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At the same time, depression involves conspicuous somatic symptoms of appetite and weight change, sleep disturbance, and sexual dysfunction (DSM-5; APA, 2013; Beck, 1967; Devlin & Walsh, 1989; Paykel, 1977; Schuyler, 1974) as well as varied non-specific complaints such as fatigue, dizziness, pain, and headache (Jain, 2009; Kapfhammer, 2006; Simon et al., 1999).
The latter are the primary indicators of depression in many cultures (Kim, 2010; Kleinman, 2004; Simon et al., 1999; Yusim et al., 2010) and are among the more common indicators of depression in children (Mc Cauley, Carlson, & Calderon, 1991; Ryan et al., 1987).
An explosion of research in the area of interoception-the perception and interpretation of bodily signals-over the last decade nonetheless holds promise for illuminating what have until now been obscure links between the social, cognitive-affective, and somatic features of depression.
This article reviews rapidly accumulating evidence that both somatic signaling and interoception are frequently altered in depression.
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Depression is also a common correlate of extreme homeostatic disturbance, as occurs in starvation (Brozek, Guetzkow, Vig Baldwin, & Cranston, 1951; Fliederbaum, Heller, Zweibaum, & Zarchi, 1979) and anorexia nervosa (e.g., Halmi et al., 1991).Despite such close association, cognitive approaches have tended to privilege the cognitive and behavioral over the somatic features of depression (e.g., Gotlib & Joormann, 2010).Neurobiological and neuropsychiatric approaches have similarly tended toward strict —assuming that the most important causes of disorder necessarily operate at the level of the brain and the neurons, circuits, and synapses therein—often to the exclusion of large portions of the physiological systems of interest (cf.This paper reviews rapidly accumulating evidence that both somatic signaling and interoception are frequently altered in depression.is a longstanding problem (e.g., Burton, 1621; Fuchs, 2005; Micali, 2011; Pollitt, 1965).