Abstract MP56: Sleep Regularity Modifies The Association Of Visceral Adiposity With Elevated Blood Pressure In Adolescents

Abstract

Introduction: Although obesity, insufficient sleep and sleep apnea are known risk factors for elevated blood pressure, the circadian timing of sleep is also involved in metabolic and blood pressure regulation. As a result, sleep irregularity, which is highly prevalent in adolescents, may be a potential risk factor for obesity-related adverse cardiovascular outcomes. Hypothesis: We hypothesize that greater sleep irregularity increases the impact of visceral adiposity on elevated blood pressure in adolescents. Methods: We analyzed cross-sectional data from the Penn State Child Cohort follow-up study, a random population-based sample of 303 adolescents (16.2 ± 2.2 year old; 47.5% female; 21.5% racial/ethnic minority) who had complete at-home 7-night (at least 5) actigraphy (ACT) data and in-lab dual-energy X-ray absorptiometry (DEXA) scan and polysomnography (PSG) data. ACT-measured sleep duration and sleep midpoint were calculated as the intra-individual mean of the 7-night total sleep time and the midpoint (zeroed to midnight) of the sleep period, respectively. ACT-measured sleep regularity was calculated as the intra-individual standard deviation of the 7-night sleep midpoint. DEXA-measured visceral adipose tissue (VAT) was the primary predictor. Systolic (SBP) and diastolic (DBP) blood pressure, measured three times in the seated position, were the primary outcomes. Multivariable linear regression models tested sleep midpoint and sleep regularity as effect modifiers of VAT on SBP/DBP levels, while simultaneously adjusting for sex, race/ethnicity, age, ACT-measured sleep duration and PSG-measured apnea/hypopnea index. Results: Significant interactions were found between sleep regularity and VAT on SBP (p-interaction=0.009) and DBP (p-interaction=0.039), while not between mean sleep midpoint and VAT (p-interactions=0.210 and 0.883). These findings remained valid even after further adjusting for body mass index percentile (p-interactions=0.006 and 0.034). Among adolescents with high sleep irregularity (≥ 45 minutes; n=124), each standard deviation increase in VAT was associated with a 5.55 (0.91) and 3.07 (0.70) mmHg increase in SBP and DBP, respectively (both p<0.001). Among those with low sleep irregularity (< 45 minutes; n=179) VAT was not significantly associated with SBP [0.69 (0.99), p=0.488] or DBP [0.04 (0.77), p=0.956]. Conclusions: An irregular circadian timing of sleep may increase the impact of visceral adiposity on elevated blood pressure in adolescents. These data support that sleep irregularity, independent of sleep apnea and insufficient sleep, may contribute to the development of cardiovascular sequelae associated with central obesity.