It is important for sleep technicians to raise public awareness about the dangers associated with obesity and its relationship with various sleep disorders
Obesity is a serious disorder resulting in significant health impairment. Obese adults are at increased risk of morbidity and mortality from acute and chronic medical conditions, including hypertension, dyslipidemia, coronary heart disease, diabetes mellitus, gallbladder disease, gout, arthritis, and respiratory disease. The National Health and Nutrition Examination Surveys (NHANES),1 conducted from 1960 to 2000, showed dramatic increases in the prevalence of overweight. The most recent survey has indicated that 34.9% of the US adult population is considered to be overweight and 2.9% to be morbidly obese. If this trend continues into the next decade, these figures are expected to reach epidemic proportion. While health care providers came to realize the toll of obesity on various organ systems, obesity-related sleep disorders remained a secondary concern. In this article, we will explore the interaction between obesity and sleep disorders with emphasis on nonsurgical treatments and prevention.
Obstructive Sleep Apnea
Large epidemiologic studies describe a compelling association between obstructive sleep apnea (OSA) and obesity. It is estimated that for every 10 kg increment in weight, the risk for OSA increases by more than twofold, and for each increase in waist or hip circumference by 13 cm to 15 cm, the OSA risk rises by approximately fourfold.2 In a recent study of morbidly obese patients with body mass index (BMI) >40 kg/m2, 33% have an apnea hypopnea index (AHI) >15 and 98% had an AHI >5.3
The mechanism of OSA in the morbidly obese relates to a change in the structural and functional characteristics of the pharyngeal anatomy. The increased fat deposits in the pharyngeal and submental regions cause soft tissue enlargement and contribute to critical narrowing of the airways. During rapid eye movement (REM) sleep, there is a decrease in the central nervous system output to the pharyngeal muscles, allowing airway occlusion to occur at lesser negative pressures compared to individuals with normal pharyngeal anatomy. These changes are exacerbated by the effect of excess body weight on respiratory mechanics. The reduction of functional residual capacity worsens the severity of hypoxemia and prolongs the time to recovery.
Several small studies have reported a significant association between the extent of weight loss and reduction in the severity of OSA. In one controlled study, 23 obese patients were assigned to receive either dietary counseling or no intervention. Those who experienced even a modest weight loss (10 kg) had significant reduction in apnea index (AI), improvement in daytime sleepiness, and decline in oxyhemoglobin saturation.4 The most impressive results of AI improvement are derived from those morbidly obese patients who underwent bariatric surgery. The single study reporting on long-term follow-up of 14 morbidly obese sleep apneic patients revealed a dramatic reduction in the AI from 40±23 per hour to 11±16 per hour in the first 4 months postsurgery.5 During that period, 48% had complete resolution of their apneas; however, 71/2 years later, the AI increased again to 24±23 per hour despite a modest increase in weight. These results demonstrate that sleep apnea can recur in the absence of weight gain possibly due to increasing age or other unexplained factors.
Morbidly obese patients with OSA tend to have more apneic episodes in the supine compared to the lateral position. This observation has been attributed in part to the positional reduction in upper airway collapsibility.6 Positional treatment has been recommended for those patients who have at least twice the number of respiratory events in the supine position than the lateral one. Among the devices available to treat this condition, Cartwright et al7 described a positional monitor that would trigger an alarm whenever the patient lies in the supine position for more than 15 seconds. In another study,8 patients were instructed to wear a backpack with a softball inside to prevent them from lying supine. Although these strategies might be effective in patients with mild disease, future trials are needed to determine the long-term effects of positional therapy.
Continuous positive airway pressure (CPAP) is the most effective method of treatment of OSA in morbidly obese patients. It acts as a pneumatic splint by exerting an outward force on the upper airways, thus preventing collapse during inspiration. Randomized controlled trials have shown that patients treated with nasal CPAP experience improvement in daytime somnolence and neuropsychiatric function, and likely a reduction in cardiovascular mortality.9 Of particular importance are the reports of weight loss and change in visceral fat distribution after long-term use of CPAP.10 Because of the high incidence of undiagnosed OSA in morbidly obese patients, CPAP may be considered in the perioperative period and postextubation to prevent hypoxic complications. In a retrospective, case-control study, Gupta et al11 reported adverse postoperative outcomes of noncompliant OSA patients undergoing hip or knee replacement compared with controls undergoing the same operations. Empiric CPAP at 10 cm H2O has been suggested for those morbidly obese patients who cannot complete an overnight polysomnography before surgery12; however, prospective studies to document the effectiveness of such a measure are lacking.
Obesity hypoventilation syndrome
Up to 12.5% of morbidly obese patients undergoing gastric surgery are found to have obesity hypoventilation syndrome (OHS).13 Although both OSA and OHS can present with excessive daytime hypersomnolence, there are fundamental differences between the two syndromes. In OSA, disordered breathing is present typically only during sleep and obesity is not always reported. By contrast, hypoventilation is present in OHS during sleep and wakefulness, and by definition, obesity is always present.
