The answer is yes. At least in terms of biochemistry. In a study published in the journal Nature Communications , researchers at the Wake Forest School of Medicine at Wake Forest Baptist Medical Center (USA) found that alcohol produces the same neural and molecular changes as drugs, substances that have proven to be very effective antidepressants.
“Due to the high comorbidity between major depressive disorder and alcoholism, there is a widely recognized self-medication hypothesis, which suggests that depressed individuals may turn to drinking as a means of treating their depression. We now have behavioral and biochemical data to support them. to support this hypothesis “comments Kimberly Raab-Graham, leader of the work.
This, however, in no way suggests that alcohol can be considered an effective treatment for depression, since the danger of self-medicating with alcohol is more than palpable. The line between using it as a useful tool or a harmful tool is very fine: “ At some point during repeated use, self-medication becomes an addiction, ” Raab-Graham says.
In their animal experiment, the researchers discovered that a single dose of alcohol was shown to block NMDA receptors (proteins associated with learning and memory), and to work in conjunction with the autism-related protein FMRP to transform an acid called GABA from an inhibitor to a stimulator of neuronal activity. These biochemical changes resulted in non-depressive behavior that lasted at least 24 hours.
The study showed that alcohol followed the same biochemical pathway as antidepressants, while producing behavioral effects comparable to those seen in people. In recent years, single doses of rapid antidepressants such as ketamine have been shown to be able to relieve depressive symptoms in a matter of hours and last up to two weeks, even in individuals who are resistant to traditional antidepressants.
“ Additional research is needed but our results provide a biological basis for the natural human instinct to self-medicate. 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.” , Raab-Graham ends.
