Sodium Intake in Populations: Assessment of Evidence (2013)
Chapter: Appendix F: Presentation of Results - Evidence Tables
Presentation of Results—Evidence Tables
This appendix contains tables summarizing the studies reviewed by the committee organized by health outcome, type of study, and alphabetically by first author. Studies that reviewed multiple health outcomes are listed in more than one table. Some studies included in these tables were not included in the committee’s final review and assessment of the evidence for associations between dietary sodium intake and outcomes discussed in Chapter 4 due to inability to meet the inclusion criteria. As described in Chapter 2, the committee reviewed peer-reviewed original research studies (excluding case studies and case series), published in the English language and published between January 1, 2003, and December 18, 2012, including those conducted in all countries and with all sample sizes, populations, and follow-up periods. Studies were excluded if they included only intermediate outcomes; did not use a food frequency questionnaire, 24-hour recall, dietary diary, or urine analysis methods to estimate dietary sodium intake; did not calculate numerical sodium levels; or did not analyze the independent association between sodium and a health outcome. Studies that reviewed multiple health outcomes are included in more than one table.
LIST OF TABLES
- Table F-1 Evidence Tables: CVD/Stroke/Mortality Randomized Controlled Trials
- Table F-2 Evidence Tables: CVD/Stroke/Mortality Cohort Studies
- Table F-3 Evidence Tables: CVD/Stroke/Mortality Case-Control Studies
- Table F-4 Evidence Tables: Congestive Heart Failure Randomized Controlled Trials
- Table F-5 Evidence Tables: Congestive Heart Failure Cohort Studies
- Table F-6 Evidence Tables: Kidney Disease Cohort Studies
- Table F-7 Evidence Tables: Diabetes Cohort Studies
- Table F-8 Evidence Tables: Metabolic Syndrome and Diabetes Cross-Sectional Studies
- Table F-9 Evidence Tables: Gastrointestinal Cancer Cohort Studies
- Table F-10 Evidence Tables: Gastrointestinal Cancer Case-Control Studies
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TABLE F-1 Evidence Tables: CVD/Stroke/Mortality Randomized Controlled Trials
| Citation | Population Studied |
Study Design | Intervention/ Control |
Sample Size |
| Chang et al., 2006 | Five kitchens at a veterans retirement home, >40 y |
RCT | Intervention K-enriched salt (49 percent sodium chloride, 49 percent potassium chloride) Control Regular salt |
Intervention 768 (mean age: 74.8±7.1 y) Control 1,213 (mean age: 74.9±6.7 y) |
NOTES FOR TABLES F-1 THROUGH F-10
*Indicates significance.
Sodium intake presented as mmol was converted to mg using 23 mg/mmol. ACE, angiotensin-converting enzyme; ACM, all-cause mortality; ADHF, acute decompensated heart failure; amt, amount; ARB, angiotension receptor blockers; ARR, absolute risk reduction; BMI, body mass index; BP, blood pressure; Ca, calcium; CHD, coronary heart disease; CHF, congestive heart failure; CI, confidence interval; CKD, chronic kidney disease; CVD, cardiovascular disease; d, day; dl, deciliter; DM, diabetes mellitus; ESRD, end-stage renal disease; FFQ, food frequency questionnaire; g, grams; h, hour; HDL, high-density-lipoprotein cholesterol; HR, hazard ratio; HSS, hypertonic saline solution; IDNT, Irbesartan Diabetic Nephropathy Trial; IHD, ischemic heart disease; IS, ischemic stroke; K, potassium; Kt/V, measurement of urea removal; L, liter; LDL, low-density-lipoprotein cholesterol; LVEF, left ventricular ejection fraction; mg, milligrams; MI, myocardial
| Sodium Exposure (method and level) |
Co-intervention | Blinding | Follow-up Period |
Health Outcome |
Results |
| Calculated from number of meals served and amount of salt used per day Intervention 3,800 mg Control 5,200 mg Urine electrolyte data available for about 25% of the subjects |
N/A | Single blind (participants) |
2.6 y (length of intervention and mean follow-up) |
ACM CVD mortality |
Use of K-enriched salt associated with significant reduction in CVD mortality; however, may be primarily due to increased K intake Intervention vs. Control ACM HR=0.90, CI: 0.79, 1.06 CVD mortality *Intervention: HR=0.59, CI: 0.37, 0.95 |
infarction; ml, milliliter; mm HG, millimeters mercury; mo, month; Na, sodium; N/A, not applicable; NCI, National Cancer Institute; NHANES, National Health and Nutrition Examination Survey; NS, not significant; NYHA, New York Heart Association; ONTARGET, ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial; OR, odds ratio; Q, quartile/quintile; RAAS, rennin-angiotensin-aldosterone system; RCT, randomized controlled trial; RENAAL, Reduction of Endpoints in NIDDM with the Angiotensiin II Antagonist Losartan Study; RR, relative risk; sat. fat, saturated fat; SD, standard deviation; T, tertile; TOHP, Trials of Hypertension Prevention; TRANSCEND, Telmisartan Randomized AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease; UK, urinary potassium; UNa, urinary sodium; USDA, U.S. Department of Agriculture; vs., versus; wk, week; y, year.