Berg et al14 showed that OHS patients are heavy users of health care resources. Compared to simple obesity, OHS results in more intensive care unit admissions, long-term placement, and higher mortality and cost of care.15 Those affected often have restrictive pulmonary defects, increased work of breathing, and diminished respiratory drive in response to hypoxemia and hypercapnea. Noninvasive positive pressure ventilation (NPPV) rapidly improves blood gas abnormalities, dyspnea symptoms, daytime sleepiness, and other complaints related to poor sleep quality. The improvement in ventilation nocturnally achieved with NPPV may persist even during the daytime.16 Medroxyprogesterone has been advanced as a means to improve the hypoxic and hypercapneic ventilatory drive. In uncontrolled study of 10 patients, medroxyprogesterone reduced significantly daytime hypercarbia and increased oxygenation after 4 to 9 months of treatment17; however, randomized controlled trials in large samples of patients are lacking, and the role of medroxyprogesterone in association with nocturnal positive airway pressure is unclear.
Nonbreathing-related Sleeping Disorders
Excessive Daytime Sleepiness
Poor sleep quality is a common complaint among morbidly obese patients that is not entirely explained by sleep-related breathing disorders. In a cross-sectional study of 78 morbidly obese patients without OSA, Resta et al18 reported that the majority of participants complained of frequent choking (25%), awakenings (50%), unrefreshing sleep (50%), and loud snoring (46.7%). Moreover, 35% had excessive daytime sleepiness (EDS) without concomitant increase in the arousal index.
The pathophysiological mechanism of these sleep disturbances in morbidly obese patients without OSA remains unclear. It has been suggested that the mechanical effects of obesity may play a role in determining sleep disturbances, but further research is needed to conform this hypothesis. The possibility that the abnormalities of sleep patterns reflect a psychological distress has been discredited by other investigators.19 One potential explanation focuses on the alteration of endocrinologic and metabolic circadian abnormalities observed in these patients. Noteworthy, plasma levels of inflammatory cytokines (tumor necrosis factor-a and interleukin-6) are elevated in subjects with excessive daytime sleepiness, and interestingly, the levels of these cytokines are higher in obese than in normal-weight healthy subjects.20
The prevalence of narcolepsy has been estimated to be about 56.3/100,000 in general, but specific prevalence of narcolepsy in the morbidly obese is not well known. New data indicate that patients with narcolepsy have higher rates of obesity, a state that may also be linked to hypocretin dysfunction.21 In knocked-out mice, the absence of genes for the ligands and its receptors has been linked to the development of excessive sleepiness, cataplexy, and obesity.22 One study also observed that relatives of people with narcolepsy had a higher incidence of excessive body weight, suggesting that there may be some genetic association between obesity and narcolepsy.23
The higher mean BMI observed in patients with narcolepsy probably explains the higher than expected rate of OSA. Until the OSA is treated, however, a reliable Multiple Sleep Latency Test cannot be obtained. Documenting undetectable hypocretin levels in the CSF is extremely useful in these circumstances, although lumbar punctures are not currently considered part of a routine diagnostic evaluation.
Most clinicians use modafinil 200 to 400 mg per day as a first-line agent for narcolepsy; however, if the patient has severe EDS or cataplexy, modafinil is unlikely to be sufficient. Methylphenidate, increasingly used in extended-release form, is the agent of choice in these cases with the amphetamines being reserved for treatment-refractory patients. The dosage is titrated upward until the patient reports satisfactory alertness, particularly when driving.
Night Eating Syndrome
One interaction of sleep and morbid obesity is illustrated by night eating syndrome. This is a non-REM sleep related behavioral disorder with poor recollection of events once awake. Those afflicted obese patients consume most of their calorie-rich diets after sleep, which further worsens their obesity. They also complain of insomnia and interestingly have poor appetite while awake. Although not consistently associated with obesity, it is important to ask the very obese with paradoxically poor awake appetite about this disorder because patients may not be forthcoming about it. A multidisciplinary approach, involving dieticians, psychiatrists, endocrinologists, and bariatric surgeons, is needed for successful treatment.24
Prevention of Obesity-related Sleep Disorders
The evidence of preventive measures to reduce sleep-related disorders is lacking in most of the aforementioned diseases. The impact of weight changes on obesity is better studied compared to modifications of the other risk factors. Weight loss in those who are obese reduces the severity of OSA regardless of the method used, although surgical procedures produce better results. Abstinence from alcohol and avoiding sedative agents are strongly recommended because they have been shown to exacerbate sleep apnea and worsen daytime sleepiness.25 The role of government, media, and food industry is central to fighting obesity and improving public health. Incorporating sleep disorders education into health-related curricula could increase clinicians’ awareness of these problems. Health providers should continue to raise awareness of the public about the dangers associated with obesity and its relationship with various sleep disorders. Once they are suspected, patients should be referred early to sleep specialists for evaluation and treatment. It is also the responsibility of the specialists to devise new treatment measures through rigorous research to improve compliance and efficacy while reducing cardiovascular complications.26
Winston Nara, MD, is Fellow, Pulmonary, Critical Care, and Sleep Medicine, and Ali El-Solh, MD, MPH, is director, James Nolan Clinical Research Center, both in the Division of Pulmonary, Critical Care, and Sleep Medicine, University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY.
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