Genetic and environmental influences on insomnia, daytime sleepiness, and obesity in twins

To better understand the relationships of insomnia, sleepiness, and obesity.

Classic twin study.

A community-based twin registry in Washington State.

One thousand forty-two monozygotic and 828 dizygotic twin pairs participating in the University of Washington Twin Registry.

N/A.

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.

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.