The Authors: Jamie CM Lam, MD, is Honorary Clinical Assistant Professor of Medicine, with expertise in sleep related breathing disorders, carcinoma of lung and bronchiectasis. Judith CW Mak, PhD, is Assistant Professor of Medicine with an interest in laboratory research of chronic obstructive pulmonary disease, asthma and intermittent hypoxia. Mary SM Ip, MD, is Mok Hing Yiu Endowed Chair Professor in Respiratory Medicine, with special interest in sleep related breathing disorders and chronic airway diseases. She is also the Chief of the Division of Respiratory Medicine, Department of Medicine, Queen Mary Hospital, The University of Hong Kong.
Obesity, obstructive sleep apnoea and metabolic syndrome
Version of Record online: 24 JAN 2012
© 2011 The Authors. Respirology © 2011 Asian Pacific Society of Respirology
Volume 17, Issue 2, pages 223–236, February 2012
How to Cite
LAM, J. C. M., MAK, J. C. W. and IP, M. S. M. (2012), Obesity, obstructive sleep apnoea and metabolic syndrome. Respirology, 17: 223–236. doi: 10.1111/j.1440-1843.2011.02081.x
SERIES EDITOR: AMANDA J. PIPER
- Issue online: 24 JAN 2012
- Version of Record online: 24 JAN 2012
- Accepted manuscript online: 12 OCT 2011 02:15PM EST
- Received 25 August 2011; invited to revise 6 September 2011; revised 9 September 2011; accepted 10 September 2011.
- mechanistic pathway;
- metabolic syndrome;
- obstructive sleep apnoea
OSA is increasingly recognized as a major health problem in developed countries. Obesity is the most common risk factor in OSA and hence, the prevalence of OSA is undoubtedly rising given the epidemic of obesity. Recent data also suggest that OSA is highly associated with the metabolic syndrome, and it is postulated that OSA contributes to cardiometabolic dysfunction, and subsequently vasculopathy.
Current evidence regarding the magnitude of impact on ultimate cardiovascular morbidity or mortality attributable to OSA-induced metabolic dysregulation is scarce. Given the known pathophysiological triggers of intermittent hypoxia and sleep fragmentation in OSA, the potential mechanisms of OSA–obesity–metabolic syndrome interaction involve sympathetic activation, oxidative stress, inflammation and neurohumoral changes. There is accumulating evidence from human and animal/cell models of intermittent hypoxia to map out these mechanistic pathways.
In spite of support for an independent role of OSA in the contribution towards metabolic dysfunction, a healthy diet and appropriate lifestyle modifications towards better control of metabolic function are equally important as CPAP treatment in the holistic management of OSA.