Evolutionary origins of depression: a review and reformulation

An evolutionary model of low mood states

“…That is a question of individual variation, beyond the scope of this paper (Nettle, 2004). Instead, this kind of ultimate reasoning might shed some light on the species-typical design of the mechanisms of mood, which sometimes make us pessimistic and risk-averse, and sometimes impulsive and risk-prone.…”

“…Since the generic trigger of low mood is loss of or lack of access to some important resource, low mood may usefully be seen as an evolved suite of responses to unpropitious or adverse situations (Allen and Badcock, 2003;Nesse, 2000;Nesse, 2006;Watson and Andrews, 2002). Note that this does not mean that clinical depression itself represents adaptive behaviour; clinical cases may represent instances where the evolved mechanisms are chronically overactive or have become dysregulated (Nesse, 2000;Nettle, 2004). However, evolutionary reasoning may still be useful for understanding why low mood has the fundamental features that it does.…”

Evolutionary genetics of affective disorders

“…The general paucity of population-genetic evidence for balancing selection on genes underling mental disorders may arise in part from ascertainment bias in SNPbased scans for selection, such that high-frequency variants are differentially detected (Kelley and Swanson 2008). At the phenotypic and epidemiological levels, psychotic-affective cognition or disorders have been associated with measures of enhanced creativity (Nettle 2001;Burch et al 2006), mating success (Nettle and Clegg 2006), socio-economic achievement (Jamison 1996;Johnson 2005) and, in several studies, higher fertility of first-order relatives (reviewed in Crespi et al 2007;Crespi and Badcock 2008), compared to controls. These findings are consistent with evolutionary benefits of alleles and genotypes underlying such disorders but they do not directly or quantitatively address any particular model based on positive or balancing selection.…”

“…Most evolutionary approaches to the analysis of human cognitive function, affective states, and mental disorders have focused on the potential adaptive significance of the phenotypes involved, in ancestral or modern environments (e. g. Nesse 1999;Nettle 2001Nettle , 2004. According to such evolutionary hypotheses, natural selection has optimized human mental phenotypes in the context of functions that are related to reproductive success, and mental disorders have been inferred to represent either unavoidable, maladaptive byproducts of such selection (e. g., Burns 2006), tails of continuous distributions of genetically-based cognitive-affective functional abilities (e. g., Nesse 2004), or manifestations of associations between enhanced abilities in some domain of performance, such as creativity, emotional sensitivity, or propensity to strive for success, and increased risk of mental illness (e. g., Nettle 2001Nettle , 2004Nettle , 2006a.…”

“…According to such evolutionary hypotheses, natural selection has optimized human mental phenotypes in the context of functions that are related to reproductive success, and mental disorders have been inferred to represent either unavoidable, maladaptive byproducts of such selection (e. g., Burns 2006), tails of continuous distributions of genetically-based cognitive-affective functional abilities (e. g., Nesse 2004), or manifestations of associations between enhanced abilities in some domain of performance, such as creativity, emotional sensitivity, or propensity to strive for success, and increased risk of mental illness (e. g., Nettle 2001Nettle , 2004Nettle , 2006a. In this context, major depression and bipolar disorder can be interpreted as forms of dysregulation of adaptive mental systems that regulate mood, where low mood and high mood are normally-adaptive states that contextually-regulate physiology, cognition and behavior to maximize fitness (Nesse 2000;Nettle 2004;Johnson 2005;Wolpert 2008).…”