Effect Of Dietary Sodium Intake Research Articles

Potential role of inflammation in relation to dietary sodium and β-carotene with non-alcoholic fatty liver disease: a mediation analysis

BackgroundHigh sodium intake has been linked to the prevalence of non-alcoholic fatty liver disease (NAFLD), but underlying mechanism remains unclear. This study aims to explore the role of chronic inflammation in the association between sodium and NAFLD. We also observed whether β-carotene, which had a strong anti-inflammatory effect, lowers the odds of NAFLD.MethodsWe performed mediation analyses to assess the mediating effects of C-reactive protein (CRP) and red cell distribution width (RDW) on the relationship between dietary sodium and NAFLD defined by the hepatic steatosis index (HSI) and the fatty liver index (FLI), respectively.ResultsA total of 6725 participants were included in this study. Compared with the high sodium-low carotene group, participants in the high sodium-high carotene group had 16% and 26% lower odds for HSI and FLI-defined NAFLD, respectively. There were positive indirect effects of dietary sodium intake on the HSI-defined NAFLD (indirect effect: 0.0057, 95% CI: 0.0021–0.0091, P < 0.0001), as well as the FLI defined NAFLD (indirect effect: 0.0081, 95% CI: 0.0024–0.0162, P < 0.0001) when C-reactive protein (CRP) was considered as a mediator. The mediating effects were somewhat attenuated after further adjusting for dietary β-carotene intake. Similar results were found when RDW was considered as a mediator in the HSI-defined NAFLD analysis.ConclusionsHigher sodium intake increases the odds of NAFLD by upregulating inflammation. Dietary β-carotene may attenuate this association by down regulating inflammation.

423.12: Dietary Protein Intake and Blood Pressure After Living Kidney Donation

Background: High dietary protein intake is associated with worsening kidney function especially in at-risk patients such as living kidney donors; high blood pressure is a known risk factor for kidney disease. Whether pre-donation protein intake contributes to post-donation blood pressure is unknown. Methods: A single-center cohort study included living kidney donors undergoing living kidney donation in 2021 and divided the patients into 2 groups: low and high pre-donation protein intake defined by dietary protein intake estimated from 24-hour urine collection <1 (LPI) and ≥1 (HPI) g/kg/day, respectively. Association between dietary protein intake and systolic blood pressure during the first two weeks post-donation was evaluated by multiple linear regression. Results: Of 14 living kidney donors, mean±SD was 44±12 and 50% were female. Half of the study population were in the LPI group with a mean dietary protein intake of 0.8±0.1 g/kg/day and the remaining seven patients in the HPI group had a dietary protein intake of 2.2±2.5 g/kg/day (meandifference HPI vs LPI 1.4; p 0.172; 95%CI -0.7, 3.5). Dietary sodium intake was not different between the two groups (mean sodium intake of LPI 3,171±1,315 and of HPI 4,058±1,135 g/day, meandifferenc HPI vs LPI 887; p 0.202; 95%CI -544, 2,318; Figure 1). Mean systolic blood pressure of LPI and HPI groups were 135±8 and 121±7 mmHg, respectively (meandifference LPI vs HPI 14; p 0.007; 95%CI 5, 23). Compared to the LPI group, the HPI group had 14 mmHg lower systolic blood pressure (β -14; p 0.007; 95%CI -23, -5; Figure 2). After adjusted by age, gender, ethnicity, pre-donation body mass index, dietary sodium intake (<4 vs ≥4 g/day), and the interaction term between dietary protein intake and dietary sodium intake, the magnitude and direction of the association between dietary protein intake and systolic blood pressure remain the same (β -13, p 0.043, 95%CI -26, -0.6) and dietary sodium intake did not modify the association (Pinteraction 0.498). Conclusions: Higher dietary protein intake during pre-donation is inversely associated with SBP level without the effect of dietary sodium intake. Although HPI is associated with adverse kidney outcomes, the protective association between HPI and high blood pressure may involve physiological change after donor nephrectomy and further studies with long-term follow-up are required.

