scholarly journals Genetic moderation of environmental risk for depression and anxiety in adolescent girls

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.

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.


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.


Author(s):  
Diego Zunino

Abstract Genetic factors influence entrepreneurial activity, but we know little about how genetic factors influence entrepreneurial activity when the institutional environment is favorable. Two theories from behavioral genetics explain the gene–environment interaction. One theory argues that a favorable environment favors the development of genetic factors and their influence. An alternative theory posits that unfavorable environment triggers the development of genetic factors and their influence. I test these two competing theories with a twin study based in Italy. I compare the influence of genetic factors in provinces where the institutional environment favors entrepreneurial activity with provinces where the institutional environment is unfavorable to entrepreneurial activity. I found consistent evidence that genetic factors exert a larger influence in favorable institutional environments, suggesting that favorable institutional environments complement genetic factors.


PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0259210
Author(s):  
Eric A. W. Slob ◽  
Cornelius A. Rietveld

Background Tobacco consumption is one of the leading causes of preventable death. In this study, we analyze whether someone’s genetic predisposition to smoking moderates the response to tobacco excise taxes. Methods We interact polygenic scores for smoking behavior with state-level tobacco excise taxes in longitudinal data (1992-2016) from the US Health and Retirement Study (N = 12,058). Results Someone’s genetic propensity to smoking moderates the effect of tobacco excise taxes on smoking behavior along the extensive margin (smoking vs. not smoking) and the intensive margin (the amount of tobacco consumed). In our analysis sample, we do not find a significant gene-environment interaction effect on smoking cessation. Conclusions When tobacco excise taxes are relatively high, those with a high genetic predisposition to smoking are less likely (i) to smoke, and (ii) to smoke heavily. While tobacco excise taxes have been effective in reducing smoking, the gene-environment interaction effects we observe in our sample suggest that policy makers could benefit from taking into account the moderating role of genes in the design of future tobacco control policies.


2014 ◽  
Vol 205 (2) ◽  
pp. 113-119 ◽  
Author(s):  
Wouter J. Peyrot ◽  
Yuri Milaneschi ◽  
Abdel Abdellaoui ◽  
Patrick F. Sullivan ◽  
Jouke J. Hottenga ◽  
...  

BackgroundResearch on gene×environment interaction in major depressive disorder (MDD) has thus far primarily focused on candidate genes, although genetic effects are known to be polygenic.AimsTo test whether the effect of polygenic risk scores on MDD is moderated by childhood trauma.MethodThe study sample consisted of 1645 participants with a DSM-IV diagnosis of MDD and 340 screened controls from The Netherlands. Chronic or remitted episodes (severe MDD) were present in 956 participants. The occurrence of childhood trauma was assessed with the Childhood Trauma Interview and the polygenic risk scores were based on genome-wide meta-analysis results from the Psychiatric Genomics Consortium.ResultsThe polygenic risk scores and childhood trauma independently affected MDD risk, and evidence was found for interaction as departure from both multiplicativity and additivity, indicating that the effect of polygenic risk scores on depression is increased in the presence of childhood trauma. The interaction effects were similar in predicting all MDD risk and severe MDD risk, and explained a proportion of variation in MDD risk comparable to the polygenic risk scores themselves.ConclusionsThe interaction effect found between polygenic risk scores and childhood trauma implies that (1) studies on direct genetic effect on MDD gain power by focusing on individuals exposed to childhood trauma, and that (2) individuals with both high polygenic risk scores and exposure to childhood trauma are particularly at risk for developing MDD.


2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Yi Hou ◽  
Yong Gao ◽  
Yan Zhang ◽  
Si-Tong Lin ◽  
Yue Yu ◽  
...  

