Neighborhood Deprivation Moderates Shared and Unique Environmental Influences on Hazardous Drinking: Findings from a Cross-Sectional Co-Twin Study.
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ABSTRACT:
SUBMITTER: Rhew IC
PROVIDER: S-EPMC7485221 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:To examine whether trauma and posttraumatic stress disorder (PTSD) are differentially associated with binge and hazardous patterns of drinking among women and men.Secondary analysis of the Wave 2 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC); the analytic sample included 31,487 respondents (54.6% female) without past-year alcohol abuse/dependence. Participants' trauma-exposure/PTSD status was characterized as: no exposure to trauma in lifetime (reference), lifetime trauma exposure, PTSD before past-year, or past-year PTSD. Past-year binge and hazardous drinking were examined with multinomial logistic regression models (past-year abstinence was modeled as the non-event); models included the main effects of trauma-exposure/PTSD status and gender, the trauma-exposure/PTSD status-by-gender interaction, psychiatric comorbidity, and socio-demographic covariates.The gender-specific effects of trauma, before past-year PTSD, and past-year PTSD were significantly elevated for all drinking behaviors in women (range of odds ratios (ORs) = 1.8-4.8), and for some drinking behaviors in men (range of ORs = 1.3-2.0), relative to no trauma exposure. Trauma exposure was more strongly associated with high-frequency binge drinking, low-frequency binge drinking, and non-binge drinking among women as compared to men. Past-year PTSD was also more strongly associated with low-frequency binge drinking and non-binge drinking among women compared to men. Findings for hazardous drinking followed a similar pattern, with significant gender-related differences in ORs for hazardous drinking and non-hazardous drinking observed with respect to trauma exposure and past-year PTSD..Mental health practitioners should be mindful of the extent to which trauma-exposed individuals both with and without PTSD engage in binge and hazardous drinking, given the negative consequences associated with these patterns of drinking..
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Project description:Neighborhood influences in the etiology of schizophrenia have been emphasized in a number of systematic reviews, but causality remains uncertain. To test the social drift hypothesis, we used three complementary genetically informed Swedish cohorts. First, we used nationwide Swedish data on approximately 760 000 full- and half-sibling pairs born between 1951 and 1974 and quantitative genetic models to study genetic and environmental influences on the overlap between schizophrenia in young adulthood and subsequent residence in socioeconomically deprived neighborhoods. Schizophrenia diagnoses were ascertained using the National Patient Registry. Second, we tested the overlap between childhood psychotic experiences and neighborhood deprivation in early adulthood in the longitudinal Twin Study of Child and Adolescent Development (TCHAD; n=2960). Third, we investigated to what extent polygenic risk scores for schizophrenia predicted residence in deprived neighborhoods during late adulthood using the TwinGene sample (n=6796). Sibling data suggested that living in deprived neighborhoods was substantially heritable; 65% (95% confidence interval (95% CI): 60-71%) of the variance was attributed to genetic influences. Although the correlation between schizophrenia and neighborhood deprivation was moderate in magnitude (r=0.22; 95% CI: 0.20-0.24), it was entirely explained by genetic influences. We replicated these findings in the TCHAD sample. Moreover, the association between polygenic risk for schizophrenia and neighborhood deprivation was statistically significant (R(2)=0.15%, P=0.002). Our findings are primarily consistent with a genetic selection interpretation where genetic liability for schizophrenia also predicts subsequent residence in socioeconomically deprived neighborhoods. Previous studies may have overemphasized the relative importance of environmental influences in the social drift of schizophrenia patients. Clinical and policy interventions will therefore benefit from the future identification of potentially causal pathways between different dimensions of cognitive functions and socioeconomic trajectories derived from studies adopting family-based research designs.