TABLE F-2 Evidence Tables: CVD/Stroke/Mortality Cohort Studies
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| Cohen et al., 2006 |
NHANES II, 30-74 y, without a history of CVD events |
Prospective cohort |
7,154 | 24-h dietary recall of Na intake at baseline Na intake levels ≥2,300 mg/d <2,300 mg/d |
| Cohen et al., 2008 |
NHANES III, ≥30 y, without a history of CVD events |
Prospective cohort |
8,699 | 24-h dietary recall of Na intake at baseline Na intake quartiles (intake level): Q1: <2,060 mg/d (1,501 mg/d) Q2: 2,060-2,921 mg/d (2,483 mg/d) Q3: 2,922-4,047 mg/d (3,441 mg/d) Q4: 4,048-9,946 |
| Cook et al., 2007 |
Subset of 2,415 participants from 2 RCTs: TOHP (United States) 30-54 y with diastolic BP 80-89 mmHg (prehypertensives) TOHP II (United States) 30-54 y with diastolic BP 83-89 mmHg and weighing 110-165% of their desirable weight (prehypertensives) |
Prospective cohort |
TOHP I Intervention: 327 (232 men; 95 women) TOHP I Control: 417 (299 men; 118 women) TOHP II Intervention: 1,191 (784 men; 407 women) TOHP II Control:1,191 (782 men; 409 women) |
TOHP I 24-h urine collection at baseline, 6, 12, and 18 mo. Net Na reduction at 18 mo.=1,012 mg/24 h (3,577 to 2,565 mg/d) TOHP II 24-h urine collection at baseline, 18, and 36 mo. Net Na reduction at 36 mo.=759 mg/24 h (4,225 to 3,466 mg/d) |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results |
| 13.7 y | ACM CVD mortality CHD mortality Cerebrovascular disease mortality |
Age, sex, race, smoking, alcohol use, systolic BP, antihypertensive treatment, BMI, education<high school, physical activity, dietary K, history of diabetes, serum cholesterol, calories |
Lower Na intake associated with increased risk of ACM and CVD mortality For Na intake <2,300 mg/d: ACM *HR=1.28, CI: 1.10, 1.50, p=0.003 CVD mortality *HR=1.37, CI: 1.03, 1.81, p=0.03 CHD mortality HR=1.21, CI: 0.87, 1.68, p=0.25 Cerebrovascular disease mortality HR=1.78, CI: 0.89, 3.55, p=0.10 |
| 8.7±2.3 y | ACM CVD mortality |
Age, sex, race, education, added table salt, exercise, alcohol use, current smoking, history of diabetes, history of cancer, systolic BP, cholesterol, dietary K, weight, treatment of hypertension, calories |
Modest associations between lower Na intake and higher mortality ACM Q1: HR=1.24, CI: 0.91, 1.70 Q2: HR=1.30, CI: 0.96, 1.76 Q3: HR=1.06, CI: 0.81, 1.40 Q4: HR=1.00 p for Q1 vs. Q4=0.17 CVD mortality Q1: HR=1.80, CI: 1.05, 3.08 Q2: HR=1.94, CI: 1.32, 2.85 Q3: HR=1.48, CI: 0.82, 2.67 Q4: HR=1.00 *p for Q1 vs. Q4=0.03 |
| 10-15 y | Total mortality Incident CVD (MI, stroke, revascularization, or death due to CV cause) |
Age, sex, race, trial, clinic, weight loss intervention |
Lower Na excretion associated with reduced mortality and CVD Mortality TOHP I HR=0.81, CI: 0.52, 1.27, p=0.35 CVD *HR=0.75, CI: 0.57, 0.99, p=0.044 |
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| Cook et al., 2009 |
Subset of 2,275 participants from 2 RCTs: TOHP (United States) 30-54 y with diastolic BP 80-89 mmHg (prehypertensives) TOHP II (United States) 30-54 y with diastolic BP 83-89 mmHg and weighing 110-165% of their desirable weight (prehypertensives) |
Prospective cohort |
2,275 | TOHP I 24-h urine collection at baseline, 6, 12, and 18 mo. TOHP II 24-h urine collection at baseline, 18, and 36 mo. Median excretion Overall: 3,634 mg/24 h (interquartile range: 2,921-4,462 mg/24 h) Men: 3,933 mg/24 h Women: 3,082 mg/24 h Na excretion quartiles (not provided) |
| Costa et al., 2012 |
Brasilia Heart Study subjects diagnosed with MI |
Prospective cohort |
372 | 62-item FFQ Na intake quantified using Brazilian Table of Food Composition, version 2 Na intake levels ≥1,200 mg/d=high; <1,200 mg/ d=low |
| Dong et al., 2010 |
Chinese patients receiving peritoneal dialysis at single clinic, mean age=59.4±14.2 y |
