consequence

This discussion has an uncomfortable economic dimension that does not require conspiracy theories or accusations of bad faith. Modern health care is exceptionally effective at creating financial structures around treatment. A pharmaceutical product can be researched, patented, manufactured, marketed, prescribed, reimbursed, monitored, and administered repeatedly. Hospitals can build programs around it. Insurers can establish coverage criteria for it. Physicians can prescribe it. Investors can calculate its market. Patients can measure its effects. The entire structure of modern medicine understands how to assign economic value to an intervention.

Prevention is different. No comparable recurring revenue stream is generated when a child grows up eating mostly minimally processed food, sleeping adequately, walking and exercising regularly, maintaining muscle, and never developing metabolic disease. No blockbuster pharmaceutical product is called adequate sleep, no patent exists on resistance exercise, and no quarterly earnings call celebrates the number of patients who never became sick. That does not mean pharmaceutical companies created the obesity epidemic. It means that our economic system has far more powerful mechanisms for rewarding treatment than for rewarding the absence of disease.

The result can emerge without anyone designing it. Industry develops products that generate returns. Physicians work within reimbursement systems built around identifiable diagnoses and interventions. Insurers reimburse treatments meeting defined criteria. Hospitals organize programs around services they can deliver and bill. Patients understandably prefer interventions that produce meaningful results, particularly after years of unsuccessful attempts at weight loss.

Each participant can behave rationally, yet the system can drift toward a remarkable destination: we construct an environment that promotes metabolic dysfunction and then build an increasingly sophisticated medical economy around helping people survive it.

Now the Government Is Buying In

This discussion became even more consequential in 2026. Beginning July 1, the Centers for Medicare & Medicaid Services launched the Medicare GLP-1 Bridge, a demonstration program providing eligible Medicare Part D beneficiaries access to certain GLP-1 drugs with a $50 copayment. The program is scheduled to continue through December 31, 2027.[19] Whatever one thinks about the policy, it represents an important transition. GLP-1 therapy for obesity is no longer simply a matter between an individual patient, physician, insurer, and manufacturer. The federal government is now directly participating in expanded access.

For many patients, this may be excellent news. Obesity disproportionately affects populations that often have the least access to effective treatment, and cost has been a substantial barrier to modern obesity pharmacotherapy. If these medications reduce cardiovascular events, diabetes, kidney disease, sleep apnea, disability, and other obesity-related complications, expanding access may ultimately prove both humane and economically rational. Those outcomes should be studied carefully, not presumed.

But public financing also creates a public obligation to ask what we are buying. Are we purchasing durable reductions in cardiovascular disease, diabetes, disability, and mortality? Are we reducing total health-care expenditure over time? Are patients becoming stronger and metabolically healthier, or simply lighter? What happens after five, ten, or twenty years of treatment? What proportion of patients remain on therapy? What happens to those who discontinue it? What are the nutritional and functional consequences in older adults? And perhaps most importantly, how much are we simultaneously investing in understanding and modifying the conditions that made treatment necessary?

Those questions are not arguments against coverage. They are precisely the questions that should accompany responsible coverage.

Medicine Must Be Able to Hold Two Ideas at Once

Public debates increasingly demand that we choose teams. Either GLP-1 drugs are miracle therapies that should be celebrated without reservation, or they are dangerous pharmaceutical shortcuts that should be rejected in favor of diet and exercise. Both positions are intellectually unsatisfying. Medicine should be able to hold two ideas simultaneously, particularly when both are supported by evidence.

The first is that GLP-1-based therapies represent a major medical advance. They produce substantial weight loss, improve important metabolic parameters, and have demonstrated benefits extending to cardiovascular outcomes, kidney outcomes, and obstructive sleep apnea in appropriately selected populations. [5,6,13] For many patients, they may prevent disease, restore mobility, improve quality of life, and possibly extend survival. Patients who benefit from them should not be ashamed for using them any more than a patient with hypertension should be shamed for taking an antihypertensive medication.

Second, a civilization in which enormous numbers of people may require lifelong pharmacological manipulation of appetite and metabolism to maintain health should be intensely curious about how that situation arose. Calling obesity a chronic disease does not relieve us of that responsibility. If anything, the scale of the disease makes the responsibility greater.

We should therefore reject the false choice between treating obesity and preventing it. Physicians must treat the patient standing in front of them with the best tools available today. Scientists and public health institutions must also investigate why so many patients present with the same problem.

Government should evaluate whether policies affecting food, cities, schools, physical activity, sleep, and environmental exposures promote metabolic health or undermine it. Medicine should study not merely how efficiently we can produce weight loss, but whether we can preserve muscle, metabolic health, function, and independence while doing so.

The Question Our Grandchildren May Ask

Medical history is filled with treatments that became so familiar that physicians stopped asking the questions that originally justified them. Sometimes the treatments were eventually shown to be wrong. Sometimes they were useful but applied too broadly. And sometimes the treatment worked exactly as intended while distracting medicine from a more fundamental cause of disease. The GLP-1 revolution may ultimately belong to an entirely different category: therapies that are genuinely transformative and beneficial, but whose very effectiveness risks concealing the magnitude of the societal failure that made them necessary.