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Project description:Alcohol is one of the most widely consumed psychoactive drugs globally. Hazardous drinking, defined by quantity and frequency of consumption, is associated with acute and chronic morbidity. Alcohol use disorders (AUDs) are psychiatric syndromes characterized by impaired control over drinking and other symptoms. Contemporary aetiological perspectives on AUDs apply a biopsychosocial framework that emphasizes the interplay of genetics, neurobiology, psychology, and an individual's social and societal context. There is strong evidence that AUDs are genetically influenced, but with a complex polygenic architecture. Likewise, there is robust evidence for environmental influences, such as adverse childhood exposures and maladaptive developmental trajectories. Well-established biological and psychological determinants of AUDs include neuroadaptive changes following persistent use, differences in brain structure and function, and motivational determinants including overvaluation of alcohol reinforcement, acute effects of environmental triggers and stress, elevations in multiple facets of impulsivity, and lack of alternative reinforcers. Social factors include bidirectional roles of social networks and sociocultural influences, such as public health control strategies and social determinants of health. An array of evidence-based approaches for reducing alcohol harms are available, including screening, pharmacotherapies, psychological interventions and policy strategies, but are substantially underused. Priorities for the field include translating advances in basic biobehavioural research into novel clinical applications and, in turn, promoting widespread implementation of evidence-based clinical approaches in practice and health-care systems.
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Project description:Background Attention deficit hyperactivity disorder (ADHD) is a common and highly heritable neurodevelopmental disorder with a complex aetiology. The identification of candidate intermediate phenotypes that are both heritable and genetically linked to ADHD may facilitate the detection of susceptibility genes and elucidate aetiological pathways. Very low-frequency (VLF; <0.5 Hz) electroencephalographic (EEG) activity represents a promising indicator of risk for ADHD, but it currently remains unclear as to whether it is heritable or genetically linked to the disorder.Methods Direct-current (DC)-EEG was recorded during a cognitive activation condition in 30 monozygotic and dizygotic adolescent twin pairs concordant or discordant for high ADHD symptom scores, and 37 monozygotic and dizygotic matched-control twin pairs with low ADHD symptom scores. Structural equation modelling was used to quantify the genetic and environmental contributions to the phenotypic covariance between ADHD and VLF activity.Results Attention deficit hyperactivity disorder was significantly associated with reduced VLF power during cognitive activation, which suggests reduced synchronization of widespread neuronal activity. Very low-frequency power demonstrated modest heritability (0.31), and the genetic correlation (-0.80) indicated a substantial degree of overlap in genetic influences on ADHD and VLF activity.Conclusions Altered VLF activity is a potential candidate intermediate phenotype of ADHD, which warrants further investigation of underlying neurobiological and genetic mechanisms.
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Project description:BackgroundResearch conducted in high-income countries has investigated influences of socioeconomic inequalities on drinking outcomes such as alcohol use disorders (AUD), however, associations between area-level neighborhood social deprivation (NSD) and individual socioeconomic status with these outcomes have not been explored in Brazil. Thus, we investigated the role of these factors on drink-related outcomes in a Brazilian population, attending to male-female variations.MethodsA multi-stage area probability sample of adult household residents in the São Paulo Metropolitan Area was assessed using the WHO Composite International Diagnostic Interview (WMH-CIDI) (n = 5,037). Estimation focused on prevalence and correlates of past-year alcohol disturbances [heavy drinking of lower frequency (HDLF), heavy drinking of higher frequency (HDHF), abuse, dependence, and DMS-5 AUD] among regular users (RU); odds ratio (OR) were obtained.ResultsHigher NSD, measured as an area-level variable with individual level variables held constant, showed an excess odds for most alcohol disturbances analyzed. Prevalence estimates for HDLF and HDHF among RU were 9% and 20%, respectively, with excess odds in higher NSD areas; schooling (inverse association) and low income were associated with male HDLF. The only individual-level association with female HDLF involved employment status. Prevalence estimates for abuse, dependence, and DSM-5 AUD among RU were 8%, 4%, and 8%, respectively, with excess odds of: dependence in higher NSD areas for males; abuse and AUD for females. Among RU, AUD was associated with unemployment, and low education with dependence and AUD.ConclusionsRegular alcohol users with alcohol-related disturbances are more likely to be found where area-level neighborhood characteristics reflect social disadvantage. Although we cannot draw inferences about causal influence, the associations are strong enough to warrant future longitudinal alcohol studies to explore causal mechanisms related to the heterogeneous patterns of association and male-female variations observed herein. Hopefully, these findings may help guide future directions for public health.
