High Salt Intake Research Articles

Association of rheumatoid arthritis and high sodium intake with major adverse cardiovascular events: a cross-sectional study from the seventh Korean National Health and Nutrition Examination Survey

ObjectivesHigh salt intake has a harmful effect on hypertension; however, the association between major adverse cardiovascular events (MACE) and salt intake is still controversial. Rheumatoid arthritis (RA) is also characterised...

Starvation and activity dependent modulation of salt taste behavior in Drosophila

Sodium present in NaCl is a fundamental nutrient required for many physiological processes but high salt consumption in western world is contributing health risk to all age individuals. Although high salt detection pathways have been studied in great detail, the mechanisms that regulate high salt consumption in animals are largely unknown. To understand how pre-exposure to high NaCl diet modulates subsequent feeding behavior, we looked into the neural mechanisms of high NaCl consumption in adult Drosophila. We used Neuro-Genetics, imaging and behavioral assays to determine how flies respond to high NaCl exposure. We studied the neural mechanism by which flies modify their acceptance of high salt as a function of diet, where a long-term high-salt exposure increases taste sensitivities of pharyngeal LSO (Labral sense organ) neurons and enhances high salt intake. We discovered that exposing flies to high NaCl diet(200mM NaCl in fly food) for three days modify their feeding responses to high levels of salt. High NaCl fed flies show decline in high salt aversion under starvation. Genetic suppression of LSO pharyngeal neurons in high NaCl fed flies inhibits excessive salt intake. We found that this modulation requires functional LSO neurons and starvation state, and that multiple independent taste receptor neurons and pathways are involved in this process. Silencing any one of multiple LSO neuronal types inhibits excessive salt intake. Our data support the idea that high dietary salt modulates and reshapes salt and other taste curves to promote over consumption of food in flies. Our study suggest flies can adapt to the amount of salt ingested over several days, indicating the presence of a critical mechanism to reset the salt appetite and related neural circuits. Identification of new molecular sensors for salt and related neural controls such as hormones, neuropeptides, and neurotransmitters may yield insights into the coordination of processes in the nervous system.

Blood pressure regulation in autonomic failure by dietary sodium, blood volume and posture

In normal subjects natriuresis is tightly coupled to dietary salt ingestion to maintain sodium balance. Likewise, blood pressure remains unchanged over a wide range of salt intake because of pressure natriuresis, whereby an increase in blood pressure stimulates renal sodium excretion to restore homeostasis. These sodium handling mechanisms are impaired in autonomic failure. When exposed to salt restriction, autonomic failure patients are unable to reduce renal sodium excretion, and their orthostatic hypotension worsens. It follows that increased dietary salt would improve orthostatic tolerance. Indeed, most clinical practice guidelines emphasize a high salt intake (6-10g/day) in the treatment of neurogenic orthostatic hypotension. This approach has been shown to improve other conditions such as syncope and postural tachycardia syndrome, but surprisingly there is no empirical evidence to support this recommendation in orthostatic hypotension. Even though there is expert opinion consensus in its favor, it would be reassuring if at least mechanistic proof of concept studies were available. Fludrocortisone is often added to a high salt diet to improve sodium retention and increase plasma volume, but these effects are transient. Fludrocortisone is contraindicated in patients with heart failure and should be used with caution, if at all, if supine hypertension is present. In patients with supine hypertension posture is an important determinant of sodium balance; blood pressure substantially increases while supine, triggering pressure natriuresis and extensive sodium loss. Thus, avoiding the supine posture may be as important as increasing dietary salt in the management of orthostatic hypotension.

ROMK channels are inhibited in the aldosterone-sensitive distal nephron of renal tubule Nedd4-2-deficient mice.

