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Review

Endocrine and metabolic effects of smoking cessation

Pages 527-534 | Accepted 12 Dec 2008, Published online: 27 Jan 2009
 

ABSTRACT

Background: Cardiovascular, pulmonary, and oncological hazards of tobacco smoking have been well studied. Smoking may also have multiple effects on endocrine and metabolic systems affecting pituitary, thyroid, and adrenal glands; testicular and ovarian function; as well as energy balance; lipid, and glucose metabolism; and insulin resistance. Less is known about hormonal and metabolic effects that patients may experience while quitting smoking.

Scope: The objective of this article is to review systematically data on the endocrine and metabolic effects of smoking cessation. Articles based upon clinical trials, randomised controlled trials, and meta-analyses were obtained via a MEDLINE search (articles published between 1 August 1998 and 31 July 2008, inclusive; English language; human subjects; including abstracts) using key search terms relating to smoking cessation and endocrine or metabolic parameters. Additional studies were identified from the bibliographies of reviewed literature. Studies related to the search criteria were reviewed, 199 papers were identified, and 57 pertinent to this review were included.

Findings: Limited data are available on the short- and long-term effects of smoking cessation on hypothalamic– and thyroid–pituitary–adrenal axes, sex hormones, energy homeostasis, and lipid and glucose metabolism. Initial data indicate that smoking cessation is associated with decreased cortisol levels and in the short-term, smoking cessation does not correct the diminished adrenocortical responses to stress caused by chronic smoking. Cessation reverses smoking's effects on thyroid disorders and may reduce the risk of osteoporosis. Finally, smoking cessation increases transiently food intake and sustained weight gain and is associated with increases in high-density lipoprotein cholesterol levels that occur rapidly on cessation.

Conclusion: Further research may provide insight into post-cessation endocrine changes that may be caused by alterations to central and peripheral systems. Such research may increase the understanding of underlying biological mechanisms that lead to symptoms and clinical features of smoking cessation.

Acknowledgements

Declaration of interest: I. B. declares having received consulting fees during the last 3 years from Pfizer and sanofi-aventis. Editorial support was provided by Ray Beck Jr, PhD, and Zoë Thornton-Jones, PhD, of Envision Pharma and was funded by Pfizer Ltd.

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