Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, 677 Huntington Ave, Boston, MA 02115, USA.
Division of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA.
Psychoneuroendocrinology. 2021 Oct;132:105341. doi: 10.1016/j.psyneuen.2021.105341. Epub 2021 Jun 25.
Posttraumatic stress disorder (PTSD) has been associated with increased cardiovascular risk, however, underlying mechanisms have not been fully specified. PTSD is associated with stress-related hormones, including dysregulated glucocorticoid activity. Dysregulation of aldosterone, a mineralocorticoid activated by psychological stress and implicated in cardiovascular damage, may be a relevant pathway linking PTSD and cardiovascular risk. Few studies to date have evaluated the association between PTSD and aldosterone, none with repeated measures of aldosterone. We examined if trauma and PTSD were associated with altered aldosterone levels relative to women unexposed to trauma.
The association of trauma exposure and chronic PTSD with plasma aldosterone levels was investigated in 521 middle-aged women in the Nurses' Health Study II. Aldosterone was assessed at two time points, 10-16 years apart, and trauma exposure and PTSD were also ascertained for both time points. Regarding exposure assessment, women were characterized based on a structured diagnostic interview as: having chronic PTSD (PTSD at both time points; n = 174); being trauma-exposed (trauma exposure at first time point but no PTSD; n = 174); and being unexposed (no trauma exposure at either time point; reference group for all analyses; n = 173). Linear mixed models examined associations of trauma and PTSD status with log-transformed aldosterone levels, adjusting for covariates and health-related variables that may confound or lie on the pathway between PTSD and altered aldosterone levels.
Across the sample, mean aldosterone concentration decreased over time. Adjusting for covariates, women with chronic PTSD had significantly lower aldosterone levels averaged over time, compared to women unexposed to trauma (β = - 0.08, p = 0.04). Interactions between trauma/PTSD group and time were not significant, indicating change in aldosterone over time did not differ by trauma/PTSD status. Post-hoc exploratory analyses suggested that menopausal status partially mediated the relationship between chronic PTSD status and aldosterone level, such that postmenopausal status explained 7% of the effect of PTSD on aldosterone.
These findings indicate that PTSD is associated with lower levels of aldosterone. Further work is needed to understand implications of this type of dysregulation in a key biological stress system for cardiovascular and other health outcomes previously linked with PTSD.
创伤后应激障碍（PTSD）与心血管风险增加有关，但潜在机制尚未完全明确。PTSD 与应激相关激素有关，包括糖皮质激素活性失调。醛固酮的失调，一种由心理应激激活并与心血管损伤有关的盐皮质激素，可能是将 PTSD 与心血管风险联系起来的相关途径。迄今为止，很少有研究评估 PTSD 与醛固酮之间的关系，且没有一项研究对醛固酮进行重复测量。我们研究了创伤和 PTSD 是否与创伤未暴露女性相比，与改变的醛固酮水平有关。
在护士健康研究 II 中，对 521 名中年女性进行了创伤暴露和慢性 PTSD 与血浆醛固酮水平之间关系的研究。在 10-16 年的时间里两次评估醛固酮水平，创伤暴露和 PTSD 也是两次时间点的评估。关于暴露评估，女性通过结构化诊断访谈来确定：患有慢性 PTSD（两次时间点都患有 PTSD；n=174）；有创伤暴露史（第一次时间点有创伤暴露但没有 PTSD；n=174）；和未暴露（两个时间点都没有创伤暴露；所有分析的参考组；n=173）。线性混合模型通过调整混杂或位于 PTSD 和改变的醛固酮水平之间的路径的健康相关变量，来研究创伤和 PTSD 状态与经对数转换的醛固酮水平之间的关联。
在整个样本中，平均醛固酮浓度随时间下降。调整混杂因素后，与未暴露于创伤的女性相比，患有慢性 PTSD 的女性平均醛固酮水平显著降低（β=-0.08，p=0.04）。创伤/PTSD 组与时间之间的交互作用不显著，表明随着时间的推移，醛固酮的变化没有因创伤/PTSD 状态而不同。事后探索性分析表明，绝经状态部分解释了慢性 PTSD 状态和醛固酮水平之间的关系，即绝经状态解释了 PTSD 对醛固酮影响的 7%。
这些发现表明 PTSD 与较低水平的醛固酮有关。需要进一步的工作来了解这种生物应激系统中失调的类型对心血管和其他以前与 PTSD 相关的健康结果的影响。
