Alcohol and rapid antidepressants have same effects on the brain
Alcohol can have the same molecular and neural changes in the body as rapid antidepressants, according to new research. The study showed that in terms of biochemistry, alcohol can help people diagnosed with clinical depression feel better.
The researchers, however, noted that this does not mean alcohol is an effective treatment for depression.
Researchers administered a single dose of an intoxicating level of alcohol to an animal model thereby blocking its NMDA receptors, which are proteins linked to learning and memory. This dose of alcohol works with FMRP receptors, which are autism-related proteins, and converts GABA acid from an inhibitor of neural activity to a stimulator.
The team found that the biochemical changes that occurred from consuming alcohol resulted in nondepressive behavior. These changes lasted for at least 24 hours.
“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,” Kimberly Raab-Graham, the study’s principal investigator from the Wake Forest School of Medicine in North Carolina, said in a statement. “We now have biochemical and behavioral data to support that hypothesis.” He added there is a danger in self-medicating using alcohol where repeated self-medication can turn into addiction.
The findings indicated that alcohol and rapid antidepressants followed the same biochemical pathway in animals. The resulting changes in animals are similar to those observed in people.
"[...] our data define a common molecular paradigm for alcohol and rapid antidepressants, and identify a mechanism for the initial antidepressant effects of alcohol.
A shift in signaling is observed with both rapid antidepressants and acute ethanol treatment, which may provide insight into the molecular basis for the high comorbidity between major depressive disorder and AUD [alcohol use disorder]."
“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.”