Effects Of High Sodium Intake Research Articles

Sodium and Human Health: What Can Be Done to Improve Sodium Balance beyond Food Processing?

Sodium plays a key role in the regulation of water balance and is also important in food formulation due to its contribution to the taste and use in the preservation of many foods. Excessive intake of any essential nutrient is problematic and this seems to be particularly the case for sodium since a high intake makes it the nutrient most strongly associated with mortality. Sodium intake has been the object of recommendations by public health agencies such as the WHO and this has resulted in efforts by the food industry to reduce the sodium content of packaged foods, although there is still room for improvement. The recent literature also emphasizes the need for other strategies, e.g., regulations and education, to promote adequate sodium intake. In the present paper, we also describe the potential benefits of a global healthy lifestyle that considers healthy eating but also physical activity habits that improve body functionality and may help to attenuate the detrimental effects of high sodium intake on body composition and cardiometabolic health. In conclusion, a reduction in sodium intake, an improvement in body functioning, and educational interventions promoting healthy eating behaviours seem to be essential for the optimal regulation of sodium balance.

Sodium intake and public health -- methodological pitfalls in assessing the relationship between sodium intake and health outcomes

Background and aims The findings on the relationship between sodium intake and health outcomes such as cardiovascular disease and all-cause mortality have been controversial. Some studies found the relationship between sodium intake and all-cause mortality was linear while others found a U-shaped or J-shaped relationship. This study aimed to identify the methodological issues contributing to the conflicting findings. Methods and results The present study investigated methodological gaps in assessing the relationship between sodium intake and health outcomes (hypertension, cardiovascular disease, and all-cause mortality). The contradictory findings appear to stem from flawed methods used in the published studies: (1) Both spot and 24-h urinary sodium collection methods underestimate the adverse effects of low sodium intake and overestimate the harmful effects of high sodium intake, (2) the linear relationship between sodium intake and all-cause mortality appears to be a result of random chance due to small sample sizes, and (3) the divergent temporal trends of sodium consumption and hypertension prevalence indicate sodium intake was not the primary cause of the worldwide hypertension epidemic. Conclusion Considering, (1) sodium is an essential nutrient, (2) the adverse effects of low and high sodium intake appear to be under- and over-estimated, respectively, (3) large studies have found a U-shaped or J-shaped relationship between sodium intake and all-cause mortality, and (4) sodium consumption is unlikely to be the major driver behind the worldwide hypertension epidemic and has little effect on the blood pressure of most normotensive individuals, the recommendation for population-wide low sodium intake merits further evaluation.

Effect of High Sodium Intake (5 mEq/kg/day) in Preterm Newborns (<35 Weeks Gestation) During the Initial 24 Hours of Life: A Non-Blinded Randomized Clinical Trial

Effect of High Sodium Intake (5 mEq/kg/day) in Preterm Newborns (<35 Weeks Gestation) During the Initial 24 Hours of Life: A Non-Blinded Randomized Clinical Trial

HDAC1 inhibition promotes pathogenic Th17 cell expansion in the context of high salt

