Gene-environment interaction in posttraumatic stress disorder

Koenen, Karestan C.; Nugent, Nicole R.; Amstadter, Ananda B.

doi:10.1007/s00406-007-0787-2

Cited by 97 publications

(38 citation statements)

References 141 publications

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“…Individual differences in the risk for developing psychiatric disorders, including PTSD and AUD, are likely the product of an individual's genetic predisposition and exposure to environmental risk (e.g., stress; Ducci & Goldman, 2008; Koenen, Nugent, & Amstadter, 2008; Sher et al, 2010; Tarter, 2002). There has been substantial interest in characterizing such genetic vulnerabilities, yet the findings have been mixed.…”

Section: Gene-by-environment (G × E) Interactionsmentioning

confidence: 99%

PTSD, alcohol dependence, and conduct problems: Distinct pathways via lability and disinhibition

Simons

O’Brien

et al. 2017

Addictive Behaviors

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This study tested the role of affect lability and disinhibition in mediating associations between PTSD symptoms and two forms of alcohol-related problems, dependence syndrome symptoms (e.g., impaired control over consumption) and conduct problems (e.g., assault, risk behaviors). Genotype at the serotonin transporter linked polymorphic region (5-HTTLPR) was hypothesized to moderate associations between traumatic stress and PTSD symptoms. In addition, the study tested whether childhood traumatic stress moderated associations between combat trauma and PTSD symptoms. Participants were 270 OIF/OEF/OND veterans. The hypothesized model was largely supported. Participants with the low expression alleles of 5-HTTLPR (S or LG) exhibited stronger associations between childhood (but not combat) traumatic stress and PTSD symptoms. Affect lability mediated the associations between PTSD symptoms and alcohol dependence symptoms. Behavioral disinhibition mediated associations between PTSD symptoms and conduct related problems. Conditional indirect effects indicated stronger associations between childhood traumatic stress and lability, behavioral disinhibition, alcohol consumption, AUD symptoms, and associated conduct problems via PTSD symptoms among those with the low expression 5-HTTLPR alleles. However, interactions between combat trauma and either childhood trauma or genotype were not significant. The results support the hypothesis that affect lability and behavioral disinhibition are potential intermediate traits with distinct associations with AUD and associated externalizing problems.

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Section: Gene-by-environment (G × E) Interactionsmentioning

confidence: 99%

PTSD, alcohol dependence, and conduct problems: Distinct pathways via lability and disinhibition

Simons

O’Brien

et al. 2017

Addictive Behaviors

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“…In addition, they share a number of criterion symptoms, as outlined by the most recent Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 2013). Various explanatory hypotheses have been put forth regarding high rates of comorbid depression and PTSD, with some studies suggesting that depression and PTSD can be explained by the same underlying factors, whether psychological or genetic (Elhai et al, 2011; Koenen, Fu, et al, 2008; Koenen, Nugent, & Amstadter, 2008), while other studies indicate that depression and PTSD are best represented as correlated but fundamentally distinct processes (Hickling, Gillen, Blanchard, Buckley, & Taylor, 1998; Kemp, Drummond, & McDermott, 2010; Post, Zoellner, Youngstrom, & Feeny, 2011). In light of this debate, one related hypothesis is that depression and PTSD are mutually reinforcing conditions (Cramer, Waldorp, van der Maas, & Borsboom, 2010), such that PTSD symptoms may lead to the development of depression symptoms, and vice versa, thus leading to the maintenance of both disorders in a traumatized population such as MSM with histories of CSA.…”

Section: Introductionmentioning

confidence: 99%

Applying network analysis to psychological comorbidity and health behavior: Depression, PTSD, and sexual risk in sexual minority men with trauma histories.

