Browsing by Author "The Psychiatric Genomics Consortium Posttraumatic Stress Disorder Working Group"

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    Differences in genetic correlations between posttraumatic stress disorder and alcohol-related problems phenotypes compared to alcohol consumption-related phenotypes
    (Cambridge University Press, 2023) Bountress, Kaitlin E.; Bustamante, Daniel; Subbie-Saenz de Viteri, Stacey; Chatzinakos, Chris; Sheerin, Christina; Daskalakis, Nikolaos P.; Edenberg, Howard J.; The Psychiatric Genomics Consortium Posttraumatic Stress Disorder Working Group; Peterson, Roseann E.; Webb, Bradley T.; Meyers, Jackie; Amstadter, Ananda; Biochemistry and Molecular Biology, School of Medicine
    Background: Posttraumatic Stress Disorder (PTSD) tends to co-occur with greater alcohol consumption as well as alcohol use disorder (AUD). However, it is unknown whether the same etiologic factors that underlie PTSD-alcohol-related problems comorbidity also contribute to PTSD- alcohol consumption. Methods: We used summary statistics from large-scale genome-wide association studies (GWAS) of European-ancestry (EA) and African-ancestry (AA) participants to estimate genetic correlations between PTSD and a range of alcohol consumption-related and alcohol-related problems phenotypes. Results: In EAs, there were positive genetic correlations between PTSD phenotypes and alcohol-related problems phenotypes (e.g. Alcohol Use Disorders Identification Test (AUDIT) problem score) (rGs: 0.132-0.533, all FDR adjusted p < 0.05). However, the genetic correlations between PTSD phenotypes and alcohol consumption -related phenotypes (e.g. drinks per week) were negatively associated or non-significant (rGs: -0.417 to -0.042, FDR adjusted p: <0.05-NS). For AAs, the direction of correlations was sometimes consistent and sometimes inconsistent with that in EAs, and the ranges were larger (rGs for alcohol-related problems: -0.275 to 0.266, FDR adjusted p: NS, alcohol consumption-related: 0.145-0.699, FDR adjusted p: NS). Conclusions: These findings illustrate that the genetic associations between consumption and problem alcohol phenotypes and PTSD differ in both strength and direction. Thus, the genetic factors that may lead someone to develop PTSD and high levels of alcohol consumption are not the same as those that lead someone to develop PTSD and alcohol-related problems. Discussion around needing improved methods to better estimate heritabilities and genetic correlations in diverse and admixed ancestry samples is provided.
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    Potential causal effect of posttraumatic stress disorder (PTSD) on alcohol use disorder and alcohol consumption in individuals of European descent: A Mendelian Randomization Study
    (Wiley, 2021) Bountress, Kaitlin E.; Wendt, Frank; Bustamante, Daniel; Agrawal, Arpana; Webb, Bradley; Gillespie, Nathan; Edenberg, Howard; Sheerin, Christina; Johnson, Emma; The Psychiatric Genomics Consortium Posttraumatic Stress Disorder Working Group; Polimanti, Renato; Amstadter, Ananda; Biochemistry and Molecular Biology, School of Medicine
    Background: Posttraumatic stress disorder (PTSD) often co-occurs with alcohol consumption (AC) and alcohol use disorder (AUD). However, it is unknown whether the same etiologic influences that underlie PTSD co-occurring with AUD are those that underlie PTSD and AC individually. Methods: This study used large-scale genome-wide association study (GWAS) data to test whether PTSD and drinks per week [DPW]/AUD are causally related to one another, and, if so, whether PTSD precedes DPW/AUD and/or vice versa. We used Mendelian Randomization methods to analyze European ancestry GWAS summary statistics from the Psychiatric Genomics Consortium (PGC; PTSD), GWAS & Sequencing Consortium of Alcohol and Nicotine Use (GSCAN; DPW), and the Million Veteran Program (MVP; AUD). Results: PTSD exerted a potentially causal effect on AUD (β = 0.039, SE = 0.014, p = 0.005), but not on DPW (β = 0.002, SE = 0.003, p = 0.414). Additionally, neither DPW (β = 0.019, SE = 0.041, p = 0.637) nor AUD (β = 8.87 × 10-4 , SE = 0.001, p = 0.441) exerted a causal effect on PTSD. Conclusions: These findings are consistent with the self-medication model, in which individuals misuse alcohol to cope with aversive trauma-related symptoms. These findings extend latent analysis and molecular findings of shared and correlated risk between PTSD and alcohol phenotypes. Given the health behaviors associated with these phenotypes, these findings are important in that they suggest groups to prioritize for prevention efforts. Further, they provide a rationale for future preclinical and clinical studies examining the biological mechanisms by which PTSD may impact AUD.