To the Editor:
I read with interest the study by Sui et al1 that was published in the November 2011 issue of Mayo Clinic Proceedings, showing an association between elevated fasting plasma glucose and increased stroke risk in men. The authors present an insightful discussion and offer several potential biological mechanisms for this association. I would like to offer an additional explanation for the phenomenon that was seen in their study: the potential contributory role of obstructive sleep apnea in both raising the fasting glucose level and increasing the risk of stroke. Indeed, studies have linked sleep-disordered breathing with impaired glucose-insulin metabolism.2 Although the mechanism of this is not well understood, it is likely that factors such as hypoxia,3 increased sympathetic activity, and counterregulatory hormones4 are involved. Furthermore, obstructive sleep apnea is well known as an independent risk factor for vascular disease, including stroke.5
Therefore, it is possible that the increased incidence of stroke observed in the hyperglycemic group may not have been directly due to glucose factors, but due to the presence of sleep apnea. Indeed, the authors did note differences in body mass index among patients with normal fasting glucose, impaired fasting glucose, and undiagnosed diabetes. Data regarding the prevalence and severity of obstructive sleep apnea were not presented in their study, but the differences in body mass index presumably may result in a higher number of patients with sleep-disordered breathing in the latter 2 groups.
Although impaired fasting glucose levels can easily be treated by means of lifestyle or pharmacologic intervention, it would be interesting to study whether improvement of fasting glucose levels in these at-risk patients would in fact decrease stroke incidence. A lack of stroke decrease might suggest that the fasting hyperglycemia may just be a surrogate marker of another underlying condition that independently contributes to a cerebrovascular event.
References
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