TWIN FAMILY STUDY OF VULNERABILITY TO SUBSTANCE ABUSE

描述：（申请人摘要） 寻求五年的更新资金，以研究物质的病因学 从发育行为遗传学的角度来看，虐待（SA）。 我们 假设SA遗传易感性可能在早期 青春期作为1）人格特征，2）心理生理 标志物; 3）精神障碍。 我们迄今为止的发现表明， 这些因素是a）强烈遗传的，B）区分个体与 c）区分具有和不具有SA亲本的个体， d）前瞻性预测早期开始使用药物和酒精， 青春期中期，和e）预测早发性药物和酒精障碍， 青春期后期 我们还发现支持我们的假设1）， 这些责任表型标记部分地通过以下方式影响SA风险： 增加了个体暴露于和受影响的可能性 在青春期的经验风险因素和2）性别可能 缓和责任标记、环境风险 因素和精神活性物质使用障碍的结果。 666个家庭组成的一对双胞胎和他们的 母亲和父亲已经完成了为期一天的全面评估， 他们的1）心理健康和物质使用史，2）个性（评估 积极情绪、消极情绪和 行为约束），3）心理生理指标（包括大脑 电位[P3和EEG]、自主神经系统测量、眨眼 惊吓和眼动跟踪），以及3）环境因素（包括家庭 气候、同伴群体和认知风险因素）。 在研究摄入时， 双胞胎要么是11岁（实验药物之前的年龄， 酒精）或17岁（成年物质使用之前的年龄 模式）。 在续约时，这些家庭将完成他们的 在14岁和20岁时进行首次面对面随访（FU 1）评估，3年 40%的人将在第一次入学评估后完成FU2， 17岁和23岁。 大约有一半的儿童因道德而处于高风险之中 父母中有非法药物滥用/依赖或酗酒者 依赖 在未来五年内，我们建议1）完成FU 2，2）启动FU 3 (at年龄20和26岁），3）分析摄入量和FU数据，将其与 我们对717个女性双胞胎家庭的平行研究（这是由 新增200个双胞胎家庭）。 主要分析是 在本供资期内开展的活动包括：1）评估 父母SA，2）双胞胎数据的单变量生物统计学分析，3）多 旨在探索基因型-环境的变量生物特征分析 相关分析; 4）基因型-环境互作效应分析。

DESCRIPTION: (Applicant's Abstract) Five years of renewal funding are sought to study the etiology of substance abuse (SA) from a developmental behavioral genetic perspective. We hypothesize that an inherited predisposition to SA may be expressed in early adolescence as 1) personality characteristics, 2) psychophysiological markers, and 3) psychiatric disorder. Our findings to date indicate that these factors are a) strongly heritable, b) differentiate individuals with and without SA, c) differentiate individuals with and without an SA parent, d) prospectively predict the early initiation of drug and alcohol use in middle adolescence, and e) predict early onset drug and alcohol disorders in late adolescence. We have also found support for our hypotheses 1) that these phenotypic markers of liability influence SA risk in part by increasing the likelihood that an individual is both exposed to and affected by experiential risk factors during adolescence and 2) that gender may moderate the association between liability markers, environmental risk factors, and a psychoactive substance use disorder outcome. Six-hundred and sixty-six families consisting of a twin pair and their mother and father have completed a daylong, comprehensive assessment of their 1) mental health and substance use history, 2) personality (assessing the broad dimensions of positive emotionality, negative emotionality, and behavioral constraint), 3) psychophysiological markers (including brain potentials [P3 and EEG], autonomic nervous system measures, eye-blink startle, and eye tracking), and 3) environmental factors (including family climate, peer group, and cognitive risk factors). At study intake, the twins were either age 11 (an age prior to experimentation with drugs and alcohol) or age 17 (an age that precedes the adoption of adult substance use patterns). At the time of renewal, these families will have completed their first in-person follow-up (FU1) assessment at ages 14 and 20, three years after their initial intake assessment, and 40% will have completed FU2 at ages 17 and 23. Approximately half the children are at high risk by virtue of their having a parent with illicit drug abuse/dependence or alcohol dependence. During the next five years we propose to 1) complete FU2, 2) initiate FU3 (at ages 20 and 26), and 3) analyze the intake and FU data, comparing it to our parallel study of 717 female twin families (which is being augmented by the addition of another 200 twin families). The primary analyses to be undertaken during this funding period involve: 1) assessing the effects of parental SA, 2) univariate biometric analyses of the twin data, 3) multi variate biometric analyses aimed at exploring genotype-environment correlation, and 4) analysis of genotype-environment interaction effects.