Differential Impact of Stress Reduction Programs upon Ambulatory Blood Pressure among African American Adolescents: Influences of Endothelin-1 Gene and Chronic Stress Exposure
Stress-activated gene × environment interactions may contribute to individual variability in blood pressure reductions from behavioral interventions. We investigated effects of endothelin-1 (ET-1) LYS198ASN SNP and discriminatory stress exposure upon impact of 12-week behavioral interventions upon ambulatory BP (ABP) among 162 prehypertensive African American adolescents. Following genotyping, completion of questionnaire battery, and 24-hour ABP monitoring, participants were randomized to health education control (HEC), life skills training (LST), or breathing awareness meditation (BAM). Postintervention ABP was obtained. Significant three-way interactions on ABP changes indicated that among ET-1 SNP carriers, the only group to show reductions was BAM from low chronic stress environments. Among ET-1 SNP noncarriers, under low chronic stress exposure, all approaches worked, especially BAM. Among high stress exposure noncarriers, only BAM resulted in reductions. If these preliminary findings are replicated via ancillary analyses of archival databases and then via efficacy trials, selection of behavioral prescriptions for prehypertensives will be edging closer to being guided by individual's underlying genetic and environmental factors incorporating the healthcare model of personalized preventive medicine. 1. Introduction Essential hypertension (EH) is a major risk factor for cardiovascular disease (CVD), and EH incidence among youth is increasing [1]. African Americans (AAs) experience a higher prevalence, earlier onset, and greater severity of EH-related complications than other ethnic groups [2]. From late childhood onward, AAs display increased levels of resting and ambulatory blood pressure (ABP) compared to other ethnic groups [3–5]. BP levels are monotonically associated with future CVD morbidity and mortality [6]. Stage I prehypertensive adults (i.e., SBP/DBP 121–129/81–84？mmHg) have a 40% increased risk and adults with stage II prehypertension (i.e., SBP/DBP 130–139/85–89？mmHg) are twice as likely to develop CVD compared to those with optimal BP (<120/<80？mmHg) [6–8]. BP percentile ranking tracks from late childhood into adulthood [9–11] placing AA adolescents with BP between the 50th and 95th percentiles for age and sex at an increased risk of future EH and CVD development [9]. EH, like other multifactorial chronic diseases, results from a complex interplay between an individual’s genetic underpinnings, lifestyle behaviors, psychosocial factors, and exposures to various environmental toxins. Over time, this dynamic interplay eventuates in adverse
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