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Background: Recent cohort studies show that salt intake below 6 g is associated with increased mortality. These findings have not changed public recommendations to lower salt intake below 6 g, which are based on assumed blood pressure (BP) effects and no side-effects., Objectives: To assess the effects of sodium reduction on BP, and on potential side-effects (hormones and lipids) SEARCH METHODS: The Cochrane Hypertension Information Specialist searched the following databases for randomized controlled trials up to April 2018 and a top-up search in March 2020: the Cochrane Hypertension Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (from 1946), Embase (from 1974), the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. We also contacted authors of relevant papers regarding further published and unpublished work. The searches had no language restrictions. The top-up search articles are recorded under "awaiting assessment.", Selection Criteria: Studies randomizing persons to low-sodium and high-sodium diets were included if they evaluated at least one of the outcome parameters (BP, renin, aldosterone, noradrenalin, adrenalin, cholesterol, high-density lipoprotein, low-density lipoprotein and triglyceride,., Data Collection and Analysis: Two review authors independently collected data, which were analysed with Review Manager 5.3. Certainty of evidence was assessed using GRADE., Main Results: Since the first review in 2003 the number of included references has increased from 96 to 195 (174 were in white participants). As a previous study found different BP outcomes in black and white study populations, we stratified the BP outcomes by race. The effect of sodium reduction (from 203 to 65 mmol/day) on BP in white participants was as follows: Normal blood pressure: SBP: mean difference (MD) -1.14 mmHg (95% confidence interval (CI): -1.65 to -0.63), 5982 participants, 95 trials; DBP: MD + 0.01 mmHg (95% CI: -0.37 to 0.39), 6276 participants, 96 trials. Hypertension: SBP: MD -5.71 mmHg (95% CI: -6.67 to -4.74), 3998 participants,88 trials; DBP: MD -2.87 mmHg (95% CI: -3.41 to -2.32), 4032 participants, 89 trials (all high-quality evidence). The largest bias contrast across studies was recorded for the detection bias element. A comparison of detection bias low-risk studies versus high/unclear risk studies showed no differences. The effect of sodium reduction (from 195 to 66 mmol/day) on BP in black participants was as follows: Normal blood pressure: SBP: mean difference (MD) -4.02 mmHg (95% CI:-7.37 to -0.68); DBP: MD -2.01 mmHg (95% CI:-4.37, 0.35), 253 participants, 7 trials. Hypertension: SBP: MD -6.64 mmHg (95% CI:-9.00, -4.27); DBP: MD -2.91 mmHg (95% CI:-4.52, -1.30), 398 participants, 8 trials (low-quality evidence). The effect of sodium reduction (from 217 to 103 mmol/day) on BP in Asian participants was as follows: Normal blood pressure: SBP: mean difference (MD) -1.50 mmHg (95% CI: -3.09, 0.10); DBP: MD -1.06 mmHg (95% CI:-2.53 to 0.41), 950 participants, 5 trials. Hypertension: SBP: MD -7.75 mmHg (95% CI:-11.44, -4.07); DBP: MD -2.68 mmHg (95% CI: -4.21 to -1.15), 254 participants, 8 trials (moderate-low-quality evidence).   During sodium reduction renin increased 1.56 ng/mL/hour (95%CI:1.39, 1.73) in 2904 participants (82 trials); aldosterone increased 104 pg/mL (95%CI:88.4,119.7) in 2506 participants (66 trials); noradrenalin increased 62.3 pg/mL: (95%CI: 41.9, 82.8) in 878 participants (35 trials); adrenalin increased 7.55 pg/mL (95%CI: 0.85, 14.26) in 331 participants (15 trials); cholesterol increased 5.19 mg/dL (95%CI:2.1, 8.3) in 917 participants (27 trials); triglyceride increased 7.10 mg/dL (95%CI: 3.1,11.1) in 712 participants (20 trials); LDL tended to increase 2.46 mg/dl (95%CI: -1, 5.9) in 696 participants (18 trials); HDL was unchanged -0.3 mg/dl (95%CI: -1.66,1.05) in 738 participants (20 trials) (All high-quality evidence except the evidence for adrenalin)., Authors' Conclusions: In white participants, sodium reduction in accordance with the public recommendations resulted in mean arterial pressure (MAP) decrease of about 0.4 mmHg in participants with normal blood pressure and a MAP decrease of about 4 mmHg in participants with hypertension. Weak evidence indicated that these effects may be a little greater in black and Asian participants. The effects of sodium reduction on potential side effects (hormones and lipids) were more consistent than the effect on BP, especially in people with normal BP., (Copyright © 2020 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.)