Histone deacetylase 1 (HDAC1) is an important regulator of chromatin conformation and cell differentiation. There is currently great interest in repurposing HDAC inhibitors for use in cardiovascular and kidney diseases. Our lab previously reported that HDAC1 in kidney tubules and endothelial cells is highly responsive to high salt diet (HSD), but it is unclear how HDAC1 regulates the T cell response in the context of HSD. It has been shown that Th17 cells may expand with HSD. However, our lab has found that HSD may also reduce intestinal Th17 cells. Th17 cells produce the cytokine interleukin‐17A (IL‐17A), are involved in barrier maintenance and homeostasis, and demonstrate substantial plasticity. Th17(23) cells require signaling with IL‐23 and display aberrant responses that promote disease in contrast to physiologic, homeostatic Th17cells. It is unclear which subset of Th17 cells drives the response to HSD. Loss of HDAC1 is known to be protective against Th17 mediated autoimmunity, but the direct effect of HDAC1 on Th17 expansion is unknown. We hypothesized that high sodium conditions promote Th17(23) expansion and HDAC1 inhibition will reduce pathogenic Th17(23) expansion. To test this hypothesis, naïve CD4+ T cells from spleens of 8‐12 weeks old male mice were seeded under in vitro polarizing conditions for 5 days in conditioned media. Conditioned media included physiologic Th17 (TGFb1, IL‐6, anti‐IFNg, anti‐IL‐4, anti‐CD28) and pathogenic Th17(23) (IL‐1b, IL‐23, IL‐6, anti‐IFNg, anti‐IL‐4, anti‐CD28) cytokines with or without high sodium (40 mM NaCl) or MS‐275, an HDAC1 inhibitor (300 nM) in the media. Following 5 days of culture, flow cytometry was used to determine IL‐17A production. We found that high NaCl supplementation significantly reduced Th17 cells, however HDAC1 inhibition in normal media significantly expanded Th17 cells. When MS‐275 was combined with high NaCl media, Th17 was reduced compared to normal NaCl MS‐275 treated cells (2‐way ANOVA, Effect of MS‐275: p=0.001, Effect of NaCl: p=0.002, Interaction: p=0.003, normal media vs 40mM NaCl: p=0.002, normal media vs 300nM MS‐275: p=0.025, 40mM NaCl vs 40mM NaCl+300nM MS‐275: p=0.053, 300nM MS‐275 vs 300nm MS‐275+40mM NaCl: p=0.058). Interestingly, high NaCl and HDAC1 inhibition both significantly increased Th17(23) cell production. When Th17(23) cells were treated with both MS‐275 and 40mM NaCl, IL‐17A production expanded further (2‐way ANOVA, Effect of MS‐275: p=0.001, Effect of NaCl: p=0.003, Interaction: p=0.003, normal media vs 40mM NaCl: p=0.024, normal media vs 300nM MS‐275: p=0.015, 40mM NaCl vs 40mM high sodium+300nM MS‐275: p=0.003, 300nM MS‐275 vs 300nm MS‐275+40mM NaCl: p=0.007). These data indicate unique microenvironment‐dependent responses by Th17 cells to NaCl. Namely, IL‐23‐pathogenic conditions support expansion of Th17s by NaCl and HDAC1 suppresses this expansion. In contrast, Th17 cells responses similarly to NaCl regardless of HDAC1 inhibition. These data indicate that NaCl‐responsive IL‐23R dependent signaling is regulated in part by HDAC1. Further investigation is necessary to understand the in vivo effects of high sodium intake on HDAC1 activity.

Deletion of renal Nedd4-2 abolishes the effect of high sodium intake (HS) on Kir4.1, ENaC, and NCC and causes hypokalemia during high HS.

Neural precursor cell expressed developmentally downregulated protein 4-2 (Nedd4-2) regulates the expression of Kir4.1, thiazide-sensitive NaCl cotransporter (NCC), and epithelial Na+ channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN), and Nedd4-2 deletion causes salt-sensitive hypertension. We now examined whether Nedd4-2 deletion compromises the effect of high-salt (HS) diet on Kir4.1, NCC, ENaC, and renal K+ excretion. Immunoblot analysis showed that HS diet decreased the expression of Kir4.1, Ca2+-activated large-conductance K+ channel subunit-α (BKα), ENaCβ, ENaCγ, total NCC, and phospho-NCC (at Thr53) in floxed neural precursor cell expressed developmentally downregulated gene 4-like (Nedd4lfl/fl) mice, whereas these effects were absent in kidney-specific Nedd4-2 knockout (Ks-Nedd4-2 KO) mice. Renal clearance experiments also demonstrated that Nedd4-2 deletion abolished the inhibitory effect of HS diet on hydrochlorothiazide-induced natriuresis. Patch-clamp experiments showed that neither HS diet nor low-salt diet had an effect on Kir4.1/Kir5.1 currents of the distal convoluted tubule in Nedd4-2-deficient mice, whereas we confirmed that HS diet inhibited and low-salt diet increased Kir4.1/Kir5.1 activity in Nedd4lflox/flox mice. Nedd4-2 deletion increased ENaC currents in the ASDN, and this increase was more robust in the cortical collecting duct than in the distal convoluted tubule. Also, HS-induced inhibition of ENaC currents in the ASDN was absent in Nedd4-2-deficient mice. Renal clearance experiments showed that HS intake for 2 wk increased the basal level of renal K+ excretion and caused hypokalemia in Ks-Nedd4-2-KO mice but not in Nedd4lflox/flox mice. In contrast, plasma Na+ concentrations were similar in Nedd4lflox/flox and Ks-Nedd4-2 KO mice on HS diet. We conclude that Nedd4-2 plays an important role in mediating the inhibitory effect of HS diet on Kir4.1, ENaC, and NCC and is essential for maintaining normal renal K+ excretion and plasma K+ ranges during long-term HS diet.NEW & NOTEWORTHY The present study suggests that Nedd4-2 is involved in mediating the inhibitory effect of high salt (HS) diet on Kir4.1/kir5.1 in the distal convoluted tubule, NaCl cotransporter function, and epithelial Na+ channel activity and that Nedd4-2 plays an essential role in maintaining K+ homeostasis in response to a long-term HS diet. This suggests the possibility that HS intake could lead to hypokalemia in subjects lacking proper Nedd4-2 E3 ubiquitin ligase activity in aldosterone-sensitive distal nephron.

