Vogel S W N, Bijlenga D, Verduijn J, Bron T I, Beekman A T F, Kooij J J S, Penninx B W J H
PsyQ Expertise Center Adult ADHD, The Hague, The Netherlands.
PsyQ Expertise Center Adult ADHD, The Hague, The Netherlands.
Psychoneuroendocrinology. 2017 May;79:31-39. doi: 10.1016/j.psyneuen.2017.02.009. Epub 2017 Feb 13.
The current study examined whether (a) Attention-Deficit/Hyperactivity Disorder (ADHD) symptoms were associated with dysregulation of stress-related mechanisms, and (b) whether ADHD symptoms interact with affective disorders in their association with dysregulated stress-related mechanisms.
Data were obtained from 2307 subjects participating in the Netherlands Study of Depression and Anxiety. Stress-related mechanisms were reflected by the following biomarkers: (1) hypothalamic-pituitary-adrenal axis indicators (salivary cortisol awakening curve, evening cortisol, cortisol suppression after a 0.5mg dexamethasone suppression test (DST)); (2) autonomic nervous system measures (heart rate, pre-ejection period, respiratory sinus arrhythmia); (3) inflammatory markers (C-reactive protein, interleukin-6, tumor necrosis factor-alpha); (4) brain-derived neurotrophic factor. ADHD symptoms were measured using Conners' Adult ADHD Rating Scale and used both dichotomous (High ADHD symptoms (yes/no)) and continuous (Inattentive symptoms, Hyperactive/Impulsive symptoms, and the ADHD index).
Regression analyses showed associations between High ADHD symptoms, Inattentive symptoms, the ADHD index and a higher cortisol awakening curve, between Hyperactive/Impulsive symptoms and less cortisol suppression after DST, and between Inattentive symptoms and a longer pre-ejection period. However, the associations with the cortisol awakening curve disappeared after adjustment for depressive and anxiety disorders. No associations were observed between ADHD symptoms and inflammatory markers or BDNF. ADHD symptoms did not interact with affective disorders in dysregulation of stress-related mechanisms.
Some associations were observed between ADHD symptoms, the HPA-axis, and the pre-ejection period, but these were mostly driven by depressive and anxiety disorders. This study found no evidence that ADHD symptomatology was associated with dysregulations in inflammatory markers and BDNF. Consequently, ADHD symptoms did not confer an added risk to the disturbances of stress-related mechanisms in an - already at-risk - population with affective disorders.
本研究探讨了以下两个问题：（a）注意缺陷多动障碍（ADHD）症状是否与应激相关机制的失调有关；（b）ADHD症状在与失调的应激相关机制的关联中是否与情感障碍相互作用。
数据来自参与荷兰抑郁与焦虑研究的2307名受试者。应激相关机制由以下生物标志物反映：（1）下丘脑 - 垂体 - 肾上腺轴指标（唾液皮质醇觉醒曲线、夜间皮质醇、0.5毫克地塞米松抑制试验（DST）后的皮质醇抑制）；（2）自主神经系统测量指标（心率、射血前期、呼吸性窦性心律不齐）；（3）炎症标志物（C反应蛋白、白细胞介素 - 6、肿瘤坏死因子 - α）；（4）脑源性神经营养因子。使用康纳斯成人ADHD评定量表测量ADHD症状，并采用二分法（高ADHD症状（是/否））和连续变量法（注意力不集中症状、多动/冲动症状以及ADHD指数）。
回归分析显示，高ADHD症状、注意力不集中症状、ADHD指数与较高的皮质醇觉醒曲线之间存在关联，多动/冲动症状与DST后较少的皮质醇抑制之间存在关联，注意力不集中症状与较长的射血前期之间存在关联。然而，在对抑郁和焦虑障碍进行调整后，与皮质醇觉醒曲线的关联消失。未观察到ADHD症状与炎症标志物或脑源性神经营养因子之间存在关联。ADHD症状在应激相关机制失调方面未与情感障碍相互作用。
在ADHD症状、下丘脑 - 垂体 - 肾上腺轴和射血前期之间观察到一些关联，但这些关联大多由抑郁和焦虑障碍驱动。本研究未发现证据表明ADHD症状学与炎症标志物和脑源性神经营养因子的失调有关。因此，在已经处于风险中的情感障碍人群中，ADHD症状并未给应激相关机制的紊乱带来额外风险。
