Abstract
The evolutionary basis for clinical depression is not well understood. A growing body of literature that is not based on evolutionary logic links inflammation to depression. Integration of these findings with an evolutionary framework for depression, however, needs to address the reasons why the body's inflammatory response would be regulated so poorly that it would result in incapacitating depression. Pathogen induction of inflammation offers an explanation, but the extent to which the association between inflammation and depression can be attributed to general inflammation as opposed to particular effects of pro-inflammatory pathogens remains unclear. This paper reports a study of sexually transmitted pathogens, which addresses this issue. Although several sexually transmitted pathogens were associated with depression according to bivariate tests, only Chlamydia trachomatis and Trichomonas vaginalis were significantly associated with depression by a multivariate analysis that accounted for correlations among the pathogens. This finding is consistent with the hypothesis that infection may contribute to depression through induction of tryptophan restriction, and a consequent depletion of serotonin. It reinforces the idea that some depression may be caused by specific pathogens in specific evolutionary arms races with their human host.
Highlights
The evolutionary reasons for the widespread presence of clinical depression are unclear
The only pathogens that were significantly correlated with depression in the multiple regression analysis were C. trachomatis and T. vaginalis
Our results show that several sexually transmitted pathogens were significantly associated with depression by bivariate analyses; only two of the tested pathogens – Chlamydia trachomatis and Trichomonas vaginalis – were significantly associated with depression after correlations among infections and pathogens were accounted for by multiple regression analysis
Summary
The evolutionary reasons for the widespread presence of clinical depression are unclear. One line of evolutionary reasoning suggests that depression may cause individuals to shift away from unattainable goals (Nesse 2019). This explanation, seems inadequate for prolonged, incapacitating depression which should be purged by natural selection (Coyne 2010; Nesse 2019). The adaptive argument for short-term depression, may help explain the presence of adaptive neurological circuitry which could function counter-productively when depression is prolonged and intractable. One hypothesis within this category of explanations invokes mismatches between modern and ancestral environments. An alternative mismatch hypothesis proposes that the neocortex is vulnerable to damaging environmental agents and that clinical depression results from the elevated presence of such hazards in modern relative to ancestral environments (Galecki and Talarowska 2017)
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