Can Sleep Apnea Cause Weight Gain?
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Sleep apnea syndrome (SAS) refers to apnea lasting more than 10 seconds per episode, repeated apnea episodes more than 30 times, or apnea-hypopnea index (AHI) more than 5 times during 7 hours of sleep per night. It is generally divided into 3 types: obstructive sleep apnea syndrome (OSAS), central SAS, and mixed SAS, with OSAS being the most common.
OSAS is defined as the disappearance of oral and nasal airflow for more than 10 seconds, accompanied by obvious chest and abdominal respiratory movements or esophageal pressure fluctuations. It is characterized by complete collapse of the airway, and disappearance of airflow, but chest respiratory movements still exist. The incidence of SAS in adults is 4%~7%, of which OSAS>90%, 4% of adult male patients, and 2% of female patients, and the incidence increases with age. The incidence of OSAS in the elderly population aged 60 and above is as high as 20%~40%.
The most important pathophysiological basis for OSAS to cause damage to the body is hypoxemia and hypercapnia caused by apnea. If it is not corrected in time, it can manifest as acute respiratory failure. The occurrence and development of OSAHS are closely related to body weight. Studies have shown that body mass index (BMI) and AHI are positively correlated. A 20% increase in weight will increase AHI by 70%, while a 20% decrease in weight will reduce AHI by 48%, which means that obese people are more susceptible to OSAS.
After weight loss treatment, the symptoms of OSAS such as the number of apnea, waking up due to suffocation, snoring, daytime sleepiness, and hypoxemia are significantly improved in obese patients with OSAS. At the same time, weight loss treatment can also improve the function of the pharynx and larynx. The reduction of AHI is related to the degree of weight loss. The more weight is lost, the more obvious the improvement of the condition. This article discusses the relationship between weight and OSAHS.
Association Between Weight Gain And OSA
Weight gain and sleep apnea can affect each other, and OSA can lead to weight gain. If you have sleep apnea, you may not only be prone to excessive fatigue, but you may also gain weight.
When you’re tired, you’ll naturally exercise less frequently. Regular exercise can help you maintain a healthy weight, but if you’re constantly tired, you may not be motivated to exercise, which can reduce your calorie deficit and make it easier to gain weight. Also, if you don’t exercise, you may feel more tired instead of more energetic even after exercise.
Feelings of fatigue can also lead you to reach for sugary snacks or high-calorie caffeinated drinks to help you wake up. While they may temporarily increase your alertness, those calories can lead to weight gain and ultimately further sleep disturbances.
Association Between Obesity And OSA
In a study of 526 patients, 474 were male (90.1%) and 52 were female (9.9%), with an age range of 5.5-86 years, and an average age of 46.27±12.91 years. The body mass index (BMI) ranged from 16.14 to 51.27, with an average of 27.17±3.76.
The distribution of patients with different BMI is shown in the table.
| BMI | Number Of Cases | Composition Ratio(%) |
|---|---|---|
|
<18.5 （Being Underweight） |
5 |
0.95 |
|
18.5-22.9（Normal Weight） |
54 |
10.27 |
|
23.0-24.9 （Pre-obesity） |
83 |
15.78 |
|
25.0-29.9 （Grade I Obesity） |
276 |
52.47 |
|
>30.0 (Grade II obesity) |
108 |
20.53 |
Obesity is one of the most important independent risk factors for OSAHS, and changes in body weight can directly affect the severity of OSAHS. According to the BMI standard for adults, they were divided into five groups: underweight, normal weight, pre-obesity, grade I obesity, and grade II obesity. It was found that the grade I obesity group had the highest case composition, followed by the grade II obesity group and the pre-obesity group. The normal weight group accounted for 10.27%, while the underweight group accounted for an extremely low proportion (0.95%). MBI and AHI have a positive linear relationship, indicating that the larger the body mass index, the more severe the condition.
Age and obesity are closely related to the severity of OSAHS. Using the AHI value as a measure of the severity of OSAHS, it was found that AHI and BMI were in a linear relationship, with MBI and AHI in a positive linear relationship and age and AHI in a negative linear relationship, indicating that the larger the BMI, the more severe the condition, while the condition is alleviated with increasing age. In addition, the absolute values of the standard partial regression coefficients of BMI and age were 0.369 and 0.115, respectively, indicating that the effect of BMI on AHI was greater than that of age on AHI, that is, weight had a greater impact on OS-AHS.
The possible reasons for the impact of obesity on OSAHS are: obesity can cause accumulation of subcutaneous fat in the neck and pharynx or fat around the airway, leading to narrowing of the upper airway. When sleeping in the supine position, the pharyngeal fat falls and the fat in the front part is compressed, causing the narrow upper airway to further collapse and occlude, leading to the occurrence of apnea and hypoventilation.
