Active and passive smoking and development of glucose intolerance among young adults in a prospective cohort: CARDIA study

Abstract

Objective To assess whether active and passive smokers are more likely than non-smokers to develop clinically relevant glucose intolerance or diabetes. Design Coronary artery risk development in young adults (CARDIA) is a prospective cohort study begun in 1985-6 with 15 years of follow-up. Setting Participants recruited from Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California, USA. Participants Black and white men and women aged 18-30 years with no glucose intolerance at baseline, including 1386 current smokers, 621 previous smokers, 1452 never smokers with reported exposure to secondhand smoke (validated by serum cotinine concentrations 1-15 ng/ml), and 1113 never smokers with no exposure to secondhand smoke. Main outcome measure Time to development of glucose intolerance (glucose ≥ 100 mg/dl or taking antidiabetic drugs) during 15 years of follow-up. Results Median age at baseline was 25, 55% of participants were women, and 50% were African-American. During follow-up, 16.7% of participants developed glucose intolerance. A graded association existed between smoking exposure and the development of glucose intolerance. The 15 year incidence of glucose intolerance was highest among smokers (21.8%), followed by never smokers with passive smoke exposure (17.2%), and then previous smokers (14.4%); it was lowest for never smokers with no passive smoke exposure (11.5%). Current smokers (hazard ratio 1.65, 95% confidence interval 1.27 to 2.13) and never smokers with passive smoke exposure (1.35, 1.06 to 1.71) remained at higher risk than never smokers without passive smoke exposure after adjustment for multiple baseline sociodemographic, biological, and behavioural factors, but risk in previous smokers was similar to that in never smokers without passive smoke exposure. Conclusion These findings support a role of both active and passive smoking in the development of glucose intolerance in young adulthood.

Dietary risk factors for the development of insulin resistance in adolescent girls: a 3-year prospective study

“…These results are consistent with prospective cohorts which have assessed PUFA intake in middle-aged women (16) and dietary fibre (12) , obesity (39) and tobacco exposure in adults (18) . Our findings extend these results by suggesting that these associations operate independently in girls in late adolescence, after adjusting for variations in macronutrient intake, habitual physical activity and pubertal onset.…”

“…We compared the distribution of study variables between our analytical sample and those who participated at ages 16-17 and 18-19 years but were excluded due to missing data. Girls in the excluded group were less likely to have parents who had attended $4 years of college than those in the analytical sample (32?0 % v. 41?5 %, P , 0?001); they were also less likely to start smoking by [18][19] We conducted sensitivity analyses to explore the potential effect of excluding participants at age 16-17 or 18-19 years who had a fasting blood glucose $100-126 mg/dl indicative of IFG or $126 mg/dl as a diagnosis of T2DM (38) (2012 definitions of the American Diabetes Association (ADA)), to focus on the role of these risk factors in prevention. All analyses were conducted using the Stata version 10 statistical software package.…”

Association between the time of length since smoking cessation and insulin resistance in asymptomatic Korean male ex-smokers

“…Many studies have shown that active smoking increases the prevalence and incidence of not only type 2 diabetes mellitus (DM) [13][14][15] but also glucose intolerance [16]. The causes of insulin resistance are not well defined, but both genetic and environmental factors including obesity, physical inactivity, and smoking may play a role.…”

Association of smoking with prevalence of common diseases and metabolic abnormalities in community-dwelling Japanese individuals

“…Previous cross-sectional studies also reported that smokers exhibited elevated GFRs compared with nonsmokers (42,43). Smoking causes glucose intolerance (38), whereas higher insulin resistance was demonstrated to be associated with increased GFR (44). These observations indicate that smoking induces a rise in GFR, at least in part, via its effects on glucose intolerance.…”

“…In addition, previous studies demonstrated a significant association between smoking and MetS (36,37). Smoking increases the risk of dyslipidemia (9,21,22) and causes glucose intolerance (38), leading to an increased risk of T2DM (10).…”