We used whole cell recording to examine the renal outer medullary K+ channel (ROMK or Kir1.1) and epithelial Na+ channel (ENaC) in the late distal convoluted tubule (DCT2)/initial connecting tubule (iCNT) and in the cortical collecting duct (CCD) of kidney tubule-specific neural precursor cell-expressed developmentally downregulated protein 4-2 (Nedd4-2) knockout mice (Ks-Nedd4-2 KO) and floxed neural precursor cell-expressed developmentally downregulated 4-like (Nedd4l) mice (control). Tertiapin Q (TPNQ)-sensitive K+ currents (ROMK) were smaller in both the DCT2/iCNT and CCD of Ks-Nedd4-2 KO mice on a normal diet than in control mice. Neither high dietary salt intake nor low dietary salt intake had a significant effect on ROMK activity in the DCT2/iCNT and CCD of control and Ks-Nedd4-2 KO mice. In contrast, high dietary K+ intake (HK) increased, whereas low dietary K+ intake (LK) decreased TPNQ-sensitive K+ currents in floxed Nedd4l mice. However, the effects of dietary K+ intake on ROMK channel activity were absent in Ks-Nedd4-2 KO mice since neither HK nor LK significantly affected TPNQ-sensitive K+ currents in the DCT2/iCNT and CCD. Moreover, TPNQ-sensitive K+ currents in the DCT2/iCNT and CCD of Ks-Nedd4-2 KO mice on HK were similar to those of control mice on LK. Amiloride-sensitive Na+ currents in the DCT2/iCNT and CCD were significantly higher in Ks-Nedd4-2 KO mice than in floxed Nedd4l mice on a normal K+ diet. HK increased ENaC activity of the DCT2/iCNT only in control mice, but HK stimulated ENaC of the CCD in both control and Ks-Nedd4-2 KO mice. Moreover, the HK-induced increase in amiloride-sensitive Na+ currents was larger in Ks-Nedd4-2 KO mice than in control mice. Deletion of Nedd4-2 increased with no lysine kinase 1 expression and abolished HK-induced inhibition of with no lysine kinase 1. We conclude that deletion of Nedd4-2 increases ENaC activity but decreases ROMK activity in the aldosterone-sensitive distal nephron and that HK fails to stimulate ROMK, but robustly increases ENaC activity in the CCD of Nedd4-2-deficient mice.NEW & NOTEWORTHY We demonstrate that renal outer medullary K+ (ROMK) channel activity is inhibited in the late distal convoluted tubule/initial connecting tubule and cortical collecting duct of neural precursor cell-expressed developmentally downregulated protein 4-2 (Nedd4-2)-deficient mice. Also, deletion of Nedd4-2 abolishes the stimulatory effect of dietary K+ intake on ROMK. The lack of high K+-induced stimulation of ROMK is associated with the absence of high K+-induced inhibition of with no lysine kinase 1.

Bilateral Paraventricular Nucleus Upregulation of Extracellular Superoxide Dismutase Decreases Blood Pressure by Regulation of the NLRP3 and Neurotransmitters in Salt-Induced Hypertensive Rats.

Aims: Long-term salt diet induces the oxidative stress in the paraventricular nucleus (PVN) and increases the blood pressure. Extracellular superoxide dismutase (Ec-SOD) is a unique antioxidant enzyme that exists in extracellular space and plays an essential role in scavenging excessive reactive oxygen species (ROS). However, the underlying mechanism of Ec-SOD in the PVN remains unclear. Methods: Sprague–Dawley rats (150–200 g) were fed either a high salt diet (8% NaCl, HS) or normal salt diet (0.9% NaCl, NS) for 6 weeks. Each group of rats was administered with bilateral PVN microinjection of AAV-Ec-SOD (Ec-SOD overexpression) or AAV-Ctrl for the next 6 weeks. Results: High salt intake not only increased mean arterial blood pressure (MAP) and the plasma noradrenaline (NE) but also elevated the NAD(P)H oxidase activity, the NAD(P)H oxidase components (NOX2 and NOX4) expression, and ROS production in the PVN. Meanwhile, the NOD-like receptor protein 3 (NLRP3)–dependent inflammatory proteins (ASC, pro-cas-1, IL-β, CXCR, CCL2) expression and the tyrosine hydroxylase (TH) expression in the PVN with high salt diet were higher, but the GSH level, Ec-SOD activity, GAD67 expression, and GABA level were lower than the NS group. Bilateral PVN microinjection of AAV-Ec-SOD decreased MAP and the plasma NE, reduced NAD(P)H oxidase activity, the NOX2 and NOX4 expression, and ROS production, attenuated NLRP3-dependent inflammatory expression and TH, but increased GSH level, Ec-SOD activity, GAD67 expression, and GABA level in the PVN compared with the high salt group. Conclusion: Excessive salt intake not only activates oxidative stress but also induces the NLRP3-depensent inflammation and breaks the balance between inhibitory and excitability neurotransmitters in the PVN. Ec-SOD, as an essential anti-oxidative enzyme, eliminates the ROS in the PVN and decreases the blood pressure, probably through inhibiting the NLRP3-dependent inflammation and improving the excitatory neurotransmitter release in the PVN in the salt-induced hypertension.

