title: No interaction between serotonin transporter gene (5-HTTLPR) polymorphism and adversity on depression among Japanese children and adolescents.
abstract: BACKGROUND
  Identification of gene × environment interactions (G × E) for depression is a crucial step in ascertaining the mechanisms underpinning the disorder. Earlier studies have indicated strong genetic influences and numerous environmental risk factors. In relation to childhood and adolescent depression, evidence is accumulating that the quality of the parental environment is associated with serotonin biology in children. We hypothesized that maternal depression is a crucial environmental risk factor associated with serotonin-regulating genes.
  
  
  METHODS
  This study was designed to ascertain the G × E interaction for diagnosis of depression in a Japanese pediatric sample. DNA samples from 55 pediatric patients with depression and 58 healthy schoolchildren were genotyped for the 5-HTT (2 short (S) alleles at the 5-HTT locus) promoter serotonin-transporter-linked polymorphic region (5-HTTLPR) polymorphism. We examined whether an adverse parental environment, operationalized as the mother's history of recurrent major depressive disorder, interacts with 5-HTTLPR polymorphism to predict patients' depression symptoms.
  
  
  RESULTS
  Binary logistic regression analyses revealed that maternal depression (adversity), gender, and FSIQ significantly affect the diagnosis of depression among children and adolescents. However, no main effect was found for adversity or genotype. Results of multivariable logistic regression analyses using stepwise procedure have elicited some models with a good fit index, which also suggests no interaction between 5-HTTLPR and adversity on depression.
  
  
  CONCLUSIONS
  To assess G × E interaction, data obtained from children and adolescents who had been carefully diagnosed categorically and data from age-matched controls were analyzed using logistic regression. Despite an equivocal interaction effect, adversity and gender showed significant main effects.
authors.affiliation: Research Center for Child Mental Development, University of Fukui, Fukui, Japan. atomoda@u-fukui.ac.jp
authors.forename: Akemi
authors.initials: A
authors.lastname: Tomoda
authors.forename: Shota
authors.initials: S
authors.lastname: Nishitani
authors.forename: Naomi
authors.initials: N
authors.lastname: Matsuura
authors.forename: Takashi X
authors.initials: TX
authors.lastname: Fujisawa
authors.forename: Junko
authors.initials: J
authors.lastname: Kawatani
authors.forename: Daiki
authors.initials: D
authors.lastname: Toyohisa
authors.forename: Mai
authors.initials: M
authors.lastname: Ono
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Shinohara
mesh_terms: D000293:Adolescent; D000483:Alleles; D044466:Asian People / Q000235:genetics / Q000523:psychology; D002648:Child; D003866:Depressive Disorder / Q000235:genetics* / Q000523:psychology; D005260:Female; D059647:Gene-Environment Interaction; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007564:Japan; D008016:Life Change Events; D008297:Male; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics*; D012931:Social Environment
chemical_list: D050486:Serotonin Plasma Membrane Transport Proteins