High Dietary Sodium Intake Research Articles

The Economic Impact of Dietary Sodium Reduction In Canada

The average Canadian sodium intake is double the amount recommended. Excess dietary sodium consumption is a risk factor for the development of high blood pressure (BP), estimated to cause about 30% of hypertension and 17% of cardiovascular disease (CVD). The cost attributable to high dietary sodium intake in Canada is unknown. Mathematical modeling can be used to explore the potential health and economic impacts of a population-wide reduction in dietary sodium. The Canadian Cardiovascular Disease Policy model (C-CVDPM) is a computer simulation state transition model, which simulates CVD events, costs and health consequences from a public payer perspective for the Canadian population. It can be used to evaluate the economic impact of population health interventions. Using the CVDPM and a 50-year time horizon, we examined the health and economic impact of a population-wide reduction in dietary sodium of 1800 mg/day. Sensitivity analyses were conducted using modest dietary sodium reductions of 500 mg/day and 1500 mg/day. Reducing dietary sodium by 1800 mg/day is projected to reduce the annual number of new cases of coronary heart disease by 199,808, stroke by 120,381, and myocardial infarction by 115,528, and to reduce the annual number of deaths from any cause, including CVD by 89,734. Overall, the model projected a gain of 24,285 quality-adjusted life years (QALYs), and a savings of $414 million, annually. Modest reductions in dietary sodium intake were also cost saving. A population-wide reduction in dietary sodium could substantially decrease healthcare costs and improve health outcomes. The results of this work may be useful to policy makers in revising Canadian sodium regulation and policy.

Novel Mechanism for Buffering Dietary Salt in Humans: Effects of Salt Loading on Skin Sodium, Vascular Endothelial Growth Factor C, and Blood Pressure.

High dietary sodium intake triggers increased blood pressure (BP). Animal studies show that dietary salt loading results in dermal Na+ accumulation and lymphangiogenesis mediated by VEGF-C (vascular endothelial growth factor C), both attenuating the rise in BP. Our objective was to determine whether these mechanisms function in humans. We assessed skin electrolytes, BP, and plasma VEGF-C in 48 healthy participants randomized to placebo (70 mmol sodium/d) and slow sodium (200 mmol/d) for 7 days. Skin Na+ and K+ concentrations were measured in mg/g of wet tissue and expressed as the ratio Na+:K+ to correct for variability in sample hydration. Skin Na+:K+ increased between placebo and slow sodium phases (2.91±0.08 versus 3.12±0.09; P=0.01). In post hoc analysis, there was a suggestion of a sex-specific effect, with a significant increase in skin Na+:K+ in men (2.59±0.09 versus 2.88±0.12; P=0.008) but not women (3.23±0.10 versus 3.36±0.12; P=0.31). Women showed a significant increase in 24-hour mean BP with salt loading (93±1 versus 91±1 mm Hg; P<0.001) while men did not (96±2 versus 96±2 mm Hg; P=0.91). Skin Na+:K+ correlated with BP, stroke volume, and peripheral vascular resistance in men but not in women. No change was noted in plasma VEGF-C. These findings suggest that the skin may buffer dietary Na+, reducing the hemodynamic consequences of increased salt, and this may be influenced by sex.

Abstract P283: Effects of High Salt Diet on Vascular Function and Renal Injury in a Novel Mouse Model of Neurogenic Hypertension

