Upside Of Depression

Two brilliant papers on the upside of depression. The idea here is not to fall under the trap of societal bias against depression nor passively accept that depression is good but to accept and act on how to use it to make oneself learn and develop from what we rumiate. 

The bright side of being blue: Depression as an adaptation for analyzing complex problems:

Abstract

Depression ranks as the primary emotional problem for which help is sought. Depressed people often have severe, complex problems, and rumination is a common feature. Depressed people often believe that their ruminations give them insight into their problems, but clinicians often view depressive rumination as pathological because it is difficult to disrupt and interferes with the ability to concentrate on other things. Abundant evidence indicates that depressive rumination involves the analysis of episode-related problems. Because analysis is time consuming and requires sustained processing, disruption would interfere with problem-solving. The analytical rumination (AR) hypothesis proposes that depression is an adaptation that evolved as a response to complex problems and whose function is to minimize disruption of rumination and sustain analysis of complex problems. It accomplishes this by giving episode-related problems priority access to limited processing resources, by reducing the desire to engage in distracting activities (anhedonia), and by producing psychomotor changes that reduce exposure to distracting stimuli. Because processing resources are limited, the inability to concentrate on other things is a tradeoff that must be made to sustain analysis of the triggering problem. The AR hypothesis is supported by evidence from many levels, including genes, neurotransmitters and their receptors, neurophysiology, neuroanatomy, neuroenergetics, pharmacology, cognition and behavior, and the efficacy of treatments. In addition, we address and provide explanations for puzzling findings in the cognitive and behavioral genetics literatures on depression. In the process, we challenge the belief that serotonin transmission is low in depression. Finally, we discuss implications of the hypothesis for understanding and treating depression.

The evolutionary significance of depression in Pathogen Host Defense:

Abstract

Given the manifold ways that depression impairs Darwinian fitness, the persistence in the human genome of risk alleles for the disorder remains a much debated mystery. Evolutionary theories that view depressive symptoms as adaptive fail to provide parsimonious explanations for why even mild depressive symptoms impair fitness-relevant social functioning, whereas theories that suggest that depression is maladaptive fail to account for the high prevalence of depression risk alleles in human populations. These limitations warrant novel explanations for the origin and persistence of depression risk alleles. Accordingly, studies on risk alleles for depression were identified using PubMed and Ovid MEDLINE to examine data supporting the hypothesis that risk alleles for depression originated and have been retained in the human genome because these alleles promote pathogen host defense, which includes an integrated suite of immunological and behavioral responses to infection. Depression risk alleles identified by both candidate gene and genome-wide association study (GWAS) methodologies were found to be regularly associated with immune responses to infection that were likely to enhance survival in the ancestral environment. Moreover, data support the role of specific depressive symptoms in pathogen host defense including hyperthermia, reduced bodily iron stores, conservation/withdrawal behavior, hypervigilance and anorexia. By shifting the adaptive context of depression risk alleles from relations with conspecifics to relations with the microbial world, the Pathogen Host Defense (PATHOS-D) hypothesis provides a novel explanation for how depression can be nonadaptive in the social realm, whereas its risk alleles are nonetheless represented at prevalence rates that bespeak an adaptive function.