Why Depression Might Be Adaptive

A very general, short review of adaptationist theories of depression.

Major depressive disorder is the most common psychiatric disorder in the United States, affecting 18% of adults (ADAA). Those with depression are lethargic, withdraw from social relationships, and don’t get pleasure from typically enjoyable activities such as eating and sex—a symptom called anhedonia (Watson & Andrews). All this might lead you to believe that depression is maladaptive, some vestigial structure that somehow slipped through the cracks of time. If depression were purely maladaptive, then yes, it would be quite perplexing that it’s so common. However, many have theorized about adaptive explanations for depression, reasons why it may have increased individuals’ fitness and thus persisted. I’ll present and review a couple of these hypotheses—the analytic rumination hypothesis and the inflammation hypothesis—and touch upon some big themes in evolutionary medicine such as tradeoffs, genetics, and evolutionary mismatch.

The analytic rumination hypothesis is part of a much broader class of social adaptationist hypotheses about depression (Gilbert). It posits that one of the hallmarks of depression, rumination, was actually adaptive because it allowed for sustained problem-solving and high-level analytical thought. The anhedonia, appetite suppression and lethargy characteristic of depression are features, not bugs, because they allow for this energetically costly problem-solving to happen uninterrupted (Andrews & Thomson Jr.). Because we are social creatures, in our evolutionary past these problems would have been social in nature: analyzing what others think of you, knowing who is allied with whom, etc. Being able to ruminate on these problems for long periods of time would have allowed for better navigation of one’s social scene, which presumably would increase fitness. This hypothesis is further strengthened by the fact that social conflict is highly correlated with the onset of a depressive period, suggesting that depressive rumination is specifically about social problem-solving (Watson & Andrews; Coyne & Downey).

While appealing, Watson and Thomson’s hypothesis needs more evidence in order for it to be a fully fleshed-out theory and not just an evolutionary “just-so story.” One such line of evidence comes from neurophysiology. Depression is often attributed to an imbalance of neurotransmitters in the brain, specifically serotonin. Those with depression have malfunctioning serotonin receptors and often take SSRI’s—a class of medications which improve one’s receptivity to serotonin—because of imbalance of neurotransmitters. Andrews and Thomson point out that this reduced serotonin receptivity in those with depression may actually make attention—an energetically costly cognitive function key to problem-solving—less energetically costly, and thus more sustainable (Andrews & Thomson Jr.). The neurophysiological literature seems to bear this out, and this evidence fits in neatly with the analytical rumination hypothesis.

While the analytical rumination hypothesis is provocative, some think that it is barking up the wrong tree and that depression’s adaptive value is immunological, not social. A meta-analysis by Barnes et al. found that genetic variations associated with depression seem to correspond with key variations in immune system function (Barnes et al.) Specifically, Gene Wide Association Studies (GWAS)—which look at the whole genome of a population and identify correlations between diseases and specific genes and polymorphisms—find that many of the polymorphisms associated with depression affect key parts of our immune system such as cytokines (Raison & Miller). They argue that in our evolutionary past, those with depression would have greater inflammatory responses to pathogens, decreasing the likelihood of the pathogen’s survival, thus improving the fitness of the depressive host. Furthermore, the behavioral symptoms of depression such as social withdrawal may have prevented our ancestors from being exposed to pathogen and increased their likelihood of survival (Raison and Miller, The Atlantic). This hypothesis is strengthened by evidence showing a high rate of co-occurrence between autoimmune diseases (which affect the immune system) and mood disorders such as depression (Benros et al.)

Obviously the etiology of depression is quite complex, as are its symptoms, and I’ve only touched the tip of the iceberg. In this blog I’ve used one term, “depression,” to cover a disorder whose symptoms range from mild lethargy to suicidality, but in reality a fully fleshed out explanation of depression would have to talk about the various gradations and intensities of depression. That said, hopefully a better understanding of the distal, evolutionary causes of depression can improve our treatment of it.


ADAA (Anxiety and Depression Association of America). 2016. “Facts and Statistics.” https://www.adaa.org/about-adaa/press-room/facts-statistics

Allen, Nicholas B., and Paul B.T. Badcock. 2006. “Darwinian models of depression: A review of evolutionary accounts of mood and mood disorders.” Progress in Neuro-Psychopharmacology & Biological Psychiatry 30: 815-826.

Andrews, Paul W., and J. Anderson Thomson Jr. 2009. “The bright side of being blue: depression as an adaptation for analyzing complex problems.” Psychological Review 116(3): 620-654.

Barnes, J., Mondelli, V., and C.M. Pariante. 2017. “Genetic contributions of inflammation to depression.” Neuropsychopharmacology 42(1): 81-98.__

Benros, Michael E., Waltoft, Berit L., Nordentoft, Merete, Østergaard, Søren D., Eaton, William E., Krogh, Jesper, and Preben B. Mortensen. 2013. “Autoimmune diseases and severe infections as risk factors for mood disorders: a nationwide study.” JAMA Psychiatry 70(8): 812-820.

Coyne, James C., and Geraldine Downey. 1991. “Social factors and psychopathology: stress, social support, and coping processes.” Annual Review of Psychology 42: 401-425.

Gilbert, Paul. 2006. “Evolution and depression: issues and implications.” Psychological Medicine 36: 287-297.

Raison, C.L., and A.H. Miller. 2013. “The evolutionary significance of depression in Pathogen Host Defense (PATHOS-D).” Molecular Psychiatry 18: 15-37.

Watson, Paul J., and Paul W. Andrews. 2002. “Toward a revised evolutionary and adaptationist analysis of depression: the social navigation hypothesis.” Journal of Affective Disorders 72: 1-14.