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Project description:There is a dearth of research exploring the moderating role of the social environment on neighborhood structural disadvantage and depressive symptoms, particularly among adolescents. Therefore, we examined if adolescent perceptions of neighborhood social cohesion and safety moderated the association between neighborhood structural disadvantage and adolescent depressive symptoms. This cross-sectional study used data from the National Longitudinal Study of Adolescent to Adult Health (Add Health). The study sample consisted of 12,105 adolescents enrolled in 9th-12th grades during the 1994-1995 school year across the United States (U.S.). Mixed effects multilevel modeling was used to determine if adolescent perceptions of neighborhoods moderated the relationship between neighborhood structural disadvantage and adolescent depressive symptoms. Results showed that perceived neighborhood social cohesion moderated the relationship between neighborhood structural disadvantage and adolescent depressive symptoms (p???0.001). At higher levels of perceived neighborhood social cohesion, neighborhood structural disadvantage was associated with decreased depressive symptoms. Findings suggest that improving perceived neighborhood social cohesion may decrease adolescent depressive symptoms, particularly in neighborhoods with high disadvantage. This aspect of the neighborhood social environment may serve as a target for structural and other interventions to address the growing burden of depression among adolescents.
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Project description:Aging-related declines occur in many different domains of cognitive function during middle and late adulthood. However, whether a global dimension underlies individual differences in changes in different domains of cognition and whether global genetic influences on cognitive changes exist is less clear. We addressed these issues by applying multivariate growth curve models to longitudinal data from 857 individuals from the Swedish Adoption/Twin Study of Aging, who had been measured on 11 cognitive variables representative of verbal, spatial, memory, and processing speed abilities up to 5 times over up to 16 years between ages 50 and 96 years. Between ages 50 and 65 years scores on different tests changed relatively independently of one another, and there was little evidence for strong underlying dimensions of change. In contrast, over the period between 65 and 96 years of age, there were strong interrelations among rates of change both within and across domains. During this age period, variability in rates of change were, on average, 52% domain-general, 8% domain-specific, and 39% test-specific. Quantitative genetic decomposition indicated that 29% of individual differences in a global domain-general dimension of cognitive changes during this age period were attributable to genetic influences, but some domain-specific genetic influences were also evident, even after accounting for domain-general contributions. These findings are consistent with a balanced global and domain-specific account of the genetics of cognitive aging.
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Project description:AimsTo investigate associations of life-time hazardous and binge drinking with biomarkers of cardiometabolic health, liver function, cardiovascular disease (CVD) and mortality.DesignProspective cohort study with median follow-up time to CVD incidence of 4.5 years.SettingLondon, UK: civil servants within the Whitehall II Study.ParticipantsA total of 4820 drinkers aged 59-83 years with biological measurements during the 2011-12 survey.MeasurementsHazardous drinking was defined as having an AUDIT-C score ≥ 5 calculated at each decade of life, forming the following groups: never hazardous drinker, former early (stopping before age 50), former later (stopping after age 50), current hazardous drinker and consistent hazardous drinker (hazardous drinker at each decade of life).FindingsMore than half the sample had been hazardous drinkers at some point during their life-time, comprising former early (< age 50) (19%), former later (≥ age 50) (11%), current (21%) and consistent hazardous drinker (AUDIT-C ≥ 5 across life (5%). After adjusting for covariates, waist circumference was larger with more persistent hazardous drinking (e.g. compared with never hazardous drinkers, former early had increased waist circumference by 1.17 cm [95% confidence interval (CI) = 0.25-2.08]; former later by 1.88 cm (CI = 0.77-2.98); current by 2.44 cm (CI = 1.50-3.34) and consistent hazardous drinker by 3.85 cm (CI = 2.23-5.47). Current hazardous drinkers had higher systolic blood pressure (2.44 mmHg, CI = 1.19-3.68) and fatty liver index scores (4.05 mmHg, CI = 2.92-5.18) than never hazardous drinkers. Current hazardous drinkers [hazard ratio (HR) = 2.75, CI = 1.44-5.22) had an elevated risk of stroke, and former later hazardous drinkers had an elevated risk of non-CVD mortality (HR = 1.93, CI = 1.19-3.14) than never hazardous drinkers. Life-time binge drinking was associated with larger waist circumferences and poorer liver function compared with never binge drinkers.ConclusionHazardous drinking may increase cardiometabolic risk factors; this is made worse by persistent hazardous drinking throughout life, particularly in relation to weight gain, suggesting benefits of early intervention.
