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01-02-2015 | Empirical Research | Uitgave 2/2015

Journal of Youth and Adolescence 2/2015

Autonomic Dysfunction: A Possible Pathophysiological Pathway Underlying the Association Between Sleep and Obesity in Children At-Risk for Obesity

Tijdschrift:
Journal of Youth and Adolescence > Uitgave 2/2015
Auteurs:
Denise C. Jarrin, Jennifer J. McGrath, Paul Poirier, QUALITY Cohort Collaborative Group
Belangrijke opmerkingen
The QUALITY (QUebec Adipose and Lifestyle InvesTigation in Youth) Cohort Collaborative Group is an inter-university research team from Université de Montréal, Concordia University, Université Laval, McGill University, and University of Toronto including (alphabetical): Tracie A. Barnett, Arnaud Chiolero, Vicky Drapeau, Josée Dubois, Katherine Gray-Donald, Melanie Henderson (PI), Marie Lambert (posthumous), Émile Lévy, Marie-Eve Mathieu, Katerina Maximova, Jennifer J. McGrath, Belinda Nicolau, Jennifer O’Loughlin, Gilles Paradis, Paul Poirier, Catherine M. Sabiston, Angelo Tremblay, and Michael Zappitelli.

Abstract

While mounting evidence suggests that sleep plays an important role in the etiology of obesity, the underlying pathogenic pathways are complex and unresolved. Experimental sleep deprivation studies demonstrate sympathovagal imbalance, indicative of diminished parasympathetic activity and/or heightened sympathetic activity, is consequent to poor sleep. Further, obese children exhibit sympathovagal imbalance, particularly during the night, compared to non-obese children. The question remains whether sympathovagal imbalance is one potential pathophysiological pathway underlying the association between sleep and obesity. The aim of the present study was to examine whether sympathovagal imbalance contributed to the association between sleep and obesity in children. Participants included 564 children aged 10 to 12 years (M = 11.67, SD = 0.95; 43.5 % girls) from the QUALITY Cohort, a longitudinal study of children at-risk for the development of obesity. While children were at-risk due to confirmed parental obesity status, 57.7 % of children were of normal body mass index (5–85th percentile). Sleep duration, sleep timing, and sleep disturbances were based on child- and parent-report. Anthropometrics were measured for central adiposity (waist circumference) and body composition (body mass index, fat mass index). Sympathovagal imbalance was derived from heart rate variability spectral analyses. Estimated path coefficients revealed that sympathovagal imbalance partially contributed to the association between poor sleep (later bedtimes, sleep-disordered breathing) and obesity. These findings highlight the importance of better understanding sympathovagal imbalance and its role in the etiology and maintenance of obesity. Future research should consider investigating nocturnal sympathovagal balance in youth.

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