Depression’s evolutionary roots

Since there are intelligent people here who follow the topic of evolutionary psychology, I’d like to hear opinions about some research from 2009. Particularly if this idea seems reasonable or not, but possibly other opinions that people might have about it.

The idea is a variation on one that’s somewhat popular here: that some conditions usually regarded as mental illnesses (Asperger’s for example) are beneficial, even adaptive. But the condition in question now is depression. Briefly, the argument is that depression, at least when it is a response to stimuli and not a permanent feature, can have the useful effect of encouraging more rational thought when this is particularly important, even at the cost of quality of life, and that this is adaptive.

Links: a Scientific American article, a journal article (which I haven’t read, behind a $12 paywall). Here’s the abstract of the journal article:

Depression is the primary emotional condition for which help is sought. Depressed people often report persistent rumination, which involves analysis, and complex social problems in their lives. Analysis is often a useful approach for solving complex problems, but it requires slow, sustained processing, so disruption would interfere with problem solving. The analytical rumination hypothesis proposes that depression is an evolved response to complex problems, whose function is to minimize disruption and sustain analysis of those problems by (a) giving the triggering problem prioritized access to processing resources, (b) reducing the desire to engage in distracting activities (anhedonia), and (c) producing psychomotor changes that reduce exposure to distracting stimuli. As processing resources are limited, sustained analysis of the triggering problem reduces the ability to concentrate on other things. The hypothesis is supported by evidence from many levels—genes, neurotransmitters and their receptors, neurophysiology, neuroanatomy, neuroenergetics, pharmacology, cognition, behavior, and efficacy of treatments. In addition, the hypothesis provides explanations for puzzling findings in the depression literature, challenges the belief that serotonin transmission is low in depression, and has implications for treatment.

The full journal citation is Andrews, Paul W., and Thomson Jr., J. Anderson; July 2009; Psychological Review 116 (3), 620–654; doi 10.1037/​a0016242.