It has been proposed that individual differences in vulnerability to maltreatment are partially genetically mediated by a common functional length polymorphism in the promoter sequence of the serotonin transporter gene (5-HTTLPR) (Caspi et al., 2003). This hypothesis was supported in a number of studies focusing on threatening events in which physical, sexual, or relational harm against children was carried out or intended (Aguilera et al., 2009; Aslund et al., 2009; Benjet et al., 2010; Cicchetti et al., 2007; Kaufman et al., 2004; Kumsta et al., 2010; Sugden et al., 2010), but inconsistent results have also been reported, especially in studies of childhood adversities other than maltreatment (Araya et al., 2009; Ritchie et al., 2009; Surtees et al., 2006; Wichers et al., 2008). Although the most recent and complete meta-analysis has confirmed that the 5-HTTLPR significantly moderates the depressogenic effects of childhood maltreatment (Karg et al., 2011), these inconsistent results require explanation.