Retrospective cohort |
305 (129 men; 176 women) |
3-d dietary records completed by patients and checked by dietitian using food models Na calculated using computer software Na intake tertiles (average intake=1,820 mg/d; range=760-5,530 mg/d) |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results |
| 10-15 y | CVD events | Age, sex, race/ethnicity, clinic, treatment assignment, education status, baseline weight, alcohol use, smoking, exercise, family history of CVD, changes in weight, smoking, exercise | Non-significant, relationship between UNa excretion and risk of CVD Q1: RR=1.0 Q2: RR=0.99, CI: 0.62, 1.58 Q3: RR=1.16, CI: 0.73, 1.84 Q4: RR=1.20, CI: 0.73, 1.97 p for trend=0.38 Adjusted for potassium excretion: *HR=1.42 (0.99-2.04) per 100 mmol/24 hr sodium, p=0.05 |
| 4 y | ACM | Age, sex, hypertension, diabetes, sedentarity, BMI |
Risk of death was higher among individuals with Na intake >1,200 mg/d *Exp(B)=2.857, CI: 1.501, 5.437, p=0.01 |
| 31.4±13.7 mo. | ACM CVD mortality |
Age, sex, BMI, history of DM or CVD, baseline total Kt/V, total creatinine clearance, mean arterial pressure, serum albumin, hemoglobin, Ca χ phosphate, LDL | Lower Na intake associated with increased risk of ACM and CVD mortality ACM *HR=0.44, CI: 0.20, 0.95, p=0.04 CVD mortality *HR=0.11, CI: 0.03, 0.48, p=0.003 |
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| Ekinci et al., 2011 | Patients attending a diabetes clinic in Melbourne, Australia 56% men; mean age= 64 y; median duration of diabetes=11 y; 47% obese |
Prospective cohort | 638 | 24-h urine collection Na excretion tertiles: T1: <3,450 mg/24 h T2: 3,450-4,784 mg/24 h T3: >4,784 mg/24 h |
| Gardener et al., 2012 | Participants from the Northern Manhattan Study (New York), excluding those with stroke and MI (mean age=69 ±10 y, 64% women; 53% Hispanic; 24% African American; 21% white) |
Population-based prospective cohort |
2,657 | Block National Cancer Institute FFQ Na intake calculated using DIETSYS software Na intake examined continuously (500 mg/d unit) and Na intake quartiles Q1: ≤1,500 mg/d Q2: 1,501-2,300 mg/d Q3: 2,301-3,999 mg/d Q4: 4,000-10,000 mg/d |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results |
| 9.9 y (median) | ACM CVD mortality |
Age, sex, duration of diabetes, atrial fibrillation, presence/ severity of CKD | Lower Na excretion associated with increased risk of ACM and CVD mortality ACM *For every 2,300 mg/d rise in 24-h UNa excretion: HR=0.72, CI: 0.55, 0.94, p=0.017 CVD mortality *For every 2,300 mg/d rise in 24-h UNa excretion: sub-HR=0.65, CI: 0.44, 0.94, p=0.026 |
| 10 y (mean) | Vascular death Stroke incidence Stroke, MI, or vascular death MI |
Age, sex, race/ethnicity, high school completion, diet, smoking, physical activity, alcohol consumption, daily energy, protein, fat, sat. fat, carbohydrates consumption | Higher Na intake associated with increased stroke risk Vascular death 500 mg/d increase HR=1.02, CI: 0.95, 1.10 By quartile Q1: HR=1.0 Q2: HR=1.39, CI: 0.95, 2.04 Q3: HR=1.37, CI: 0.91, 22.07 Q4: HR=1.49, CI: 0.82, 2.72 Stroke: 500 mg/d increase *HR=1.17, CI: 1.07, 1.27 By quartile Q1: HR=1.0 Q2: HR=1.33, CI: 0.81, 2.18 Q3: HR=1.31, CI: 0.78, 2.22 *Q4: HR=2.50, CI: 1.23, 5.07 |
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| Gardener et al., 2012 continued | ||||
| Geleijnse et al., 2007 | Randomly selected Dutch Rotterdam Study subjects, >55 y (41% men; mean age=69.2 y) | Population-based prospective cohort |
1,448 | Overnight urine sample UNa excretion concentration standardized from 24-h values using recorded collection times and urinary volumes Analyses per 1 SD increase in UNa excretion |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results |
