The evolutionary genetics of the creativity – psychosis connection

Schizophrenia, a debilitating mental illness affecting roughly 1 percent of the population worldwide, is widely accepted as being highly genetically influenced (Cardno et al., 1999; Gershon et al., 1988; Kendler and Diehl, 1993). Schizophrenia is often marked by distortions of reality, disorganized thought, emotional blunting, and/or social isolation that may interfere with optimal functioning (Cornblatt et al., 2012). Schizophrenia may be associated with creativity, although research findings are mixed (e.g., Andreasen, 2011; Kyaga et al., 2013). Evidence also points to adverse effects on fertility and reproductive success among (particularly) males with schizophrenia (Svensson et al. 2007), in part accounted for by marital status (McCabe et al., 2009), suggesting potential biological and social influences. Collectively, this raises an intriguing potential evolutionary puzzle: How does schizophrenia persist in the population at a stable prevalence rate too high to be explained by simple random mutation? (Doi et al., 2009; see Del Giudice et al., 2010). Among various hypotheses, including in the context of the emerging field of evolutionary epidemiology, schizophrenia may represent “one extreme of a sexually selected fitness factor” (Shaner et al., 2004). One possibility, which we explore in this chapter, is that schizophrenia remains in the human population (in part via the gene pool) because of shared genetic linkages to creativity (Andreasen, 2011; Carson, 2011), with acknowledgement of likely concurrent environmental (e.g., epigenetic) influences. Available evidence – particularly from twin