TY - JOUR
T1 - Tobacco use, insulin resistance, and risk of type 2 diabetes
T2 - Results from the multi-ethnic study of atherosclerosis
AU - Keith, Rachel J.
AU - Al Rifai, Mahmoud
AU - Carruba, Christopher
AU - De Jarnett, Natasha
AU - McEvoy, John W.
AU - Bhatnagar, Aruni
AU - Blaha, Michael J.
AU - Defilippis, Andrew P.
N1 - Funding Information:
Research reported in this publication was supported by the AHA Tobacco Regulation and Addiction Center (A-TRAC) and FDA Center for Tobacco Products (CTP). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH or the Food and Drug Administration. The authors thank the other investigators, the staff, and the participants of the MESA study for their valuable contributions. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org . Exam 1 and 5 Urinary Cotinine measurements are available to the MESA study courtesy of MESA Lung contract HL077612.
Publisher Copyright:
© 2016 Keith et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2016/6
Y1 - 2016/6
N2 - Introduction: Tobacco use is associated with insulin resistance and incident diabetes. Given the racial/ethnic differences in smoking patterns and incident type 2 diabetes our objective was to evaluate the association between tobacco use and insulin resistance (IR) as well as incident type 2 diabetes mellitus in a contemporary multiethnic cohort. Methods and Results: We studied 5,931 Multi- Ethnic Study of Atherosclerosis (MESA) participants who at base-line were free of type 2 diabetes (fasting glucose ≥7.0 mmol/l (126 mg/dl) and/or use of insulin or oral hypoglycemic medications) categorized by self-reported tobacco status and reclassified by urinary cotinine (available in 58% of participants) as never, current or former tobacco users. The association between tobacco use, IR (fasting plasma glucose, insulin, and the homeostatic model assessment of insulin resistance (HOMA-IR)) and incident diabetes over 10 years was evaluated using multivariable linear regression and Cox proportional hazards models, respectively. Mean age of the participants was 62 (±10) years, 46% were male, 41% Caucasian, 12% Chinese, 26% African American and 21% Hispanic/Latino. IR biomarkers did not significantly differ between current, former, and never cigarette users (P >0.10) but showed limited unadjusted differences for users of cigar, pipe and smokeless tobacco (All P <0.05). Fully adjusted models showed no association between dose or intensity of tobacco exposure and any index of IR. When stratified into participants that quit smoking vs. those who continued smoking during the 10-year study there was no difference in serum glucose levels or frequency of diabetes. In fully adjusted models, there was no significant difference in diabetes risk between former or current cigarette smokers compared to never smokers [HR (95% CI) 1.02 (0.77,1.37) and 0.81 (0.52,1.26) respectively]. Conclusion: In a contemporary multi-ethnic cohort, there was no independent association between tobacco use and IR or incident type 2 diabetes. The role smoking plays in causing diabetes may be more complicated than originally thought and warrants more in-depth large contemporary multi-ethnic studies.
AB - Introduction: Tobacco use is associated with insulin resistance and incident diabetes. Given the racial/ethnic differences in smoking patterns and incident type 2 diabetes our objective was to evaluate the association between tobacco use and insulin resistance (IR) as well as incident type 2 diabetes mellitus in a contemporary multiethnic cohort. Methods and Results: We studied 5,931 Multi- Ethnic Study of Atherosclerosis (MESA) participants who at base-line were free of type 2 diabetes (fasting glucose ≥7.0 mmol/l (126 mg/dl) and/or use of insulin or oral hypoglycemic medications) categorized by self-reported tobacco status and reclassified by urinary cotinine (available in 58% of participants) as never, current or former tobacco users. The association between tobacco use, IR (fasting plasma glucose, insulin, and the homeostatic model assessment of insulin resistance (HOMA-IR)) and incident diabetes over 10 years was evaluated using multivariable linear regression and Cox proportional hazards models, respectively. Mean age of the participants was 62 (±10) years, 46% were male, 41% Caucasian, 12% Chinese, 26% African American and 21% Hispanic/Latino. IR biomarkers did not significantly differ between current, former, and never cigarette users (P >0.10) but showed limited unadjusted differences for users of cigar, pipe and smokeless tobacco (All P <0.05). Fully adjusted models showed no association between dose or intensity of tobacco exposure and any index of IR. When stratified into participants that quit smoking vs. those who continued smoking during the 10-year study there was no difference in serum glucose levels or frequency of diabetes. In fully adjusted models, there was no significant difference in diabetes risk between former or current cigarette smokers compared to never smokers [HR (95% CI) 1.02 (0.77,1.37) and 0.81 (0.52,1.26) respectively]. Conclusion: In a contemporary multi-ethnic cohort, there was no independent association between tobacco use and IR or incident type 2 diabetes. The role smoking plays in causing diabetes may be more complicated than originally thought and warrants more in-depth large contemporary multi-ethnic studies.
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U2 - 10.1371/journal.pone.0157592
DO - 10.1371/journal.pone.0157592
M3 - Article
C2 - 27322410
AN - SCOPUS:84976891162
SN - 1932-6203
VL - 11
JO - PloS one
JF - PloS one
IS - 6
M1 - e0157592
ER -