Sleep Apnea and Sleep Habits: Relationships with Metabolic Syndrome

Anne-Laure Borel, Anne-Laure Borel

Abstract

Excess visceral adiposity is a primary cause of metabolic syndrome and often results from excess caloric intake and a lack of physical activity. Beyond these well-known etiologic factors, however, sleep habits and sleep apnea also seem to contribute to abdominal obesity and metabolic syndrome: Evidence suggests that sleep deprivation and behaviors linked to evening chronotype and social jetlag affect eating behaviors like meal preferences and eating times. When circadian rest and activity rhythms are disrupted, hormonal and metabolic regulations also become desynchronized, and this is known to contribute to the development of metabolic syndrome. The metabolic consequences of obstructive sleep apnea syndrome (OSAS) also contribute to incident metabolic syndrome. These observations, along with the first sleep intervention studies, have demonstrated that sleep is a relevant lifestyle factor that needs to be addressed along with diet and physical activity. Personalized lifestyle interventions should be tested in subjects with metabolic syndrome, based on their specific diet and physical activity habits, but also according to their circadian preference. The present review therefore focuses (i) on the role of sleep habits in the development of metabolic syndrome, (ii) on the reciprocal relationship between sleep apnea and metabolic syndrome, and (iii) on the results of sleep intervention studies.

Keywords: chronotype; metabolic syndrome; sleep; sleep apnea; sleep duration; sleep habit; social jetlag.

Conflict of interest statement

The author declares no conflict of interest.

Figures

Figure 1
Figure 1
Schema showing the roles of intrinsic and extrinsic factors associated with evening chronotype in the risk of developing metabolic syndrome.
Figure 2
Figure 2
Bidirectional relationship between obstructive sleep apnea syndrome and metabolic syndrome. ROS, reactive oxygen species; IGF-1, insulin-like growth factor 1.

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Source: PubMed

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