Tight glycemic control in diabetes is one of the cornerstones of management. Glycemic control is usually assessed with HbA1c. The Diabetes Control and Complications Trial showed that in type 1 diabetes, decreasing HbA1c from 9.0 to 7.2% resulted in a 50–75% reduction in retinopathy, nephropathy, and neuropathy (1). The U.K. Prospective Diabetes Study (UKPDS) showed that in type 2 diabetes, decreasing HbA1c from 7.9 to 7.0% decreased retinopathy and nephropathy (2).
Increased insulin resistance occurs in smokers with and without diabetes (3,4). Smoking is also a risk factor for development of type 2 diabetes. The aim of this study was to determine whether smoking cessation was associated with improved glycemic control.
This study was a prospective cohort design and included 34 patients who ceased smoking, were followed for 1 year, and continued not to smoke at 1 year. Two control groups were randomly selected from patients participating in a prospective diabetes complications study (DCS). A DCS includes history, examination, ophthalmological review, and investigations, including HbA1c. The control groups were 34 never smokers and 34 current smokers. Smoking status was assigned based on patient self report. HbA1c was measured by high-performance liquid chromatography, with 3.5–5.7% as the normal range. Results are presented as means ± 1 SD. The study was approved by the institutional ethics committee.
Average consumption before cessation was 24 cigarettes per day. Mean age for the group who stopped smoking was 60 ± 15 years. A total of 7 subjects had type 1 diabetes, and 27 had type 2 diabetes. Mean HbA1c was 7.7 ± 2.2% while smoking and 7.0 ± 1.6% after smoking cessation (P = 0.048) (Fig. 1). Thus, the change in HbA1c was −0.70% (P < 0.0001 vs. expected change of 0%). Mean change was 0.07% for never smokers (P = 0.036) and 0.12% for continuing smokers (P < 0.01).
Some studies have shown increased insulin resistance in association with cigarette smoking (3,4). It is possible that cigarette smoking may affect glycosylation of hemoglobin, although no studies were found with a literature search. It is possible that some patients may report smoking cessation when they continue to smoke. However, it seems unlikely that patients with diabetes would report continuing to smoke after stopping. Patients incorrectly reporting nonsmoking would tend to make the observed difference smaller than the true difference.
To our knowledge, this is the first study documenting improvement in HbA1c with smoking cessation. It may reflect a change in lifestyle factors, with the decision to stop smoking, or a direct effect. The 0.7% decrease is clinically significant, approaching the 0.9% in the UKPDS (2). The small but significant increases in other groups parallel the 0.12% rise per year in the UKPDS metformin group (2). These results constitute yet another reason why patients with diabetes should not smoke.
Address correspondence to Dr. Jenny Gunton, Department of Endocrinology, Royal North Shore Hospital, St. Leonards 2065, Australia. E-mail:.
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