STUDY OBJECTIVES: To better understand the relationships of insomnia, sleepiness, and obesity. DESIGN: Classic twin study. SETTING: A community-based twin registry in Washington State. PATIENTS OR PARTICIPANTS: One thousand forty-two monozygotic and 828 dizygotic twin pairs participating in the University of Washington Twin Registry. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Twins were, on average, 32 years old; 61% were women, and 19.5% were obese, defined as a body mass index > or = 28. Insomnia and sleepiness were endorsed by 19.3% and 3.7% of twins, respectively. Twin correlations were higher in monozygotic than dizygotic twins for insomnia (0.47 versus 0.15), sleepiness (0.37 versus 0.14), and obesity (0.82 versus 0.46). Heritability estimates were 57% for insomnia (p < .001; 95% confidence interval 47-63), 38% for sleepiness (p < .01; 95% confidence interval 16-46), and 73% for obesity (p < .001; 95% confidence interval 49-87). Multivariate genetic model fitting revealed that common additive genetic effects comprised 12.8% of the phenotypic correlation between insomnia and sleepiness (p < .01) and 10% of the phenotypic correlation between insomnia and obesity (p < .01). The phenotypic correlation between sleepiness and obesity was not due to common additive genetic effects. CONCLUSIONS: Insomnia, sleepiness, and obesity are under strong genetic influence. Common genetic effects were observed between insomnia and both sleepiness and obesity, suggesting shared genetic contributions to these phenomena.
STUDY OBJECTIVES: To better understand the relationships of insomnia, sleepiness, and obesity. DESIGN: Classic twin study. SETTING: A community-based twin registry in Washington State. PATIENTS OR PARTICIPANTS: One thousand forty-two monozygotic and 828 dizygotic twin pairs participating in the University of Washington Twin Registry. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Twins were, on average, 32 years old; 61% were women, and 19.5% were obese, defined as a body mass index > or = 28. Insomnia and sleepiness were endorsed by 19.3% and 3.7% of twins, respectively. Twin correlations were higher in monozygotic than dizygotic twins for insomnia (0.47 versus 0.15), sleepiness (0.37 versus 0.14), and obesity (0.82 versus 0.46). Heritability estimates were 57% for insomnia (p < .001; 95% confidence interval 47-63), 38% for sleepiness (p < .01; 95% confidence interval 16-46), and 73% for obesity (p < .001; 95% confidence interval 49-87). Multivariate genetic model fitting revealed that common additive genetic effects comprised 12.8% of the phenotypic correlation between insomnia and sleepiness (p < .01) and 10% of the phenotypic correlation between insomnia and obesity (p < .01). The phenotypic correlation between sleepiness and obesity was not due to common additive genetic effects. CONCLUSIONS:Insomnia, sleepiness, and obesity are under strong genetic influence. Common genetic effects were observed between insomnia and both sleepiness and obesity, suggesting shared genetic contributions to these phenomena.
Authors: Tracey L Sletten; Shantha M W Rajaratnam; Margaret J Wright; Gu Zhu; Sharon Naismith; Nicholas G Martin; Ian Hickie Journal: Sleep Date: 2013-11-01 Impact factor: 5.849
Authors: Emily J McAllister; Nikhil V Dhurandhar; Scott W Keith; Louis J Aronne; Jamie Barger; Monica Baskin; Ruth M Benca; Joseph Biggio; Mary M Boggiano; Joe C Eisenmann; Mai Elobeid; Kevin R Fontaine; Peter Gluckman; Erin C Hanlon; Peter Katzmarzyk; Angelo Pietrobelli; David T Redden; Douglas M Ruden; Chenxi Wang; Robert A Waterland; Suzanne M Wright; David B Allison Journal: Crit Rev Food Sci Nutr Date: 2009-11 Impact factor: 11.176