Correlation study of socio-demographic factors like gender, age, body mass index and some cardiovascular parameters in hypertensive subjects of Yenagoa, Bayelsa state, Nigeria

Hypertension is defined as a sustained elevated arterial pressure to a level that places the patient at increased risk of organ damage. It is a non-communicable disease which constitutes a public health importance. Its risk factors include advancing age, high salt intake, excessive alcohol consumption and stress. This study was performed to determine the correlation between some socio-demographic factors like gender, age, body mass index (BMI) and some cardiovascular parameters in hypertensive patients of Yenagoa, Bayelsa State, Nigeria. The study was carried out with 400 hypertensive subjects, whose blood pressures were determined using palpatory and auscultatory methods. The gender, age and body mass index of the subjects were also determined. Statistical analysis was done using Z-statistics. We found a significant positive relationship between the age and cardiovascular parameters. Gender and BMI were found to have an insignificant positive correlation with the cardiovascular parameters. The study demonstrated that body mass index, age and gender are closely associated with cardiovascular parameters, though the degree of correlation differed. The risk of hypertension is therefore expected to be higher among the aged and populations who are overweight or obese.

Differential biomechanics in resistance arteries of male compared with female Dahl hypertensive rats.

Background:Increase in vascular stiffness is associated with a higher risk of cardiovascular morbidity and mortality and is likely sex-specific.Method:Our objectives were to compare structural and functional alterations in small resistance arteries as related to vascular stiffness from Dahl salt-sensitive male and female rats (n = 8, mean ± s.e.m.).Results:Arterial blood pressure and pulse wave velocity were significantly (P < 0.05) elevated in males (161 ± 3 mmHg; 6.4 ± 0.2 m/s) and females (147 ± 2 mmHg; 5.5 ± 0.1 m/s) on a high (H) salt compared with regular (R) diets but were significantly higher in males (H) than in all others. Significant increases in collagen and smooth muscle cell areas were evident in ultrastructure of mesenteric arteries of hypertensive males compared to normotensive or corresponding females. There were no significant differences in composite Young's modulus (CYM) between groups. Vasoconstriction resulted in significantly higher CYM in male (H: 8.6 ± 1 KPa) than R (4.5 ± 0.8 KPa), and the corresponding females (H: 5.6 ± 0.6 KPa and R: 5 ± 0.9 KPa). In contrast, vasodilation significantly reduced CYM in the male groups (H: 2.5 ± 0.4 KPa and R: 2.7 ± 0.5 KPa) compared with the corresponding values in females (H: 4.2 ± 0.6 KPa and R: 5 ± 0.5 KPa). Moreover, the slope of pressure-volume curves revealed significantly greater distended vascular compliance in male H than R, and the corresponding females.Conclusion:Our findings are supportive of a link between high salt intake and elevated blood pressure as being sex specific, likely involving sex-dependent changes in ultrastructure of the vessels, which ultimately may alter the biomechanics, and thus, the haemodynamic functions of both macro-circulation and micro-circulations.

Effects of almonds on ameliorating salt-induced hypertension in dahl salt-sensitive rats.