Competing Interests: Competing interests: We have read and understood BMJ policy on declaration of interests and have the following interests to declare: NRC has received past research funding from the National Institutes of Health and the American Heart Association, and consultancy fees from Jazz Pharmaceuticals and OptumCare. She was a member of the Committee to Review the Dietary Reference Intakes for Sodium and Potassium, National Academies of Sciences, Engineering, and Medicine, 2019. FJH is a member of Consensus Action on Salt and Health (CASH) and World Action on Salt and Health (WASH). Both CASH and WASH are non-profit charitable organisations and FJH does not receive any financial support from CASH or WASH. GAM is chairman of Blood Pressure UK (BPUK), chairman of CASH and chairman of WASH. BPUK, CASH, and WASH are non-profit charitable organisations. GAM does not receive any financial support from any of these organisations. NG has no competing interests to declare.

Background: The projected reduced mortality effect of reduced sodium intake in model-based studies conflicts with the observed increased mortality associated with low sodium intake in population studies. This may reflect an overestimation of the dose-response relation between sodium reduction (SR) and blood pressure (BP) used in mortality modeling studies., Objectives: The present meta-regression analysis sought to estimate the dose-response relations between SR and BP in study groups with mean BP above or below the 75th percentile of the general population., Methods: Based on a literature search from 1 January 1946 to 11 April 2018, we identified 133 randomized controlled trials allocating healthy or hypertensive individuals to SR or usual sodium intake. Multivariable regression analyses of the mean SR versus the mean blood pressure effect adjusted for effect modifiers were performed., Results: In study groups with mean BP above the 75th percentile [131/78 mm Hg systolic BP (SBP)/diastolic BP (DBP)], there was strong evidence of a linear dose-response relation between SR and BP. For SBP, the dose-response relation was -7.7 mm Hg/100 mmol SR (95% CI: -10.4, -5.0), and for DBP it was -3.0 mm Hg/100 mmol SR (95% CI: -4.6, -1.4). In study groups with mean BP ≤ 131/78 mm Hg, the relation between SR and BP was weak. For SBP it was -1.46 mm Hg/100 mmol SR (95% CI: -2.7, -0.20) and for DBP it was: -0.07 mm Hg/100 mmol SR (95% CI: -1.5, 1.4)., Conclusions: Only study groups with a BP in the highest 25th percentile of the population showed a clinically significant drop in BP with SR. The policy of lowering dietary sodium intake in the general population may need to be reframed to target patients with hypertension. This study was registered at PROSPERO 2015 as CRD42015017773., (Copyright © American Society for Nutrition 2019.)

