| Literature DB >> 24148106 |
M Nobile1, A Greco2, G Perna3, P Colombo1, V Bianchi1, M Bellina1, R Giorda1, D Monzani2, O Carlet4, E Griez5, M Molteni1.
Abstract
Aims. Many studies of various stress reactive phenotypes suggest that 5-HTTLPR short allele carriers (S-carriers) are characterised by the stable trait of negative affectivity that is converted to psychopathology only under conditions of stress. In this study, we examined the moderating role of the 5-HTTLPR on the relationship between two objective chronic risk factors, i.e. socioeconomic status (SES) and family structure, and internalising symptoms across adolescence. Methods. A multigroup path analysis was employed in a general adolescent population sample of a 5-year follow-up study. Results. Internalising problems were significantly more stable in the S-carriers. The focus on the main dimensions of internalising problems, i.e. anxiety and depression, revealed two different developmental patterns. In the S-carriers Anxiety problems seemed to be more stable and to predict a possible evolution towards the development of Depressive problems. In the long allele homozygotes (LL-subjects) the anxiety trait was significantly less stable, and, in late-adolescence, seemed to be significantly predicted by SES, suggesting a possible gene-environment interaction (G × E). Family structure seemed to play a role in a G × E perspective only until early-adolescence, while during late-adolescence SES seemed to play a pivotal role in interaction with 5-HTTLPR, with the S-allele playing a protective role. Conclusions. Future models of the developmental link between environmental adversities and internalising behaviour therefore need to consider that the effect of G × E interaction, may be associated with internalising behaviour via different mechanisms during different time frames and that shifts in the strength of this effect should be expected across development.Entities:
Year: 2013 PMID: 24148106 PMCID: PMC7192166 DOI: 10.1017/S2045796013000565
Source DB: PubMed Journal: Epidemiol Psychiatr Sci ISSN: 2045-7960 Impact factor: 6.892