Deletion of Kir5.1 abolishes the effect of high Na+ intake on Kir4.1 and Na+-Cl- cotransporter.

High sodium (HS) intake inhibited epithelial Na+ channel (ENaC) in the aldosterone-sensitive distal nephron and Na+-Cl- cotransporter (NCC) by suppressing basolateral Kir4.1/Kir5.1 in the distal convoluted tubule (DCT), thereby increasing renal Na+ excretion but not affecting K+ excretion. The aim of the present study was to explore whether deletion of Kir5.1 compromises the inhibitory effect of HS on NCC expression/activity and renal K+ excretion. Patch-clamp experiments demonstrated that HS failed to inhibit DCT basolateral K+ channels and did not depolarize K+ current reversal potential of the DCT in Kir5.1 knockout (KO) mice. Moreover, deletion of Kir5.1 not only increased the expression of Kir4.1, phospho-NCC, and total NCC but also abolished the inhibitory effect of HS on the expression of Kir4.1, phospho-NCC, and total NCC and thiazide-induced natriuresis. Also, low sodium-induced stimulation of NCC expression/activity and basolateral K+ channels in the DCT were absent in Kir5.1 KO mice. Deletion of Kir5.1 decreased ENaC currents in the late DCT, and HS further inhibited ENaC activity in Kir5.1 KO mice. Finally, measurement of the basal renal K+ excretion rate with the modified renal clearance method demonstrated that long-term HS inhibited the renal K+ excretion rate and steadily increased plasma K+ levels in Kir5.1 KO mice but not in wild-type mice. We conclude that Kir5.1 plays an important role in mediating the effect of HS intake on basolateral K+ channels in the DCT and NCC activity/expression. Kir5.1 is involved in maintaining renal ability of K+ excretion during HS intake. NEW & NOTEWORTHY Kir5.1 plays an important role in mediating the effect of high sodium intake on basolateral K+ channels in the distal convoluted tubule and Na+-Cl- cotransporter activity/expression.

DETERMINANT ANALYSIS OF TRIGGER RISK OF DEATH FATHER BECAUSE NON-COMMUNICABLE DISEASES IN FAMILY THAT IS IN SEMANDING DISTRICT TUBAN

The tendency of Non-Communicable Diseases is chronic, the impact of disability including permanent disability. The purpose of this study is to analyze the determinants of the risk of father's death due to Non-Communicable Diseases in families in Semanding District, Tuban Regency. This type of research is observational analytic with case control design. 437 samples were taken by cluster sampling. In the second stage the sample was taken by determining the highest Non-Communicable Diseases in the family, 0.82%, then the sample size was 182 with a case group of 82 (the highest Non-Communicable Diseases) and a control of 100 (the father Non-Communicable Diseases risk). Data collection techniques are done by interview. OR = 5,863 95% CI 3,087-11,136) with p value = 0,000, consumption of foods high in excess salt (OR = 7,653 CI 95 % 3,951-14,821) p value = 0,000, consumption of food and drink high in excess sugar (OR 5, 582 CI 95% 2.9478-10.57) p value = 0.000, smoking (OR = 4.849 CI 95% 2.545-9.238) p value = 0,000. The effect of high sodium intake on the incidence of primary hypertension increases plasma volume so that cardiac output increases which is directly proportional to the increase in blood pressure. This can be overcome by consuming fruits and vegetables as the main source of Potassium. Potassium is a mineral that maintains fluid and electrolyte balance which has the effect of releasing sodium to prevent hypertension.

Dietary Sodium Intake and Risk of Cardiovascular Disease: A Systematic Review and Dose-Response Meta-Analysis.

