Jacobson K C, Prescott C A, Kendler K S
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Medical College of Virginia of Virginia Commonwealth University, Richmond 23298-0126, USA.
Psychol Med. 2000 Nov;30(6):1315-25. doi: 10.1017/s0033291799002780.
There is conflicting evidence concerning the magnitude of genetic and shared environmental influences on juvenile antisocial behaviour (AB). The use of more than one assessment of AB may yield more accurate estimates of these influences.
Retrospective reports of antisocial behaviour prior to age 18 were obtained on two occasions from a population-based sample of 3522 adult males from male-male twin pairs: phone interviews (wave 1) and self-report questionnaires obtained 19 months later (wave 2). Structural equation modelling estimated the genetic and environmental influences on reliably-measured AB. Factors related to participation of co-twin at wave 1, attrition between waves 1 and 2, and reliability of wave 1 and wave 2 assessments were also investigated.
Twin analyses revealed that genetic, shared environmental, and non-shared environmental influences accounted for approximately 33% (95% CI = 9-57%), 31% (95% CI = 10-51%) and 36% (95% CI = 29-44%) of the variance of reliably measured AB, respectively. We also found significant occasion-specific genetic influences on wave 1 AB. Wave 1 AB did not predict wave 1 participation of co-twin or attrition, but was related to reliability. Co-twins of MZ twins and younger twins were more likely to participate at wave 1; attrition was predicted by being a DZ twin, lack of initial participation of co-twin, fewer years of education, and fewer children. Being older, being unmarried, and having less psychopathology were associated with greater reliability.
When measurement error is taken into account, both genetic and shared environmental factors are significant influences on juvenile AB, accounting for approximately one-third of variation. The origin of the specific genetic influences on wave 1 AB is unclear, but may be due to factors related to measurement.
关于遗传和共同环境因素对青少年反社会行为(AB)影响程度的证据存在冲突。使用多种反社会行为评估方法可能会更准确地估计这些影响。
从3522对成年男性同卵双胞胎的基于人群的样本中,分两次获取18岁之前反社会行为的回顾性报告:电话访谈(第1波)以及19个月后获得的自我报告问卷(第2波)。结构方程模型估计了对可靠测量的反社会行为的遗传和环境影响。还研究了与第1波中双胞胎参与情况、第1波和第2波之间的损耗以及第1波和第2波评估的可靠性相关的因素。
双胞胎分析显示,遗传、共同环境和非共同环境影响分别占可靠测量的反社会行为方差的约33%(95%置信区间 = 9 - 57%)、31%(95%置信区间 = 10 - 51%)和36%(95%置信区间 = 29 - 44%)。我们还发现了对第1波反社会行为的显著特定场合遗传影响。第1波反社会行为并不能预测双胞胎在第1波中的参与情况或损耗,但与可靠性相关。同卵双胞胎的双胞胎和较年轻的双胞胎在第1波中更有可能参与;损耗可通过异卵双胞胎、双胞胎初始参与度低、受教育年限少和孩子数量少来预测。年龄较大、未婚以及心理病理学症状较少与更高的可靠性相关。
当考虑测量误差时,遗传和共同环境因素对青少年反社会行为均有显著影响,约占变异的三分之一。对第1波反社会行为的特定遗传影响的来源尚不清楚,但可能与测量相关因素有关。