Obesity and Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is a disorder that negatively affects many parts of the body. Medical conditions linked to OSA include hypertension, insulin resistance, visceral fat deposition, and systemic inflammation.

Sleep apnea is believed to affect 25% of the adult population and as high as 45% of individuals with obesity.

Obesity is a major risk factor for the development and progression of OSA, and it is the only truly reversible risk factor. About 70% of adult OSA patients have obesity, and the higher the BMI, the greater the prevalence. The prevalence of sleep apnea is also significant in the pediatric population. Children with obesity have a 46% increased risk of OSA compared to their normal-weight peers.

Patients with mild OSA who gain 10% of their body weight are at a six-fold risk of disease progression. Conversely, a 10% weight loss correlates with a 20% improvement in OSA severity. Obesity may worsen OSA because of fat deposition in tissues of the upper airway, resulting in a smaller lumen and increased collapsibility, and in the thorax, reducing chest compliance and functional residual capacity.

Obstructive sleep apnea is associated with glucose intolerance and insulin resistance. Lipid abnormalities associated with OSA include high triglycerides and low HDL. Hormones related to obesity are also altered by OSA. Ghrelin, an appetite stimulant, is higher in patients with OSA. Leptin is a hormone produced by adipose tissue functions in the hypothalamus to signal satiety to the brain. Sleep deprivation tends to inhibit leptin production, a possible reason that poor sleep may contribute to obesity. Adiponectin is another adipokine that improves glucose control and lipid metabolism and may reduce inflammation and atherosclerosis. Levels of adiponectin are reduced in both obesity and obstructive sleep apnea.

Treatment of OSA with CPAP (Continuous Positive Airway Pressure) has shown benefits in lowering blood pressure and improving quality of life. It may also improve some of the cardio-metabolic complications of OSA. In a trial of 86 patients with metabolic syndrome and OSA randomized to treatment with CPAP and “sham” CPAP, three-month results showed partial reversal of metabolic abnormalities and reduced blood pressure in the CPAP group (Sharma, et al, NEJM Dec 15, 2011).

CPAP combined with weight loss showed reduction in insulin resistance, triglyceride levels, and blood pressure (Chirinor et al, NEJM June 12, 2014).

In summary, there is a complex relationship between obesity and obstructive sleep apnea. It should be considered in patients with obesity. Losing weight can improve OSA, and treating OSA may help with weight loss. Hopefully, continued research will clarify this interrelationship and lead to improved treatments for both conditions.