For four years the press has reported GLP-1 drugs reducing one behavior after another: drinking, smoking, gambling, compulsive shopping, and now violence. Read as a stack, the disconnected headlines are one finding being confirmed by fields that do not read each other. The drugs turn down wanting, and food was only the first thing we wanted less.
In June 2026 two criminologists at Rutgers published a paper in the journal Criminology that asked, in effect, whether a diabetes drug reduces violence. They surveyed 7,521 American adults, 821 of whom had used a GLP-1 medication. Among current users the statistical link between impulsivity and violent behavior was about 62 percent weaker than among former users. The authors reached for an analogy from the clinic: the drug behaved like cognitive behavioral therapy, weakening the path from impulse to action rather than removing the impulse. It is an odd sentence to encounter. A molecule marketed for weight loss now has a footnote in a criminology journal.
It is not, though, a surprise, if you have been collecting these stories the way I have. For roughly four years the press has run the same article over and over with a different word in one slot: GLP-1 drugs reduce ____. Alcohol. Cigarettes. Compulsive shopping. Gambling. Binge eating. Now impulsive aggression. Each version arrives as its own small wonder, written by the reporter who covers that beat and read by the people who follow that topic, then filed under curiosities about Ozempic. Read one at a time, they are anecdotes. Read in a stack, they are something else.
They are one finding, reported by people who do not read each other's journals. The addiction researchers, the criminologists, the retail analysts watching snack sales, and the diet writers are each describing the same mechanism from inside their own vertical, and none of them is positioned to notice that the others are describing it too.
The mechanism is not exotic. GLP-1 receptor agonists, the class that includes semaglutide and tirzepatide, do not act only on the gut and the pancreas. They reach receptors in the brain's reward circuitry and turn down mesolimbic dopamine signaling. In preclinical work the same compounds reduce intake and seeking across alcohol, nicotine, opioids, and stimulants. The drugs do not make a meal, or a drink, or a bet less pleasant. They make it less wanted.
That distinction is older than the drugs. Neuroscientists separate liking, the pleasure of a thing in the moment, from wanting, the pull toward it beforehand, and dopamine belongs mostly to wanting. People on these drugs report that the cheeseburger still tastes good; what is gone is the second cheeseburger, the reach for it, the loop that says more. Obesity, alcohol use disorder, compulsive shopping, and the impulse that turns an argument into a shove are different behaviors sitting on one circuit. Turn down the circuit and they sag together.
What makes the stack worth taking seriously is that it has begun to firm up from anecdote into trial. In 2024 a group reading 5,859 threads and comments across six GLP-1 subreddits found that 29.75 percent of the alcohol-related comments described stopping drinking after starting the drug, and 21.35 percent described an interruption in compulsive shopping. That is Reddit, and the authors said so plainly. But in early 2025 a randomized, double-blind, placebo-controlled trial in JAMA Psychiatry put 48 adults with alcohol use disorder on low-dose semaglutide for nine weeks and measured less craving, smaller drinking quantities, fewer heavy-drinking days, and, unprompted, fewer cigarettes. By 2026 the question had escalated to a larger randomized trial in the Lancet, for patients carrying alcohol use disorder and obesity at once.
Obesity was simply the first compulsion with a market large enough and a regulatory path clear enough to pull the drug through. The molecule was filed as a weight-loss drug because weight is what we knew how to measure, bill, and sell. Had the first large trials been run in addiction clinics, the same compound might have reached the public as an anti-craving drug that happens to shrink waistlines.
Which frame you pick decides what counts as a side effect. Call it a metabolic drug and the drop in drinking is a happy accident buried in the safety data. Call it a compulsion dampener and the weight loss is the accident, the first and most visible symptom of an off-switch we noticed because it showed up on the scale. The two framings are not cosmetic. They route billions of dollars of trial design, they decide which indications the FDA will entertain, and they determine whether the next decade of these drugs is aimed at fat or at appetite in the larger sense.
The market is already sliding toward the broader frame without saying so. In December 2025 the FDA approved an oral version of semaglutide for weight management, the first GLP-1 pill of its kind; the supporting OASIS 4 trial showed roughly 13.6 percent average weight loss over 64 weeks against 2.2 percent on placebo. A pill is not a better injection. A pill is a bet on chronic, casual, lifelong use by people who would never inject themselves weekly. You do not build that delivery system for a disease you mean to cure. You build it for a habit you mean to manage.
Here is the part that held my attention, and the reason this is a reading list and not a single citation. The stack of disconnected headlines is itself the experiment. It is enormous, uncontrolled, badly designed, and spread across populations no ethics board would have assembled on purpose, and it has been running in public for years. The signal is not in any one article. The signal is that the same result keeps arriving from fields that have no reason to speak to each other.
And the people least able to read that signal are the specialists. The criminologist sees a violence result. The hepatologist sees a drinking result. The retail analyst sees softer snack-food sales. Each is a careful reader of one line. The pattern lives between the lines, in the white space between journals, which is the one stretch of territory no single expert is paid to cover.
It would be easy to overclaim, so the honest caveats: the Reddit study is self-report, the criminology paper is correlational and admits it, the alcohol trial was small and brief, and an off-switch on wanting is not obviously a gift. A drug that blunts the pull toward the next drink also blunts the pull toward the next anything, including the wanted ones. Some users describe food going gray, then hobbies, then ambition. We have learned to turn down the volume on the circuit before we have learned what the circuit is for.
But the thing I did not believe before I read the stack, and believe now, is that we did not invent a weight-loss drug that turned out to have surprising side effects. We invented a drug that turns down wanting, and the first thing we happened to want less was food. Everything since has been the same discovery, made again, by someone who did not know it had already been made.
Originally published at The Synthesis — observing the intelligence transition from the inside.