In the brain, transcription of the renin gene is initiated from an alternative promoter within exon 1b resulting in the expression of Renin-b, a renin isoform lacking the signal peptide and first third of the prosegment. The specific deletion of Renin-b paradoxically induces neurogenic hypertension concomitant with increased brain renin-angiotensin system and renal sympathetic nerve activation. High dietary sodium intake has been associated with hypertension, endothelial dysfunction, and renal complications especially in salt-sensitive populations. We hypothesized that deletion of Renin-b causes vascular dysfunction and induces renal damage. In addition, high dietary sodium intake further exacerbates end-organ damage in Renin-b deficient mice (Ren-b KO). To evaluate vascular function, acetycholine (Ach) and nitroprusside (SNP)-induced dose-dependent vasorelaxation was assessed in aorta, carotid and basilar arteries isolated from Ren-b KO or littermate controls fed normal or high sodium diet (4% NaCl) for 4 weeks. Urinary protein excretion was measured at baseline and after 4 weeks on high sodium diet in control and Ren-b KO mice. At baseline, Ren-b KO exhibited impaired Ach-induced vasorelaxation in the aorta (logEC50 control: 0.88mM vs Ren-b KO: 1.1mM; p = 0.014; n=4) while SNP dose-response curve was unaltered. Urinary protein levels were increased in Ren-b KO (control: 11.0±3.7 vs Ren-b KO: 45.8±9.3 mg/day; p = 0.007; n=6-8). In control mice, 4 weeks high sodium diet increased urinary protein levels compared to baseline (baseline: 11.0±3.7 vs high salt: 31.6±7.4 mg/day); however high salt diet did not worsen proteinuria in Ren-b KO (baseline: 45.8±9.3 vs high salt: 44.1±4.5 mg/day). Similarly, Ren-b KO fed high sodium diet did not exhibit higher degrees of vascular dysfunction in comparison with control mice on high sodium diet. Our data indicates that Renin-b deletion promotes end-organ damage, likely as a consequence of high blood pressure or sympathetic nerve activation or both. Surprisingly, high sodium diet failed to exacerbate vascular dysfunction or proteinuria in Ren-b KO. Studies are in progress to evaluate the blood pressure response to high sodium diet in Ren-b KO mice to assess if Ren-b KO mice are salt sensitive.

No association between dietary sodium intake and the risk of multiple sclerosis.

To prospectively investigate the association between dietary sodium intake and multiple sclerosis (MS) risk. In this cohort study, we assessed dietary sodium intake by a validated food frequency questionnaire administered every 4 years to 80,920 nurses in the Nurses' Health Study (NHS) (1984-2002) and to 94,511 in the Nurses' Health Study II (NHSII) (1991-2007), and calibrated it using data from a validation study. There were 479 new MS cases during follow-up. We used Cox proportional hazards models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the effect of energy-adjusted dietary sodium on MS risk, adjusting also for age, latitude of residence at age 15, ancestry, body mass index at age 18, supplemental vitamin D intake, cigarette smoking, and total energy intake in each cohort. The results in both cohorts were pooled using fixed effects models. Total dietary intake of sodium at baseline was not associated with MS risk (highest [medians: 3.2 g/d NHS; 3.5 g/d NHSII] vs lowest [medians: 2.5 g/d NHS; 2.8 g/d NHSII] quintile: HRpooled 0.98, 95% CI 0.74-1.30, p for trend = 0.75). Cumulative average sodium intake during follow-up was also not associated with MS risk (highest [medians: 3.3 g/d NHS; 3.4 g/d NHSII] vs lowest [medians: 2.7 g/d NHS; 2.8 g/d NHSII] quintile: HRpooled 1.02, 95% CI 0.76-1.37, p for trend = 0.76). Comparing more extreme sodium intake in deciles yielded similar results (p for trend = 0.95). Our findings suggest that higher dietary sodium intake does not increase the risk of developing MS.

Central systolic blood pressure and aortic stiffness response to dietary sodium in young and middle-aged adults

High dietary sodium intake can lead to hypertension and increased incidence of cardiovascular disease. We sought to determine the effect of short-term dietary sodium loading on central blood pressure and arterial stiffness in young (YG; 22–40 years) and middle-aged (MA; 41–60 years) normotensive adults. YG (n = 49; age: 27 ± 1 years) and MA (n = 36; age: 52 ± 1 years) subjects were randomized, in a cross-over design, to 7 days of low-sodium (LS; 20 mmol/d) or high-sodium (HS; 300 mmol/d) diet. On the last day of each diet, central pressures, forward and reflected wave amplitudes (via radial artery applanation tonometry), and carotid-femoral pulse wave velocity were assessed. Central systolic blood pressure (cSBP) was greater after HS in both YG (LS: 96 ± 1 vs. HS: 99 ± 1 mm Hg; P = .012) and MA (LS: 106 ± 2 vs. HS: 115 ± 3 mm Hg; P < .001). However, the increase in cSBP was greater in MA (YG: 4 ± 1 vs. MA: 9 ± 2; P = .02). In MA subjects, HS elicited greater forward (LS: 25 ± 1 vs. HS: 29 ± 1 mm Hg; P < .001) and reflected (LS: 19 ± 1 vs. HS: 23 ± 1 mm Hg; P < .001) wave amplitudes. Carotid-femoral pulse wave velocity was also greater in MA on HS but after adjustment for mean arterial pressure, the difference was no longer significant. Our data indicate that HS intake leads to a greater increase in cSBP in MA adults, which may be the result of increased forward and reflected wave amplitudes.

