Question What is the impact of dietary sodium intake on blood pressure in middle-aged to elderly individuals?
Findings In this prospectively allocated diet order crossover study of 213 individuals, 1 week of a low-sodium diet resulted in an average 8–mm Hg reduction in systolic blood pressure vs a high-sodium diet, with few adverse events. The low-sodium diet lowered systolic blood pressure in nearly 75% of individuals compared with the high-sodium diet.
Meaning In this trial, the blood pressure–lowering effect of dietary sodium reduction was comparable with a commonly used first-line antihypertensive medication.
Importance Dietary sodium recommendations are debated partly due to variable blood pressure (BP) response to sodium intake. Furthermore, the BP effect of dietary sodium among individuals taking antihypertensive medications is understudied.
Objectives To examine the distribution of within-individual BP response to dietary sodium, the difference in BP between individuals allocated to consume a high- or low-sodium diet first, and whether these varied according to baseline BP and antihypertensive medication use.
Design, Setting, and Participants Prospectively allocated diet order with crossover in community-based participants enrolled between April 2021 and February 2023 in 2 US cities. A total of 213 individuals aged 50 to 75 years, including those with normotension (25%), controlled hypertension (20%), uncontrolled hypertension (31%), and untreated hypertension (25%), attended a baseline visit while consuming their usual diet, then completed 1-week high- and low-sodium diets.
Intervention High-sodium (approximately 2200 mg sodium added daily to usual diet) and low-sodium (approximately 500 mg daily total) diets.
Main Outcomes and Measures Average 24-hour ambulatory systolic and diastolic BP, mean arterial pressure, and pulse pressure.
Results Among the 213 participants who completed both high- and low-sodium diet visits, the median age was 61 years, 65% were female and 64% were Black. While consuming usual, high-sodium, and low-sodium diets, participants’ median systolic BP measures were 125, 126, and 119 mm Hg, respectively. The median within-individual change in mean arterial pressure between high- and low-sodium diets was 4 mm Hg (IQR, 0-8 mm Hg; P < .001), which did not significantly differ by hypertension status. Compared with the high-sodium diet, the low-sodium diet induced a decline in mean arterial pressure in 73.4% of individuals. The commonly used threshold of a 5 mm Hg or greater decline in mean arterial pressure between a high-sodium and a low-sodium diet classified 46% of individuals as “salt sensitive.” At the end of the first dietary intervention week, the mean systolic BP difference between individuals allocated to a high-sodium vs a low-sodium diet was 8 mm Hg (95% CI, 4-11 mm Hg; P < .001), which was mostly similar across subgroups of age, sex, race, hypertension, baseline BP, diabetes, and body mass index. Adverse events were mild, reported by 9.9% and 8.0% of individuals while consuming the high- and low-sodium diets, respectively.
Conclusions and Relevance Dietary sodium reduction significantly lowered BP in the majority of middle-aged to elderly adults. The decline in BP from a high- to low-sodium diet was independent of hypertension status and antihypertensive medication use, was generally consistent across subgroups, and did not result in excess adverse events.
Trial Registration ClinicalTrials.gov Identifier: NCT04258332
Introduction
Sodium is a dietary component that substantially contributes to blood pressure (BP).1,2 Estimated daily average sodium intake in middle-aged to elderly US adults is 3.5 g, exceeding World Health Organization, US Department of Health and Human Services, and American Heart Association recommendations, and in the prior decade, deaths attributable to excess dietary sodium increased.3-7 Randomized trials inform recommendations to reduce sodium consumption to lower BP; however, individual variability in the BP response to dietary sodium can make determining personalized treatment responses from clinical trials challenging.7-16
The within-individual BP response to variation in sodium intake, known as salt sensitivity of BP (SSBP), has been used to define individuals who experience meaningful BP differences with sodium intake reduction.17,18 Estimates suggest that approximately 50% and 25% of individuals with and without hypertension exhibit SSBP, respectively; however, few contemporary data exist and thresholds for defining SSBP may underestimate the impact of dietary sodium reduction on BP.17-19 Most randomized trials testing dietary sodium reduction excluded individuals taking antihypertensive medications.9-11 Thus, among individuals with treated hypertension, uncertainty persists regarding the extent to which dietary sodium reduction lowers BP and whether antihypertensive pharmacotherapies are associated with lessening of SSBP.8-11,20
We conducted the Coronary Artery Risk Development in Young Adults (CARDIA)–SSBP study in a contemporary community dwelling population of middle-aged to elderly persons including the spectrum of individuals with normotension through treated and untreated hypertension. Using a prospectively allocated diet order crossover design of 1-week high-sodium and low-sodium diets, we examined (1) the distribution of within-individual BP response to dietary sodium, (2) the difference in BP between individuals allocated to high- or low-sodium diet first, and (3) whether these varied by baseline BP and antihypertensive medication use.