Effects Of Dietary Sodium Intake On Blood Flow Regulation During Exercise In Salt Resistant Individuals

PURPOSE: Dietary guidelines for sodium intake is less than 2,300 mg/day, yet 90% of Americans exceed this value. This study examined individuals resistant to salt-induced changes in blood pressure to determine the impact of a high sodium diet on blood flow regulation during upper and lower limb exercise. METHODS: Six young (25 ± 2 years) males followed recommended dietary sodium intake guidelines on two separate weeks, with one week supplemented with salt capsules (HS: 6,900 mg/day of sodium) and the other week supplemented with placebo capsules (LS: 2,300 mg/day of sodium). Resting central hemodynamic measurements [heart rate (HR), heart rate variability (HRV), and mean arterial pressure (MAP)] were evaluated the end of each diet. Peripheral hemodynamic measurements [blood flow (BF), shear rate (SR), and flow mediated dilation (FMD)/SR)] of the brachial and superficial femoral artery were taken during rhythmic (1 Hz), progressive handgrip (HG) and plantar flexion (PF) exercise, respectively. Exercise workloads were three minutes in length and increased by increments of 8 kilograms until exhaustion. RESULTS: Between each diet (LS and HS) there were no significant differences in resting MAP (82 ± 4 v 80 ± 5 mmHg; p = 0.3), HR (56 ± 6 v 59 ± 10 bpm; p = 0.4), or HRV (2.7 ± 1.9 v 8.3 ± 15.1 LF/HF; p = 0.4). During progressive HG and PF exercise the BF, SR, and FMD/SR were significantly increased by workload (p < 0.03 for all), but not different between diets (p > 0.05 for all). CONCLUSION: Despite previous evidence reporting a HS diet can impair resting vascular function, this study revealed that peripheral vascular function and blood flow regulation during exercise is not impacted by a HS diet in salt resistant individuals.

Effect of dietary sodium intake on residual renal function in patients undergoing peritoneal dialysis: a prospective study of 33 cases

To explore the impact of dietary sodium-intake on residual renal function in patients undergoing peritoneal dialysis (PD). Thirty-three patients on PD with stable dialysis were regularly followed up for 12 months. The daily sodium intake of the patients was calculated based on the 3-day dietary record. Based on the mean daily sodium intake, the patients enrolled were divided into low-salt group (sodium intake≤3.0 g/day, 19 patients) and high-salt group (sodium intake&gt;3.0 g/day, 14 patients). The baseline data of the patients were recorded, and the indicators of residual renal function and peritoneal function were regularly tested. The patients were followed-up at 3-month intervals, and their urine volume, peritoneal ultrafiltration volume and other clinical indicators were recorded and the biochemical indexes were detected to evaluate the changes in the residual renal function and peritoneal function. There was a positive correlation between the total sodium excretion and dietary sodium intake in these patients (r=0.536, P=0.0013), and sodium excretion by dialysis was positively correlated with their sodium intake (r=0.901, P=0.000). Regression analysis suggested that the total sodium excretion was correlated with dietary sodium intake (β=0.416, 95% CI: 0.170-0.666; P &lt; 0.0018); sodium excretion by dialysis was associated with dietary sodium intake (β=0.489, 95% CI: 0.395-0.582; P &lt; 0.001). The residual renal function was reduced by 17.48±11.22 L /(w·1.73 m2) in the low-salt group, as compared to 30.20±18.30 L /(w·1.73 m2) in the high-salt group (P=0.032). The reduction in the residual renal function was correlated with sodium intake in the PD patients (r=0.409, P=0.018). Multivariate regression analysis showed that sodium intake was an independent factor contributing to the reduction of residual renal function (β=14.646, 95% CI 7.426-21.866, P &lt; 0.001). Sodium excretion by PD in patients with continuous ambulatory PD is positively correlated with their dietary sodium intake, which contribute to the decrease of residual renal function. A high dietary sodium intake may accelerate the reduction of residual renal function in these patients.

A Novel Meta-Analytic Approach with Applications to Nutrition Research: A Comprehensive Analysis of Sodium Restriction (OR06-05-19)

ObjectivesSince the application of meta-analysis to biomedical research, the breadth of evidence covered in published meta-analyses has diminished. Despite the imperative of literature reviews to present “state of the art” knowledge, current meta-analyses are confined to pooling only select evidence. Imposing a priori criteria on scientific evidence results in biased and myopic conclusions. These current practices, in addition to the vastness of the literature base, ensure that research evidence remains opaque, and unusable to guide research and clinical practice. For example, whether and how much dietary sodium should be restricted for healthy or at-risk populations remains controversial. New epidemiological data suggest a striking increase in mortality with sodium intake <3 g/day, confounding this discussion. Thus, a system enabling investigators to access, review, and interpret all evidence is needed. MethodsMedAware Systems, Inc. is a platform that continuously identifies, extracts and organizes medical research data from multiple repositories. A blinded, cross-validated data extraction process, using artificial intelligence, guides two research scientists to process each study with near 100% accuracy. Intelligent software compares each data field for matches, prompting a senior scientist to review and reconcile any mismatched data fields. Over 200 methodological and clinical parameters are coded and organized, supporting comprehensive meta-analytic reviews of any medical topic.We demonstrate this innovative technology by addressing the effects of dietary sodium intake. We identify and analyze the complete domain of studies pertaining to sodium intake and cardiovascular outcomes. ResultsTo date, 368 studies have been identified. Initial review of patients, interventions, and outcomes data show extreme heterogeneity of this literature domain. This confirms the need for comprehensive evidence review, data extraction, and pooling. ConclusionsSodium intake literature is vast and difficult to interpret. We introduce a comprehensive process to analyze thousands of studies that traditional approaches cannot match. Our database and meta-analytic methodology profile the domain of evidence, summarizing the diversity and efficacy of sodium restriction recommendations. Funding SourcesMedAware Systems, Inc.

