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Social and economic consequences of alcohol use disorder: a longitudinal cohort and co-relative analysis.

ABSTRACT: Although alcohol use disorder (AUD) is associated with future risk for psychosocial dysfunction, the degree to which this arises from a direct causal effect of AUD on functioning v. from correlated risk factors (also known as confounders) is less clearly established.AUD was assessed from Swedish medical, criminal and pharmacy registries. In a large general population cohort, using Cox proportional hazard and regression models, we predicted from the onset of AUD four outcomes: early retirement, unemployment, social assistance, and individual income. We then examined the degree to which these associations were attenuated by relevant confounders as well as by the use of discordant cousin, half-sibling, full-sibling, and monozygotic twin pairs.In males, AUD most strongly predicted social assistance [hazard ratio (HR) 8.27, 95% confidence interval (CI) 7.96-8.59], followed by early retirement (HR 5.63, 95% CI 5.53-5.72) and unemployment (HR 2.75, 95% CI 2.65-2.85). For income at age 50, AUD was associated with a decrease in income of 0.24 s.d.s (95% CI -0.25 to -0.23). Results were similar in females. Modest to moderate attenuation of these associations was seen in both sexes after the addition of relevant covariates. These associations were reduced but remained robust in discordant co-relative pairs, including monozygotic twins.Our results suggest that AUD has a causal impact on a range of measures reflective of psychosocial dysfunction. These findings provide strong support for the drift hypothesis. However, some of the associations between AUD and dysfunction appear to be non-causal and result from shared risk factors, many of which are likely familial.

SUBMITTER: Kendler KS

PROVIDER: S-EPMC5340576 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature

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Social and economic consequences of alcohol use disorder: a longitudinal cohort and co-relative analysis.

Kendler K S KS Ohlsson H H Karriker-Jaffe K J KJ Sundquist J J Sundquist K K

Psychological medicine 20161205 5

<h4>Background</h4>Although alcohol use disorder (AUD) is associated with future risk for psychosocial dysfunction, the degree to which this arises from a direct causal effect of AUD on functioning v. from correlated risk factors (also known as confounders) is less clearly established.<h4>Method</h4>AUD was assessed from Swedish medical, criminal and pharmacy registries. In a large general population cohort, using Cox proportional hazard and regression models, we predicted from the onset of AUD ...[more]

PMID: 27917730

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Project description:Excess alcohol consumption and alcohol use disorders (AUDs) are associated with substantially increased mortality. Efforts to reduce this toll require an understanding of their causes.To clarify the degree to which the excess mortality associated with AUDs arises (1) from the predispositions of the person who develops AUD (and which would likely be shared by close relatives) and (2) as a direct result of AUD itself.A prospective cohort and co-relative design study involving all individuals born in Sweden from 1940 to 1965 who had neither died nor migrated prior to 1973 or age 15 years (N?=?2?821?036). They were followed up from January 1, 1973, until December 31, 2010. Alcohol use disorder was assessed from medical, criminal, and pharmacy registries. Half-siblings, full-siblings, and monozygotic twin pairs discordant for AUD were obtained from the Multi-Generation and Twin Register.Death obtained from the Swedish Death registry.Our cohort (1?447?887 males and 1?373?149 females) included 131?895 males and 42?163 females registered with AUD. The mean (SD) age at first AUD registration was 39 (13.4) years. We ascertained 127?347 and 76?325 deaths in the male and female subsamples, respectively. Controlling for sex, educational status, and year of birth, the mortality hazard ratio associated with AUD was 5.83 (95% CI, 5.76-5.90) and varied-with an inverted U-shaped function-by age. Examining the AUD-mortality association in the general population and in relative pairs discordant for AUD exposure demonstrated substantial familial confounding in early to mid-adulthood: the AUD-associated mortality hazard ratio was much lower in discordant close relatives than in the general population. In middle to late adulthood, evidence for familial confounding decreased with increasing evidence for a direct effect of AUD on elevated mortality. In the oldest age group (65-70 years), the mortality hazard ratios were similar across the population and all relative pairs, suggesting that the excess mortality was largely a result of having AUD. Adding years since onset of AUD to the model showed that both increasing age and increasing years of duration of AUD contributed to the reduction of familial confounding in the association between AUD and elevated mortality.Excess mortality associated with AUD arises both from the predispositions of the person who develops AUD and the direct result of having AUD. The effect of predisposition is more prominent early in the life course and in the early years of AUD. The direct effect of AUD becomes progressively more important later in life and with longer duration of AUD. These results have implications for interventions seeking to reduce the elevated AUD-associated mortality.

