STRESS AND RISK FOR SUBSTANCE ABUSE IN ADOLESCENTS

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目及 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 压力和物质使用障碍（SUD）的发展之间的相互作用往往始于创伤的早期经历。 经历过童年虐待的人一贯报告较高的药物使用率，其中许多人也倾向于参与越轨和犯罪行为。 由于儿童虐待的人除了滥用药物外，还在多个社会领域受到损害，因此针对这一群体的治疗和预防方案将产生重大的社会经济影响。 然而，为了制定更有效的干预措施，至关重要的是要了解儿童虐待和易受SUD之间的关联的基本机制。 本研究采用对照纵向设计，通过在SUD发病前招募有和无儿童期虐待史的青少年，探讨早期生活压力、HPA反应性和SUD易感性之间的关系。 我们假设在前瞻性随访中，与未受童年虐待的青少年相比，受童年虐待的青少年发生SUD的比例更高，并且SUD易感性的增加至少部分是由基线时测量的HPA失调介导的。 除了检查发病前压力和HPA失调与SUD发展的易感性之间的关联外，还将从多维度的角度评估已知影响这些过程的其他因素。 识别特定的脆弱性和相关的生物学改变将有助于制定更有针对性和有效的药理学和心理社会干预措施，以减少这些青年的SUD风险。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The interaction between stress and the development of substance use disorders (SUD) often begins with the early experience of trauma. Individuals who experienced childhood abuse consistently report higher rates of substance use, and many of them also tend to participate in deviant and criminal behaviors. Because persons with childhood abuse are impaired in multiple social domains in addition to substance abuse, targeting this group of individuals for treatment and prevention programs will have significant socioeconomic impact. However, in order to develop more effective interventions, it is critical to understand the underlying mechanisms of association between childhood abuse and vulnerability to SUD. Using a controlled longitudinal design, this study will examine the relationships among early-life stress, HPA responsivity and vulnerability to SUD in adolescents with and without a history of childhood maltreatment by recruiting them prior to the onset of SUD. We hypothesize that a higher proportion of adolescents with childhood maltreatment will develop SUD during prospective follow-up compared withadolescents without childhood maltreatment, and that this increase in vulnerability to SUD will be mediated, at least in part, by HPA dysregulation measured at baseline. In addition to examing the association between premorbid stress and HPA dysregulation as related to susceptibility for the development of SUD, other factors that are known to influence these processes will be assessed from a multi-dimensional perspective. The identification of specific vulnerabilities and associated biological alterations will aid in the development of more focused and effective pharmacological and psychosocial interventions to reduce the risk of SUD in such youth.