Kir4.1/Kir5.1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter.

Dietary sodium intake regulates the thiazide-sensitive Na-Cl cotransporter (NCC) in the distal convoluted tubule (DCT). Whether the basolateral, inwardly rectifying potassium channel Kir4.1/Kir5.1 (a heterotetramer of Kir4.1/Kir5.1) in the DCT is essential for mediating the effect of dietary sodium intake on NCC activity is unknown. We used electrophysiology, renal clearance techniques, and immunoblotting to examine effects of Kir4.1/Kir5.1 in the DCT and NCC in wild-type and kidney-specific Kir4.1 knockout mice. Low sodium intake stimulated basolateral Kir4.1/Kir5.1 activity, increased basolateral K+ conductance, and hyperpolarized the membrane. Conversely, high sodium intake inhibited the potassium channel, decreased basolateral K+ currents, and depolarized the membrane. Low sodium intake increased total and phosphorylated NCC expression and augmented hydrochlorothiazide-induced natriuresis; high sodium intake had opposite effects. Thus, elevated NCC activity induced by low sodium intake was associated with upregulation of Kir4.1/Kir5.1 activity in the DCT, whereas inhibition of NCC activity by high sodium intake was associated with diminished Kir4.1/Kir5.1 activity. In contrast, dietary sodium intake did not affect NCC activity in knockout mice. Further, Kir4.1 deletion not only abolished basolateral K+ conductance and depolarized the DCT membrane, but also abrogated the stimulating effects induced by low sodium intake on basolateral K+ conductance and hyperpolarization. Finally, dietary sodium intake did not alter urinary potassium excretion rate in hypokalemic knockout and wild-type mice. Stimulation of Kir4.1/Kir5.1 by low intake of dietary sodium is essential for NCC upregulation, and inhibition of Kir4.1/Kir5.1 induced by high sodium intake is a key step for downregulation of NCC.

A11100 Effects of Chronic Salt Loading on Plasma Inflammatory Factors in Normotensive Adults

Objectives: To observe the effects of dietary sodium intake on plasma inflammatory factors tumor necrosis factor alpha (TNF-α), high-sensitivity C-reactive protein (CRP) and monocyte chemoattractant protein -1 (MCP-1) in normotensive adults. Methods: Thirty normotensive volunteers, aged 18 to 60, were selected to undergo a baseline survey, a low-sodium diet (51.3 mmol per day) for 7 days, a high-sodium diet (307.8 mmol per day) for an additional 7days. Thirty subjects were classified as salt sensitive group (SS, 10 subjects) or non-salt sensitive group (NSS, 20 subjects) on the basis of their mean arterial blood pressure (MAP) increase more than 10 percent at the end of the high-sodium phase compared with the low-sodium phase. Fasting blood samples were taken on the first day of baseline and on the sixth day of the two intervention phases. Plasma TNF-α and MCP-1 concentration was measured using an enzyme-linked immunosorbent assay system, plasma hsCRP concentration was measured by immune nephelometry. Results: The prevalence of SS is 33%. After salt loading, no significant change was found in the plasma hsCRP concentrations; Whereas plasma TNF-α level increased significantly in both of the two groups [(168.4 ± 67.8 vs. 42.1 ± 26.7)pg/ml, P < 0.01 and (129.8 ± 24.1 vs. 37.7 ± 15.8)pg/ml, P < 0.01, respectively]; Plasma MCP-1 was significantly higher during the high-sodium than the low-sodium phase in both of the two groups[(205.2 ± 64.2 vs. 166.3 ± 48.5)pg/ml, P < 0.01and (212.3 ± 52.2 vs. 143.6 ± 55.9)pg/ml, P < 0.01]. Conclusion: High-sodium diet can induce an inflammatory state, which may be independent of the salt sensitivity.

