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Sökning: WFRF:(GRILL V) > (2010-2014)

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  • Ostenson, CG, et al. (författare)
  • High consumption of smokeless tobacco ("snus") predicts increased risk of type 2 diabetes in a 10-year prospective study of middle-aged Swedish men
  • 2012
  • Ingår i: Scandinavian journal of public health. - : SAGE Publications. - 1651-1905 .- 1403-4948. ; 40:8, s. 730-737
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims: Cigarette smoking increases the risk of type 2 diabetes (T2D). In Sweden and the US, people shift from smoking cigarettes to smokeless tobacco, i.e. oral moist snuff, “snus”, to attain harm-reduction. There are limited and conflicting data as to whether snus increases the risk of T2D. The present study investigated if snus use predicts the risk of T2D incidence. Methods: This is a prospective population-based study where middle-aged Swedish men ( n=2,383), without previously diagnosed T2D, were investigated with oral glucose tolerance test (OGTT) at baseline in 1992–94 and at follow-up 10 years later. Odds ratios (ORs) for newly diagnosed T2D at follow-up were assessed among those using snus, or cigarettes, at both baseline and follow-up, adjusted for major confounders. Results: The OR for T2D was not significantly increased in the whole group of snus users. However, the risk of diabetes increased with increasing weekly snus consumption; ORs (CIs) for >four boxes of snus/week were 2.1 (CI 0.9–4.9), and for >five boxes/week 3.3 (CI 1.4–8.1). For comparison, men smoking at baseline and still smoking at follow-up had an increased risk of diabetes compared with never smokers, OR 1.5 (CI 0.8–3.0), most evident for those smoking >15 cigarettes per day, OR 2.4 (CI 1.0–5.8). Tobacco use was associated with estimations of low insulin response (OGTT), but not low insulin sensitivity (HOMA). Conclusions: High consumption of snus, like smoking, predicts risk of developing T2D. This should be considered when seeking harm-reduction by changing from use of cigarettes to snus. T2D risk from tobacco use may be mediated by effects on beta-cell function.
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