The Downside

While I agree with Nick Tiller’s skepticism about the new weight loss drugs coming along in his piece at Skeptical Inquirer:

Semaglutide is a breakthrough in the noninvasive treatment of obesity. First made available in 2017 under the brand name Ozempic for treating type II diabetes, it was re-approved by the FDA in 2021, with a distinct dosing regimen, under the brand name Wegovy as a therapeutic aid for obesity. Both drugs mimic glucagon-like peptide-1 (GLP-1)—a hormone secreted during digestion to suppress appetite. More specifically, by acting through the central and peripheral nervous system, semaglutide slows the rate at which food empties from the stomach, increases insulin release from the pancreas (for better blood glucose control), and alters the perception of taste (thereby causing “taste aversion”). The drug can effectively restore the GLP-1 signaling pathway, which is thought to be dysfunctional in certain obese patients. As with all medications, Ozempic and Wegovy come with side effects. Nausea, abdominal pain, constipation, diarrhea, and vomiting are all common. But for clinically obese patients or diabetics, who have a considerably greater risk of cardiometabolic disease, the risk-to-benefit ratio is generally thought to be favorable.

But not for everyone. Experts broadly categorize obesity into one-of-four subtypes: people who need to eat more food than normal to become full (referred to as “hungry brain”); people who become full with a regular meal but with short-lived effects (“hungry gut”); people who eat to cope with difficult emotions (“emotional hunger”); and people with a relatively slow metabolism (“slow burn”). Semaglutide, as a GLP-1 analog, is an effective intervention for those with “hungry gut,” but it may not be appropriate for people with obesity classified as “slow burn” or “emotional hunger.” Chronic depression and anxiety are two of the most common psychopathologies that trigger binge eating, and many people eat to transiently improve their mood. These behaviors won’t simply subside along with one’s appetite. In such cases, semaglutide may bury the symptoms, leaving the causes to root.

For all its clinical efficacy, semaglutide doesn’t show people how to change their relationship with food or eat in a healthy, sustainable way. Studies show that people who stopped the therapy after twenty weeks regained most of the weight they’d initially lost because the appetite suppressant reduces diet quantity without improving quality. What’s more, “yo-yo dieting”—large and periodic fluctuations in body weight—poses a considerable risk of cardiovascular disease and life dissatisfaction. For optimal outcomes, semaglutide must be taken alongside the dietary and lifestyle changes that obese patients have historically been unable to do implement. Where they have previously failed, semaglutide may provide the conditions to succeed.

I still don’t think he gets to the biggest problem. Maybe my understanding is flawed but as I understand it these drugs function by reducing the appetite. They don’t make you eat the things you need to eat to sustain life and health. Unless there’s a lot more to your regimen that taking these drugs, won’t you gravitate to eating what you like rather than what you need?

I won’t be at all surprised if we start seeing a rash of cases of scurvy, pellagra, rickets, osteoporosis, etc. in rich countries.