Abstract
Introduction: Chronic stress conditions associate with a greater incidence of hypertension (HTN). Hypothesis: We tested whether genetic risk for or neurobiological features of vulnerability to chronic stress associate with the risk for and timing of HTN. Methods: Data were obtained from Mass General Brigham Biobank participants. HTN was defined as > 2 International Classification of Disease codes at least one week apart. Those with secondary HTN and those diagnosed at age <18 years were excluded. Of this parent dataset, a validated polygenic risk score for neuroticism reflecting stress sensitivity (ssPRS) was assessed in 11,320 participants. Of the same parent dataset, stress-related neural network activity (SNNA), defined as a ratio of amygdalar to regulatory medial prefrontal cortical activity, was measured in 867 individuals who had undergone clinical 18 F-flurodeoxyglucose positron emission tomography imaging. Results: In the genetic subgroup, the median age [interquartile range] of participants was 60 [34-86] years and 56.3% were female. In a Cox regression model, standardized ssPRS predicted incident HTN (hazard ratio [95% confidence interval (CI)]: 1.05 [1.02, 1.08], p<0.001), when adjusted for principal components, age, and sex (Figure 1A). Similarly, standardized SNNA predicted incident HTN (1.44 [1.11, 1.85], p = 0.006) when adjusted for age and sex. The age of onset of HTN was significantly lower in those with high vs. low ssPRS (difference (years) [95% CI]: -1.65 (-2.45, -0.85], p < 0.001) and in those with high vs. low SNNA (-4.67 [-7.68, -1.66], p = 0.002, Figure 1B) in unadjusted models with findings of a similar magnitude and significance in multivariable models. Conclusions: This study identifies genetic and neurobiological factors linking chronic stress to HTN risk and its age of onset. Future studies should evaluate whether therapies targeting this neurobiological pathway may reduce HTN risk.
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