Abstract

ObjectiveTo assess the distribution of autonomic nervous system (ANS) dysfunction in overweight and obese children.MethodsParasympathetic and sympathetic ANS function was assessed in children and adolescents with no evidence of impaired glucose metabolism by analysis of heart rate variability (low frequency power ln(LF), high frequency power, ln(HF); ln(LF/HF) ratio, ratio of longest RR interval during expiration to shortest interval during inspiration (E/I ratio), root mean square of successive differences (RMSSD); sympathetic skin response (SSR); and quantitative pupillography (pupil diameter in darkness, light reflex amplitude, latency, constriction velocity, re-dilation velocity). The relationship of each ANS variable to the standard deviation score of body mass index (BMI-SDS) was assessed in a linear model considering age, gender and pubertal stage as co-variates and employing an F-statistic to compare the fit of nested models. Group comparisons between normal weight and obese children as well as an analysis of dependence on insulin resistance (as indexed by the Homeostasis Model Assessment of Insulin Resistance, HOMA-IR) were performed for parameters shown to correlate with BMI-SDS. Statistical significance was set at 5%.ResultsMeasurements were performed in 149 individuals (mean age 12.0 y; 90 obese 45 boys; 59 normal weight, 34 boys). E/I ratio (p = 0.003), ln(HF) (p = 0.03), pupil diameter in darkness (p = 0.01) were negatively correlated with BMI-SDS, whereas ln(LF/HF) was positively correlated (p = 0.05). Early re-dilation velocity was in trend negatively correlated to BMI-SDS (p = 0.08). None of the parameters that depended significantly on BMI-SDS was found to be significantly correlated with HOMA-IR.ConclusionThese findings demonstrate extended ANS dysfunction in obese children and adolescents, affecting several organ systems. Both parasympathetic activity and sympathetic activity are reduced. The conspicuous pattern of ANS dysfunction raises the possibility that obesity may give rise to dysfunction of the peripheral autonomic nerves resembling that observed in normal-weight diabetic children and adolescents.

Highlights

  • Obesity has reached global epidemic proportions [1] with prevalence remaining high, despite some evidence of stabilisation [2]

  • Out of 95 obese children, 5 had to be excluded due to impaired glucose metabolism, which is in line with previously published prevalence rates of impaired glucose tolerance among children and adolescents with marked obesity [25]

  • Within the obese study group, 7 candidates (6.3%) presented with elevated blood pressure measurements according to the recommendations of the American Heart Association [26], candidates (15.3%) had elevated serum ASAT serum levels, candidates (16.2%) had one pathological lipid measures, 5 candidates (4.5%) had 2 pathological lipid measures, none of the obese candidates had more than 3 pathological lipid findings, and 6 obese candidates presented with hyperuricaemia (5.4%)

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Summary

Introduction

Obesity has reached global epidemic proportions [1] with prevalence remaining high, despite some evidence of stabilisation [2]. Because dysfunction of the autonomic nervous system (ANS) may contribute to development or stabilization of obesity and is associated with cardiovascular mortality [4], the study of ANS function in obesity is of considerable clinical interest. Most previous studies of ANS function in obese children have been limited to investigations of cardiac autonomic function through analysis of heart rate variability. These studies have generally revealed a decrease in parasympathetic activity. It remains unclear, whether abnormalities of ANS can be found in the sympathetic nervous system, and outside of the cardiac autonomic nerve function in overweight and obese children and adolescents

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