Obstructive sleep apnea and metabolic syndrome

Metabolic syndrome (MS) is a heterogeneous condition associated with increased cardiovascular risk. There is growing evidence from experimental, translational, and clinical investigations that has suggested that obstructive sleep apnea (OSA) is associated with prevalent and incident components of MS and MS itself. The biological plausibility is supportive, primarily related to one of the main features of OSA, namely intermittent hypoxia: increased sympathetic activation with hemodynamic repercussions, increased hepatic glucose output, insulin resistance through adipose tissue inflammation, pancreatic beta-cell dysfunction, hyperlipidemia through the worsening of fasting lipid profiles, and the reduced clearance of triglyceride-rich lipoproteins. Although there are multiple related pathways, the clinical evidence relies mainly on cross-sectional data preventing any causality assumptions. The overlapping presence of visceral obesity or other confounders such as medications challenges the ability to understand the independent contribution of OSA on MS. In this review, we revisit the evidence on how OSA/intermittent hypoxia could mediate adverse effects of MS parameters independent of adiposity. Particular attention is devoted to discussing recent evidence from interventional studies. This review describes the research gaps, the challenges in the field, perspectives, and the need for additional high-quality data from interventional studies addressing the impact of not only established but promising therapies for OSA/obesity.

Automated summary

Metabolic syndrome (MS) is associated with increased cardiovascular risk, and there is evidence suggesting that obstructive sleep apnea (OSA) is associated with MS and its components. The biological plausibility of this association is supported by the intermittent hypoxia seen in OSA, which leads to various physiological effects related to MS. However, the clinical evidence is mainly based on cross-sectional data, and confounders such as obesity and medication use pose challenges in determining the independent contribution of OSA to MS. This review discusses the evidence on how OSA/intermittent hypoxia may affect MS parameters independently of adiposity and highlights the need for further high-quality interventional studies.