Trial Oversight
The CARDIA Executive Committee, Observational Study Monitoring Board, and University of Alabama at Birmingham (UAB) Institutional Review Board, serving as the single institutional review board, approved the study protocol (eAppendix 1 in Supplement 1). All participants provided written informed consent. Participants received stipends.
Participants
Briefly, CARDIA is a prospective, multicenter, observational cohort study that aims to identify the factors in young adulthood influencing development of cardiovascular disease.21 Participant enrollment occurred in 1985-1986 and was balanced by sex, self-identified race (Black or White), age (18-24 or 25-30 years), and education (high school or more than high school) subgroups from 4 study sites across the US: Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California. Longitudinal follow-up since enrollment is ongoing.
Between April 2021 and February 2023, enrollment into CARDIA-SSBP occurred through 2 sources, initially the CARDIA year 35 core examination, and then an amendment in 2022 allowing for non-CARDIA participants from Chicago and Birmingham. Detailed eligibility criteria are in eAppendix 1 in Supplement 1. Briefly, the inclusion criterion was age 50 to 75 years and key exclusion criteria were enrollment visit systolic or diastolic BP outside of 90 to 160 mm Hg or 50 to 100 mm Hg, respectively, resistant hypertension, or contraindications to high- or low-sodium diets.
Study Protocol
Sodium content and 1-week duration of diets, use of 24-hour ambulatory BP monitoring (ABPM), and 24-hour urine collections for assessment of dietary adherence were based on the American Heart Association’s SSBP recommendations.18 Participants attended 4 study visits: enrollment, baseline, end of the first diet week, and end of the second diet week, with the latter 3 occurring over consecutive 1-week intervals. Study visits occurred at the UAB and Northwestern University CARDIA field centers. Allocation to diet order alternated by weekday at each site. The high-sodium diet was achieved pragmatically by daily supplementation of each participant’s usual diet with 2 bullion packets, each containing 1100 mg of sodium. The low-sodium diet was standardized across sites and prepared in metabolic kitchens at the University of Illinois–Chicago and UAB. One week of low-sodium meals, snacks, and beverages were provided at no cost to participants with instructions not to consume anything outside that provided. The low-sodium diet was designed to provide daily averages of approximately 500 mg of sodium, approximately 4500 mg of potassium, and approximately 1000 mg of calcium, with an individual’s caloric need estimated using the Mifflin-St Jeor formula (eAppendix 2 in Supplement 1).22 The potassium and calcium content of the prepared meals aligns with US dietary guideline recommendations.4
Twenty-four-hour ABPM (OnTrak, Spacelabs Healthcare) and 24-hour urine collections were performed beginning the day before each of the baseline, end of first diet week, and end of second diet week visits. For study visits, participants were instructed to arrive fasting for 6 hours or longer. Participant-reported adverse events while consuming study diets were recorded. Twenty-four-hour ABPM results were transmitted to Vanderbilt University Medical Center (VUMC) for safety review and BP outcomes. For each individual, systolic BP, diastolic BP, mean arterial pressure, and pulse pressure at the end of each diet week were calculated as the averages from 24-hour ABPM. Urine collections were processed on study visit days, stored frozen at −80 °C, then batch shipped overnight on dry ice to VUMC. Urine sodium and creatinine were measured using flame photometry (Jenway PFP7/C, Cole-Parmer) and ELISA (Exocell, Ethos Biosciences), respectively. Assessors for 24-hour ABPM and urinalysis results were masked to diet order.
Statistical Analysis
Salt sensitivity of BP, calculated as 24-hour BP during a high-sodium diet minus 24-hour BP during a low-sodium diet, provides a continuous measure of within-individual BP response to variation in sodium loading. The precision of the estimate of SSBP for mean arterial pressure, the primary outcome, was estimated a priori, and a sample size of 200 individuals at an SD of 7 mm Hg yielded a margin of error of 1 mm Hg.