Background: In spite of more than 100 years of investigations the question of whether a reduced sodium intake improves health is still unsolved., Objectives: To estimate the effects of low sodium intake versus high sodium intake on systolic and diastolic blood pressure (SBP and DBP), plasma or serum levels of renin, aldosterone, catecholamines, cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglycerides., Search Methods: The Cochrane Hypertension Information Specialist searched the following databases for randomized controlled trials up to March 2016: the Cochrane Hypertension Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL) (2016, Issue 3), MEDLINE (from 1946), Embase (from 1974), the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. We also searched the reference lists of relevant articles., Selection Criteria: Studies randomising persons to low-sodium and high-sodium diets were included if they evaluated at least one of the above outcome parameters., Data Collection and Analysis: Two review authors independently collected data, which were analysed with Review Manager 5.3., Main Results: A total of 185 studies were included. The average sodium intake was reduced from 201 mmol/day (corresponding to high usual level) to 66 mmol/day (corresponding to the recommended level).The effect of sodium reduction on blood pressure (BP) was as follows: white people with normotension: SBP: mean difference (MD) -1.09 mmHg (95% confidence interval (CI): -1.63 to -0.56; P = 0.0001); 89 studies, 8569 participants; DBP: + 0.03 mmHg (MD 95% CI: -0.37 to 0.43; P = 0.89); 90 studies, 8833 participants. High-quality evidence. Black people with normotension: SBP: MD -4.02 mmHg (95% CI:-7.37 to -0.68; P = 0.002); seven studies, 506 participants; DBP: MD -2.01 mmHg (95% CI:-4.37 to 0.35; P = 0.09); seven studies, 506 participants. Moderate-quality evidence. Asian people with normotension: SBP: MD -0.72 mmHg (95% CI: -3.86 to 2.41; P = 0.65); DBP: MD -1.63 mmHg (95% CI:-3.35 to 0.08; P =0.06); three studies, 393 participants. Moderate-quality evidence.White people with hypertension: SBP: MD -5.51 mmHg (95% CI: -6.45 to -4.57; P < 0.00001); 84 studies, 5925 participants; DBP: MD -2.88 mmHg (95% CI: -3.44 to -2.32; P < 0.00001); 85 studies, 6001 participants. High-quality evidence. Black people with hypertension: SBP MD -6.64 mmHg (95% CI:-9.00 to -4.27; P = 0.00001); eight studies, 619 participants; DBP -2.91 mmHg (95% CI:-4.52, -1.30; P = 0.0004); eight studies, 619 participants. Moderate-quality evidence. Asian people with hypertension: SBP: MD -7.75 mmHg (95% CI:-11,44 to -4.07; P < 0.0001) nine studies, 501 participants; DBP: MD -2.68 mmHg (95% CI: -4.21 to -1.15; P = 0.0006). Moderate-quality evidence.In plasma or serum, there was a significant increase in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.03), cholesterol (P < 0.0005) and triglyceride (P < 0.0006) with low sodium intake as compared with high sodium intake. All effects were stable in 125 study populations with a sodium intake below 250 mmol/day and a sodium reduction intervention of at least one week., Authors' Conclusions: Sodium reduction from an average high usual sodium intake level (201 mmol/day) to an average level of 66 mmol/day, which is below the recommended upper level of 100 mmol/day (5.8 g salt), resulted in a decrease in SBP/DBP of 1/0 mmHg in white participants with normotension and a decrease in SBP/DBP of 5.5/2.9 mmHg in white participants with hypertension. A few studies showed that these effects in black and Asian populations were greater. The effects on hormones and lipids were similar in people with normotension and hypertension. Renin increased 1.60 ng/mL/hour (55%); aldosterone increased 97.81 pg/mL (127%); adrenalin increased 7.55 pg/mL (14%); noradrenalin increased 63.56 pg/mL: (27%); cholesterol increased 5.59 mg/dL (2.9%); triglyceride increased 7.04 mg/dL (6.3%).

Scientific evidence to support the recommended salt intake of < 5.8 g/day is virtually non-existingent. There are no randomized controlled trials (RCTs) to investigate the effect of salt reduction (SR) below 5.8 g on health outcomes. The effect of SR on blood pressure (BP) reaches maximal efficacy at 1 week. RCTs in healthy individuals lasting at least 1 week show that the effect of SR on BP is <1 mmHg, but that SR has significant side effects, including increases in renin, aldosterone, noradrenalin, adrenalin, cholesterol and triglyceride. Still, disregarding confounders and side effects, health authorities use BP effects obtained in studies of pre-hypertensive and hypertensive patients to recommend SR in the healthy population and use these biased BP effects in statistical models indirectly to project millions of saved lives. These fantasy projections are in contrast to real data from prospective observational population studies directly associating salt intake with mortality, which show that salt intake <5.8 g/day is associated with an increased mortality of ∼15%. The population studies also show that a very high salt intake >12.2 g is associated with increased mortality. However, since <5% of populations consume such high amounts of salt, SR at the population level should not be a public health priority. Consequently, this policy should be abolished, not because any attempt to implement it has failed, and not because it costs taxpayers and food consumers unnecessary billions of dollars, but because-if implemented-it might kill people instead of saving them., (© The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)

Several health institutions recommend sodium intake be reduced to below 2,300 mg, which means that 6-7 billion individuals should alter their diet to accommodate. Such a radical recommendation should be based on solid evidence. However, this review reveals that (i) there are no randomized controlled trials (RCTs) allocating individuals to below 2,300 mg and measuring health outcomes; (ii) RCTs allocating risk groups such as obese prehypertensive individuals and hypertensive individuals down to (but not below) 2,300 mg show no effect of sodium reduction on all-cause mortality; (iii) RCTs allocating individuals to below 2,300 mg show a minimal effect on blood pressure in the healthy population (less than 1mm Hg) and significant increases in renin, aldosterone, noradrenalin cholesterol, and triglyceride; and (iv) observational studies show that sodium intakes below 2,645 and above 4,945 mg are associated with increased mortality. Given that 90% of the worlds' population currently consumes sodium within the optimal range of 2,645-4,945 mg, there is no scientific basis for a public health recommendation to alter sodium intake., (© American Journal of Hypertension, Ltd 2016. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

