Associations Between Blood Pressure and Accelerated DNA Methylation Aging

Abstract

Background Individuals of the same chronological age may exhibit diverse susceptibilities to death. However, few studies have investigated the associations between blood pressure and the accelerated aging. Methods and Results A cross‐sectional study was conducted in 288 adults aged ≥50 years. We assessed the DNA methylation‐based measures of biological age using CpG sites on the Illumina HumanMethylationEPIC BeadChip. Epigenetic age acceleration metrics were derived by regressing residuals (ΔAge) and ratios (aging rate) of DNA methylation age on chronological age. Dose‐response relationships between blood pressure and epigenetic age acceleration were quantified using multiple linear regression and restricted cubic regression models. We found that each 10–mm Hg increase in systolic blood pressure was associated with 0.608 (95% CI, 0.231–0.984) years increase in ΔAge and 0.007 (95% CI, 0.002–0.012) increase in aging rate; meanwhile, for pulse pressure, the increase was 1.12 (95% CI, 0.625–1.61) years for ΔAge and 0.013 (95% CI, 0.007–0.020) for aging rate. Subgroup analysis showed that the significant associations of systolic blood pressure and pulse pressure with epigenetic age acceleration appeared to be limited to women, although interactions between blood pressure and sex were not significant ( P values for interaction >0.05). The combination of women and hypertension was associated with a much higher increase in ΔAge (β [95% CI], 4.05 [1.07–7.02]) and aging rate (β [95% CI], 0.047 [0.008–0.087]), compared with male participants without hypertension. Conclusions Our findings suggested that high systolic blood pressure and pulse pressure were associated with the epigenetic age acceleration, providing important clues for relationships between blood pressure and epigenetic aging.

Association between Serum Soluble α-Klotho and Urinary Albumin Excretion in Middle-Aged and Older US Adults: NHANES 2007–2016

“…It is undeniable that most studies have focused on mid- to end-of-life applications, and data from early-life interventions are sparse and require a more robust evaluation. Additionally, we found that elevated PP and the presence of hypertension or diabetes were potential effect modifiers as well, possibly because these states inherently accelerate senescence [ 59 , 60 ]. The enhanced senescence of renal tubules and vascular cells leads to endothelial dysfunction and impaired vasculogenesis [ 61 ], suggesting the presence of complex physiologically relevant feedback loops.…”

Alcohol consumption and epigenetic age acceleration across human adulthood

“…Moreover, two previous studies demonstrated that the alcohol use disorder was associated with Horvath’s age acceleration and PhenoAge acceleration (PAA) [ 19 , 20 ]. Hypertension, which was often linked to chronic alcohol consumption, was also found to be positively associated with Horvath’s age acceleration in the elderly [ 21 , 22 ]. The hypertensive target organ damage (e.g., higher left ventricular mass index) was also associated with Intrinsic epigenetic age acceleration (IEAA) and extrinsic epigenetic age acceleration (EEAA) in older African Americans [ 23 ].…”

Better Life’s Essential 8 contributes to slowing the biological aging process: a cross-sectional study based on NHANES 2007–2010 data

“…Blood pressure exhibits alterations with advancing age, generally characterized by an increase in systolic pressure while diastolic pressure remains stable or even reduces, potentially associating these periodic dynamic changes in blood pressure with biological aging. Research by Xiao et al ( 57 ) disclosed that higher systolic and pulse pressures are related to accelerated epigenetic aging. Dintica et al ( 58 ) proposed that elevated blood pressure during middle age associates with premature brain aging.…”