Prospective allocation to either diet order with a crossover design enabled not only within-individual analysis examining SSBP between high- and low-sodium diets, but also between parallel-group analysis examining contrast in BP between groups at the end of the first diet week. Analyses were performed using an intention-to-treat approach. Baseline characteristics were calculated as medians and IQRs or counts and percentages.
The distribution of SSBP for mean arterial pressure was summarized as medians and IQRs in the overall cohort and within prespecified subgroups by age, sex (self-report), race (self-report), hypertension status, antihypertensive medication use, baseline BP, body mass index, study site, diabetes, and enrollment source, and analyzed using the Wilcoxon signed rank test. The SSBP for mean arterial pressure was then compared between subgroups using the Wilcoxon rank sum test. Distributions of SSBP for systolic BP, diastolic BP, and pulse pressure in the overall cohort were also examined, summarized as medians and IQRs and analyzed using the Wilcoxon signed rank test. Whether SSBP differed by allocated diet order was tested using unadjusted ordinary least-squares regression. In prespecified exploratory analysis, whether SSBP differed between individuals with baseline normotension, controlled hypertension, untreated hypertension, and uncontrolled hypertension was analyzed by the Kruskal-Wallis test. In additional exploratory analysis, associations between classes of antihypertensive medications and SSBP were examined in ordinary least-squares models adjusted for demographic and clinical covariates. The proportion of individuals with any decline, no change, or any increase in BP between high- and low-sodium diets was quantified and then repeated using commonly used thresholds of a 5–mm Hg or greater decrease and a 7–mm Hg or greater increase in mean arterial pressure to define salt sensitivity and inverse salt sensitivity, respectively.18,19,23 The analysis for within-individual BP changes was also recalculated between the usual and low-sodium diets and between the usual and high-sodium diets.
Next, we performed parallel-group analysis to examine contrast in BP at the end of just the first diet week between the groups of individuals allocated to either high- or low-sodium diet first. Primary unadjusted then multivariable-adjusted ordinary least-squares regression was used to calculate mean between-group differences and 95% CIs. Adjustment covariates included age, sex, race, baseline BP, history of hypertension, number of antihypertensive medications, diabetes, body mass index, end of first diet week urine potassium, study site, and CARDIA vs non-CARDIA participants. The overall between-group parallel analysis was then repeated using just the BP from the end of the second diet week. Crossover analysis was performed to assess for interindividual sequence, intra-individual period, or carryover effects, which were all nonsignificant at P = .89, P = .78, and P = .98, respectively. Variation in the difference in systolic BP at the end of the first diet week between the high- and low-sodium diet groups was examined in the aforementioned subgroups by including interaction terms with first diet assignment.
The proportion of participants reporting adverse events while consuming high- and low-sodium diets was tabulated. Analyses were performed using Stata version 15.1 (StataCorp). Statistical significance threshold was set at a 2-sided α ≤ .05. Subgroup analyses were prespecified but considered exploratory, without a priori Bonferroni P value correction. Post hoc, for subgroup analyses we calculated a Bonferroni corrected significance threshold of P < .002.
Of 281 individuals who consented, 232 met eligibility and 228 were randomized and attended the baseline visit (eFigure 1 in Supplement 1). Enrollment characteristics for the 213 individuals who completed both high- and low-sodium diet visits according to allocation are shown in the Table.
Assessed by 24-hour urine excretion, the high-sodium diet significantly increased sodium intake above the low-sodium and usual diets (eTable 1 in Supplement 1). The subset of individuals not taking antihypertensive medications at baseline provides population estimates of usual sodium consumption and the contrast between high- and low-sodium diets. Participants’ usual diets were already high in sodium (median, 4.45 g/d; IQR, 2.57-6.93 g/d), which was significantly raised and lowered to medians of 5.00 and 1.27 g/d while participants were consuming the high- and low-sodium diets, respectively.
Figure 1 shows 24-hour ABPM results according to allocated diet order and study visit. Figure 2 shows distributions of SSBP calculated as the within-individual difference in 24-hour ABP for the high-sodium diet minus the low-sodium diet. For the primary outcome of SSBP for mean arterial pressure, the median was 4 mm Hg (IQR, 0-8 mm Hg; P < .001). The SSBP for mean arterial pressure did not significantly differ between subgroups, except by diastolic BP, in whom individuals with baseline diastolic BP of 74 mm Hg or lower had a relatively smaller but still significant decline in mean arterial pressure while consuming a low-sodium diet vs a high-sodium diet, compared with individuals whose baseline diastolic BP was above 74 mm Hg (Figure 3). The SSBP did not differ according to diet order (eTable 2 in Supplement 1).