| Stroke, MI, or vascular death: 500 mg/d increase *HR=1.06, CI: 1.00, 1.12 By quartile Q1: HR=1.0 Q2: HR=1.32, CI: 0.98, 1.78 Q3: HR=1.21, CI: 0.87, 1.67 *Q4: HR=1.70, CI: 1.08, 2.68 MI: 500 mg/d increase HR=0.95, CI: 0.86, 1.04 By quartile Q1: HR=1.0 Q2: HR=0.93, CI: 0.58, 1.51 Q3: HR=0.68, CI: 0.40, 1.15 Q4: HR=0.79, CI: 0.37, 1.69 |
|||
| 5.5 y (median) | ACM CVD mortality Incident MI Incident stroke |
Age, sex, 24-h urinary creatinine excretion, 24-h urinary potassium, BMI, smoking status, DM, use of diuretics, highest completed education, dietary confounders (intake of total energy, alcohol, Ca, sat. fat) | No association between Na intake and mortality UNa excretion not significantly associated with incident MI or stroke ACM HR=0.95, CI: 0.81, 1.12 CVD mortality HR=0.77, CI: 0.60, 1.01 (borderline significant inverse association was reduced when subjects with a history of CVD/ hypertension were excluded) Incident MI HR=1.19, CI: 0.97, 1.46 Incident stroke HR=1.08, CI: 0.80, 1.46 |
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| Heerspink et al., 2012 | Subjects from the RENAAL (250 centers in 28 countries in the Americas, Asia, Australia, and Europe) and IDNT trials (210 centers in the Americas, Europe, Israel, and Australia) (intervention was therapy with angiotensin receptor blockers), 30-70 y, with type 2 diabetic nephropathy, proteinuria (>500 mg/d, RENAAL; >900 mg/d, IDNT), and serum creatinine levels 1.3-3.0 mg/dl (RENAAL) or 1.0-30 mg/dl (IDNT) Randomized to ARB vs. non-RAAS therapy |
Prospective cohort | 1,177 (769 men; 408 women) |
Multiple 24-h urine collections Na intake tertiles based on 24-h Na/creatinine ratios: T1: <2,783 mg/d T2: 2,783-3,519 mg/d T3: >3,519 mg/d |
| Jafar, 2006 Kono et al., 2011 |
Pashtun ethnic subgroup in Pakistan, mean age=51.5 y Japanese with acute IS who met the criteria for emergent admission to an acute hospital, mean age=63.9±9.1 y |
Prospective cohort Prospective cohort |
500 102 (78 men; 24 women) Analysis performed on 89 patients |
FFQ that included a question on use of extra salt on food in addition to salt used in cooking Salt intake measured using a self-monitoring device Urine collected daily for 3 consecutive days for approximately 8 h/d |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results | |
| 30 mo. 4-wk intervals until 3 mo. Then at 3-mo. intervals |
CVD (CVD mortality, MI, stroke, hospitalization for heart failure or revascularization procedure) |
None listed | ARBs were significantly more effective at decreasing CVD when Na intake was in the lowest tertile (<2,783 mg/day) T1: HR=0.63 CI: 0.43, 0.92 T2: HR=1.02, CI: 0.73, 1.43 T3: HR=1.25, CI: 0.89, 1.75 *p for interaction=0.021 |
|
| 1 y | Stroke | Not listed | *OR=3.66, CI: 1.06, 12.60 | |
| 3 y | Recurrence rate for vascular events | Age, medication | Higher salt intake predictive for stroke recurrence *HR=1.98, CI: 1.02, 4.22, p=0.028 |
|
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| Larsson et al., 2008 | Finnish men in the Alpha-Tocopheral, Beta-Carotene Cancer Prevention (ATBC) Study, 50-69 y who smoked ≤5 cigarettes/d at baseline | Prospective cohort | 26,556 | Self-administered 276-item FFQ Nutrient intake calculated using food composition database at the National Public Health Institute Na intake quintiles (median) adjusted for energy intake: Q1: 3,909 mg/d Q2: 4,438 mg/d Q3: 4,810 mg/d Q4: 5,212 mg/d Q5: 5,848 mg/d |
| Nagata et al., 2004 | Nonhospitalized Japanese in Takayama City, Gifu, ≥35 y Exclude people who reported having stroke, IHD, or cancer |
Population-based prospective cohort |
29,079 (13,355 men; 15,724 women) |
Semi-quantitative 169-item FFQ Na intake estimated from Standard Tables of Food Composition in Japan Na intake tertiles: Men: T1: 4,070 mg/d T2: 5,209 mg/d T3: 6,613 mg/d Women: T1: 3,799 mg/d T2: 4,801 mg/d T3: 5,930 mg/d |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results |
