ok so i was reading about tirzepatide and how it can reduce inflammation, which is kinda cool. but what caught my eye was that it also removes the desire to smoke or drink.
has anyone else noticed this? is there a reason why peptides would affect substance use like that?
reduced food noise and changes in appetite signals can sometimes affect other reward pathways, and thatās a plausible mechanistic hypothesis for some people reporting a decreased interest in substances. but āremoves the desireā as a specific, established effect of GLP-1s, particularly tirz, isnāt something supported by controlled trial data on addiction pathways. an observed correlation isnāt the same as a proven mechanism.
The āremoves the desire to smoke or drinkā piece is a common observation with GLP-1s, and itās because they address neurological pathways beyond just metabolism. The distinction most telehealth platforms use is binge eating
itās not quite āremoving desireā in a direct sense. glp-1 agonists influence reward pathways and alter the subjective experience of consumption, and the gastric emptying effect plays a larger, often underspecified, role in how that manifests.
itās really something, isnāt it? that observation about āremoves the desire to smoke or drinkā is one iāve heard from others too, though often phrased more as a general quieting of the constant mental pull towards certain habits. i think the mechanism isnāt a direct anti-craving signal, but more likely
appetite suppression, not just food š
That āremoves the desire to smoke or drinkā observation you mentioned is common with GLP-1s; itās thought to be due to their action on neurological reward pathways, not just metabolic ones.
inflammation reduction is pretty cool but what about the nicotine receptor interaction
something about tirzepatide reducing inflammation is really interesting, and that phrase āremoves the desire to smoke or drinkā you mentioned is what iāve heard from others too, though often in the context of appetite suppression plateauing, not necessarily a direct effect on substance use, fwiw.
That āremoves the desireā point is a pretty consistent observation for a lot of people on tirz, fwiw. The CNS effects of GLP-1s donāt just hit the satiety centers; they also modulate dopamine signaling in the brainās reward pathways, so itās a known mechanism for reducing cravings for things like alcohol and nicotine.
That observation about āremoves the desireā is something many people report on tirz, and itās definitely interesting how those effects manifest. Where Iād gently push back is on the idea of a direct āremovalā of desire itself; fwiw, for GLP-1s, the shifts in central nervous system signaling often precede the appetite changes, which means the reduction in desire might be a downstream effect of other, more foundational changes in brain chemistry, rather than a direct erasure of craving. Itās less about a willpower assist and more about the pharmacology adjusting how those signals are processed in the first place, which is a key distinction when thinking about how these meds actually work.
definitely seen people report that āremoves the desire to smoke or drinkā effect with tirz. for alcohol, the gastric emptying timing explains that window better than a direct dopamine hit, especially since conditioned aversions outlast the acute mechanism, so the durable version doesnāt need the acute mechanism still running. inflammation is a common claim but thatās
i definitely noticed that with alcohol. my intake dropped probably 80% once tirz really kicked in, and iād tracked daily drinks in the app i use, CareClinic, so the trend line was pretty clear. itās the same general satiety mechanism at play, not specific to just food cravings, which affects those reward pathways.