Potassium Chloride-Based Salt Substitutes: A Critical Review with a Focus on the Patent Literature.

High dietary sodium intake (DSI) represents a major health-related public issue in most countries all over the world. Such a diet can lead to increased risk of hypertension and related cardiovascular diseases. This situation has resulted in important public policies for various salt reduction strategies. One of these is based on the use of salt substitutes or salts with reduced sodium content. Among several options, potassium chloride (KCl) has proved to be a key nutritional ingredient for this purpose. It provides similar properties like common salt (NaCl), but with several unwanted side effects, of which the most important have relatively offensive side tastes: bitter, acrid, and metallic. To successfully formulate KCl-based salt substitutes, numerous taste-improving agents and formulation concepts have been used. The field of salt substitutes is mainly described in the patent literature. Since patents are both scientific and legal documents, careful and critical consideration is required when using them as a source of scientific information. This review brings a deep insight into the area of KCl-based salt substitutes with a focus on the patent literature through the eyes of food science and technology. The most important classes of taste-improving agents that have been employed in numerous formulation concepts of KCl-based salt substitutes are nutritionally acceptable mineral salts; food acids, amino acids, and their nutritionally acceptable salts; simple carbohydrates and sugar substitutes; food polymers; umami ingredients; spices, vegetables, and flavors; miscellaneous taste improvers; as well as a plethora of their specific combinations. A critical review of the respective patent literature is given.

Factors Predicting Sodium Intake of Korean Americans with Type 2 Diabetes.

The increasing prevalence of type 2 diabetes mellitus (T2DM) and its complications including cardiovascular disease and chronic kidney disease threaten Korean Americans (KAs). High dietary sodium intake contributes to both conditions. The purpose of the study was to assess dietary sodium consumption and to examine the predictors of sodium intake among KA with T2DM. A total 232 KA who had uncontrolled diabetes participated in this study. The majority of the sample (69%) consumed more sodium than current national guidelines. A high level of energy intake was the strongest predictor for sodium intake with gender and marital status also related. Our findings identified predictive factors to excessive sodium intake and these data support the need for culturally-tailored education about appropriate dietary sodium and energy intake are needed for patients about T2DM.

Drinking Water Salinity and Raised Blood Pressure: Evidence from a Cohort Study in Coastal Bangladesh.

Background:Millions of coastal inhabitants in Southeast Asia have been experiencing increasing sodium concentrations in their drinking-water sources, likely partially due to climate change. High (dietary) sodium intake has convincingly been proven to increase risk of hypertension; it remains unknown, however, whether consumption of sodium in drinking water could have similar effects on health.Objectives:We present the results of a cohort study in which we assessed the effects of drinking-water sodium (DWS) on blood pressure (BP) in coastal populations in Bangladesh.Methods:DWS, BP, and information on personal, lifestyle, and environmental factors were collected from 581 participants. We used generalized linear latent and mixed methods to model the effects of DWS on BP and assessed the associations between changes in DWS and BP when participants experienced changing sodium levels in water, switched from “conventional” ponds or tube wells to alternatives [managed aquifer recharge (MAR) and rainwater harvesting] that aimed to reduce sodium levels, or experienced a combination of these changes.Results:DWS concentrations were highly associated with BP after adjustments for confounding factors. Furthermore, for each reduction in sodium in drinking water, systolic/diastolic BP was lower on average by , and odds of hypertension were lower by 14%. However, MAR did not consistently lower sodium levels.Conclusions:DWS is an important source of daily sodium intake in salinity-affected areas and is a risk factor for hypertension. Considering the likely increasing trend in coastal salinity, prompt action is required. Because MAR showed variable effects, alternative technologies for providing reliable, safe, low-sodium fresh water should be developed alongside improvements in MAR and evaluated in “real-life” salinity-affected settings. https://doi.org/10.1289/EHP659

Dietary sodium intake relates to vascular health in children with type 1 diabetes.

