Genetic and Environmental Associations Between Objective Sleep and Weight Indicators in 8-year-old Twins

Previous research has established associations between sleep and weight indictors (e.g., body mass index [BMI]; Gregory et al., 2006). For example, twin studies suggest that sleep indicators may be as high as 70% heritable,... [ view full abstract ]

Previous research has established associations between sleep and weight indictors (e.g., body mass index [BMI]; Gregory et al., 2006). For example, twin studies suggest that sleep indicators may be as high as 70% heritable, and BMI between 60 and 70% heritable in middle childhood (Fernandez et al., 2012; Maes et al., 1997). One adult twin study found that associations between self-reported sleep duration and BMI may be accounted for by environmental effects rather than shared genetics (Watson et al., 2010). However, it is unclear whether objective sleep indicators (sleep duration, efficiency) are associated with objective weight indicators in children (BMI, waist circumference, and percent body fat), and the extent to which these associations may be genetic or environmental.

The sample included 203 twin pairs (28.6% MZ, 37.6% same-sex DZ, 33.5% opposite-sex DZ; 54.4% Caucasian, 26.1% Hispanic; M_age = 8.5 years) drawn from the Arizona Twin Project (Lemery-Chalfant et al., 2013). Objective sleep indicators were collected using wrist-based accelerometers (Ambulatory Monitoring Inc.). Weight and percent body fat measurements were collected at home visits using a Tanita scale with bioelectrical impedance, and waist circumference was collected using Gulick tape measures. BMI was computed using height and weight, accounting for age and sex. Bivariate models were fit in OpenMx after regressing out the effects of age and sex. Phenotypic correlations between sleep duration/efficiency and weight ranged from .18-.23. Heritability for sleep ranged from .47 to .50, and from .90 to .91 for weight indicators. Thus, the best fitting model for all bivariate models was an ACE-AE model, with no reduction in model fit. Covariance between sleep duration and all weight indicators were primarily accounted for by shared additive genetic factors. For sleep duration models, shared additive genetics accounted for 8% of the variance in BMI, 7% of the variance in waist circumference, and 11% of the variance in percent body fat . In sleep efficiency models, shared additive genetics accounted for 9% of the variance in BMI, 8% of the variance in waist circumference, and 10% of the variance in percent body fat. Future studies should test possible environmental moderators of genetic associations between sleep and weight.

References

Fernandez, J. R., Klimentidis, Y. C., Dulin-Keita, a, & Casazza, K. (2012). Genetic influences in childhood obesity: recent progress and recommendations for experimental designs. International Journal of Obesity, 36(4), 479–484.

Gregory, A. M., Rijsdijk, F. V., & Eley, T. C. (2006). A twin-study of sleep difficulties in school-aged children. Child Development, 77(6). 1668-1679.

Lemery-Chalfant, K., Clifford, C., McDonald, K., O’Brien, T. C., Valiente, C. (2013). Arizona twin project: A focus on early resilience. Twin Research and Human Genetics, 16(1), 404-411.

Maes, H. M. H., Neale, M. C., & Eaves, L. J. (1997). Genetic and environmental factors in relative body weight and human adiposity. Behavior Genetics, 27(4), 325–348.

Watson, N. F., Buchwald, D., Vitiello, M. V., Noonan, C., & Goldberg, J. (2010). A twin study of sleep duration and body mass index. Journal of Clinical Sleep Medicine, 15(6), 11-17.