Obstructive Sleep Apnea (OSA) and Gastroesophageal Reflux Disease (GERD) are two common health issues, and research suggests a connection between them. While OSA and GERD are distinct conditions, they are closely linked.
In recent years, a growing number of studies have confirmed a potential link between obstructive sleep apnea (OSA) and GERD. GERD is much more common in patients with OSAHS than in the general population, and is more common in obese individuals and those with alcoholism.
Research results confirm that approximately 70% of patients with OSAHS have pathological GERD, and upper airway obstruction can induce and exacerbate GERD.
Theoretically, OSAS may cause GERD, and GERD may cause OSAS, and the two are causally related.
Definitions of Sleep Apnea and GERD
Sleep-related breathing disorders are considered a major cause of death. Sleep apnea syndrome (SAS) is defined as episodes of breathing pauses lasting more than 10 seconds per episode, recurring 30 or more times per hour, or an apnea/hypopnea index (AHI) exceeding 5 during a seven-hour sleep period.
SAS is more common than asthma in adults. It is categorized into obstructive sleep apnea (OSA), central sleep apnea (CSA), and mixed sleep apnea (MSA).
Gastroesophageal reflux (GERD) refers to the backflow of gastric and duodenal contents into the esophagus through the lower esophageal sphincter. It occurs regularly in everyone every day, but does not necessarily cause clinical symptoms or tissue damage.
In pathological conditions, GER damages the esophageal mucosa through hydrochloric acid and pepsin. GER is the most common gastrointestinal disease, affecting approximately 7% to 15% of the population.
Interaction Between Sleep Apnea and GERD
The comorbidity rate of OSA and GERD is high. Studies have shown that the prevalence of GERD in OSA patients is high, approximately 58-62%, significantly higher than that in the general population (approximately 20%).
A study based on the National Inpatient Database (NIS) of the United States from 2016 to 2019 found that among 22,677,620 GERD patients, 12.21% also suffered from OSA, while the prevalence of OSA in the non-GERD population was only 4.79%.
Another study showed that the incidence of GERD in OSA patients was 32.3%, which was significantly higher than the 15.0% in non-OSA patients.
A survey showed that 59% of patients with obstructive sleep apnea syndrome (OSAHS) experience significant GERD symptoms. During sleep, especially in the supine position, OSAHS prolongs esophageal clearance time, leading to esophageal reflux.
OSAHS causes airway obstruction, leading to a significant increase in negative thoracic and esophageal pressure during inspiration. This increases the pressure gradient across the esophageal sphincter, making it easier for gastric contents to reflux into the esophagus, causing GERD.
Furthermore, during apnea, due to increased upper airway resistance, the patient’s work of inspiration increases, leading to frequent awakenings and swallowing, which in turn induces transient relaxation of the esophageal sphincter.
Continuous reflux of gastric and duodenal contents weakens the esophageal epithelial defense mechanism, causing damage to the esophageal mucosa by acid, pepsin, bile acid, and pancreatic enzymes, ultimately leading to GERD.
When reflux occurs, aspiration of refluxed material into the airways causes airway inflammation and edema, and stimulates chemoreceptors in the airways, leading to bronchoconstriction and vagal hyperreflexia, ultimately causing and exacerbating apnea and hypopnea.
Therefore, theoretically, OSAHS may cause GERD, and GERD may also cause OSAHS, with a causal relationship between the two.
However, the relationship between OSAHS and GERD remains controversial in some research reports. Other scholars believe that OSAHS and GERD are both common clinical conditions with similar risk factors and that their coexistence is common. GERD is a common complication of OSAHS.
Physiological Relationship Between Esophagus and Trachea
The esophagus and respiratory system are closely related. From embryogenesis to function, the two share many similarities and interactions.
During human embryonic development, the respiratory tract, esophagus, and stomach all originate from the posterior foregut, placing them in close anatomical proximity.
Dysfunction of one organ can lead to certain changes in another organ. For example, changes in pressure in the pleural cavity can be transmitted to the esophagus. Similarly, the transport of food bolus and its peristaltic waves in the esophagus can also affect lung function.
The trachea and esophagus both originate from a common lumen, the pharynx. The esophagus transports food to the digestive organs, while the trachea transports air to the alveoli.
Therefore, a precise and quantitative regulatory mechanism is required within the central nervous system to coordinate the activities of the trachea and esophagus.
Failure of this protective coordination mechanism can lead to various serious consequences for the body.
OSA Causes GER
OSA can cause gastroesophageal reflux.
Negative pressure effect: In OSA, patients need to continuously inhale to overcome upper airway obstruction. This not only causes intrathoracic pressure to drop to -80 cmH2O but also increases diaphragmatic pressure, both of which can lead to GER.
The negative pressure in the thoracic cavity increases the transdiaphragmatic pressure gradient, potentially pulling gastric acid back into the esophagus.
LES relaxation: Increased nighttime awakenings and decreased sleep efficiency in OSA patients can trigger transient LES relaxation, leading to acid reflux.
Decreased esophageal clearance: During sleep, swallowing reflexes, salivation, and esophageal motility decrease, causing gastric acid to remain in the esophagus for a longer time, increasing the risk of GERD. The supine position also prolongs esophageal clearance, leading to GERD.
