Posted by linkadge on May 20, 2021, at 17:42:00
In reply to Attn: Linkadge(?) Can you elaborate on this study?, posted by PeterMartin on May 20, 2021, at 12:10:50
So reading over the study, it seems that GLP-1 agonism *decreases* the release of dopamine in the nucleus accumbens that results from cocaine administration.
I.e. cocaine increases dopamine release in the nucleus accumbens and GLP-1 agonists (i.e. potentially Semaglutide) would reduce this.
As to whether it decreases the (possible) addictive effects of ritalin is unclear (but would seem logical). Ritalin also activates the reward system, but to a lesser extent than cocaine. The study suggested that the decrease was not due to effects on dopamine transporter binding (i.e. it is not directly counteracting the drug's effect). I would be interested to find out if GLP-1 agonists decrease dopamine release in other brain regions. If so, it may mean an overall decrease in the efficacy of ritalin (i.e. requiring a higher dose). However, I wouldn't necessarily assume that this would happen. Ritalin's actions are complex. Although dopamine plays a role in it's effects, it may have additional effects that go beyond increasing dopamine. Also, I wouldn't assume that Semaglutide is decreases overall dopamine function (unless a study indicated this).
If the decrease in dopamine release from Semaglutide was selective to the nucleus accumbens, then I would think that it could counteract some of the addictive potential of ritalin. That being said, some studies link ADHD to reward deficits (which ritalin may help counteract).
This being said, I wouldn't read into it too much. What happens on paper doesn't always directly translate to what occurs in real life. I would go based on your response to the medications. For example:
Do you notice any less ups / downs when taking ritalin?
Do you notice any loss of efficacy?
Linkadge
poster:linkadge
thread:1115174
URL: http://www.dr-bob.org/babble/20210418/msgs/1115181.html