Project description:BACKGROUND:Recent reviews of associations of alcohol availability with alcohol outcomes suggest findings are highly inconsistent and highlight a lack of longitudinal and causal evidence. Effect modification (moderation or statistical interaction), which could contribute to the inconsistent picture in the existing literature, has not been systematically assessed. We examined associations of alcohol availability with onset and recurrence of alcohol use disorder (AUD) using multilevel, longitudinal population data from Sweden and tested hypothesized effect modifiers to identify groups for whom increased alcohol availability may be particularly risky. We also employed cosibling models to assess potential causality for AUD onset by accounting for genetic and shared-environment confounders. METHODS:Data come from all individuals born in Sweden between 1950 and 1975 who were registered in a residential neighborhood at the end of 2005 (N = 2,633,922). We used Cox proportional hazards models to investigate time to AUD onset and logistic regression to assess the odds of AUD recurrence over an 8-year period. RESULTS:Living in a neighborhood with at least 1 alcohol outlet of any type was associated with a small increase in the likelihood of developing AUD, with an adjusted hazard ratio (HR) of 1.16 (95% CI: 1.13 to 1.19). Among people with a prior AUD registration, alcohol availability was not significantly associated with recurrence of AUD, with an adjusted odds ratio of 1.02 (95% CI: 1.00 to 1.05). Associations of alcohol availability with AUD onset varied according to sex, age, education, neighborhood deprivation, and urbanicity. HRs from the sibling models were similar to those in the general population models, with an adjusted HR = 1.19 (95% CI: 1.15 to 1.24). CONCLUSIONS:Effects varied among neighborhood residents, but greater alcohol availability was a risk factor for AUD onset (but not relapse) in all groups examined except women. Cosibling models suggest there may be a causal relationship of greater alcohol availability with adult-onset AUD.

Project description:BackgroundExtensive research indicates that having a positive family history of alcohol use disorder (FHP) and impulsivity are 2 risk factors for problem drinking. To our knowledge, no study has investigated which facets of impulsivity interact with family history to increase risk for problem drinking. The goal of this study was to: (i) examine whether FHP individuals with higher levels of impulsivity are more likely to engage in problematic drinking, and (ii) identify which facets of impulsivity interact with FHP to increase risk for problems.MethodsThe data consisted of a combined sample of 757 participants (50% female, 73% White, mean age = 32.85, SD = 11.31) drawn from the Transdisciplinary Tobacco Use Research Center and the Center for the Translational Neuroscience of Alcohol. Analyses of covariance and cumulative logistic regression models investigated the association of family history and impulsivity-related traits with drinking quantity, frequency, and alcohol-related problems. Models were adjusted for age, sex, race, ethnic group, education level, and data source.ResultsSignificant interactions between impulsivity and family history were found for measures of alcohol-related problems. Specifically, there was a stronger positive association of Barratt Impulsiveness Scale (BIS) poor self-regulation with interpersonal, F(1, 504) = 6.27, p = 0.01, and impulse control alcohol-related problems, F(1, 504) = 6.00, p = 0.01, among FHP compared to FHN individuals. Main effects of family history and impulsivity on alcohol quantity and frequency of use and problems were also found.ConclusionsThese findings suggest that having both a family history of AUD and high BIS poor self-regulation is more strongly associated with alcohol-related consequences in the interpersonal and impulse control domains. Given the heterogeneity of impulsivity, these findings highlight the need for additional research to examine which facets of impulsivity are associated with which alcohol outcomes to narrow phenotypic risk for alcohol misuse.

Dataset Information

Social and economic consequences of alcohol use disorder: a longitudinal cohort and co-relative analysis.

Publications

Social and economic consequences of alcohol use disorder: a longitudinal cohort and co-relative analysis.

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