scholarly journals Is too much salt harmful? Yes

2019 ◽  
Vol 35 (9) ◽  
pp. 1777-1785 ◽  
Author(s):  
Róbert Agócs ◽  
Dániel Sugár ◽  
Attila J. Szabó

AbstractThe contribution of high sodium intake to hypertension and to the severity of immune-mediated diseases is still being heatedly debated in medical literature and in the lay media. This review aims to demonstrate two conflicting views on the topic, with the first part citing the detrimental effects of excessive salt consumption. Sodium plays a central role in volume and blood pressure homeostasis, and the positive correlation between sodium intake and blood pressure has been extensively researched. Despite the fact that the average of global daily salt consumption exceeds recommendations of international associations, health damage from excessive salt intake is still controversial. Individual differences in salt sensitivity are in great part attributed to this contradiction. Patients suffering from certain diseases as well as other vulnerable groups—either minors or individuals of full age—exhibit more pronounced blood pressure reduction when consuming a low-sodium diet. Furthermore, findings from the last two decades give insight into the concept of extrarenal sodium storage; however, the long-term consequences of this phenomenon are lesser known. Evidence of the relationship between sodium and autoimmune diseases are cited in the review, too. Nevertheless, further clinical trials are needed to clarify their interplay. In conclusion, for salt-sensitive risk groups in the population, even stricter limits of sodium consumption should be set than for young, healthy individuals. Therefore, the question raised in the title should be rephrased as follows: “how much salt is harmful” and “for whom is elevated salt intake harmful?”

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1970 ◽  
Author(s):  
Grillo ◽  
Salvi ◽  
Coruzzi ◽  
Salvi ◽  
Parati

The close relationship between hypertension and dietary sodium intake is widely recognized and supported by several studies. A reduction in dietary sodium not only decreases the blood pressure and the incidence of hypertension, but is also associated with a reduction in morbidity and mortality from cardiovascular diseases. Prolonged modest reduction in salt intake induces a relevant fall in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group, with larger falls in systolic blood pressure for larger reductions in dietary salt. The high sodium intake and the increase in blood pressure levels are related to water retention, increase in systemic peripheral resistance, alterations in the endothelial function, changes in the structure and function of large elastic arteries, modification in sympathetic activity, and in the autonomic neuronal modulation of the cardiovascular system. In this review, we have focused on the effects of sodium intake on vascular hemodynamics and their implication in the pathogenesis of hypertension.


Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3177
Author(s):  
David A. Jaques ◽  
Gregoire Wuerzner ◽  
Belen Ponte

While sodium is essential for human homeostasis, current salt consumption far exceeds physiological needs. Strong evidence suggests a direct causal relationship between sodium intake and blood pressure (BP) and a modest reduction in salt consumption is associated with a meaningful reduction in BP in hypertensive as well as normotensive individuals. Moreover, while long-term randomized controlled trials are still lacking, it is reasonable to assume a direct relationship between sodium intake and cardiovascular outcomes. However, a consensus has yet to be reached on the effectiveness, safety and feasibility of sodium intake reduction on an individual level. Beyond indirect BP-mediated effects, detrimental consequences of high sodium intake are manifold and pathways involving vascular damage, oxidative stress, hormonal alterations, the immune system and the gut microbiome have been described. Globally, while individual response to salt intake is variable, sodium should be perceived as a cardiovascular risk factor when consumed in excess. Reduction of sodium intake on a population level thus presents a potential strategy to reduce the burden of cardiovascular disease worldwide. In this review, we provide an update on the consequences of salt intake on human health, focusing on BP and cardiovascular outcomes as well as underlying pathophysiological hypotheses.


1982 ◽  
Vol 63 (s8) ◽  
pp. 447s-450s ◽  
Author(s):  
Gloria Valdés ◽  
M. Eugenia Soto ◽  
Hector R. Croxatto ◽  
Teresa Bellolio ◽  
Ramón Corbalán ◽  
...  

