Table 1.
Study (Country) | Study Design | Participants | Study Duration | Dietary Salt “Dose” (Actual Mean Intake per d)a | Method of Sodium Intake Measurement | Outcomes | Results |
---|---|---|---|---|---|---|---|
Cardiovascular major morbid events | |||||||
Doukky et al. (US)12 | Prospective cohort | N=833 HF patients overall, 42% male, mean age 63 y; N=260 in propensity‐matched analysis by sodium restriction; 45% male; mean age 64 y | 36 mo |
Overall: 8.3 g salt/d (range: 3.1–39.2 g salt/d). Mean salt intake for sodium‐restricted and sodium‐unrestricted groups not reported |
57‐item FFQ |
Primary outcome: composite of death and HF hospitalization; secondary outcomes: cardiac death and HF hospitalization |
Sodium restriction was associated with an increased risk of death or HF hospitalization (HR 1.85; 95% CI 1.21–2.84) and HF hospitalization (HR, 1.82; 95% CI, 1.11–2.96). |
Blood Pressure | |||||||
Correia‐Costa et al. (Portugal)13 | Cross‐sectional | N=298 children aged 8–9 y (sampled from “Generation XXI, Porto, Portugal” cohort); 53% male; mean age 8.8 y | Cross‐sectional |
Total sample: 6.5 g salt/d Boys: 6.8 g salt/d Girls: 6.1 g salt/d |
24‐h urine sodium excretion | 24‐h ABPM | Every 1 g of salt intake was associated with an increase in daytime SBP by 0.56 mm Hg (95% CI, 0.11–1.01) in boys. No significant association in girls. |
Ito et al. (Japan)14 | Cross‐sectional | N=1501 adults (Shimane CoHRE study); 38% male; age 40–74 y. n=1005 without antihypertensive therapy; n=491 treated with antihypertensive therapy | Cross‐sectional |
Taking diuretics: 10.5 g salt/d Without diuretics: 9.6 g salt/d |
Spot urine sodium, estimated by Tanaka equation | SBP and DBP, using automatic sphygmomanometer | Sodium intake was positively associated with SBP in untreated (β=1.45, 95% CI, 0.93–1.96) and treated patients (β=0.75; 95% CI, 0.21–1.29). Sodium intake was positively associated with pulse pressure. |
Iuchi et al. (Japan)15 | Nonrandomized intervention study (pre‐/post‐study) | N=10 adults with type 2 diabetes and hypertension not treated with antihypertensive agents (7DACS); 70% male; mean age 60 y | 7 d |
Day 1: 9.8 g salt/d Day 7: 6.8 g salt/d |
Urine sodium from casual urine samples, collected daily for 7 d, estimated using Tanaka equation | BP variability, using ABPM; body weight; plasma glucose and continuous glucose monitoring; ratio of low‐ to high‐frequency power; glycated hemoglobin, cholesterol, creatinine, plasma, and urinary C‐peptide | Short‐term salt restriction was not associated with significant change in SBP variability. There was a reduction in median SBP (–15 mm Hg, IQR −24 to −13 mm Hg). |
Krupp et al. (Germany)16 | Prospective cohort | N=206 young adults (DONALD study); 52% male; mean age 12 y during data collection at adolescence | Mean follow‐up not reported; study followed participants from infancy to young adulthood (age 18–25 y) |
Boys: 6.7 g salt/d Girls: 6.1 g salt/d |
Three 24‐h urine collections and three 3‐d food records (1 each per annum) | Office BP in young adulthood, using random‐zero or standard mercury sphygmomanometer | Sodium intake was associated with SBP in young adult men only (adjusted β coefficient 0.10 mm Hg per 1 mmol NaCl; 95% CI, 0.03–0.18), and was not associated with DBP. |
Noh et al. (Korea)17 | Cross‐sectional | N=24 096 adults (KNHANES 2007–2012); high BP group: 66.9% male, mean age 49.9 y; normal BP group: 48.1% male, mean age 40.8 y | Cross‐sectional |
High BP group: 2585 mg sodium/1000 kcal Normal BP group: 2563 mg sodium/1000 kcal |
24‐h dietary recall; high‐ and low‐sodium and potassium intake defined as above and below medians | Office BP, using a mercury sphygmomanometer; hypertension prevalence, defined as SBP ≥140 mm Hg or DBP ≥90 mm Hg | Low‐sodium:low‐potassium intake ratio and high‐sodium:low‐potassium intake ratio were associated with increased risk of high BP compared with low‐sodium:high‐potassium intake ratio (adjusted OR, 1.19; 95% CI, 1.01–1.40 and OR, 1.21; 95% CI, 1.02–1.44, respectively). |
Thuesen et al. (Denmark)18 | Cross‐sectional | N=3294 adults (Health 2006 study); 44.8% male; mean age 49.4 y | Cross‐sectional | Total sample: 8.99 g/d of salt | Random spot urine sodium, estimated using the Danish model formula | Office BP and fasting serum lipids | Estimated salt intake was positively associated with BP. Association was attenuated by adjustment for obesity (β 0.58 mm Hg/g salt; 95% CI, 0.20–0.97 for SBP, and 0.25 mm Hg/g salt 95% CI, 0.01–0.49 for DBP). |
Umesawa et al. (Japan)19 | Prospective cohort study | N=889 normotensive adults from Kyowa (CIRCS study); 33% male; mean age 75.3 y | Mean follow‐up: 5.8 y |
Median urine sodium concentration: Quartile 1: 66 mmol/L Quartile 2: 107 mmol/L Quartile 3: 145 mmol/L Quartile 4: 193 mmol/L |
Random spot urine sodium concentration at baseline | BP change from baseline, measured by sphygmomanometer | High urine sodium concentrations were associated with subsequent SBP increases (+7.0 mm Hg in highest quartile; +4.2 mm Hg in lowest quartile, P=.047) in patients with BMI <25, but not overweight patients. |
