Interactions of child maltreatment and serotonin transporter and monoamine oxidase A polymorphisms: Depressive symptomatology among adolescents from low socioeconomic status backgrounds

2007 ◽  
Vol 19 (4) ◽  
pp. 1161-1180 ◽  
Author(s):  
Dante Cicchetti ◽  
Fred A. Rogosch ◽  
Melissa L. Sturge-Apple

AbstractChild maltreatment and polymorphisms of the serotonin transporter (5-HTT) and monoamine oxidase A (MAOA) genes were examined in relation to depressive symptomatology. Adolescents (Mage = 16.7 years) from low socioeconomic backgrounds with a history of child maltreatment (n= 207) or no such history (n= 132) were interviewed and provided buccal cells for genetic analysis. Gene × environment interactions were observed. Heightened depressive symptoms were found only among extensively maltreated youth with lowMAOAactivity. Among comparably maltreated youth with highMAOAactivity, self-coping strategies related to lower symptoms. Sexual abuse and the5-HTT short/shortgenotype predicted higher depression, anxiety, and somatic symptoms. This Gene × Environment interaction was further moderated byMAOAactivity level. The results highlight the protective functions of genetic polymorphisms and coping strategies in high risk youth and offer direction for understanding resilience and its promotion from a multiple levels of analysis perspective.

2012 ◽  
Vol 24 (3) ◽  
pp. 907-928 ◽  
Author(s):  
Dante Cicchetti ◽  
Fred A. Rogosch ◽  
Eric L. Thibodeau

AbstractGene–environment interaction effects in predicting antisocial behavior in late childhood were investigated among maltreated and nonmaltreated low-income children (N= 627,Mage = 11.27). Variants in three genes were examined: tryptophan hydroxylase 1 (TPH1), serotonin transporter linked polymorphic region (5-HTTLPR), and monoamine oxidase A (MAOA) upstream variable number tandem repeat. In addition to child maltreatment status, we considered the impact of maltreatment subtypes, developmental timing of maltreatment, and chronicity. Indicators of antisocial behavior were obtained from self-, peer, and adult counselor reports. In a series of analyses of covariance, child maltreatment and its parameters demonstrated strong main effects on early antisocial behavior as assessed by all report forms. Genetic effects operated primarily in the context of gene–environment interactions, moderating the impact of child maltreatment on outcomes. Across the three genes, among nonmaltreated children no differences in antisocial behavior were found based on genetic variation. In contrast, among maltreated children specific polymorphisms ofTPH1,5-HTTLPR, andMAOAwere each related to heightened self-report of antisocial behavior; the interaction of5-HTTLPRand developmental timing of maltreatment also indicated more severe antisocial outcomes for children with early onset and recurrent maltreatment based on genotype.TPH1and5-HTTLPRinteracted with maltreatment subtype to predict peer reports of antisocial behavior; genetic variation contributed to larger differences in antisocial behavior among abused children. TheTPH1and5-HTTLPRpolymorphisms also moderated the effects of maltreatment subtype on adult reports of antisocial behavior; again, the genetic effects were strongest for children who were abused. In addition,TPH1moderated the effect of developmental timing of maltreatment and chronicity on adult reports of antisocial behavior. The findings elucidate how genetic variation contributes to identifying which maltreated children are most vulnerable to antisocial development.


2013 ◽  
Vol 25 (3) ◽  
pp. 599-614 ◽  
Author(s):  
Adrienne M. Banny ◽  
Dante Cicchetti ◽  
Fred A. Rogosch ◽  
Assaf Oshri ◽  
Nicki R. Crick

AbstractChild maltreatment, peer victimization, and a polymorphism of the serotonin transporter gene (5-HTTLPR) were examined as predictors of depressive symptomatology. Children (Mage = 11.26,SD= 1.65), including 156 maltreated and 145 nonmaltreated children from comparable low socioeconomic backgrounds, provided DNA samples and self-reports of relational peer victimization, overt peer victimization, and depressive symptoms. Path analysis showed that relational and overt victimization mediated the association between child maltreatment and depressive symptoms. Bootstrapping procedures were used to test moderated mediation and demonstrated that genotype moderated the indirect effects of relational and overt victimization on child depressive symptoms, such that victimized children with the long/long variation were at an increased risk for depressive symptoms compared to victimized children carrying a short allele. Results highlight the utility of examining process models that incorporate biological and psychological factors contributing to the development of depressive symptomatology and provide direction toward understanding and promoting resilience among high-risk youth from a multiple levels of analysis approach.