Children with type 1 diabetes (T1D) have vascular dysfunction and frequently struggle to adhere to dietary recommendations. Limited data exist for the vascular consequences of poor diet quality in children. We aimed to evaluate the association between dietary components and vascular function in children with T1D. Cross-sectional study including 90 children (13.6 [3.5] years, 41 boys) with T1D. They had evaluation of dietary micro and macronutrients (Australian Child and Adolescent Eating Survey), vascular endothelial and smooth muscle function (flow-mediated dilatation and glyceryl trinitrate mediated dilatation [GTN], respectively), clinical and biochemical variables. Children had a sodium intake of 3.013 (0.76) (mean [SD]) g/day. Vascular smooth muscle dysfunction, as measured by GTN, related to higher daily sodium intake (r = -0.31, P = .003), independent of the inverse relationships between GTN and total energy (r = -0.30, P = .005) and fat intake (r = -0.28, P = .007). Multiregression model showed that an increase in 1 g of daily sodium intake was independently associated with a deterioration of 3 percentage units in GTN (95% CI -4.3, -0.9; P = .003). There was an association between sodium intake and systolic blood pressure after adjustment for age and gender (regression coefficient 2.4; 95% CI 0.5, 4.3; P = .01). High dietary sodium intake in children with T1D is common and relates to vascular dysfunction, independently of other dietary intake, blood pressure, and glycemic control.

Distinctive Risk Factors and Phenotype of Younger Patients With Resistant Hypertension

Resistant hypertension, defined as blood pressure &gt;140/90 mm Hg despite using ≥3 antihypertensive medications, is a well-recognized clinical entity. Patients with resistant hypertension are at an increased risk of cardiovascular disease compared with those with more easily controlled hypertension. Coronary heart disease mortality rates of younger adults are stagnating or on the rise. The purpose of our study was to characterize the phenotype and risk factors of younger patients with resistant hypertension, given the dearth of data on cardiovascular risk profile in this cohort. We conducted a cross-sectional analysis with predefined age groups of a large, ethnically diverse cohort of 2170 patients referred to the Hypertension Clinic at the University of Alabama at Birmingham. Patients (n=2068) met the inclusion criteria and were classified by age groups, that is, ≤40 years (12.7% of total cohort), 41 to 55 years (32.1%), 56 to 70 years (36.1%), and ≥71 years (19.1%). Patients aged ≤40 years compared with those aged ≥71 years had significantly earlier onset of hypertension (24.7±7.4 versus 55.0±14.1 years; P &lt;0.0001), higher rates of obesity (53.4% versus 26.9%; P &lt;0.0001), and significantly higher levels of plasma aldosterone (11.3±9.8 versus 8.9±7.4 ng/dL; P =0.005), plasma renin activity (4.9±10.2 versus 2.5±5.0 ng/mL per hour; P =0.001), 24-hour urinary aldosterone (13.4±10.0 versus 8.2±6.2 µg/24 h; P &lt;0.0001), and sodium excretion (195.9±92.0 versus 146.8±67.1 mEq/24 h; P &lt;0.0001). Among patients with resistant hypertension, younger individuals have a distinct phenotype characterized by overlapping risk factors and comorbidities, including obesity, high aldosterone, and high dietary sodium intake compared with elderly.