| 13.6 y (mean) | Cerebral infarction Intracerebral hemorrhage Subarachnoid hemorrhage |
Age, supplementation group, number of cigarettes/d, BMI, systolic and diastolic BP, serum total cholesterol, serum HDL, history of diabetes, history of CHD, leisure time physical activity, alcohol intake, total energy intake | Na intake not significantly associated with stroke or subarachnoid hemorrhage Cerebral infarction Q1: RR=1.00 Q2: RR=1.08, CI: 0.96, 1.22 Q3: RR=1.05, CI: 0.93, 1.18 Q4: RR=0.99, CI: 0.87, 1.13 Q5: RR=1.04, CI: 0.92, 1.18 p for trend=0.99 Intracerebral hemorrhage Q1: RR=1.00 Q2: RR=0.81, CI: 0.58, 1.13 Q3: RR=0.99, CI: 0.71, 1.37 Q4: RR=1.04, CI: 0.75, 1.44 Q5: RR=1.28, CI: 0.93, 1.75 p for trend=0.06 Subarachnoid hemorrhage Q1: RR=1.00 Q2: RR=0.69, CI: 0.44, 1.08 Q3: RR=0.81, CI: 0.52, 1.24 Q4: RR=0.74, CI: 0.48, 1.16 Q5: RR=0.84, CI: 0.54, 1.30 p for trend=0.55 |
| 7 y | Stroke mortality | Age, level of education, marital status, BMI, smoking status, alcohol consumption, histories of diabetes and hypertension, energy | Increased Na intake associated with increased risk of stroke mortality Men T2: HR=1.60, CI: 0.92, 2.80 T3: HR=2.33, CI: 1.23, 4.45 *p for trend: 0.009 Women T2: HR=1.33, CI: 0.80, 2.21 T3: HR=1.70, CI: 0.96, 3.02 p for trend: 0.07 |
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| O’Donnell et al., 2011 | Participants in the ONTARGET and TRANSCEND trials, at high risk of CVD (with CVD or DM), >55 y (mean age=66.52 y) Recruited from 733 centers in 40 countries Ineligible if they had CHF, low ejection fraction, significant valvular disease, serum creatinine >3.0 mg/L, renal artery stenosis, nephritic range proteinuria, BP >160/100 mmHG |
Follow-up of two RCT cohorts treated with ACE inhibitor or AGII antagonist | 28,880 (20,376 men; 8,504 women) |
Morning fasting urine sample used to estimate 24-h Na excretion using the Kawasaki formula 7 Na excretion levels: 1: <2,000 mg/d 2: 2,000-2,999 mg/d 3: 3,000-3,999 mg/d 4: 4,000-5,999 mg/d 5: 6,000-6,999 mg/d 6: 7,000-8,000 mg/d 7: >8,000 mg/d |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results |
| 56 mo. (median) | ACM CVD mortality Non-CVD mortality Stroke MI CHF hospitalization |
Age, sex, race/ ethnicity, prior stroke or MI, creatinine, BMI, hypertension, DM, atrial fibrillation, smoking, LDL, HDL, treatment allocation (with ramipril, telmitarsan or both, statins, β-blockers, diuretics, Ca antagonist, antithrombotic therapy), fruit and vegetable consumption, level of exercise, UNa and UK excretion, baseline BP, changes in systolic BP from baseline to last follow-up | J-shaped association between Na excretion and CVD mortality Higher Na intake associated with increased risk of stroke, MI, and CHF hospitalization. Lower Na intake associated with increased risk of CHF hospitalization. MCM 1: HR=1.19, CI: 0.99, 1.45 2: HR=1.11, CI: 0.99, 1.26 3: HR=1.06, CI: 0.96, 1.16 4: HR=1.00 *5: HR=1.14, CI: 1.02, 1.28 *6: HR=1.29, CI: 1.10, 1.52 *7: HR=1.56, CI: 1.30, 1.89 CVD mortality *1: HR=1.37, CI: 1.09, 1.73 *2: HR=1.19, CI: 1.02, 1.39 3: HR=1.09, CI: 0.96, 1.23 4: HR=1.00 5: HR=1.11, CI: 0.96, 1.29 *6: HR=1.53, CI: 1.26, 1.86 *7: HR=1.66, CI: 1.31, 2.10 Non-CVD mortality 1: HR=0.92, CI: 0.65, 1.29 2: HR=1.00, CI: 0.83, 1.21 3: HR=1.02, CI: 0.88, 1.18 4: HR=1.00 5: HR=1.18, CI: 0.99, 1.40 6: HR=0.95, CI: 0.71, 1.27 *7: HR=1.42, CI: 1.04, 1.94 Stroke 1: HR=1.06, CI: 0.76, 1.46 2: HR=1.05, CI: 0.86, 1.28 3: HR=0.97, CI: 0.83, 1.13 4: HR=1.00 5: HR=0.95, CI: 0.79, 1.15 6: HR=1.06, CI: 0.81, 1.40 *7: HR=1.48, CI: 1.09, 2.01 MI 1: HR=1.10, CI: 0.80, -1.53 2: HR=1.04, CI: 0.85, 1.27 3: HR=1.11, CI: 0.96, 1.28 4: HR=1.00 *5: HR=1.21, CI: 1.03, 1.43 6: R=1.11, CI: 0.85, 1.44 *7: HR=1.48, CI: 1.11, 1.98 |
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| O’Donnell et al., 2011 continued | ||||