Effect of Dietary Sodium Intake on Blood Pressure Variability

PurposeStudies in rodents have demonstrated that increased dietary sodium intake elevates blood pressure variability (BPV), independent of changes in resting blood pressure. Clinical studies have shown that increased BPV independently contributes to target organ damage and cardiovascular events. However, the effects of high dietary sodium intake on BPV in young, normotensive adults remains unknown. Therefore, the purpose of this study was to test the hypothesis that increased dietary sodium intake alters BPV in young, healthy adults.MethodsFourteen healthy, normotensive adults (7M/7W; age: 25±4 yrs; BMI: 24.7±0.9 kg/m2, Mean‐±SEM) participated in a controlled feeding study that consisted of 10 days of either low‐(LS:1 g sodium/day), medium‐ (MS: 2.3 g sodium/day), or high‐sodium (HS: 7 g sodium/day) diets, in randomized order. The diets were separated by at least a month. Urinary sodium excretion was determined to ensure compliance on diets. Resting beat‐to‐beat BPV was assessed in the laboratory in the supine position for ten minutes. BPV was also derived from 24‐hour ambulatory blood pressure monitoring (ABPM) to assess BPV under free‐living conditions. BPV was calculated as the average real variability index (ARV; the average of the absolute differences between consecutive blood pressure measurements) and as standard deviation (SD).ResultsTwenty‐four‐hour urinary sodium excretion increased in a step‐wise manner from low, to the medium, to the high sodium diets (LS: 34±6 mmol/24 hours, MS: 93±9 mmol/24, HS:275±29 mmol/24 hours, p&lt;0.05). Dietary sodium did not alter laboratory beat‐to‐beat systolic ARV (LS=2.2±0.2 mmHg, MS= 2.0±0.2 mmHg, HS= 2.1±0.2 mmHg, p&gt;0.05) or 24h ABPM systolic ARV (LS=9.4±0.5 mmHg, MS= 9.9±0.4 mmHg, HS=10.3±0.7 mmHg, p&gt;0.05). Dietary sodium also did not alter laboratory beat‐to‐beat systolic SD (LS= 5.4±0.5 mmHg, MS=5.1±0.3 mmHg, HS=5.8±0.6 mmHg, p&gt;0.05) or 24h ABPM systolic SD (LS= 12.1±0.9 mmHg, MS= 13.9±0.7 mmHg, HS= 13.1±0.9 mmHg, p&gt;0.05).ConclusionThese preliminary data suggest that 10 days of high dietary sodium intake does not alter systolic BPV in young, healthy adults.Support or Funding InformationNIH Grant 1RO1HL128388This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The role of dietary sodium intake on the modulation of T helper 17 cells and regulatory T cells in patients with rheumatoid arthritis and systemic lupus erythematosus.

We aimed at investigating whether the frequency and function of T helper 17 (Th17) and regulatory T cells (Treg) are affected by a restriction of dietary sodium intake in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). We enrolled RA and SLE patients not receiving drugs known to increase urinary sodium excretion. Patients underwent a dietary regimen starting with a restricted daily sodium intake followed by a normal-sodium daily intake. The timepoints were identified at baseline (T0), after 3 weeks of low-sodium dietary regimen (T3), after 2 weeks of normal-sodium dietary regimen (T5). On these visits, we measured the 24-hour urinary sodium excretion, the frequency and function of Th17 and Treg cells in the peripheral blood, the serum levels of cytokines. Analysis of urinary sodium excretion confirmed adherence to the dietary regimen. In RA patients, a trend toward a reduction in the frequencies of Th17 cells over the low-sodium dietary regimen followed by an increase at T5 was observed, while Treg cells exhibited the opposite trend. SLE patients showed a progressive reduction in the percentage of Th17 cells that reached a significance at T5 compared to T0 (p = 0.01) and an increase in the percentage of Treg cells following the low-sodium dietary regimen at both T1 and T3 compared to T0 (p = 0.04 and p = 0.02, respectively). No significant apoptosis or proliferation modulation was found. In RA patients, we found a reduction at T5 compared to T0 in serum levels of both TGFβ (p = 0.0016) and IL-9 (p = 0.0007); serum IL-9 levels were also reduced in SLE patients at T5 with respect to T0 (p = 0.03). This is the first study investigating the effects of dietary sodium intake on adaptive immunity. Based on the results, we hypothesize that a restricted sodium dietary intake may dampen the inflammatory response in RA and SLE patients.

