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When did obesity become a drug deficiency?

By Joseph Varon - posted Thursday, 8 October 2026


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.

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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.

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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.

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  1. Fryar CD, Afful J, Saif NT. Prevalence of overweight, obesity, and severe obesity among adults age 20 and older: United States, 1960-1962 through August 2021-August 2023. NCHS Health E-Stat. Hyattsville (MD): National Center for Health Statistics; 2026.
  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.
  3. Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384(11):989-1002. doi:10.1056/NEJMoa2032183.
  4. Jastreboff AM, Aronne LJ, Ahmad NN, et al. Tirzepatide Once Weekly for the Treatment of Obesity. N Engl J Med. 2022;387(3):205-216. doi:10.1056/NEJMoa2206038.
  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.
  6. Malhotra A, Grunstein RR, Fietze I, et al. Tirzepatide for the Treatment of Obstructive Sleep Apnea and Obesity. N Engl J Med. 2024;391(13):1193-1205. doi:10.1056/NEJMoa2404881.
  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.
  12. Heindel JJ, Lustig RH, Howard S, Corkey BE. Obesogens: a unifying theory for the global rise in obesity. Int J Obes (Lond). 2024;48(4):449-460. doi:10.1038/s41366-024-01460-3.
  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.

This article is published under a Creative Commons Licence and was first published by The Brownstone Institute.

 



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About the Author

Joseph Varon, MD, is a critical care physician, professor, and President of the Independent Medical Alliance. He has authored over 980 peer-reviewed publications and serves as Editor-in-Chief of the Journal of Independent Medicine.

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