Upper airway inflammation: Snoring and airway vibrations caused by OSA may stimulate the vagus nerve, affect the function of the lower esophageal sphincter (LES), and increase reflux.
GER Causes OSA
GER often causes pulmonary symptoms through microaspiration of the respiratory tract. In recent years, a clear link between asthma, chronic bronchitis, chronic cough, pulmonary fibrosis, and GER has been established. Apnea caused by GER is often fatal.
There are two possible mechanisms by which GER causes OSA.
First, a small amount of gastric contents is aspirated into the glottis, subglottis, and tracheobronchial tree, stimulating the acid sensors in the throat and airways, causing laryngeal spasm.
The second mechanism is that the acidic contents of the stomach stimulate the mucosal receptors in the distal esophagus, causing bronchospasm and respiratory apnea through the vagal reflex.
Acid reflux may cause inflammation or edema in the throat, further aggravating upper airway obstruction and worsening OSA symptoms. Nocturnal awakenings caused by GERD may disrupt sleep structure and exacerbate OSA-related symptoms such as daytime sleepiness.
Shared Risk Factors Between Sleep Apnea and GERD
Obesity: Obesity is a common risk factor for both OSA and GERD. Abdominal fat increases pressure on the stomach, promoting reflux; at the same time, fat deposits in the throat worsen airway obstruction.
Other factors: Smoking, diabetes, sleeping in a supine position, and excessive alcohol use increase the risk of both.
Risk of complications:
OSA patients are more likely to develop GERD-related complications, such as non-erosive reflux disease (NERD), erosive esophagitis, esophageal strictures, and Barrett’s esophagus.
Long-term untreated GERD may lead to an increased risk of esophageal cancer, and OSA may exacerbate these complications through repeated hypoxic states.
Association Between OSA and GER Treatment
OSA and GER are not only linked in their etiology but also require complementary treatment. Studies have shown that in patients with OSA and GER, OSA symptoms are significantly alleviated after treatment with antireflux medications or surgery.
Conversely, in patients with GER and OSA, reflux symptoms are significantly improved after treatment targeting OSA.
1. Treatment of OSA
OSA treatment includes medications (to increase upper airway patency and reduce upper airway resistance), such as respiratory stimulants and vasoconstrictors; continuous positive airway pressure (CPAP); mandibular reshaping; uvulopalatopharyngoplasty; and hyoid bone suspension.
2. Treatment of GER
GERD can be treated with gastrointestinal stimulants, acid suppressants, mucosal protective agents, endoscopic dilatation, and fundo-reentry surgery.
3. Treatment of OSA and GER
Research has shown that CPAP can significantly reduce the incidence of gastroesophageal reflux and apnea. CPAP primarily affects various body systems in the following ways:
(1) Respiratory system: After CPAP treatment, patients’ alveolar ventilation increased significantly, oxygen partial pressure increased significantly, and carbon dioxide partial pressure decreased significantly in patients with hypercapnia.
Researchers believe that after CPAP treatment, the sensitivity of patients’ chemoreceptors increases, ventilation drive is enhanced, alveolar ventilation improves, and blood gas levels are enhanced.
Additionally, during CPAP treatment, the introduction of positive air pressure into the respiratory tract can increase the patient’s functional residual capacity, reduce upper airway resistance, stimulate upper airway mechanical receptors, increase upper airway muscle tension, and prevent upper airway collapse during sleep.
(2) Digestive system: CPAP can effectively eliminate the GER of OSA patients, normalize the esophageal pH value at night, and significantly reduce the frequency of gastroesophageal reflux.
The mechanism may be that CPAP corrects apnea while removing the abnormal pressure gradient of the lower esophageal sphincter caused by awakening and body activity, thereby increasing the pressure in the esophagus and causing the contraction of the LES, thus eliminating the reflux.
(3) Other systems: In the cardiovascular system, CPAP can effectively eliminate arrhythmias and hypertension associated with OSA patients, and can also reduce the mortality rate of OSA patients.
In the blood system, CPAP can significantly reduce the red blood cell count and hematocrit of OSA patients. The main mechanism is that after treatment, the plasma level of ANP decreases, body fluids enter the blood vessels from outside the blood vessels, and the blood is diluted.
In the nervous system, CPAP can significantly improve the patient’s alertness and perception function, both of which can improve the patient’s nocturnal hypoxia and sleep structure.
Conclusion
Sleep apnea (OSA) and gastroesophageal reflux disease (GERD) are significantly associated.
The high comorbidity rate (GERD prevalence in OSA patients ranges from 58% to 62%) suggests that the two may influence each other through shared risk factors (such as obesity) or bidirectional mechanisms.
CPAP therapy significantly improves both conditions, while antireflux medications and lifestyle interventions can also indirectly alleviate OSA symptoms.
Although further research is needed on a causal relationship, bidirectional screening for OSA or GERD and comprehensive treatment are recommended to improve symptoms and quality of life.
We must prioritize the treatment of both OSA and GERD. Only by combining the two can we achieve optimal results. While many treatments are currently available for both OSA and GERD, CPAP therapy is undoubtedly the most commonly used and effective.
Long-term use can not only improve OSA symptoms, such as a significant reduction in apnea episodes, daytime sleepiness, and hypoxemia, but also significantly reduce daytime sleepiness and hypoxia.
