Obesity is a global epidemic that has far-reaching economic and public health implications . Excess body weight is associated with multiple comorbidities including type 2 diabetes (T2DM), hypertension, obstructive sleep apnea (OSA), and cardiovascular disease (CVD) . Dysglycemia andOSA share common risk factors such as age and obesity; hence it is not surprising that OSA and glycemic abnormalities often coexist.
Despite the close association between OSA and dysglycemia, the direction of this association and whether obesity modulates the association remain unclear. The interaction between multiple genetic and environmental factors gives rise to a heterogeneous and progressive condition with variable degrees of insulin resistance (IR) and pancreatic β-cell dysfunction . When β cells are no longer able to secrete sufficient insulin to overcome IR, impaired glucose tolerance (IGT) progresses to T2DM . OSA is associated with different factors that alter IR and β-cell function suggesting that OSA can result in glycemic abnormalities. On the other hand, dysglycemia and its association with inflammation and autonomic dysfunction can lead to or worsen pre-existing sleep apnea .
An increasing number of human and animal studies have expanded our understanding of the association between OSA and dysglycemia and how each condition modulates the metabolic impacts of the other . In this chapter we aim to review the evidence for the association between OSA and dysglycemia, to explore the underlying mechanisms and to assess the metabolic impacts of OSA in the presence of dysglycemia and vice versa. The mainstay of this chapter will focus on OSA, rather than central sleep apnea (CSA), as it is the most common type of sleep apnea and the one that is closely related to obesity and T2DM. We will, however, highlight some important issues in relation to CSA when needed.
Sleep apnea can be either central or obstructive. OSA is a common medical disorder that is characterized by instability of the upper airway during sleep, which results in markedly reduced (hypopnea) or absent (apnea) airflow at the nose or mouth . These apnea/hypopnea episodes are usually accompanied with oxygen desaturations and micro arousals that cause sleep fragmentation and reduction in slow wave and rapid eye movement (REM) sleep . The American Academy of Sleep Medicine (AASM) 2007 guideline has defined sleep events apnea as cessation or ≥90% reduction in airflow for a period of ≥10 seconds and hypopnea as ≥30% reduction in airflow for ≥10 seconds associated with ≥4% drop in oxygen saturations; an alternative definition of hypopnea based on ≥50% reduction in airflow with ≥3% drop in oxygen saturations can also be used . The updated AASM 2012 guidelines defined hypopnea in adults as ≥30% drop of air flow of pre-event baseline for ≥10 seconds in association with either ≥3% arterial oxygen desaturation or an arousal . Apneas are classified into obstructive or central based on the presence or absence of respiratory/abdominal efforts. An example of apneas and hypopneas can be found in Figure 22.1.
The apnea-hypopnea index (AHI) is the average number of apnea and hypopnea episodes per hour during sleep and is a marker of the severity of OSA . An AHI of ≥5 events per hour is consistent with the diagnosis of OSA . OSA can be classified to mild, moderate, and severe based on AHI 5 to <15, 15 to <30, and ≥30 events per hour. The respiratory disturbance index (RDI) is another OSA measure that includes the AHI in addition to respiratory effort-related arousal, which is defined as a sequence of breaths characterized by increasing respiratory effort leading to an arousal from sleep, but which does not meet criteria for an apnea or hypopnea . Another measure of OSA is the oxygen desaturation index (ODI), which is the average number of oxygen desaturations per hour during sleep.