1. Nifedipine (20 mg) was given by mouth to seven patients with moderate essential hypertension receiving a low, normal or high sodium intake. The drug produced an important hypotensive effect. Normal sodium intake enhanced the hypotensive action of the drug compared with that during the low and high sodium regimens. Blood pressure remained significantly lower 3 h after drug ingestion. 2. Increases in heart rate and plasma renin activity under all conditions reflected enhanced adrenergic activity. 3. A short-term natriuresis followed nifedipine ingestion in spite of increased aldosterone excretion during the low sodium diet and a decrease in urinary kallikrein during the low and high sodium diets. 4. Nifedipine increased urinary volume only during the high sodium intake. 5. Apart from vasodilatation, nifedipine induces important changes in neurogenic, renal and adrenal mechanisms that regulate blood pressure homoeostasis. Different conditions of sodium balance modulate most of these effects.


2021 ◽  
Author(s):  
Sai Sidharth Manikandan ◽  
Murali Dhar

Abstract Background: Non-pharmacological strategies such as lowering sodium intake aim to protect renal function and delay the initiation of renal replacement therapy. It might also be a cost-effective method to improve chronic kidney disease (CKD) prognosis. We decided to perform a meta-analysis of randomized controlled trials (RCTs) to evaluate the effects of low versus high sodium intake in adults with CKD. Results:Our search strategy yielded seven studies from six countries with 465 participants. The overall effect on restricted sodium intake favored reduction in systolic blood pressure with an overall mean difference of -6.14(95% CI: -9.52, -2.76) and reduction in diastolic blood pressure with a mean difference of -3.08 (95% CI: -4.62, -1.55). There was lowering of estimated glomerular filtration rate (eGFR), however the same was not statistically significant.Conclusion:The study found that restricted salt intake could significantly reduce systolic and diastolic BP. Further, multi-center RCTs for longer durations across different stages of CKD could effectively assess the effects of restricted sodium intake on vital parameters. Such study designs could also help clinicians identify the optimal intake of dietary sodium to achieve better renal and cardio vascular outcomes.


2017 ◽  
Vol 18 (s1) ◽  
pp. 55-60
Author(s):  
Nebojsa Tasic ◽  
Danijela Tasic ◽  
Dalibor Dragisic ◽  
Miroslav Mitrovic

Abstract Plasma-renin values vary in normotensive and hypertensive populations. Some studies consider renin to be a key factor in the aetiology of hypertension, but other studies note that renin is an important factor in cardiovascular homeostasis and functions more as a growth factor than as a pressor hormone. The aim of this study was to assess the PRA and aldosterone values under different salt intake regimes in patients with essential hypertension. The study group consisted of 50 untreated patients (27 women and 23 men; average age 42±9,2 yrs.; average BMI 27,91±4,6 kg/m2) with essential hypertension. All patients were put on a high-sodium diet (200 mmol NaCl per day) for one week after a week on a low-sodium diet (20 mmol NaCl per day). Sodium sensitivity (SS) was defined as a 10-mmHg increase in the mean blood pressure at the end of the high- vs. the low-sodium diet. The SS group consisted of 26 patients, and the sodiuminsensitive group consisted of 24 patients. The PRA and aldosterone levels were determined in 12 patients. PRA values in the SS group during rest were significantly lower compared with the salt-resistant group during all regimes of salt intake (F=10,56, p=0,0012). Salt loading in SS patients causes a significant decrease in PRA (in rest and effort) values in comparison to values during a low salt intake regime (rest: t=4,49, p<0,001; effort: t=3,45, p<0,01). The PRA values in the salt-resistant group did not vary significantly under the different salt intake regimes. The aldosterone values followed the pattern of the PRA values. It is necessary to distinguish investigations on salt intake effects based on incidence and value of blood pressure and investigations on salt restriction’s effects on of blood pressure levels (i.e., non-pharmacological hypertension therapy).


