Behavioral Strategies to Reduce Stress Reactivity in Opioid Use Disorder

项目概要/摘要 作为对RFA-RM-17-028的回应，我们建议调查行为策略对减少 阿片类药物使用障碍成年人应激反应阿片类药物滥用在美国已经达到流行病的水平 美国，2015年有超过1250万人滥用处方阿片类药物，超过90万人使用海洛因。在 2015年，超过33，000人死于阿片类药物过量，自2015年以来，死亡人数继续有增无减。 90年代末虽然治疗，如丁丙诺啡维持已被证明是有效的， 在阿片类药物使用障碍的治疗方面，复发仍然非常普遍。对压力的反应性增强（即， 对压力源的情感和生理反应）与复发风险密切相关;然而， 治疗对应激反应性几乎没有影响。因此，显然需要新的干预措施， 减少阿片类药物使用障碍患者的应激反应。与一个以机制为中心的实验一致 医学方法的行为改变研究，我们建议测试的效果，简短的认知行为 影响调节干预对（1）情感和生理标志物的反应，以压力（目标 参与），和（2）短期行为改变（压力背景下的行为持续性）。 参与者将被随机分配到一个控制条件或两个简短的情感调节之一 干预，包括故意的影响调节策略（认知重新评价）或 附带影响调节策略（影响标签）。这两种策略已被证明产生类似的 减少对情感刺激的反应，但需要不同水平的认知资源，因此， 代表了两种不同的降低应激反应的方法。第一个目标是确定 相对于对照条件，有意和偶然影响对压力源反应性的调节策略。 第二个目标是确定这些情绪调节策略和行为之间的联系 对压力的耐受性。作为次要目标，我们将调查基线（即，干预前）水平 的自我调节与这些影响调节策略的影响。具体来说，我们将 调查那些自我调节缺陷的人是否对影响调节的反应降低 干预以及它们是否对有意策略和偶然策略有不同的反应（例如，无论这些 自我调节赤字表现出更大的反应，一个偶然的影响调节策略，这需要 更少的认知资源）。如果我们的假设得到支持，这些信息可以用来通知 开发全剂量的多疗程认知行为治疗，以改善这些患者的结局 阿片类药物使用障碍重要的是，由于压力反应在一系列精神疾病中的相关性， 这些发现可能也会影响到 其他心理健康状况的行为改变。

Project Summary/Abstract In response to RFA-RM-17-028, we propose to investigate the impact of behavioral strategies for reducing stress reactivity in adults with opioid use disorder. Opioid misuse has reached an epidemic level in the United States, with over 12.5 million people misusing prescription opioids and over 900,000 using heroin in 2015. In 2015, over 33,000 people died from opioid overdose, continuing the unabated escalation of deaths since the late 1990s. Although treatments such as buprenorphine maintenance have been shown to be effective for the treatment of opioid use disorder, relapse remains highly prevalent. Heightened reactivity to stress (i.e., affective and physiological response to stressors) is robustly associated with risk for relapse; however, existing treatments have little impact on stress reactivity. Accordingly, there is a clear need for novel interventions to reduce stress reactivity in those with opioid use disorder. Consistent with a mechanisms-focused experimental medicine approach to behavior change research, we propose to test the effect of brief cognitive-behavioral affect regulation interventions on (1) affective and physiological markers of reactivity to stress (target engagement), and (2) short-term behavior change (behavioral persistence in the context of stress). Participants will be randomly assigned to either a control condition or one of two brief affect regulation interventions, consisting of either an intentional affect regulation strategy (cognitive reappraisal) or an incidental affect regulation strategy (affect labeling). These two strategies have been shown to yield similar reductions in response to affective stimuli, but require different levels of cognitive resources, and thus represent two distinct approaches to reducing stress reactivity. The first aim is to determine the impact of intentional and incidental affect regulation strategies on reactivity to a stressor relative to a control condition. The second aim is to determine the association between these affect regulation strategies and behavioral tolerance to a stressor. As a secondary aim, we will investigate whether baseline (i.e., pre-intervention) levels of self-regulation are associated with the impact of these affect regulation strategies. Specifically, we will investigate whether those with self-regulatory deficits have a reduced response to affect regulation interventions and whether they respond differently to intentional vs. incidental strategies (e.g., whether those with self-regulatory deficits exhibit greater responding to an incidental affect regulation strategy, which requires fewer cognitive resources). If our hypotheses are supported, this information can be used to inform the development of a full dose of multi-session cognitive-behavioral therapy for improving outcomes among those with opioid use disorder. Critically, because of the relevance of stress reactivity across an array of psychiatric disorders (alcohol use disorder, posttraumatic stress disorder), these findings may also have implications for behavior change for other mental health conditions.