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Posttraumatic stress disorder (PTSD) and insomnia are comorbid clinical conditions that are thought to result from genetic and environmental effects. Though studies have established the heritability of these disorders independently, no study to date has examined the genetic contributions to the relation between insomnia and PTSD symptoms (PTSS). The present study assessed this gap in the literature using a behavioral genetics approach to symptom dimensions. The sample consisted of 242 twin pairs who endorsed lifetime trauma exposure. Insomnia symptoms were assessed with the Women's Health Initiative Survey, and intrusion and avoidance PTSS were assessed with the Impact of Events Scale. Structural equation modeling was then employed to test the relative contributions of genetic, shared environmental, and nonshared environmental components to the relations between insomnia symptoms and intrusions and avoidance. Results indicated a significant association between insomnia symptoms and intrusions (r = 0.33, p < 0.01) and insomnia symptoms and avoidance (r = 0.20, p < 0.01), and 36-44% of phenotypic variance was accounted for by genetic contributions. These findings highlight a significant role for genetic factors in the mechanisms underlying the comorbidity between insomnia and PTSS. The implications for current etiological models of PTSD and insomnia are discussed., Competing Interests: Declaration of Competing Interest None, (Copyright © 2019 Elsevier B.V. All rights reserved.)

It has been over 5 years since the last special issue of Twin Research and Human Genetics on 'Twin Registries Worldwide: An Important Resource for Scientific Research' was published. Much progress has been made in the broad field of twin research since that time, and the current special issue is a follow-up to update the scientific community about twin registries around the globe. The present article builds upon our 2013 Registry description by summarizing current information on the Washington State Twin Registry (WSTR), including history and construction methods, member characteristics, available data, and major research goals. We also provide a section with brief summaries of recently completed studies and discuss the future research directions of the WSTR. The Registry has grown in terms of size and scope since 2013; highlights include recruitment of youth pairs under 18 years of age, extensive geocoding work to develop environmental exposures that can be linked to survey and administrative health data such as death records, and expansion of a biobank with specimens collected for genotyping, DNA methylation, and microbiome based-studies.

Objectives: Pain is a complex phenomenon influenced by context and person-specific factors. Affective dimensions of pain involve both enduring personality traits and fleeting emotional states. We examined how personality traits and emotional states are linked with clinical and evoked pain in a twin sample., Methods: 99 female twin pairs were evaluated for clinical and evoked pain using the McGill Pain Questionnaire (MPQ) and dolorimetry, and completed the 120-item International Personality Item Pool (IPIP), the Positive and Negative Affect Scale (PANAS), and ratings of stress and mood. Using a co-twin control design we examined a) the relationship of personality traits and emotional states with clinical and evoked pain and b) whether genetics and common environment (i.e. familial factors) may account for the associations., Results: Neuroticism was associated with the sensory component of the MPQ; this relationship was not confounded by familial factors. None of the emotional state measures was associated with the MPQ. PANAS negative affect was associated with lower evoked pressure pain threshold and tolerance; these associations were confounded by familial factors. There were no associations between IPIP traits and evoked pain., Conclusions: A relationship exists between neuroticism and clinical pain that is not confounded by familial factors. There is no similar relationship between negative emotional states and clinical pain. In contrast, the relationship between negative emotional states and evoked pain is strong while the relationship with enduring personality traits is weak. The relationship between negative emotional states and evoked pain appears to be non-causal and due to familial factors., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Informal caregiving can be deleterious to mental health, but research results are inconsistent and may reflect an interaction between caregiving and vulnerability to stress., Methods: We examined psychological distress among 1,228 female caregiving and non-caregiving twins. By examining monozygotic and dizygotic twin pairs discordant for caregiving, we assessed the extent to which distress is directly related to caregiving or confounded by common genes and environmental exposures., Results: Caregiving was associated with distress as measured by mental health functioning, anxiety, perceived stress, and depression. The overall association between caregiving and distress was confounded by common genes and environment for mental health functioning, anxiety, and depression. Common environment also confounded the association of caregiving and perceived stress., Conclusions: Vulnerability to distress is a factor in predicting caregivers' psychosocial functioning. Additional research is needed to explicate the mechanisms by which common genes and environment increase the risk of distress among informal caregivers.

Background: There is a dearth of knowledge about the link between cortisol and pain sensitivity., Purpose: We examined the association of salivary cortisol with indices of cold pain sensitivity in 198 female twins and explored the role of familial confounding., Methods: Three-day saliva samples were collected for cortisol levels and a cold pressor test was used to collect pain ratings and time to threshold and tolerance. Linear regression modeling with generalized estimating equations examined the overall and within-pair associations., Results: Lower diurnal variation of cortisol was associated with higher pain ratings at threshold (p = 0.02) and tolerance (p < 0.01). The relationship of diurnal variation with pain ratings at threshold and tolerance was minimally influenced by familial factors (i.e., genetics and common environment)., Conclusions: Understanding the genetic and non-genetic mechanisms underlying the link between HPA axis dysregulation and pain sensitivity may help to prevent chronic pain development and maintenance.

