Obstructive Sleep Apnea; Cause or Concequence

Obstructive sleep apnea (OSA) is a common disorder in the western world. OSA patients suffer from repetitive collapses of the upper airway tract during sleep, resulting in hypoxemia and arousal from sleep. 2-7% of general adult population is found to suffer from OSA. Incidence of OSA in the obese population exceeds these numbers by far; the numbers increase up to 30% and even as far as 70% in obese diabetic individuals. The idea that there is a correlation between OSA and obesity is a commonly shared idea since years. But what is the chicken and what is the egg in this story? Some researchers say crenialfacial abnormalaties cause the upper airways to collapse during the night. During the day, the activation of mucles that dilate the airways would protect the airway against collapsing. Though not all researchers support these hypothesis, they all agree on the idea that fat deposition in the neck region makes one vulnerable for the development of OSA. Fat depositioning in the upper airway region would promote changes is muscle orientation and alter the firing rate of neurons of the dilatory mucles. Neckcircumference correlates with prevalence of OSA; a neck circumference of 43 cm or more increases the risk on OSA significantly. Some, though not all, studies found a wider neck in OSA patients compaired with BMI matched non-OSA patiets. Besides, weight loss is associated with a decrease in OSA severity and vice versa. But OSA severity appears to be not the only factor correlating with neck circumference. The same accounts for other obesity associated factors. Recently the proposed direct causal relationship between fat depositioning in the neck region and the development of OSA is questioned and a reverse relationship is proposed. Short sleep duration is associated with an increase in BMI. OSA patients, because of the frequent arousal from sleep, both adequate sleep duration and sleep quality are reduced. Indeed increased weightgain in OSA patients has been found compaired with non-OSA patients. Besides that, an increase in both calloric intake and fat deposition in OSA patients compaired with non-OSA patients is seen, making OSA patients more susceptible for weight gain. This is caused by several factors. First of al, repetitive waking causes activation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis promoting a chronic state of inflammation in the body. Besides that, both sleep restriction and sympathetic nervous activation causes upregulation of leptin levels but in the same time, the body becomes insensative for leptin, deminishing its restriction on caloric intake. Ghrelin is also elevated due to sleep restriction and seems to cause an increase in caloric intake. All these changes together induce insulin resistance. Treatment of OSA using continous positive airway pressure appears to normalize all impaired values noted above and promotes weight loss, suggesting OSA causes obesity. Whether obesity causes OSA or vice versa is hard to say; for both statements plausible evidence is present. But regarding all evidence presented in this review, I would say OSA causes obesity. But before conclusions can be drawn, more research should be performed.