Excessive dietary salt intake is related to an increased risk of hypertension. Dietary functional foods probably could help to improve salt-induced hypertension. In this study, Dahl salt-sensitive (DSS) rats were used to investigate their metabolic differences from those of salt-resistant SS.13BN rats and determine whether dietary protein-rich almonds could ameliorate salt-induced elevation of blood pressure in DSS rats. After high-salt intake, the systolic blood pressure and mean arterial pressure of the DSS rats increased dramatically. Metabolomics analysis indicated abnormal amino acid metabolism in their kidneys. Their renal nitric oxide (NO) content and nitric oxide synthase activity decreased significantly after high-salt diet. Oxidative stress also occurred in DSS rats. After the DSS rats received almond supplementation, the levels of various amino acids in their kidney increased, and renal arginine and NO contents were upregulated. Their renal hydrogen peroxide and malonaldehyde levels decreased, whereas renal catalase, superoxide dismutase and glutathione peroxidase activities and glutathione levels increased. The renal abnormal amino acid metabolism of DSS rats contributed to the impaired NO production in response to high-salt intake. Together with salt-induced oxidative stress, high-salt diet intake ultimately led to an increase in the blood pressure of DSS rats. Protein-rich almond supplementation might prevent the development of salt-induced hypertension by restoring arginine and NO regeneration and alleviating salt-induced oxidative stress. © 2021 Society of Chemical Industry.

Perturbed body fluid distribution and osmoregulation in response to high salt intake in patients with hereditary multiple exostoses

SummaryBackgroundHereditary Multiple Exostoses (HME) is a rare autosomal disorder characterized by the presence of multiple exostoses (osteochondromas) caused by a heterozygous loss of function mutation in EXT1 or EXT2; genes involved in heparan sulfate (HS) chain elongation. Considering that HS and other glycosaminoglycans play an important role in sodium and water homeostasis, we hypothesized that HME patients have perturbed whole body volume regulation and osmolality in response to high sodium conditions.MethodsWe performed a randomized cross-over study in 7 male HME patients and 12 healthy controls, matched for age, BMI, blood pressure and renal function. All subjects followed both an 8-day low sodium diet (LSD, <50 mmol/d) and high sodium diet (HSD, >200 mmol/d) in randomized order. After each diet, blood and urine samples were collected. Body fluid compartment measurements were performed by using the distribution curve of iohexol and 125I-albumin.ResultsIn HME patients, HSD resulted in significant increase of intracellular fluid volume (ICFV) (1.2 L, p = 0.01). In this group, solute-mediated water clearance was significantly lower after HSD, and no changes in interstitial fluid volume (IFV), plasma sodium, and effective osmolality were observed. In healthy controls, HSD did not influence ICFV, but expanded IFV (1.8 L, p = 0.058) and increased plasma sodium and effective osmolality.ConclusionHME patients show altered body fluid distribution and osmoregulation after HSD compared to controls. Our results might indicate reduced interstitial sodium accumulation capacity in HME, leading to ICFV increase. Therefore, this study provides additional support that HS is crucial for maintaining constancy of the internal environment.

High salt diet impairs dermal tissue remodeling in a mouse model of IMQ induced dermatitis.

Recent animal studies, as well as quantitative sodium MRI observations on humans demonstrated that remarkable amounts of sodium can be stored in the skin. It is also known that excess sodium in the tissues leads to inflammation in various organs, but its role in dermal pathophysiology has not been elucidated. Therefore, our aim was to study the effect of dietary salt loading on inflammatory process and related extracellular matrix (ECM) remodeling in the skin. To investigate the effect of high salt consumption on inflammation and ECM production in the skin mice were kept on normal (NSD) or high salt (HSD) diet and then dermatitis was induced with imiquimod (IMQ) treatment. The effect of high salt concentration on dermal fibroblasts (DF) and peripheral blood mononuclear cells (PBMC) was also investigated in vitro. The HSD resulted in increased sodium content in the skin of mice. Inflammatory cytokine Il17 expression was elevated in the skin of HSD mice. Expression of anti-inflammatory Il10 and Il13 decreased in the skin of HSD or HSD IMQ mice. The fibroblast marker Acta2 and ECM component Fn and Col1a1 decreased in HSD IMQ mice. Expression of ECM remodeling related Pdgfb and activation phosphorylated (p)-SMAD2/3 was lower in HSD IMQ mice. In PBMCs, production of IL10, IL13 and PDGFB was reduced due to high salt loading. In cultured DFs high salt concentration resulted in decreased cell motility and ECM production, as well. Our results demonstrate that high dietary salt intake is associated with increased dermal pro-inflammatory status. Interestingly, although inflammation induces the synthesis of ECM in most organs, the expression of ECM decreased in the inflamed skin of mice on high salt diet. Our data suggest that salt intake may alter the process of skin remodeling.