Assessment of Sodium and Potassium Intake by 24 h Urinary Excretion in a Healthy Mexican Cohort

A high dietary sodium intake and a low potassium intake are associated with adverse cardiovascular health. Data on these nutrients consumption in Mexico is limited. The aim of this study was to assess sodium and potassium intake by 24h urinary excretion in a clinically healthy Mexican population. We additionally explored their association with blood pressure. 711 clinically healthy participants aged 20-50years old recruited in the Tlalpan 2020 cohort from September 2014-December 2015, were included in this cross-sectional analysis. All participants provided a 24h urine sample and underwent anthropometric, biochemical, and blood pressure evaluations. Univariate and multivariate linear regression analyses were used to assess the association of urinary sodium, potassium, and Na/K ratio with blood pressure. Mean (95% confidence interval [CI]) urinary sodium and potassium in the overall population was 3150.1 (3054.2-3246.0) mg/d and 1909.5 (1859.3-1959.6) mg/d, respectively. Overall, only 121 (17%) met the WHO recommendation for sodium intake (<2000mg/d) and 16 (2.3%) met the goal for potassium intake (≥3510mg/d). Urinary sodium (β coefficient 1.3, 95% CI: 0.7, 1.8, p <0.001) and potassium (β coefficient 2.1, 95% CI: 1.0, 3.2, p <0.001) were found to be associated with systolic blood pressure in the univariate analysis but not in the multivariate analysis. Sodium intake was higher and potassium intake was lower than the WHO recommendations in this healthy Mexican population. Sodium and potassium intakes were not associated with blood pressure at the mean levels of intake observed in this population, after adjusting for key variables.

High dietary sodium intake is associated with low bone mass in postmenopausal women: Korea National Health and Nutrition Examination Survey, 2008-2011.

Several studies have reported that large amount of dietary sodium intake is highly associated with elevated urinary calcium. However, the direct effect of excessive dietary sodium intake on bone mass, as a risk factor for osteoporosis, is still a controversial issue. The aim of the present study was to assess the relationship between high intake of sodium and lower bone mass and risk of osteoporosis in adult women. This cross-sectional study was performed using data from the Korea National Health and Nutrition Examination Survey (KNHANES), 2008-2011. Participants (n=9526 women older than 18years) were divided into a premenopausal (n=4793) and postmenopausal (n=4733) group. Both groups were subdivided into five groups according to quintiles of energy-adjusted sodium intake. Multiple regression analysis was performed to assess relationships between sodium intake and lower bone mass. Multivariate linear regression analysis showed that high sodium intake was negatively associated with bone mineral content (BMC) and bone mineral density (BMD) in postmenopausal women. After adjusting confounding factors, high sodium intake was negatively associated with BMC and BMD of the lumbar spine in postmenopausal women. Postmenopausal women, whose sodium intake was ≥2000mg/day (odds ratio 1.284, 95% CI 1.029-1.603, P=0.027), were at risk of developing osteoporosis after adjustment of confounding variables. The present study suggested that high sodium intake could be a potential risk factor for low bone mass after adjusting for confounding factors in postmenopausal women.

Abstract P106: Effects of Aldosterone Excess and Sodium on Dipping Patterns in Resistant Hypertensive Patients

Background: High dietary sodium intake and aldosterone excess have been independently linked to increased cardiovascular morbidity and mortality. In addition, a large body of literature indicates that aldosterone excess contributes importantly to antihypertensive treatment resistance and is associated with higher 24- hour ambulatory blood pressure (BP) levels. Objective: This study was designed to determine if high dietary sodium intake, and hyperaldosteronism combine to mediate the development of abnormal diurnal BP patterns including nocturnal hypertension and dipping BP patterns. Methods: A single-center cohort of 326 African American (AA) and Caucasian resistant hypertensive patients were prospectively evaluated by assessing 24-hr urinary aldosterone (UAldo), plasma renin activity (PRA), sodium (UNa + ) levels, and 24-hr ambulatory blood pressure monitoring (ABPM). Daytime, night-time, and 24-hr BP and dipping patterns were determined. High sodium excretion was defined as UNa + = 200 mEq/24hr and hyperaldosteronism was defined as UAldo = 12 μg/24hr and PRA ≤ 1 ng/ml/hr. Results: There was no difference in ABPM and dipping patterns when comparing the normal versus high sodium group. However, patients without high sodium excretion had better nocturnal (p=0.024) and 24- hour BP control (p=0.036). Furthermore, there was no difference in ABPM patterns when comparing patients with high versus normal sodium excretion with hyper versus non- hyperaldosteronism. Interestingly, in the group with hyperaldosteronism, patients with normal sodium excretion had improved dipping patterns, but only in the dipper group (p=0.016). Conclusions: High dietary sodium intake contributes to increased nocturnal hypertension and poor 24-h BP control, but there does not seem to be a significant relationship between hyperaldosteronism and high dietary sodium intake. This data suggests that improvements in dietary sodium intake will lead to better control of nighttime BP and 24-h BP control and therefore reduces the risk of cardiovascular disease. Further studies are underway comparing these relationships in males versus females, and AAs versus Caucasians.

