In the August 2005 issue of Diabetes Care, Oh et al. (1) reported that, in a representative population-based sample of 3,452 Korean men, cigarette smoking is associated with the metabolic syndrome. They also show a dose-dependent effect, with prevalence of the syndrome progressively increasing with the number of cigarettes smoked. Of the components of the syndrome, dyslipidemia (high triglycerides and low HDL cholesterol) and abdominal obesity are shown to be the main contributors to this association. The underlying mechanisms of this association are not explored. Insulin resistance and compensatory hyperinsulinemia are considered central features of the metabolic syndrome, yet neither factor is measured in this study.
We have explored this same issue in a large population-based sample of 2,370 nondiabetic men, aged 35–65 years, in whom the components of the metabolic syndrome, defined according to Adult Treatment Panel III criteria, were evaluated together with fasting plasma insulin; homeostasis model assessment of insulin resistance index was also calculated as a validated surrogate measure of insulin resistance.
In agreement with Oh et al., we find that chronic smoking is associated with higher triglycerides and lower HDL cholesterol with a dose effect. However, other key components of the metabolic syndrome, such as hypertension and hyperglycemia, were less common in smokers. These results were not modified after correction for BMI, alcohol and coffee consumption, and use of antihypertensive medication. Furthermore, fasting plasma insulin concentrations were very similar in smokers and never-smokers (8.02 ± 4.63 vs. 8.34 ± 3.35 μU/ml), whereas homeostasis model assessment of insulin resistance index was significantly lower in smokers (1.99 ± 1.12 vs. 2.12 ± 0.91, P < 0.01) due to the lower glucose values observed in this group.
Our data therefore confirm the finding by Oh et al. of an increased prevalence of the metabolic syndrome in smokers but suggest that this is mainly driven by higher prevalence of dyslipidemia. Furthermore, our findings expand the interpretation by providing evidence that smoking-associated dyslipidemia may be mediated by mechanisms other than insulin resistance.