Impact of salt intake on inflammation markers in cardiovascular disease: a retrospective observational case-control study

Background. Salt intake currently poses a serious threat due to the cardiovascular challenge incurred by excessive sodium consumption.Objectives. The identification of markers associated with high salt intake in hypertensive patients.Methods. A retrospective observational case-control study surveyed 251 persons, including 194 hypertensive patients with stable salt intake. The intake was assessed in the “Charlton: SaltScreener” questionnaire. General, biochemical blood panels and interleukin levels (IL-1, IL-2, IL-4, IL-6, IL-8, IL-10, IL-18) were evaluated in the outcome of medical examination. Statistical data processing was performed with R using the RStudio software.Results. The mean patient age in survey was 72.47 ± 9.8 years, women prevailed in the selected cohort (n = 151, 60.1%). All patients were assigned in cohorts by the daily salt intake rate, ≤5 g (n = 12), 6–10 g (n = 144), &gt;10 g salt per day (n = 38). The largest cohort (74.2%) united patients consuming 6–10 g salt per day, whereas only 6.2% patients consumed salt &lt;5 g/day. Final analysis included patients consuming ≥6 g/day and having a C-reactive protein (CRP) level &lt;20 mg/L. The analysis elicited an association between the monocyte count, CRP and salt intake towards the statement that higher salt intake leads to higher monocyte counts at CRP &lt;20 mg/L in blood. Modelling revealed a close monocyte count–salt intake relationship, with a low-to-high intake transition sharply increasing the probability of elevated absolute monocyte count in blood provided the CRP level is &lt;20 mg/L.Conclusion. The study infers a direct relationship between salt intake &gt;10 g/day and blood monocyte count. However, its significance ceases at CRP rising to ≥20 mg/L.

Salt-Sensitive Hypertension, Renal Injury, and Renal Vasodysfunction Associated With Dahl Salt-Sensitive Rats Are Abolished in Consomic SS.BN1 Rats.

BackgroundAbnormal renal hemodynamic responses to salt‐loading are thought to contribute to salt‐sensitive (SS) hypertension. However, this is based largely on studies in anesthetized animals, and little data are available in conscious SS and salt‐resistant rats.Methods and ResultsWe assessed arterial blood pressure, renal function, and renal blood flow during administration of a 0.4% NaCl and a high‐salt (4.0% NaCl) diet in conscious, chronically instrumented 10‐ to 14‐week‐old Dahl SS and consomic SS rats in which chromosome 1 from the salt‐resistant Brown‐Norway strain was introgressed into the genome of the SS strain (SS.BN1). Three weeks of high salt intake significantly increased blood pressure (20%) and exacerbated renal injury in SS rats. In contrast, the increase in blood pressure (5%) was similarly attenuated in Brown‐Norway and SS.BN1 rats, and both strains were completely protected against renal injury. In SS.BN1 rats, 1 week of high salt intake was associated with a significant decrease in renal vascular resistance (−8%) and increase in renal blood flow (15%). In contrast, renal vascular resistance failed to decrease, and renal blood flow remained unchanged in SS rats during high salt intake. Finally, urinary sodium excretion and glomerular filtration rate were similar between SS and SS.BN1 rats during 0.4% NaCl and high salt intake.ConclusionsOur data support the concept that renal vasodysfunction contributes to blood pressure salt sensitivity in Dahl SS rats, and that genes on rat chromosome 1 play a major role in modulating renal hemodynamic responses to salt loading and salt‐induced hypertension.