Relationship between sodium and potassium intake and blood pressure in a sample of overweight adults

ObjectiveThe aim of this study was to examine the relationship between sodium and potassium intakes and blood pressure (BP) in a clinical sample. MethodsSecondary analysis of baseline data from 328 participants (mean age: 43.6 ± 8 y, mean body mass index [BMI]: 32.4 ± 4.2 kg/m2, mean systolic BP [SBP]/diastolic BP [DBP]: 124.9 ± 14.5/73.3 ± 9.9 mm Hg) of the 12-mo HealthTrack randomized controlled weight loss trial was conducted. Resting BP and 24-h urine sodium and potassium were measured. Dietary intake was evaluated with 4-d food records and self-reported diet histories. ResultsUrinary sodium was positively correlated (Spearman's rho) with SBP (r = 0.176; P = 0.001) and DBP (r = 0.150; P = 0.003). The ratio of sodium to potassium was positively correlated with SBP (r = 0.1; P = 0.035). Urinary sodium (F [4,323] = 20.381; P < 0.0005; adjusted R2 = 0.231) and sodium-to-potassium ratio (F[4,323] = 25.008; P < 0.0005; adjusted R2 = 0.227) significantly predicted SBP after controlling for age, sex, BMI, and hypertension medication use. Dietary sodium and potassium significantly predicted urinary sodium (B = 0.33, t = 4.032, P < 0.01) and potassium (B = 0.67, t = 8.537, P < 0.01) excretion, respectively, after adjustment for energy and BMI. Median dietary sodium intake was 3197 mg/d and median dietary potassium intake was 2886 mg/d. Cereal-based products and dishes were the major contributors (22%) to total sodium intake. ConclusionsIn the present study, a high dietary sodium intake and high sodium-to-potassium ratio predicted high SBP. This suggests a need to focus dietary advice on reduction of sources of sodium and increasing sources of potassium in weight loss interventions to improve BP control.

The effect of zinc deficiency on salt taste acuity, preference, and dietary sodium intake in hemodialysis patients.

Introduction High sodium intake is the main cause of fluid overload in hemodialysis (HD) patients, leading to increased cardiovascular mortality. High sodium intake is known to be associated with low salt taste acuity and/or high preference. As the zinc status could influence taste acuity, we analyzed the effect of zinc deficiency on salt taste acuity, preference, and dietary sodium intake in HD patients. Methods A total of 77 HD patients was enrolled in this cross-sectional study. Zinc deficiency was defined as serum zinc level with below 70 µg/mL. The patients were divided into two groups based on serum zinc level. Salt taste acuity and preference were determined by a sensory test using varying concentrations of NaCl solution, and dietary sodium intake was estimated using 3-day dietary recall surveys. Findings The mean salt recognition threshold and salt taste preference were significantly higher in the zinc deficient group than in the non-zinc deficient group. And there was significant positive correlation between salt taste preference and dietary sodium intake in zinc deficient group (r = 0.43, P = 0.002). Although, the dietary sodium intake showed a high tendency with no significance (P = 0.052), interdialytic weight gain was significantly higher in the zinc deficient group than in the non-zinc deficient group (2.68 ± 1.02 kg vs. 3.18 ± 1.02 kg; P = 0.047). Discussion Zinc deficiency may be related to low salt taste acuity and high salt preference, leading to high dietary sodium intake in HD patients.

