Serotonin transporter gene and childhood trauma - a G × E effect on anxiety sensitivity

Klauke, Benedikt; Deckert, Jürgen; Reif, Andreas; Pauli, Paul; Zwanzger, Peter; Baumann, Christian; Arolt, Volker; Glöckner-Rist, Angelika; Domschke, Katharina

doi:10.1002/da.20840

Cited by 59 publications

(42 citation statements)

References 111 publications

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“…The current investigation uses data from the second, third, and fourth wave of data collection and will be referred to as time 1, 2, and 3, respectively from here on for ease of presentation. Mean age and range (in parenthesis) at times 1, 2, and 3 was 15 years (12-21), 17 years (14-23), and 20 years (18)(19)(20)(21)(22)(23)(24)(25)(26)(27) …”

Section: Methods Participantsmentioning

confidence: 99%

“…To date (to our knowledge), there have only been two published studies of gene-environment interactions in anxiety sensitivity. [23,24] In both studies, results showed that 5HTTLPR genotype moderated the effect of childhood emotional maltreatment on anxiety sensitivity. However, the direction of effect varied across the two studies.…”

Section: Introductionmentioning

confidence: 91%

“…[23] Although in the second study, an interaction was observed between the "LL" genotype and childhood maltreatment on anxiety sensitivity. [24] No study to date has examined the interplay between 5HTTLPR and stressful life events on anxiety sensitivity.…”

Section: Introductionmentioning

confidence: 99%

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Anxiety Sensitivity in Adolescence and Young Adulthood: The Role of Stressful Life Events, 5httlpr and Their Interaction

et al. 2012

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Background: Cognitive biases have long been hypothesized to influence the development and maintenance of symptoms of internalizing problems. Anxiety sensitivity represents one such bias and refers to sensitivity to the physical and emotional symptoms of anxiety and the belief that these are harmful. Twin studies indicate a role for both environmental and genetic influences on anxiety sensitivity. However, little work has been done specifying environments or genes involved in this phenotype. In light of this, we looked at the association between stressful life events, the serotonin transporter gene polymorphism (5HTTLPR), and anxiety sensitivity in a longitudinal sample of adolescents. Methods: Stressful life events and anxiety sensitivity were measured in over 1,500 individuals at three time points (mean ages 15, 17, and 20 years). 5HTTLPR was genotyped in 1,109 participants. Results: There was consistent evidence for an association between stressful life events and both anxiety sensitivity and change in anxiety sensitivity over time. Although the effect of independent stressful life events was relatively short lived, dependent stressful life events were associated with anxiety sensitivity over time. There was no evidence for a main effect of 5HTTLPR on anxiety sensitivity. 5HTTLPR genotype did not moderate the effect of stressful life events on anxiety sensitivity. Conclusions: The current study extends previous work by showing that stressful life events, independent of the individual, explained change in cognitions associated with anxiety and depression. This effect does not, however, appear to be moderated by genotype. Depression and Anxiety 29:400-408, 2012.C 2012 Wiley Periodicals, Inc.

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Section: Methods Participantsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 91%

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Anxiety Sensitivity in Adolescence and Young Adulthood: The Role of Stressful Life Events, 5httlpr and Their Interaction

et al. 2012

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“…Furthermore, these results extend findings of the role of BDNF and CM on AS. Previous studies have focused on convenience samples of college students, or adults, and predominantly on the effects of the 5-HTTLPR polymorphism (Hemmings et al, 2016; Kim et al, 2009; Klauke et al, 2011; Laucht et al, 2009; Stein et al, 2008). Our results suggest that the influence of CM on adolescent AS levels is not moderated by the BDNF Val66Met polymorphism.…”

Section: Discussionmentioning

confidence: 99%

“…There is support for the role of gene-environment interaction in the aetiology of youth and adult anxiety, including panic and separation anxiety, anxiety symptoms, anxious mood and anxious temperament (Baumann et al, 2013; Chen et al, 2015; Gunthert et al, 2007; Ibarra et al, 2014; Klauke et al, 2011; Lau, Gregory, Goldwin, Pine, & Eley, 2007; Stein, Schork, & Gelernter, 2008; Vendlinski, Lemery-Chalfant, Essex, & Goldsmith, 2011). CM and AS have both consistently been implicated as risk factors for psychopathology, including anxiety disorders (Collishaw et al, 2007; Kessler, McLaughlin et al, 2010; McLaughlin et al, 2007, 2012).…”

Section: Introductionmentioning

confidence: 99%

No gene-by-environment interaction of BDNF Val66Met polymorphism and childhood maltreatment on anxiety sensitivity in a mixed race adolescent sample

