Potential Causal Influence of Neighborhood Disadvantage on Disordered Gambling: Evidence From a Multilevel Discordant Twin Design.
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ABSTRACT:
SUBMITTER: Slutske WS
PROVIDER: S-EPMC6521693 | biostudies-literature | 2019 May
REPOSITORIES: biostudies-literature
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Project description:Marriage and parenthood are associated with alcohol use and use disorder (AUD), although they are confounded such that many studies struggle to identify their unique and/or causal effects. The present study utilized a genetically informed discordant twin design that strengthens the putative causal role of marital and parental status in the presentation of AUD symptoms by using each individual's cotwin as their own control while simultaneously modeling both predictors among men and women. Participants were 980 complete same-sex twin pairs from the Australian Twin Registry (Mage = 31.70 [SD = 2.48]; 71% women). Marital status, parental status, and past year AUD symptoms were assessed via semistructured interview. Three random-intercept generalized linear mixed models were fit in men and women including (a) marital status only, (b) parental status only, and (c) both marital and parental status; demographics, past year pregnancy, age of first drink, age of regular drinking, personality traits, and antisociality were included as covariates. Models tested for quasi-causal and familial effects. The sole-predictor marital status model (Model 1) provided the best fit among men, while the simultaneous-predictor marital and parental status model (Model 3) provided the best fit among women. Sole-predictor models showed familial effects of both predictors among men and quasi-causal and familial effects of both predictors among women; the simultaneous-predictor model revealed familial effects of marital status only among men and quasi-causal effects of parental status only among women. The present study elucidates important sex differences in the presentation of AUD among midlife adults in the context of notable developmental milestones. (PsycInfo Database Record (c) 2020 APA, all rights reserved).
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Project description:Human laboratory studies and twin research investigating relationships between alcohol use/pathology and gambling generally have yielded contradictory results, sometimes suggesting causal relationships and common genetic risk factors. 2860 individuals (mean age: 25.60, s.d = 3.21, 50.62% female) from separate clinical (n = 636) and community based (twin) samples (n = 2224) were used to assess associations between past year alcohol use and frequency of past year gambling behaviors (gambling frequency). After adjustment for demographic and psychiatric covariates, individual-level analyses detected that increased alcohol use was associated with more frequent gambling behaviors in twin and clinical samples. Co-twin control models were then used to test potential causal (direct) relationships between alcohol use and gambling frequency. Controlling for all covariates and shared genetic/environmental factors, we found increased alcohol use directly predicted more frequent gambling behaviors (consistent with causality). Our study also suggests shared genetic and/or environmental risk factors contribute to the association between increased alcohol use and frequent gambling behavior, a finding that may be more pronounced in males. The present study helps bridge the gap between twin research and human laboratory studies on gambling and alcohol use and corroborates findings across community and clinical samples. Overall, our findings support both common risk factors between alcohol use and gambling as well as a direct relationship between alcohol use and gambling frequency. Recognizing these dual processes could prove useful for gambling-related prevention/intervention programs.
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Project description:BackgroundDespite abundant research on the potential causal influence of childhood maltreatment (CM) on psychological maladaptation in adulthood, almost none has implemented the discordant twin design as a means of examining the role of such experiences in later disordered gambling (DG) while accounting for genetic and family environmental confounds. The present study implemented such an approach to disentangle the potential causal and familial factors that may account for the association between CM and DG.MethodsParticipants were 3750 twins from the Australian Twin Registry [Mage = 37.60 (s.d. = 2.31); 58% female]. CM and DG were assessed separately via two semi-structured telephone interviews. Random-intercept generalized linear mixed models were fit to the data; zygosity, sex, educational attainment, childhood psychiatric disorder, adult antisocial behavior, and alcohol use disorder (AUD) were included as covariates.ResultsNeither quasi-causal nor familial effects of CM predicted DG after adjusting for covariates. Educational attainment appeared to reduce the risk of DG while AUD appeared to increase risk; evidence also emerged for familial effects of antisocial behavior on DG. Post-hoc analyses revealed a familial effect of CM on antisocial behavior, indicating that the association between CM and DG identified in unadjusted models and in prior studies may be accounted for by genetic and shared family environmental effects of antisociality.ConclusionsThese findings add to the meager literature showing that CM does not exert a causal effect on DG, and present novel evidence that familial effects of antisocial behavior may account for the association between CM and DG identified in extant non-twin research.
