Sleep Quality Moderates the Relationship between Anxiety Sensitivity and PTSD Symptoms in Combat-exposed Veterans.

Objective/Background: Posttraumatic stress disorder (PTSD) and related conditions (e.g., depression) are common in Operation Enduring Freedom, Operation Iraqi Freedom, and Operation New Dawn (OEF/OIF/OND) veterans. High anxiety sensitivity (AS), defined as fear of anxiety and anxiety-related consequences, is related to greater PTSD and depressive symptoms; however, few studies have identified possible modifiers of these associations. The current study examined the moderating role of sleep quality in the associations between AS and PTSD and depressive symptoms. Participants: Participants were 155 OEF/OIF/OND community veterans ages 21-40 (12.3% women). Methods: Participants completed a semi-structured clinical interview for DSM-IV PTSD symptoms (Clinician Administered PTSD Scale; CAPS) and self-report measures of anxiety sensitivity (Anxiety Sensitivity Index), sleep quality (Pittsburgh Sleep Quality Index global score; PSQI), and depressive symptoms (Beck Depression Inventory-II; BDI-II). Results: Results of hierarchical linear regression models indicated that the main effects of AS and global PSQI score were significantly associated with greater PTSD and depressive symptoms (both with sleep items removed), above and beyond the covariates of trauma load and military rank. Sleep quality moderated the relationship between AS and PTSD symptoms (but not depressive symptoms), such that greater AS was associated with greater PTSD symptoms for individuals with good sleep quality, but not poor sleep quality. Conclusions: Sleep quality and AS account for unique variance in PTSD and depressive symptoms in combat-exposed veterans. AS may be less relevant to understanding risk for PTSD among combat-exposed veterans experiencing poor sleep quality.

Longitudinal Examination of the Impact of Resilience and Stressful Life Events on Alcohol Use Disorder Outcomes.

Stressful life events (SLEs) are a risk factor for alcohol use problems, and there is a need for identification of factors that may offset this risk. Resilience is uniquely, inversely associated with alcohol use, but there remains a dearth of research examining the buffering effect of resilience toward alcohol use problems in the context of SLEs. Objectives: This study used prospective data from an epidemiological twin sample (N = 7441) to test whether resilience at Time 1 would act as a buffer for new onset SLEs (e.g. assault, marital problems) against risk for alcohol dependence (AD) symptoms at Time 2. Results: The final model, adjusted for familial relatedness and controlling for demographic covariates and Time 1 (lifetime) AD symptoms, identified significant main effects of resilience and SLEs; those with greater resilience at Time 1 reported fewer symptoms (ß=-.087, p<.001) and those with greater new-onset SLEs reported greater symptoms (ß=.116, p<.001) at Time 2. However, there was no significant interaction (ß=-.008, p>.05). Conclusions: Although findings further support the association of resilience and SLEs with AD, results do not support the conceptualization of resilience as a buffer against the impact of future life stressors on alcohol use outcomes. This suggests other factors may be more relevant for understanding protective factors for alcohol use problems or the relation between resilience and SLEs on alcohol use outcomes.

Meta-Analysis of Associations Between Hypothalamic-Pituitary-Adrenal Axis Genes and Risk of Posttraumatic Stress Disorder.

The hypothalamic-pituitary-adrenal (HPA) axis has been of interest in attempts to identify genetic vulnerability for posttraumatic stress disorder (PTSD). Although numerous HPA-axis genes have been implicated in candidate gene studies, the findings are mixed and interpretation is limited by study design and methodological inconsistencies. To address these inconsistencies in the PTSD candidate gene literature, we conducted meta-analyses of HPA-related genes from both a traditional single nucleotide polymorphism (SNP)-level analysis and a gene-level analysis, using novel methods aggregating markers in the same gene. Database searches (PubMed and PsycINFO) identified 24 unique articles examining six HPA-axis genes in PTSD; analyses were conducted on four genes (ADCYAP1R1, CRHR1, FKBP5, NR3C1) that met study eligibility criteria (original research, human subjects, main effect association study of selected genes, PTSD as an outcome, trauma-exposed control group) and had sufficient data and number of studies for use in meta-analysis, within 20 unique articles. Findings from SNP-level analyses indicated that two variants (rs9296158 in FKBP5 and rs258747 in NR3C1) were nominally associated with PTSD, ps = .001 and .001, respectively, following multiple testing correction. At the gene level, significant relations between PTSD and both NR3C1 and FKBP5 were detected and robust to sensitivity analyses. Although study limitations exist (e.g., varied outcomes, inability to test moderators), taken together, these results provide support for FKBP5 and NR3C1 in risk for PTSD. Overall, this work highlights the utility of meta-analyses in resolving discrepancies in the literature and the value of adopting gene-level approaches to investigate the etiology of PTSD.

