Comparison of the association with sleep apnoea of obesity<i>versus</i>insulin resistance

Liu, Alice; Ariel, Danit; Lamendola, Cindy; Kim, Sun H.; Cardell, James; Tomasso, Vanessa; Mojaddidi, Hafasa; Grove, Kaylene; Kushida, Clete A.; Reaven, Gerald M.

doi:10.1183/13993003.01087-2015

Cited by 1 publication

(1 citation statement)

References 17 publications

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“…Furthermore, a "bidirectional" or "reciprocal" relationship, or the possibility that OSA is a manifestation of the metabolic syndrome, has been discussed in several publications [7][8][9][10]. However, while evidence continues to grow that sleep-disordered breathing and sleep disruption can worsen metabolic function including insulin resistance [11], there is currently limited direct evidence to support the concept that early biomarkers of metabolic dysfunction such as insulin resistance predispose to OSA [12,13]. Thus, the chicken or the egg causality dilemma remains.…”

Section: @Erspublicationsmentioning

confidence: 99%

When insulin has to work hard to keep the sugar at bay the upper airway collapses away

Eckert

Oliven

2016

Eur Respir J

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@ERSpublicationsInsulin resistance may increase upper airway collapsibility and directly contribute to sleep apnoea pathogenesis http://ow.ly/10BTf9Obesity is a major risk factor for both obstructive sleep apnoea (OSA) and metabolic disease. As obesity rates continue to rise, so too does the prevalence of OSA and metabolic disorders. Indeed, recent community sample data from over 2000 adults aged 40-85 years in Switzerland indicate that up to 50% of men and almost a quarter of women have apnoea-hypopnoea indices (AHI) within the moderate to severe range (>15 events·h −1 sleep) [1]. Insulin resistance, a strong predictor for the development of type 2 diabetes [2], is being recognised earlier with prevalence rates in children varying between 3 and 44% [3]. Thus, OSA and insulin resistance are major health issues.Given the shared link with obesity, the connection between metabolic disruption and OSA is not new. Indeed, OSA has been implicated in the pathogenesis of metabolic dysfunction [4][5][6]. Furthermore, a "bidirectional" or "reciprocal" relationship, or the possibility that OSA is a manifestation of the metabolic syndrome, has been discussed in several publications [7][8][9][10]. However, while evidence continues to grow that sleep-disordered breathing and sleep disruption can worsen metabolic function including insulin resistance [11], there is currently limited direct evidence to support the concept that early biomarkers of metabolic dysfunction such as insulin resistance predispose to OSA [12,13]. Thus, the chicken or the egg causality dilemma remains.The new study by LLANOS et al. [14] in this issue of the European Respiratory Journal takes us one step closer to solving this dilemma. Specifically, the authors have provided elegant insight into this question by going to the source; evaluating the relationship between pre-diabetes (i.e. insulin resistance), and "pre-OSA" (i.e. individuals with vulnerable upper airways due to high mechanical load from morbid obesity but without frank OSA (AHI <10 events/h sleep)). This unique approach has allowed the investigators to study upper airway collapsibility during sleep, using the gold standard critical closing pressure or "Pcrit" technique, without the confounding effects of prior exposure to repetitive severe hypoxaemia and sleep fragmentation, both of which contribute to metabolic sequelae [5,15]. Accordingly, consistent with insulin resistance preceding the decline in pharyngeal stability, the reported positive correlation between insulin resistance and upper airway collapsibility and the ∼4 cmH 2 O increase in Pcrit when the group was dichotomised according to high versus low insulin resistance cannot be explained by the presence of severe sleep-disordered breathing.

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