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BDNF Val⁶⁶Met polymorphism to generalized anxiety disorder pathways: Indirect effects via attenuated parasympathetic stress-relaxation reactivity.
Journal of Psychopathology and Clinical Science ( IF 4.6 ) Pub Date : 2020-04-01 , DOI: 10.1037/abn0000507
Hsin-An Chang 1 , Wen-Hui Fang 2 , Yia-Ping Liu 1 , Nian-Sheng Tzeng 1 , Jia-Fwu Shyu 3 , Fang-Jung Wan 1 , San-Yuan Huang 1 , Tieh-Ching Chang 1 , Chuan-Chia Chang 1
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The valine⁶⁶methionine (Val⁶⁶Met) polymorphism (rs6265) of the brain-derived neurotrophic factor (BDNF) gene has been shown to influence autonomic arousal pathways, which in turn predict elevated syndromal anxiety in healthy humans. We examined whether the BDNF variant is associated with an increased risk of generalized anxiety disorder (GAD), one of the most prevalent anxiety disorders, through altering parasympathetic stress/relaxation reactivity. A total of 2,250 Han Chinese adults (750 GAD patients and 1,500 healthy controls) were included in the genotyping. High-frequency heart rate variability, an index of vagal (parasympathetic) activity, was measured during the supine-standing-supine test (5 min in each position); vagal withdrawal and vagal activation were calculated as baseline supine minus standing and recovery supine minus standing, respectively. Analysis of healthy participants indicated that Val/Val homozygotes displayed significantly blunted vagal withdrawal and vagal activation compared with Met allele carriers. After analyzing the entire sample, these effects remained significant. Furthermore, both attenuated vagal response patterns were found to be significantly associated with a higher incidence of GAD. Lastly, the path analysis identified a significant indirect effect of BDNF on the risk of GAD via diminishing vagal response to either orthostatic stress or supine relaxation. Even when further testing the subsample comprising only comorbidity- and medication-free GAD patients and healthy controls to minimize the confounding bias, the results still remained. Our findings demonstrate that individuals carrying the BDNF Val/Val genotype, compared to Met-carriers, may be at higher risk of GAD due to blunted vagal reactivity in response to both stress and relaxation. (PsycINFO Database Record (c) 2020 APA, all rights reserved).

中文翻译:

BDNFVal⁶⁶Met多态性与广泛性焦虑症途径的关系:副交感神经应力松弛反应减弱引起的间接作用。

脑源性神经营养因子(BDNF)基因的缬氨酸蛋氨酸(Val⁶⁶Met)多态性(rs6265)已显示会影响自主觉醒途径,从而预示着健康人的综合症焦虑症会升高。我们检查了BDNF变异是否通过改变副交感神经应激/放松反应性而与增加的广泛性焦虑症(GAD)(一种最普遍的焦虑症)的风险相关。共有2250名汉族成年人(750名GAD患者和1500名健康对照)参与了基因分型。仰卧站立仰卧位测试(每个位置5分钟)测量高频心率变异性,这是迷走神经(副交感神经)活动的指标。迷走神经退缩和迷走神经激活计算为基线仰卧减去站立和恢复仰卧减去站立,分别。健康参与者的分析表明,与Met等位基因携带者相比,Val / Val纯合子表现出明显的迷走神经退缩和迷走神经激活。在分析了整个样本之后,这些影响仍然很明显。此外,发现两种迷走神经减退反应模式均与较高的GAD发生率显着相关。最后,路径分析确定了BDNF通过减少对立位应力或仰卧放松的迷走神经反应对GAD风险的显着间接作用。即使在进一步测试仅包含无合并症和药物治疗的GAD患者和健康对照组的子样本以最小化混杂偏差时,结果仍然保留。我们的发现表明,与Met携带者相比,携带BDNF Val / Val基因型的个体,由于对压力和松弛的反应使迷走神经反应钝化,因此GAD的风险可能更高。(PsycINFO数据库记录(c)2020 APA,保留所有权利)。
更新日期:2020-04-01
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