We appreciate Dr. Kawada’s comments (1) on our study demonstrating that 6 weeks of mild sleep restriction (SR) adversely affected insulin sensitivity compared with maintenance of adequate habitual sleep in women (2). Dr. Kawada reiterates the constraints of the trial noted in the Discussion section of the article. Here, we expand upon these points.

We agree with Dr. Kawada that the relationship between chronic insufficient sleep and type 2 diabetes (T2D) is complex. The findings of our trial expand our understanding of the impact of short sleep on T2D risk by establishing a causal relationship between prolonged, mildly short sleep, an ecologically valid representation of chronic insufficient sleep, and prominent risk factors for T2D in women. However, the study cannot confirm that short sleep directly causes T2D. Indeed, to draw such a conclusion would be neither feasible nor ethical in the context of a human clinical trial. Observational studies, however, clearly and consistently demonstrate elevated T2D incidence in adults with habitual short versus adequate sleep under free-living circumstances (35).

We further agree with Dr. Kawada’s postulation that other factors, such as adiposity, sex hormones, and comorbid insomnia, could influence the relationship between chronic short sleep and T2D risk. To the degree possible, we aimed to isolate the effect of sleep duration on glucose metabolism by 1) employing a crossover design for within-person comparisons under different sleep conditions, 2) evaluating the effects of sleep condition on within-person changes in outcomes separately in pre- and postmenopausal women, 3) applying gold-standard measures of adiposity and systematically testing for a mediating role of adiposity changes in the effects of sleep restriction on outcomes (null) and then controlling for adiposity changes in statistical models, and 5) enrolling individuals who had habitual adequate sleep and no concomitant sleep disorder, including insomnia and obstructive sleep apnea. Nevertheless, we acknowledge that other factors may contribute to, or exacerbate, risk for T2D as a consequence of reduced sleep duration. For example, our study results highlight a more marked adverse impact of sleep restriction on insulin sensitivity in postmenopausal compared with premenopausal women, suggesting a role for sex hormones in the deleterious effects of insufficient sleep. As we described in our article, elucidation of mediators and moderators of the effects observed in our study is of great scientific interest. Similarly, identification of individual differences in the response to perturbations in sleep duration could have important clinical implications.

Finally, Dr. Kawada’s commentary underscores an avenue of future research that we strongly endorse: systematic evaluation of the feasibility and efficacy of improving sleep to prevent cardiometabolic disease and promote health. Clinical trials testing interventions to improve sleep health among individuals with existing sleep deficits are desperately needed. These interventions should be applied to populations with, or at elevated risk for, T2D to determine whether insulin sensitivity is improved by ameliorating sleep health. Only findings from such studies can inform public health guidance to reduce T2D risk in those with poor sleep health.

Funding. M.P.S.-O. receives support from National Institutes of Health (NIH), National Heart, Lung, and Blood, grants R01HL128226, R01DK128154, and R35HL155670. F.M.Z. is supported by NIH grant R01DK128154. B.L. is supported by NIH, National Institute on Aging, grant R01AG065569 and NIH, National Institute of Diabetes and Digestive and Kidney Disease, grants P30DK063608 and R01DK128154. S.J. is supported by NIH grants R01HL106041 and R01HL137234. B.A. is supported by American Heart Association grant AHA811531.

The funding sources were not involved in this letter.

Duality of Interest. No potential conflicts of interest relevant to this article were reported.

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