| Stolarz-Skrzypek et al., 2011 | Individuals >20 y invited to participate in 2 studies: (1) Flemish Study on Environment, Genes, and Health Outcome; (2) European Project on Genes in Hypertension | Population-based prospective cohort |
3,681 | 24-h urine collection Na excretion tertiles: T1: 2,461 mg/d T2: 3,864 mg/d T3: 5,980 mg/d |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results |
| CHF hospitalization 1: HR=1.29, CI:0.95, 1.74 *2: HR=1.23, CI: 1.01, 1.49 3: HR=1.07, CI: 0.91, 1.25 4: HR=1.00 5: HR=1.04, CI: 0.79, 1.42 6: HR=1.06, CI: 0.79, 1.42 *7: HR=1.51, CI: 1.12, 2.05 |
|||
| 7.9 y (median) | ACM CVD mortality Noncardiovascular mortality Fatal and nonfatal CVD Fatal and nonfatal coronary Fatal and nonfatal stroke |
Study population, sex, age, BMI, systolic BP, 24-h UK excretion, antihypertensive drug treatment, smoking, alcohol, diabetes, total cholesterol, educational attainment | Lower Na intake associated with higher CVD mortality Na intake not significantly associated with CVD events ACM T1: HR=1.14, CI: 0.87, 1.50 T2: HR=0.94, CI: 0.75, 1.18 T3: HR=1.06, CI: 0.84, 1.33 p for trend=0.10 CVD mortality T1: HR=1.56, CI: 1.02, 2.36 T2: HR=1.05, CI: 0.72, 1.53 T3: HR=0.95, CI: 0.66, 1.38 *p for trend=0.02 Noncardiovascular mortality T1: HR=0.98, CI: 0.71, 1.36 T2: HR=0.90, CI: 0.68, 1.20 T3: HR=1.11, CI: 0.83, 1.47 p for trend=0.64 Fatal and nonfatal CVD T1: HR=1.13, CI: 0.90, 1.42 T2: HR=1.11, CI: 0.90, 1.36 T3: HR=0.90, CI: 0.73, 1.11 p for trend=0.55 Fatal and nonfatal coronary T1: HR=1.42, CI: 0.99, 2.04 T2: HR=1.17, CI: 0.89, 1.54 T3: HR=0.86, CI: 0.65, 1.13 p for trend=0.10 Fatal and nonfatal stroke T1: HR=1.07, CI: 0.57, 2.00 T2: HR=1.29, CI: 0.75, 2.20 T3: HR=0.78, CI: 0.45, 1.33 p for trend=0.64 |
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| Takachi et al., 2010 | Japanese subjects in the two cohorts of the Japan Public Health Center-based Prospective Study 40-59 y (cohort I) and 40-69 y (cohort II) | Prospective cohort | 77,500 (35,730 men; 41,770 women) |
138-item FFQ Na intake calculated using the Standardized Tables of Food Composition, 5th edition revised Validated with 24-h UNa excretion in subsamples Na intake quintiles based on median intake Q1: 3,084 mg/d Q2: 4,005 mg/d Q3: 4,709 mg/d Q4: 5,503 mg/d Q5: 6,844 mg/d |
| Thomas et al., 2011 | Finnish, diagnosed with type 1 diabetes diagnosed before 35 y, without ESRD at baseline Mean age=39 y; median duration of diabetes=20y |
Prospective cohort | 2,807 | Single 24-h urine collection Na excretion tertiles T1: <2,346 mg/d T2: 2,346-4,301 mg/d T3: >4,301 mg/d |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results |
| 10 y (cohort I) 7 y (cohort II) |
CVD Stroke MI |
Sex, age, BMI, smoking status, alcohol consumption, physical activity, quintiles of energy, K, and Ca | Higher Na intake associated with increased risk of CVD, significant increase in stroke, but not MI CVC Q1: HR=1.00 Q2: HR=1.11, CI: 0.96, 1.29 Q3: HR=1.02, CI: 0.87, 1.19 Q4: HR=1.10, CI: 0.94, 1.29 Q5: HR=1.19, CI: 1.01, 1.40 p for trend=0.06 Stroke Q1: HR=1.00 Q2: HR=1.05, CI: 0.90, 1.24 Q3: HR=0.97, CI: 0.82, 1.14 Q4: HR=1.08, CI: 0.92, 1.28 Q5: HR=1.21, CI: 1.01, 1.43 *p for trend=0.03 MI Q1: HR=1.00 Q2: HR=1.50, CI: 1.05, 2.14 Q3: HR=1.34, CI: 0.92, 1.96 Q4: HR=1.26, CI: 0.85, 1.88 Q5: HR=1.09, CI: 0.71, 1.68 p for trend=0.91 |
| 10 y (median) | ACM | Age, sex, duration of diabetes, presence/ severity of CKD, presence of established CVD, systolic BP | UNa excretion significantly associated with ACM (*p<0.001). T1 and T3 had reduced cumulative survival |
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| Tikellis et al., 2013 | Finnish Diabetic Nephropathy Study subjects with type 1 diabetes (onset before 40 y) without prior CVD or ESRD Subpopulation of Thomas et al., 2011 (above) excluding those with prior CVD |
