RISK FOR SUBSTANCE ABUSE IN DEPRESSED ADOLESCENTS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 青春期物质使用障碍(SUD)的发展是一个重大的公共卫生问题，不仅关系到年轻人，而且关系到成年人的长期心理健康。在青少年中，SUD常与抑郁症并存，在一些青少年中，抑郁可能是SUD的先兆。伴发抑郁症和SUD与显著增加的社会心理和经济负担有关，因此强调了确定增加这些疾病风险的因素的必要性。有几条研究路线提出了一些假设，以检验抑郁、SUD、心理社会应激和下丘脑-垂体-肾上腺(HPA)系统之间的关系。为了支持这一假设，在两项初步研究中，我们已经证明，在抑郁的年轻人中，皮质醇升高或高水平的生活压力与SUD风险增加有关。这项研究采用纵向设计，旨在通过在抑郁青少年出现这些问题之前招募你来检查他们发展为SUD的风险。这项研究还旨在评估HPA失调与该队列中的SUD风险之间的关系。心理社会压力在预测SUD风险中的作用将在那些有或没有HPA调节失调的患者中进行评估。除了评估患有HPA失调和/或心理社会压力的人罹患SUD的风险大小外，还将确定在这些易受伤害的人中提供保护以抵御SUD的因素。该项目还旨在评估SUD对抑郁症临床病程和社会适应的影响。如果我们最初的结果--显示高皮质醇与SUD风险之间的关系--在更大规模的抑郁青少年样本中重复，那么这一发现可能有助于识别可能从抗抑郁或抗糖皮质激素治疗策略中受益最大的年轻人亚群。有证据表明，对抗抑郁药物的良好反应可能是由于HPA轴的Do-Ww调节。如果压力导致一些抑郁青年罹患SUD的风险，他们可能会从辅助性心理社会干预中受益。更有针对性和更有效的治疗可能有助于降低抑郁青年的SUD风险。此外，这种治疗策略可以推广到非抑郁症青年身上进行测试。

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 development of substance use disorder (SUD) during adolescence is a major public health problem which not only relates to the younger population, but also for the long-term mental health of adults. SUD often co-occurs with depression in adolescents and in some youth, depression may be a precursor to SUD. Comorbid depression and SUD is associated with significant added psychosocial and economic burden, thus highlighting the need to identify factors that increase the risk for these disorders. Several lines of investigation suggest hypotheses for examining the associations among depression, SUD, psychosocial stress and hypothalamic-pituitary-adrenal (HPA) system. In support of this hypothesis, in two preliminary studies, we have shown that elevated cortisol, or high level of life stress, is associated with increased risk for SUD in depressed youth. Using a longitudinal design, this investigation aims to examine the risk for development of SUD in depressed adolescents by recruiting you th before they develop these problems. The study also aims to evaluate the association between HPA dysregulation and risk for SUD in this cohort. The contribution of psychosocial stress in predicting risk for SUD will be assessed in those with and without HPA dysregulation. In addition to estimating the magnitude of risk for SUD in those with HPA dysregulation and/or psychosocial stress, factors that confer protection against SUD in such vulnerable individuals will be identified. The project is also designed to assess the effects of SUD on clinical course of depression and on social adjustment. If our initial results, showing a relationship between high cortisol and risk for SUD, are replicated in a larger sample of depressed adolescents, the findings potentially might be helpful in identifying the subgroup of youth who might benefit most from antidepressant or anti-glucocorticoid treatment strategies. Evidence suggests that a good response to antidepressant agents may be due to the do wn-regulation of the HPA axis. If stress contributes to the risk for SUD in some depressed youth, they might benefit from adjunctive psychosocial interventions. More focused and effective treatments potentially might be helpful in reducing the risk for SUD in depressed youth. Moreover, such treatment strategies can be extended for testing in non-depressed youth.