Validation of spot urine in predicting 24-h sodium excretion at the individual level ,

Background: Evidence for the effect of dietary sodium intake on the risk of cardiovascular disease has been controversial. One of the main explanations for the conflicting results lies in the great variability associated with measurement methods for sodium intake. Spot urine collection is a convenient method commonly used for sodium estimation, but its validity for predicting 24-h urinary sodium excretion at the individual level has not been well evaluated among the general population.Objective: The aim of this study was to evaluate the validity of the Kawasaki, the International Cooperative Study on Salt, Other Factors, and Blood Pressure (INTERSALT), and the Tanaka formulas in predicting 24-h urinary sodium excretion by using spot urine samples in Chinese adults.Design: We analyzed the relative and absolute differences and misclassification at the individual level from 3 commonly used methods for estimating sodium intake among 141 Chinese community residents.Results: The mean measured 24-h sodium excretion was 220.8 mmol/d. The median (95% CIs) differences between measured sodium and those estimated from the Kawasaki, INTERSALT, and Tanaka methods were 6.4 mmol/d (-17.5, 36.8 mmol/d), -67.3 mmol/d (-96.5, -46.9 mmol/d), and -42.9 mmol/d (-59.1, -24.8 mmol/d), respectively. The proportions of relative differences >40% with the Kawasaki, INTERSALT, and Tanaka methods were 31.2%, 41.1%, and 22.0%, respectively; and the absolute difference for the 3 methods was >51.3 mmol/d (3 g salt) in approximately half of the participants. The misclassification rate was 63.1% for the Kawasaki method, 78.7% for the INTERSALT method, and 66.0% for the Tanaka method at the individual level.Conclusion: The results from our study do not support the use of spot urine to estimate 24-h urinary sodium excretion at the individual level because of its poor performance with respect to misclassification. This trial was registered at www.chictr.org.cn as ChiCTR-IOR-16010278.

Salt Loading on QT Dispersion and the Protective Role of Potassium Supplement in Normotensive Adults

QT interval dispersion (QTd) has been suggested to reflect the heterogeneity of myocardial repolarization and widely used in hypertension, coronary heart disease, arrhythmia, evaluation of a drug and so on. The aim of this study was to investigate the effects of dietary sodium intake on QTd and T peak -T end interval (Tp-Te) in normotensive healthy adults and the protective effect of dietary potassium. Sixty-four normotensive subjects aged 20~60 were selected and involved in a 3-week test in chronic salt loading and potassium supplementation, including baseline survey (baseline phase) for 3 d, low-salt diet (3g/day, NaCl, low-salt phase), high-salt diet (18g/day, salt loading phase) and high-salt with potassium supplementation diet (4.5g/day, KCl, salt and potassium supplement phase) each for 7 d. Blood pressure was measured and ECG was recorded at the last day of each phase, QT interval, QTd, corrected QTd (QTcd) and Tp-Te were measured and calculated. QTd, QTcd and Tp-Te at low-salt phase were less than those at baseline phase (QTd, 45.6±7.6ms vs. 52.1±9.4ms; QTcd, 53.4±8.4ms vs. 62.9±10.1ms; Tp-Te, 75.2±8.2ms vs. 85.0±9.6ms, P±0.05); QTcd and Tp-Te after salt loading were greater than those at low-salt phase (QTcd, 62.3±7.9ms vs. 53.4±8.4ms; Tp-Te, 84.7±10.0ms vs. 75.2±8.2ms, P<0.05); compared with those at salt loading phase, QTd, QTcd and Tp-Te were all reduced by large doses of oral potassium supplementation(QTd, 42.6±8.3ms vs. 53.4±9.1ms; QTcd, 52.2±6.2ms vs. 62.3±7.9ms; Tp-Te, 75.1± 8.5ms vs. 84.7±10.0ms, P±0.05). Salt loading increases blood pressure and prolongs QTd, QTcd and Tp-Te, while potassium supplementation reduces the influences of high salt on QTd, QTcd and Tp-Te, suggesting that high potassium intake may decrease the heterogeneity of cardiac repolarization and prevent arrhythmia by shortening repolarization time.

Effects of a high salt intake and potassium supplementation on QT interval dispersion in normotensive healthy subjects.