2019 ◽  
Vol 160 (2) ◽  
pp. 43-49
Author(s):  
Endre Sulyok

Abstract: This article shortly outlines the evolution of hypertonia from risk factors to end-organ damage. The pathogenetic role of salt intake is underlined and in the light of recent clinical and experimental observations, the importance of renal and extrarenal mechanism in the development of salt-sensitive hypertension is analysed. The generally accepted concept that the inefficient renal sodium excretion and the subsequent expansion of the extracellular space is the major factor in blood pressure elevation is challenged. Evidences have been provided that the retained sodium dissociates from the volume of extracellular space and, also from the blood pressure. It has been shown that the negatively charged macromolecules in the subcutaneous interstitium bind sodium ions in osmotically inactive form and store sodium reversibly. The local tissue hypertonicity induces monocytes/macrophages invasion and activation that causes increased expression of tonicity-responsive enhancer binding protein (TonEBP) and the secretion of vascular endothelial growth factor C that result in enhanced lymphangiogenesis. The expanded lymphatic system drains the excess sodium and volume back to the circulation. The reduction of buffer function of this system may contribute to the development or to worsening of hypertension. Similar buffer and barrier functions are attributed to the glycocalyx that covers the luminal surface of vascular endothelium. It is also recognised that the high sodium intake alone is an important pathogenetic factor in end-organ damage independent of hypertension. This may be accounted for by the induction and activation of Th17 cells as well as by the increased production of several pro-inflammatory and pro-fibrotic cytokines. Orv Hetil. 2019; 160(2): 43–49.


Reproduction ◽  
2006 ◽  
Vol 131 (2) ◽  
pp. 331-339 ◽  
Author(s):  
Jean St-Louis ◽  
Benoît Sicotte ◽  
Annie Beauséjour ◽  
Michèle Brochu

Lowering and increasing sodium intake in pregnant rats evoke opposite changes in renin–angiotensin–aldosterone system (RAAS) activity and are associated with alterations of blood volume expansion. As augmented uterine blood flow during gestation is linked to increased circulatory volume, we wanted to determine if low- and high-sodium intakes affect the mechanical properties and angiotensin II (AngII) responses of the uterine vasculature. Non-pregnant and pregnant rats received a normal sodium (0.22% Na+) diet. On the 15th day of gestation some animals were moved to a low-sodium (0.03%) diet, whereas others were given NaCl supplementation as beverage (saline, 0.9% or 1.8%) for 7 days. All rats were killed after 7 days of treatment (eve of parturition). Uterine arcuate arteries (>100 μm) were set up in wire myographs under a tension equivalent to 50 mmHg transmural pressure. The pregnancy-associated increase in diameter of the uterine arteries was significantly attenuated on the low-sodium diet and 1.8% NaCl supplementation. The arcuate arteries of non-pregnant rats on the low-sodium diet showed markedly increased responses to AngII and phenylephrine (Phe). Pregnancy also resulted in heightened responses to AngII and Phe that were significantly reduced for the former agent in rats on the low-sodium diet. Sodium supplementation of non-pregnant rats did not affect the reactivity of the uterine arteries to AngII, but significantly reduced the effect of Phe (1 μmol/l). High salt also significantly diminished the elevated responses to AngII in the arteries of pregnant animals. It was observed that altered sodium intake affects the mechanical and reactive properties of the uterine arcuate arteries more importantly in pregnant than in non-pregnant rats. Low-salt intake similarly affected the reactivity of the uterine arcuate arteries to AngII and Phe, whereas high-salt intake more specifically affected AngII responses. These results showed that perturbations of sodium intake have major impacts on the structure and functions of the uterine arterial circulation, indicating RAAS involvement in uterine vascular remodeling and function during gestation.


2020 ◽  
Author(s):  
R Jayatissa ◽  
Y Yamori ◽  
AH De Silva ◽  
M Mori ◽  
PC De Silva ◽  
...  

