Obesity is an important risk factor for the development of OSA. Some 50-60% of adults with OSA are overweight. Women of reproductive age snore less than post menopausal women, due to the decrease in estrogen level in post menopause. Estrogen has got a protective effect in maintaining the upper airway patency.
Obstructive sleep apnea syndrome characterized by repetitive episodes of upper airway obstruction that occur during sleep. Associated features include loud snoring, fragmented sleep, hypoxemia, hypercarbia, daytime sleepiness, memory loss, sexual dysfunction and cardiovascular complications.
Metabolic responses in Obstructive Sleep Apnea
There are several mechanisms responsible for the increased risk of OSA and obesity. These include reduced pharyngeal lumen size due to fatty tissue infiltration within the airway or in its lateral walls and decreased upper airway muscle protective force due to fatty deposits in the muscle. The neck obesity is more important than peripheral obesity in producing narrow airway. There is increase in collar size along with higher BMI in these obese sleep apnea patients.
OSA is associated with increased sympathetic activation, sleep fragmentation, ineffective sleep, and insulin resistance, potentially leading to type 2 diabetes and aggravation of obesity.
Also in OSA, sleep is fragmented with excessive daytime somnolence, consequently resulting in higher incidence of occupational and traffic accidents.
The reasons for gaining in weight in OSA patients are multifactorial. Excessive daytime sleepiness may result in decreased mood and decreased physical activity, which if not associated with reduced caloric intake, will obviously worsen obesity.
When treated withy CPAP or Surgery, patients manage to improve alertness and daytime activity and also an improvement in loosing weight. But if remained untreated, patients tend to gain more weight and the sleep apnea becomes worse.
The mechanism of insulin resistance in OSA
It is well established that sleep deprivation decreases glucose tolerance and results in insulin resistance. There is a close association between sleep apnea and the risk for obesity, insulin resistance, and diabetes.
Sleep deprivation can result in decreased insulin sensitivity at peripheral receptor sites, which can eventually lead to insulin exhaustion at pancreatic sites.
After treatment with CPAP or Surgery there is an improvement in insulin sensitivity and there by improvement in diabetes.
Sleep Apnea Surgery
Leptin, Ghrelin, and Orexin levels in Sleep Apnea and Obesity
These are newly described hormones that regulate appetite and obesity. OSA may be associated with changes in leptin, ghrelin, and orexin levels, increased appetite and caloric intake and again exacerbating obesity. Thus, it appears that obesity and OSA form a vicious cycle where each results in worsening of the other.
Leptin is a protein produced by adipose tissue that circulates to the brain and interacts with receptors in the hypothalamus to inhibit eating and control of body weight and fat distribution. There is growing evidence that leptin regulation is altered in OSA. Most studies reported on increased leptin levels in patients with OSA, which were commonly correlated with an apnea-hypopnea index.
Ghrelin- Another relatively recently discovered hormone that regulates appetite and body weight is ghrelin. In a recent study of patients with OSA, the ghrelin levels were shown to be significantly higher in patients with OSA. CPAP treatment significantly reduced ghrelin levels in these patients. The appetite stimulating effects of ghrelin may well contribute to increased caloric intake and weight gain in patients with OSA.
Orexin- an additional appetite-stimulating neuropeptide produced by lateral hypothalamic neurons and participates in the control of feeding, sleep, wakefulness, neuroendocrine homeostasis, and autonomic regulation.
