Published online Apr 28, 2020. doi: 10.13105/wjma.v8.i2.119
Peer-review started: February 5, 2020
First decision: March 21, 2020
Revised: April 8, 2020
Accepted: April 21, 2020
Article in press: April 21, 2020
Published online: April 28, 2020
Processing time: 82 Days and 22.8 Hours
Evidence relating tobacco smoking to type 2 diabetes has accumulated rapidly in the last few years, rendering earlier reviews considerably incomplete.
To review and meta-analyse evidence from prospective studies of the relationship between smoking and the onset of type 2 diabetes.
Prospective studies were selected if the population was free of type 2 diabetes at baseline and evidence was available relating smoking to onset of the disease. Papers were identified from previous reviews, searches on Medline and Embase and reference lists. Data were extracted on a range of study characteristics and relative risks (RRs) were extracted comparing current, ever or former smokers with never smokers, and current smokers with non-current smokers, as well as by amount currently smoked and duration of quitting. Fixed- and random-effects estimates summarized RRs for each index of smoking overall and by various subdivisions of the data: Sex; continent; publication year; method of diagnosis; nature of the baseline population (inclusion/exclusion of pre-diabetes); number of adjustment factors; cohort size; number of type 2 diabetes cases; age; length of follow-up; definition of smoking; and whether or not various factors were adjusted for. Tests of heterogeneity and publication bias were also conducted.
The literature searches identified 157 relevant publications providing results from 145 studies. Fifty-three studies were conducted in Asia and 53 in Europe, with 32 in North America, and seven elsewhere. Twenty-four were in males, 10 in females and the rest in both sexes. Fifteen diagnosed type 2 diabetes from self-report by the individuals, 79 on medical records, and 51 on both. Studies varied widely in size of the cohort, number of cases, length of follow-up, and age. Overall, random-effects estimates of the RR were 1.33 [95% confidence interval (CI): 1.28-1.38] for current vs never smoking, 1.28 (95%CI: 1.24-1.32) for current vs non-smoking, 1.13 (95%CI: 1.11-1.16) for former vs never smoking, and 1.25 (95%CI: 1.21-1.28) for ever vs never smoking based on, respectively, 99, 156, 100 and 100 individual risk estimates. Risk estimates were generally elevated in each subdivision of the data by the various factors considered (exceptions being where numbers of estimates in the subsets were very low), though there was significant (P < 0.05) evidence of variation by level for some factors. Dose-response analysis showed a clear trend of increasing risk with increasing amount smoked by current smokers and of decreasing risk with increasing time quit. There was limited evidence of publication bias.
The analyses confirmed earlier reports of a modest dose-related association of current smoking and a weaker dose-related association of former smoking with type 2 diabetes risk.
Core tip: Based on data from 145 follow-up studies of individuals free of type 2 diabetes at baseline, we confirm evidence of a modest association of smoking with subsequent onset of the disease. Meta-analysis showed relative risks of 1.33 [95% confidence interval (CI): 1.28-1.38] for current vs never smoking, 1.28 (95%CI: 1.24-1.32) for current vs non-smoking, and 1.13 (95%CI: 1.11-1.16) for former smoking. Risks increased with amount smoked and decreased with time quit. Elevated risks were consistently seen when the data were subdivided by various factors, suggesting that the associations are not a result of uncontrolled confounding.