Abstract MP26: Visceral Obesity and Systemic Inflammation Predict Sleep Disordered Breathing in Normal Weight, Never Obese Adolescents: A Longitudinal, Population-Based Study

Abstract

Introduction: Although obesity is a known risk factor for sleep disordered breathing (SDB), a significant proportion of children with SDB are not obese or overweight as per body mass index percentile (BMI%) for age-and-sex. It is unknown whether premorbid or concurrent adiposity phenotypes are associated with SDB in normal weight youth. Hypothesis: We hypothesize that central obesity is a predictor of apnea/hypopnea index (AHI) in adolescents who have been otherwise normal weight since childhood. Methods: We analyzed data from the Penn State Child Cohort (N=421), a random population-based sample of 8.7 (1.7) year old children followed-up as 17.0 (2.3) year old adolescents. Of these, 242 subjects (49.2% female, 18.2% minority) were classified as persistently normal weight based on BMI%<85 at both baseline and follow-up. Neck, hip and waist circumference (WC) were measured and “central obesity” was defined as a WC%≥85 for age-and-sex at baseline. During the follow-up exam, android and gynoid distribution and subcutaneous (SAT) and visceral (VAT) adipose tissue composition were assessed via DEXA scan, while inflammatory biomarkers were assayed from a fasting blood sample. The AHI was obtained from 9-hour, in-lab polysomnography at baseline and follow-up. Multivariable linear regression models examined the association between adiposity and inflammation with AHI at follow-up while adjusting for sex, race, adenotonsillectomy, age and AHI at baseline. Results: The average AHI at baseline was 0.7 (0.9) events/hour and 2.3 (6.3) events/hour at follow-up. Unadjusted analyses showed that WC (β=0.159) and central obesity (β=0.227) at baseline, but not BMI%, neck or hip circumference, and VAT (β=0.307), IL-6 (β=0.245), SAT (β=0.235), CRP (β=0.222), and android distribution (β=0.195) at follow-up were significantly (P<0.05) associated with a higher follow-up AHI. Multivariable-adjusted analyses showed that VAT (β=0.299), IL-6 (β=0.191), central obesity (β=0.185) and CRP (β=0.163) were independently associated with a higher follow-up AHI. Conclusions: This is the first study to demonstrate that central obesity in childhood is a strong predictor of SDB in adolescence, even in individuals who have been persistently normal weight since childhood as per BMI% standards. These data support the clinical utility of simple measures of central obesity in childhood (i.e., WC) as early surrogate markers of increased risk of future development of SDB in the transition to adolescence. Furthermore, our study demonstrates that increased visceral adiposity and systemic inflammation are strong correlates of adolescent SDB, which supports the clinical utility of these biomarkers in predicting the cardiometabolic risk associated with adolescent SDB.