Commentary: Childhood abuse: new insights into its association with posttraumatic stress, suicidal ideation, and aggression.

The publication of the Battered Child Syndrome (Kempe, Silverman, Steele, Droegemueller, & Silver, 1962) opened our eyes to the large number of abused children. With this awareness came the dawning realization that exposure to early adversity is a major risk factor for psychopathology and poor health. The most sobering statistics arise from the Adverse Childhood Experiences Study. Based on retrospective reports from 17,337 adult HMO members they concluded that exposure to early abuse and adversity accounted for 50–78% of the population attributable risk for drug abuse, depression, alcoholism, and suicide attempts [see (Anda et al., 2006) for a review]. Further, early adversity leads to the adoption of unhealthy habits (e.g., smoking, risky sex) associated with premature death. To paraphrase Fellitti, ‘‘what we recognize as common disorders in adult medicine and psychiatry are likely the result of what we fail to recognize or address in childhood (Felitti, 2002).’’ Developmental traumatology is still in its infancy. We do not understand why exposure to abuse appears to profoundly affect some individuals but not others, or why it may be associated with posttraumatic stress disorder (PTSD) in some; depression, substance abuse, or antisocial behaviors in others still. The articles in this issue bring new findings to bear on these questions. Cicchetti and colleagues (2010) addresses two key factors likely to influence outcome: genetic polymorphisms and the number of different types of adversity endured. They provided evidence for a gene environment (G E) interaction involving abuse, the serotonin transporter promoter polymorphisms (5HTTLPR), and suicidal ideation. They found that the short form of the 5HTTLPR gene conveyed vulnerability while two copies of the high efficiency long form provided protection. However, this protective effect was only apparent in individuals with moderate levels of exposure, but not in individuals exposed to three or four different types of abuse. Dose-dependent protection also emerged in a recent paper by Weder et al., (2009). Hence, it is likely that some polymorphisms act to right or left shift the dose-response relationship between trauma and outcome, predominantly affecting individuals with moderate levels of exposure. Gordis and colleagues (2010) explored the hypothesis that autonomic nervous system (ANS) activity buffers the effects of maltreatment on aggression. They presented interesting findings that presume that the ANS was unaffected by abuse. This premise is reasonable as they failed to observe ANS differences associated with maltreatment. However, there is an important alternative. Exposure to early stress may program some individuals to have an enhanced sympathetic fight–flight reaction (Heim et al., 2000), and others to have a blunted response (Macmillan et al., 2009). We suspect that heightened sympathetic responses emerge in situations where fight or flight is adaptive. In contrast, a submissive parasympathetic response may be lifesaving in other situations. Hence, the association between ANS and aggression may depend on the adaptive programming of the ANS to foster aggressive, avoidant, or submissive responses. Carrión and colleagues (2010) and De Bellis (2001) focused on the relationship between abuse, PTSD, and hippocampal function. This is an intriguing area as at least five studies have shown an association between childhood abuse and reduced hippocampal volume in adults while at least three studies have failed to find a similar association in children. It is likely, as we proposed (Teicher, Andersen, Polcari, Anderson, & Navalta, 2002),