Lycett, Deborah, Nichols, Linda, Ryan, Ronan, Farley, Amanda, Roalfe, Andrea, Mohammed, Mohammed A., Szatkowski, Lisa, Coleman, Tim, Morriss, Richard K., Farmer, Andrew and Aveyard, Paul
(2015)
The association between smoking cessation and glycaemic control in patients with type 2 diabetes: a THIN database cohort study.
Lancet Diabetes & Endocrinology, 3
(6).
pp. 423-430.
ISSN 2213-8595
Full text not available from this repository.
Abstract
Background
Smoking increases the risk of developing type 2 diabetes. However, several population studies also show a higher risk in people 3–5 years after smoking cessation than in continuing smokers. After 10–12 years the risk equates to that of never-smokers. Small cohort studies suggest diabetes control deteriorates temporarily during the first year after quitting. We examined whether or not quitting smoking was associated with altered diabetes control in a population study, for how long this association persisted, and whether or not this association was mediated by weight change.
Methods
We did a retrospective cohort study (Jan 1, 2005, to Dec 31, 2010) of adult smokers with type 2 diabetes using The Health Improvement Network (THIN), a large UK primary care database. We developed adjusted multilevel regression models to investigate the association between a quit event, smoking abstinence duration, change in HbA1c, and the mediating effect of weight change.
Findings
10 692 adult smokers with type 2 diabetes were included. 3131 (29%) quit smoking and remained abstinent for at least 1 year. After adjustment for potential confounders, HbA1c increased by 0·21% (95% CI 0·17–0·25; p<0·001; [2·34 mmol/mol (95% CI 1·91–2·77)]) within the first year after quitting. HbA1c decreased as abstinence continued and became comparable to that of continual smokers after 3 years. This increase in HbA1c was not mediated by weight change.
Interpretation
In type 2 diabetes, smoking cessation is associated with deterioration in glycaemic control that lasts for 3 years and is unrelated to weight gain. At a population level, this temporary rise could increase microvascular complications.
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