Sleep Apnoea & Hypertension: Physiological bases for a causal relation Sleep and the metabolic syndrome
Experimental Physiology 92.1 pp 67-78
DOI: 10.1113/expphysiol.2006.033787
© The Physiological Society 2007

Themed Issue Papers
Sleep Apnoea & Hypertension: Physiological bases for a causal relation
Sleep and the metabolic syndrome
Robert Wolk1,2 and Virend K. Somers2

1 Cardiovascular/Metabolic Diseases, Pfizer Global Research & Development, Pfizer Inc., Groton, CT, USA 2 Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA

The metabolic syndrome represents a clustering of several interrelated risk factors of metabolic origin that are thought to increase cardiovascular risk. It is still uncertain whether this clustering results from multiple underlying risk factors or whether it has a single cause. One metabolic abnormality that may underlie several clinical characteristics of the metabolic syndrome is insulin resistance. This review discusses the evidence that sleep disturbances (obstructive sleep apnoea, sleep deprivation and shift work) may independently lead to the development of both insulin resistance and individual clinical components of the metabolic syndrome. The converse may also be true, in that metabolic abnormalities associated with the metabolic syndrome and insulin resistance may potentially exacerbate sleep disorders. The notion that sleep disturbances exert detrimental metabolic effects may help explain the increasing prevalence of the metabolic syndrome and insulin resistance in the general population and may have important implications for population-based approaches to combat the increasing epidemic of metabolic and cardiovascular disease.

(Received 3 August 2006; accepted after revision 30 October 2006; first published online 3 November 2006)

Corresponding author R. Wolk: Cardiovascular/Metabolic Diseases, Pfizer Global Research & Development, Eastern Point Road, MS 8260-2506, Groton, CT 06340, USA. Email: robert.wolk@pfizer.com
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