Lack of impairment in glucose tolerance: support for further investigation of sleep restriction in older long sleepers

Dear Sir We thank Drs Knutson and Leproult for their interest in our paper. This response allows us to further clarify our rationale and findings. Because long sleep is associated with increased mortality (indeed, with more excess mortality than short sleep), our longterm goal is to test the hypothesis that voluntary restriction of time in bed (TIB) or total sleep time (TST) could improve the survival of those with long sleep (Youngstedt and Kripke, 2004). If sleep restriction improved survival among those with long sleep, it could potentially prolong survival for millions. Before a major long-term trial can be planned, much pilot work is needed. The immediate goal of our pilot study (Zielinski et al., 2008; Youngstedt et al., 2009) was to explore whether the TIB of long sleepers could be restricted without excessive adverse effects that would preclude a large-scale long-term trial of sleep restriction. If long sleep was a consequence of sleep apnea or other ill health, sleep restriction might make acute symptoms so much worse that sleep restriction could not be maintained safely. Because virtually all epidemiological studies reporting associations of long sleep with mortality ⁄morbidity have defined sleep duration based on self-reports, we similarly selected long sleepers based on self-reports. Participants in our study overestimated their TST compared to objective assessment, but this was consistent with other recent data indicating similar overestimation of TST (approximately 1 h) in large population cohorts (Lauderdale et al., 2008; Silva et al., 2007). In our study, the participants objective TST was approximately 60 min longer than age-matched normative data and 30 min longer than normative data for young adults (Ohayon et al., 2004). So, the participants were, indeed, long sleepers as defined both by objective and epidemiological criteria. Contrary to speculation by Knutson and Leproult, our sample did not have poor glucose tolerance or particularly poor sleep, poor health or symptoms suggestive of sleep apnea. Their glucose tolerance and insulin sensitivity were notably better than average for their ages. Baseline sleep efficiency in the sleep restriction group (83.1%) was comparable with age-matched normative data (Ohayon et al., 2004), and similar to the sleep efficiency of the young, healthy sample assessed by Spiegel et al. (1999) (85.8%). Moreover, the participants in our study reported remarkably high satisfaction with their sleep, and they had levels of sleepiness, depression, obesity, neurobehavioral performance and quality of life that were similar to or better than age-matched normative data. Consistent with our long-term goals, we were hoping that we would not find that sleep restriction would cause problems with glucose tolerance or insulin sensitivity, and we were delighted to find no significant impairment. Contrary to what was stated in the letter, we assessed glucose ⁄ insulin at 2 h post-glucose consumption, as well as at baseline. This standardized procedure is accepted widely as adequate for detecting clinically significant changes in glucose metabolism. These results will help to make a major long-term trial feasible. We agree with Drs Knutson and Leproult that there are many factors which could explain why our results do not resemble those of experimental studies restricting sleep below average amounts (see pp. 416–417 of Zielinski et al., 2008). We also agree that, based on epidemiological evidence linking sleep duration with diabetes and poor glucose tolerance, we would not necessarily predict unfavorable effects of sleep restriction for long sleepers. As there seems to be a U-shaped association of sleep duration with glucose intolerance (Gottlieb et al., 2005), there would be a rationale to hypothesize that modest sleep restriction might elicit improvement in glucose tolerance and insulin sensitivity in long sleepers, by moving their pattern towards the bottom of the U. Whether or not there are negative effects of modest chronic sleep restriction, which is a far more common experience than dramatic sleep restriction, is certainly a relevant question. Knutson and Leproult understated the degree of sleep restriction that we obtained, which was 62 min in the experimental group and 20 min in the control group. For many years, it has been argued that such a modest decrease in sleep duration is a probable culprit in the growing rates of obesity and diabetes that have been observed over the last few decades (Spiegel et al., 2005), so it was necessary to test this degree of restriction. We did not assume that we would obtain similar results to those produced experimentally with short sleep, but we had to exclude that obvious possibility. Indeed, our assumption is that modest sleep restriction for long sleepers will be safe, but this has to be proven before large-scale studies addressing the mortality issue can be undertaken. We are happy that, so far, our pilot work does not suggest that modest experimental sleep restriction for long sleepers would be unsafe (Youngstedt et al., 2009; Zielinski et al., 2008). J. Sleep Res. (2010) 19, 116–117 Letter to the Editor