It is the discovery of a stress risk gene, but ambivalent, which sheds light on the development of depression, due to various factors, social or financial: because this same gene has a protective effect when it comes to social factors and aggravating when it comes to financial factors. Conclusions presented at the 31st Congress of the European College of Neuropsychopharmacology which, in addition to possible indications for better management of depression, provide a possible answer to a question that has long perplexed scientists: why depression has survived through evolution?
Indeed, these researchers from the University of Budapest found that the same gene, 5-HTTLPR, present on chromosome 17, increases the risk of depression with financial stress and also reduces the risk of depression associated with friendship and to social relationships.
5-HTTLPR is a variant of the gene that codes for the production of the serotonin transporter protein, essential to the pharmacology of depression. Thus, antidepressants such as selective serotonin reuptake inhibitors (SSRIs, including, for example, Prozac, Paxil, Zoloft) form the mainstay of drug treatment for depression. One of the two variants of 5-HTTLPR, “the short variant” is already documented to promote a tendency towards depression, to some extent however, since depression is associated with many genes.
5-HTTLPR vs 4 different types of stress: this new work is conducted with 1,081 participants, aged under 30, asked about 4 different types of stress related to relationship problems, illness or trauma and financial difficulties. This analysis finds that the short variant of 5-HTTLPR, present in approximately 37-40% of the population, confers statistically significant protection against the risk of depression as a result of social difficulties, but not against the other stressors taken into account. account in the study.
Depression has survived through evolution: This gene could explain why depression has survived when for an inherited trait to survive over time it must normally have an advantage. In the case of depression, there was previously no obvious reason. The study shows that the 5-HTTLPRs variant also has an advantage, it can also help protect against depression associated with social stressors, which may also explain its persistence. On the other hand, previous research, cited by the authors, shows that the same variant may also increase the risk of depression following financial stress, particularly in older men.
The scientists comment: “ What we see is that the same gene has opposite effects on the development of depression, depending on different environmental factors and even at different times of life. For people under 30, the social network is vital. At this time of life, the “s” variant of 5-HTTLPR protects them against depression. The same variant increases the risk of depression in the event of financial difficulties during aging .
And on a therapeutic level, the study has implications: Depression is not a single disease, it is linked to different types of genes and different environmental factors. The disease can therefore respond to different types of pharmacological and psychotherapeutic treatments. For example, patients with higher social sensitivity conferred by the s allele may respond better to psychotherapy than those who do not carry this variant…
The message to remember is therefore that “depressogenic” genes are not always so, it depends on their environmental context, gender, age and type of stress.
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