Medical Psychology & Medical Sociology, University Medical Center Mainz Johannes Gutenberg University of Mainz, Mainz, Germany; Clinic of Psychotherapy and Psychosomatic Medicine, University Hospital Carl Gustav Carus Dresden, Technical University Dresden, Germany.
Medical Psychology & Medical Sociology, University Medical Center Mainz Johannes Gutenberg University of Mainz, Mainz, Germany; University Hospital Carl Gustav Carus Dresden, Medical Psychology and Medical Sociology, Dresden, Germany.
Psychoneuroendocrinology. 2021 Jan;123:104913. doi: 10.1016/j.psyneuen.2020.104913. Epub 2020 Oct 15.
In order to understand the psychopathology of the social anxiety disorder (SAD) at the neuroendocrine level, standardized experimental studies on endocrine and physiological markers are necessary, especially since empirical data are still ambiguous. Hence, differences in both, the autonomic nervous system (ANS) and the endocrine stress responses (ACTH, salivary and plasma cortisol) were investigated in a particularly homogenous sample after a standardized stressor (Trier Social Stress Test). The sample consisted of n = 35 patients with SAD, age, and gender matched to n = 35 healthy controls (HC). In terms of the heart rate, the response pattern was comparable in both groups. Concerning ACTH, no significant group differences in the response pattern nor in the total output (AUC) were exhibited. Significant differences were noticeable only in the plasma cortisol response pattern with less total output (AUC) in patients suggesting a blunted response. The salivary cortisol response indicated comparable patterns between groups. However, the patients' total output (AUC) was significantly smaller relative to the controls. In sum, evidence for a hypo-responsiveness of the HPA-axis in SAD by means of blood cortisol was observed, with no differences in ACTH between the two groups. This reduced reactivity of the HPA-axis might be associated with an inability to elicit an adequate hormone release, possibly accompanied by an enhanced perception of the stress stimulus. This might be explained by an adaptation of the adrenocortical system due to prolonged repeated stress exposure such as social evaluation.
为了从神经内分泌层面理解社交焦虑障碍（SAD）的心理病理学，有必要进行标准化的内分泌和生理标志物实验研究，特别是因为实证数据仍然存在分歧。因此，在对一组特别同质的样本进行标准化应激源（特里尔社会应激测试）后，研究了自主神经系统（ANS）和内分泌应激反应（ACTH、唾液和血浆皮质醇）的差异。该样本由 n = 35 名 SAD 患者组成，年龄和性别与 n = 35 名健康对照组（HC）相匹配。就心率而言，两组的反应模式相似。关于 ACTH，两组的反应模式和总输出（AUC）均无显著差异。只有在血浆皮质醇反应模式中，患者的总输出（AUC）明显较小，表明反应迟钝，才会出现显著差异。唾液皮质醇反应表明两组之间的模式相似。然而，与对照组相比，患者的总输出（AUC）明显较小。总的来说，通过血液皮质醇观察到 SAD 患者的 HPA 轴反应迟钝，两组之间的 ACTH 没有差异。HPA 轴的这种低反应性可能与无法引发足够的激素释放有关，这可能伴随着对压力刺激的增强感知。这可能是由于肾上腺皮质系统对长期重复的社会评价等应激暴露的适应。