Prospective cohort | 2,648 Subset of 2,807 included in Thomas et al., 2011 (above) |
24-h urine collection at baseline Na excretion quartiles T1: <2,346 mg/d T2: 2,346-4,301 mg/d T3: >4,301 mg/d |
| Umesawa et al., 2008 | Japanese subjects in the Japan Collaborative Study for Evaluation of Cancer Risk, 40-79 y with no history of stroke, CHD, or cancer | Prospective cohort; mortality follow-up on population study | 58,730 (23,119 men; 35,611 women) |
35-item FFQ Responses were *Rarely *1-2 d/mo *1-2 d/wk *3-4 d/wk *Almost every day Based on results of validation study comparing FFQ to four 3-d dietary records for 85 people, intake values calibrated by multiplying by 2 Calibrated Na intake quintiles Q1: 2,323 mg/d Q2: 3,358 mg/d Q3: 4,186 mg/d Q4: 5,060 mg/d Q5: 6,256 mg/d |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results |
| 10 y (median) | ACM CVD |
Parameters associated with daily UNa excretion, age, sex, glycemic control, presence/severity of CKD, lipid levels | After adjustment, UNa excretion significantly associated with increased risk of ACM and incidence CVD event Nonlinear association, individuals with highest and lowest Na excretion had reduced cumulative survival Na excretion not significantly associated with stroke or new coronary event (Rates and p values not provided) |
| 12.7 y (mean) | Total stroke mortality CVD mortality CHD mortality |
Age, sex, BMI, smoking status, alcohol intake, history of hypertension, history of diabetes, menopause, hormone replacement therapy, time spent on sports activities, walking time, educational status, perceived mental stress, Ca intake, K intake (quintiles) | Higher Na intake associated with increased risk of stroke and CVD mortality Stroke mortality Q1: HR=1.00 Q2: HR=0.96, CI: 0.76, 1.22 Q3: HR=1.26, CI: 1.00, 1.59 Q4: HR=1.42, CI: 1.12, 1.80 Q5: HR=1.55, CI: 1.21, 2.00 *p for trend<0.001 CVD mortality Q1: HR=1.00) Q2: HR=1.04, CI: 0.89, 1.22 Q3: HR=1.19, CI: 1.01, 1.39 Q4: HR=1.29, CI: 1.10, 1.52 Q5: HR=1.42, CI: 1.20, 1.69 *p for trend<0.001 CHD mortality Q1: HR=1.00 Q2: HR=0.92, CI: 0.66, 1.28 Q3: HR=1.05, CI: 0.75, 1.46 Q4: HR=1.09, CI: 0.77, 1.54 Q5: HR=1.19, CI: 0.82, 1.73 p for trend=0.230 |
| Citation | Population Studied | Study Design | Sample Size | Sodium Exposure (method and level) |
| Yang et al., 2011 |
NHANES III, 76% <60 y | Prospective cohort | 12,267 (5,899 men; 6,368 women) |
24-h dietary recall of Na intake Na intake quartiles by midvalue of quartile of estimated usual intake in population: Q1: 2,176 mg/d Q2: 3,040 mg/d Q3: 3,864 mg/d Q4: 5,135 mg/d |
| Follow-up Period |
Health Outcome | Confounders Adjusted for |
Results |
| 14.8 y (mean) | ACM CVD mortality IHD mortality |
Sex, race/ethnicity, educational attainment, BMI, smoking status, alcohol intake, total cholesterol, HDL cholesterol, physical activity, family history of CVD, total calorie intake | Higher Na intake associated with increased ACM ACM Q1: HR=1.00 Q2: HR=1.17, CI: 1.13, 1.33 Q3: HR=1.37, CI: 1.28, 1.74 Q4: HR=1.73, CI: 1.54, 2.63 *p for trend=0.02 CVD mortality Q1: HR=1.00 Q2: HR=0.95, CI: 0.71, 1.27 Q3: HR=0.90, CI: 0.51, 1.60 Q4: HR=0.83, CI: 0.31, 2.28 p for trend=0.72 IHD mortality Q1: HR=1.00 Q2: HR=1.17, CI: 0.84-1.62 Q3: HR=1.36, CI: 0.71, 2.58 Q4: HR=1.70, CI: 0.55, 5.27 p for trend=0.36 |
TABLE F-3 Evidence Tables: CVD/Stroke/Mortality Case-Control Studies
| Citation | Population Studied | Study Design | Sample Size (case/control) |
|
| Baune et al., 2005 | Cases: Patients in the Gaza Strip who had been hospitalized for acute stroke and history of hypertension, 40-69 y, 52% men Controls: Patients in the Gaza Strip with hypertension and no history of stroke, 40-69 y, 52% men |
Hospital-based case-control | 112 cases 224 controls |
