Externalizing Disorders : Genetics or Prenatal Alcohol Exposure?

• Main Author: Wetherill, Leah
• Other Authors: Goodlett, Charles
• Language: en_US
• Published: 2018
• Subjects: ADHD; Prenatal alcohol exposure; Externalizing disorders; Alcohol dependence; Genetics
• Online Access: http://hdl.handle.net/1805/17960

Indiana University-Purdue University Indianapolis (IUPUI) === Introduction: Externalizing disorders such as attention deficit hyperactivity disorder (ADHD), conduct disorder (CD), and oppositional defiant disorder (ODD) have a high prevalence rate in both children of alcoholics and in those with prenatal alcohol exposure (PAE). These disorders are also predictors of alcohol dependence (alcdep), heritable, and share an underlying genetic liability with alcdep. Furthermore, a mother who drinks while pregnant is likely to be alcohol dependent (AD), and vice-versa. This study incorporated these factors into one model, including as well as a measure of broad genetic risk for ADHD and alcdep to test for the contributions of these effects simultaneously. An independent sample was used to confirm the results for PAE and broad genetic risk. The hypothesis is that PAE will increase the risk to ADHD but not to CD or ODD. Methods: Each of these factors was evaluated independently to test if that effect on its own, significantly contributed to each disorder. Another model included several demographic covariates, to determine which of these environmental effects also contributed to the disorder. The final model for each disorder included environmental effects along with the primary effects of interest. Results: PAE resulted in increased risk for the inattentive (INATT) sub-type of ADHD and conduct disorder (CD) in the discovery sample and for the hyperactive-impulsive (HYPIMP), INATT and CD in the replication sample. PAE and the PAE*maternal alcohol dependence interaction increased the risk for ADHD and INATT. A broad genetic risk for ADHD was associated with all disorders except HYPIMP in the replication sample. Conclusion: This study further supports the trending evidence of a unique etiology of ADHD in those with PAE, and more specifically, that INATT and HYPIMP are affected according to two different mechanisms of action, independent of a genetic contribution due to either ADHD or alcohol dependence, both of which also were associated with a risk for INATT. The contribution of PAE to INATT and CD were the only consistent results across all definitions of alcohol exposure and in both datasets, indicating that PAE is a veritable risk for INATT and CD.