Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine , Houston, TX , USA.
Human Neuroscience Institute, Department of Human Development, Cornell University , Ithaca, NY , USA.
Front Psychiatry. 2014 Jul 17;5:83. doi: 10.3389/fpsyt.2014.00083. eCollection 2014.
Childhood trauma and post-childhood chronic/repeated stress could increase the risk of a substance use disorder by affecting five stages of addiction illness-course: (a) initial experimentation with substances; (b) shifting from experimental to regular use; (c) escalation from regular use to abuse or dependence; (d) motivation to quit; and (e) risk of (re-)lapse. We reviewed the human literature on relationships between stress and addiction illness-course. We explored per illness-course stage: (i) whether childhood trauma and post-childhood chronic/repeated stress have comparable effects and (ii) whether effects cut across classes of substances of abuse. We further discuss potential underlying mechanisms by which stressors may affect illness-course stages for which we relied on evidence from studies in animals and humans. Stress and substances of abuse both activate stress and dopaminergic motivation systems, and childhood trauma and post-childhood stressful events are more chronic and occur more frequently in people who use substances. Stressors increase risk to initiate early use potentially by affecting trait-like factors of risk-taking, decision making, and behavioral control. Stressors also accelerate transition to regular use potentially due to prior effects of stress on sensitization of dopaminergic motivation systems, cross-sensitizing with substances of abuse, especially in people with high trait impulsivity who are more prone to sensitization. Finally, stressors increase risk for abuse and dependence, attenuate motivation to quit, and increase relapse risk potentially by intensified sensitization of motivational systems, by a shift from positive to negative reinforcement due to sensitization of the amygdala by corticotropin releasing factor, and by increased sensitization of noradrenergic systems. Stress generally affects addiction illness-course across stressor types and across classes of substances of abuse.
儿童期创伤和儿童期后慢性/反复应激可通过影响成瘾疾病进程的五个阶段，增加物质使用障碍的风险：(a) 最初尝试使用物质；(b) 从实验性使用转变为常规使用；(c) 从常规使用升级为滥用或依赖；(d) 戒除的动机；以及 (e) (复)发的风险。我们回顾了关于应激与成瘾疾病进程之间关系的人类文献。我们探讨了每个疾病进程阶段：(i) 儿童期创伤和儿童期后慢性/反复应激是否具有可比的影响，以及 (ii) 影响是否跨越滥用物质的类别。我们进一步讨论了应激源可能通过影响我们依赖于动物和人类研究证据的疾病进程阶段的潜在机制。应激和滥用物质都会激活应激和多巴胺能动机系统，而儿童期创伤和儿童期后应激事件在使用物质的人群中更常见且更频繁。应激源通过影响冒险、决策和行为控制等特质因素，增加了早期使用的风险。应激源还可能通过先前对多巴胺能动机系统致敏的影响，以及与滥用物质的交叉致敏作用，加速向常规使用的转变，尤其是在具有高特质冲动性的人群中，他们更容易致敏。最后，应激源通过强化动机系统的致敏作用，通过由于促肾上腺皮质释放因子对杏仁核的致敏作用导致正强化向负强化的转变，以及通过增加去甲肾上腺素能系统的致敏作用，增加滥用和依赖的风险，减弱戒除的动机，并增加复发的风险。一般来说，应激源会影响所有应激源类型和滥用物质类别的成瘾疾病进程。
