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Time-specific and cumulative effects of exposure to parental externalizing behavior on risk for young adult alcohol use disorder
Institution:1. Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Department of Psychiatry, Richmond, VA, USA;2. Center for Primary Health Care Research, Lund University, Malmö, Sweden;3. Alcohol Research Group, Public Health Institute, Emeryville, CA, USA;4. Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, CA, USA;5. Department of Family Medicine and Community Health, Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, USA;1. Department of Experimental and Clinical Pharmacology, College of Pharmacy, University of Minnesota, 7-153 Weaver Densford Hall, 308 Harvard St SE, Minneapolis, MN 55455, United States;2. Department of Psychiatry, University of Minnesota, 2450 Riverside Ave, Minneapolis, MN 55454, United States;3. Masonic Cancer Center, University of Minnesota, Mayo Mail Code 806 420 Delaware Street SE, Minneapolis, MN 55455, United States;4. Tobacco Research Programs, University of Minnesota, 717 Delaware Street SE, Minnneapolis, MN 55414, United States;1. Tactus Addiction Treatment, P.O. Box 154, 7400 AD Deventer, The Netherlands;2. Nijmegen Institute for Scientist-Practitioners in Addiction (NISPA), Radboud University Nijmegen, 6525 ED Nijmegen, The Netherlands
Abstract:BackgroundPrevious studies indicate that parental externalizing behavior (EB) is a robust risk factor for alcohol use disorder (AUD) in their children, and that this is due to both inherited genetic liability and environmental exposure. However, it remains unclear whether the effects of exposure to parental EB vary as a function of timing and/or chronicity.MethodsWe identified biological parents with an alcohol use disorder, drug abuse, or criminal behavior, during different periods of their child's upbringing, using Swedish national registries. Logistic regression was used to determine whether the effect of parental EB exposure during different developmental periods differentially impacted children's risk for young adult AUD (ages 19–24). In addition, we tested how multiply affected parents and/or sustained exposure to affected parents impacted risk.ResultsWhile parental EB increased risk for young adult AUD, timing of exposure did not differentially impact risk. Having a second affected parent increased the risk of AUD additionally, and sustained exposure to parental EB across multiple periods resulted in a higher risk of young adult AUD than exposure in only one period.ConclusionsIn this well-powered population study, there was no evidence of “sensitive periods” of exposure to national registry-ascertained parental EB with respect to impact on young adult AUD, but sustained exposure was more pathogenic than limited exposure. These findings suggest developmental timing does not meaningfully vary the impact, but rather there is a pervasive risk for development of young adult AUD for children and adolescents exposed to parental EB.
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