The purpose of this meta-analysis was to establish the time for achievement of maximal blood pressure (BP) efficacy of a sodium reduction (SR) intervention and the relation between the amount of SR and the BP response in individuals with hypertension and normal BP. Relevant studies were retrieved from a pool of 167 randomized controlled trials (RCTs) published in the period 1973-2010 and integrated in meta-analyses. Fifteen relevant RCTs were included in the maximal efficacy analysis. After initiation of sodium reduction (range: 55-118 mmol/d), there were no significant differences in systolic blood pressure (SBP) or diastolic blood pressure (DBP) between measurements at weeks 1 and 2 (∆SBP: -0.18 mmHg/∆DBP: 0.12 mmHg), weeks 1 and 4 (∆SBP: -0.50 mmHg/∆DBP: 0.35 mmHg), weeks 2 and 4 (∆SBP: -0.20 mmHg/∆DBP: -0.10 mmHg), weeks 2 and 6 (∆SBP: -0.50 mmHg/∆DBP: -0.42 mmHg), and weeks 4 and 6 (∆SBP: 0.39 mmHg/∆DBP: -0.22 mmHg). Eight relevant RCTs were included in the dose-response analysis, which showed that within the established usual range of sodium intake [<248 mmol/d (5700 mg/d)], there was no relation between the amount of SR (range: 136-188 mmol) and BP outcome in normotensive populations [∆SBP: 0.99 mm Hg (95% CI: -2.12, 4.10 mm Hg), [corrected] P = 0.53; ∆DBP: -0.49 mm Hg (95% CI: -4.0, 3.03), P = 0.79]. In contrast, prehypertensive and hypertensive populations showed a significant dose-response relation (range of sodium reduction: 77-140 mmol/d) [∆SBP: 6.87 mmHg (95% CI: 5.61, 8.12, P < 0.00001); ∆DBP: 3.61 mmHg (95% CI: 2.83, 4.39, P < 0.00001)]. Consequently, the importance of kinetic and dynamic properties of sodium reduction, as well as baseline BP, should probably be considered when establishing a policy of sodium reduction., (© 2015 American Society for Nutrition.)

Background: The effect of sodium intake on population health remains controversial. The objective was to investigate the incidence of all-cause mortality (ACM) and cardiovascular disease events (CVDEs) in populations exposed to dietary intakes of low sodium (<115 mmol), usual sodium (low usual sodium: 115-165 mmol; high usual sodium: 166-215 mmol), and high sodium (>215 mmol)., Methods: The relationship between individual measures of dietary sodium intake vs. outcome in cohort studies and randomized controlled trials (RCTs) measured as hazard ratios (HRs) were integrated in meta-analyses., Results: No RCTs in healthy population samples were identified. Data from 23 cohort studies and 2 follow-up studies of RCTs (n = 274,683) showed that the risks of ACM and CVDEs were decreased in usual sodium vs. low sodium intake (ACM: HR = 0.91, 95% confidence interval (CI) = 0.82-0.99; CVDEs: HR = 0.90, 95% CI = 0.82-0.99) and increased in high sodium vs. usual sodium intake (ACM: HR = 1.16, 95% CI = 1.03-1.30; CVDEs: HR = 1.12, 95% CI = 1.02-1.24). In population representative samples adjusted for multiple confounders, the HR for ACM was consistently decreased in usual sodium vs. low sodium intake (HR = 0.86; 95% CI = 0.81-0.92), but not increased in high sodium vs. usual sodium intake (HR = 1.04; 95% CI = 0.91-1.18). Within the usual sodium intake range, the number of events was stable (high usual sodium vs. low usual sodium: HR = 0.98; 95% CI = 0.92-1.03)., Conclusions: Both low sodium intakes and high sodium intakes are associated with increased mortality, consistent with a U-shaped association between sodium intake and health outcomes., (© American Journal of Hypertension, Ltd 2014. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Background: The question of whether reduced sodium intake is effective as a health prophylaxis initiative is unsolved. The purpose was to estimate the effects of low-sodium vs. high-sodium intake on blood pressure (BP), renin, aldosterone, catecholamines, and lipids., Methods: Studies randomizing persons to low-sodium and high-sodium diets evaluating at least one of the above outcome parameters were included. Data were analyzed with Review Manager 5.1., Results: A total of 167 studies were included. The effect of sodium reduction in: (i) Normotensives: Caucasians: systolic BP (SBP) -1.27 mm Hg (95% confidence interval (CI): -1.88, -0.66; P = 0.0001), diastolic BP (DBP) -0.05 mm Hg (95% CI: -0.51, 0.42; P = 0.85). Blacks: SBP -4.02 mm Hg (95% CI: -7.37, -0.68; P = 0.002), DBP -2.01 mm Hg (95% CI: -4.37, 0.35; P = 0.09). Asians: SBP -1.27 mm Hg (95% CI: -3.07, 0.54; P = 0.17), DBP -1.68 mm Hg (95% CI: -3.29, -0.06; P = 0.04). (ii) Hypertensives: Caucasians: SBP -5.48 mm Hg (95% CI: -6.53, -4.43; P < 0.00001), DBP -2.75 mm Hg (95% CI: -3.34, -2.17; P < 0.00001). Blacks: SBP -6.44 mm Hg (95% CI: -8.85, -4.03; P = 0.00001), DBP -2.40 mm Hg (95% CI: -4.68, -0.12; P = 0.04). Asians: SBP -10.21 mm Hg (95% CI: -16.98, -3.44; P = 0.003), DBP -2.60 mm Hg (95% CI: -4.03, -1.16; P = 0.0004). Sodium reduction resulted in significant increases in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.0002), cholesterol (P < 0.001), and triglyceride (P < 0.0008)., Conclusions: Sodium reduction resulted in a significant decrease in BP of 1% (normotensives), 3.5% (hypertensives), and a significant increase in plasma renin, plasma aldosterone, plasma adrenaline, and plasma noradrenaline, a 2.5% increase in cholesterol, and a 7% increase in triglyceride.