Insomnia Disorder and Behaviorally Induced Insufficient Sleep Syndrome: Prevalence and Relationship to Depression in College Students.

Background: College students are at increased risk for sleep disorders, including insomnia disorder and obtaining less than 6.5 hr of sleep per night by choice, or behaviorally induced insufficient sleep syndrome (BIISS). These disorders can have deleterious daytime consequences, including depression. This study aims to establish the prevalence of insomnia and BIISS disorders and examine associations of insomnia and BIISS with other sleep characteristics and depression. Methods: A subset of data from Spit for Science, a college risk behaviors and health study (n = 989) was used. Insomnia and BIISS were defined as mutually exclusive disorders, based on diagnostic criteria. Results: A majority (68%) of students were categorized as normal sleepers, followed by insomnia (22%), and BIISS (10%). Sleep duration was comparable between BIISS and insomnia, while daytime sleepiness was significantly higher in BIISS, and sleep latency was longer in insomnia (m = 44 vs. m = 13 min). Insomnia was associated with the highest depression symptoms, followed by BIISS, and normal sleep, controlling for demographics. Insomnia was associated with twice the risk of moderate or higher depression compared to normal sleep (CI: 1.60, 2.70, p < .001). Conclusion: These findings highlight the sleep difficulties endemic to college populations. Further, this study provides the first prevalence estimation of BIISS in college students and the first comparison of insomnia and BIISS on sleep characteristics and depressive symptoms. This study underscores the importance of targeted screening and intervention to improve both sleep and depression in this vulnerable population.

The impact of resilience and subsequent stressful life events on MDD and GAD.

BACKGROUND: There remains a dearth of research examining the "buffering" effect of resilience, wherein resilience at one point in time would be expected to protect an individual against development of psychopathology following future adverse life events. METHODS: Using longitudinal data from an epidemiological twin sample (N = 7463), this study tested whether resilience would act as a buffer for stressful life events (SLEs) against risk for major depressive disorder (MDD) and generalized anxiety disorder (GAD). Resilience, demographics, and psychopathology were measured at Time 1 and recent SLEs and current MDD and GAD were measured at Time 2. RESULTS: Final models, controlling for demographic covariates and Time 1 diagnosis, examined the impact of Time 1 resilience, recent SLEs, their interaction, and a three-way interaction adding sex on MDD and GAD. CONCLUSIONS: The pattern of findings was the same for MDD and GAD, wherein main effects and two-way interactions of resilience and SLEs were significant, such that greater resilience was protective even in the context of high numbers of past-year SLEs. The three-way interaction was not significant, suggesting that the relationship between SLEs and resilience on psychopathology was the same for both men and women. Findings support the conceptualization of resilience as a buffer against the impact of future life stressors on common internalizing psychopathology. Longitudinal designs and trajectory-based studies that include recurring measures of SLEs could inform conceptualizations of resilience in the context of ongoing adversity and aid in developing interventions aimed at fostering healthy adaptation in the face of stressors.

Does Parenting Influence the Enduring Impact of Severe Childhood Sexual Abuse on Psychiatric Resilience in Adulthood?

This study examined the effect of parenting on the association between childhood sexual abuse (CSA) and psychiatric resilience in adulthood in a large female twin sample (n = 1423) assessed for severe CSA (i.e., attempted or completed intercourse before age 16). Severe CSA was associated with lower resilience to recent stressors in adulthood (defined as the difference between their internalizing symptoms and their predicted level of symptoms based on cumulative exposure to stressful life events). Subscales of the Parental Bonding Instrument were significantly associated with resilience. Specifically, parental warmth was associated with increased resilience while parental protectiveness was associated with decreased resilience. The interaction between severe CSA and parental authoritarianism was significant, such that individuals with CSA history and higher authoritarianism scores had lower resilience. Results suggest that CSA assessment remains important for therapeutic work in adulthood and that addressing parenting may be useful for interventions in children with a CSA history.

