1.
Salt Reduction to Prevent Hypertension and Cardiovascular Disease: JACC State-of-the-Art Review.
He, FJ, Tan, M, Ma, Y, MacGregor, GA
Journal of the American College of Cardiology. 2020;(6):632-647
Abstract
There is strong evidence for a causal relationship between salt intake and blood pressure. Randomized trials demonstrate that salt reduction lowers blood pressure in both individuals who are hypertensive and those who are normotensive, additively to antihypertensive treatments. Methodologically robust studies with accurate salt intake assessment have shown that a lower salt intake is associated with a reduced risk of cardiovascular disease, all-cause mortality, and other conditions, such as kidney disease, stomach cancer, and osteoporosis. Multiple complex and interconnected physiological mechanisms are implicated, including fluid homeostasis, hormonal and inflammatory mechanisms, as well as more novel pathways such as the immune response and the gut microbiome. High salt intake is a top dietary risk factor. Salt reduction programs are cost-effective and should be implemented or accelerated in all countries. This review provides an update on the evidence relating salt to health, with a particular focus on blood pressure and cardiovascular disease, as well as the potential mechanisms.
2.
Body Fluid-Independent Effects of Dietary Salt Consumption in Chronic Kidney Disease.
Oppelaar, JJ, Vogt, L
Nutrients. 2019;(11)
Abstract
The average dietary salt (i.e., sodium chloride) intake in Western society is about 10 g per day. This greatly exceeds the lifestyle recommendations by the WHO to limit dietary salt intake to 5 g. There is robust evidence that excess salt intake is associated with deleterious effects including hypertension, kidney damage and adverse cardiovascular health. In patients with chronic kidney disease, moderate reduction of dietary salt intake has important renoprotective effects and positively influences the efficacy of common pharmacological treatment regimens. During the past several years, it has become clear that besides influencing body fluid volume high salt also induces tissue remodelling and activates immune cell homeostasis. The exact pathophysiological pathway in which these salt-induced fluid-independent effects contribute to CKD is not fully elucidated, nonetheless it is clear that inflammation and the development of fibrosis play a major role in the pathogenic mechanisms of renal diseases. This review focuses on body fluid-independent effects of salt contributing to CKD pathogenesis and cardiovascular health. Additionally, the question whether better understanding of these pathophysiological pathways, related to high salt consumption, might identify new potential treatment options will be discussed.
3.
Salt Intake and Immunity.
Afsar, B, Kuwabara, M, Ortiz, A, Yerlikaya, A, Siriopol, D, Covic, A, Rodriguez-Iturbe, B, Johnson, RJ, Kanbay, M
Hypertension (Dallas, Tex. : 1979). 2018;(1):19-23
4.
Analysis of Sodium Chloride Intake and Treg/Th17 Lymphocytes in Healthy Individuals and Patients with Rheumatoid Arthritis or Systemic Lupus Erythematosus.
Vitales-Noyola, M, Layseca-Espinosa, E, Baranda, L, Abud-Mendoza, C, Niño-Moreno, P, Monsiváis-Urenda, A, Rosenstein, Y, González-Amaro, R
Journal of immunology research. 2018;:9627806
Abstract
We assessed different immune parameters in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) with low (LSI) and high (HSI) sodium intake. Thirty-eight patients with RA, thirty-seven with SLE, and twenty-eight healthy subjects were studied and classified as LSI or HSI. Levels and suppressive function of CD4+CD25+Foxp3+ and CD4+CD69+Foxp3- Treg cells were determined by flow cytometry in blood samples. Levels and in vitro differentiation of Th17 cells were also assessed. Similar levels of CD4+CD25+Foxp3+ and CD4+CD69+Foxp3- Treg cells were observed in LSI and HSI patients or controls. However, a positive correlation was detected between sodium intake and levels of CD4+CD25+Foxp3+ Treg cells in SLE and a negative association between CD4+CD69+Foxp3- Treg cells and sodium intake in RA. No other significant associations were detected, including disease activity and sodium intake. Moreover, the suppressor activity of CD4+CD25+Foxp3+ and CD4+CD69+Foxp3- Treg cells was similar in LSI and HSI patients or controls. The levels and in vitro differentiation of Th17 cells were also similar in LSI and HSI individuals. Our results suggest that, in the population studied (Mexican mestizo), the level of sodium intake is not apparently associated with different relevant immune parameters in healthy subjects or patients with SLE or RA.