Department of Psychology, Louisiana State University, USA.
Psychiatry Res. 2010 Jun 30;178(1):79-83. doi: 10.1016/j.psychres.2008.07.018. Epub 2010 May 8.
Mounting evidence suggests that social anhedonia may be a marker of genetic liability for schizophrenia-spectrum pathology. To examine this hypothesis, we conducted a study of severity of schizotypal, schizoid and paranoid pathology (i.e., Cluster A personality disorders) in the biological parents of individuals with high levels of social anhedonia and healthy controls. Eighty-six individuals with social anhedonia, 89 healthy controls and their biological parents were recruited from a large community. Structured clinical interviews were conducted to obtain Cluster A diagnoses and symptom ratings for parents. The biological parents of socially anhedonic probands had elevated rates of Cluster A disorders (24%) compared with the parents of control probands (12%). Post hoc analyses revealed that these group differences were the result of elevated rates of diagnoses in the fathers of social anhedonic probands, but not the mothers. This finding was replicated when Cluster A symptoms were examined dimensionally. These findings are consistent with the hypothesis that social anhedonia is a promising indicator of the genetic vulnerability to schizophrenia-spectrum pathology. The unexpected findings of elevated pathology in fathers, but not mothers of socially anhedonic probands, require further exploration.
越来越多的证据表明,社交快感缺失可能是精神分裂症谱系病理遗传易感性的标志物。为了检验这一假设,我们对社交快感缺失程度较高的个体和健康对照组的个体的生物父母的类精神分裂型、类分裂型和偏执型病理(即 A 类人格障碍)严重程度进行了研究。从一个大型社区招募了 86 名社交快感缺失者、89 名健康对照者及其生物父母。通过结构化临床访谈获得了父母的 A 类诊断和症状评分。与对照组的父母(12%)相比,社交快感缺失者的生物父母的 A 类障碍发生率较高(24%)。事后分析表明,这些组间差异是由于社交快感缺失者的父亲的诊断率升高所致,而母亲的诊断率则没有升高。当从维度上检查 A 类症状时,发现了同样的结果。这些发现与社交快感缺失是精神分裂症谱系病理遗传易感性的一个有前途的指标的假设一致。令人意外的是,社交快感缺失者的父亲而非母亲的病理程度升高,这需要进一步探索。