Background: In spite of more than 100 years of investigations the question of reduced sodium intake as a health prophylaxis initiative is still unsolved., Objectives: To estimate the effects of low sodium versus high sodium intake on systolic and diastolic blood pressure (SBP and DBP), plasma or serum levels of renin, aldosterone, catecholamines, cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglycerides., Search Methods: PUBMED, EMBASE and Cochrane Central and reference lists of relevant articles were searched from 1950 to July 2011., Selection Criteria: Studies randomizing persons to low sodium and high sodium diets were included if they evaluated at least one of the above outcome parameters., Data Collection and Analysis: Two authors independently collected data, which were analysed with Review Manager 5.1., Main Results: A total of 167 studies were included in this 2011 update.The effect of sodium reduction in normotensive Caucasians was SBP -1.27 mmHg (95% CI: -1.88, -0.66; p=0.0001), DBP -0.05 mmHg (95% CI: -0.51, 0.42; p=0.85). The effect of sodium reduction in normotensive Blacks was SBP -4.02 mmHg (95% CI:-7.37, -0.68; p=0.002), DBP -2.01 mmHg (95% CI:-4.37, 0.35; p=0.09). The effect of sodium reduction in normotensive Asians was SBP -1.27 mmHg (95% CI: -3.07, 0.54; p=0.17), DBP -1.68 mmHg (95% CI:-3.29, -0.06; p=0.04). The effect of sodium reduction in hypertensive Caucasians was SBP -5.48 mmHg (95% CI: -6.53, -4.43; p<0.00001), DBP -2.75 mmHg (95% CI: -3.34, -2.17; p<0.00001). The effect of sodium reduction in hypertensive Blacks was SBP -6.44 mmHg (95% CI:-8.85, -4.03; p=0.00001), DBP -2.40 mmHg (95% CI:-4.68, -0.12; p=0.04). The effect of sodium reduction in hypertensive Asians was SBP -10.21 mmHg (95% CI:-16.98, -3.44; p=0.003), DBP -2.60 mmHg (95% CI: -4.03, -1.16; p=0.0004).In plasma or serum there was a significant increase in renin (p<0.00001), aldosterone (p<0.00001), noradrenaline (p<0.00001), adrenaline (p<0.0002), cholesterol (p<0.001) and triglyceride (p<0.0008) with low sodium intake as compared with high sodium intake. In general the results were similar in studies with a duration of at least 2 weeks., Authors' Conclusions: Sodium reduction resulted in a 1% decrease in blood pressure in normotensives, a 3.5% decrease in hypertensives, a significant increase in plasma renin, plasma aldosterone, plasma adrenaline and plasma noradrenaline, a 2.5% increase in cholesterol, and a 7% increase in triglyceride. In general, these effects were stable in studies lasting for 2 weeks or more.