Imagine medicine 20 or 30 years from now. The drugs will almost certainly be better. Oral formulations, combinations of incretin and other metabolic pathways, agents that better preserve lean mass, and therapies we cannot yet imagine may make obesity increasingly controllable. Perhaps cardiovascular disease and diabetes will decline dramatically as a result. That would be a genuine triumph of medical science.

But imagine another possibility as well. Suppose half of the adult population requires continuous pharmacological intervention to maintain metabolic health while children continue entering the same environment that produced the epidemic.

Suppose we become extraordinarily proficient at altering the individual’s biology while leaving the biology-disrupting environment essentially untouched. Would we call that prevention? Would we call it health? Or would we have become very good at treating the consequences of something we never dared to confront?

Those are not reasons to take an effective drug away from a patient who needs it. They are reasons to refuse the complacency that can accompany therapeutic success. The physician’s responsibility is to treat disease. Medicine’s responsibility is larger. It must also remain curious about why disease occurs, particularly when its prevalence changes before our eyes.

The great irony of the GLP-1 era may therefore be that the medications are not the problem at all. They may be among the best tools we have ever developed for treating obesity. The real problem will arise if their success convinces us that the epidemic itself has been solved. A weekly injection can change appetite, body weight, glucose metabolism, cardiovascular risk, and perhaps the trajectory of an individual patient’s life. What it cannot do is explain why a condition that affected a relatively small minority of Americans 60 years ago now affects roughly four in ten adults.

We should use these medications when they improve our patients’ lives. We should study them rigorously, monitor their long-term consequences, make access rational and equitable, and resist both their demonization and their indiscriminate use. But every prescription should coexist with a much larger scientific question, one that medicine should have been asking with far greater urgency for decades: what did we change that made so many people sick?

The tragedy of the GLP-1 era will not be that these drugs failed. The tragedy will be if they succeed so spectacularly that an entire generation of physicians stops asking why we needed them in the first place.

References

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2. NCD Risk Factor Collaboration (NCD-RisC). Worldwide trends in underweight and obesity from 1990 to 2022: a pooled analysis of 3663 population-representative studies with 222 million children, adolescents, and adults. Lancet. 2024;403(10431):1027-1050. doi:10.1016/S0140-6736(23)02750-2.

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5. Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and Cardiovascular Outcomes in Obesity Without Diabetes. N Engl J Med. 2023;389(24):2221-2232. doi:10.1056/NEJMoa2307563.

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7. Rubino F, Cummings DE, Eckel RH, et al. Definition and diagnostic criteria of clinical obesity. Lancet Diabetes Endocrinol. 2025;13(3):221-262. doi:10.1016/S2213-8587(24)00316-4.

8. Varon J. The Comfortable Collapse: How America Learned to Pretend Obesity Is Normal. Brownstone Institute. 2025 Oct 21.

9. Hall KD, Ayuketah A, Brychta R, et al. Ultra-processed Diets Cause Excess Calorie Intake and Weight Gain: an Inpatient Randomized Controlled Trial of Ad Libitum Food Intake. Cell Metab. 2019;30(1):67-77.e3. doi:10.1016/j.cmet.2019.05.008.

10. Strain T, Flaxman S, Guthold R, et al. National, regional, and global trends in insufficient physical activity among adults from 2000 to 2022: a pooled analysis of 507 population-based surveys with 5.7 million participants. Lancet Glob Health. 2024;12(8):e1232-e1243. doi:10.1016/S2214-109X(24)00150-5.

11. Wu Y, Zhai L, Zhang D. Sleep duration and obesity among adults: a meta-analysis of prospective studies. Sleep Med. 2014;15(12):1456-1462. doi:10.1016/j.sleep.2014.07.018.

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13. Colhoun HM, Lingvay I, Brown PM, et al. Long-term kidney outcomes of semaglutide in obesity and cardiovascular disease in the SELECT trial. Nat Med. 2024;30(7):2058-2066. doi:10.1038/s41591-024-03015-5.

14. Wilding JPH, Batterham RL, Davies M, et al. Weight regain and cardiometabolic effects after withdrawal of semaglutide: the STEP 1 trial extension. Diabetes Obes Metab. 2022;24(8):1553-1564. doi:10.1111/dom.14725.

15. Aronne LJ, Sattar N, Horn DB, et al. Continued Treatment With Tirzepatide for Maintenance of Weight Reduction in Adults with Obesity: the SURMOUNT-4 Randomized Clinical Trial. JAMA. 2024;331(1):38-48. doi:10.1001/jama.2023.24945.

16. American Diabetes Association Professional Practice Committee. 8. Obesity and Weight Management for the Prevention and Treatment of Diabetes: Standards of Care in Diabetes-2026. Diabetes Care. 2026;49(Suppl 1). doi:10.2337/dc26-S008.

17. Celletti F, Farrar J, De Regil LM. World Health Organization Guideline on the Use and Indications of Glucagon-Like peptide-1 Therapies for the Treatment of Obesity in Adults. JAMA.2026;335(5):434-438. doi:10.1001/jama.2025.24288.

18. Look M, Dunn JP, Kushner RF, et al. Body composition changes during weight reduction with tirzepatide in the SURMOUNT-1 study of adults with obesity or overweight. Diabetes Obes Metab. 2025;27(5):2720-2729. doi:10.1111/dom.16275.

19. Centers for Medicare & Medicaid Services. Medicare GLP-1 Bridge. Baltimore (MD): Centers for Medicare & Medicaid Services; 2026.

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