Fighting Fire with Fire: GLP-1s and the Political Economy of Population Health

Glucagon-like peptide-1 (GLP-1) receptor agonists have been adopted faster and more widely than any anti-obesity therapy prior. Within a few years of approval, nearly 1 in 5 US adults report having used one, and 1 in 8 is currently using it, with these numbers only likely to increase. Notably, these drugs produce average weight loss of 15% to 21% of body weight, a magnitude comparable only to bariatric surgery. While their broader health impact remains unknown, their potential to reduce obesity, and numerous other morbidities, at the population level is seemingly unprecedented.

The natural question, in turn, is what about this GLP-1 era feels different, or, to put it another way, what is the cause for optimism after decades of losing the “war on obesity”? The superficial answer is that we finally have drugs that work, but many interventions that succeed at the individual level fail to live up to their population-level promise. The fuller story — and the argument advanced here — is that they are poised to succeed because they operate within the same structural logic as the industries that engender obesity and so much chronic disease in the United States: profit-seeking, scalability, and reprogramming individuals’ default decisions and behaviors.

In a sense, GLP-1s are fighting fire with fire, which presents a dilemma for those concerned with population health. If the most promising solution succeeds because it leverages market logic, the more pressing concern for population health shifts from prevention alone toward intervening in how this market distributes GLP-1s to maximize population benefit. That is, left to its own devices, we have every reason to believe that a solely market-driven approach to GLP-1s as a population health intervention would fail to live up to the promise and potential of these transformative medications.

Leveling the Playing Field

The diseases of modernity are, perversely, a product of tremendous societal success. They are, in no small part, the product of lifestyles of excess that abundance and technology have enabled. But they should not be conflated with mass failure of willpower. Even if we now view them with disdain vis-à-vis population health, these markers of success — automobiles and their commensurate built environment, less physically demanding work, food engineered to maximize taste and convenience — have made excess the path of least resistance, absent any value judgment. Namely, to the extent that this is now the “default” lifestyle, it is the path that society selects for you unless you actively override it, which takes knowledge, resources, and self-efficacy, all of which are unequally distributed. Given this broader societal context, obesity is not inevitable per se, but it is often inescapable.

In turn, public health has been fighting on highly unequal terms, and the food environment is the clearest case: industrial-scale optimization for palatability, convenience, and hyperconsumption, precision-engineered to hijack the reward system (e.g., the tobacco conglomerate that owned Kraft applied its cigarette product-development methods directly to food). In a controlled trial, people ate roughly 500 more calories a day on an ultra-processed diet, unprompted. Public health’s (rightful) focus on prevention counters this with a fraction of the resources. No society has reversed its obesity epidemic, and there is little evidence that healthy-eating and activity policies move population-level weight. This is not a failure of population health science or efforts, but a reflection of the unfair playing field.

It is perhaps a bit strange to then argue that biomedical interventions like GLP-1s help us level said playing field, but it’s an important reminder that biomedicine has long been population health’s active — if softly spurned — partner. Over the past forty years, drugs like statins and antihypertensives, among other innovations, have built a robust population-mortality record alongside efforts targeting prevention. Population health’s wariness of biomedicine is understandable — it is downstream, individualized, and commercial — but it also risks overcorrecting. Whatever the gap in intentions between selling a drug and improving a population’s health, the impact of biomedical innovation has consistently aligned with the goals of prevention. Even if it’s not the preferred way to attain better population health, we are, at least in this sense, playing on the same side.

This is not an entirely novel point: Mehta and Dowd make a similar case for an alliance between medicine and population health when it comes to GLP-1s, despite their operating downstream of the social determinants of health. The stronger claim here is that GLP-1s succeed not despite being downstream but because they are more structurally on par with the disease(s) they treat. Against an obesogenic environment sustained by industrial optimization, biomedicine is arguably the more equal opponent. It meets those industries on their own terms, precisely because it plays by the same rules of optimization, profit, and convenience. For instance, linking GLP-1 use to household grocery purchases, one analysis found that spending fell about 5.3% within six months of a member starting the drug — concentrated in calorie-dense, processed foods — even as food manufacturers began reformulating in response. In effect, the food industry now treats these medications as a competitor for the same consumer demand: the clearest sign yet that biomedicine and the obesogenic industries are playing on the same field.

And this brings some nuance to a central claim in population health. Namely, the commercial determinants of health literature contends that the profit motive is as fundamental a driver of disease as any social determinant and calls for confronting it directly rather than accommodating industry. It is hard to argue with this point, but it is perhaps too aspirational given the realities of the political economy that give rise to obesity, including but not limited to the power and influence of the food industry. From that realist perspective, a downstream intervention that works because it shares the disease’s market logic is something population health should not ignore. Lest this sound like a resigned version of “if you can’t beat ’em, join ’em,” the greater goal should always be to change the rules of the game and shift the focus upstream. But, in recognizing the long-term nature of this goal, figuring out how to use existing rules to population health’s advantage can be valuable, too.

The Satisfaction Mechanism

The structural compatibility between GLP-1s — as a tool of biomedicine — and the larger societal forces that lead to obesity and chronic disease is not the only domain where these drugs have an advantage over extant prevention efforts. Namely, the actual mechanism of action through which GLP-1s work is crucial for understanding their population health potential. Lifestyle interventions ask people to resist the aforementioned “default” indefinitely, whether as a function of resources, willpower, or any number of material and psychosocial factors. But even the most intensive (and, often, impractical) interventions have a limit, and sustained lifestyle interventions that lead to weight loss may not improve cardiovascular health. GLP-1s act directly on appetite and reward, reducing the demand for consumption rather than asking individuals to resist it. Unlike prior anti-obesity drugs — and critical to their potential for large-scale success — they interfere with the innate drive to consume. We see this beyond food, too, in their attenuation of alcohol and cigarette use. The real significance here is that it acts on the biophysiological circuitry of consumption itself — the very mechanisms the default environment, and industries within it, exploit. Prevention-oriented efforts, by design, cannot target these reward/satisfaction-based pathways and, if anything, heighten their salience when asking people to relearn habits or change behaviors, however well-intentioned.

