Justin J. Verlinden , Mairead E. Moloney , Olga A. Vsevolozhskaya , Lauren N. Whitehurst , Jessica Weafer
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引用次数: 0
Abstract
Insomnia is a risk factor for hazardous drinking, yet the mechanisms underlying this risk are not well characterized. Two factors that might contribute to the relationship between insomnia and drinking are stress and depression. Insomnia is strongly associated with increased stress and depression, which are, in turn, strongly linked to hazardous drinking. Here we conducted a preliminary investigation to determine whether perceived stress and depression indirectly explain the relationship between insomnia and hazardous drinking. Heavy drinkers with self-reported insomnia (n = 405: 270 women, 134 men, 1 non-binary) completed self-report measures of hazardous drinking, insomnia, perceived stress, and depression. Results from our primary cross-sectional parallel mediation model with insomnia as the predictor and hazardous drinking as the outcome showed that, when accounting for the influence of both perceived stress and depression, there was a partial indirect effect of insomnia on hazardous drinking through perceived stress, 95% CI [0.014, 0.205], but not depression, 95% CI [-0.080, 0.172]. In our competing cross-sectional parallel mediation model with hazardous drinking as the predictor and insomnia as the outcome, there was a partial indirect effect of hazardous drinking on insomnia through depression 95% CI [0.016, 0.059], but not perceived stress 95% CI: [-0.026, 0.011]. Results suggest that insomnia may be related to hazardous drinking through its effects on stress and that hazardous drinking may be related to insomnia through its effects on depression. These findings lay the groundwork for future longitudinal studies assessing the causal roles of stress and depression in the insomnia-AUD relationship.
期刊介绍:
Alcohol is an international, peer-reviewed journal that is devoted to publishing multi-disciplinary biomedical research on all aspects of the actions or effects of alcohol on the nervous system or on other organ systems. Emphasis is given to studies into the causes and consequences of alcohol abuse and alcoholism, and biomedical aspects of diagnosis, etiology, treatment or prevention of alcohol-related health effects.
Intended for both research scientists and practicing clinicians, the journal publishes original research on the neurobiological, neurobehavioral, and pathophysiological processes associated with alcohol drinking, alcohol abuse, alcohol-seeking behavior, tolerance, dependence, withdrawal, protracted abstinence, and relapse. In addition, the journal reports studies on the effects alcohol on brain mechanisms of neuroplasticity over the life span, biological factors associated with adolescent alcohol abuse, pharmacotherapeutic strategies in the treatment of alcoholism, biological and biochemical markers of alcohol abuse and alcoholism, pathological effects of uncontrolled drinking, biomedical and molecular factors in the effects on liver, immune system, and other organ systems, and biomedical aspects of fetal alcohol spectrum disorder including mechanisms of damage, diagnosis and early detection, treatment, and prevention. Articles are published from all levels of biomedical inquiry, including the following: molecular and cellular studies of alcohol''s actions in vitro and in vivo; animal model studies of genetic, pharmacological, behavioral, developmental or pathophysiological aspects of alcohol; human studies of genetic, behavioral, cognitive, neuroimaging, or pathological aspects of alcohol drinking; clinical studies of diagnosis (including dual diagnosis), treatment, prevention, and epidemiology. The journal will publish 9 issues per year; the accepted abbreviation for Alcohol for bibliographic citation is Alcohol.