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Project description:Gambling disorder is associated with suicidal behaviors, but it is not clear whether the association is due to common etiologic factors or to gambling disorder being causally related to suicidality. This question was examined from epidemiologic, longitudinal, and discordant twin study perspectives. The results suggested that the causes of the association with disordered gambling differed for suicidal ideation, plan, and attempt, and differed for men and women. The association of suicidal thoughts with disordered gambling was non-causally explained by common genetic influences among women (but not men). Conversely, there was evidence consistent with a potentially causal influence of disordered gambling on suicide attempt among men (but not women), which might have been related to gambling-related financial problems. The use of monetary data to identify individuals experiencing financial harms associated with their gambling may represent a more practicable target for screening, intervention, and prevention and may reduce gambling-related financial crises, thereby warding off a potential gambling-related suicide attempt.
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Project description:OBJECTIVE:Childhood adverse experiences are known to engender persistent changes in stress-related systems and brain structures involved in mood, cognition, and behavior in animal models. Uncertainty remains about the causal effect of early stressful experiences on physiological response to stress in human beings, as the impact of these experiences has rarely been investigated while controlling for both genetic and shared environmental influences. METHOD:We tested whether bullying victimization, a repeated adverse experience in childhood, influences cortisol responses to a psychosocial stress test (PST) using a discordant monozygotic (MZ) twin design. Thirty pairs (43.3% males) of 12-year-old MZ twins discordant for bullying victimization were identified in the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative 1994-1995 cohort of families with twins. RESULTS:Bullied and nonbullied MZ twins showed distinct patterns of cortisol secretion after the PST. Specifically, bullied twins exhibited a blunted cortisol response compared with their nonbullied MZ co-twins, who showed the expected increase. This difference in cortisol response to stress could not be attributed to children's genetic makeup, their familial environments, pre-existing and concomitant individual factors, or the perception of stress and emotional response to the PST. CONCLUSION:Results from this natural experiment provide support for a causal effect of adverse childhood experiences on the neuroendocrine response to stress.
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Project description:This study examined associations between neighborhood disadvantage and body mass index (BMI), and tested whether this differed by level of individual socioeconomic position (SEP). Data were from 9953 residents living in 200 neighborhoods in Brisbane, Australia in 2007. Multilevel linear regression analyses were undertaken by gender to determine associations between neighborhood disadvantage, individual SEP (education, occupation and household income) and BMI (from self-reported height and weight); with cross-level interactions testing whether the relationship between neighborhood disadvantage and BMI differed by level of individual SEP. Both men (Quintile 4, where Quintile 5 is the most disadvantaged β = 0.66 95%CI 0.20, 1.12) and women (Quintile 5 β = 1.32 95%CI 0.76, 1.87) from more disadvantaged neighborhoods had a higher BMI. BMI was significantly higher for those with lower educational attainment (men β = 0.71 95%CI 0.36, 1.07 and women β = 1.66 95%CI 0.78, 1.54), and significantly lower for those in blue collar occupations (men β = -0.67 95%CI -1.09, -0.25 and women β = -0.71 95%CI -1.40, -0.01). Among men, those with a lower income had a significantly lower BMI, while the opposite was found among women. None of the interaction models had a significantly better fit than the random intercept models. The relationship between neighborhood disadvantage and BMI did not differ by level of education, occupation, or household income. This suggests that individual SEP is unlikely to be an effector modifier of the relationship between neighborhood disadvantage and BMI. Further research is required to assist policy-makers to make more informed decisions about where to intervene to counteract BMI-inequalities.
