Interaction between dietary sodium and smoking increases the risk for rheumatoid arthritis: results from a nested case-control study

Sundström, Björn; Johansson, Ingegerd; Rantapää-Dahlqvist, Solbritt

doi:10.1093/rheumatology/keu330

Cited by 112 publications

(89 citation statements)

References 25 publications

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“…The significant associations found for a carbohydrate-restricted diet among anti-CCP-positive cases, as well as the protein consumption among smokers, were no longer significant after additional adjustment for sodium intake. This is consistent with our previous results showing that sodium intake is associated with the odds for developing RA among smokers [26]. In that study, sodium intake had its strongest positive association with protein intake and its strongest negative association with the intake of carbohydrates.…”

Section: Discussionsupporting

confidence: 93%

“…Subgroup analyses were performed on cases developing RF-positive RA and/or anti-CCP-positive RA, as well as on the presence or absence of HLA-SE among the patient cohort. Furthermore, subgroup analyses were also performed among smokers since in a previous study based on the same cohort, we showed a significant association between sodium intake and the OR for developing RA among smokers [26]. Statistical calculations were performed using SPSS (version 20, IBM Corp, NY, USA) and Stata (version 13.1, StataCorp, Lakeway, USA).…”

Section: Statistical Analysesmentioning

confidence: 99%

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Diet and alcohol as risk factors for rheumatoid arthritis: a nested case–control study

2014

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The aim of this study was to investigate whether alcohol and diet, assessed as both macronutrients and dietary patterns, increased the risk of development of rheumatoid arthritis (RA) through a nested case-control design in the Västerbotten Intervention Program (VIP) cohort. Individuals in the VIP who had developed RA after the dietary survey were identified from medical records at the department of rheumatology at the University Hospital, Umeå (n = 386), and matched to 1,886 controls from the same database. Diet was assessed as food groups, as macronutrients and as scores of dietary patterns, namely the carbohydrate-restricted diet score, the Mediterranean diet score and the healthy diet indicator score. When analysing the dietary patterns, consumption of food groups and different macronutrients, a significant association was found in the highest tertile of carbohydrate-restricted diet among the cases with a subsequent anti-CCP-positive disease 1.40 (1.02-1.92), as well as in the highest tertile of protein consumption among smokers (OR = 1.80, 95% CI 1.09-2.95). However, after additional adjustment for sodium intake, these associations were no longer statistically significant. No association was observed between alcohol consumption and the risk of RA. To summarize, there were no significant associations between diet, or alcohol consumption, and the risk of development of RA within this cohort. The lack of any significant associations of alcohol consumption may be explained by a low consumption in the studied population overall or alternatively by methodological issues raised recently.

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Section: Discussionsupporting

confidence: 93%

Section: Statistical Analysesmentioning

confidence: 99%

Diet and alcohol as risk factors for rheumatoid arthritis: a nested case–control study

2014

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“…Increases in dietary salt intake worsen animal models of MS (experimental autoimmune encephalomyelitis [EAE]), and is associated with increased in vivo induction of proinflammatory Th17 cells (24,25). Of note, recent studies in patients with autoimmune diseases indicated that higher salt intake is associated with increased clinical and radiological disease activity in MS patients and with increased risk of developing rheumatoid arthritis (28,29). Moreover, a recent longitudinal study under highly controlled conditions in humans indicated that changes in dietary salt levels could significantly impact cellularity of cells of the innate immune system and secreted levels of pro-and antiinflammatory cytokines such as IL-6, IL-23, and IL-10 in vivo (30).…”

Section: Secretion Of Ifnγ By Foxp3mentioning

confidence: 99%

Sodium chloride inhibits the suppressive function of FOXP3+ regulatory T cells

Hernandez¹,

Kitz²,

Wu³

et al. 2015

Journal of Clinical Investigation

300

318

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“…One such study found a positive correlation between sodium intake and disease activity in patients with relapsing-remitting MS, as patients with higher salt intake had higher lesion load by MRI and higher disability scores (105). Similarly, the combination of high sodium intake and smoking was associated with a significantly increased incidence of developing RA (106). Thus, high salt concentrations can promote the differentiation of pathogenic Th17 cells, and increased dietary salt intake may promote autoimmune disease in both mice and humans.…”

