It’s not you, it’s your set point: Societal considerations of GLP-1 drugs
Rodent snacks don’t trigger the headshaking that human indulgence does. Scientist Randy Seeley says will power is no match for biology when it comes to controlling obesity. (Pickpik photo)
In a research lab somewhere, a lab mouse overeats and sleeps. Meanwhile, at an apartment nearby, a person decides to stay in and order pizza. While we might agree that mice will be mice, we might shake our heads about the weak willpower behind that late-night pizza.
New research questions this double standard, asking whether humans’ food intake is also limited by our their biology.
Speaking at the ScienceWriters2026 conference in Corvallis, Ore., on Sept. 27, Randy Seeley, a professor of surgery, internal medicine, and nutritional sciences at the University of Michigan, argued that human body weight is maintained at a set point, a state that the body always wants to get back to. This set point is mainly defined by a person’s genetics. However, it is not static and can be altered by factors such as food availability.
Addressing science writers as part of the annual Council for the Advancement of Science Writing’s New Horizons in Science briefings, Seeley explained why GLP-1 drugs must be taken for a lifetime to maintain weight loss. In experiments that involve both undereating and overeating, he said, the body returns to its set point. When mice were either overfed or underfed for a few months, they returned to a baseline weight comparable to other control mice.
Seeley compared trying to lose weight through sheer willpower to “holding a life preserver under water”: it is possible to move your set point as long as you do not lose focus or strength, but as soon as you get even a little distracted, the life preserver pops back up to the surface.
Environmental factors also play a role. In experiments where mice slept next to their food, they were more likely to eat more and gain weight. If they slept away from their food, this did not happen.
On the flipside, even in mice that appear the same, genetics influence weight gain. In an experiment with two mouse strains — one bred with diet-resistant genes and a second sensitive to diet-induced obesity — the diet-resistant mice did not gain weight after 12 weeks of overfeeding, while the sensitive mice more than doubled their size.
GLP-1 drugs such as semaglutide and tirzepatide (marketed under brand names including Ozempic, Wegovy, and Mounjaro) help the body adjust to a lower set point so that appetite can be satisfied with less food. They work by slowing down the pace at which food passes through the gut, increasing insulin production, and reducing cravings. Many of the details of how they work are still unknown, including their effect on inflammation and on the brain. Patients must continue taking GLP-1s for a lifetime to maintain weight loss, what Seeley called a “chronic solution for a chronic illness.”
Other models of weight regulation also exist, each somewhat different in the roles played by genetics, biology, and the environment. A newer model considers a set range rather than a specific set point. Differences among these models affect how scientists and society discuss obesity.
Simply eating healthy and making better lifestyle choices, Seeley said, are not good enough mechanisms for everyone, including those who are obese.
As we debate the roles of biology, diet, lifestyle, and policy, the one certainty is that society’s headshaking will continue.
