The pathophysiological relationship and treatment progress of obstructive sleep apnea syndrome, obesity, and metabolic syndrome

Cardiovascular diseases remain a leading cause of mortality globally, particularly among individuals with both obstructive sleep apnea (OSA) and metabolic syndrome (MetS). These two conditions exacerbate each other, creating a vicious cycle that increases the risk of cardiovascular diseases. Understanding the pathophysiological relationship between OSA and MetS is crucial for developing effective prevention and treatment strategies. This review explores current knowledge on the connection between OSA and MetS and discusses the progress in treatment options.

Concepts and Epidemiology of OSA and MetS

OSA is characterized by repeated upper airway collapse during sleep, leading to intermittent hypoxia and fragmented sleep patterns. Affecting 14% of the global population, OSA is more prevalent among adults aged 30–69. Symptoms include daytime sleepiness, memory issues, and headaches, significantly reducing patients' quality of life.

MetS is a cluster of metabolic abnormalities that include central obesity, high blood pressure, dyslipidemia, and insulin resistance. The prevalence of MetS is estimated at 24% in the U.S., with obesity being a key contributing factor.

The Relationship Between OSA and MetS

OSA and MetS share common risk factors like obesity and aging, and they often coexist. Studies show that patients with severe OSA are more likely to have MetS, and vice versa. The bidirectional nature of their relationship suggests that these conditions reinforce each other, further aggravating metabolic and cardiovascular risks. Obesity, particularly visceral fat, plays a central role in worsening OSA, while OSA exacerbates metabolic disturbances through intermittent hypoxia and sympathetic nervous system activation.

The Correlation Between OSA and Obesity

Visceral fat accumulation in obese individuals significantly increases the risk of OSA. Research shows that obese individuals with OSA have larger visceral fat areas compared to those without OSA. Hormonal disruptions, including lowered leptin levels and increased ghrelin levels, are associated with OSA and contribute to heightened appetite and further weight gain.

The Connection Between OSA and Hypertension

OSA is strongly associated with hypertension. The intermittent hypoxia seen in OSA triggers increased sympathetic nervous activity, which leads to spikes in blood pressure and disrupts the natural nocturnal “dipping” pattern of blood pressure. This effect contributes to elevated cardiovascular risks among OSA patients.

The Connection Between OSA and Diabetes

OSA is linked to an increased risk of developing type 2 diabetes mellitus (T2DM). Intermittent hypoxia impairs glucose regulation and insulin sensitivity, contributing to the development and worsening of T2DM. OSA patients also experience elevated inflammatory cytokine levels, which are associated with insulin resistance.

The Connection Between OSA and Dyslipidemia

Dyslipidemia is common in OSA patients, with studies showing reduced levels of high-density lipoprotein (HDL) and increased triglycerides (TG) and low-density lipoprotein (LDL) levels. Intermittent hypoxia and heightened sympathetic activity contribute to these lipid abnormalities, further increasing the risk of cardiovascular diseases.

The Influence of Various Treatments on MetS and Its Components

Continuous positive airway pressure (CPAP) therapy is the primary treatment for OSA. While CPAP effectively alleviates OSA symptoms, its impact on MetS components is limited. CPAP has shown modest effects in reducing blood pressure, total cholesterol, and insulin resistance, but long-term improvements in metabolic markers are often insufficient.

Weight management and lifestyle interventions remain critical for reversing MetS. Combining CPAP with weight loss strategies has been shown to improve inflammatory markers, insulin sensitivity, and triglyceride levels. Metabolic surgeries, such as gastric bypass, offer more substantial improvements in both OSA symptoms and metabolic health by addressing the root cause of obesity.

For patients with mild to moderate OSA, mandibular advancement devices (MADs) provide an alternative treatment option. MADs improve sleep quality and may help reduce blood pressure, though their impact on metabolic markers is less significant.

Conclusions

OSA and MetS form a complex, mutually reinforcing cycle that significantly elevates cardiovascular risks. Breaking this cycle through weight management, lifestyle interventions, and targeted therapies like CPAP and metabolic surgery can improve patient outcomes. However, more research is needed to fully understand the metabolic benefits of these treatments and optimize care for patients with both OSA and MetS.

 

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The study was recently published in the Chronic Metabolic Diseases

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