In a previous study, we demonstrated sleep-disordered breathing and nocturnal oxygen desaturation in a significant proportion of morbidly obese men scheduled for bypass surgery to control obesity. In that study, 14 morbidly obese subjects who were at least 200 percent of ideal body weight were monitored during a single night of sleep. Six of the seven men experienced oxygen desaturation or abnormal breathing. Two of these subjects were symptomatic with daytime somnolence.
The relationship of obesity to the sleep apnea syndrome is not clear. Although the incidence of sleep apnea in men has been shown by Block et al to increase with increasing body weight, obese patients accounted for only 40 percent of one large series of patients with sleep apnea. In a recent review of the cardiorespiratory effects of obesity, the authors noted that weight loss in obese patients with the sleep apnea syndrome resulted in relief of hypersomnolence, shortened apneic periods, and improved levels of arterial oxygen saturation while awake and asleep. Remmers and colleagues also reported complete resolution of airway obstruction and normalization of the genioglossus EMG in two subjects after moderate weight loss. Others have noted that a small number of patients with sleep apnea, restudied after moderate weight loss, continued to have significant episodes of obstructive sleep apnea. Guilleminault and Dement suggested that upper airway obstruction is the primary event, with weight gain occurring later. If this were the case, one would expect no change in sleep apnea after weight reduction.
While weight loss in morbidly obese subjects improves lung volume and oxygenation, it probably does not affect hypoxemic or hypercapnic ventilatory drives. The sleep apnea syndrome in obesity may be due to central neurogenic mechanisms, the mechanical effects of fat in the upper airway and chest wall, or the interaction of the two. Thus, the effect of weight loss on the frequency of sleep-disordered breathing events might be expected to shed some light on the pathogenesis of the syndrome, particularly the question of whether the obesity is a primary or secondary factor in its development. This report records our observation of repeat sleep studies on four morbidly obese men with sleep apnea after massive weight reduction.