Choi¹,

Batchelder²,

Ehlinger³

et al. 2017

Journal of Consulting and Clinical Psychology

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Objective High rates of depression and PTSD contribute to sexual risk, particularly in men who have sex with men (MSM) who have experienced childhood sexual abuse. The comorbidity between depression and PTSD and mechanisms by which they contribute to sexual risk in MSM remain unclear. This study sought to demonstrate the feasibility and utility of a novel network approach to (1) characterize symptom interconnections between depression and PTSD in MSM, (2) identify specific symptoms related to sexual risk behavior, and (3) compare symptom networks across groups at different levels of risk. Method Cross-sectional baseline data were collected from 296 HIV-negative urban MSM as part of a multi-site randomized intervention trial. Symptoms of depression and PTSD were self-reported along with sexual risk behavior. Analyses were performed in R using regularized partial correlation network modeling. Results Network analyses revealed complex associations between depression and PTSD symptoms and in relation to sexual risk behavior. While symptoms clustered within their respective disorders, depression and PTSD were connected at key symptom nodes (e.g., sleep, concentration). Specific symptoms (e.g., avoiding thoughts and feelings) were linked to sexual risk behavior. Network comparisons across risk groups suggested avoidant processes could be more readily activated in higher-risk individuals, whereas hyperarousal symptoms may be more salient for lower-risk individuals. Conclusions This study is one of the earliest network analyses of depression and PTSD, and first to extend this inquiry to health behavior. Symptom-level investigations may clarify mechanisms underlying psychological comorbidity and behavioral risk in MSM and refine targets for intervention/prevention.

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“…Although a substantial proportion (50–90%; [1,2]) of Americans are exposed to traumatic events in their lifetime, only a minority (8–20%) go on to develop PTSD. [1] Trauma exposure characteristics such as type or severity do not fully explain differences in risk of PTSD, suggesting that additional factors, both genetic and environmental, [3] contribute to risk of PTSD following trauma exposure.…”

Section: Introductionmentioning

confidence: 99%

ADCYAP1R1GENOTYPE, POSTTRAUMATIC STRESS DISORDER, AND DEPRESSION AMONG WOMEN EXPOSED TO CHILDHOOD MALTREATMENT

et al. 2012

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Background A growing literature indicates that genetic variation, in combination with adverse early life experiences, shapes risk for later mental illness. Recent work also suggests that molecular variation at the ADCYAP1R1 locus is associated with posttraumatic stress disorder (PTSD) in women. We sought to test whether childhood maltreatment (CM) interacts with ADCYAP1R1 geno-type to predict PTSD in women. Methods Data were obtained from 495 adult female participants from the Detroit Neighborhood Health Study. Genotyping of rs2267735, an ADCYAP1R1 variant, was conducted via TaqMan assay. PTSD, depression, and CM exposure were assessed via structured interviews. Main and interacting effects of ADCYAP1R1 and CM levels on past month PTSD and post-traumatic stress (PTS) severity were examined using logistic regression and a general linear model, respectively. As a secondary analysis, we also assessed main and interacting effects of ADCYAP1R1 and CM variation on risk of past-month depression diagnosis and symptom severity. Results No significant main effects were observed for ADCYAP1R1 genotype on either PTSD/PTS severity. In contrast, a significant ADCYAP1R1 × CM interaction was observed for both past month PTSD and PTS severity, with carriers of the “C” allele showing enhanced risk for these outcomes among women exposed to CM. No significant main or interaction effects were observed for past month depression/depression severity. Conclusions Genetic variation at the ADCYAP1R1 locus interacts with CM to shape risk of later PTSD, but not depression, among women. The molecular mechanisms contributing to this interaction require further investigation.

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Gene-environment interaction in posttraumatic stress disorder

Cited by 97 publications

References 141 publications

PTSD, alcohol dependence, and conduct problems: Distinct pathways via lability and disinhibition

PTSD, alcohol dependence, and conduct problems: Distinct pathways via lability and disinhibition

Applying network analysis to psychological comorbidity and health behavior: Depression, PTSD, and sexual risk in sexual minority men with trauma histories.

ADCYAP1R1GENOTYPE, POSTTRAUMATIC STRESS DISORDER, AND DEPRESSION AMONG WOMEN EXPOSED TO CHILDHOOD MALTREATMENT

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