Obesity and Sleep Disorders: Implications for Bariatric Patients

Sleep Apnea

Sleep deprivation can be due to a number of common sleep disorders, including obstructive sleep apnea (OSA), insufficient sleep syndrome, restless leg syndrome, narcolepsy, and insomnia. Sleep apnea is as common as adult type 2 diabetes and affects more than 12 million Americans, according to the National Institutes of Health. ⁵ Risk factors include being male, overweight, and over the age of 40, but sleep apnea can strike anyone at any age—even children.

However, due to the lack of awareness by the public and healthcare professionals the vast majority of sleep apnea patients remain undiagnosed and therefore untreated, despite the fact that this disorder can have significant consequences. One study estimated that 93% of women and 82% of men with moderate to severe sleep apnea remain undiagnosed. ⁶ The consequences of sleep apnea include heart attacks, heart failure, stroke, hypertension, accelerated development of coronary artery disease, abnormal heart rhythms, convulsions, memory problems, slowed thinking, irritability, mood swings, depression, and high-speed highway crashes. ³

Apnea, which means “without breath,” includes three types: obstructive, central, and mixed. Of the three, obstructive is the most common. In all three, people with untreated sleep apnea stop breathing repeatedly during their sleep. These repeated pauses in breathing last at least 10 seconds. In more severe cases, hundreds of episodes of apnea may occur every night. A bed partner familiar with the person experiencing apnea may report cessation of breathing, choking, gasping, and frequent awakenings. The daytime manifestations of OSA include excessive daytime sleepiness (EDS) and decreased concentration.

Obstructive sleep apnea is caused by a blockage of the airway, usually when the soft tissue in the rear of the throat collapses and closes during sleep. Blockage of the airway can be partial or complete and results in ventilation that is decreased (hypopnea) or absent (apnea) (Figure 1). If normal inspiration is from 70% to 100%, an apnea occurs when breathing is stopped completely or when one takes in less than 25% of a normal breath (for a period that lasts 10 seconds or more). This definition includes complete stoppage of airflow. Apneas are usually measured during sleep over a 2-hour period. An estimate of the severity of apnea is calculated by dividing the number of apneas by the number of hours of sleep, giving an apnea index (AI). The greater the AI, the more severe the apnea.

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FIG. 1.

Obstructive sleep apnea.

A hypopnea is a decrease in breathing that is not as severe as an apnea. If normal breath airflow is from 70% to 100%, a hypopnea is from 26% to 69% of a normal breath. Hypopneas, like apneas are also associated with a 4% or greater drop in the saturation of oxygen in the blood, occurring usually during sleep. Also like apneas, hypopneas usually disrupt the level of sleep. A hypopnea index (HI) can be calculated by dividing the number of hypopneas by the number of hours of sleep.

The apnea-hypopnea index (AHI) is an index of severity that combines apneas and hypopneas. Combining them both gives an overall severity of sleep apnea including sleep disruptions and desaturations (a low level of oxygen in the blood). The AHI, like the AI and HI, is calculated by dividing the number of apneas and hypopneas by the number of hours of sleep. Sleep apnea is formally defined as an AHI of at least 15 episodes per hour (the equivalent of one episode every 4 minutes) in a patient without medical problems that may be related to the sleep apnea. ⁷ In a patient with concomitant diseases, such as hypertension and other cardiovascular diseases, insomnia, or mood disorders, sleep apnea is defined as an AHI of at least 5 episodes per hour. ⁷ This is a more rigorous criterion because the patient may be already experiencing the negative medical effects of sleep apnea; therefore, it may be important to begin treatment at a lower AHI.

In central sleep apnea (CSA), the airway is not blocked but the brain fails to signal the muscles to breathe (i.e., there is erratic brain activity in the area that controls breathing). With polysomnography (PSG), CSA is conventionally defined as a cessation of airflow for 10 seconds or longer without an identifiable respiratory effort. In contrast, an obstructive apnea has a discernible ventilatory effort during the period of airflow cessation. The vast majority of patients with CSA have concomitant OSA.

Indeed, there is significant overlap regarding the pathophysiology of OSA and CSA. During normal inspiration, neuronal discharge to the diaphragm and dilator muscles of the pharynx increases. When pharyngeal dilatation is not achieved in the presence of diaphragmatic contraction, an obstructive apnea is the consequence. If there are diminished contractions of the diaphragm, a central sleep apnea occurs. During CSA the hypopharynx may or may not be open. If the hypopharynx is closed during central apnea and diaphragmatic activity resumes before pharyngeal dilator muscle tone is restored, a mixed apnea results.

Upper airway resistance syndrome (UARS) shares the daytime symptoms with OSA, but based on polysomnography (PSG), patients do not have apneas or hypopneas. UARS patients have a pattern of progressively negative intrathoracic pressure, resulting in an arousal from sleep or have respiratory effort–related arousals (RERA). Both OSA and UARS are obstructive sleep–related breathing disorders (OSRBD).

A 2003 study ⁸ found that the incidence of OSRBD for patients being evaluated for bariatric surgery was very high based on polysomnography findings. OSRBD was present in 88% of the patients: OSA was present in 71% and upper-airway UARS was present in 17%. In this particular study, the majority of the patients were women with a mean body mass index (BMI) of 47 kg/m².