The SSBP was also similar among individuals with normotension, controlled hypertension, untreated hypertension, and uncontrolled hypertension (Figure 4; eTables 3 and 4 in Supplement 1). In exploratory multivariable analysis, antihypertensive drug classes (ie, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, β-blockers, calcium channel blockers, and diuretics) were not consistently associated with SSBP (eTable 5 in Supplement 1).
In the overall cohort, while consuming the low-sodium diet compared with the high-sodium diet, mean arterial pressure declined, was unchanged, or increased in 73.4%, 1.0%, and 25.6% of individuals, respectively, with similar patterns for systolic BP, diastolic BP, and pulse pressure (eTable 6 in Supplement 1). The commonly used threshold of a 5–mm Hg or greater decline in mean arterial pressure from high- to low-sodium diets classified 46% of individuals as “salt sensitive.” This group had a median difference in 24-hour urine sodium in high-sodium minus low-sodium diet of 3.4 g (IQR, 1.4-4.9 g; P < .001). Using a threshold of a 7–mm Hg or greater increase in mean arterial pressure from a high- to a low-sodium diet, 5% of individuals exhibited inverse salt sensitivity. These individuals had a median difference in 24-hour urine sodium in high-sodium minus low-sodium diet of 0.3 g (IQR, −4.6 to 1.4 g; P = .92).
Compared with usual diet, the low-sodium diet reduced daily sodium intake by a median of 2.3 g (IQR, 0.4- g; P < .001), which was similar to the 7–mm Hg median difference between high- and low-sodium diets (eTable 7 in Supplement 1). Compared with usual diet, 71.7% of individuals demonstrated a decline in systolic BP with the low-sodium diet (eTable 6 in Supplement 1). In contrast, the high-sodium diet raised dietary sodium intake by a median of 1.1 g (IQR, −0.4 to 2.7 g; P < .001), but without significant changes in BP (eTable 6 in Supplement 1).
In the parallel-group analysis performed to examine the differences in BP at the end of the first diet week between the groups of individuals allocated to either high- or low-sodium diets first, systolic BP was 8 mm Hg lower (95% CI, 4-11 mm Hg; P < .001) in those allocated to a low-sodium diet first compared with a high-sodium diet first (Figure 1), which was similar following multivariable adjustment (8 mm Hg; 95% CI, 5-11 mm Hg; P < .001). This between-group effect was also consistent comparing low- and high-sodium diet groups using just the end of the second diet week BP (7 mm Hg; 95% CI, 3-11 mm Hg; P < .001), without evidence for interindividual sequence or carryover effects. Mean differences in diastolic BP, mean arterial pressure, and pulse pressure between individuals randomized to a high- vs low-sodium diet first were also significant (Figure 1). The reduction in systolic BP resulting from a low-sodium diet compared with a high-sodium diet was largely consistent across subgroups, including age, sex, and race, with relatively greater effects in individuals with higher baseline BP and diabetes (eFigure 2 in Supplement 1).
A total of 35 and 24 adverse events were reported in 21 (9.9%) and 17 (8.0%) individuals while consuming high- and low-sodium diets, respectively (eTable 8 in Supplement 1). These were generally mild and self-remitted. The most frequent symptoms while consuming the high-sodium diet were headache, gastrointestinal discomfort, and edema; while consuming the low-sodium diet, these were cramping and weakness.
Discussion
In this sample of community-dwelling middle-aged to elderly individuals, sodium reduction significantly lowered BP compared with a high-sodium diet after a 1-week diet study period. Furthermore, the within-individual and between-group declines in BP from a high-sodium to a low-sodium diet were independent of hypertension status and antihypertensive medication use, were generally consistent across subgroups, and did not result in excess adverse events.
