OBJECTIVE There is growing interest in how peers' genotypes may influence health (i.e., peer social genetic effects). The authors sought to clarify the nature of peer social genetic effects on risk for drug use disorder, alcohol use disorder (AUD), major depression, and anxiety disorder. METHOD Cox models were used with data from a population-based Swedish cohort (N=655,327). Outcomes were drug use disorder, AUD, major depression, and anxiety disorder registrations between ages 17 and 30 from medical, criminal, and pharmacy registries. The authors indexed peer social genetic effects with peers' family genetic risk scores (FGRSs) for the same disorders, which are personalized measures of genetic risk inferred from diagnoses in first- to fifth-degree relatives. RESULTS Across disorders, peer FGRSs predicted increased risks of proband registration (hazard ratio range, 1.01-1.59), with stronger effects for drug use disorder and AUD than for major depression and anxiety disorder. Peer social genetic effects were stronger for school classmates than for geographically proximal peers, and for peers from upper secondary school (ages 16-19) versus peers from lower secondary school (ages 7-16). Peer social genetic effects remained significant following statistical control for sociodemographic confounders, whether peers were affected, and peers' FGRS for educational attainment. Peer social genetic effects were more pronounced for probands at higher genetic risk. CONCLUSIONS The genetic makeup of adolescents' peers has long-reaching consequences on risks for drug use disorder, AUD, major depression, and anxiety disorder. Individuals at high genetic risk are more sensitive to social genetic effects. Alternative hypotheses such as sociodemographic stratification, exposure to affected peers, and genetic predispositions for educational attainment did not explain the risk associated with peer social genetic effects for substance use and psychiatric disorders.

中文翻译：

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瑞典全国样本中的同伴社会遗传效应和药物使用障碍、重度抑郁症和焦虑症的病因学。


目的 人们越来越关注同龄人的基因型如何影响健康（即同龄人的社会遗传效应）。作者试图阐明同伴社会遗传对吸毒障碍、酒精使用障碍 (AUD)、重度抑郁症和焦虑症风险的影响的本质。方法 Cox 模型与基于人口的瑞典队列 (N=655,327) 的数据一起使用。结果是医疗、刑事和药房登记处 17 岁至 30 岁之间的吸毒障碍、AUD、重度抑郁症和焦虑症登记。作者将同龄人社会遗传效应与同龄人针对相同疾病的家庭遗传风险评分（FGRS）建立了索引，这是根据一级至五级亲属的诊断推断出的遗传风险的个性化测量。结果 在各种疾病中，同行 FGRS 预测先证者登记的风险增加（风险比范围，1.01-1.59），对吸毒障碍和 AUD 的影响比对重度抑郁症和焦虑症的影响更强。学校同学的同侪社会遗传效应比地理位置相近的同龄人更强，高中生（16-19 岁）的同龄人比初中同龄人（7-16 岁）的同辈社会遗传效应更强。在对社会人口统计学混杂因素、同龄人是否受到影响以及同龄人教育程度的 FGRS 进行统计控制后，同龄人社会遗传效应仍然显着。对于遗传风险较高的先证者，同伴社会遗传效应更为明显。结论 青少年同龄人的基因构成对吸毒障碍、AUD、重度抑郁症和焦虑症的风险具有长期影响。具有高遗传风险的个体对社会遗传效应更加敏感。 其他假设，如社会人口分层、与受影响同龄人的接触以及受教育程度的遗传倾向等，并不能解释与同龄人社会遗传效应对物质使用和精神疾病相关的风险。