To examine the relationship between adverse childhood experiences (ACE) and health perception in adulthood, and to explore the contribution of shared familial factors to these associations. Data were collected from 180 female twins (90 pairs) from the community-based University of Washington Twin Registry. Participants completed questionnaires including the modified ACE Questionnaire, Traumatic Life Events Questionnaire, McGill Pain Questionnaire-Short Form, and the SF-36. Mixed effects linear regression modeling investigated the effects of ACE on indices of health perception controlling for correlated twin data. Additional models examined the associations while controlling for the experience of physical and/or sexual abuse in childhood; within-twin pair models that inherently adjust for familial factors explored shared familial influences. After controlling for relevant demographic variables, more ACE was associated with worse perceptions of general health (p=.01) and vitality (p=.05) on the SF-36. After controlling for childhood physical and/or sexual abuse, the relationship between ACE and general health remained significant (p=.01) while vitality was no longer significant. None of the associations remained significant after accounting for the influence of familial factors. These results support previous findings on the negative link between ACE and perceived health in adulthood. The detrimental effects of ACE on vitality may be accounted for by the experience of childhood physical and/or sexual abuse. Shared familial factors might play a partial role in the relationship between ACE and health perception. Future research should further investigate the genetic and environmental mechanisms that may explain this relationship., (Published by Elsevier Ltd.)

Background: The etiology of chronic fatigue syndrome (CFS) remains unknown. Personality traits influence well-being and may play a role in CFS and unexplained chronic fatigue., Purpose: This study aimed to examine the association of emotional instability and extraversion with chronic fatigue and CFS in a genetically informative sample., Methods: We evaluated 245 twin pairs for two definitions of chronic fatigue. They completed the Neuroticism and Extraversion subscales of the NEO Five Factor Inventory. Using a co-twin control design, we examined the association between personality and chronic fatigue., Results: Higher emotional instability was associated with both definitions of chronic fatigue and was confounded by shared genetics. Lower extraversion was also associated with both definitions of fatigue, but was not confounded by familial factors., Conclusions: Both emotional instability and extraversion are related to chronic fatigue and CFS. Whereas emotional instability and chronic fatigue are linked by shared genetic mechanisms, the relationship with extraversion may be causal and bidirectional.

Background: Systemic inflammation and pain sensitivity may contribute to the development and maintenance of chronic pain conditions., Purpose: We examined the relationship between systemic inflammation as measured by C-reactive protein (CRP) and cold pain sensitivity in 198 female twins from the University of Washington Twin Registry. We also explored the potential role of familial factors in this relationship., Methods: Linear regression modeling with generalized estimating equations examined the overall and within-pair associations., Results: Higher levels of CRP were associated with higher pain sensitivity ratings at pain threshold (p = 0.02) and tolerance (p = 0.03) after adjusting for age, body mass index, time to reach pain threshold or tolerance, and clinical pain status. The magnitude of the associations remained the same in within-pair analyses controlling for familial factors., Conclusions: The link between CRP and pain sensitivity may be due to non-shared environmental factors. CRP and pain sensitivity can be examined as potential biomarkers for chronic pain and other inflammatory conditions.

BackgroundDepression is a significant problem and it is vital to understand its underlying causes and related policy implications. Neighborhood characteristics are implicated in depression but the nature of this association is unclear. Unobserved or unmeasured factors may confound the relationship. This study addresses confounding in a twin study investigating neighborhood-level effects on depression controlling for genetics, common environment, and gene×environment (G × E) interactions.MethodData on neighborhood deprivation and depression were gathered from 3155 monozygotic twin pairs and 1275 dizygotic pairs (65.7% female) between 2006 and 2013. The variance for both depression and neighborhood deprivation was decomposed into three components: additive genetic variance (A); shared environmental variance (C); and non-shared environmental variance (E). Depression was then regressed on neighborhood deprivation to test the direct association and whether that association was confounded. We also tested for a G × E interaction in which the heritability of depression was modified by the level of neighborhood deprivation.ResultsDepression and neighborhood deprivation showed evidence of significant A (21.8% and 15.9%, respectively) and C (13.9% and 32.7%, respectively) variance. Depression increased with increasing neighborhood deprivation across all twins (p = 0.009), but this regression was not significant after controlling for A and C variance common to both phenotypes (p = 0.615). The G × E model showed genetic influences on depression increasing with increasing neighborhood deprivation (p < 0.001).ConclusionsNeighborhood deprivation is an important contributor to depression via increasing the genetic risk. Modifiable pathways that link neighborhoods to depression have been proposed and should serve as targets for intervention and research. [ABSTRACT FROM AUTHOR]