Mortimore et al. performed airway MRI examinations on obese patients with OSAHS and obese patients without OSAHS. They found that the upper airway cross-sectional area was reduced in both groups, but the reduction was more obvious in obese patients with OSAHS, indicating that this structural change in the upper airway plays an important role in the occurrence and development of OSAHS. In addition, obese people have decreased respiratory function during sleep, insufficient alveolar ventilation, increased carbon dioxide in the body, insensitivity to hypoxia, decreased ventilation drive of the respiratory center, and aggravated OSAHS.
At the same time, people with central obesity have increased intra-abdominal pressure, the diaphragm shifts toward the head, and their vital capacity, expiratory volume, total lung volume and oxygen content are significantly reduced. The weight load on the airway is increased when lying down, and airway obstruction is more likely to occur during sleep.
Association Between Neck Circumference And OSA
Neck circumference is also an effective objective indicator for determining the degree of obesity. The size of the neck circumference can reflect the caliber and function of the upper airway during sleep. Potential causes of OSA include changes in the structure and function of the upper airway. Neck obesity can increase the instability of the pharynx and even collapse it, while fat accumulation can cause changes in upper airway pressure and fatty degeneration, resulting in compression of the upper airway during sleep, making it more likely to cause upper airway obstruction and cause OSA. Shepard and Hoffstein of Canada studied the measurement data of 1,351 patients and found that among many variables, neck circumference and AHI had the strongest correlation, and found that the correlation was stronger in men than in women.
In 1999, Sergi et al. showed that among BMI, waist circumference, waist-to-hip ratio, and other factors, neck circumference is the only data related to AHI. A study of 670 cases showed that patients with OSA had larger BMI, neck circumference, and abdominal circumference than those without OSA, but there was no difference in abdominal circumference between OSA patients with the same BMI, while neck circumference was significantly increased in OSAS patients with obesity. Therefore, neck circumference may be one of the determining factors of apnea and snoring.
Obese patients have more fat accumulation in the upper airway, such as the neck, pharynx, tongue, and jaw, which can easily lead to apnea and hypopnea. However, the amount of fat in the upper airway and jaw varies among patients with the same degree of obesity. Obese patients with OSA have a lot of fat accumulation in this area. The mechanism of this selective preferential distribution of fat needs further study. However, in the research results of Millman et al., male patients did not show a direct connection between neck circumference and AHI, so it is believed that the reason may be that neck circumference is only a data related to neck muscles, fat and other tissues, and has no correlation with OSA.
Waist Circumference, Intra-abdominal Fat And OSA
Excessive accumulation of visceral fat is another important risk factor for OSA in obese patients. Waist circumference and waist-to-hip ratio can be used to roughly estimate the indicators of visceral fat, and their increase indicates excessive accumulation of visceral fat.
A sleep study of 1464 overweight men showed that waist circumference was a better predictor of OSA than BMI. Shinohara et al. studied 37 patients with primary obesity and found that 27 obese patients were diagnosed with OSA. After analyzing the abdominal visceral fat area, the results showed that the total visceral fat area and the ratio of visceral fat area to total fat area in obese patients with OSA were significantly larger than those without OSA. The size of the visceral fat area was positively correlated with AHI. The larger the visceral fat area, the more likely OSA was to occur, and the more severe the OSA was.
People with visceral fat tissue >220 cm² are more likely to suffer from OSAS, while those with <120 cm² rarely suffer from OSA. Vgontzas et al. accurately measured visceral fat accumulation and confirmed through CT that obese male patients with OSAS had more visceral fat tissue in the abdomen, which was significantly higher than the control group with the same BMI index but without OSA. Therefore, visceral fat tissue is a more dangerous factor for OSA.
Schafer et al. used linear regression analysis to show that intra-abdominal fat was correlated with OSA, while parapharyngeal fat and AHI did not show a correlation; intra-abdominal fat and intra-thoracic fat deposition coexist in obese patients and are two different aspects of visceral obesity. A close connection between abdominal visceral fat accumulation and intra-thoracic visceral fat was also found.
There is a close connection between visceral fat and OSA, but visceral fat accumulation can be manifested in two ways. Waist circumference is its most important manifestation, and neck circumference is also affected by visceral fat. Waist circumference seems to have a greater impact, because excessive accumulation of visceral fat pushes up on the diaphragm, affects the movement of the calves, and hinders the stretching of the upper airway and lungs, causing OSA. However, Resta et al. questioned whether intra-abdominal fat tissue is a good predictor of OSA in morbidly obese men, and believed that neck circumference is more likely to play this predictive role.
Conclusion
At present, the treatment of OSAHS includes weight loss, drugs, surgery, non-invasive positive airway pressure ventilation, oral appliances, etc. Drugs are rarely used in clinical practice due to their large side effects and poor efficacy. Surgery, non-invasive positive airway pressure ventilation, wearing oral appliances, etc. all have their advantages and disadvantages, while weight loss is a simple, economical, safe, and effective method.
The larger the body mass index, the more serious the condition. Many kinds of literature report that after significant weight loss, the patient’s AHI decreases, which can produce positive effects and is an important means of treating sleep apnea-hypopnea syndrome.
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