To evaluate the effects of dietary sodium intake on QT interval dispersion (QTd) in normotensive healthy subjects and assess the protective effects of dietary potassium. Methods All subjects were sequentially maintained on a protocol with a three-day baseline investigation, seven-day low-salt period (3 g/day (d), NaCL), seven-day salt loading period (18 g/d, NaCL) and a seven-day salt loading with potassium supplementation period (4.5 g/d, KCL). On the last day of each period, 24-hour urine samples were collected, the blood pressure values were measured and an electrocardiogram was recorded. The QT interval, QTd and T peak-T end interval (Tp-Te) were subsequently measured and calculated. Patients Sixty-four normotensive subjects, men and women, ranging from 28 to 60 years of age, were enrolled. Results There were no great fluctuations in heart rate after salt loading, whereas the systolic blood pressure (SBP, mmHg) and diastolic blood pressure (DBP, mmHg) increased and the corrected QT interval (QTc), corrected QT interval dispersion (QTdc) and Tp-Te values were significantly prolonged compared to that observed in the low-salt period (SBP, 118.6 ± 13.5 vs. 111.7 ± 11.3, p<0.01; DBP, 76.9 ± 8.6 vs. 71.7 ± 7.7, p<0.01; QTdc, 60.3 ± 19.4 vs. 55.6 ± 19.4, p<0.05; Tp-Te, 83.0 ± 10.1 vs. 79.8 ± 8.5, p<0.01). Surprisingly, all of these changes were reversed by potassium supplementation (SBP, 114.5 ± 12.3 vs.118.6 ± 13.5, p<0.01; DBP, 72.2 ± 7.9 vs.76.9 ± 8.6, p<0.01;QTd, 42.6 ± 15.1 vs. 47.4 ± 19.0, p<0.05; QTdc, 52.2 ± 18.0 vs. 60.3 ± 19.4, p<0.05; Tp-Te, 79.1 ± 8.5 vs. 83.0 ± 10.1, p<0.01). Conclusion Salt loading prolongs the QT interval, QTd and Tp-Te, while dietary potassium supplementation reverses these alterations. These findings suggest that potassium supplementation may improve variation in the healing time and prevent arrhythmia.

Risk factors for high blood pressure in low income children aged 3–4 years

This study aimed to evaluate the effect of dietary sodium intake on blood pressure among low income children aged 3-4 years. Data were collected during a randomized trial conducted in São Leopoldo, Brazil, with 500 mother-child pairs recruited from the maternity ward of a local hospital. Breastfeeding data were obtained during the children's first year of life. At 3 to 4 years of age, children's anthropometric, dietary, and blood pressure assessments were obtained. Sodium intake was estimated from two multiple-pass 24-h dietary recalls. Systolic blood pressure > 90th percentile for age, sex, and height was classified as high systolic blood pressure, according to the population-based percentiles provided by the Task Force on Hypertension Control in Children and Adolescents. Blood pressure data were obtained from 331 children at 3 to 4 years. The mean value of systolic blood pressure was 91.31 mmHg (SD = 8.30 mmHg) and 5.2% (n = 17) presented high systolic blood pressure. The results of the multivariable analyses showed that children who consumed more than 1,200 mg of sodium/day and with waist-to-height ratio higher than 0.5 presented, respectively, 3.32 (95%CI 0.98-11.22) and 8.81 (95%CI 2.13-36.31) greater risk of having high systolic blood pressure. Exclusive breastfeeding, child overweight and change in body mass index z score during the first year of life were not associated with the outcome. The results of this study suggest that at preschool age sodium intake and high waist-to-height ratio are risk factors for high systolic blood pressure.