Abstract Background The association of diabetic nephropathy (DN) risk with single nucleotide polymorphisms (SNPs) within Engulfment and Cell Motility 1 (ELMO1) gene and gene–environment synergistic effect have not been extensively examined in, therefore, the purpose of this study is to explore the association between multiple SNPs in ELMO1 gene, and the relationship between gene–environment synergy effect and the risk of DN. Methods Genotyping for 4 SNPs was performed with polymerase chain reaction (PCR) and following restriction fragment length polymorphism (RFLP) methods. Hardy–Weinberg balance of the control group was tested by SNPstats (online software: http://bioinfo.iconologia.net/snpstats). The best combination of four SNPs of ELMO1 gene and environmental factors was screened by GMDR model. Logistic regression was used to calculating the OR values between different genotypes of ELMO1 gene and DN. Results The rs741301-G allele and the rs10255208-GG genotype were associated with an increased risk of DN risk, adjusted ORs (95% CI) were 1.75 (1.19–2.28) and 1.41 (1.06–1.92), respectively, both p-values were < 0.001. We also found that the others SNPs-rs1345365 and rs7782979 were not significantly associated with susceptibility to DN. GMDR model found a significant gene–alcohol drinking interaction combination (p = 0.0107), but no significant gene–hypertension interaction combinations. Alcohol drinkers with rs741301-AG/GG genotype also have the highest DN risk, compared to never drinkers with rs741301-AA genotype, OR (95% CI) 3.52 (1.93–4.98). Conclusions The rs741301-G allele and the rs10255208-GG genotype, gene–environment interaction between rs741301 and alcohol drinking were all associated with increased DN risk.


2011 ◽  
Vol 14 (6) ◽  
pp. 544-552 ◽  
Author(s):  
Venla S. Laitala ◽  
Jacob Hjelmborg ◽  
Markku Koskenvuo ◽  
Ismo Räihä ◽  
Juha O. Rinne ◽  
...  

We analyzed the association between mean height and old age cognition in two Nordic twin cohorts with different childhood living conditions. The cognitive performance of 4720 twin individuals from Denmark (mean age 81.6 years, SD = 4.59) and Finland (mean age 74.4 years, SD = 5.26) was measured using validated cognitive screens. Taller height was associated with better cognitive performance in Finland (β-estimates 0.18 SD/10cm, p value < .001, for men and 0.13 SD, p = .008, for women), but this association was not significant in Denmark (β-estimates 0.0093 SD, p value = .16, for men and 0.0075 SD, p value = .016, for women) when adjusted for age and education/social class. Among Finnish participants higher variability of cognitive performance within shorter height quintiles was observed. Analysis using gene-environment interaction models showed that environmental factors exerted a greater impact on cognitive performance in shorter participants, whereas in taller participants' it was explained mainly by genetic factors. Our results suggest that shorter participants with childhood adversity are more vulnerable to environmental risk factors for cognitive impairment.


2020 ◽  
Author(s):  
Arunabha Majumdar ◽  
Kathryn S. Burch ◽  
Sriram Sankararaman ◽  
Bogdan Pasaniuc ◽  
W. James Gauderman ◽  
...  

AbstractWhile gene-environment (GxE) interactions contribute importantly to many different phenotypes, detecting such interactions requires well-powered studies and has proven difficult. To address this, we combine two approaches to improve GxE power: simultaneously evaluating multiple phenotypes and using a two-step analysis approach. Previous work shows that the power to identify a main genetic effect can be improved by simultaneously analyzing multiple related phenotypes. For a univariate phenotype, two-step methods produce higher power for detecting a GxE interaction compared to single step analysis. Therefore, we propose a two-step approach to test for an overall GxE effect for multiple phenotypes. Using simulations we demonstrate that, when more than one phenotype has GxE effect (i.e., GxE pleiotropy), our approach offers substantial gain in power (18% – 43%) to detect an aggregate-level GxE effect for a multivariate phenotype compared to an analogous two-step method to identify GxE effect for a univariate phenotype. We applied the proposed approach to simultaneously analyze three lipids, LDL, HDL and Triglyceride with the frequency of alcohol consumption as environmental factor in the UK Biobank. The method identified two independent genome-wide significant signals of an overall GxE effect on the vector of lipids.


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