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Gene–lifecourse interaction for alcohol consumption in adolescence and young adulthood: Five monoamine genes
Author(s) -
Guo Guang,
Wilhelmsen Kirk,
Hamilton Nathan
Publication year - 2007
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.30340
Subject(s) - affect (linguistics) , alcohol , association (psychology) , psychology , young adult , life course approach , monoamine neurotransmitter , alcohol consumption , developmental psychology , genetic association , genotype , genetics , gene , clinical psychology , biology , single nucleotide polymorphism , biochemistry , receptor , communication , serotonin , psychotherapist
Association analysis has suggested that common sequence variants of genes that affect monoamine function can affect substance use and abuse. Demonstration of these associations has been inconsistent because of limited sample sizes and phenotype definition. Drawing on the life course perspective, we predicted a stronger association between the polymorphisms in 5HTT, DAT1, DRD4, DRD2 , and MAOA and alcohol consumption in young adulthood than adolescence. This analysis tested for the gene–lifecourse interaction for the frequency of alcohol consumption in a nationally representative non‐alcohol‐dependent sample of 2,466 individuals that were visited during adolescence and young adulthood for four times between 1994 and 2002. All five genes are significantly associated with the frequency of alcohol consumption, with the genotype effects ranging 7%–20% of the mean score of alcohol consumption and their P values being 0.014, 0.0003, 0.003, 0.007, 0.005, and 0.003, respectively. The association is only observed in the life stage of young adulthood and not in adolescence. This analysis has demonstrated the potential usefulness of the life course perspective in genetic studies of human behaviors such as alcohol consumption. © 2007 Wiley‐Liss, Inc.