Cousins Center for Psychoneuroimmunology and Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, California.
Department of Developmental Psychology, Tilburg University, Tilburg, The Netherlands.
Depress Anxiety. 2020 Feb;37(2):179-193. doi: 10.1002/da.22987.
Depression rates increase markedly for girls across the adolescent transition, but the social-environmental and biological processes underlying this phenomenon remain unclear. To address this issue, we tested a key hypothesis from Social Signal Transduction Theory of Depression, which posits that individuals who mount stronger inflammatory responses to social stress should exhibit greater increases in depressive symptoms following interpersonal life stress exposure than those who mount weaker inflammatory responses to such stress.
Participants were 116 adolescent girls (M = 14.71) at risk for psychopathology, defined as having a history of mental health concerns (e.g., psychiatric treatment, significant symptoms) over the past 2 years. At baseline, we characterized their inflammatory reactivity to social stress by quantifying their salivary proinflammatory cytokine responses to a laboratory-based social stressor. Then, 9 months later, we assessed the interpersonal and noninterpersonal stressful life events that they experienced over the prior 9 months using an interview-based measure of life stress.
As hypothesized, greater interpersonal life stress exposure was associated with significant increases in depression over time, but only for girls exhibiting stronger salivary tumor necrosis factor-α and interleukin-1β reactivity to social stress. In contrast, noninterpersonal stress exposure was unrelated to changes in depression longitudinally, both alone and when combined with youths' cytokine reactivity scores.
These results are consistent with Social Signal Transduction Theory of Depression and suggest that heightened inflammatory reactivity to social stress may increase adolescents' risk for depression. Consequently, it may be possible to reduce depression risk by modifying inflammatory responses to social stress.
在青少年过渡期间，女孩的抑郁率显著增加，但这种现象背后的社会环境和生物学过程仍不清楚。为了解决这个问题，我们检验了抑郁的社会信号转导理论中的一个关键假设，该假设认为，对社会压力产生更强炎症反应的个体在经历人际生活压力暴露后，其抑郁症状的增加应该比那些对这种压力产生较弱炎症反应的个体更大。
参与者是 116 名有心理病理学风险的青春期女孩（M = 14.71），定义为在过去 2 年内有心理健康问题的病史（例如，精神科治疗，明显症状）。在基线时，我们通过量化唾液促炎细胞因子对基于实验室的社会应激源的反应，来描述她们的炎症反应性。然后，9 个月后，我们使用基于访谈的生活压力测量方法评估她们在过去 9 个月中经历的人际和非人际生活压力事件。
正如假设的那样，更多的人际生活压力暴露与随着时间的推移抑郁的显著增加有关，但仅对于对社会压力表现出更强唾液肿瘤坏死因子-α和白细胞介素-1β反应的女孩。相比之下，非人际压力暴露与纵向抑郁变化无关，无论是单独还是与年轻人的细胞因子反应评分相结合时。
这些结果与抑郁的社会信号转导理论一致，表明对社会压力的炎症反应增强可能会增加青少年患抑郁症的风险。因此，通过改变对社会压力的炎症反应，可能有可能降低抑郁症的风险。