Based on 24-hour urine sodium excretion, during the 1-week low-sodium dietary intervention, median sodium intake was approximately 1.3 g/d. Compared with usual diet, the low-sodium diet resulted in a median reduction of about 1 tsp of table salt (2.3 g of sodium) per day with a corresponding median 6–mm Hg reduction in systolic BP. The magnitude of this 24-hour ABP effect is similar to the mean 6.7–mm Hg reduction in clinic systolic BP via a low-sodium diet of 1.5 g/d observed in the DASH-Sodium trial, in which individuals consumed fully controlled sodium diets for 30 days each.10 The 6–mm Hg reduction in systolic BP achieved with dietary sodium reduction compared with usual diet in the overall cohort is also similar to the average effect observed with 12.5 mg of hydrochlorothiazide.24 The low-sodium diet was well tolerated, with 8% of individuals reporting any adverse event vs 9.9% consuming the high-sodium diet. Collectively, these data may inform recommendations to patients; namely, clinically meaningful lowering of BP through dietary sodium reduction can be achieved safely and rapidly within 1 week; an effect comparable with that of a common first-line antihypertensive medication.
In participants in this study, the estimated median daily sodium intake during usual diet was approximately 4.5 g. Although further increase in daily sodium intake achieved a significant increase of approximately 0.5 tsp of table salt (approximately 1.1 g of sodium), parallel increases in BP were not observed. This approach of supplementing dietary sodium above each individual’s usual diet was not only pragmatic but also designed to reflect real-life variability in sodium intake. It also contrasts with the DASH-Sodium and GenSalt studies, in which the “high-sodium” diets did not, on average, surpass the sodium intake of usual diets.10,13 This distinction in study design enabled us to address the impact of sodium supplementation beyond usual diet, providing complementary information to the existing literature. That further sodium supplementation did not increase BP in the participants of this study suggests that usual diets may already have been sodium saturated. We caution against the interpretation that added sodium beyond usual diet does not adversely contribute to health.25 Rather, our data demonstrate that the greatest impact on BP compared with usual diet is achieved through lowering sodium intake. Once a low-sodium diet is attained, returning to a higher-sodium diet afterward did raise BP, consistent with findings from others.11,13
Conventional thresholds for defining SSBP may underestimate the proportion of individuals who experience clinically meaningful lowering of BP with sodium reduction. Using a difference in mean arterial pressure threshold of 5 mm Hg or greater in high-sodium minus low-sodium diets to define SSBP, 46% of participants met this criterion.18 This contrasts with the 73.4% of individuals who experienced any reduction in mean arterial pressure with a low-sodium diet. Furthermore, we found that the reduction in mean arterial pressure between individuals allocated to a high- vs a low-sodium diet first was largely consistent across subgroups. We also appreciate the concept of inverse salt sensitivity, in which BP appears to increase with sodium reduction.23 An increase in BP with the low-sodium diet occurred in some individuals, with 5% meeting the inverse SSBP for mean arterial pressure threshold of 7 mm Hg or greater, in whom we found a smaller difference in 24-hour urine sodium between high- and low-sodium diets, raising consideration for dietary nonadherence. Fully observed dietary studies may be needed to confirm whether and to what extent BP rises in response to sodium reduction in some individuals, and its prevalence.
In contrast to most prior studies evaluating dietary sodium’s effect on BP, we included individuals across the spectrum of normotensive to hypertensive, treated and untreated, controlled and uncontrolled.11,13 The reduction in BP between high- and low-sodium diets was similar across these groups. Moreover, in exploratory analyses, we did not find different classes of antihypertensive medications consistently associated with the BP response to variation in dietary sodium. That none of the classes of antihypertensive medications was consistently associated with the BP response to dietary sodium emphasizes the importance of continued lifestyle modification even among individuals with treated hypertension.
Limitations
There are some limitations to this study. The 24-hour urine sodium levels on the low-sodium diet were higher than expected for the provided standardized low-sodium meals, suggesting that there was dietary nonadherence, that equilibrium had not yet been obtained, or both. This reflects what is likely to occur in an individual’s life even if attempts are made to adhere to a low-sodium diet because sodium content of food and day-to-day dietary patterns vary. It does not, however, negate the contrast achieved between usual or high-sodium diet and low-sodium diet and the BP effects attained, and may suggest underestimation of the magnitude of difference in BP. The usual, high-sodium, and low-sodium diets were not fully controlled; thus, we cannot exclude contributions of nonsodium dietary components, but reassuringly, the magnitude of effect observed from high- to low-sodium diets was independent of differences in 24-hour urine potassium between high- and low-sodium diets and on par with that of fully controlled sodium feeding trials, eg, DASH-Sodium.11,26 Intra-individual variability in BP over time may also contribute to overestimation or underestimation of the observed BP effects attributed to contrasts between diets. We also acknowledge that intra-individual variability in BP can make interpreting individual treatment responses from parallel-design trials challenging. Our study design enabled us to assess both the between-group and within-individual BP difference between high- and low-sodium diets, and we are reassured by the similar magnitudes of effect, ie, medians of 8 mm Hg and 7 mm Hg, respectively, and that we did not observe carryover effects. Our study design does not allow assessment of BP effects of longer time consuming high- or low-sodium diets, but this does not negate the effects observed at 1 week, which was when the majority of BP effect of dietary sodium reduction was observed in DASH-Sodium.27 Our study does not address sustainability of a low-sodium diet, but the magnitudes of BP effects were similar to longer feeding studies, ie, DASH-Sodium, and are consistent with a meta-analysis demonstrating similar effects of 1-week dietary interventions to those of 1 to 6 months’ duration.10,15 Null findings for differences in SSBP between subgroups by hypertension status or antihypertensive medication class might be related to insufficient power for subgroup analysis. Evaluating the effect of dietary sodium on daytime and nocturnal BP is a future direction. Our results may not be generalizable outside of the community-based population studied.
