RTI uses cookies to offer you the best experience online. By clicking “accept” on this website, you opt in and you agree to the use of cookies. If you would like to know more about how RTI uses cookies and how to manage them please view our Privacy Policy here. You can “opt out” or change your mind by visiting: http://optout.aboutads.info/. Click “accept” to agree.
Replication of the interaction of PRKG1 and trauma exposure on alcohol misuse in an independent African American sample
Hawn, S. E., Sheerin, C. M., Webb, B. T., Peterson, R. E., Do, E. K., Dick, D., Kendler, K. S., Bacanu, S.-A., & Amstadter, A. B. (2018). Replication of the interaction of PRKG1 and trauma exposure on alcohol misuse in an independent African American sample. Journal of Traumatic Stress, 31(6), 927-932. https://doi.org/10.1002/jts.22339
In the present study, we sought to replicate recent findings of Polimanti et al. (2017), who conducted a genome-wide gene-by-environment interaction study (GEWIS) and identified a gene-by-trauma interaction that predicts alcohol misuse among African Americans. Consistent with the findings published by Polimanti and colleagues, results of the current study demonstrated an interaction effect, b = 0.41, of trauma exposure and rs1729578 in the intron of PRKG1 on alcohol misuse in a subsample of ancestral African Americans. The minor allele (rs1729578*C) was positively associated with increased alcohol use disorder symptoms in trauma-exposed subjects and negatively associated in non-trauma-exposed subjects. This effect, however, was only significant for one out of three alcohol outcome measures we investigated, suggesting the interaction may be most salient when predicting higher severity of alcohol misuse. Additionally, the effect did not remain significant after we accounted for testing the effect on three different outcome variables. Also in line with the original study, the gene-by-environment effect was not demonstrated among the ancestral European subsample. The findings suggest this gene variant may increase an individual's susceptibility to environmental influences, both adverse and supportive.