This is an observational analysis of NHANES 2015-2018 data, examining the association between smoking status and HbA1c in U.S. adults. The study included N=9,214 full population participants and N=7,328 adults without diabetes.
In the full population, after adjustment for cardiometabolic covariates, no significant association was found between smoking and HbA1c. For former smokers, the effect size was β=0.029% (p=0.30); for current smokers, β=0.053% (p=0.13). Among adults without diabetes, current smoking was significantly associated with higher HbA1c (β=0.067%, p<0.001), while former smoking was not (β=-0.001%, p=0.923). Using serum cotinine, active smoking (≥3.0 ng/mL) was associated with higher HbA1c in non-diabetic adults (p<0.001), but not in the full population.
The authors note key limitations: the observational design cannot establish causality, self-reported smoking may have recall bias, and NHANES data may not be generalizable to all populations. No adverse events or follow-up duration were reported.
Practice relevance is restrained; the findings support early cessation interventions and may inform counseling, but causality cannot be inferred. The analysis is based on adjusted regression models, with uncertainty preserved as reported.
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AimWe examined associations between smoking and HbA1c among U.S. adults, and whether these associations vary by diabetes status.
MethodsWe analyzed NHANES data from 2015-2018 for adults aged [≥]20 years. Smoking was assessed by self-report and serum cotinine. Survey-weighted multivariable linear regression was used to evaluate the association between smoking and HbA1c in the full population (N=9,214) and in adults without diabetes (N=7,328), adjusting for demographics, blood pressure, waist circumference, lipids, and C-reactive protein.
ResultsAfter adjustment for cardiometabolic covariates, there was no significant association between smoking and HbA1c in the full population (former: {beta}=0.029%, p=0.30; current: {beta}=0.053%, p=0.13). Among adults without diabetes, former smoking was not associated with HbA1c, whereas current smoking remained significantly associated (former: {beta}=-0.001%, p=0.923; current: {beta}=0.067%, p<0.001). These findings were similar when cotinine was used as the exposure measure, with active smoking ([≥]3.0 ng/mL) associated with higher HbA1c among non-diabetic adults (p<0.001), but not in the full population.
ConclusionsAmong adults without diabetes, current but not former smoking was associated with higher HbA1c. The absence of an association in former smokers suggests that this effect may attenuate following cessation. These findings support early cessation interventions and may inform cessation counseling and diabetes screening.