Conclusions
In conclusion, sodium reduction significantly lowered BP in the majority of middle-aged to elderly adults in this study. The decline in BP from a high-sodium diet to a low-sodium diet was independent of hypertension status and antihypertensive medication use, generally consistent across subgroups, and did not result in excess adverse events.
Accepted for Publication: October 29, 2023.
Published Online: November 11, 2023. doi:10.1001/jama.2023.23651
Concept and design: Gupta, Wang, Lloyd-Jones, Allen.
Acquisition, analysis, or interpretation of data: Gupta, Lewis, Varady, Su, Madhur, Lackland, Reis, Lloyd-Jones, Allen.
Drafting of the manuscript: Gupta, Varady, Allen.
Critical review of the manuscript for important intellectual content: Gupta, Lewis, Varady, Su, Madhur, Lackland, Reis, Wang, Lloyd-Jones, Allen.
Statistical analysis: Gupta, Allen.
Obtained funding: Gupta, Lewis, Allen.
Administrative, technical, or material support: Lewis, Varady, Su, Lackland, Reis, Lloyd-Jones, Allen.
Supervision: Madhur, Wang, Lloyd-Jones, Allen.
Conflict of Interest Disclosures: Dr Allen reported receipt of grants from the American Heart Association during the conduct of the study. No other disclosures were reported.
Funding/Support: This study was supported by grants K23-HL128928 and R01HL148661 from the National Heart, Lung, and Blood Institute (NHLBI) to Dr Gupta; grant R01HL148661 and contract 75N92023D00005 from the NHLBI to Dr Lewis; grants R01DK128180, R01CA257807, R01DK119783, and R01HL148661 from the National Institutes of Health to Dr Varady; grant 1R01HL161212 from the NHLBI and grant AHA19EIA34480023 from the American Heart Association to Dr Madhur; grant R01HL148661 from the NHLBI to Dr Lloyd-Jones; and grant R01HL148661 from the NHLBI to Dr Allen. The CARDIA study is supported by contracts 75N92023D00002, 75N92023D00003, 75N92023D00004, 75N92023D00005, and 75N92023D00006 from the NHLBI. The project described was supported by Clinical and Translational Science Awards UL1TR002243 and UL1TR003096 from the National Center for Advancing Translational Sciences.
Role of the Funder/Sponsor: The funding bodies had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; or decision to submit the manuscript for publication.
Disclaimer: The contents and views expressed in this article are those of the authors and do not necessarily represent the views of the NHLBI, National Center for Advancing Translational Sciences, National Institutes of Health, or US Department of Health and Human Services.
Data Sharing Statement: See Supplement 2.
Additional Contributions: We thank all participants and study staff of CARDIA-SSBP for their time and invaluable contributions.
References
World Health Organization. WHO Guideline: Sodium Intake for Adults and Children. World Health Organization; 2012.
Department of Agriculture and Department of Health and Human Services. Dietary Guidelines for Americans, 2020-2025. 9th ed. Dept of Agriculture and Dept of Health and Human Services; 2020.
Effect of Dietary Sodium on Blood Pressure: A Crossover Trial | Cardiology | JAMA - JAMA Network
Read More
Bagikan Berita Ini
0 Response to "Effect of Dietary Sodium on Blood Pressure: A Crossover Trial | Cardiology | JAMA - JAMA Network"
Post a Comment