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Epidemiol Psychiatr Sci. 2014 Dec;23(4):399-409. doi: 10.1017/S2045796013000565. Epub 2013 Oct 22.

Effect of the serotonin transporter gene and of environment on the continuity of anxiety and depression traits throughout adolescence.

Epidemiology and psychiatric sciences

M Nobile, A Greco, G Perna, P Colombo, V Bianchi, M Bellina, R Giorda, D Monzani, O Carlet, E Griez, M Molteni

Affiliations

  1. Department of Child Psychiatry,'Eugenio Medea' Scientific Institute,Bosisio Parini,Italy.
  2. Department of Psychology,Università degli Studi di Milano Bicocca,Milan,Italy.
  3. Department of Clinical Neurosciences, Hermanas Hospitalarias,FoRiPsi,Albese con Cassano,Italy.
  4. Department of Child Psychiatry,'Eugenio Medea' Scientific Institute,Conegliano,Italy.
  5. Department of Psychiatry and Neuropsychology,University of Maastricht,The Netherlands.

PMID: 24148106 PMCID: PMC7192166 DOI: 10.1017/S2045796013000565

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.

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