Maltreated Children
The role of genotype in the cycle of violence in maltreated children
Caspi, Avshalom, Joseph McClay, Terrie E. Moffitt, Jonathan Mill, Judy Martin, Ian W. Craig,
Alan Taylor & Richie Poulton. (2002). The role of genotype in the cycle of violence in maltreated children. Science, 297: 851-853.
The study "the role of genotype in the cycle of violence in maltreated children" (Caspi et al. 2002) addresses a commonly-observed phenomenon seen in anecdotal experience. Although maltreatment in childhood may seem to predispose some adolescents to act out later in life, not all maltreated children engage in delinquent or criminal behavior. "Maltreatment increases the risk of later criminality by about 50%" (Caspi et al. 2002: 851). The study proposes that certain genetic markers predispose individuals towards criminality while other acted as a buffer against antisocial behavior. "Individual differences at a functional polymorphism in the promoter...
2002: 851).
The MAOA gene is responsible for metabolizing the neurotransmitters norepinephrine (NE), serotonin (5-HT), and dopamine (DA). Having enough of these 'feel good' chemicals has been linked to guarding against depression, anxiety, and other mental disorders. In the case of individuals who manifested antisocial tendencies later in life, a deficiency in the MAOA gene was strongly linked to more aggressive behaviors.
But the mechanism of MAOA is more complex than simply causing aggression when there is a deficit of the chemical. Stress itself, not simply genetics, can cause abnormalities in MAOA's impact upon human development. "Maltreatment stress (e.g., maternal deprivation, peer rearing) in early life alters NE, 5-HT,…
, 2002). It is now widely believed that vulnerability to bad behavior is conditional and depends on genetic susceptibility (Kendler, 2001; Rutter & Silberg 2001; in Caspi et al., 2002). This theory was tested by Caspi et al. (2001) when they attempted to predict antisocial behavior among more than 1000 male maltreated children by genotyping their polymorphism at the MAOA gene. Their findings provided epidemiological evidence that high MAOA expression moderates