What sleep abnormalities are associated with abnormal glucose metabolism?
Snoring, sleep duration, and OSA have all been linked to hyperglycemia and T2DM risk.
a. Interestingly just snoring , in nonobese Asians and especially in those who are obese, has been independently associated with abnormal oral glucose tolerance tests and higher hemoglobin A 1c (HbA 1c ) levels.
b. In epidemiologic studies, sleep duration has been both negatively and positively correlated with the risk of developing T2DM. Observational studies have shown that patients who report < 6 hours of sleep per night have an increased prevalence of glucose intolerance and T2DM. Very recently, it was found that the duration of sleep (< 6 and > 8 hours per night) was predictive of an increased incidence of T2DM.
c . OSA , as diagnosed with PSG, is independently associated with abnormal glucose metabolism. A recent study extends this independent association through rigorous assessment of the potential confounders of overweight/obesity. In this cross-sectional analysis of 2588 patients, it was shown that impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and occult diabetes are associated (but to different degrees) with OSA in both the normal-weight (BMI < 25 kg/m 2 ) and overweight/obese subgroups. This suggests that individuals with OSA are at special risk for T2DM. Importantly, sleep fragmentation and hypoxemia are likely OSA culprits leading to hyperglycemia. A 2009 study comparing subjects without diabetes who had OSA with patients without diabetes who had mild, moderate, and severe OSA showed 27%, 37%, and 44% decreases, respectively, in insulin sensitivity caused by OSA; this contribution to reduced insulin sensitivity was found to be independent of age, gender, ethnicity, and percent body fat. Furthermore, there were no increases in insulin concentrations. Unfortunately, at present the relative contributions of sleep restriction, sleep fragmentation, and hypoxia cannot be ascertained. The risk of hyperglycemia is likely proportional to OSA severity; data from diverse patient populations suggest that OSA severity is a risk for T2DM development. The prevalence of OSA in patients with T2DM is 60% to 80% based on an evaluation of 12 clinic or community-based cohorts from 2003 to 2016. The prevalence of T2DM in patients with OSA is reported to be 15% to 30%.