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142 EFFECTS OF EARLY MALTREATMENT AND STRESSDifferential vulnerability to early neglect and maltreatment and differential responsivenessto intervention are not simply noise in our research, but are potentialclues that may aid our understanding of the mechanisms of early experienceeffects and thus our ability to intervene more effectively with the difficult-to-helpcases. It is unlikely that these individual differences can be reduced to variationin genetic vulnerabilities; on the other hand, it is also likely that genetics play arole. Recently, studies of variations (polymorphisms) in the serotonin transportergene provide evidence that this major neurotransmitter system is involved in mediatingthe impact of early adverse caregiving.Both humans and rhesus monkeys have similar functional variations in the serotonintransporter, or SERT, gene (Bennett et al., 2002). The variations involve thepromoter region of the gene—that is the region that regulates gene transcription.One version of the SERT gene (short) appears to reduce the efficiency of serotoninregulation. Individuals carrying at least one short SERT allele may be at higher riskof impairments in stress-emotion system functioning under conditions of adversity,particularly perhaps, adversity during early development. Caspi and colleagues(Caspi, Sugden, & Moffit, 2003), for example, have shown that the onset of depressionis associated with the short SERT allele, but only for individuals who experiencemore stressful life events, including being maltreated prior to puberty.Conversely, carrying two long versions of the gene seems to protect maltreatedchildren from depression as a consequence of their maltreatment history.In studies of rhesus monkeys, animals carrying one short copy of the SERT genewere found to be at risk for low serotonin production (Higley, Suomi, & Linnoila,1992), high HPA axis stress responses (Fahlke et al., 2000), and an affinity for alcoholconsumption if they were reared without mothers (i.e., with only other infantmonkeys as attachment figures), but not if they were mother reared (Bennett et al.,2002). Conversely, monkeys with two long versions of the gene seemed relativelyprotected from these adverse consequences of peer-only rearing. Finally, in the repeated,unpredictable separation paradigm described earlier, it was the infants withtwo short SERT alleles that exhibited heightened HPA axis stress responses as aconsequence of this early adversity (Sanchez et al., 2005). It is likely that the SERT–stress story is only one of many gene-environment interactions that play a role inindividual differences in vulnerability to early adverse care and susceptibility tointervention. Understanding these stories should help us identify the neural systemsimpacted by early adverse care and may potentially help guide the selection of interventionexperiences that will be most helpful for different children.Future DirectionsThe work outlined above is an example of the emerging field of translational studiesfocused on bringing basic science to bear on clinically significant problems. When