The significance of homocysteine in patients with hypertension

Abstract Cardiovascular disease is the most common cause of death in developed countries. Important factors leading to ischemic heart disease and strokes are hypertension and high levels of homocysteine in blood serum. The coexistence of these two factors significantly increases the risk of these diseases and premature deaths. Many studies indicate that patients with hypertension are significantly more likely to demonstrate increased blood serum homocysteine levels than those with normal blood pressure. This may be caused by a higher incidence of overweight, high intake of salt and increased uric acid levels. It has been shown that both these factors increase the prevalence of hypertension and lead to higher homocysteine levels. However, the results of some studies indicate that arterial hypertension and homocysteinemia are causally related. It was shown, among other things, that high homocysteine levels damage the endothelium and reduce nitric oxide synthesis, which may directly lead to hypertension. Serum homocysteine levels are slightly higher in patients with white coat hypertension than they are in healthy individuals and may therefore also increase the risk of cardiovascular diseases. Several authors have also shown that the levels of homocysteine in blood serum are higher in so-called non-dippers, i.e., patients with no night-time pressure drop. The lack of a 10%–20% decrease in blood pressure at night is associated with increased cardiovascular complications. Strokes occur especially frequently in older people with arterial hypertension and hyperhomocysteinemia. The administration of B vitamins and folic acid significantly reduces serum homocysteine levels. The administration of this acid also slightly, but statistically significantly, increases the effectiveness of hypotensive drugs. Large meta-analyses meta-analysis indicate that the increased supply of folic acid in patients with hypertension significantly reduces the risk of stroke. Such management is particularly effective in patients with hypertension and hyperhomocysteinemia.

Nutritional risk factors in Hungarian elderly-Biomarker2019 survey

Abstract In Hungary, about a quarter of the population is over the age of 60 and their proportion is projected to increase considerably within a few decades. According to the 2009 and 2014 European Health Interview Survey data, 87% of Hungarian older adults suffer from at least one non-communicable disease (NCD). Many of the NCDs are associated with poor nutrition. Reliable data on nutritional status of this age group is scarce. The Biomarker2019 survey provides comprehensive data on the nutritional status of this vulnerable age group. The cross-sectional survey was carried out in western Hungary. Participants aged ≥60y were selected from non-institutionalized patients of general practitioners' practicing in Western Hungary (n = 200). Data collection involved a questionnaire, physical examinations, three-day dietary record, and a collection of biological samples (fasting blood and 24-hour urine). 77% of the participants had high blood pressure diagnosed by a physician. 85% of men and 76% of women were overweight or obese, according to the BMIs. The mean proportion of energy from fat was higher (men: 39 E%, women: 37 E%), that from carbohydrates was lower in men (43 E%) than recommended, while it was adequate in women (47 E%). The mean protein intake was adequate in both sexes. Cholesterol intake was 433 mg/day for men and 317 mg/day for women, both higher than the Hungarian recommendations. The fiber intake was 23.8 g/day for men and 23.6 g/day for women, both below the recommended values. Based on the estimates of salt intake from 24-hour urine, 90% of participants had a higher salt intake than recommended. Nutritional risk factors predisposing to the development of NCDs were identified in the sample. The results of the study contributed to the development of a food-based dietary guideline tailor made to the Hungarian elderly population (60+ Health - Dietary Guideline for the Elderly), its dissemination to the target audience has been started. Key messages The identification of nutritional risk factors in a sample of older adults contributed to the development of a new food-based dietary guideline for the elderly population. The results can form the basis of further public health interventions.

An assessment of ethnic and environmental influences on the phenotypes of hypertension

