Abstract

Insulin resistance can be affected directly or indirectly by smoking. This cross-sectional study aimed at examining the association between smoking patterns and insulin resistance using objective biomarkers. Data from 4043 participants sourced from the Korea National Health and Nutrition Examination Survey, conducted from 2016 to 2018, were examined. Short-term smoking patterns were used to classify participants according to urine levels of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and cotinine as continuous-smokers, past-smokers, current-smokers, and non-smokers. Insulin resistance was calculated using the triglyceride-glucose index from blood samples and was defined as either high or low. Multiple logistic regression analysis was performed to investigate the association between smoking behavior and insulin resistance. Men and women who were continuous-smokers (men: odds ratio [OR] = 1.74, p = 0.001; women: OR = 2.01, p = 0.001) and past-smokers (men: OR = 1.47, p = 0.033; women: OR = 1.37, p = 0.050) were more likely to have high insulin resistance than their non-smoking counterparts. Long-term smokers (≥ 40 days) are at an increased risk of insulin resistance in short-term smoking patterns. Smoking cessation may protect against insulin resistance. Therefore, first-time smokers should be educated about the health benefits of quitting smoking.

Highlights

  • Insulin resistance can be affected directly or indirectly by smoking

  • Several previous studies have examined the relationship between smoking and insulin resistance using selfreported data; studies on this relationship using biomarkers remain rare

  • Our study found that NNAL and cotinine concentrations in short-term smoking patterns were associated with insulin resistance risk in continuous- and past-smokers who met the smoking criteria

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Summary

Introduction

Insulin resistance can be affected directly or indirectly by smoking This cross-sectional study aimed at examining the association between smoking patterns and insulin resistance using objective biomarkers. Direct methods of assessing insulin resistance include euglycemic-hyperinsulinemia clamp and insulin suppression tests and simple indirect indicators are estimated by the homeostasis model assessment of insulin resistance (HOMA-IR)[2–4] These tests are invasive, complex, and expensive, making their application difficult in large-scale population studies and clinical p­ ractice[5]. Several prospective studies on the relationship between smoking and insulin resistance have shown that smoking is a risk factor for insulin r­ esistance[10–13] These studies have mostly used self-reporting as a method of measuring exposure to smoking, and this may have led to incorrect measurement, as self-reported and biomarker results show a consistency of only 46–53%; in addition, self-reports tend to be unreliable for quantitative assessments of smoking ­volume[14,15]. Intake, facilitation of consistent detection of people exposed to tobacco, and evaluation of long-term exposure to harmful s­ ubstances[23]

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