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Integrating genome-wide information and wearable device data to explore the link of anxiety and antidepressants with pulse rate variability
Molecular Psychiatry ( IF 9.6 ) Pub Date : 2024-11-18 , DOI: 10.1038/s41380-024-02836-7
Eleni Friligkou, Dora Koller, Gita A. Pathak, Edward J. Miller, Rachel Lampert, Murray B. Stein, Renato Polimanti

This study explores the genetic and epidemiologic correlates of long-term photoplethysmography-derived pulse rate variability (PRV) measurements with anxiety disorders. Individuals with whole-genome sequencing, Fitbit, and electronic health record data (N = 920; 61,333 data points) were selected from the All of Us Research Program. Anxiety polygenic risk scores (PRS) were derived with PRS-CS after meta-analyzing anxiety genome-wide association studies from three major cohorts- UK Biobank, FinnGen, and the Million Veterans Program (NTotal =364,550). PRV was estimated as the standard deviation of average five-minute pulse wave intervals over full 24-hour pulse rate measurements (SDANN). Antidepressant exposure was defined as an active antidepressant prescription at the time of the PRV measurement in the EHR. Anxiety PRS and antidepressant use were tested for association with daily SDANN. The potential causal effect of anxiety on PRV was assessed with one-sample Mendelian randomization (MR). Anxiety PRS was independently associated with reduced SDANN (beta = −0.08; p = 0.003). Of the eight antidepressant medications and four classes tested, venlafaxine (beta = −0.12, p = 0.002) and bupropion (beta = −0.071, p = 0.01), tricyclic antidepressants (beta = −0.177, p = 0.0008), selective serotonin reuptake inhibitors (beta = −0.069; p = 0.0008) and serotonin and norepinephrine reuptake inhibitors (beta = −0.16; p = 2×10−6) were associated with decreased SDANN. One-sample MR indicated an inverse effect of anxiety on SDANN (beta = −2.22, p = 0.03). Anxiety and antidepressants are independently associated with decreased PRV, and anxiety appears to exert a causal effect on reduced PRV. Those observational findings provide insights into the impact of anxiety on PRV.



中文翻译:


整合全基因组信息和可穿戴设备数据,探索焦虑和抗抑郁药与脉率变异性的联系



本研究探讨了长期光电容积脉搏波衍生的脉率变异性 (PRV) 测量与焦虑症的遗传和流行病学相关性。具有全基因组测序、Fitbit 和电子健康记录数据(N = 920;61,333 个数据点)的个体是从 All of Us 研究计划中选出的。在对来自三个主要队列 - 英国生物银行、FinnGen 和百万退伍军人计划 (N总计 = 364,550) 的焦虑全基因组关联研究进行荟萃分析后,使用 PRS-CS 得出焦虑多基因风险评分 (PRS)。PRV 估计为完整 24 小时脉率测量 (SDANN) 中平均 5 分钟脉搏波间隔的标准差。抗抑郁药暴露被定义为在 EHR 中测量 PRV 时有效的抗抑郁药处方。测试焦虑 PRS 和抗抑郁药的使用与每日 SDANN 的相关性。通过单样本孟德尔随机化 (MR) 评估焦虑对 PRV 的潜在因果效应。焦虑 PRS 与 SDANN 降低独立相关 (beta = -0.08;p = 0.003)。在测试的八种抗抑郁药物和四类抗抑郁药中,文拉法辛 (beta = -0.12, p = 0.002) 和安非他酮 (beta = -0.071, p = 0.01)、三环类抗抑郁药 (beta = -0.177, p = 0.0008)、选择性血清素再摄取抑制剂 (β = -0.069;p = 0.0008) 以及血清素和去甲肾上腺素再摄取抑制剂 (β = -0.16;p = 2×10-6) 与 SDANN 降低相关。单样本 MR 表明焦虑对 SDANN 有负效应 (beta = -2.22,p = 0.03)。焦虑和抗抑郁药与 PRV 降低独立相关,焦虑似乎对 PRV 降低产生因果效应。 这些观察结果提供了对焦虑对 PRV 影响的见解。

更新日期:2024-11-18
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