The formula used to decide whether you have obesity was invented in the 1830s by a Belgian astronomer. Adolphe Quetelet was studying populations, not patients. He wanted a mathematical description of the "average man," and dividing weight by height squared gave him a tidy way to do it. He never meant it to measure any individual's health, and it didn't get the name "body mass index" until 1972, when the physiologist Ancel Keys coined it (Eknoyan, Nephrology Dialysis Transplantation, 2008, DOI (external link); Keys et al., Journal of Chronic Diseases, 1972, DOI (external link)). Nearly two centuries later, that same ratio is still the number on the chart that sorts people into "normal," "overweight," and "obese."
That origin says a lot. Much of what we assume about obesity rests on tools and ideas that weren't designed for the job, and making sense of how it's diagnosed, why medicine calls it a disease, and why it's considered chronic means separating the science from a century of moral baggage.
From moral failing to medical diagnosis
For most of the twentieth century, obesity wasn't treated as a medical condition at all. It was treated as a character problem: eat less, move more, and if you couldn't, you lacked willpower. Medicine largely went along with that, which is why "treatment" for decades meant being told to try harder.
The framing began to shift as the biology accumulated. In 2013 the American Medical Association formally recognized obesity as a disease. The vote was contested at the time, but it put on record that obesity is a medical condition with biological drivers, not simply the sum of a person's choices.
In 2025 a global commission of 58 experts, published in The Lancet Diabetes & Endocrinology and endorsed by 76 medical organizations worldwide, proposed an overhaul of how obesity is defined and diagnosed.
How obesity is diagnosed
This is where Quetelet's formula comes back. BMI is cheap, fast, and useful across large populations, but for one person it's crude. It can't tell muscle from fat, it doesn't show where fat sits (the visceral fat around your organs is the dangerous kind), and its cutoffs don't translate cleanly across age, sex, or ethnicity. A muscular athlete and a sedentary person can share a BMI, and so can two people in very different health. (For what a direct body-fat measurement looks like in practice, see DXA scans for tracking progress.)
The 2025 Lancet commission recommends that BMI no longer be used as a diagnosis on its own. BMI becomes a screening signal, and excess body fat is confirmed by a direct measurement or at least one additional measure such as waist circumference. The commission also splits obesity into two states:
- Preclinical obesity: excess fat, but organs and tissues still working normally. A risk state, not an illness in itself.
- Clinical obesity: excess fat that is already impairing how the body works, with signs, symptoms, or organ damage that trace back to the fat itself.
The distinction aims treatment at the people whose health is affected, instead of at a number on a chart.
Why it counts as a disease
The case rests on what excess fat does inside the body. In clinical obesity, fat tissue acts like a dysfunctional organ. It disrupts hormones, inflammation, blood sugar, blood pressure, and cardiovascular function, and it can cause serious, sometimes life-threatening damage like heart attack, stroke, and organ failure. A condition that impairs the body's normal function fits the definition of a disease.
Body weight is also biologically regulated. The body defends a weight range through hunger and satiety hormones, energy expenditure, and brain circuitry, the same systems the GLP-1 medications act on. That's why "just eat less" so reliably fails as a long-term prescription: it asks someone to consciously override a system built to resist exactly that.
Why "chronic" matters
When someone loses weight, the body doesn't accept the new number as the target. It responds much as it would to starvation: appetite hormones shift toward hunger and the drive to eat increases. Those changes can last. In one study of 50 people who lost an average of 13.5 kg on a 10-week diet, hormones such as leptin, ghrelin and peptide YY were still changed a year later, and hunger was still higher than before the diet (Sumithran et al., New England Journal of Medicine, 2011, DOI (external link)). The regain that so often follows a diet is what you'd expect from a body defending its weight. It says nothing about character.
That's what makes obesity a chronic, relapsing condition that you manage over time. It's also why the medications are understood as long-term treatment: stop them, and the underlying biology they were managing returns, along with the weight. You wouldn't treat high blood pressure for three months and call it cured, and obesity works the same way. (Our guide on what to realistically expect on a GLP-1 gets into this directly.)
The stigma that sits on top of the science
Weight stigma, the assumption that body size reflects discipline or worth, is widespread, and it does damage. A 2020 international consensus statement in Nature Medicine, backed by dozens of scientific organizations, laid out the evidence that weight stigma causes physical and psychological harm and makes people less likely to receive good medical care. People avoid appointments, and clinicians attribute unrelated symptoms to weight and miss the actual problem.
This is where the science and the framing meet. Recognizing obesity as a biologically driven disease directly challenges the "just try harder" story that feeds the stigma. (For the deeper argument on how that framing shapes everything from insurance to how you're treated in an exam room, see Obesity as a chronic disease vs. a lifestyle choice; for handling bias in clinical settings, see Weight stigma in healthcare settings.)
Study findings above are attributed to their authors and were located via PubMed.
This is general education, not medical advice. Whether and how obesity should be diagnosed or treated in your case is a conversation for you and your clinician.