Dietary sodium intake has received considerable attention as a potential risk factor of cardiovascular disease. However, evidence on the dose-response association between dietary sodium intake and cardiovascular disease risk is unclear. Embase and PubMed were searched from their inception to 17 August 2020 and studies that examined the association between sodium intake and cardiovascular disease in adolescents were not included in this review. We conducted a meta-analysis to estimate the effect of high sodium intake using a random effects model. The Newcastle-Ottawa Scale assessment was performed. A random-effects dose-response model was used to estimate the linear and nonlinear dose-response relationships. Subgroup analyses and meta-regression were conducted to explain the observed heterogeneity. We identified 36 reports, which included a total of 616,905 participants, and 20 of these reports were also used for a dose-response meta-analysis. Compared with individuals with low sodium intake, individuals with high sodium intake had a higher adjusted risk of cardiovascular disease (Rate ratio: 1.19, 95% confidence intervals = 1.08–1.30). Our findings suggest that there is a significant linear relationship between dietary sodium intake and cardiovascular disease risk. The risk of cardiovascular disease increased up to 6% for every 1 g increase in dietary sodium intake. A low-sodium diet should be encouraged and education regarding reduced sodium intake should be provided.

Interactive effect of high sodium intake with increased serum triglycerides on hypertension.

BackgroundA high salt diet is associated with the development of hypertension, one of the most important cardiovascular risk factors. A reduction in sodium intake seems to have an effect on increasing serum triglycerides (TGs). Elevated TGs are independently linked to cardiovascular risk. However, there is limited evidence of a possible interactive effect of sodium intake and serum TGs on high blood pressure (BP).MethodsWe conducted a nationwide, population-based interaction analysis using the Kawasaki method for estimating 24-h urinary sodium excretion (e24hUNaEKawasaki) as a candidate indicator of dietary sodium intake. All native Koreans aged 20 years or older without significant medical illness were eligible for inclusion.ResultsA total of 16936 participants were divided into quintiles according to their e24hUNaEKawasaki results. Participants in the highest quintile were more obese and hypertensive and had higher white blood cell count, lower hemoglobin, greater glycemic exposure, and poor lipid profiles compared to the same parameters of individuals in other quintiles. Linear regression revealed that e24UNaEKawasaki was related to systolic BP, diastolic BP, and TGs. Multiple logistic regression, adjusted for dietary sodium intake and various conventional risk factors for chronic vascular diseases, showed that both e24UNaEKawasaki and TGs were significant predictors of hypertension. Our interaction analysis demonstrated that increased sodium intake was associated with higher risk of hypertension in participants with elevated TGs than in those without (adjusted RERI = 0.022, 95% CI = 0.017–0.027; adjusted AP = 0.017, 95% CI = 0.006–0.028; adjusted SI = 1.010, 95% CI = 1.007–1.014).ConclusionOur findings suggest that the interaction between a high salt diet and elevated TGs may exert synergistic biological effects on the risk of hypertension.

Sodium Intake, Blood Pressure and Cardiovascular Disease.

Sodium intake reduction has been emphasized because sodium adversely impacts health, especially blood pressure (BP), and the cardiovascular (CV) disease risk. However, data obtained from several cohort studies have raised questions regarding the effects of high sodium intake on BP and the CV disease risk. In the present study, we systematically reviewed the literature to evaluate these associations. Studies showing negative associations between urine sodium and BP and CV outcomes relied on estimated 24-hour urine sodium from spot urine that is inappropriate for determining sodium intake at an individual level. Furthermore, controversy about the association between 24-hour urine sodium and BP may have been caused by different characteristics of study populations, such as age distribution, ethnicity, potassium intake and the inclusion of patients with hypertension, the different statistical methods and BP measurement methods. Regarding the association between sodium intake and the CV disease risk, studies showing negative or J- or U-shaped associations used a single baseline measurement of 24-hour urine sodium in their analyses. However, recent studies that employed average of subsequently measured 24-hour urine sodium showed positive, linear associations between sodium intake and CV outcomes, indicating that controversies are caused by the different sodium intake measurement methods and analytic designs. In conclusion, the study shows that positive associations exist between sodium intake and BP, CV outcomes, and mortality, and that the argument that reducing sodium intake is dangerous is invalid. Sodium intake reduction should be recommended to all, and not limited to patients with hypertension or CV disease.

