OBJECTIVESmoking is an established risk factor for type 2 diabetes. In contrast, it has been proposed that smoking may reduce the risk of latent autoimmune diabetes in adults (LADA), but studies are scarce. We aimed to study the impact of smoking on LADA and type 2 diabetes risks.
RESEARCH DESIGN AND METHODSWe used data from a Swedish case-control study including incident case patients with LADA (GAD antibody [GADA] positive, n = 377) and type 2 diabetes (GADA negative, n = 1,188) and control subjects randomly selected from the population (n = 1,472). We calculated odds ratios (ORs) with 95% CIs by logistic regression, adjusted for age, sex, BMI, family history of diabetes, and alcohol consumption.
RESULTSThere was no indication of reduced risk of LADA in smokers; instead, heavy smoking was associated with an increased risk of LADA (OR 1.37, 95% CI 1.02-1.84). Heavy smokers had higher levels of HOMA of insulin resistance (9.89 vs. 4.38, P = 0.0479) and HOMA of b-cell function (55.7 vs. 42.5, P = 0.0204), but lower levels of GADA (75 vs. 250, P = 0.0445), compared with never smokers. Smokers also displayed an increased risk of type 2 diabetes (OR in ever smokers 1.53, 95% CI 1.25-1.88).
CONCLUSIONSIn this large population of LADA patients, we did not observe a protective effect of smoking on autoimmunity and the risk of LADA. A protective effect could possibly be masked by a smoking-induced aggravation of insulin resistance, akin to the diabetogenic effect seen in individuals with type 2 diabetes.Smoking increases the risk of type 2 diabetes (1). This effect is exerted mainly through a decrease in insulin sensitivity (2). Knowledge about the impact of smoking on other forms of diabetes is limited. In a study based on the Norwegian HUNT study (3), we showed that smoking is associated with a reduced risk of latent autoimmune diabetes in adults (LADA). These findings fit with previous observations (4,5) in individuals with type 1 diabetes, indicating a reduced risk in the offspring of smoking parents. A suggested mechanism behind a protective effect could be the modulating effect of smoking/exposure to nicotine on immune response and an inflammatory process (6,7). The clinical impact of such a biological mechanism has been debated