Pillar Giora, Shehadeh Naim
Sleep Lab, Meyer Children's Hospital, Rambam Medical Center, Haifa, Israel.
Diabetes Care. 2008 Feb;31 Suppl 2(7):S303-9. doi: 10.2337/dc08-s272.
Obstructive sleep apnea (OSA) syndrome is a disorder characterized by repetitive episodes of upper airway obstruction that occur during sleep. Associated features include loud snoring, fragmented sleep, repetitive hypoxemia/hypercapnia, daytime sleepiness, and cardiovascular complications. The prevalence of OSA is 2-3% and 4-5% in middle-aged women and men, respectively. The prevalence of OSA among obese patients exceeds 30%, reaching as high as 50-98% in the morbidly obese population. Obesity is probably the most important risk factor for the development of OSA. Some 60-90% of adults with OSA are overweight, and the relative risk of OSA in obesity (BMI >29 kg/m(2)) is >or=10. Numerous studies have shown the development or worsening of OSA with increasing weight, as opposed to substantial improvement with weight reduction. There are several mechanisms responsible for the increased risk of OSA with obesity. These include reduced pharyngeal lumen size due to fatty tissue within the airway or in its lateral walls, decreased upper airway muscle protective force due to fatty deposits in the muscle, and reduced upper airway size secondary to mass effect of the large abdomen on the chest wall and tracheal traction. These mechanisms emphasize the great importance of fat accumulated in the abdomen and neck regions compared with the peripheral one. It is the abdomen much more than the thighs that affect the upper airway size and function. Hence, obesity is associated with increased upper airway collapsibility (even in nonapneic subjects), with dramatic improvement after weight reduction. Conversely, OSA may itself predispose individuals to worsening obesity because of sleep deprivation, daytime somnolence, and disrupted metabolism. OSA is associated with increased sympathetic activation, sleep fragmentation, ineffective sleep, and insulin resistance, potentially leading to diabetes and aggravation of obesity. Furthermore, 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.
阻塞性睡眠呼吸暂停（OSA）综合征是一种以睡眠期间上气道反复阻塞发作的病症。相关特征包括大声打鼾、睡眠片段化、反复低氧血症/高碳酸血症、日间嗜睡和心血管并发症。中年女性和男性中OSA的患病率分别为2% - 3%和4% - 5%。肥胖患者中OSA的患病率超过30%，在病态肥胖人群中高达50% - 98%。肥胖可能是OSA发生发展的最重要危险因素。约60% - 90%的成年OSA患者超重，肥胖（BMI>29kg/m²）者患OSA的相对风险≥10。大量研究表明，随着体重增加，OSA病情会发展或加重，而体重减轻则会有显著改善。肥胖导致OSA风险增加有多种机制。这些机制包括气道内或其侧壁的脂肪组织导致咽腔尺寸减小、肌肉内脂肪沉积导致上气道肌肉保护力下降，以及大腹部对胸壁的质量效应和气管牵引导致上气道尺寸减小。这些机制强调了腹部和颈部区域积累的脂肪相较于外周脂肪的重要性。影响上气道尺寸和功能的是腹部而非大腿。因此，肥胖与上气道可塌陷性增加相关（即使在非呼吸暂停受试者中），体重减轻后会有显著改善。相反，OSA本身可能因睡眠剥夺、日间嗜睡和代谢紊乱使个体更容易肥胖。OSA与交感神经激活增加、睡眠片段化、无效睡眠和胰岛素抵抗相关，可能导致糖尿病和肥胖加重。此外，OSA可能与瘦素、胃饥饿素和食欲素水平变化、食欲和热量摄入增加有关，进而加重肥胖。因此，肥胖和OSA似乎形成了一个恶性循环，二者相互恶化。
