The idea that we drink to forget our sorrows is now, apparently, a scientifically-proven fact. Everyone who’s ever enjoyed a glass of booze after a rough day knows the release that comes with every sip, but it’s still surprising to find that your nightcap is just about as therapeutic as taking antidepressants. Which goes a long way toward explaining why we always turn to it.
The new discovery comes from Wake Forest Baptist Medical Center’s Wake Forest School of Medicine. The study, which was published under the incredibly exciting name, “FMRP regulates an ethanol-dependent shift in GABABR function and expression with rapid antidepressant properties” in the most recent issue of Nature Communications, was headed by School of Medicine associate professor of physiology and pharmacology Kimberly Raab-Graham, PhD., who said, “Because of the high comorbidity between major depressive disorder and alcoholism, there is the widely recognized self-medication hypothesis, suggesting that depressed individuals may turn to drinking as a means to treat their depression. We now have biochemical and behavioral data to support that hypothesis.”
Basically, we drink to be happy. Or to be less sad.
If you really want to get technical, the study, which used an animal model, found that a single dose of an intoxicating level of alcohol worked with the protein FMRP (which, interestingly enough, is associated with autism) to transform an acid called GABA from an inhibitor of neural activity into a stimulator of neural activity.