2013 ◽  
Vol 25 (2) ◽  
pp. 555-575 ◽  
Author(s):  
John V. Lavigne ◽  
Laura B. K. Herzing ◽  
Edwin H. Cook ◽  
Susan A. Lebailly ◽  
Karen R. Gouze ◽  
...  

AbstractGenetic factors can play a key role in the multiple level of analyses approach to understanding the development of child psychopathology. The present study examined gene–environment correlations and Gene × Environment interactions for polymorphisms of three target genes, the serotonin transporter gene, the D4 dopamine receptor gene, and the monoamine oxidase A gene in relation to symptoms of anxiety, depression, and oppositional behavior. Saliva samples were collected from 175 non-Hispanic White, 4-year-old children. Psychosocial risk factors included socioeconomic status, life stress, caretaker depression, parental support, hostility, and scaffolding skills. In comparison with the short forms (s/s, s/l) of the serotonin transporter linked polymorphic repeat, the long form (l/l) was associated with greater increases in symptoms of oppositional defiant disorder in interaction with family stress and with greater increases in symptoms of child depression and anxiety in interaction with caretaker depression, family conflict, and socioeconomic status. In boys, low-activity monoamine oxidase A gene was associated with increases in child anxiety and depression in interaction with caretaker depression, hostility, family conflict, and family stress. The results highlight the important of gene–environment interplay in the development of symptoms of child psychopathology in young children.


2008 ◽  
Vol 39 (4) ◽  
pp. 579-590 ◽  
Author(s):  
E. C. Prom-Wormley ◽  
L. J. Eaves ◽  
D. L. Foley ◽  
C. O. Gardner ◽  
K. J. Archer ◽  
...  

BackgroundRecent studies among males have reported a genotype–environment interaction (G×E) in which low-activity alleles at the monoamine oxidase A (MAOA) locus conferred greater sensitivity to the effects of childhood adversity on risk for conduct disorder (CD). So far, few studies of females have controlled for gene–environment correlation or used females heterozygous for this X-linked gene.MethodLogistic regression analysis of a sample of 721 females ages 8–17 years from the longitudinal Virginia Twin Study of Adolescent Behavioral Development (VTSABD) assessed the additive effects of MAOA genotypes on risk for CD, together with the main effect of childhood adversity and parental antisocial personality disorder (ASP), as well as the interaction of MAOA with childhood adversity on risk for CD.ResultsA significant main effect of genotype on risk for CD was detected, where low-activity MAOA imparted the greatest risk to CD in girls while controlling for the significant effects of maternal ASP and childhood adversity. Significant G×E with weak effect was detected when environmental exposure was untransformed, indicating a higher sensitivity to childhood adversity in the presence of the high-activity MAOA allele. The interaction was no longer statistically significant after applying a ridit transformation to reflect the sample sizes exposed at each level of childhood adversity.ConclusionsThe main effect of MAOA on risk for CD in females, its absence in males and directional difference of interaction is suggestive of genotype–sex interaction. As the effect of G×E on risk for CD was weak, its inclusion is not justified.


2020 ◽  
Author(s):  
Andrea Bonassi ◽  
Ilaria Cataldo ◽  
Giulio Gabrieli ◽  
Moses Tandiono ◽  
Jia Nee Foo ◽  
...  

Human social interactions ensure recognition and approval from others, both in offline and online environments. This study applies a model from behavioural genetics on Instagram sociability to explore the impact of individual development on the behaviour on social networks.We hypothesize that sociable attitudes on Instagram resulted from an interaction between serotonin transporter gene alleles and the individual’s social relationship with caregivers. We assess environmental and genetic components of 57 Instagram users. The self-report questionnaire Parental Bonding Instrument is adopted to determine the quality of parental bonding. The number of posts, followed users (“followings”), and followers are collected from Instagram as measures of online social activity. Additionally, the ratio between the number of followers and followings (“Social Desirability Index”) was calculated to estimate the asymmetry of each user’s social network. Finally, buccal mucosa cell samples were acquired, and the polymorphism rs25531 (T/T homozygotes vs C-carriers) within the serotonin transporter gene was examined.In the preliminary analysis, we identified a gender effect on the number of followings. In line with our predictions, we specifically found a gene- environment interaction on the standardized Instagram “Social Desirability Index”: users with the genotype more sensitive to environmental influences (T/T homozygotes) showed a higher Instagram “Social Desirability Index” than non-sensitive ones (C-carriers) when they experienced positive maternal care.This result may contribute to the understanding of online social behaviour from a gene*environment perspective.


2012 ◽  
Vol 136 ◽  
pp. S147
Author(s):  
Ximena Goldberg ◽  
Mar Fatjó-Vilas ◽  
Silvia Alemany ◽  
Aldo Córdova ◽  
Igor Nenadic ◽  
...  

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