AbstractBackgroundSodium intakes of different populations around the world became of interest after a positive correlation was drawn between dietary sodium intake and prevalence of hypertension. Sri Lanka has adopted a salt reduction strategy to combat high blood pressure in the population with escalation of non-communicable diseases.ObjectiveTo measure intake of salt, potassium and sodium/potassium ratio of adults in urban and rural settings.DesignA community based study of 328 adults between 30-59 years, including equal numbers from urban and rural sectors. Weight, height and waist circumference were measured. Blood pressure was measured by a standardized automated measurement system and the mean of two readings was used for analysis. 24-hour urine was collected and measured for creatinine, sodium, potassium levels.ResultsMean daily salt consumption was 8.3g (95%CI:7.9,8.8), which is 1.6 times higher than WHO recommendation. Mean daily potassium intake was 1,265g (95%CI:1191.0,1339.3), which is 2.8 times lower and sodium/potassium ratio was 4.3 (95%CI:4.2,4.5), which is 7 times higher than WHO recommendation. Daily salt consumption was significantly higher in males (9.0g;95%CI:8.3,9.8) than females (7.7g;95%CI:7.2,8.2); rural (8.9g;95%CI:8.2-9.6,) than urban (7.7g;95%CI:7.2,8.3) with increasing body mass index (8.2g;95%CI:6.1,10.2 to 10.0g;95%CI:8.5,11.6). Systolic blood pressure was significantly positively correlated with high BMI and waist circumference.ConclusionsHigh salt consumption, low potassium intake and high sodium/potassium ratio was found in this population. This information can be used to set targets to reduce salt intake in the population. Need to create awareness to enhance the consumption of potassium rich food while reducing salt intake to minimize future NCD burden.


Author(s):  
Sai Sidharth M ◽  
◽  
Dhar M ◽  

Introduction: Non-pharmacological strategies such as lowering sodium intake aim to protect renal function and delay the initiation of renal replacement therapy. It might also be a cost-effective method to improve Chronic Kidney Disease (CKD) prognosis. We decided to perform a meta-analysis of Randomized Controlled Trials (RCTs) to evaluate the effects of low versus high sodium intake in adults with CKD. Methodology: We searched the online databases – PUBMED, Cochrane Kidney and Transplant Specialized Register, Cochrane Library and Google Scholar to 31st December 2020 for RCTs to be included in the study. Meta- Analysis was performed for the intervention groups for each arm against the control. Inverse variance methods were applied for analysis using random effects models due to the high heterogeneity among the studies. Results: Our search strategy yielded seven studies from six countries with 465 participants. The overall effect on restricted sodium intake favored reduction in systolic blood pressure with an overall mean difference of -6.14(95% CI: -9.52, -2.76) and reduction in diastolic blood pressure with a mean difference of -3.08 (95% CI: -4.62, -1.55). There was lowering of estimated Glomerular Filtration Rate (eGFR), however the same was not statistically significant. Conclusion: The study found that restricted salt intake could significantly reduce systolic and diastolic BP. Further, multi-center RCTs for longer durations across different stages of CKD could effectively assess the effects of restricted sodium intake on vital parameters. Such study designs could also help clinicians identify the optimal intake of dietary sodium to achieve better renal and cardio vascular outcomes.


2019 ◽  
Vol 23 (6) ◽  
pp. 92-99
Author(s):  
I. G. Kayukov ◽  
O. N. Beresneva ◽  
M. M. Parastaeva ◽  
G. T. Ivanova ◽  
A. N. Kulikov ◽  
...  

BACKGROUND. Increased salt intake is associated with a number of cardiovascular events, including increased blood pressure (BP) and the development of left ventricular hypertrophy (LVH). However, there is much evidence that a high content of sodium chloride in the diet does not always lead to an increase in BP, but almost inevitably causes cardiac remodeling, in particular, LVH. Many aspects of myocardial remodeling induced by high sodium content in the food have not been studied enough. THE AIM of the study was to trace the echocardiographic changes in Wistar rats fed the high salt ration and the high salt ration supplemented with soy proteins.MATERIAL AND METHODS. Echocardiography and BP measurements were performed on male Wistar rats, divided into three groups. The first (control; n = 8) included rats that received standard laboratory feed (20.16 % animal protein and 0.34 % NaCl); the second (n = 10) – animals that received standard feed and 8 % NaCl (high salt ration). The third group (n = 10) consisted of rats who consumed a low-protein diet containing 10 % soy protein isolate (SUPRO 760) and 8 % NaCl. The follow-up period was 2 and 4 months.THE RESULTS of the study showed that: (1) the intake of a large amount of salt with a diet does not necessarily lead to the formation of arterial hypertension; (2) despite the absence of a distinct increase in BP, under these conditions signs of cardiac remodeling, in particular, LVH, appear rather quickly; (3) supplementing a high-salt diet with soy isolates counteracts the development of LVH.CONCLUSION. High salt intake with food can cause heart remodeling, regardless of blood pressure, while soy proteins can counteract this process.


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