Does Limiting Salt Intake Prevent Heart Failure? A Critical Appraisal

Reducing the incidence of heart failure (HF) and its associated morbidity is a major goal for public health authorities. In this review, we evaluate the evidence supporting sodium restriction as a means to prevent HF. High dietary sodium intake is associated with several factors that promote the development of HF including systemic hypertension, ventricular hypertrophy, diastolic dysfunction, vascular stiffness, and endothelial dysfunction. Some argue that sodium restriction actually may contribute to the development of HF through increased neurohormonal activation. The effect of sodium intake on HF risk may depend on an individual’s “salt-sensitivity.” Due in part to methodological limitations, currently available cohort studies have not fully clarified the links between sodium intake and incident HF. Future research is needed to determine accurate and reproducible methods of measuring sodium intake and to identify factors which may make specific individuals more vulnerable to developing HF in the setting of high sodium intake.

High Dietary Sodium Intake Assessed by Estimated 24-h Urinary Sodium Excretion Is Associated with NAFLD and Hepatic Fibrosis.

BackgroundAlthough high sodium intake is associated with obesity and hypertension, few studies have investigated the relationship between sodium intake and non-alcoholic fatty liver disease (NAFLD). We evaluated the association between sodium intake assessed by estimated 24-h urinary sodium excretion and NAFLD in healthy Koreans.MethodsWe analyzed data from 27,433 participants in the Korea National Health and Nutrition Examination Surveys (2008–2010). The total amount of sodium excretion in 24-h urine was estimated using Tanaka’s equations from spot urine specimens. Subjects were defined as having NAFLD when they had high scores in previously validated NAFLD prediction models such as the hepatic steatosis index (HSI) and fatty liver index (FLI). BARD scores and FIB-4 were used to define advanced fibrosis in subjects with NAFLD.ResultsThe participants were classified into three groups according to estimated 24-h urinary excretion tertiles. The prevalence of NAFLD as assessed by both FLI and HSI was significantly higher in the highest estimated 24-h urinary sodium excretion tertile group. Even after adjustment for confounding factors including body fat and hypertension, the association between higher estimated 24-h urinary sodium excretion and NAFLD remained significant (Odds ratios (OR) 1.39, 95% confidence interval (CI) 1.26–1.55, in HSI; OR 1.75, CI 1.39–2.20, in FLI, both P < 0.001). Further, subjects with hepatic fibrosis as assessed by BARD score and FIB-4 in NAFLD patients had higher estimated 24-h urinary sodium values.ConclusionsHigh sodium intake was independently associated with an increased risk of NAFLD and advanced liver fibrosis.

Carotid intima media thickness is independently associated with urinary sodium excretion in patients with chronic kidney disease

Atherosclerosis-induced premature vascular diseases are the leading cause of mortality among patients with chronic kidney disease (CKD). The pathogenetic mechanism of atherosclerosis in patients with CKD has not been fully explained. Experimental studies have demonstrated that high dietary sodium intake not only increases circulatory volume and blood pressure, but also facilitates development of atherosclerosis by reducing production-bioavailability of nitric oxide due to oxidative stress and accordingly by enhancing endothelial and arterial stiffness. In this study, we investigated the relationship between sodium consumption and carotid artery intima-media thickness, which is the indicator of atherosclerosis, by determining daily urinary sodium excretion, which is a reliable indicator of sodium consumption, in our patient group. Our patient group included 193 patients with stage 2–4 non-diabetic CKD and without a history of atherosclerotic disease. We determined that 77% of our patients have been consuming more than 2 g of sodium per day, which is the upper limit of sodium consumption recommended for patients with CKD. We determined a positive linear correlation between carotid artery intima-media thickness and patient age (p < 0.001), C-reactive protein (p < 0.001), urinary sodium excretion (p < 0.001), body mass index (p = 0.002), systolic blood pressure (p = 0.002), hemoglobin (p = 0.030), triglycerides (p = 0.043), and diastolic blood pressure (p = 0.049). We also found a negative linear correlation between carotid artery intima-media thickness and glomerular filtration rate (p = 0.008). We found that urinary sodium excretion is the determinant of intima-media thickness even if all factors associated with intima-media thickness are adjusted, and that intima-media thickness increases by 0.031 (0.004–0.059) mm per 2 g increase in daily sodium excretion, independent from overall factors (p = 0.025). Our results reveal a relation between urinary sodium excretion and carotid artery intima-media thickness and suggest that excessive sodium consumption predisposes development of atherosclerosis in patients with CKD.