High Sodium Intake Impairs Small Artery Vasoreactivity in vivo in Dahl Salt-Sensitive Rats

The effects of high sodium intake on the functionality of resistance arteries have been repeatedly studied in vitro, but no study has focused on salt-sensitive hypertension in vivo. We studied the in vivo reactivity of mesenteric small arteries (MSAs) to vasoactive agents in Dahl salt-sensitive (DS) rats with various sodium diets. Twenty-four male DS rats were randomized into 3 groups: LS (0.3% NaCl diet), NS (0.6% NaCl diet), and HS (8% NaCl diet). After a 12-week intervention, the diameter changes of the MSAs after noradrenaline (NA) and acetylcholine (ACh) exposure were detected by a microscope, and changes in blood perfusion through the MSAs were measured by full-field laser perfusion imaging. HS enhanced the constrictive response of the MSAs to NA and attenuated the relaxing response to ACh. Low sodium intake reduced the response of the MSAs to NA and promoted ACh-induced vasodilatation. HS also aggravated NA-induced blood perfusion reduction and impaired ACh-induced hyperperfusion of the MSAs. Pathologically, HS was associated with arteriolar structural damage and fibrosis of the MSAs. We conclude that sodium intake affects the responsiveness of the MSAs to vasoactive agents in DS rats and might play important roles in modulating blood pressure in hypertensive individuals.

Male Mice Heterozygous LSD1 Knockout Gene Prevented the Effect of High Sodium Intake on Renal Fibrosis and AT1 Conformational Status

AimTo evaluate the effects of dietary salt overload or restriction on renal structure and AT1 conformational status in wild type and LSD1 (lysine specific demethylase 1) deficient mice.MethodsLSD1 deficient (Het) and wild type (WT) mice were maintained on high (HS), low (LS) or normal (NS) sodium intake, for 12 months. Renal fibrosis, glomerular volume, glomerular diameter and AT1 and AT2 receptor conformational status (activated or not activated by agonist ligation) were evaluated at the end of the study.Results: (n=6–17/group) LS‐WT LS‐HET NS‐WT NS‐HET HS‐WT HS‐HET Renal Fibrosis (%) 1.08±0.03* 1.13±0.04 1.14±0.03* 1.20±0.03 1.23±0.02 1.22±0.02 Glomerular Volume (×106 μm3) 0.25±0.01 0.27±0.01 0.25±0.01 0.23±0.01 0.27±0.01 0.27±0.01 Glomerular Diameter (μm) 82.4±1.78 84.3±2.92 84.0±1.63 81.0±1.31 84.1±1.58 84.7±2.98 Conformational Status AT1R (FI) 16.9±0.81 19.8±1.43 18.8±0.83 21.2±2.10 19.8±0.84& 21.4±0.67 Conformational Status AT2R (FI) 7.08±0.33 7.27±0.38 6.71±0.28 7.12±0.50 7.69±0.32 6.97±0.38 Data are reported as mean±SEM. p<0.05 vs. HS‐WT and p<0.05 vs. LS‐WT ConclusionsInterestingly, high salt intake stimulated renal fibrosis only in WT mice. The same phenomenon was observed in AT1 conformational status. In addition, the dietary salt content did not influence the glomerular volume and diameter in both WT and Het models suggesting that: renal fibrosis development and AT1 conformational status in response to dietary salt overload occur through different mechanisms in WT and Het animals stimulating further studies to elucidate this phenomenon.Support or Funding InformationSupported by FAPESP, CAPES and American Heart AssociationThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Cardiovascular Diseases Deaths Attributable to High Sodium Intake in Shandong Province, China.

BackgroundHigh sodium intake elevates blood pressure and thereby raises cardiovascular diseases (CVDs). Sodium intake is high in northern China, including Shandong province where the SMASH (Shandong‐Ministry of Health Action on Sodium and Hypertension) is currently underway.Methods and ResultsBlood pressure values and sodium intake measurements using 24‐hour urinary excretion were collected from the 2011 SMASH baseline survey, which was conducted in 20 counties/districts using a multistage stratified cluster random sampling method. We derived cause‐specific mortality from the Shandong Death Registration System (SDRS) during the same year and used population‐attributable fraction to estimate annual CVDs deaths attributable to high sodium intake (mediated through elevated systolic blood pressure) and CVD deaths averted by achieving different sodium‐reduction targets. Overall, 16 100 (95% uncertainty intervals, 11 000–22 600) CVD deaths among adults aged 25 to 69 years, including 5600 (4000–6500) for ischemic heart disease and 9000 (6700–11 600) for stroke, were attributable to higher sodium intake (2000 mg/day or 5.0 g/day of salt as a reference) in Shandong in 2011, accounting for 19.9% (13.7–25.0%) of total CVD deaths. The benefit of CVD deaths from sodium reduction is considerable with 8800 (6400–13 600), 6700 (4900–11 600), and 8500 (6000–10 800) averted, respectively, if sodium intake was reduced from the 2011 baseline to 3500 mg/day, 4000 mg/day, or reduced by 30%.ConclusionsNearly 20% of CVD deaths among adults aged 25 to 69 years could be attributable to the systolic blood pressure–raising effect of high sodium intake in Shandong in 2011. Potential benefits from population reduction of sodium intake are considerable.