Sodium Intake and Hypertension Risk in Children

Yang Y, Zhang Z, et al. Sodium intake and blood pressure among US children and adolescents. Pediatrics. 2012; 130(4): 611-619; doi: 10.1542/peds.2011-3870Investigators from the Centers for Disease Control and Prevention utilized 2003 to 2008 data from the National Health and Nutrition Examination Survey (NHANES) to determine the association between dietary sodium intake and blood pressure in children aged 8 to 18 years. In addition, the investigators evaluated the joint effect of dietary sodium intake and weight on the risk for pre-hypertension (P-HTN) and hypertension (HTN). Dietary sodium intake was estimated from 24-hour dietary recalls that were adjusted to minimize measurement error. Patients were classified as having normal blood pressure, P-HTN or HTN based on the average of three blood pressure measurements. Overweight was defined as 85th to 95th BMI percentile and obese as >95th percentile. Other covariates accounted for were race and gender.A total of 6,235 children were included in the study, 49% of whom were female. The prevalence of overweight and obesity combined was 37% and the prevalence of P-HTN and HTN combined was 15%. Children consumed an average of 3,387 mg of sodium per day. Among all participants, the systolic blood pressure increased by approximately 1 mm Hg for every 1,000 mg per day of sodium intake (P = .037). Diastolic blood pressure was not associated with sodium intake. There was a nonsignificant trend for children in the highest quartile of sodium intake to be more likely to have P-HTN or HTN than children who were in the lowest quartile of sodium intake (adjusted odds ratio [aOR]=2.0; 95% CI, 0.95-4.10). Children in the highest quartile of sodium intake who were also overweight or obese were at higher risk (aOR=3.5; 95% CI, 1.34-9.20). The risk for P-HTN or HTN increased by 74% for every 1,000 mg/day increase in sodium among overweight or obese children but increased by only 6% among normal weight children.The authors conclude that sodium intake is associated with systolic blood pressure and risk of P-HTN or HTN in a nationally representative sample of US children. Furthermore, overweight and obese children with high sodium intake may have a higher risk for P-HTN/HTN compared to normal weight children.Elevated blood pressure in childhood is a risk factor for the development of HTN and cardiovascular disease in adulthood. The prevalence of HTN in children has increased in recent years due partly to obesity and other lifestyle factors such as physical inactivity and consumption of high-calorie and -sodium foods.1 In the current study, investigators were able to demonstrate that sodium intake was associated with systolic blood pressure and risk of P-HTN or HTN in children, which is consistent with previous studies in children and adults. A novel finding of the study is the joint synergy between sodium intake and weight, suggesting that high sodium intake in overweight/obese children may have a greater effect on risk for P-HTN or HTN than in normal weight children. The authors suggest that sodium sensitivity in obesity may be related to hyperinsulinemia, hyperaldosteronism, and activity of the sympathetic nervous system.The authors of this study also found that children in the United States consume roughly the same amount of sodium as the average adult, around 3400 mg/day. The 2010 Dietary Guidelines for Americans advise reducing daily sodium intake to less than 2,300 milligrams for most individuals aged 2 years and older, and cutting back to 1,500 milligrams for people aged ≥51 years and those of any age who are African American or have hypertension, diabetes, or chronic kidney disease.2 In 2008, Congress asked the Institute of Medicine to suggest strategies to reduce sodium consumption to the recommended allowance. The Institute of Medicine released a brief report in 2010 that recommended a coordinated effort by government agencies, health industry, consumer agencies, and the food industry to support FDA-set mandatory national standards for sodium content in foods by gradually reducing excess sodium in processed foods and menu items.3 Further interventions to prevent HTN should be aimed at reducing sodium intake, increasing physical activity, and maintaining a healthy weight for all children and adolescents.As noted over 2 years ago in these pages, current levels of dietary salt intake impose a costly public health burden (see AAP Grand Rounds, June 2010;23[6]:664). Isn't it time for pediatricians to inform their patients that salt – as well as calories – counts?

Differential effects of dietary sodium intake on blood pressure and atherosclerosis in hypercholesterolemic mice

The amount of dietary sodium intake regulates the renin angiotensin system (RAS) and blood pressure, both of which play critical roles in atherosclerosis. However, there are conflicting findings regarding the effects of dietary sodium intake on atherosclerosis. This study applied a broad range of dietary sodium concentrations to determine the concomitant effects of dietary sodium intake on the RAS, blood pressure, and atherosclerosis in mice. Eight-week-old male low-density lipoprotein receptor −/− mice were fed a saturated fat-enriched diet containing selected sodium concentrations (Na 0.01%, 0.1%, or 2% w/w) for 12 weeks. Mice in these three groups were all hypercholesterolemic, although mice fed Na 0.01% and Na 0.1% had higher plasma cholesterol concentrations than mice fed Na 2%. Mice fed Na 0.01% had greater abundances of renal renin mRNA than those fed Na 0.1% and 2%. Plasma renin concentrations were higher in mice fed Na 0.01% (14.2±1.7 ng/ml/30 min) than those fed Na 0.1% or 2% (6.2±0.6 and 5.8±1.6 ng/ml per 30 min, respectively). However, systolic blood pressure at 12 weeks was higher in mice fed Na 2% (138±3 mm Hg) than those fed Na 0.01% and 0.1% (129±3 and 128±4 mmHg, respectively). In contrast, mice fed Na 0.01% (0.17±0.02 mm2) had larger atherosclerotic lesion areas in aortic roots than those fed Na 2% (0.09±0.01 mm2), whereas lesion areas in mice fed Na 0.1% (0.12±0.02 mm2) were intermediate between and not significantly different from those in Na 0.01% and Na 2% groups. In conclusion, while high dietary sodium intake led to higher systolic blood pressure, low dietary sodium intake augmented atherosclerosis in hypercholesterolemic mice.

Effects of chronic salt loading on plasma inflammatory factors in normotensive adults

Objective: To observe the effects of dietary sodium intake on plasma inflammatory factors tumor necrosis factor alpha (TNF-α), high-sensitivity C-reactive protein (HS-CRP) and MCP-1 in normotensive adults and to investigate the effect of inflammation induced by salt loading on the development of salt sensitivity. Methods: Thirty normotensive volunteers, aged 16 to 60years, were selected to undergo a baseline survey, a low-sodium diet (51.3mmol per day) for 7days, a high-sodium diet (307.8mmol per day) for an additional 7days.

