Luo J, Rossouw J, Margolis KL. Smoking Cessation, Weight Change, and Coronary Heart Disease Among Postmenopausal Women With and Without Diabetes. JAMA. 2013;310(1):94-96. doi:10.1001/jama.2013.6871
Cigarette smoking is an important cause of cardiovascular disease, and smoking cessation reduces the risk.1,2 However, weight gain after smoking cessation may increase the risk of diabetes and weaken the benefit of quitting.3 One study4 found an association between smoking cessation and a lower risk of cardiovascular events among participants without diabetes that was not modified by weight gain. However, this study4 had limited power for participants with diabetes and the more specific outcome of coronary heart disease (CHD). We used data from the Women’s Health Initiative (WHI)5 to assess the association between smoking cessation, weight gain, and subsequent CHD risk among postmenopausal women with and without diabetes.
In the WHI, 161 808 postmenopausal women aged 50 through 79 years were recruited from 40 sites between 1993 and 1998 and followed up every 6 to 12 months. Loss to follow-up was 3% to 5%. Smoking status was defined by self-report at baseline and year 3. Never smokers and former smokers did not smoke at either time point, current smokers smoked at both time points, and those who had newly quit smoked at baseline but not at year 3.
Women without known cancer or cardiovascular disease at baseline or CHD at year 3 were followed up until CHD diagnosis, date of death, loss to follow-up, or September 30, 2010, whichever occurred first. Cases of CHD were adjudicated by physicians and defined as the first occurrence of clinical myocardial infarction, silent myocardial infarction, or death due to CHD.
Diabetes was self-reported and defined as either having diabetes at baseline or year 3. Self-reported diabetes in the WHI has been validated as an indicator of diagnosed diabetes.6 Cox proportional hazards regression models were used to estimate hazard ratios (HRs) for risk of CHD in relation to smoking status stratified by diabetes status and weight gain between baseline and year 3 (categorized as <5 kg, 5-<10 kg, or ≥10 kg), with and without additional adjustment for covariates.
Statistical analyses were performed using SAS version 9.3 (SAS Institute Inc). The WHI study was approved by institutional review boards at all participating centers. All participants gave written informed consent.
Of 104 391 women followed up, 3381 developed CHD during a mean (SD) of 8.8 (2.8) years. Baseline characteristics appear in Table 1. The incidence rates of CHD per 1000 person-years were 3.3 in never smokers, 3.7 in former smokers, 7.6 in current smokers, and 5.3 in those who had newly quit. Among 98 053 women without diabetes, those who had newly quit had an adjusted HR for CHD of 0.74 (95% CI, 0.57-0.95) compared with current smokers; for former smokers, the adjusted HR was 0.39 (95% CI, 0.34-0.45). Among 6338 women with diabetes, those who had newly quit had a lower risk for CHD (HR, 0.36; 95% CI, 0.17-0.78), as did former smokers (HR, 0.41; 95% CI: 0.29-0.59) compared with current smokers. These associations were unchanged after further adjustment for weight change (Table 2).
Among women who gained less than 5 kg, the association between smoking status and CHD risk was similar to the overall results in both women with and without diabetes (Table 2). Among women without diabetes who gained 5 kg to less than 10 kg or 10 kg or more, former smokers had a lower CHD risk than current smokers. In women with diabetes who gained 5 kg to less than 10 kg, neither those who had newly quit nor former smokers had a statistically significantly lower CHD risk than current smokers. The number of women with diabetes and a weight gain of 10 kg or more was too small to allow modeling.
In this study, smoking cessation was associated with a lower risk of CHD among postmenopausal women with and without diabetes. Weight gain following smoking cessation weakened this association, especially for women with diabetes who gained 5 kg or more, although power was limited in this subgroup due to the small number of cases. Other limitations of the study are that it included only postmenopausal women and did not account for further changes in smoking, weight, or diabetes status after year 3.
Corresponding Author: Juhua Luo, PhD, Indiana University School of Public Health, 1025 E Seventh St, Bloomington, IN 47405 (firstname.lastname@example.org).
Author Contributions: Dr Luo had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Luo, Rossouw, Margolis.
Acquisition of data: Luo, Margolis.
Analysis and interpretation of data: Luo, Rossouw, Margolis.
Drafting of the manuscript: Luo.
Critical revision of the manuscript for important intellectual content: Rossouw, Margolis.
Statistical analysis: Luo.
Obtained funding: Rossouw.
Study supervision: Rossouw, Margolis.
Conflict of Interest Disclosures: The authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
Funding/Support: The Women’s Health Initiative is funded by the National Heart, Lung, and Blood Institute, National Institutes of Health, US Department of Health and Human Services through contracts N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122, 42107-26, 42129-32, and 44221.
Role of the Sponsors: The funding agency oversaw the design and conduct of the overall Women’s Health Initiative study. Other than Dr Rossouw’s role as an author, the funding agency had no role in the collection, management, analysis and interpretation of the data for this manuscript, in the preparation or approval of the manuscript, or the decision to submit the manuscript for publication.