An examination of the etiologic overlap between the genetic and environmental influences on insomnia and common psychopathology.

BACKGROUND: Insomnia is comorbid with internalizing and externalizing psychiatric disorders. However, the extent to which the etiologic influences on insomnia and common psychopathology overlap is unclear. There are limited genetically informed studies of insomnia and internalizing disorders and few studies of overlap exist with externalizing disorders. METHODS: We utilized twin data from the Virginia Adult Twin Studies of Psychiatric and Substance Use Disorders (total n = 7,500). Insomnia, internalizing disorders (major depressive disorder [MDD], generalized anxiety disorder [GAD]), and alcohol abuse or dependence (AAD) were assessed at two time points, while antisocial personality disorder (ASPD) was assessed once. Cholesky decompositions were performed in OpenMx and longitudinal measurement models were run on available phenotypes to reduce measurement error. RESULTS: The latent additive genetic influences on insomnia overlapped significantly (56% for females, 74% for males) with MDD and were shared completely (100%) with GAD. There was significant overlap of latent unique environmental influences, with overlap ranging from 38 to 100% across disorders. In contrast, there was less genetic overlap between insomnia and externalizing disorders, with 18% of insomnia's heritability shared with AAD and 23% with ASPD. Latent unique environmental overlap between insomnia and both externalizing disorders was negligible. CONCLUSIONS: The evidence for substantial genetic overlap between insomnia and stable aspects of both internalizing disorders suggests that there may be few insomnia-specific genes and investigation into unique environmental factors is important for understanding insomnia development. The modest overlap between insomnia and externalizing disorders indicates that these disorders are genetically related, but largely etiologically distinct.

The Effects of a BDNF Val66Met Polymorphism on Posttraumatic Stress Disorder: A Meta-Analysis.

OBJECTIVE: Given evidence that posttraumatic stress disorder (PTSD) is moderately heritable, a number of studies utilizing candidate gene approaches have attempted to examine the potential contributions of theoretically relevant genetic variation. Some of these studies have found sup port for a brain-derived neurotrophic factor (BDNF) variant, Val66Met, in the risk of developing PTSD, while others have failed to find this link. METHODS: This study sought to reconcile these conflicting findings using a meta-analysis framework. Analyses were also used to determine whether there is significant heterogeneity in the link between this variant and PTSD. We conducted a systematic review of the literature on BDNF and PTSD from the PsycINFO and PubMed databases. A total of 11 studies were included in the analysis. RESULTS: Findings indicate a marginally significant effect of the BDNF Val66Met variant on PTSD (p < 0.1). However, of the 11 studies included, only 2 suggested an effect with a non-zero confidence interval, one of which showed a z score of 3.31. We did not find any evidence for heterogeneity. CONCLUSIONS: Findings from this meta-analytic investigation of the published literature provide little support for the Val66Met variant of BDNF as a predictor of PTSD. Future well-powered agnostic genome-wide association studies with more refined phenotyping are needed to clarify genetic influences on PTSD.

Association of Posttraumatic Stress Disorder With rs2267735 in the ADCYAP1R1 Gene: A Meta-Analysis.

Recent studies point to the potential role of the (pituitary) adenylate cyclase activating polypeptide receptor 1 (ADCYAP1R1) gene, which has been implicated in stress response, in posttraumatic stress disorder (PTSD). Multiple genetic association studies have examined potential PTSD risk related to this gene, with mixed results. We conducted a meta-analysis of rs2267735 in ADCYAP1R1 in PTSD. A literature search was conducted using PubMed and PsycINFO, resulting in nine studies that met criteria for inclusion in analysis. Biostat's Comprehensive Meta-Analysis was used to conduct the main meta-analysis on the combined sex sample, as well as two subanalyses examining effects separately in female and male participants. Results indicated that the C allele of rs2267735 conferred significant risk for PTSD in the combined sex data, OR = 1.210, 95% CI [1.007, 1.454], p = .042, and in the subsample of women and girls, OR = 1.328, 95% CI [1.026, 1.719], p = .031; but not in the subsample of men and boys, OR = 0.964, 95% CI [0.733, 1.269], p = .796. These results provide evidence for an association between ADCYAP1R1 and PTSD and indicate that there may indeed be sex differences. Implications of these findings, including the role of rs2267735 as one modulator of the stress system, are discussed.

Molecular genetic overlap between posttraumatic stress disorder and sleep phenotypes.