The relation between ACE D/I and CYP11B2 C-344T polymorphisms and parameters of arterial stiffness in the context of renal sodium handling

Background. Sodium overload is related to the development of primary hypertension and its complications. Methods. In 131 (65 female) treated hypertensives (average blood pressure 144/82 mmHg and duration of hypertension 11.7 years), we measured peripheral and central arterial pressures, peripheral (AIxP) and central (AIxC1, AIxC2) augmentation indices, pulse-wave velocity (PWV) and daily urinary sodium excretion, and conducted genetic studies of ACE D/I and CYP11B2 C-344T polymorphisms. Proximal (FELi) and distal (FDRNa) sodium reabsorption measurements were performed using endogenous lithium clearance. Results. We found statistically significant interactions between FELi and ACE D/I polymorphism with respect to AIxC2 (PINT = 0.05) and between FELi and CYP11B2 C-344T polymorphism with respect to AIxC1 (PINT = 0.01), AIxC2 (PINT = 0.04) and AIxP (PINT = 0.01). In the group of ACE I allele carriers compared with DD homozygotes, the AIxC1 (154.1 vs 140.6%; p = 0.02), AIxC2 (33.3 vs 26.9%; p = 0.02) and AIxP (94.6 vs 85.2%; p = 0.01) were higher in the subgroup with FELi below the median value (FELi1), but not in the subgroup with FELi above the median value (FELi2). In the group of CYP11B2 TT homozygotes compared with C allele carriers, we observed higher values of AIxC1 (158.5 vs 146.4%; p = 0.03), AIxC2 (36.0 vs 29.4%; p = 0.01) and AIxP (99.0 vs 88.7%; p = 0.005) in the FELi1 but not the FELi2 subgroup. Conclusions. In the population with assumed high dietary sodium intake and long-standing history of hypertension, the relation between proximal sodium reabsorption and the development of arterial stiffness depends on the genetic context of the selected genetic polymorphisms of the renin—angiotensin—aldosterone system, independent of blood pressure.

Does pragmatically structured outpatient dietary counselling reduce sodium intake in hypertensive patients? Study protocol for a randomized controlled trial.

BackgroundHypertension is highly prevalent among adults, and is the most important modifiable risk factor for cardiovascular events, in particular stroke. Decreasing sodium intake has the potential to prevent or delay the development of hypertension and improve blood pressure control, independently of blood pressure lowering drugs, among hypertensive patients. Despite guidelines recommending a low sodium diet, especially for hypertensive individuals, sodium intake remains higher than recommended. A recent systematic review indicated that the efficacious counselling methods described in published trials are not suitable for hypertension management by primary care providers in Canada in the present form. The primary reason for the lack of feasibility is that interventions for sodium restriction in these trials was not limited to counselling, but included provision of food, prepared meals, or intensive inpatient training sessions.Methods/designThis is a parallel, randomized, controlled, open-label trial with blinded endpoints. Inclusion criteria are adult patients with hypertension with high dietary sodium intake (defined as ≥100 mmol/day). The control arm will receive usual care, and the intervention arm will receive usual care and an additional structured counselling session by a registered dietitian, with four follow-up telephone support sessions over four weeks. The two primary outcomes are change in sodium intake from baseline, as measured by a change in 24-hour urinary sodium measurements at four weeks and one year. Secondary outcomes include change in blood pressure (as measured by 24-hour ambulatory monitoring), change in 24-hour urinary potassium, and change in body weight at the same time points.DiscussionThough decreasing sodium intake has been reported to be efficacious in lowering blood pressure, there exists a gap in the evidence for an effective intervention that could be easily translated into clinical practice. If successful, our intervention would be suitable for outpatient programs such as hypertension clinics or interprofessional family practices (family health teams). A negative, or partially negative (positive effect at four weeks with attrition by 12 months) trial outcome also has significant implications for healthcare delivery and use of resources.Trial registrationThe trial was registered with Clinicaltrials.gov (identifier: NCT02283697) on 2 November 2014.Electronic supplementary materialThe online version of this article (doi:10.1186/s13063-015-0794-y) contains supplementary material, which is available to authorized users.