GW29-e0030 Potassium Supplement blunts the effects of high sodium intake on serum retinol-binding protein 4 levels in humans

GW29-e0030 Potassium Supplement blunts the effects of high sodium intake on serum retinol-binding protein 4 levels in humans

Effects of high-sodium intake on systemic blood pressure andvascular responses in spontaneously diabetic WBN/Kob-Leprfa/fa rats.

SummaryThe prevalence of type 2 diabetes mellitus (T2DM) and hypertension has markedly increased worldwide. The purpose of the present study was to examine the effects of a high‐salt intake on the systolic blood pressure (SBP) and vascular responses in WBN/Kob‐Lepr fa/fa (WBKDF) rats, a new spontaneous animal model of T2DM. Male WBKDF rats and age‐matched Wistar rats at 6 weeks of age were each divided into two groups and fed either a normal‐sodium (NS, 0.26%) diet or high‐sodium (HS, 8%) diet for 14 weeks: (i) Wistar rats on NS diet (Wistar‐NS); (ii) Wistar rats on HS diet (Wistar‐HS); (iii) WBKDF rats on NS diet (WBKDF‐NS); (iv) WBKDF rats on HS diets (WBKDF‐HS). Neither WBKDF‐NS nor Wistar‐NS rats showed significant changes in SBP throughout the experiment, but both WBKDF‐HS and Wistar‐HS exhibited significant elevation of SBP, which was more prominent (P<.01) in WBKDF‐HS than in Wistar‐HS. Phenylephrine‐induced contractions of isolated thoracic aortic rings were significantly (P<.01) enhanced in WBKDF‐HS and Wistar‐HS compared with the respective strain of rats on the NS diet. In contrast, acetylcholine‐ and nitroprusside‐induced relaxation were significantly (P<.01) diminished in both WBKDF‐HS and Wistar‐HS, and these HS diet‐induced changes were more profound (P<.01) in WBKDF rats than in Wistar rats. Significantly (P<.05) higher plasma concentrations of 8‐iso‐prostaglandin F2α and sodium ions were observed in WBKDF‐HS than in Wistar‐HS. The current study demonstrated that WBKDF‐HS rats developed salt‐sensitive hypertension associated with vascular dysfunction. The WBKDF rat may be a useful model for investigating the etiology of hypertension with T2DM.

Sodium and Potassium Content of Meals Served in University Canteens

A high sodium intake is associated with high blood pressure, an important risk factor for noncommunicable diseases (NCDs). In contrast, the ingestion of high levels of potassium counteracts this negative effect of high sodium intake on blood pressure, thus reducing the sodium-to-potassium ratio. The aim of this work was to determine the sodium and potassium content of meals served in university canteens in Portugal. The analysis included 35 samples of soup and 35 samples of main dish collected at 5 random days from a total of 7 university canteens. The samples were analyzed for sodium and potassium by atomic emission spectrometry technique. On average, a meal (soup and main dish) had a sodium content of 1,069.4 mg (mean sodium content was 671.4 ± 374.5 mg/portion in the main dish and 398.0 ± 153.0 mg/portion in the soup) and a potassium content of 1,004 mg (mean potassium content was 731.4 ± 385.9 mg/serving in the main dish and 272.6 ± 272.6 mg/serving in the soup). Our results revealed that with a single university meal, students can reach 53% of the maximum daily value recommended for sodium and 27% of the minimum daily value recommended for potassium. An investment to decrease sodium and increase potassium in meals served is imperative in order to prevent NCDs.

