A new study showed that Semaglutide, a drug used to treat obesity and diabetes, significantly reduced alcohol consumption and the rate of relapses in alcohol-dependent rats, offering promise for its use in human alcohol dependency treatment. The drug appears to block alcohol-induced dopamine release in the brain’s reward system, which could potentially curb the rewarding effects of alcohol, although clinical studies on humans are needed to confirm these findings.
The medication Semaglutide, also known by brand names like Ozempic, has been approved to treat obesity, leading to an upsurge in demand that’s caused recent procurement issues. Some patients struggling with obesity or diabetes have informally reported that their alcohol cravings diminished after starting this medication.
Currently, a blend of assorted psychosocial techniques and drugs is used to treat individuals suffering from alcohol dependence. There are four approved medications on the market. Given the multifaceted nature of alcohol dependence as a disease with numerous origins, these medications’ effectiveness can vary. Therefore, the development of additional treatment options is crucial.
Reduced relapses
Semaglutide is a long-acting substance that only needs to be taken once a week. This is the first medication to act on the GLP-1 receptor that can be taken in tablet form.
The results of the study are published in the scientific journal eBioMedicine. In the study, alcohol-dependent rats were treated with semaglutide, which significantly reduced their alcohol consumption and even reduced the drinking of alcohol in conjunction with relapses. Relapses comprise a major problem for individuals with alcohol dependence, as an individual who has abstained from alcohol for a period relapses and drinks more than before the withdrawal.
Elisabet Jerlhag Holm and Cajsa Aranäs, Sahlgrenska Academy at the University of Gothenburg. Credit: Johan Wingborg, Elin Lindström
In the study, the treated rats cut their alcohol intake in half compared to animals that did not receive treatment. One interesting finding in the study was that semaglutide reduced alcohol intake equally in both male and female rats.
Animals and humans
The study reports a strikingly good effect, although clinical studies will be required before the medication can be used for alcohol dependence, and such studies take time. Moving forward, the medication may be of most benefit to patients suffering from both overweight and alcohol dependence. According to the researchers, it is likely that these results will carry over to humans, as results from other studies on alcohol dependency medications made with the same research model have shown similar effects in humans as in rats.
“There are, of course, differences in conducting studies on animals and humans, and these must always be taken into account. However, in this case, there is a previous study on humans in which an older version of the diabetes medications that act on GLP-1 was found to reduce alcohol intake in overweight individuals with alcohol dependence,” says Elisabet Jerlhag, professor of pharmacology at Sahlgrenska Academy at the University of Gothenburg.
Mechanisms in the brain
The current study also examined why the medication reduces alcohol drinking. The results indicate that reduced alcohol-induced reward could be a contributing factor. In the study, semaglutide affected the brain’s reward system in mice, to be more exact the nucleus accumbens area of the brain, which is part of the limbic system.
“Alcohol activates the brain’s reward system, resulting in the release of dopamine, something that is seen in both humans and animals. This process is blocked by the medication in mice, and with our interpretation, this could cause a reduction in the alcohol-induced reward,” says Cajsa Aranäs, a doctoral student at Sahlgrenska Academy at the University of Gothenburg, who is responsible for much of the work behind the study presented here.
Reference: “Semaglutide reduces alcohol intake and relapse-like drinking in male and female rats” by Cajsa Aranäs, Christian E. Edvardsson, Olesya T. Shevchouk, Qian Zhang, Sarah Witley, Sebastian Blid Sköldheden, Lindsay Zentveld, Daniel Vallöf, Maximilian Tufvesson-Alm and Elisabet Jerlhag, 7 June 2023, eBioMedicine.
DOI: 10.1016/j.ebiom.2023.104642
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