Ninety-five percent of the World's populations have a mean salt intake between 6 and 12 g, which is much lower than the tolerated daily level of up to 55 g/d. In spite of this, the recommended upper level by many health institutions is as low as 5.8 g/day. When reviewing the evidence for an upper level of 5.8 g/day, it becomes apparent that neither the supporting studies selected by the health institutions, nor randomized controlled trials and prospective observational studies disregarded by the health institutions, document that a salt intake below this 5.8 g, has beneficial health effects. Although there is an association between salt intake and blood pressure, both in randomized controlled trials and in observational studies, this association is weak, especially in non-obese individuals with normal blood pressure. Furthermore a salt intake below 5.8 g is associated with the activation of the renin-angiotensin-aldosteron system, an increase in plasma lipids and increased mortality. A redesign of the salt dietary guidelines, therefore, seems to be needed. [ABSTRACT FROM AUTHOR]

Reduced dietary sodium intake (sodium reduction) increases heart rate in some studies of animals and humans. As heart rate is independently associated with the development of heart failure and increased risk of premature death a potential increase in heart rate could be a harmful side-effect of sodium reduction. The purpose of the present meta-analysis was to investigate the effect of sodium reduction on heart rate. Relevant studies were retrieved from an updated pool of 176 randomized controlled trials (RCTs) published in the period 1973-2014. Sixty-three of the RCTs including 72 study populations reported data on heart rate. In a meta-analysis of these data sodium reduction increased heart rate with 1.65 beats per minute [95% CI: 1.19, 2.11], p < 0.00001, corresponding to 2.4% of the baseline heart rate. This effect was independent of baseline blood pressure. In conclusion sodium reduction increases heart rate by as much (2.4%) as it decreases blood pressure (2.5%). This side-effect, which may cause harmful health effects, contributes to the need for a revision of the present dietary guidelines. [ABSTRACT FROM AUTHOR]

The purpose of the meta-analysis of randomized trials was to analyze the significance of ethnicity on the effect of sodium reduction (SR) on blood pressure (BP) by estimating the effect of SR on BP in Asians, Blacks and Whites under conditions, which were adjusted with respect to baseline BP, baseline sodium intake and quantity of SR. Relevant studies were retrieved from a pool of 167 RCTs published in the period 1973-2010 and identified in a previous Cochrane review. 9 Asian, 9 Black, and 74 White populations standardized with respect to the range of baseline blood pressure, the range of baseline sodium, duration of SR (at least 7 days) and baseline sodium intake (at maximum 250 mmol) intake were included. In the cross-sectional analysis, there was no difference in change in SBP to SR between the ethnic groups, but there was a small difference in SR induced change in DBP between Blacks and Whites (p = 0.04). The comparison of changes in SBP and DBP to SR in ethnic groups compared in identical studies showed no statistically significant differences between the groups. [ABSTRACT FROM AUTHOR]

BACKGROUND The recommendation to restrict dietary sodium for management of hypertensive cardiovascular disease assumes that sodium intake exceeds physiologic need, that it can be significantly reduced, and that the reduction can be maintained over time. In contrast, neuroscientists have identified neural circuits in vertebrate animals that regulate sodium appetite within a narrow physiologic range. This study further validates our previous report that sodium intake, consistent with the neuroscience, tracks within a narrow range, consistent over time and across cultures. METHODS Peer-reviewed publications reporting 24-hour urinary sodium excretion (UNaV) in a defined population that were not included in our 2009 publication were identified from the medical literature. These datasets were combined with those in our previous report of worldwide dietary sodium consumption. RESULTS The new data included 129 surveys, representing 50,060 participants. The mean value and range of 24-hour UNaV in each of these datasets were within 1 SD of our previous estimate. The combined mean and normal range of sodium intake of the 129 datasets were nearly identical to that we previously reported (mean = 158.3±22.5 vs. 162.4±22.4 mmol/d). Merging the previous and new datasets (n = 190) yielded sodium consumption of 159.4±22.3 mmol/d (range = 114–210 mmol/d; 2,622–4,830mg/d). CONCLUSIONS Human sodium intake, as defined by 24-hour UNaV, is characterized by a narrow range that is remarkably reproducible over at least 5 decades and across 45 countries. As documented here, this range is determined by physiologic needs rather than environmental factors. Future guidelines should be based on this biologically determined range. [ABSTRACT FROM AUTHOR]

A letter to the editor in response to the article related to effect of sodium intake on blood pressure in the previous issue and a response from the author on same is presented.