Latent Trajectories of Adolescent Antisocial Behavior: Serotonin Transporter Linked Polymorphic Region (5-Httlpr) Genotype Influences Sensitivity to Perceived Parental Support  

Oleh:

Tung, Irene ; Lee, Steve S.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Development and Psychopathology vol. 29 no. 1 (Feb. 2017), page 185-201.
Topik: ASB; developmental trajectories; Adolescent Health; Controlling for sex; Furthermore; 5-HTTLPR; Gene ×

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Perpustakaan Pusat (Semanggi) Nomor Panggil: DD21 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Although prevailing theories of antisocial behavior (ASB) emphasize distinct developmental trajectories, few studies have explored gene–environment interplay underlying membership in empirically derived trajectories. To improve knowledge about the development of overt (e.g., aggression) and covert (e.g., delinquency) ASB, we tested the association of the 44-base pair promoter polymorphism in the serotonin transporter linked polymorphic region gene (5-HTTLPR), perceived parental support (e.g., closeness and warmth), and their interaction with ASB trajectories derived using latent class growth analysis in 2,558 adolescents followed prospectively into adulthood from the National Longitudinal Study of Adolescent Health. Three distinct trajectories emerged for overt (low desisting, adolescent peak, and late onset) and covert ASB (high stable, low stable, and nonoffending). Controlling for sex, parental support inversely predicted membership in the adolescent-peak overt ASB trajectory (vs. low desisting), but was unrelated to class membership for covert ASB. Furthermore, the 5-HTTLPR genotype significantly moderated the association of parental support on overt ASB trajectory membership. It is interesting that the pattern of Gene × Environment interaction differed by trajectory class: whereas short allele carriers were more sensitive to parental support in predicting the late-onset trajectory, the long/long genotype functioned as a potential “plasticity genotype” for the adolescent-peak trajectory group. We discuss these preliminary findings in the context of the differential susceptibility hypothesis and discuss the need for future studies to integrate gene–environment interplay and prospective longitudinal designs.

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