Benca-Bachman Chelsie E, Cassidy Samantha, Syed Rameez A, Barfield Whitney L, Jaume-Feliciosi Natalia, Smith Alicia K, Katrinli Seyma, Powers Abigail, Mekawi Yara, Palmer Rohan H C
Behavioral Genetics of Addiction laboratory, Department of Psychology at Emory University, Atlanta, GA, USA.
Department of Psychiatry & Human Behavior, Brown University, Providence, RI, USA.
medRxiv. 2025 May 14:2025.05.13.25327255. doi: 10.1101/2025.05.13.25327255.
To estimate polygenic and polygene x environment contributions to alcohol consumption and problems in the context of childhood maltreatment and lifetime trauma.
Main and interaction effects models predicting alcohol consumption and problems were estimated using multiple linear regression. Covariates included age, sex, education, employment status, and ancestral principal components.
USA.
A sample of 2,114 Black adults (75% female; M=39.88, SD=13.92) recruited from the Grady Trauma Hospital in Atlanta, Georgia.
Polygenic scores (PGS) for trauma-related symptoms (re-experiencing: PGS, avoidance: PGS, hyperarousal: PGS, PTSD symptom score: PGS) and alcohol consumption (PGS) and use disorder (AUD; PGS) were derived using genome-wide association Million Veterans Program summary statistics with PRS-CS.
Childhood maltreatment and lifetime trauma (excluding childhood abuse) were positively associated with alcohol consumption (AUDIT-C) (β=0.17, SE=0.02; β=0.28, SE=0.02) and alcohol problems (AUDIT-P) (β=0.25, SE=0.02; β=0.27, SE=0.02). None of the PGSs were associated with AUDIT-C, but both the PGSs for re-experiencing (β=0.1, SE=0.03) and avoidance (β=0.08, SE=0.03) were positively associated with AUDIT-P. Experiencing lifetime trauma and being at elevated genetic risk for AUD (interaction-β=0.17, SE=0.05) and hyperarousal (interaction-β=0.11, SE=0.06) were associated with higher AUDIT-P scores; while more lifetime trauma and higher genetic risk for AUD were associated with higher AUDIT-C scores (interaction-β=0.12, SE=0.05).
Individuals with elevated genetic risk for AUD are more likely to consume alcohol and to develop worse alcohol problems in the context of lifetime trauma. Interventions focused on also minimizing the effects of trauma-exposure would be particularly beneficial among individuals at risk for AUD.
在童年期虐待和终生创伤的背景下，评估多基因以及多基因与环境的交互作用对饮酒及饮酒问题的影响。
使用多元线性回归估计预测饮酒及饮酒问题的主效应和交互效应模型。协变量包括年龄、性别、教育程度、就业状况和祖先主成分。
美国。
从佐治亚州亚特兰大市格雷迪创伤医院招募的2114名黑人成年人样本（75%为女性；平均年龄M = 39.88，标准差SD = 13.92）。
使用全基因组关联百万退伍军人计划汇总统计数据和PRS-CS得出创伤相关症状（重新体验：多基因评分、回避：多基因评分、过度警觉：多基因评分、创伤后应激障碍症状评分：多基因评分）、饮酒量（多基因评分）和使用障碍（酒精使用障碍；多基因评分）的多基因分数（PGS）。
童年期虐待和终生创伤（不包括童年期虐待）与饮酒量（酒精使用障碍识别测试简版，AUDIT-C）呈正相关（β = 0.17，标准误SE = 0.02；β = 0.28，标准误SE = 0.02），与饮酒问题（酒精使用障碍识别测试问题部分，AUDIT-P）也呈正相关（β = 0.25，标准误SE = 0.02；β = 数据缺失，原文有误，推测为β = 0.27，标准误SE = 0.02）。没有一个多基因分数与AUDIT-C相关，但重新体验（β = 0.1，标准误SE = 0.03）和回避（β = 0.08，标准误SE = 0.03）的多基因分数均与AUDIT-P呈正相关。经历终生创伤且酒精使用障碍遗传风险较高（交互作用β = 0.17，标准误SE = 0.05）以及过度警觉（交互作用β = 0.11，标准误SE =数据缺失，原文有误，推测为0.06）与更高的AUDIT-P分数相关；而更多的终生创伤和更高的酒精使用障碍遗传风险与更高的AUDIT-C分数相关（交互作用β = 0.12，标准误SE = 0.05）。
酒精使用障碍遗传风险较高的个体在终生创伤的背景下更有可能饮酒且出现更严重的饮酒问题。对于有酒精使用障碍风险的个体，侧重于尽量减少创伤暴露影响的干预措施将特别有益。
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