Effects of High- and Low-Sodium Diets on Ambulatory Blood Pressure in Patients With Hypertension Receiving Aliskiren

Dietary sodium reduction and, as necessary, pharmacologic treatment are recommended for hypertension management. This prospective, randomized, open-label, blinded-end point, multicenter, crossover study investigated the effect of dietary sodium intake on mean ambulatory systolic blood pressure (maSBP) in patients with hypertension receiving aliskiren 300 mg once daily. Following a 2- to 4-week washout period, patients were randomized to a high- (≥ 200 mmol/d) or low- (≤ 100 mmol/d) sodium diet and were started on aliskiren, 300 mg/d. After 4 weeks, patients were crossed over to the alternate diet for an additional 4 weeks. The primary efficacy variable was change in maSBP between diets. During treatment with aliskiren, maSBP was significantly lower with the low-sodium diet compared with the high-sodium diet (least squares mean difference, 9.4 mm Hg; 95% CI, 7.5-11.4; P < .0001). The percentage of patients achieving a maSBP response to aliskiren (<130 mm Hg or a ≥ 20-mm Hg reduction from baseline) was greater with the low- (76.5%) versus the high-sodium diet (42.6%; P < .0001). Overall, 40.9% patients had ≥ 1 adverse event and the rates were similar between groups. In this study, aliskiren was well tolerated and a low-sodium diet accentuated its antihypertensive effect.

Long-Term Effects of Dietary Sodium Intake on Cytokines and Neurohormonal Activation in Patients With Recently Compensated Congestive Heart Failure

Long-Term Effects of Dietary Sodium Intake on Cytokines and Neurohormonal Activation in Patients With Recently Compensated Congestive Heart Failure

Long-Term Effects of Dietary Sodium Intake on Cytokines and Neurohormonal Activation in Patients With Recently Compensated Congestive Heart Failure

Background A growing body of evidence suggests that the fluid accumulation plays a key role in the pathophysiology of heart failure (HF) and that the inflammatory and neurohormonal activation contribute strongly to the progression of this disorder. Methods and Results The study evaluated the long-term effects of 2 different sodium diets on cytokines neurohormones, body hydration and clinical outcome in compensated HF outpatients (New York Heart Association Class II). A total of 173 patients (105 males, mean age 72.5 ± 7) recently hospitalized for worsening advanced HF and discharged in normal hydration and in clinical compensation were randomized in 2 groups (double blind). In Group 1, 86 patients received a moderate restriction in sodium (120 mmol to 2.8 g/day) plus oral furosemide (125 to 250 mg bid); in Group 2, 87 patients: received a low-sodium diet (80 mmol to 1.8 g/day) plus oral furosemide (125 to 250 mg bid). Both groups were followed for 12 months and the treatment was associated with a drink intake of 1000 mL daily. Neurohormonal (brain natriuretic peptide, aldosterone, plasma rennin activity) and cytokines values (tumor necrosis factor-α, interleukin-6) were significantly reduced with a significant increase of the anti-inflammatory cytokine interleukin-10 at 12 months in normal, P < .0001) than low-sodium group. The low-sodium diet showed a significant activation of neurohormones and cytokines and worsening the body hydration, whereas moderate sodium restriction maintained dry weigh and improved outcome in the long term. Conclusions Our results appear to suggest a surprising efficacy of a new strategy to improve the chronic diuretic response by increasing Na intake and limiting fluid intake. This counterintuitive approach underlines the need for a better understanding of factors that regulate sodium and water handling in chronic congestive HF. A larger sample of patients and further studies are required to evaluate whether this is due to the high dose of diuretic used or the low-sodium diet.

Dietary sodium effects on heart rate variability in salt sensitivity of blood pressure

High dietary sodium intake is a risk factor for hypertension, and heart rate variability (HRV) is decreased in hypertension. Effects of dietary sodium intake on HRV of normotensive persons have not, however, been investigated to date. The present study examined effects of low and high sodium diets on blood pressure, heart rate, and HRV in 36 healthy, normotensive women, ages 40-70. Each was placed on a low sodium diet for 6 days followed by a high sodium diet for 6 days. The high salt diet increased mean systolic blood pressure, decreased heart rate, and increased high frequency HRV (HF). Cardiac vagal tone, estimated at baseline from heart period and a time domain estimate of respiratory sinus arrhythmia, was higher in salt-sensitive than salt-insensitive subjects. The finding of increased vagal tone in normotensive persons on high salt intake indicates that dietary sodium status should be considered in behavioral studies of HRV.