大家好，我是新来的，最近看到不少关于服用Reta后戒酒的讨论。
这是因为服用Reta后整体健康状况有所改善吗？还是说身体对酒精产生了某种特定的反应，导致饮酒的乐趣降低？
这是因为服用Reta后整体健康状况有所改善吗？还是说身体对酒精产生了某种特定的反应，导致饮酒的乐趣降低？
零售和酒精
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他说的话。tubby said:
哈哈，那我姑且把它理解为两者兼有吧？tubby said:
This is an example of that complexity. Eating less can cause alcohol to hit you stronger and harder (as anybody who has had a drink on an empty stomach can tell you), so it might be tempting to say that's the cause.b69ca said:
At the same time, GLP agonism is a signal to your body that glucose (or other forms of food energy) is about to hit your bloodstream and to start to scale back nutrition levels in the blood in general. This is the same reason that a diabetic (not taking GLPs) will note that drinking alcohol seems to lower their blood sugar slightly (well, to the extent it's not a high-carb drink), as the body prioritizes metabolizing the alcohol (as its the greatest threat) VS the body's usual configuration to prioritize metabolizing glucose (which is normally its greatest threat).
And then presumably there are even more downstream pathways one could unpack if they cared to do so....
Think all cravings, like sweets, alcohol and other stuff, are turned down. I’m on a pretty low dose of reta and feel no need to snack while I had the constant desire before I started. Personally not much of a alcohol consumer.
tubby said:
What they said.BNLFL said:
Reta has had zero effect on my desire for alcohol... Is it five o'clock yet?
I've had two beers in 8 months on Reta, and each of those took an hour to drink. This is after having been a hard drinker for over 20 years. It wasn't even anything that I was aware of, or consciously trying to do, but I have lost all desire for alcohol. People can drink in front of me, or try to twist my arm, and they are no longer triggers for me. I'm just not interested anymore. I'll always have some around for this effect alone, because I like that alcohol, or the absence of it, isn't a driving force in my life any longer.
1. alcohol is poison. And very high calorie. You should be limiting it regardless, if you’re trying to lose weight.
2. Reta and other GLP1s mess with your reward system so you simply do not crave the things that gave you a dopamine hit before. They are studying these drugs as possible treatments for addiction.
2. Reta and other GLP1s mess with your reward system so you simply do not crave the things that gave you a dopamine hit before. They are studying these drugs as possible treatments for addiction.
This is exactly me. I didn't set out to stop drinking alcohol, but that's what happened. My desire for it just disappeared. Also, I don't get that dopamine hit or feel the 'chill out' with the first drink of the day like I used after a hard day of work or after a long drive. It just kind of makes me tired. Every couple of weeks, I still have a drink or 2 (at most) with coworkers just to be social but I could take it or leave it. Before reta, I was putting down 3-4 drinks/ day (or more). One of the best unexpected side effects along with the expected 30% loss of body weight.Chili777 said:
GLP-1's are the biggest threat to big alcohol over the next few decades. Drinking is already on the decline for may of the younger generations, cannabis is now legal in many states and TCHA (same thing as cannabis once heated) is available across almost all states because of the farm bill. Kids smoke now and don't drink.
Now, add on that millions will take glps to lose weight and a side effect for many will be lack of interesting in drinking. Big alcohol is literally done in terms of growth. I am sure they will go all in on thc and ......peptides if they can.
Now, add on that millions will take glps to lose weight and a side effect for many will be lack of interesting in drinking. Big alcohol is literally done in terms of growth. I am sure they will go all in on thc and ......peptides if they can.
Was cutting back alcohol, taking gym time and health more seriously (and realizing it takes more of a toll on you as you age) and Reta just lowers all the craving "noise". Still imbibe but much less and much happier for it.
There's actual biology behind the "I just don't feel like drinking anymore" thing people report on retatrutide and the other GLP-1 class drugs. It's not placebo and it's not just because you're eating less, although that plays a role too.
