Assessing gene–environment interactions on anxiety symptom subtypes across childhood and adolescence

2007 ◽  
Vol 19 (4) ◽  
pp. 1129-1146 ◽  
Author(s):  
Jennifer Y. F. Lau ◽  
Alice M. Gregory ◽  
Michelle A. Goldwin ◽  
Daniel S. Pine ◽  
Thalia C. Eley

AbstractConsistent evidence shows both genetic and stress-related risks on child and adolescent anxiety, yet few studies have considered the degree to which genetic effects are moderated by stress (gene–environment interaction). We used longitudinal data from both a child and adolescent sample of twins to examine three novel issues on the presence of gene–environment interaction on anxiety symptoms. First, we assessed moderation of genetic risks on anxiety symptoms by negative life events in each age group. Second, by distinguishing between “stable” and “age-specific” genetic factors, we explored the continuity of gene–environment interaction across time and/or its emergence at specific ages. Third, we compared the presence of gene–environment interaction across different symptom types (general, panic, social, and separation). Genetic effects on separation anxiety symptoms in childhood (mean age = 8 years, 6 months) and panic anxiety symptoms in adolescence (mean age = 15 years) increased across independent negative life events. Shared environmental effects on separation anxiety symptoms and nonshared environmental effects on general anxiety symptoms in adolescence were also moderated by negative life events. We interpret these preliminary findings tentatively in the context of gene–environment interaction on anxiety in general, and on early separation and later panic anxiety in particular.

2001 ◽  
Vol 179 (2) ◽  
pp. 116-121 ◽  
Author(s):  
Judy Silberg ◽  
Michael Rutter ◽  
Michael Neale ◽  
Lindon Eaves

BackgroundThere is huge individual variation in people's response to negative life events.AimsTo test the hypothesis that genetic factors moderate susceptibility to the environmentally mediated risks associated with negative life events.MethodThe Virginia Twin Study of Adolescent Behavioral Development (VTSABD) was used to study the effects of independent life events (assessed from maternal interview) on depression/anxiety (assessed from child interview) in 184 same-gender female twin pairs, aged 14–17 years, measured on two occasions.ResultsThere was no genetic effect on the independent negative life events studied. A significant gene–environment interaction was found using structural equation modelling. There was no effect of independent life events on adolescents' depression in the absence of parental emotional disorder, but a significant effect in its presence.ConclusionsThere is an environmentally mediated effect of life events on depression/anxiety. Genetic factors play a significant role in individual differences in susceptibility to these environmentally mediated risks.


2013 ◽  
Vol 43 (5) ◽  
pp. 402-414 ◽  
Author(s):  
Brea L. Perry ◽  
Bernice A. Pescosolido ◽  
Kathleen Bucholz ◽  
Howard Edenberg ◽  
John Kramer ◽  
...  

2009 ◽  
Vol 39 (9) ◽  
pp. 1407-1411 ◽  
Author(s):  
W. El Hage ◽  
J. F. Powell ◽  
S. A. Surguladze

Vulnerability to depression has been linked to the interaction of genetic predisposition with stressful life events. This review considers the associations between serotonergic and hypothalamic–pituitary–adrenal (HPA) systems. We follow the standpoint of a previous Editorial Review (Bhagwagar & Cowen, Psychological Medicine 2008, 38, 307–313) and consider another possible mechanism of vulnerability to depressive disorder, that is we suggest that the gene×environment interaction involves complex participation of serotonergic genes modulating response to stress through the HPA system.


PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e100935 ◽  
Author(s):  
Ehsan Pishva ◽  
Marjan Drukker ◽  
Wolfgang Viechtbauer ◽  
Jeroen Decoster ◽  
Dina Collip ◽  
...  

2010 ◽  
Vol 41 (4) ◽  
pp. 849-860 ◽  
Author(s):  
M. A. Distel ◽  
C. M. Middeldorp ◽  
T. J. Trull ◽  
C. A. Derom ◽  
G. Willemsen ◽  
...  

