Schreier Hannah M C, Chen Edith
From the Department of Biobehavioral Health (Schreier), The Pennsylvania State University, University Park, PA, and Department of Psychology and Cells to Society (C2S): The Center on Social Disparities and Health (Chen), Institute for Policy Research, Northwestern University, Evanston, IL.
Psychosom Med. 2017 Feb-Mar;79(2):133-142. doi: 10.1097/PSY.0000000000000377.
To determine whether the association between self-rated or interviewer-rated recent acute stress exposures and low-grade inflammation and daily cortisol production in adolescents is moderated by chronic stress ratings.
Acute and chronic stress exposures were assessed in 261 adolescents aged 13 to 16 years using a semistructured life stress interview. The negative impact of acute stressors was independently rated by both adolescents (self-rated) and interviewers (interviewer-rated). Markers of inflammation (interleukin (IL)-6, IL-1ra, C-reactive protein) were measured from peripheral blood samples obtained via antecubital venipuncture. Participants collected 4 saliva samples at home on each of 6 consecutive days for the analysis of diurnal salivary cortisol profiles.
There were no main effects of acute stressors (self- and interviewer-rated) and chronic family or peer stress on adolescent inflammation markers and cortisol (p values > .10). However, the interaction between interviewer-rated acute stress and chronic family stress was significantly associated with adolescent inflammation markers (IL-6, IL-1ra). Specifically, as chronic family stress increased, the association between acute stressor impact (interviewer-rated) and inflammation markers became more positive (IL-6 (B = .054, SE = .023, p = .022); IL-1ra (B = .030, SE = .014, p = .034)). Interactions between self-rated acute stress and chronic family stress were not associated with any biological measures (p values > .10). Interactions between acute stressor impact (both self- and interviewer-rated) and chronic peer stress were also not significantly associated with any biological measures (p values > .05).
Among adolescents, interviewer-based ratings of acute stressor impact may allow for better prediction of health-relevant inflammation markers than adolescents' own ratings.
确定青少年自评或访谈者评定的近期急性应激暴露与低度炎症及每日皮质醇分泌之间的关联是否受慢性应激评定的调节。
采用半结构化生活应激访谈对261名13至16岁青少年的急性和慢性应激暴露进行评估。青少年(自评)和访谈者(访谈者评定)分别独立评定急性应激源的负面影响。通过肘前静脉穿刺采集外周血样本,检测炎症标志物(白细胞介素(IL)-6、IL-1受体拮抗剂、C反应蛋白)。参与者在连续6天的每一天在家中采集4份唾液样本,用于分析唾液皮质醇昼夜变化情况。
急性应激源(自评和访谈者评定)以及慢性家庭或同伴应激对青少年炎症标志物和皮质醇均无主效应(p值>.10)。然而,访谈者评定的急性应激与慢性家庭应激之间的交互作用与青少年炎症标志物(IL-6、IL-1受体拮抗剂)显著相关。具体而言,随着慢性家庭应激增加,急性应激源影响(访谈者评定)与炎症标志物之间的关联变得更加正向(IL-6(B = .054,SE = .023,p = .022);IL-1受体拮抗剂(B = .)。自评急性应激与慢性家庭应激之间的交互作用与任何生物学指标均无关联(p值>.10)。急性应激源影响(自评和访谈者评定)与慢性同伴应激之间的交互作用也与任何生物学指标均无显著关联(p值>.05)。
在青少年中,基于访谈者的急性应激源影响评定可能比青少年自身评定更能准确预测与健康相关的炎症标志物。