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Obstructive sleep apnea (OSA) has been found to be associated with increased incidence of cardiovascular and cerebrovascular diseases. It has also been found to be associated with features of metabolic syndrome also known as “insulin resistance syndrome” comprising of hyperinsulinemia, glucose intolerance, dyslipidemia, central obesity, and hypertension.

 

It has been postulated that the episodic occlusion of the upper airway due to obstructive sleep apnea may lead to certain pathophysiological changes which may in turn increase the chances of developing vascular diseases.

 

A study was conducted to prove that OSA represents a stress that promotes insulin resistance, hence atherogenesis. The study was lead by Mary S, Bing Lam and colleagues and published in the American Journal of Respiratory and Critical Care Medicine. It investigated the relationship between sleep-disordered breathing and insulin resistance. There were a total of 270 participants and their fasting serum insulin level and insulin resistance index was used as a measure. 185 of these participants had OSA. It was seen during the course of the study that the OSA subjects were more insulin resistant, as indicated by higher levels of fasting serum insulin; they were also older and more obese. Stepwise multiple linear regression analysis showed that obesity was the major determinant of insulin resistance but sleep-disordered breathing parameters were also independent determinants of insulin resistance. The association between OSA and insulin resistance was present in both obese and non obese participants. Further analysis of the relationship of insulin resistance and hypertension confirmed that insulin resistance was a significant factor for hypertension in this group.

 

The cerebral activation and increased sympathetic output due to obstructive sleep apnea may provide a stress stimulus that triggers or aggravates hypertension. The study establishes the fact that OSA is independently associated with insulin resistance, and further studies can be carried out to explore the atherogenic potential of OSA.

References:

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