The main mechanism is central. GLP-1 receptors are expressed in the mesolimbic dopamine system, specifically the VTA and nucleus accumbens, which is the same reward circuitry alcohol hijacks to produce its buzz. When you're on a GLP-1 agonist, dopamine release in response to alcohol gets blunted, so the hedonic payoff just isn't there the way it used to be. You drink and your brain doesn't fire the reward signal properly, and over time the cue-driven craving fades because the behavior stops being reinforced. This is well documented in preclinical models and is showing up in human trials now, with semaglutide being studied specifically for alcohol use disorder. Retatrutide is a triple agonist (GLP-1 + GIP + glucagon) so the effect is probably even stronger, though dedicated AUD trials haven't been published yet.
On top of that, these drugs slow gastric emptying significantly, which changes how alcohol is absorbed. Normally alcohol absorption depends on how fast it reaches the small intestine, and when the stomach empties slowly, the absorption becomes slower and more erratic. The rapid onset that makes drinking feel rewarding is essentially gone.
The worse tolerance part is where people get caught off guard. Several things stack at once. You're eating much less overall, so when alcohol does pass through there's less food buffering it. Dehydration is more common on these compounds because thirst signaling drops and you're consuming less fluid with smaller meals, and alcohol compounds that. The glucagon agonism (which is the unique piece of retatrutide compared to pure GLP-1 drugs) shifts hepatic metabolism and increases glucose output, and how that interacts with ethanol metabolism isn't fully characterized yet. And the same mechanism in the area postrema that suppresses appetite also lowers your nausea threshold, so a drink or two that used to do nothing can now genuinely make you sick.
The net experience is less desire to drink in the first place, less reward when you do, and worse physical consequences per gram of ethanol. Hangovers tend to be disproportionately bad for the amount consumed. Most people just naturally drift toward drinking much less or stopping altogether without trying. If you do drink, hydration matters more than usual and starting low is smart, because your old tolerance is not a reliable reference point anymore.
The main mechanism is central. GLP-1 receptors are expressed in the mesolimbic dopamine system, specifically the VTA and nucleus accumbens, which is the same reward circuitry alcohol hijacks to produce its buzz. When you're on a GLP-1 agonist, dopamine release in response to alcohol gets blunted, so the hedonic payoff just isn't there the way it used to be. You drink and your brain doesn't fire the reward signal properly, and over time the cue-driven craving fades because the behavior stops being reinforced. This is well documented in preclinical models and is showing up in human trials now, with semaglutide being studied specifically for alcohol use disorder. Retatrutide is a triple agonist (GLP-1 + GIP + glucagon) so the effect is probably even stronger, though dedicated AUD trials haven't been published yet.
On top of that, these drugs slow gastric emptying significantly, which changes how alcohol is absorbed. Normally alcohol absorption depends on how fast it reaches the small intestine, and when the stomach empties slowly, the absorption becomes slower and more erratic. The rapid onset that makes drinking feel rewarding is essentially gone.
The worse tolerance part is where people get caught off guard. Several things stack at once. You're eating much less overall, so when alcohol does pass through there's less food buffering it. Dehydration is more common on these compounds because thirst signaling drops and you're consuming less fluid with smaller meals, and alcohol compounds that. The glucagon agonism (which is the unique piece of retatrutide compared to pure GLP-1 drugs) shifts hepatic metabolism and increases glucose output, and how that interacts with ethanol metabolism isn't fully characterized yet. And the same mechanism in the area postrema that suppresses appetite also lowers your nausea threshold, so a drink or two that used to do nothing can now genuinely make you sick.
The net experience is less desire to drink in the first place, less reward when you do, and worse physical consequences per gram of ethanol. Hangovers tend to be disproportionately bad for the amount consumed. Most people just naturally drift toward drinking much less or stopping altogether without trying. If you do drink, hydration matters more than usual and starting low is smart, because your old tolerance is not a reliable reference point anymore.
SAME!!Sarsippius said:
I find it’s harder to just get a beer down due to the “fullness” vs not craving it. Pairing with the weight food or activity a cold beer is still very tempting. I’ve also been waiting for the Reta to help curb the nicotine pouch addiction I’ve read about. I’m only on week 5 so maybe that has something to do with it as well.
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