STUDY OBJECTIVES: Sleep problems are common, serving as both a predictor and symptom of posttraumatic stress disorder (PTSD), with these bidirectional relationships well established in the literature. While both sleep phenotypes and PTSD are moderately heritable, there has been a paucity of investigation into potential genetic overlap between sleep and PTSD. Here, we estimate genetic correlations between multiple sleep phenotypes (including insomnia symptoms, sleep duration, daytime sleepiness, and chronotype) and PTSD, using results from the largest genome-wide association study (GWAS) to date of PTSD, as well as publicly available GWAS results for sleep phenotypes within UK Biobank data (23 variations, encompassing four main phenotypes). METHODS: Genetic correlations were estimated utilizing linkage disequilibrium score regression (LDSC), an approach that uses GWAS summary statistics to compute genetic correlations across traits, and Mendelian randomization (MR) analyses were conducted to follow up on significant correlations. RESULTS: Significant, moderate genetic correlations were found between insomnia symptoms (rg range 0.36-0.49), oversleeping (rg range 0.32-0.44), undersleeping (rg range 0.48-0.49), and PTSD. In contrast, there were mixed results for continuous sleep duration and daytime sleepiness phenotypes, and chronotype was not correlated with PTSD. MR analyses did not provide evidence for casual effects of sleep phenotypes on PTSD. CONCLUSION: Sleep phenotypes, particularly insomnia symptoms and extremes of sleep duration, have shared genetic etiology with PTSD, but causal relationships were not identified. This highlights the importance of further investigation into the overlapping influences on these phenotypes as sample sizes increase and new methods to investigate directionality and causality become available.

GxE effects of FKBP5 and traumatic life events on PTSD: A meta-analysis.

BACKGROUND: Twin studies have demonstrated that both genetic and environmental factors influence risk for posttraumatic stress disorder (PTSD), and there is some evidence supporting the interplay of genes and environment (GxE). Many GxE studies within the PTSD literature have focused on genes implicated in the stress response system, such as FK506 binding protein 51 (FKBP5). Given inconsistencies across GxE literature as a whole, a meta-analysis to synthesize results is warranted. METHODS: Studies were identified through PubMed and PsycINFO. A meta-analysis was conducted using a random effects model in the MAc package in R. Heterogeneity of the effect size distribution was examined with Cochran's Q statistic. A Simes procedure was used to test the gene-level GxE effect for FKBP5 interacting with trauma. RESULTS: A significant gene-level GxE gene effect was demonstrated for FKBP5 when pooled across all four examined variants (rs1360780, rs3800373, rs9296158, rs9470080) when interacting with trauma exposure on PTSD. Significant large GxE effect sizes were also found for each independent variant. There was no evidence for heterogeneity of variance. LIMITATIONS: Limitations include reduced power for detecting variability across moderators, potential bias due to failure of meta-analyzed studies to account for two-way covariate x gene and covariate x environment influences, and a high false discovery rate that is characteristic of GxE analyses. CONCLUSIONS: This is the first study to quantify an overall gene-level effect of FKBP5 in a GxE analysis of PTSD, evidence which may be used to address current issues in the FKBP5 GxE literature (e.g., disparate variants, low sample sizes and power), as well as inform follow-up functional research.

Effects of social support on the association between precollege sexual assault and college-onset victimization.

OBJECTIVE: This study examined the moderating and mediating effects of perceived social support on the association between precollege sexual assault (SA) and college-onset SA. PARTICIPANTS: A representative sample of 6,132 undergraduates. METHODS: The PLUM procedure in SPSS was used to test the moderation model, with individual regressions conducted in a hierarchical fashion. A weighted least squared mean and variance adjusted (WLSMV) mediation model was used to examine the mediating effect of social support. RESULTS: Precollege SA significantly predicted college-onset SA. Social support significantly mediated the relation between precollege SA and college-onset SA. Social support was not a significant moderator of this relationship. CONCLUSIONS: Given the high prevalence of SA among college populations, as well as the high rates of SA revictimization, identification of factors that may be related to repeated SA (eg, low social support) within this population are essential and may inform intervention, policy, and university student services.

Relation between coping and posttrauma cognitions on PTSD in a combat-trauma population.

