The Vicious Cycle of Sleep Disorders and Obesity: Obstructive Sleep Apnea and Intervention Strategies

I. Overview Sleep is a vital physiological phenomenon for regulating and restoring bodily functions. Good sleep quality eliminates fatigue, promotes physical recovery, and enhances immunity. However, if sleep disorders persist, they can lead to a series of developmental problems affecting the nervous, psychological, intellectual, and behavioral systems. Sleep disorders can cause inflammatory reactions in various systems and organs, resulting in a series of complications that affect the central nervous system, cardiovascular system, metabolic system, and growth and development. Sleep disorders refer to abnormalities in the quantity and quality of sleep, or the occurrence of certain clinical symptoms during sleep, such as reduced or excessive sleep, sleepwalking, etc. Sleep disorders can manifest as abnormal sleep volume and abnormal behaviors during sleep, and are also a manifestation of the disruption of the normal rhythmic alternation between sleep and wakefulness. They can be caused by various factors and are often related to physical illnesses, including sleep disorders and parasomnias. Sleep is closely related to human health. Surveys show that many people suffer from sleep disorders or sleep-related diseases, with the proportion of adults experiencing sleep disorders reaching as high as 30%. Many studies have found that sleep disorders are a significant risk factor for obesity, and good sleep is a necessary condition for ensuring healthy growth in children. Sleep quality is fundamental to achieving physiological, psychological, and social balance. Obesity can cause sleep disorders, creating a vicious cycle between the two. Studies have shown a potential correlation between obesity and sleep disorders, leading to many shared health risks, including obstructive sleep apnea-hypopnea syndrome (OSAHS), cardiovascular disease, type 2 diabetes, and related retinal and kidney diseases. Obese individuals are more likely to experience daytime sleepiness and nighttime sleep disturbances compared to those of normal weight. OSAHS, the most common form of breathing disorder characterized by repetitive or complete upper airway collapse, is highly correlated with obesity, and BMI is associated with OSAHS severity. Research indicates that OSAHS severity decreases with decreasing BMI, suggesting a causal effect between obesity and OSAHS. A systematically averaged study involving 40 cohorts and 2 million participants suggests that both excessive and insufficient nighttime sleep, relative to 7 hours per night, may increase the risk of all-cause mortality. Reduced sleep duration may also increase the risk of diabetes by approximately 37%, hypertension by approximately 17%, and cardiovascular disease by approximately 16%. Obesity is considered one of the most important intermediate processes in this process. As early as 2008, a systematic review involving 600,000 adults and 30,000 children indicated that insufficient sleep may increase the risk of obesity by approximately 55% in adults and approximately 89% in children. II. Pathophysiological Changes: According to changes in electroencephalograms (EEGs) and eye movements, normal sleep is divided into two phases: non-rapid eye movement (HREM) and rapid eye movement (REM). During HREM, muscle tone decreases, there is no obvious eye movement following the eyeball, and the EEG shows slow and synchronous movements. Awakening during this phase results in a feeling of drowsiness. During REM, muscle tone decreases significantly, and rapid horizontal eye movements occur. The EEG shows a state similar to that during wakefulness. Awakening during this phase results in clear consciousness and no feeling of fatigue. Research has found that the caudal portion of the brainstem has a very important relationship with sleep and is considered the location of the sleep center. Various irritative lesions in this area can cause excessive sleep, while destructive lesions can cause reduced sleep. Furthermore, it was found that central nervous system neurotransmitters are involved in sleep. Stimulation of serotonergic neurons or injection of serotonin can induce non-rapid eye movement (NREM) sleep, while administration of serotonin antagonists reduces sleep. Norepinephrine antagonists reduce REM sleep, while norepinephrine agonists increase REM sleep. In obese individuals, the accumulation of adipose tissue in the pharynx can narrow the pharyngeal cavity. Adipose tissue mainly accumulates on the lateral walls of the pharynx, reducing the pharyngeal opening during respiration. Simultaneously, this loose adipose tissue, under the negative pressure of inhalation, is more likely to cause the soft oropharyngeal wall between the soft palate and epiglottis to collapse, exacerbating airway obstruction. Additionally, because obese patients have thicker adipose tissue in the neck and mandible, the external pressure in the oropharynx and laryngopharynx increases, resulting in upper airway compression. Therefore, pharyngeal airway compression in obese patients is another important reason why the pharynx is prone to collapse during inhalation. During the day, when awake, compensatory contractions of the throat muscles keep the airway open, so there are generally no symptoms. However, during sleep at night, nerve excitability decreases, muscles relax, and pharyngeal tissues become obstructed, causing the upper airway to collapse. When airflow passes through the narrowed area, turbulence is created and vibrations occur, resulting in snoring. In severe cases, breathing may temporarily stop. Patients with obstructive sleep apnea syndrome often experience difficulty inspiring, cessation of airflow, snoring, and decreased oxygen saturation during sleep. This leads to frequent awakenings, disrupting normal sleep and causing daytime sleepiness and altered respiratory and circulatory functions. The upper airway obstruction and hypoxemia in patients with obstructive sleep apnea syndrome cause frequent awakenings, resulting in insufficient sleep and poor sleep quality. This also promotes insulin resistance, ultimately leading to weight gain. Frequent nighttime awakenings and hypoxia in patients with obstructive sleep apnea syndrome lead to daytime fatigue, increased appetite, and decreased physical activity. These factors interact, creating a vicious cycle. As weight gradually increases, the severity of sleep-disordered breathing also increases. III. Treatment and Prognosis Sleep disorders are often caused by long-term mental conflicts or excessive psychological burden, mental labor, improper work-life balance, and post-illness weakness. First, the above causes must be addressed, and work and life should be readjusted. It's important to understand the nature of the disorder: the onset is slow, the course is long, and relapses are common, but the prognosis is good. Relieving psychological burden and engaging in appropriate physical labor and exercise can help with recovery. Sleep disorders caused by obesity often involve snoring; tracheostomy can be an effective treatment for sleep apnea. Simultaneously, patients must control their weight, engaging in more outdoor aerobic exercise and strictly adhering to a diet to lose weight. This can effectively aid recovery. Avoid caffeinated beverages and foods, drink alcohol in moderation, avoid gas-producing and spicy foods, and eat more foods rich in tryptophan, B vitamins, calcium, and magnesium. Under the guidance of a doctor, medications to regulate blood pressure and blood lipids may be used.