Sleep Apnea and Obesity:
Short sleep duration leads to metabolic changes, likely linked to obesity.
Insufficient sleep during childhood may adversely affect the function of a region of the brain known as the hypothalamus, which regulates appetite and the expenditure of energy.
Snoring and sleep apnea should not be taken lightly! If you believe that you or your loved one may have sleep apnea, contact your physician or sleep apnea dentist today.
Obesity is considered a major risk factor for the development and progression of Obstructive Sleep Apnea (OSA). The prevalence of OSA in obese or severely obese patients is nearly twice that of normal-weight adults. Also, patients with mild OSA who gain 10% of their baseline weight are at a sixfold-increased risk of progression of OSA, and an equivalent weight loss can result in a more than 20% improvement in OSA severity.
It is possible that obesity may worsen OSA because of fat deposition at specific sites. Fat deposition in the tissues surrounding the upper airway seem to restrict the diameter of the trachea. Furthermore, fat deposits around the thorax (truncal obesity) reduce chest compliance and functional lung residual capacity, and can increase oxygen demand.
Visceral obesity – a form of obesity due to excessive deposition of fat in the abdominal viscera and omentum, rather than subcutaneously
Omentum – a fold of peritoneum (membrane lining the walls of the abdominal and pelvic cavities) extending from the stomach to adjacent abdominal organs
Subcutaneously – located or placed just beneath the skin
Visceral obesity is common in subjects with OSA. Although, the relationship between OSA and obesity is complex. There is convincing evidence showing that obesity, as well as visceral obesity, may predispose a patient to OSA and that losing weight results in OSA improvement. But, recent studies suggest that OSA may itself cause weight gain.
Wait Gain because of OSA?
In 2004 a Stanford University and University of Wisconsin study found that sleep-deprived people had higher levels of a hormone that triggers appetite and lower levels of a hormone that suppresses it.
Overweight sleep apnea patients usually know that the extra pounds they carry are contributing to their OSA problem. However, with barely enough energy to stay awake even during simple conversation, exercise often does not happen.
Factors such as reduced physical activity levels and increased appetite, particularly for refined carbohydrates, may possibly contribute to weight gain in OSA patients. Whether OSA predisposes to preferential accumulation of visceral fat remains to be determined. CPAP treatment of OSA reduces the amount of visceral fat (as measured by abdominal CT scanning), even in patients without significant weight loss
Studies show a dose-response relationship between self-reported short sleep duration and increased body weight, suggesting that sleep duration may be an important regulator of body weight and metabolic and endocrine function. The close interactions between obesity, sleep deprivation, and OSA share the common pathophysiologic feature of metabolic dysregulation. Weight loss may improve all of these conditions and can start an important potential intervention for these patients. In fact, research in sleep after weight loss achieved through bariatric surgery suggest that, 1 year later, there are significant increases in rapid eye movement and slow-wave sleep, with reduced daytime sleepiness. In other words, patients who lost weight through bariatric surgery got better sleep.
Other metabolic troubles present in OSA that could potentially improve with weight loss include lipid abnormalities. OSA patients have increased triglycerides, total cholesterol/high-density lipoprotein (HDL) ratio and low-density lipoprotein and lower HDL values. Intermittent reduction in oxygen causes an increase in the liver content of triglycerides.
- Lack of sleep affects our ability to control weight has a lot to do with our hormones.
- Two key hormones involved are ghrelin and leptin.
- Ghrelin is a “go” hormone. It tells us to GO EAT. When we are sleep-deprived our bodies produce more ghrelin.
- Leptin, is a “stop” hormone. It tells us that we are full and satisfied, and that we can STOP EATING. When we’re sleep-deprived, we make less leptin.
Another hormone affected by sleep apnea is insulin. When we don’t sleep well, our cells block insulin’s efforts to transport glucose into our cells. This mimics diabetes. Also, insulin promotes the release of leptin, the “stop eating” hormone. Thus when we are sleep deprived and our cells are rejecting insulin, our bodies make less leptin, which means more eating, and more weight gain.