Abstract Background Hypertension is a growing global concern with developing countries now having the highest prevalence. Environmental factors such as socioeconomic status and diet, together with ethnicity-related factors may influence the development of hypertension and its complications such as left ventricular hypertrophy (LVH). However, the relative contributions of environment and ethnicity to these outcomes remain poorly understood. Purpose To test the hypothesis that black hypertensives living in Nigeria would have a higher prevalence of hypertensive target organ damage (i.e. LVH and dysfunction) compared with black hypertensives living in the UK. Methods We conducted a three-arm comparative study based on self-defined ethnicity and country of residence. We carried out detailed cardiovascular phenotyping in untreated Black hypertensives (n=53) living in Nigeria (BNig), untreated Black (BUK) hypertensives (n=25), and untreated White (WUK) hypertensives (n=59) living in the UK. We measured brachial and central blood pressure and undertook 2D echocardiography in all the participants. In addition, we collected serum and 24-hour urine biochemistry. Results The three groups had similar mean age and BMI (Table 1). The BNig group had significantly higher brachial SBP (P=0.01) and LV mass index (LVMI); P&amp;lt;0.001) compared with the BUK group. Furthermore, both BNig &amp; BUK groups each had significantly higher brachial SBP (BNig: 162mmHg, BUK: 151mmHg) and LVMI (BNig: 100.9g/m2, BUK:86.4 g/m2) compared with the WUK group (Brachial SBP: 144mmHg, LVMI: 82.2g/m2). The prevalence of concentric LVH was similar in the two UK groups (BUK: 10%, WUK: 12%) but higher in the BNig group (41%). Septal early diastolic velocity was significantly lower in BNig group (7.0cm/s) compared to BUK (10.0cm/s) and WUK (10.0 cm/s). After adjusting for 24-hour sodium, brachial SBP (162mmHg) in the BNig group was still significantly higher compared with the other two groups [F(2,109)=13.805, BK (151mmHg, P=0.032), White UK (145mmHg, P&amp;lt;0.001)). However, after controlling for SBP, difference in LVMI persisted only between the BNig (EMM: 98.4 g/m2) versus WUK (EMM: 84.2 g/m2) groups, with no significant difference in BNig vs BUK (86.6g/m2, P=0.156) [F(2,128)=4.245, p=0.016]. Conclusion Our data suggest that higher SBP and salt intake do not explain all of the environmental differences in the prevalence of LVH and LV dysfunction in hypertensive patients drawn from different ethnicities and environments, suggesting that other factors are likely to play an important role. Further work is in a larger group is required to confirm these findings. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Niger Delta Development Commission

Hypertensive heart disease burden attributable to high salt intake in the United States compared to the European Union and the global status: trends from 1990 to 2019

Abstract Background Hypertensive heart disease (HHD) is a major cause of heart failure, cardiovascular related hospitalizations, and mortality. Diet high in salt is one of modifiable risk factors of HHD that can be controlled by appropriate policies. Purpose This study aims to provide the HHD burden attributable to diet high in sodium in the United States compared to European and the global trends from 1990 to 2019. Methods Using the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 methodology, we calculated the HHD, mortality, years lived with disability, years of life lost, and disability-adjusted life-years (DALYs). Diet high in sodium was defined as a diet with more than 1,000 milligrams of sodium per day. HHD deaths attributable to the diet high in sodium was estimated based on risk exposure, relative risks, and the theoretical minimum risk exposure level Trends of HHD attributable to diet high in sodium was estimated from 1990 to 2019. Results Globally, there were 170·3 thousand (95% uncertainty interval [UI] 31.2 to 459.5) deaths, YLLs, YLDs, DALYs due to HHD attributable to diet high in sodium, in 2019. In the United States, 4525 deaths happened because of HHD caused by the diet high in sodium, with 208.4% rise from 1990. In the European Union, 18,143 deaths happened because of HHD caused by the diet high in sodium, with 78.0% rise from 1990. To address the impact of population aging and population growth, we estimated the age standardized values for burden of HHD attributable to the diet high in sodium. From 1990 to 2019, worldwide age standardized YLL, YLD, and DALY rates per 100,000 for HHD attributable to the diet high in sodium changed by −44.0% (−63.6 to −30.6), +3.7% (−14.3 to +13.6), and −41.8% (−61.3 to −28.8), respectively (Figure 1). In the European Union, age standardized YLL, YLD, and DALY rates per 100,000 for HHD attributable to the diet high in sodium changed by −14.8% (−44.6 to −0.2), −13.5% (−45.8 to −14.0), and −14.8% (−43.5 to −0.9), respectively. Compared to the European Union and the worldwide trends, United Sates had the opposite increasing trend of HHD caused by the diet high in sodium. In the United States, age standardized YLL, YLD, and DALY rates per 100,000 for HHD attributable to the diet high in sodium changed by +110.4% (+42.0 to +631.0), +44.2% (+106.4 to +300.5), and −14.8% (−43.5 to −0.9), respectively. As shown in figure 2, the United States' increasing trend of HHD attributable to the diet high in sodium was caused mainly by the increasing trend observed in men. Conclusions Despite worldwide success in the restriction of the diet high in sodium, HHD burden attributable to high consumption of sodium is rising in the United States. This warning results requires public health attention to taking actions such as advocating for healthy diet, restricting foods high in sodium such as fast foods, and increasing the access to low salt foods for working groups. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Bill &amp; Melinda Gates Foundation Annual % DALY change of HHD due to saltTrend of HHD DALY in men vs women

