Background Studies in animal models and on human cells have suggested that sodium chloride may affect autoimmunity by the induction of pathogenic Th17 cells mediated through salt-sensing kinase-1. Since Th17 cells may play a role in the early stages of disease development of rheumatoid arthritis (RA), the dietary intake of sodium is of interest to analyse as a risk factor for the development of RA.
Objectives To investigate if sodium intake is associated with increased risk for developing RA.
Methods A nested case–control study was performed using the population based prospective data from the Västerbotten Intervention Programme (VIP). The study included 386 individuals (271 women, 115 men) who had stated their dietary habits as part of a community intervention programme before the onset of symptoms of RA. Sodium intake was assessed on basis of food frequency questions and analysed as tertiles adjusted by total energy intake. For comparison, 1886 matched controls were identified from the same database and co-analysed. Data were analysed for the outcome of rheumatoid factor (RF) and/or antibodies against cyclic citrullinated peptides (anti-CCP) or human leukocyte antigen shared epitope (HLA-SE) positive RA.
Results In analysis of all cases as a homogeneous group no significant associations between sodium intake and the risk of developing RA could be seen. In stratified analyses for smoking status at the time of the survey (smokers and non-smokers), smokers within the highest tertile of sodium intake had more than double the risk for developing RA compared to smokers within the lowest tertile of sodium consumption (OR=2.26, 95% CI 1.06–4.81). This was not seen in non–smokers. Furthermore, smokers with low sodium consumption revealed no significantly increased risk for developing RA compared to non-smokers. Interaction analysis of smoking and sodium intake revealed that among cases with the highest tertile of sodium intake, 54% of the attributable proportion (AP) of developing RA from these exposures was due to interaction (AP=0.54, 95% CI 0.26-0.82). The corresponding relative excess risk of the interaction (RERI) between smoking and highest sodium intake was also significant (RERI=1.34, 95% CI 0.37 to 2.32). These associations was further increased with the outcome of anti-CCP positive or HLA-SE positive RA disease (OR=2.42, 95% CI 1.07-5.49; and OR=3.28, 95% CI 1.24-8.67, respectively).
Conclusions A higher sodium consumption among smokers was associated with an increased risk for developing RA. This interaction between sodium intake and smoking can provide new insights into the pathogenesis of RA.
Disclosure of Interest : None declared
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