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Project description:BACKGROUND: Social support is frequently linked to positive parenting behavior. Similarly, studies increasingly show a link between neighborhood residential environment and positive parenting behavior. However, less is known about how the residential environment influences parental social support. To address this gap, we examine the relationship between neighborhood concentrated disadvantage and collective efficacy and the level and change in parental caregiver perceptions of non-familial social support. METHODOLOGY/PRINCIPAL FINDINGS: The data for this study came from three data sources, the Project on Human Development in Chicago Neighborhoods (PHDCN) Study's Longitudinal Cohort Survey of caregivers and their offspring, a Community Survey of adult residents in these same neighborhoods and the 1990 Census. Social support is measured at Wave 1 and Wave 3 and neighborhood characteristics are measured at Wave 1. Multilevel linear regression models are fit. The results show that neighborhood collective efficacy is a significant (ß = .04; SE = .02; p = .03), predictor of the positive change in perceived social support over a 7 year period, however, not of the level of social support, adjusting for key compositional variables and neighborhood concentrated disadvantage. In contrast concentrated neighborhood disadvantage is not a significant predictor of either the level or change in social support. CONCLUSION: Our finding suggests that neighborhood collective efficacy may be important for inducing the perception of support from friends in parental caregivers over time.
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Project description:Parent and teacher ratings of attention deficit hyperactivity disorder (ADHD) symptoms yield high estimates of heritability whereas self-ratings typically yield lower estimates. To understand why, the present study examined the etiological overlap between parent, teacher and self-ratings of ADHD symptoms in a population-based sample of 11-12-year-old twins. Method Participants were from the Twins Early Development Study (TEDS). ADHD symptoms were assessed using the Strengths and Difficulties Questionnaire (SDQ) hyperactivity scale completed by parents, teachers and children. Structural equation modeling was used to examine genetic and environmental contributions to phenotypic variance/covariance.The broad-sense heritability of ADHD symptoms was 82% for parent ratings, 60% for teacher ratings and 48% for self-ratings. Post-hoc analyses revealed significantly higher heritability for same-teacher than different-teacher ratings of ADHD (76% v. 49%). A common pathway model best explained the relationship between different informant ratings, with common genetic influences accounting for 84% of the covariance between parent, teacher and self-rated ADHD symptoms. The remaining variance was explained by rater-specific genetic and non-shared environmental influences.Despite different heritabilities, there were shared genetic influences for parent, teacher and self-ratings of ADHD symptoms, indicating that different informants rated some of the same aspects of behavior. The low heritability estimated for self-ratings and different-teacher ratings may reflect increased measurement error when different informants rate each twin from a pair, and/or greater non-shared environmental influences. Future studies into the genetic influences on ADHD should incorporate informant data in addition to self-ratings to capture a pervasive, heritable component of ADHD symptomatology.
| S-EPMC3818571 | biostudies-literature