Sugar is Sweet, but Snoring is Boring

Abstract & Commentary

Comment by Barbara A. Phillips, MD, Professor of Medicine, University of Kentucky; Director, Sleep Disorders Center, Samaritan Hospital, Lexington, KY; Associate Editor, Internal Medicine Alert.

Synopsis: Sleep apnea can exacerbate diabetes, and Continuous Positive Airway Pressure (CPAP) can improve glucose control in diabetic patients with sleep apnea.

Source: Babu AR, et al. Arch Intern Med. 2005;165:447-452.

This study included 25 patients who had type 2 diabetes and sleep apnea. Their mean age was 50.7 years, and 16 of the 25 patients were men. They were recruited from a sleep clinic, and had fairly severe sleep apnea, with mean Apnea Plus Hypopnea Indices of 56 events/hr, mean lowest oxygen saturations of 76%, and mean Epworth Sleepiness Scores of 14 (normals for these variables are < 5 events/hr, > 90%, and < 10). Their diabetes was also fairly longstanding and severe; their mean baseline hemoglobin A1C’s were 8.3%, Body Mass Indices were 42.7 kg/m2, and duration of diabetes was 8.3 years. Seventeen of these patients used oral agents, 4 used insulin, and 4 required both oral agents and insulin. After recruitment, participants underwent baseline testing of glucose, HbA1c, food diaries, and 72-hour continuous glucose monitoring. They also had standard in-laboratory polysomnography (sleep studies) and completed questionnaires. Patients were then treated with continuous positive airway pressure for at least 3 months. Half of the patients were compliant with CPAP, defined as use for an average of 4 hours/night. These patients tended to be heavier and male. One-hour post-meal glucose values were significantly lower after all 3 meals for those who were compliant with CPAP, but only after breakfast for the noncompliant group. HbA1C was significantly reduced for the 17 participants with an initial level greater than 7%; there was a highly significant correlation between HbA1c improvement and the number of days of CPAP use in the compliant group, but not in the noncompliant group. Fasting glucose levels fell for the group as a whole, but the change was not significant. There was a significant reduction in the number of glucose values greater than 200 mg/dL in the entire study population.


We have known for awhile that sleep disturbance and sleep apnea are associated with an increased risk of glucose intolerance and insulin resistance.1-4

Full-blown sleep apnea is not necessary in order to develop glucose intolerance or insulin resistance. In fact, snoring5 and sleep deprivation6 are associated with disruption in glucose homeostasis. In clinical practice, the relationship between sleep and glucose control is obviously most relevant for patients with diabetes. Most recently, Harsch et al demonstrated a rapid improvement in insulin responsiveness in 40 sleep apnea patients who were treated with CPAP, but not all of these patients were diabetics.7 The current study advances our understanding of the relationship between sleep apnea and diabetes because all of the patients studied were diabetic, and because Babu and colleagues were able to measure CPAP compliance. Strong correlations between compliance and outcome have been reported in other studies of the benefits of CPAP. For example, Pepperell8 and Becker9 demonstrated that 4 or 5 hours (respectively) of CPAP use was necessary to lower blood pressure in patients with sleep apnea. The proven benefits of CPAP continue to accrue. Although it is burdensome treatment, it is highly effective treatment for patients who can comply. Reminding patients that effective CPAP use can help improve glucose control and blood pressure should become part of our management of the fast-growing segment of the population who have both the Metabolic Syndrome and sleep apnea.10


1. Brooks B, et al. J Clin Endocrinol Metab. 1994;79: 1681-1685.

2. Stoohs RA, et al. Am J Respir Crit Care Med. 1996; 154:170-174.

3. Vgontzas AN, et al. J Clin Endocrinol Metab. 2000; 85:1151-1158.

4. Ip MS, et al. Am J Respir Crit Care Med. 2002;165: 670-676.

5. Al-Delaimy WK, et al. Am J Epidemiol. 2002;155: 387-393.

6. Scheen AJ, Van Cauter E. Horm Res. 1998;49:191-201.

7. Harsch I, et al. Am J Respir Crit Care Med. 2004;169: 156-162.

8. Pepperell JCT, et al. Lancet. 2002;359:204-214.

9. Becker HF, et al. Circ. 2003;107:68-78.

10. Coughlin SR, et al. Eur Heart J. 2004;25(9):735-741.