Background: Type 2 diabetes is a major epidemic in the United States, with an estimated 23.6 million diabetics or 7.8% of the population according to the National Diabetic Information Clearinghouse. Obstructive Sleep Apnea is also a major epidemic affecting 4-17% of the population. Each of these disorders, independently, can lead to increased morbidity and mortality. Rapidly developing research suggests these disorders share many important factors that must be investigated further.
Purpose of Study: To determine if continuous positive airway pressure (CPAP) will improve glucose control and insulin sensitivity in diabetic patients with Obstructive Sleep Apnea (OSA).
Hypothesis: Studies have shown sympathetic activation with hypoxic episodes in sleep apnea. In addition, sleep loss has been shown to alter glucose tolerance and possibly increases insulin resistance. Will CPAP prevent hypoxic episodes thereby stopping the sympathetic activation during sleep and improve resistance and tolerance?
Study Design/Methods: Exhaustive search of available medical literature using the following search engines; Medline, Pub Med, EBMRM, CINAHL and MDconsult. The study must have been published in English and contain the following search terms; Type 2 diabetes, obstructive sleep apnea and CPAP. Due to the rapid release if research data in this area, the search was also limited to studies published in the last six years.
Results: Obstructive Sleep Apnea and type 2 diabetes have long shared one common denominator, obesity. The five studies included in this systematic review attempted to limit discussion to factors that may suggest a causal relationship between these two disorders. There was only one study that offered a randomized, double-blinded, placebo controlled study by using a sham CPAP machine and was able to weigh the results independently against a control group and subsequently raise important questions regarding the other studies. The four other studies all reported significant positive results in glycemic and insulin control when implementing CPAP. They were single arm, single center non randomized prospective studies.
Conclusion: Many cardiovascular, metabolic, endocrinological, and neurovascular variables exist that would slow or inhibit a prompt response to a therapy. Other authors noted conflicting results could be attributed to differences in sample sizes, duration of study, lack of objective adherence to data and possible changes in body composition. Only one study suggest there is no causal or therapeutic relationship between these two disorders and therefore treating OSA with CPAP will not independently affect diabetic outcomes. Previous research presented strong conclusions suggesting such a relationship however were weak in study design. Intuitively it seems that activation of the sympathetic nervous system and sleep loss would affect diabetic control however this was not reliably proven in these studies. Given the equivocal results it would be too early for the clinician to modify treatment in reliance on research to date although this area of study has some promise and further research might reveal some more definitive answers in the future.
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