What This Means for the Field

The takeaway from a population health perspective is not that prevention is outdated or futile, but that this “either/or” framing oversimplifies the complexity of addressing obesity and chronic disease at a population level. Prevention and treatment are fundamentally different domains. The former is almost always forward-looking and oriented towards a longer time horizon, while the latter prioritizes those affected in the here and now; they are not substitutes nor are they at odds with one another. And this directly speaks to the concern that (over)medicalizing health issues displaces upstream work intended to address them. It’s true that medicalization is the “easy way out” when a disease is amenable to structural intervention at scale, but perhaps we should be asking if/when medicalization is appropriate — such as when it is a necessary response to the kind of industrial-scale optimization that public health prevention cannot counter and, critically, when the affected population already exists and requires intervention. For all its limitations, medicalization confers a legitimacy that unlocks otherwise-unavailable responses. In the case of obesity and multiple chronic diseases, absent some degree of medicalization — at both the individual and population level — there is no reimbursable, scalable treatment to distribute, which can result in denying an efficacious therapy to those who most need it.

Doing What the Market Won’t Do

Population health research and perspectives can go a long way in mitigating concerns about the overmedicalization of obesity and chronic disease in the GLP-1 era, reminding us that prevention efforts have a role to play. But perhaps population health’s greater utility is grappling with the fundamental nature of GLP-1s as an agentic intervention, and the pitfalls therein. The default environment works passively and that is precisely what makes it so pernicious — obesity can arise from “going with its flow,” which asks nothing of the public at large. For all their strengths, GLP-1s are at a deficit in requiring sustained action to obtain, afford, tolerate, and stay on them indefinitely. This runs counter to a basic tenet of health equity — that interventions requiring individual effort widen disparities, while those that change the default narrow them. Overriding the default requires the exact kind of capacities — knowledge, money, time, self-efficacy — that are most unequally distributed, which is why new health technologies often widen the gaps instead of closing them. GLP-1s reduce the agency needed to resist the obesogenic environment, which is central to why they work, but they still require the agency to obtain and sustain their use, which follows a social gradient. Access alone — the solution Mehta and Dowd rightly call for — risks widening gaps long before it narrows them.†

The problem is that we cannot make an agentic intervention passive. We cannot put GLP-1s in the water, as some jokingly suggest, nor can we force it on anyone no matter the benefits. But this nebulous space between coercion and the market is exactly where population health perspectives and policy are needed most. And decades of insights from the field tell us that the task is to minimize the agency it demands — default enrollment and refills, zero cost-sharing, delivery embedded in routine care, adherence support, and, critically, friction removed first for the most disadvantaged. Mass COVID-19 vaccination taught us, at a substantial cost, what does and does not work for equitable uptake of a voluntary intervention with tremendous population health benefit. Minimizing (or eliminating) cost, distance, and appointments narrowed the gaps, while mandates eroded trust, and, in the end, both existing and novel forms of stratification emerged. While not a one-to-one comparison, we are about to embark on a similar experiment. Medicare is beginning to bring GLP-1s to the masses (or a large subset thereof) through a time-limited demonstration that caps out-of-pocket cost and pairs the drugs with lifestyle support — the largest test yet of GLP-1s as public policy.‡ The design might work, or not, but what matters is that our ability to evaluate these drugs’ population health effects — hopefully for the best — is contingent on policy and its capacity to amplify their individual benefits in an effective and egalitarian way, rather than market forces alone.

Population health-oriented policy is critical because the industry that produced these drugs has no mandate to distribute their benefits equitably; indeed, in answering to shareholders, it often does the opposite. Doing the work of making a market-made solution reach people the way the disease reaches them — by default rather than by agency — is what population health is built for, and what the market will not do. Fighting fire with fire, in using the industries’ tools, may not be desirable but it seems necessary considering the lack of progress with prevention-based interventions. Yet, using these tools does not mean being beholden to the same underlying market logic, too. Obesity has spread by “default” and the goal should be to make the cure spread by default as well. Population health can — and should — play the market’s game, but it can do so on its own terms and by its own rules. In turn, the extent to which the promise of GLP-1s is broadly shared or quietly hoarded is where population health principles, perspective, and policy can make a difference.

† Granted, according to Mirowsky and Ross, GLP-1s constitute “medical dependency” — which is itself an aspect of the “default lifestyle,” in which health maintenance is replaced by reliance on medication. But the kind of dependency they describe is presented as a poor substitute for addressing the upstream causes, whereas I argue GLP-1s help counteract the demand induced by those upstream causes in the first place. The agency problem, as described above, remains a concern.

‡ The Medicare GLP-1 Bridge, a national demonstration running July 1, 2026, through December 31, 2027, caps out-of-pocket cost at roughly $50 per month for Wegovy, Zepbound, and Foundayo for beneficiaries with a body mass index ≥27 plus a qualifying condition (or ≥35 automatically), operating outside the standard Part D benefit. It is the near-term vehicle for the broader BALANCE Model, under which CMS negotiates GLP-1 prices directly with manufacturers for Medicaid and Part D and bundles a no-cost lifestyle-support program. Sources: CMS, Medicare GLP-1 Bridge; CMS, BALANCE Model.