Does eating less food reduce addiction to tobacco, alcohol and other substances? Because there is mounting (but not conclusive) evidence that GLP-1 agonists do just that.
I have one friend in particular who started a GLP-1 drug solely to assist in drinking less - she certainly does not need to lose any weight. It worked like a light switch for her and turned moderately problematic drinking into easily achieved light social drinking. No impact on appetite since she is on a very low dose.
I have had the same experience, even though I took it for weight loss to start with.
I do know that drinking can be downright unpleasant for me if I push through the aversion after my first drink and try to go for a few more. I have noticed a strong correlation to drinking and my blood sugar crashing rapidly afterwards while on Tirzepatide while wearing a glucose monitor.
A single cold beer on hot day with friends is still quite pleasant. Sitting in a bar for hours on end drinking heavily is simply downright uninteresting now before you get into any unpleasant side effects.
Is this based on your survey or her self assessment?
> Sitting in a bar for hours on end drinking heavily is simply downright uninteresting
Yet it used to be? You don't find this situation suspect?
Both? Being around her, and her self-assessment. Not sure how else one could interpret such a statement. This is all anecdotal evidence and should be taken as such.
> Yet it used to be? You don't find this situation suspect?
Yes, it used to be moderately interesting sometimes with the right people. Suspect in what manner? That it removes the desire to get inebriated? Perhaps so, since we do not understand the mechanism at play. What we don't know can certainly hurt us.
Overall the desire to drink less seems very similar to the impact it has on appetite and hunger levels. In that way, it is not so surprising to me.
For example we see the same behaviors in mice
https://www.niaaa.nih.gov/news-events/research-update/semagl...
>In the current study, the researchers demonstrated that semaglutide reduced binge-like alcohol drinking in both male and female mice, and that the effect was dose-dependent (i.e., greater amounts of semaglutide led to greater reductions in binge alcohol intake). The researchers also tested semaglutide in rats that were made dependent on alcohol through long-term exposure to alcohol vapor. They found that semaglutide reduced alcohol intake in this animal model, again with no sex differences.
It is not documented, so no, it is not. Which is why I questioned if it was entirely based on self assessment or not and left the door open either way as the question was based out of curiosity and if his anecdote was public I wanted the answer to be as well. Is that not fair?
> when those pieces of data come together it provides evidence.
When you properly document them it literally stops being an anecdote and then becomes evidence.
> The researchers also tested semaglutide in rats that were made dependent on alcohol through long-term exposure to alcohol vapor.
So.. what are we actually measuring then? Isn't alcoholism a disease and not some acquired exposure based dependency? The idea that "GLP-1 for Everything" is even floated in this way is unusual in and of itself. I'm uncomfortable with all this and am once again annoyed at the way we use rats in research.