Individual differences in cognitive processes and coping behaviors play a role in the development and maintenance of posttraumatic stress disorder (PTSD). Given the large numbers of combat-exposed service members returning from the Operation Enduring Freedom (OEF), Operation Iraqi Freedom (OIF), and Operation New Dawn (OND) conflicts, exploring individual differences in cognitive-affective processes is important for informing our understanding of PTSD etiology and early intervention in military samples. The present study examined the unique main and interactive effects of negative posttrauma cognitions (i.e., negative beliefs about self [NS], the world [NW], and self-blame [SB]) and coping strategies (i.e., positive behavioral, positive cognitive, avoidant coping, and social and emotional coping) on PTSD diagnosis within 155 (Mage = 30.7, SD = 4.48) OEF/OIF/OND combat trauma-exposed veterans recruited from an ongoing study examining the effects of combat trauma and stress reactivity. In the final, stepwise logistic regression analysis, avoidant coping, but no other coping strategy, was significantly positively related to PTSD diagnosis in the initial step. Higher levels of NS, but not NW, were significantly associated with having a PTSD diagnosis, while SB was associated with decreased likelihood of PTSD, above and beyond coping strategies. A significant interaction effect was found between NS and positive cognitive coping, such that greater positive cognitive coping weakened the relationship between NS and PTSD. Examining and addressing coping behaviors and negative thoughts of self jointly may benefit assessment and intervention approaches in a combat-trauma population.

The genetics and epigenetics of PTSD: overview, recent advances, and future directions.

This paper provides a brief summary and commentary on the growing literature and current developments related to the genetic underpinnings of posttraumatic stress disorder (PTSD). We first briefly provide an overview of the behavioral genetic literature on PTSD, followed by a short synopsis of the substantial candidate gene literature with a focus on genes that have been meta-analyzed. We then discuss the genome-wide association studies (GWAS) that have been conducted, followed by an introduction to other molecular platforms used in PTSD genomic studies, such as epigenetic and expression approaches. We close with a discussion of developments in the field that include the creation of the PTSD workgroup of the Psychiatric Genomics Consortium, statistical advances that can be applied to GWAS data to answer questions of heritability and genetic overlap across phenotypes, and bioinformatics techniques such as gene pathway analyses which will further advance our understanding of the etiology of PTSD.

The Genetics and Epigenetics of PTSD: Overview, Recent Advances, and Future Directions.

This paper provides a brief summary and commentary on the growing literature and current developments related to the genetic underpinnings of posttraumatic stress disorder (PTSD). We first briefly provide an overview of the behavioral genetic literature on PTSD, followed by a short synopsis of the substantial candidate gene literature with a focus on genes that have been meta-analyzed. We then discuss the genome-wide association studies (GWAS) that have been conducted, followed by an introduction to other molecular platforms used in PTSD genomic studies, such as epigenetic and expression approaches. We close with a discussion of developments in the field that include the creation of the PTSD workgroup of the Psychiatric Genomics Consortium, statistical advances that can be applied to GWAS data to answer questions of heritability and genetic overlap across phenotypes, and bioinformatics techniques such as gene pathway analyses which will further advance our understanding of the etiology of PTSD.

Relationships between potentially traumatic events, sleep disturbances, and symptoms of PTSD and alcohol use disorder in a young adult sample.

OBJECTIVE: Traumatic events, particularly those that are interpersonal in nature, are associated with increased risk for co-occurring sequelae, including sleep disturbances, posttraumatic stress disorder (PTSD), and alcohol use disorder (AUD). However, the associations between these phenotypes have not been explored among college students. METHODS: We examined relationships between type of potentially traumatic event (PTE) exposure (pre-college) and sleep disturbances, as well as mediating effects of lifetime PTSD and AUD symptoms on these relationships, in a large undergraduate sample (N = 1599, 64.7% female). Hierarchical linear regressions were conducted, beginning with demographics and then adding interpersonal and accidental PTEs in a stepwise regression; mediation analyses were run. RESULTS: Within the sample, 33.7% endorsed at least one interpersonal PTE, while 64.4% endorsed at least one accidental PTE. Hierarchical regressions demonstrated that interpersonal (ß = 0.202, p = 0.000), but not accidental PTE exposure significantly predicted disturbed sleep. Both PTSD and AUD symptoms significantly mediated (p values < 0.001) the relationship between interpersonal PTE exposure and sleep, with indirect effects accounting for 61% and 17% of total effects, respectively. In the correlated mediation model, both disorders remained significant mediators (p < 0.001), with indirect effects accounting for 56% (PTSD symptoms) and 14% (AUD symptoms) of total effects on sleep. CONCLUSIONS: Results suggest that interpersonal PTEs are more potent predictors of sleep problems than accidental PTEs. Further, trauma exposure psychiatric symptom sequelae (PTSD, AUD) account for part of the relationship between interpersonal PTE exposure and disturbed sleep, which both independently and jointly suggests that treating PTSD and AUD symptoms in college students may also improve sleep.

