causal variants. As such, these results suggest that common additive genetic variants account for little of the variation in Cloninger's personality traits, and therefore rare genetic variants and/or some combination of dominance and epistasis are likely to account for most of the variation. This is consistent with the hypothesis that genetic variation in human personality traits has been maintained by mutation-selection balance, but is less consistent with it being selectively neutral or maintained by pleiotropic balancing selection or balancing selection via environmental heterogeneity. Overdominance might also be consistent with these results because it predicts high levels of dominance variation, but it also predicts that genetic variation is due to common alleles at a relatively small number of loci per trait (Curtsinger et al. 1994; Burger 2000), which is inconsistent with previous research on these and other personality scales (de Moor et al. 2010; Verweij et al. 2010). The contribution of common additive genetic variants to genetic variation in personality traits is less than that of some other traits that have been subject to the same analysis - for example, the proportion of the genetic variation that can be explained by common SNPs is around half for height (Yang et al.