Sex-Dependent Regulation of the WNK-NCC Pathway via Ubiquitination in Response to Dietary High Salt Intake in Young Sprague-Dawley Rats

Sex-Dependent Regulation of the WNK-NCC Pathway via Ubiquitination in Response to Dietary High Salt Intake in Young Sprague-Dawley Rats

Effect of Salt Content Reduction on Food Processing Technology.

Higher salt intake is associated with the risk of cardiovascular and kidney diseases, hypertension and gastric cancer. Salt intake reduction represents an effective way to improve people’s health, either by the right choice of food or by a reduction of added salt. Salt substitutes are often used and also herb homogenates are treated by high pressure technology. Salt reduction significantly influences the shelf life, texture, pH, taste, and aroma of cheese. The composition of emulsifying salts or starter cultures must be modified to enact changes in microbial diversity, protease activity and the ripening process. The texture becomes softer and aroma atypical. In bakery products, a salt reduction of only 20–30% is acceptable. Water absorption, dough development, length and intensity of kneading and stability of dough are changed. Gluten development and its viscoelastic properties are affected. The salt reduction promotes yeast growth and CO2 production. Specific volume and crust colour intensity decreased, and the crumb porosity changed. In meat products, salt provides flavour, texture, and shelf life, and water activity increases. In this case, myofibrillar proteins’ solubility, water binding activity and colour intensity changes were found. The composition of curing nitrite salt mixtures and starter cultures must be modified.

Animal, Human, and 23Na MRI Imaging Evidence for the Negative Impact of High Dietary Salt in Children.

Purpose of the ReviewConditions typically prevalent in adults such as hypertension, kidney stones, osteoporosis, and chronic kidney disease are increasing among adolescents and young adults (AYA). The purpose of this review is to describe the association of these conditions to a high salt diet among pediatric patients.Recent FindingsWe present animal, human, and 23Na MRI evidence associated with the negative impact of high dietary salt in children. Special focus is placed on novel 23Na MRI imaging which reveals the important concept of a third compartment for sodium storage in soft tissue. Finally, we make recommendations on who should not be on a low salt diet.SummaryA high salt intake predisposes children and AYA to considerable morbidity. We exhort the reader to engage in advocacy efforts to curve the incidence and prevalence of high salt-related life-limiting conditions.

High-Salt Diet Accelerated the Decline of Residual Renal Function in Patients With Peritoneal Dialysis

Objective: This study aims to investigate the relationship between dietary salt intake and residual renal function in peritoneal dialysis (PD) patients.Methods: The daily salt intake of the patients was calculated based on a 3 day dietary record. Sixty-two patients were divided into three groups: 33 patients in the low salt intake group (salt intake <6.0 g/day), 17 in the medium salt intake group (salt intake 6.0 to <8.0 g/day), and 12 in the high salt intake group (salt intake ≥8.0 g/day). Regular follow-up was conducted every 3 months. Urine volume, peritoneal ultrafiltration volume, and other clinical indicators were recorded. Biochemical indexes were detected to evaluate the changes in residual renal function and peritoneal function during follow-up.Results: A positive correlation between dietary sodium intake and sodium excretion was found. During 12-month follow-up, a decrease of residual renal function showed a significant difference among the three groups (p = 0.041) (15.3 ± 27.5 vs. 12.5 ± 11.5 vs. 32.9 ± 18.4 L/W/1.73 m2 in the low-, medium-, and high salt intake groups, respectively). Consistently, a higher decline of residual renal function (adjusted β, 20.37; 95% CI, 2.83, 37.91) was found in participants with high salt intake (salt intake ≥8 g/day) compared with those in non-high salt intake.Conclusion: Our study showed that the sodium excretion by peritoneal dialysis was positively correlated with dietary sodium intake in PD patients. The high salt intake diet (salt intake ≥8 g/day) may lead to a faster decline of residual renal function in PD patients.