Section: Il-23 and Autoimmunitymentioning

confidence: 99%

Pouring fuel on the fire: Th17 cells, the environment, and autoimmunity

Burkett¹,

Hörste²,

Kuchroo³

2015

J. Clin. Invest.

204

137

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R e v i e w S e R i e S : A u t o i m m u n i t y2 2 1 2 jci.org Volume 125 Number 6 June 2015Murine Th17 differentiation can also be induced in the absence of TGF-β1 signaling, via the combination either of IL-1β, IL-6, and IL-23 or of 42). These TGF-β1-independent Th17 cells can efficiently induce autoimmune tissue inflammation upon adoptive transfer, a trait that led to them being termed "pathogenic" Th17 cells. Additionally, they possess a gene expression profile distinct from that of "nonpathogenic" Th17 cells, which are differentiated with TGF-β1 and IL-6. These observations have led to two competing hypotheses. The first posits that IL-23 cements Th17 lineage commitment such that Th17 cells induced with TGF-β1 and IL-6 are insufficiently committed to the lineage and cannot induce autoimmune tissue inflammation. The second suggests that there are distinct subtypes of Th17 cells whose differentiation is dependent on distinct combinations of cytokines. The latter hypothesis is supported by the finding that pathogenic Th17 cells express higher levels of several Th1 lineage-associated transcripts, such as the transcription factor T-bet and IFN-γ, and have been shown to be derived from IL-17 single producers by fate mapping experiments (43,44). Similarly, an important feature of human Th17 cells, as well as those isolated from inflamed tissues in mouse models of Th17-mediated disease, is that they coproduce IL-17 with other cytokines, leading to distinct functional roles (45)(46)(47). For instance, human Th17 cells that produce both IL-10 and IL-17 preferentially respond to Staphylococcus aureus, while those that produce both IL-17 and IFN-γ recognize Candida albicans, suggesting that distinct pathogens induce distinct subtypes of Th17 cells (40). IL-17/IFN-γ coproducers have been ascribed pathogenic functions in the CNS during EAE; however, it has been difficult to reliably differentiate such cells in vitro. Repeated rounds of in vitro culture in the presence of either Th1-inducing cytokines or IL-23 can induce IL-17/IFN-γ coproducers, albeit at moderate percentages. The transcription factors T-bet, RUNX1, and RUNX3 appear to be important in the acquisition of this phenotype (48,49).Large-scale transcriptional analysis of Th17 differentiation at very high temporal resolution has begun to elucidate the molecular networks that control this process, and is a promising approach to the identification of novel regulatory molecules that control pathogenic Th17 differentiation (50, 51). In fact, Th17 development is controlled induction of this lineage. The combination of TGF-β1 and IL-6 efficiently induces IL-17-producing murine T cells in vitro and highlights the reciprocal relationship between induced Tregs, which are generated by TGF-β1 alone, and Th17 cells (19,20). A series of studies demonstrated that IL-21, a γ c -dependent cytokine, could promote the differentiation of Th17 cells (21-23). In combination with TGF-β, IL-21 induces IL-17 production from naive Th cells and promotes the expression of both RORγt, th...

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Interaction between dietary sodium and smoking increases the risk for rheumatoid arthritis: results from a nested case-control study

Abstract: Although we were unable to confirm our stated hypothesis, our results that high sodium consumption among smokers was associated with the risk of RA may provide new insights into the impact of smoking in RA development.

Cited by 112 publications

References 25 publications

Diet and alcohol as risk factors for rheumatoid arthritis: a nested case–control study

Diet and alcohol as risk factors for rheumatoid arthritis: a nested case–control study

Sodium chloride inhibits the suppressive function of FOXP3+ regulatory T cells

Pouring fuel on the fire: Th17 cells, the environment, and autoimmunity

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