Sleep time of seven hours and 18 minutes is linked to lower risk of pre-diabetes

 Analysis of more than 23,000 adults has identified an optimal nightly sleep duration associated with improved glucose metabolism, while excessive weekend catch-up sleep may undermine metabolic health in some groups 

Sleeping for seven hours and 18 minutes each night may represent an optimal threshold to reduce the risk of insulin resistance, a metabolic disturbance that precedes type 2 diabetes (T2DM), according to a large observational study.

The analysis has also indicated that weekend catch-up sleep may confer metabolic benefit for those who sleep too little during the working week but can also be associated with impaired glucose regulation in those who already exceed the apparent optimal duration.

Researchers have long recognised a close association between sleep duration and metabolic health. Both short and prolonged sleep have been linked to insulin resistance, T2DM and related cardiometabolic disorders. Yet uncertainty has remained as to whether compensatory weekend sleep modifies these risks.

To explore this question, investigators examined data from 23,475 adults aged between 20 and 80 years who participated in serial waves of the US National Health and Nutrition Examination Survey between 2009 and 2023. Of these, 10,817 had complete data on weekend sleep duration. The US National Health and Nutrition Examination Survey is a long-running programme in the USA that assesses health and nutritional status through interviews and clinical measurements.

The team used ‘estimated glucose disposal rate’ as a surrogate marker for insulin resistance. This metric derives from a formula that incorporates waist circumference, fasting blood glucose and blood pressure. Lower values of estimated glucose disposal rate, such as less than 6 to 7 milligrams per kilogram per minute, indicate a higher likelihood of insulin resistance. Higher values, such as more than 10 milligrams per kilogram per minute, suggest lower risk.

Across the cohort, the mean estimated glucose disposal rate was 8.23 milligrams per kilogram per minute. On weekdays, participants reported an average sleep duration of seven hours and 30 minutes. Just more than 48 per cent reported some degree of weekend catch-up sleep. Among those with weekend data, average weekend sleep reached eight hours.

Weekend catch-up sleep fell into four categories:

• no catch-up sleep
• up to one hour
• one to two hours
• more than two hours.

Statistical modelling revealed an inverted U-shaped association between weekday sleep duration and estimated glucose disposal rate. The peak of this curve, which represented the most favourable metabolic profile, corresponded to seven hours and 18 minutes of nightly sleep.

Below this threshold, longer sleep during the week associated with higher estimated glucose disposal rate, which implies improved insulin sensitivity. Above this threshold, additional sleep associated with lower estimated glucose disposal rate, particularly among women and among adults aged 40 to 59 years.

Further analysis suggested that for individuals who slept less than the optimal duration during the week, one to two hours of weekend catch-up sleep associated with a higher estimated glucose disposal rate compared with no catch-up sleep. In contrast, for those who already exceeded the optimal weekday duration, more than two hours of weekend catch-up sleep associated with a lower estimated glucose disposal rate after adjustment for lifestyle factors, ethnicity, marital status and educational attainment.

“Importantly, there appears to be a bidirectional relationship between sleep and metabolism. For instance, poor glycaemic status itself has been linked to a higher likelihood of both short and extended sleep durations, as well as sleep disorders,” the researchers wrote.

“This creates a potential vicious cycle wherein metabolic dysregulation disrupts normal sleep patterns, and the resultant abnormal sleep, including extended duration, further aggravates metabolic health,” they added.

As an observational study, the analysis cannot establish cause and effect. The authors acknowledged reliance on self-reported sleep duration and the possibility of reverse causation, in which altered glucose metabolism influences sleep patterns rather than sleep disturbance driving metabolic dysfunction.

Nevertheless, the findings have suggested that sleep duration, and in particular weekend recovery sleep, may have relevance for metabolic regulation in people with or at risk of diabetes. The investigators concluded that such correlational evidence could inform clinical consideration of sleep habits as part of comprehensive metabolic care.

The results reinforce a wider body of evidence that sleep is not a passive state but an active regulator of endocrine and metabolic processes.

For further reading please visit: 10.1136/bmjdrc-2025-005692