Reduction of Salt in Haddock Mince: Effect of Different Salts on the Solubility of Proteins

ABSTRACTDue to negative health effects of high sodium intake, it is recommended to reduce the daily salt intake by around 50%. To reduce the sodium content, sodium salts can be exchanged with potassium or magnesium salts. The effect of sodium, potassium, and magnesium chlorides on extractability of proteins from fresh and frozen haddock muscle and minces was studied. Salting with KCl and MgCl2 instead of NaCl changed protein extractability. The highest solubility of the proteins was achieved using Na+. However, at low concentrations, extractability in K+ and Mg2+ is on the same level as Na+, showing that partial substitution of NaCl with KCl or MgCl2 is possible. Freezing affected the structure of tissue and protein properties, resulting in decreased amount of salt soluble proteins.

Effects of High Salt Intake on Blood Pressure and Cardiovascular Disease: The Role of COX Inhibitors.

Sodium has a bidirectional effect on blood pressure (BP) and cardiovascular disease (CVD). High sodium intake increases both BP and CVD, whereas low sodium intake decreases them. The significance of this association has been debated for years, mostly due to the inconsistency of data, but recently it has been revived due to new evidence about the harmful effects of sodium. Recent studies have indicated that high sodium intake was associated with an increase in BP and CVD, which in 2010 was estimated to have accounted for 1.65 million deaths worldwide. Based on this evidence, the American Heart Association has issued a Science Advisory statement regarding the significance of high sodium intake in relation to the incidence of hypertension and CVD. In addition to high sodium intake, experimental studies have shown that the coadministration of nonsteroidal anti-inflammatory drugs further aggravates the harmful effects of high sodium intake. The interrelationship of high sodium intake and nonsteroidal anti-inflammatory drugs will be discussed in this commentary.

Effects of High Sodium Intake on Plasma Volume and Physical Fitness in Patients with Postural Tachycardia Syndrome and Healthy Females

Background: Patients with postural tachycardia syndrome (POTS) oftenhave lowblood volumeand are advised to increase sodium intake to restore intravascular volume. However, the benefit of a high-sodium diet has not been systematically examined in POTS. Methods: We studied 12 female POTS patients (mean± SD; 34 ±9 years, BMI 23 ± 3 kg/m) and 8 female healthy control subjects (HC; 29 ± 4 years, BMI 24 ± 3 kg/m) randomly assigned to 6 days of low (LS; 10 mEq/day) or high sodium (HS; 300 mEq/day) diet and then crossed-over. Procedures performed on Day 6 included: posture study, plasma volume (PV) measurement by I-albumin, maximal oxygen consumption (VO2max) using a supine bicycle ergometer, and cardiac output (CO) and stroke volume (SV) assessments by the inert gases rebreathing technique in the flat and tilted head-up positions. Results: PV was significantly higher after HS than LS in POTS patients (PV: 2706 ± 110 ml vs. 2390 ± 89 ml, P b 0.001). Orthostatic tachycardia was reduced in POTS with HS (49 ± 16 bpm vs. 63 ±11 bpm, P = 0.001), but still increased compared with HC (49 ± 16 bpm vs. 23 ± 11 bpm, P = 0.001). Upright SV was significantly higher after HS than LS in POTS (35 ± 11ml vs. 25 ± 7ml, P = 0.023) but remained lower than HC (35 ± 11 ml vs. 52 ± 16ml, P = 0.033). Upright CO and VO2max did not differ significantly between POTS for either LS or HS. Conclusions: HS diet caused a reduction in orthostatic tachycardia, and increased PV and SV in POTS patients. Patients with POTS experienced improvement in their condition in association with higher sodium intake, but did not ‘normalize’ compared with HC.

Novel utilization of milk-based ingredients in salt reduced fish pudding

Both the food industry and the health authorities have increased their focus on salt reduction in food, due to the known negative health effect of high sodium intake. For this reason, there is great interest in developing products with reduced salt content without affecting properties related to sensory parameters, texture, yield and shelf-life. Whey and milk based permeates with favorable combinations of milk minerals and lactose can be used as natural ingredients in for instance meat and fish products and work as salt replacers. The aim of this study was to investigate how two different types of milk minerals; low mineral permeate, based on whey obtained in cheese production, and high mineral permeate, based on milk, affect the quality of comminuted fish products, using fish pudding as a model. Results showed that low mineral permeate can improve textural and water-holding properties of puddings at salt concentrations down to 0.8%, while it does not affect salt flavor. High mineral permeate contributes to changes in the textural and water-holding properties, and also increases salt flavor. Based on investigated factors, high mineral permeate is regarded as a promising salt replacer allowing for considerable salt reduction in fish puddings.