Not only does obesity contribute to sleep problems, but sleep problems can also contribute to obesity. Researchers at the University of Chicago ⁹ have found that building up a sleep debt over a matter of days can impair metabolism and disrupt hormone levels. After restricting 11 healthy young adults to 4 hours of sleep for 6 nights, researchers found that their ability to process glucose in the blood had declined—in some cases to the level of diabetics. Other cross-sectional studies have also demonstrated that sleep-disordered breathing is associated with glucose intolerance and insulin resistance.^10,11

Sleep Deprivation and Hormone Imbalance

Sleep deprivation activates a small part of the hypothalamus, the region of the brain that is also involved in appetite regulation. Two critical hormones involved in regulating food intake are ghrelin and leptin. These hormones influence eating in different ways. Ghrelin is an appetite-stimulating hormone released mostly by the stomach. When ghrelin levels are up, people feel hungry. On the other hand, leptin, considered a satiety or fullness hormone, is released by the fat cells and informs the brain about the current energy balance of the body. When leptin levels are high, that sends a message to the brain that the body has enough food and hence the person feels full. Low levels indicate starvation and increase one's appetite. Both leptin and ghrelin levels are markedly dependent on sleep duration. In fact, poor sleep results in a lower leptin levels and higher ghrelin levels. This in turn causes an increase in appetite.

Researchers at the University of Chicago School of Medicine examined the effect of sleep deprivation on these two hormones. ¹ In this study, 12 healthy, normal-weight men with an average age of 22, came into a hospital laboratory to sleep and eat dinner and breakfast. On one occasion, they were limited to 4 hours in bed for each of two consecutive nights. At another time, they were allowed up to 10 hours in bed for two nights. Their blood was drawn at regular intervals, and they were asked about their hunger. This study found that leptin levels were 18% lower and ghrelin levels were 28% higher after the men slept 4 hours. The sleep-deprived men who had the biggest hormonal changes also said they felt the most hungry and craved carbohydrate-rich foods including cakes, candy, ice cream, pasta, and bread. Those who had the smallest changes reported being the least hungry.

Implications for Bariatric Patients: Diagnosis and Treatment

Because the vast majority of patients qualified for bariatric surgery are likely to have sleep apnea, it is important that a diagnosis is established in a sleep center as part of a preoperative evaluation. Although the importance of OSA is mentioned in the guidelines of the American Society for Metabolic and Bariatric Surgery, ¹² more detailed postoperative treatment plan regarding OSA in bariatric patients needs to be incorporated in these guidelines. The success of surgical outcomes in these patients is likely to depend on the proper management of OSA.

The gold standard for OSA diagnosis is overnight polysomnography that typically includes monitoring of snoring, pulse oximetry, electrocardiogram (EKG), muscle tone, chest and abdominal wall movement (to detect respiratory effort), and electroencephalogram (EEG, to detect sleep stage). Once the establishment of OSA has been confirmed, nasal continuous positive airway pressure (CPAP) is the first line of therapy. Pressurized air is delivered through an oral mask that prevents collapse of the airway regardless of the site of obstruction. If used correctly, CPAP is highly effective in eradicating sleep-disordered breathing.

Patients should be put on CPAP prior to surgery. Continued use of CPAP postoperatively will minimize mortality and morbidity associated with sleep apnea. The patient should continue to use CPAP therapy until significant weight reduction has been achieved. However, a recent study found that even after substantial weight loss following bariatric surgery, 71% of patients reported persistent somnolence and snoring, implying that OSA had not been resolved. ¹³ The implications of this study are that patients should continue to receive treatment for OSA even after significant weight reduction. Although weight reduction is often recommended as a second-line therapy for OSA treatment, it should not be viewed as a “cure” for OSA.

Failure to treat OSA could lead to increased cardiovascular risk and ensuing weight gain in the long run. Indeed, a long-term follow-up study of morbidly obese sleep apnea patients who had bariatric surgery found that although there was a massive weight reduction in the first few years after surgery, weight gain ensued after 7 years along with symptoms of sleep apnea. ¹⁴

In addition to the above treatment guidelines, the patient should adhere to the sleep hygiene tips listed below:

Avoid alcohol within 5 hours of bedtime. Alcohol is a poor hypnotic and causes nighttime awakening.

Summary and Conclusion

Obesity is associated with various sleep disorders, including OSA. The vast majority of bariatric patients have OSA. However, OSA remains underdiagnosed, and therefore untreated, not only in the general population but also among bariatric patients. Untreated OSA can have serious cardiovascular effects, decrease the patient's quality of life, and negate the benefits of bariatric surgery in the long run by causing weight gain. As part of a preoperative evaluation, bariatric patients should be referred to a sleep center to establish a diagnosis of OSA. Once the establishment of OSA has been confirmed, the first line of therapy is to use nasal CPAP. CPAP should be continued postoperatively, even if the patient has lost substantial weight and does not report symptoms of sleep deprivation. Continued use of CPAP will significantly decrease morbidity and mortality associated with OSA and preserve the benefits of bariatric surgery.

Author Disclosure Statement

Mahmood Siddique, D.O., Iftekhar Mahmud, M.D., and Reshmi Siddique, Ph.D. have disclosed no relevant financial relationships.