Department of Psychiatry and the EMGO Institute for Health and Care Research, VU University Medical Center Amsterdam, The Netherlands.
Br J Psychiatry. 2010 Sep;197(3):180-5. doi: 10.1192/bjp.bp.109.076869.
It is unclear whether altered hypothalamic-pituitary-adrenal (HPA) axis regulation, which frequently accompanies depression and anxiety disorders, represents a trait rather than a state factor.
To examine whether HPA axis dysregulation represents a biological vulnerability for these disorders, we compared cortisol levels in unaffected people with and without a parental history of depressive or anxiety disorders. We additionally examined whether possible HPA axis dysregulations resemble those observed in participants with depression or anxiety disorders.
Data were from the Netherlands Study of Depression and Anxiety. Within the participants without a lifetime diagnoses of depression or anxiety disorders, three groups were distinguished: 180 people without parental history, 114 with self-reported parental history and 74 with CIDI-diagnosed parental history. These groups were additionally compared with people with major depressive disorder or panic disorder with agoraphobia (n = 1262). Salivary cortisol samples were obtained upon awakening, and 30, 45 and 60 min later.
As compared with unaffected participants without parental history, unaffected individuals with diagnosed parental history of depression or anxiety showed a significantly higher cortisol awakening curve (effect size (d) = 0.50), which was similar to that observed in the participants with depression or anxiety disorders. Unaffected people with self-reported parental history did not differ in awakening cortisol levels from unaffected people without parental history.
Unaffected individuals with parental history of depression or anxiety showed a higher cortisol awakening curve, similar to that of the participants with depression or anxiety disorders. This suggests that a higher cortisol awakening curve reflects a trait marker, indicating an underlying biological vulnerability for the development of depressive and anxiety disorders.
目前尚不清楚伴随抑郁和焦虑障碍的下丘脑-垂体-肾上腺(HPA)轴调节改变是特质因素还是状态因素。
为了检验 HPA 轴失调是否代表这些障碍的生物学易感性,我们比较了无抑郁或焦虑障碍家族史和有抑郁或焦虑障碍家族史的未受影响人群的皮质醇水平。我们还检查了 HPA 轴失调是否类似于抑郁或焦虑障碍患者中观察到的失调。
数据来自荷兰抑郁和焦虑研究。在无终生抑郁或焦虑障碍诊断的参与者中,区分出三组:180 名无父母病史者、114 名自我报告父母病史者和 74 名经 CIDI 诊断为父母病史者。这些组还与患有重性抑郁障碍或伴有广场恐怖症的惊恐障碍患者(n = 1262)进行了比较。在觉醒时、30 分钟、45 分钟和 60 分钟后采集唾液皮质醇样本。
与无父母病史的未受影响参与者相比,有经诊断的父母抑郁或焦虑病史的未受影响个体的皮质醇觉醒曲线显著升高(效应大小(d)= 0.50),与抑郁或焦虑障碍患者观察到的曲线相似。有自我报告父母病史的未受影响个体与无父母病史的未受影响个体在觉醒皮质醇水平上无差异。
有抑郁或焦虑障碍家族史的未受影响个体表现出较高的皮质醇觉醒曲线,与抑郁或焦虑障碍患者相似。这表明较高的皮质醇觉醒曲线反映了特质标志物,表明存在发展为抑郁和焦虑障碍的潜在生物学易感性。