A widely recognized self-medication hypothesis suggests that individuals that are depressed may treat their depression by using alcohol. This hypothesis is supported by the high comorbidity between alcoholism and major depressive disorder.
In a new study, researchers have found that on a biochemistry level, drugs that are known to be effective as rapidly effective antidepressants produce the same molecular and neural changes as alcohol. Kimberly Raab-Graham, Ph.D., associate professor of physiology and pharmacology at Wake Forest School of Medicine, a part of the Wake Forest Baptist Medical Center and the study’s principal investigator, notes that the hypothesis is now supported by behavioral and biochemical data. She does however caution that alcohol should not be viewed as an effective treatment for depression based on these findings.
She adds that self-medicating with alcohol is dangerous, as there is a very fine line between alcohol being harmful and helpful, and that with repeated use, self-medication will most likely turn into an addiction.
Raab-Graham and her colleagues conducted experiments with animals and found that a single dose of an intoxicating level of alcohol resulted in non-depressive behavior lasting for at least 24 hours. The alcohol blocks proteins associated with learning and memory (NMDA receptors). This works in combination with the autism-related protein FMRP and transforms an acid called GABA from an inhibitor to a stimulator of neural activity. These biochemical changes lead to the non-depressive behavior.
This study proved that alcohol induced the same biochemical reaction as rapid antidepressants do in the animals. The result is behavioral changes that can be compared to those observed in people. Ketamine is an example of one rapid antidepressant that has been proven capable of relieving depressive symptoms within hours with a single dose. Even in individuals who have proven to be resistant to traditional antidepressants, the effect can last for up to two weeks.
Raab-Graham notes that the natural human instinct to self-medicate with alcohol has been validated by the biological basis found in the research, but cautions that more research is needed in this area.
A specific molecular mechanism has also been defined in the study. This mechanism is possibly a critical contributor to the comorbidity that occurs with major depressive disorder and alcohol use disorder.
Full study has been published in the Nature Communications.