Seglem Karoline Brobakke, Waaktaar Trine, Ask Helga, Torgersen Svenn
Centre for Child and Adolescent Mental Health, Eastern and Southern Norway, Oslo, Norway,
Behav Genet. 2015 Mar;45(2):171-80. doi: 10.1007/s10519-015-9706-x. Epub 2015 Jan 21.
Studying monozygotic and dizygotic adolescent twin pairs of both sexes reared together, the present study examined the extent to which the variance in smoking involvement is attributable to genetic and environmental effects, and to what extent there are sex differences in the etiology. Questionnaire data on how often the adolescent had ever smoked tobacco was collected from a population-based twin sample consisting of seven national birth cohorts (ages 12-18), their mothers, and their fathers (N = 1,394 families). The data was analyzed with multivariate genetic modeling, using a multi-informant design. The etiological structure of smoking involvement was best represented in an ACE common pathway model, with smoking defined as a latent factor loading onto all three informants' reports. Estimates could be set equal across sexes. Results showed that adolescent lifetime smoking involvement was moderately heritable (37 %). The largest influence was from the shared environment (56 %), while environmental effects unique to each twin had minimal influence (7 %).
本研究通过对共同抚养的同性别和不同性别的单卵及双卵青少年双胞胎进行研究，考察了吸烟参与度的差异在多大程度上可归因于遗传和环境影响，以及病因在多大程度上存在性别差异。我们从一个基于人群的双胞胎样本中收集了关于青少年吸烟频率的问卷数据，该样本包括七个全国出生队列（年龄在12 - 18岁）、他们的母亲和父亲（N = 1394个家庭）。使用多信息者设计，通过多变量遗传模型对数据进行分析。吸烟参与度的病因结构在ACE共同路径模型中得到了最佳体现，其中吸烟被定义为一个潜在因素，加载到所有三位信息提供者的报告中。估计值在不同性别间可以设定为相等。结果表明，青少年一生的吸烟参与度具有中等遗传性（37%）。最大的影响来自共同环境（56%），而每个双胞胎特有的环境影响最小（7%）。