Wang et al. (China)23 | Meta‐analysis of quasi‐experimental studies and RCTs |
N=3153 from 6 salt‐restriction studies N=3715 from 4 salt‐restriction spoon studies N=1730 from 4 salt‐substitute studies |
Range: 1–8 wk for salt‐restriction studies Range: 3–12 mo for salt‐restriction spoon studies Range: 12–24 mo for salt‐substitute studies |
For salt‐restriction studies: 1.8–7.7 g salt/d For salt‐restriction spoon studies: 5.3–11.2 g salt/d For salt‐substitute studies: 7.0–10.2 g salt/d |
24‐h urine sodium excretion for salt‐restriction studies 24‐h urine sodium or salt weighing for salt‐restriction spoon studies First morning urine collection for salt‐substitute studies |
BP; salt intake |
Salt restriction was associated with 0.94 mm Hg/0.62 mm Hg reduction per 1 g of dietary salt restriction in hypertensive individuals. Use of salt‐restriction spoons with education was associated with a 1.46 g/d reduction in salt intake. Use of salt‐substitute reduced BP (–4.2/–0.6 mm Hg) in hypertensive individuals. |
Yokokawa et al. (Thailand)20 | Cross‐sectional | N=793 adults at high risk for cardiovascular disease (baseline data from RESIP‐CVD study); 51.8% male; mean age 66.5 y | Cross‐sectional |
Total sample: 9.9 g salt/d Low salt intake (<10 g/d salt group): 8.3 g salt/d High salt intake (≥10.0 g/d salt group): 11.9 g salt/d |
Overnight urine sodium (averaged over 3 consecutive d) | BP, measured with oscillometric device; presence of cardiovascular risk factors | Higher salt intake was associated with greater use of antihypertensive medications, family history of hypertension, and less awareness of high salt intake, compared with lower salt intake. |
Kidney disease | |||||||
Liu et al. (China)24 | Meta‐analysis of observational studies | N=5638 from 9 studies (6 prospective, 3 cross‐sectional) | Range: 11 mo to 10 y for prospective studies; N/A for cross‐sectional studies | Only highest category of salt intake was extracted and this was variably reported | Various: food intake questionnaire, 24‐h recall, 24‐h urine sodium | CKD (defined as eGFR <60 mL/min/1.73 m2 or eGFR ≥60 mL/min/1.73 m2 with albuminuria) | Compared with the lowest sodium intake, highest sodium intake level was associated with an increased risk of CKD (pooled relative risk, 1.09; 95% CI, 1.01–1.19). |
Other health outcomes | |||||||
Huh et al. (Korea)21 | Cross‐sectional | N=27 433 from South Korea (KNHANES 2008–2010); 42.9% male; mean age 51.5 y | Cross‐sectional |
Lowest tertile: 6.1 g salt/d Middle tertile: 8.2 g salt/d Highest tertile: 10.8 g salt/d |
Random spot urine sodium, estimated using Tanaka equation |
NAFLD, assessed by HSI and FLI prediction scores; Hepatic fibrosis, assessed by BARD and FIB‐4 score in patients with FLI ≥60 |
High sodium intake was associated with an increased risk of NAFLD (adjusted OR, 1.39; 95% CI, 1.26–1.55 for HSI; OR, 1.75; 95% CI, 1.39–2.20 for FLI). |
Lee et al. (Korea)22 | Cross‐sectional | N=1467 children (KNHANES 2010–2011); 57.4% male; mean age 13.4 y | Cross‐sectional |
Overall: 10.8 g salt/d Boys: 12.0 g salt/d Girls: 9.1 g salt/d |
24‐h dietary recall; UNa/Cr measured by single spot urine |
Overweight/obesity, by BMI; Central adiposity, by waist circumference; % body fat, by dual‐energy x‐ray absorptiometry |
Sodium intake by recall was associated with BMI (OR for obesity 2.79; 95% CI, 1.66–4.68) and central adiposity (OR, 2.14; 95% CI, 1.25–3.67), but not % body fat. UNa/Cr was associated with obesity, central adiposity, and % body fat. |
Abbreviations: ABPM, ambulatory blood pressure monitoring; BMI, body mass index; BP, blood pressure; CIRCS, Circulatory Risk in Communities Study; CKD, chronic kidney disease; CI, confidence interval; DBP, diastolic blood pressure; DONALD, Dortmund Nutritional and Anthropometric Longitudinally Designed Study; FFQ, food frequency questionnaire; FIB‐4, Fibrosis‐4 index; FLI, fatty liver index; eGFR, estimated glomerular filtration rate; HF, heart failure; HR, hazard ratio; HSI, hepatic steatosis index; IQR, interquartile range; KNHANES, Korea National Health and Nutrition Examination Survey; NaCl, sodium chloride; N/A, not applicable; NAFLD, nonalcoholic fatty liver disease; RCT, randomized controlled trial; RESIP‐CVD, Reducing Salt Intake for Prevention of Cardiovascular Diseases in High‐Risk Patients by Advanced Health Education Intervention study; SBP, systolic blood pressure; Shimane CoHRE, Center for the Community‐based Health Research and Education of Shimane University; UNa/Cr, urine sodium‐to‐creatinine ratio; US, United States; 7DACS, 7‐day Ambulatory Blood Pressure Monitoring and Continuous Glucose Monitoring Study.
Unless otherwise stated, units are in g per day of salt (sodium chloride) intake. To convert to mg per day of sodium, multiply by 400. To convert to mmol per day of sodium, multiply by 17.4.