Cardiovascular (CV) comorbid conditions are common in IH and include hyperlipidemia (30%), the use of diabetes and obesity medications (19.8%), hypertension (15%), and a history of CV disease (14.3%).¹ Elevated odds of multiple CV conditions have been identified in patients with IH, with an increased risk of any major CV event more than double compared to patients without the disease.²

In the first National Health and Nutrition Examination Survey (NHANES) study daytime sleepiness was associated with stroke and to a lesser extent coronary heart disease (CHD) events in subjects over the age of 32 years.³ In another study of more than 7000 individuals aged ≥65 years, subjects were assessed to determine whether excessive daytime sleepiness (EDS) was associated with subsequent CHD and stroke.⁴ Subjects self-reporting frequent EDS at baseline had a 1.73-fold increase in the risk of CHD and stroke events versus those who reported never having EDS at baseline. Other studies have shown similar results.^5,6

The relationship between EDS and CV risk may result from several origins (Figure 1):⁷

• Dietary origins: A study by Melaku et al showed that replacing 5% of protein intake with saturated fat increased the likelihood of EDS by 57% and that substitution of saturated fat with unsaturated fat reduced the odds of EDS by 26%.⁸ Consuming processed food such as prepackaged noodles, deli meats, candy, and sugar-sweetened beverages increased the likelihood of EDS by 55% in another study.⁹
• Dysbiosis of gut microbiome: Diets mimicking those common in Western societies (eg, high in fat, sugar, and sodium) promote dysbiosis of gut microbial health, which is a strong stimulus for systemic inflammation. EDS has been linked with elevated inflammatory cytokines for decades; it is plausible that the gut microbiome may be a common bond, linking diet, sleepiness, and CV risk through the promotion of systemic inflammation.
• Genetic predisposition: Genetic predispositions for sleep disorders have been previously reported.¹⁰At this time multiple genome-wide association studies have identified a role for predispositions in the etiology of EDS.⁷