Obstructive sleep apnea and dyslipidemia are common medical disorders that independently increase vascular morbidity and mortality. Current animal and human data show that, indeed, obstructive sleep apnea may mediate pathological alterations in cholesterol and triglyceride metabolism. The mechanisms involved are increased lipolysis, decreased lipoprotein clearance, and enhanced lipid output from the liver. Human evidence shows that the treatment of obstructive sleep apnea with continuous positive airway pressure leads to an improvement of postprandial hyperlipidemia. However, more studies are needed, to clarify the pathophysiology of the interrelationship between obstructive sleep apnea and dyslipidemia and whether treatment of obstructive sleep apnea will lead to an improvement in the lipid profile and, more importantly, reduce hyperlipidemia-related vascular outcomes. 1. Introduction Obstructive sleep apnea (OSA) is a common medical disorder affecting up to 24% of the general US population [1]. The disorder is characterized by repetitive complete and/or partial collapse of the upper airways. OSA is strongly associated with vascular [2, 3], metabolic [4], and kidney diseases [5]. Therefore, OSA has to be approached not just as a simple snoring problem, but rather should be considered as a medical disorder with systemic features. This notion is supported by the fact that OSA treatment may improve the function of target organs [6]. Current evidence suggests that OSA disturbs fundamental biochemical processes and is associated with low-grade systemic inflammation and oxidative stress [7]. Indeed, this may underlie the fact of why individuals affected with OSA are at increased risk for comorbid diseases, particularly for vascular diseases. Dyslipidemia, on the other hand, is the group of disorders of cholesterol (Ch) and/or triglyceride (TG) metabolism with a well-known detrimental impact on increased cardiovascular risk [8]. Furthermore, clinical evidence shows that OSA may be independently associated with dyslipidemia [9–18] and functional abnormalities of high-density lipoproteins (HDL) [19]. Moreover, OSA-targeted therapeutic intervention leads toward an improvement in the lipid profile [20–24]. However, others have failed to find any association between OSA and dyslipidemia in humans [25]. Differences in research methodology and the studied population may explain these conflicting results in clinical research on OSA and dyslipidemia. The goal of this paper is to summarize the current knowledge on the pathogenesis of the potential interrelationship
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