Sleep Disturbances in OEF/OIF/OND Veterans: Associations with PTSD, Personality, and Coping.

STUDY OBJECTIVES: Sleep disturbances are well documented in relation to trauma exposure and posttraumatic stress disorder (PTSD), but correlates of such disturbances remain understudied in veteran populations. We conducted a preliminary study of sleep disturbances in Operation Enduring Freedom, Operation Iraqi Freedom, and Operation New Dawn veterans (n = 133; mean [standard deviation] age = 29.8 [4.7] y). METHODS: Veterans were assigned to one of three groups based on responses to the Clinician Administered PTSD Scale: control (no trauma-exposure [TE] or PTSD), TE, and PTSD. Sleep disturbance was assessed using the Pittsburgh Sleep Quality Index (PSQI). Measures of resilience, trauma load, personality, coping, alcohol use, and mild traumatic brain injury were also assessed via self-report. RESULTS: The PTSD group had significantly more disturbed sleep (PSQI global score mean = 8.94, standard deviation = 3.12) than control (mean = 5.27, standard deviation = 3.23) and TE (mean = 5.34, standard deviation = 3.17) groups, but there were no differences between TE and control. The same pattern emerged across most PSQI subscales. Results of linear regression analyses indicated that current smoking, Army (versus other military branches), neuroticism, and using substances to cope were all significant correlates of higher sleep disturbance, whereas post-deployment social support was associated with less sleep disturbance. However, when combined together into a model with PTSD status, only neuroticism and substance use coping remained significant as predictors of more disturbed sleep. CONCLUSIONS: These initial findings suggest that TE itself may not be an independent risk factor for disturbed sleep in veterans, and that neurotic personality and a tendency to cope by using substances may partially explain sleep disturbance, above and beyond a diagnosis of PTSD.

Genetic Pathways to Insomnia.

This review summarizes current research on the genetics of insomnia, as genetic contributions are thought to be important for insomnia etiology. We begin by providing an overview of genetic methods (both quantitative and measured gene), followed by a discussion of the insomnia genetics literature with regard to each of the following common methodologies: twin and family studies, candidate gene studies, and genome-wide association studies (GWAS). Next, we summarize the most recent gene identification efforts (primarily GWAS results) and propose several potential mechanisms through which identified genes may contribute to the disorder. Finally, we discuss new genetic approaches and how these may prove useful for insomnia, proposing an agenda for future insomnia genetics research.

An epidemiologic study of childhood sexual abuse and adult sleep disturbances.

Childhood sexual abuse (CSA) is linked to negative consequences, including insomnia. Few studies have examined the enduring effects of CSA on adult insomnia. Given the relationship between sleep and poor health, a better understanding of these effects has clinical implications. We used a representative adult twin sample. Both sexes were assessed with a broad CSA variable, with a subset of females (n = 424) given additional items capturing escalating physical contact and abuse characteristics. A sum score of past-month insomnia symptoms was calculated from the Symptom Checklist-90 (shortened version). Logistic regression was used to estimate the effects of CSA, physical contact, and incident characteristics on insomnia symptoms. Of the full sample (N = 8,184), 9.8% reported CSA. CSA significantly predicted insomnia symptoms in the female sample (n = 1,407; odds ratio [OR] = 1.67, 95% confidence interval [CI] = 1.35-2.06, p < .0001) but the continuum of physical contact did not. Individually, more than 1 perpetrator and feeling forced/threatened increased sleep risk, whereas having a male perpetrator (vs. female or multiple) decreased risk. These associations did not hold when combined. In the mixed-sex sample (n = 6,777), we replicated our CSA finding (OR = 1.65, 95% CI = 1.34-2.04, p < .0001) and found that female gender (OR = 1.16, 95% CI = 1.03-1.30, p = .0125), but not the gender*CSA interaction, was significant. CSA predicts adult insomnia symptoms decades after abuse, but the small sample size for incident characteristics (n = 424) resulted in limited conclusions about associated risk.