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Meta‐Analyses of Externalizing Disorders: Genetics or Prenatal Alcohol Exposure?
Author(s) -
Wetherill Leah,
Foroud Tatiana,
Goodlett Charles
Publication year - 2018
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.13535
Subject(s) - odds ratio , conduct disorder , odds , alcohol dependence , alcohol , fetal alcohol syndrome , etiology , attention deficit hyperactivity disorder , medicine , psychiatry , psychology , biology , biochemistry , logistic regression
Background Externalizing disorders are heritable precursors to alcohol dependence, common in children of alcoholics ( COA ), and in children with prenatal alcohol exposure ( PAE ). Pregnancies involving alcohol exposure sufficient to affect the fetus may involve women with genetic risk for alcohol dependence . We hypothesized that known PAE will increase the odds of having an externalizing disorder compared to COA . Methods The odds ratios of 3 externalizing disorders (attention‐deficit hyperactivity disorder [ ADHD ], conduct disorder [ CD ], and oppositional defiant disorder [ ODD ]) were obtained for 2 domains: (i) PAE and (ii) COA , by estimating the logged odds ratio ( LOR ) for each study. Permutation tests were implemented to compare LOR s for PAE versus COA studies within each disorder, including PAE versus an alcohol dependent (AD) mother and PAE versus an AD father. Results In PAE studies, the odds of ADHD and CD were elevated. Rates of all 3 disorders were elevated in COA studies. Permutation tests revealed that the mean LOR for ADHD was significantly higher in PAE studies compared to: COA ( p  = 0.01), AD mother ( p  < 0.05), and AD father ( p  = 0.03). No differences were found for ODD ( p  = 0.09) or CD ( p  = 0.21). Conclusions These results provide compelling evidence of an increased risk of ADHD in those with PAE beyond that due to parental alcohol dependence or a genetic liability, consistent with a unique etiology most likely due to direct alcohol exposure during prenatal development.

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