Does Sodium Intake Induce Systemic Inflammatory Response? A Systematic Review and Meta-Analysis of Randomized Studies in Humans

Basdeki, Eirini D.; Mitrou, Panagiota; Tsirimiagkou, Christiana; Georgakis, Marios K.; Chatzigeorgiou, Antonios; Argyris, Antonis; Karatzi, Kalliopi; Μanios, Yannis; Sfikakis, Petros P.; Protogerou, Athanase D.

doi:10.3390/nu13082632

Cited by 7 publications

(4 citation statements)

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“…Several cross-sectional studies associated a higher salt intake with higher CRP levels in adults and elderly people [ 70 , 71 ], although this association was not found in adolescents [ 72 ]. A recent meta-analysis also found no associations between dietary sodium level and markers of inflammation, although it should be noted that the researchers pointed out that their findings were likely due to methodological errors [ 73 ].…”

Section: Possible Mechanisms Explaining the Relationship Between Upf ...mentioning

confidence: 99%

Low-Grade Inflammation and Ultra-Processed Foods Consumption: A Review

et al. 2023

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Low-grade inflammation alters the homeostasis of the organism and favors the onset of many chronic diseases. The global growth in the prevalence of noncommunicable diseases in recent years has been accompanied by an increase in the consumption of ultra-processed foods (UPF). Known to be hyperpalatable, economic and ready-to-eat, increased consumption of UPF has already been recognized as a risk factor for several chronic diseases. Different research groups have tried to investigate whether UPF consumption could promote low-grade inflammation and thus favor the development of noncommunicable diseases. Current evidence highlights the adverse health effects of UPF characteristics, not only due to the nutrients provided by a diet rich in UPF, but also due to the non-nutritive components present in UPF and the effect they may have on gut health. This review aims to summarize the available evidence on the possible relationship between excessive UPF consumption and modulation of low-grade inflammation, as potential promoters of chronic disease.

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Section: Possible Mechanisms Explaining the Relationship Between Upf ...mentioning

confidence: 99%

Low-Grade Inflammation and Ultra-Processed Foods Consumption: A Review

et al. 2023

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“…Persistent smoldering inflammation causes an enhanced release of reactive oxygen and nitrogen species, resulting in DNA damage and pro-oncogenic transcription factor dysregulation, leading to tumorigenesis, proliferation, and metastasis [ 3 ]. High salt (sodium chloride, NaCl) is a well-known mediator of chronic inflammation [ 4 ]. Previous studies in our laboratory have demonstrated that murine breast tumors, compared to the surrounding soft tissue, accumulate 30–70% higher sodium content [ 5 ].…”

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confidence: 99%

Chronic High-Salt Diet Activates Tumor-Initiating Stem Cells Leading to Breast Cancer Proliferation

Tucker,

Ali,

Zent

et al. 2024

Cells

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Several chronic inflammatory diseases have been linked to high-salt (HS) diets. Chronic inflammation is an established causative hallmark of cancer. However, a direct role of HS diets in tumorigenesis is yet to be defined. Previous orthotopic murine breast tumor studies have shown that short-term HS diets caused inhibition of tumor growth through the activation of cytotoxic adaptive immune responses. However, there have been experimental challenges in developing a viable chronic HS-diet-based murine tumor model. To address this, we have developed a novel chronic HS diet tumor model through the sequential passaging of tumor cells in mice under HS dietary conditions. Two orthotopic murine triple-negative breast cancer models, 4T1 tumor cells injected into BALB/c mice and Py230 tumor cells injected into C57Bl/6 mice, were utilized in our study. For the HS diet cohort, prior to orthotopic injection with tumor cells, the mice were kept on a 4% NaCl diet for 2 weeks. For the regular salt (RS) diet cohort, the mice were kept on a 1% NaCl diet. Following syngeneic cancer cell injection, tumors were allowed to grow for 28 days, following which they were collected to isolate immune cell-depleted cancer cells (passage 1, P1). The tumor cells from P1 were reinjected into the next set of non-tumor-bearing mice. This procedure was repeated for three cycles (P2–P4). In P1, compared to the RS diet cohort, we observed reduced tumor kinetics in both murine tumor models on the HS diet. In contrast, by P4, there was significantly higher tumor progression in the HS diet cohort over the RS diet cohort. Flow cytometry analysis demonstrated an 8-fold increase in tumor-initiating stem cells (TISCs) from P1 to P4 of the HS diet cohort, while there were no significant change in TISC frequency with sequential passaging in the RS diet cohort. Molecular studies showed enhanced expression of TGFβR2 and CD80 on TISCs isolated from the P4 HS diet cohort. In vitro studies demonstrated that TGFβ stimulation of these TISCs increased the cellular expression of CD80 molecules. Further, the chronic HS diet selectively induced the glycolytic metabolic phenotype over the mitochondrial oxidative phosphorylation phenotype in TISCs, which is needed for the production of metabolites during tumor cell differentiation and proliferation. The infiltrating CD8 and CD4 T-lymphocytes in P4 tumors demonstrated increased expression of the immune checkpoint inhibitor (ICI) CTLA4, a known binding partner of CD80, to cause immune exhaustion and pro-tumorigenic effects. Interestingly, anti-TGFβ monoclonal antibodies (mAbs) played a synergistic role in further enhancing the anti-tumor effect of anti-CTLA4 mAb. In summary, our findings demonstrated that chronic HS diet increased the frequency of TISCs in tumors leading to blunting of cytotoxic adaptive immune responses causing tumor proliferation. Furthermore, a combination of anti-TGFβ with current ICI-based immunotherapies could exert more favorable anti-cancer clinical outcomes.

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“…As a result, the concentration of folic acid should be often evaluated in patients with IBD and given as a supplement in cases of insufficient dietary intake and/or absorption [ 5 ]. Basdeki et al performed a systematic review and meta-analysis of previously published randomized controlled trials (RCTs) investigating the relationship of sodium intake with systemic inflammation [ 6 ]. Although the study did not verify the hypothesis that sodium intake can induce a systemic inflammatory response in humans in a dose–response manner, it highlighted major issues that could be addressed in future relevant RCTs [ 6 ].…”

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confidence: 99%

“…Basdeki et al performed a systematic review and meta-analysis of previously published randomized controlled trials (RCTs) investigating the relationship of sodium intake with systemic inflammation [ 6 ]. Although the study did not verify the hypothesis that sodium intake can induce a systemic inflammatory response in humans in a dose–response manner, it highlighted major issues that could be addressed in future relevant RCTs [ 6 ]. In a systematic review, Tsiogkas et al summarized the current evidence regarding the efficacy of Crocus sativus (Saffron) supplementation in patients with rheumatic diseases (RDs) [ 7 ].…”

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confidence: 99%