Abstract
The diathesis-stress model of psychiatric conditions has recently been challenged by the view that it might be more accurate to speak of 'differential susceptibility' or 'plasticity' genes, rather than one-sidedly focusing on individual vulnerability. That is, the same allelic variation that predisposes to a psychiatric disorder if associated with (developmentally early) environmental adversity may lead to a better-than-average functional outcome in the same domain under thriving (or favourable) environmental conditions. Studies of polymorphic variations of the serotonin transporter gene, the monoamino-oxidase-inhibitor A coding gene or the dopamine D4 receptor gene indicate that the early environment plays a crucial role in the development of favourable versus unfavourable outcomes. Current evidence is limited, however, to establishing a link between genetic variation and behavioural phenotypes. In contrast, little is known about how plasticity may be expressed at the neuroanatomical level as a 'hard-wired' correlate of observable behaviour. The present review article seeks to further strengthen the argument in favour of the differential susceptibility theory by incorporating findings from behavioural and neuroanatomical studies in relation to genetic variation of the oxytocin receptor gene. It is suggested that polymorphic variation at the oxytocin receptor gene (rs2254298) is associated with sociability, amygdala volume and differential risk for psychiatric conditions including autism, depression and anxiety disorder, depending on the quality of early environmental experiences. Seeing genetic variation at the core of developmental plasticity can explain, in contrast to the diathesis-stress perspective, why evolution by natural selection has maintained such 'risk' alleles in the gene pool of a population.Please see related manuscript: http://www.biomedcentral.com/1741-7015/10/37
Highlights
The idea that individuals are at elevated risk of developing a psychopathological condition due to their genetic make-up, when exposed to adverse environmental conditions, known as the diathesis-stress model [1], has become the prevailing theoretical concept in psychiatry
Lesch and colleagues have shown that, while carrying the s-allele of the HTTLPR predisposes to depression if associated with adverse events, the same variation is linked to superior cognitive performance in several domains and increases social conformity [9,10]. The latter example is prototypical for a ‘balanced polymorphism’, that is, a single nucleotide polymorphism (SNP) may exert disadvantageous effects in one domain, which are compensated by advantageous effects in another domain
The present article sought to explore the question whether a polymorphic variation of the oxytocin receptor gene (OXTR) coding gene could be associated with differential susceptibility to psychiatric disorders
Summary
The idea that individuals are at elevated risk of developing a psychopathological condition due to their genetic make-up, when exposed to adverse environmental conditions, known as the diathesis-stress model [1], has become the prevailing theoretical concept in psychiatry. Based on observations that intranasal application of supra-physiological dosages of OXT improves ‘mindreading’ abilities [25], fear recognition [26] and trust in healthy subjects [27,28], as well as studies demonstrating the role of OXT in establishing secure attachment and bonding [29,30], research on the effect of OXT on psychopathological parameters and cognition in adult psychiatric disorders has seen a recent resurgence after a long period of lying dormant It was shown in the early 1970s that OXT has the potential to reduce psychotic symptoms in schizophrenia [31]. The number of people in one’s social network, as well as the number of different groups these contacts belonged to, correlated significantly with the volume of the left (and slightly less the right) amygdala in younger and older psychologically healthy adults of both sexes [68] Taken together, these findings support the view that diathesis-stress models of individual SNPs are often just one side of the coin [12]
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