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Project description:Emerging evidence suggests socioeconomic disadvantage may increase risk for eating disorders (EDs). However, there are very few studies on the association between disadvantage and EDs, and all have focused on individual-level risk factors (e.g., family income). Neighborhood disadvantage (i.e., elevated poverty and reduced resources in one's neighborhood) is associated with increased risk for anxiety/depression and poor physical health. To date, no studies have examined phenotypic associations between neighborhood disadvantage and disordered eating, or how any form of disadvantage may interact with genetic individual differences in risk for EDs. We examined phenotypic and etiologic associations between neighborhood disadvantage and disordered eating in 2,922 girls ages 8-17 from same-sex twin pairs recruited through the Michigan State University Twin Registry. Parents rated the twins on nine items assessing core disordered eating symptoms (e.g., weight preoccupation, binge eating), and neighborhood disadvantage was calculated from 17 indicators of contextual disadvantage (e.g., median home value, neighborhood unemployment). Puberty was measured using the Pubertal Development Scale to examine whether associations were consistent across development. At a phenotypic level, greater neighborhood disadvantage was associated with significantly greater disordered eating symptoms in girls at all stages of puberty (β = .07). Moreover, Genotype × Environment models showed that girls living in more disadvantaged neighborhoods exhibited stronger and earlier (i.e., during pre/early puberty) activation of genetic influences on disordered eating. Results highlight the critical importance of considering contextual disadvantage in research on etiology and risk for disordered eating, and the need for increased screening and treatment for EDs in disadvantaged youth. (PsycInfo Database Record (c) 2021 APA, all rights reserved).
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Project description:ObjectiveTo assess the relationship between a composite measure of neighborhood disadvantage, the Area Deprivation Index (ADI), and control of blood pressure, diabetes, and cholesterol in the Medicare Advantage (MA) population.Data sourcesSecondary analysis of 2013 Medicare Healthcare Effectiveness Data and Information Set, Medicare enrollment data, and a neighborhood disadvantage indicator.Study designWe tested the association of neighborhood disadvantage with intermediate health outcomes. Generalized estimating equations were used to adjust for geographic and individual factors including region, sex, race/ethnicity, dual eligibility, disability, and rurality.Data collectionData were linked by ZIP+4, representing compact geographic areas that can be linked to Census block groups.Principal findingsCompared with enrollees residing in the least disadvantaged neighborhoods, enrollees in the most disadvantaged neighborhoods were 5 percentage points (P < 0.05) less likely to have controlled blood pressure, 6.9 percentage points (P < 0.05) less likely to have controlled diabetes, and 9.9 percentage points (P < 0.05) less likely to have controlled cholesterol. Adjustment attenuated this relationship, but the association remained.ConclusionsThe ADI is a strong, independent predictor of diabetes and cholesterol control, a moderate predictor of blood pressure control, and could be used to track neighborhood-level disparities and to target disparities-focused interventions in the MA population.
| S-EPMC6341202 | biostudies-literature
Project description:Using data from a large Australian twin sample we examined the extent to which genetic variation in the Big Three personality dimensions (positive emotionality, negative emotionality, and constraint) and their lower-order components explained genetic variation in the risk for disordered gambling (DG) among men and women. Genetic influences contributing to individual differences in normal-range personality traits explained over 40% of the genetic risk for DG, with a larger contribution among women than among men. The largest and most robust contributions came from the higher-order personality dimension of negative emotionality and its two lower-order dimensions of alienation and aggression. Surprisingly, low self-control was associated with the genetic risk for DG only among women, and risk-taking/sensation-seeking did not explain genetic risk for DG in either sex. The results of this study have implications for the causes of comorbidity between DG and other psychiatric disorders, the search for genes associated with DG risk, and the possibility of sex differences in the etiology of DG. Using a broad-band inventory of personality supports the conclusion that there probably is a substantial proportion of genetic variation in DG that cannot be explained by individual differences in personality.
| S-EPMC7671713 | biostudies-literature