%0 Journal Article
%T Does the oxytocin receptor polymorphism (rs2254298) confer 'vulnerability' for psychopathology or 'differential susceptibility'? insights from evolution
%A Martin Brščne
%J BMC Medicine
%D 2012
%I BioMed Central
%R 10.1186/1741-7015-10-38
%X Please see related manuscript: http://www.biomedcentral.com/1741-7015/10/37 webciteThe idea that individuals are at elevated risk of developing a psychopathological condition due to their genetic make-up, particularly when exposed to adverse environmental conditions, known as the diathesis-stress model [1], has become the prevailing theoretical concept in psychiatry. The model further entails that people who do not carry 'vulnerability genes' are less susceptible to adversity. One of the most widely cited examples of gene-environment-interaction was published by Caspi et al. [2] who demonstrated that persons carrying the low-activity variant of the monoamine oxidase A (MAO-A) enzyme are more likely to develop antisocial personality disorder under adverse environmental conditions during childhood compared to individuals endowed with the high-activity allele. Put differently, subjects who degrade biogenic amines like dopamine and noradrenaline slowly are more vulnerable to develop, as children, attention-deficit hyperactivity disorder (ADHD) and conduct disorder, and, as adults, antisocial personality disorder when having suffered early adversity such as maltreatment or abuse. Conversely, it has been argued that the absence of adversity has the potential to compensate the genetic vulnerability, also known as 'maternal buffering' [3]. Other examples of gene-environment interaction include the s-allele of the serotonin transporter gene (5-HTTLPR), which predisposes to depression if accompanied by stressful life-events [4], and the seven-repeat variant of the dopamine receptor D4 gene (DRD4), which increases the vulnerability for externalizing problems and ADHD in children whose mothers are insensitive to their children's needs [5].While it is indisputable that this line of research has greatly advanced our understanding of the role of gene-environment interaction in psychopathology, the diathesis-stress model, as currently conceived, falls short of explaining why many o
%U http://www.biomedcentral.com/1741-7015/10/38