BackgroundTraumatic life events are generally more common in patients with borderline personality disorder (BPD) than in non-patients or patients with other personality disorders. This study investigates whether exposure to life events moderates the genetic architecture of BPD features. As the presence of genotype–environment correlation (rGE) can lead to spurious findings of genotype–environment interaction (G×E), we also test whether BPD features increase the likelihood of exposure to life events.MethodThe extent to which an individual is at risk to develop BPD was assessed with the Personality Assessment Inventory – Borderline features scale (PAI-BOR). Life events under study were a divorce/break-up, traffic accident, violent assault, sexual assault, robbery and job loss. Data were available for 5083 twins and 1285 non-twin siblings. Gene–environment interaction and correlation were assessed by using structural equation modelling (SEM) and the co-twin control design.ResultsThere was evidence for both gene–environment interaction and correlation. Additive genetic influences on BPD features interacted with the exposure to sexual assault, with genetic variance being lower in exposed individuals. In individuals who had experienced a divorce/break-up, violent assault, sexual assault or job loss, environmental variance for BPD features was higher, leading to a lower heritability of BPD features in exposed individuals. Gene–environment correlation was present for some life events. The genes that influence BPD features thus also increased the likelihood of being exposed to certain life events.ConclusionsTo our knowledge, this study is the first to test the joint effect of genetic and environmental influences and the exposure to life events on BPD features in the general population. Our results indicate the importance of both genetic vulnerability and life events.


2017 ◽  
Author(s):  
Jinho Kim

By incorporating molecular genetic variants and the fetal origins of obesity hypothesis into a gene-environment interaction framework, this study investigates the potential interactive effects of variation in the obesity-associated gene (FTO) and intrauterine environment on body mass index (BMI) in adulthood. This study draws on data from the Wisconsin Longitudinal Study, and uses sibling comparisons that allow for quasi-experimental variations in both genetic and environmental factors. Findings demonstrated that even after controlling for unobserved family background, the FTO variants and birth weight are generally associated with adult BMI. Moreover, this study found that the effects of having a risk allele of the FTO gene are largely concentrated on those who were heavier at birth, providing evidence for a gene-environment interaction on BMI and the development of obesity. Results of this study suggest that genes are not destiny and environmental factors may offset the effects of obesity-promoting genes. In particular, efforts to counteract genetic effects on obesity may begin as early as in utero. Interventions to prevent higher birth weight may help reduce the risk of obesity later in life, by directly addressing the programming effects of the in utero environment and also indirectly moderating the obesity-promoting genetic effects.


2006 ◽  
Vol 188 (3) ◽  
pp. 210-215 ◽  
Author(s):  
Kay Wilhelm ◽  
Philip B. Mitchell ◽  
Heather Niven ◽  
Adam Finch ◽  
Lucinda Wedgwood ◽  
...  

BackgroundA relationship between the serotonin transporter gene, adverse events and onset of major depression has been reported.AimsTo replicate a gene × environment interaction in a cohort with longitudinal data for life events, experience of depression, parental bonding and neuroticism.MethodAtthe 25-year follow-up, genomic DNA was obtained from 127 cohort members (mean age 48 years) to determine the genotype of the serotonin transporter gene-linked promoter region (5-HTTLPR). Associations were investigated between the 5-HTTLPR genotype, positive and adverse life events and the gene × environment interaction, and also between the 5-HTTLPR genotype and risk factors for depression.ResultsNo relationship was found between 5-HTTLPR genotype and either risk factors for depression or positive life events. Adverse life events had a significantly greater impact on the onset of depression for individuals with the s/s genotype.ConclusionsThe 5-HTTLPR genotype is a significant predictor of onset of major depression following multiple adverse events. This is one of the more robust findings concerning specific biological risk factors for depression.


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