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Abstract
Objective: To assess the distribution of autonomic nervous system (ANS) dysfunction in overweight and obese children.
Methods: Parasympathetic 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%.
Results: Measurements 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.
Conclusion: These 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.