Can having a few
drinks help people with clinical depression feel better?
Yes. At least in terms of biochemistry.
In a study published in the current issue of the journal
Nature Communications, researchers found that alcohol produces the same neural
and molecular changes as drugs that have proven to be rapidly effective
“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,” said the study’s principal investigator,
Kimberly Raab-Graham, Ph.D., associate professor of physiology and pharmacology
at Wake Forest School of Medicine, part of Wake Forest Baptist Medical Center. “We
now have biochemical and behavioral data to support that hypothesis.”
This, however, does not at all suggest that alcohol can
be regarded as an effective treatment for depression.
“There’s definitely a danger in self-medicating with
alcohol,” Raab-Graham said. “There’s a very fine line between it being helpful
and harmful, and at some point during repeated use self-medication turns into
In their study using an animal model, Raab-Graham and her
colleagues found that a single dose of an intoxicating level of alcohol, which
has been shown to block NMDA receptors (proteins associated with learning and
memory), worked in conjunction with the autism-related protein FMRP to
transform an acid called GABA from an inhibitor to a stimulator of neural
activity. In addition, the research team found that these biochemical changes
resulted in non-depressive behavior lasting at least 24 hours.
This study demonstrated that alcohol followed the same biochemical
pathway as rapid antidepressants in the animals, while producing behavioral
effects comparable to those observed in people. In recent years, single
doses of rapid antidepressants such as Ketamine have proven capable of relieving
depressive symptoms within hours and lasting for up to two weeks, even in
individuals who are resistant to traditional antidepressants.
“Additional research is needed in this area, but our
findings do provide a biological basis for the natural human instinct to
self-medicate,” Raab-Graham said. “They also define a molecular mechanism that
may be a critical contributor to the comorbidity that occurs with alcohol use
disorder and major depressive disorder.”
The study was supported by an National Institutes of
Health/National Institute on Alcohol Abuse and Alcoholism pilot grant provided
by the Integrated Neuroscience Initiative on Alcoholism; National Science
Foundation grant I0S-1355158; Department of Defense USAMRMC Award W81XWH-14;
NIA/NIAA grants AA012404, AA013517 and 5T32AA007471; and NSF Postdoctoral
Research Fellowship in Biology awards DBI-2306528 and DBI-1103738.
Co-authors of the study are Chelcie F. Heaney, Ph.D., of
Wake Forest Baptist and Sara A. Wolfe, M.A., Emily R. Workman, M.A., Farr
Niere, Ph.D., Sanjeev Namjoshi, B.S., Luisa P. Cacheaux, Ph.D., Sean P. Farris,
Ph.D., Michael R. Drew, Ph.D., Boris V. Zemelman, Ph.D., and R. Adron Harris,
Ph.D., of the University of Texas at Austin.