Martin

Hemmings

Kidd

et al. 2018

European Journal of Psychotraumatology

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Background: Anxiety disorders in youth are attributable to multiple causal mechanisms, comprising biological vulnerabilities, such as genetics and temperament, and unfavourable environmental influences, such as childhood maltreatment (CM).Objective: A gene-environment (G x E) interaction study was conducted to determine the interactive effect of the BDNF Val66Met polymorphism and CM to increase susceptibility to anxiety sensitivity (AS) in a sample of mixed race adolescents.Method: Participants (n = 308, mean age = 15.8 years) who were all secondary school students and who completed measures for AS and CM were genotyped for the BDNF Val66Met polymorphism. Hierarchical multiple regression analysis was conducted to assess G x E influences on AS. Age and gender were included in the models as covariates as age was significantly associated with AS total score (p < .05), and females had significantly higher AS scores than males (p < .05).Results: A main effect of CM on AS was evident (p < .05), however, no main effect of BDNF genotype on AS was observed (p > .05). A non-significant G x E effect on AS was revealed (p < .05).Conclusions: Our results suggest that CM does not have a moderating role in the relationship between the BDNF Val66Met genotype and the increased risk of anxiety-related phenotypes, such as AS. Given the exploratory nature of this study, findings require replication in larger samples and adjustment for population stratification to further explore the role of BDNF Val66Met and CM on AS in mixed race adolescents.

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Genetic Factors and Gene–Environment Interactions

Maron

Shlik

2014

The Wiley Handbook of Anxiety Disorders

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Previous genome-wide association studies (GWAS) have identified hundreds of genetic loci to be associated with body mass index (BMI) and risk of obesity. Genetic effects can differ between individuals depending on lifestyle or environmental factors due to gene-environment interactions. In this study, we examine gene-environment interactions in 362,496 unrelated participants with Caucasian ancestry from the UK Biobank resource. A total of 94 BMI-associated SNPs, selected from a previous GWAS on BMI, were used to construct weighted genetic scores for BMI (GS BMI). Linear regression modeling was used to estimate the effect of gene-environment interactions on BMI for 131 lifestyle factors related to: dietary habits, smoking and alcohol consumption, physical activity, socioeconomic status, mental health, sleeping patterns, as well as female-specific factors such as menopause and childbirth. In total, 15 lifestyle factors were observed to interact with GS BMI , of which alcohol intake frequency , usual walking pace, and Townsend deprivation index, a measure of socioeconomic status, were all highly significant (p = 1.45*10 −29 , p = 3.83*10 −26 , p = 4.66*10 −11 , respectively). Interestingly, the frequency of alcohol consumption, rather than the total weekly amount resulted in a significant interaction. The FTO locus was the strongest single locus interacting with any of the lifestyle factors. However, 13 significant interactions were also observed after omitting the FTO locus from the genetic score. Our analyses indicate that many lifestyle factors modify the genetic effects on BMI with some groups of individuals having more than double the effect of the genetic score. However, the underlying causal mechanisms of gene-environmental interactions are difficult to deduce from cross-sectional data alone and controlled experiments are required to fully characterise the causal factors. Author summary Genome-wide association studies (GWAS) have identified hundreds of genes as being associated with body mass index (BMI). How these genetic effects are modulated by lifestyle factors has not been extensively investigated previously. Here we utilise data from PLOS Genetics | https://doi.org/10.1371/journal.pgen.approximately 360,000 participants from the UK Biobank, aged 40-69 years old, to identify interactions between genetic and lifestyle factors in relation to BMI. We investigated 131 lifestyle factors, of which 15 influence the genetic effects on BMI. The most significant factors were those related to physical activity, alcohol consumption, and socioeconomic status. For example, the effect of a genetic score for BMI was almost twice as high in participants who reported never drinking alcohol compared to everyday drinkers. Similarly, the effect of the genetic score for BMI was 2.5 times higher in participants who reported having a slow walking pace compared to participants who reported having a brisk walking pace. Our results show that many lifestyle factors influence the genetic effects, which suggests that changing our lif...

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Serotonin transporter gene and childhood trauma - a G × E effect on anxiety sensitivity

Abstract: Results indicate a G × E effect of the more active 5-HTT genotypes and childhood maltreatment on AS, with particular impact on its somatic subcomponent.

Cited by 59 publications

References 111 publications

Anxiety Sensitivity in Adolescence and Young Adulthood: The Role of Stressful Life Events, 5httlpr and Their Interaction

Anxiety Sensitivity in Adolescence and Young Adulthood: The Role of Stressful Life Events, 5httlpr and Their Interaction

No gene-by-environment interaction of BDNF Val66Met polymorphism and childhood maltreatment on anxiety sensitivity in a mixed race adolescent sample

Genetic Factors and Gene–Environment Interactions

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