Compound
Everything we've written on Semaglutide — 9 articles covering the mechanism, the evidence, comparisons, and practical considerations.
9 articles
Cagrilintide and the amylin story — why CagriSema is generating interest
For about a decade, obesity pharmacology was a field that kept almost delivering. The compounds that made it through the regulatory process were real drugs with real effects, but the effect sizes were modest by the standard of what the clinical need demanded — five percent body weight, eight percent, numbers that mattered medically but didn't shift the felt experience of treatment from incremental to transformative. Then the GLP-1 receptor agonists arrived at full dose in obesity indications, and the conversation changed. Fifteen to twenty percent body weight reduction in clinical trials was a number that made physicians and patients alike recalibrate their model of what was pharmacologically achievable. The question that immediately followed — among researchers, clinicians, and the industry watching closely — was not whether this was sufficient, but what would come next.
Food noise — the obsession with eating you can't think your way out of
It starts before breakfast is over. You're still eating and already thinking about lunch — what you'll have, whether that's too much, whether you should have eaten what you just ate, what you'll do to compensate. By mid-morning there's a quiet negotiation running in the background: if you skip the afternoon snack, you can have a real dinner. If you have the good lunch, maybe just a small dinner. You're not even hungry. You're just... in it. The loop is running whether you want it to or not.
GLP-1s and alcohol — the off-label effect nobody planned for
You started semaglutide for your weight, and somewhere around week six you noticed something nobody warned you about. The glass of wine you poured at the end of the workday sat on the counter. Not because you decided not to drink it. You just forgot it was there. The craving that usually showed up around 6 PM — specific, familiar, a little impatient — didn't. And then the next night, same thing. And the night after that. You mentioned it to a friend who was also on a GLP-1 and she laughed and said she'd stopped buying wine entirely because she kept letting bottles go bad.
GLP-1s in perimenopause — when nothing else is working
You are eating the way you ate at thirty-five. You're training four days a week, sometimes five. You sleep reasonably well, you don't drink much, you track your food on and off and it's not dramatic. And the weight is still going in the wrong direction, or it isn't moving at all, or it's moving to your abdomen and waist in a way it never did before and no amount of core work touches it. You've been told it's stress. You've been told it's perimenopause and to just wait it out. You've been told your labs are normal. And you're standing in a body that feels like it's operating on entirely different rules than the one you've lived in for the last two decades.
Weight regain after stopping a GLP-1 — what's biological, what's behavioral, what to do
You lost thirty pounds over nine months. You ate less without fighting yourself about it, which was new. The background noise of food — the constant low-level negotiation between wanting something and deciding not to have it — went quiet in a way it never had before. And then, for whatever reason — cost, the medication becoming unavailable, your provider recommending a break, your own decision — you stopped. The quiet lasted maybe three weeks. And then the noise came back.
Microdose GLP-1: who it's actually for, and what "microdose" really means
You lost the weight. Not all of it, but enough — and then life happened, or the stress came back, or perimenopause shifted the whole calculus, and slowly the scale started moving in the wrong direction again. Not dramatically. Five pounds, then eight. The cravings that had gotten quiet started getting louder. You've heard about GLP-1 medications, but the idea of full-dose — the nausea, the muscle loss concerns, the appetite suppression so aggressive you stop eating enough protein — feels like more than the problem warrants. There should be something in between, and you're not sure whether that's a real clinical option or just wishful thinking.
Microdose vs full-dose GLP-1 — picking the right intensity for the right goal
You've done the reading. You know GLP-1 receptor agonists exist. You know they work. But the conversation around them — the before-and-afters, the celebrity speculation, the prescribing provider ads — all seems to point at one thing: the full dose, the dramatic weight loss, the transformation narrative. And that's not quite what you're looking for. Or maybe it is, and you're not sure. You're trying to figure out whether the intensity of the intervention matches the intensity of your situation, and nobody has given you a framework for that.
The decades arc of peptide research — what's changed and what's recurred
In 1921, Frederick Banting was a twenty-nine-year-old Canadian surgeon with a research idea that his department chairman at the University of Toronto considered unpromising. The idea was that insulin — the pancreatic secretion that had been hypothesized for decades to regulate blood sugar — could be isolated and used to treat diabetic patients who would otherwise die. Banting had read a paper about the pancreatic islet cells and had a method in mind for isolating their secretion without contaminating it with the destructive enzymes produced by surrounding tissue. His chairman, J.J.R. Macleod, gave him a laboratory, a summer, a young biochemist named Charles Best, and a collection of experimental dogs. By the end of that summer, the extract worked in dogs. By January 1922, Leonard Thompson — a fourteen-year-old diabetic patient near death in Toronto General Hospital — received the first injection in a human being. By the end of the century, the compound that Banting and Best partially purified in that summer laboratory had been re-engineered through recombinant DNA technology, was being produced by bacteria carrying a human gene, and was keeping approximately nine million Americans alive.
Semaglutide vs. tirzepatide: how to actually decide between them
You've done enough research to know that both medications are weekly injectables, that both work through GLP-1, that both have produced results in trials that made headlines. And now you're at the actual decision point — which one, and why — and the information available online tends to either oversimplify it ("tirzepatide is stronger, tirzepatide wins") or hedge so thoroughly it says nothing useful. The honest answer is that it depends on specific things about you, and those things can be named.