|
| Sodium Exposure (method and level) |
Health Outcome | Confounders Adjusted for |
Results |
| Questionnaire including 1 question on "excessive use of salt" (yes/no) | Stroke | Age, sex Significant differences in education not controlled for |
Significant association between stroke and excessive use of salt at meals *OR=4.51, CI: 2.059.90, p=0.0002 |
TABLE F-4 Evidence Tables: Congestive Heart Failure Randomized Controlled Trials
| Citation | Population Studied | Intervention/ Control |
Sample Size | Sodium Exposure (method and level) |
| Parrinello et al., 2009 |
Italian decom-pensated CHF patients (NYHA class II), 53-86 y LVEF <35%; Serum creatinine <2 mg/dl; blood urea nitrogen ≤60 mg/dL, urinary volume <500 mL/24 h; low natriuresis (<60 mEq/24 h) |
Intervention 1,840 mg/d Na Control 2,760 mg/d Na |
Intervention 87 (53 men; 34 women) Control 86 (56 men; 30 women) |
Intervention Diets containing 1,840 mg Na Control Intervention group diet + 920 mg/d Na (same amt of sat fat, fruit, etc.) Diaries to record fluid intake and diet variations |
| Paterna et al., 2008 |
Italian compensated CHF patients (NYHA class II to IV), 53-86 y Ejection fraction <35% Serum creatinine <2 mg/dl |
Intervention 1,840 mg/d Na Control 2,760 mg/d Na |
Intervention 114 (71 men; 43 women) Control 118 (73 men; 45 women) |
Intervention Diets containing 1,840 mg Na Control Intervention group diet + 920 mg/d Na (same amt of sat fat, fruit, etc.) Diaries to record fluid intake and diet variations |
| Co-intervention | Blinding | Follow-up Period |
Health Outcome | Result |
| 1,000 ml/d fluid + 125 or 250 mg furosemide twice a day | Double blind | 12 mo Weekly (after 30 d post-discharge) for the first mo, every 2 wks for the next 2 mo, then every mo for the remainder of the study period Length of intervention= 180 d |
Mortality Readmissions for worsening CHF |
Significantly fewer deaths and readmissions in control group MoTtol-ity *ARR=14.2, CI: 5.65, 22.7, p<0.005 Readmissions *ARR=21.2, CI: 10.8, 31.6, p<0.001 |
| 1,000 or 2,000 ml/d fluid + 125 or 250 mg furosemide twice a day | Evaluations by two physicians blinded to the study | Weekly (after 30 d postdischarge) for the first mo, every 2 wks for the next 2 mo, then every mo for the remainder of the study period Length of intervention and follow-up period=180 d |
Mortality Readmission for worsening CHF |
Fewer deaths and readmissions in control MonoUay ARR=8.07%, CI: 0.71, 15.43%, p=NS Readmissions *ARR=18.69%, CI: 9.29, 28.08%, p<0.05 |
| Citation | Population Studied |
Intervention/ Control |
Sample Size | Sodium Exposure (method and level) |
| Paterna et al., 2009 |
Italian compensated CHF patients (NYHA class II to IV), 55-83 y Ejection fraction <35% Serum creatinine <2 mg/dl |
Intervention 1,840 mg/d Na (low) Control 2,760 mg/d Na (normal) |
Intervention 205 (77 men; 128 women) Control: 205 (75 men; 130 women) |
Intervention Diets containing 1,840 mg Na Control Intervention group diet + 920 mg/d Na (same amt of sat fat, fruit, etc.) |
| Paterna et al., 2011 |
Italian compensated CHF patients (NYHA class III to IV), 53-86 y Ejection fraction <40% Serum creatinine <2.5 mg/dl |
Intervention 1,840 mg/d Na Control 2,760 mg/d Na |
1,771 patients, 881 (intervention) and 890 (control) |
Intervention Diets containing 1,840 mg Na Control Intervention group diet + 920 mg/d Na (same amt of sat fat, fruit, etc.) Diaries to record fluid intake and diet variations |
| Co-intervention | Blinding | Follow-up Period |
Health Outcome | Results |
| 1,000 ml/d fluid + 250-500 mg/d furosemide twice a day | Evaluations by two physicians blinded to the study | Weekly (after 30 d post-discharge) for the first mo, every 2 wks for the next 2 mo, then every mo for the remainder of the study period Length of intervention and follow-up period=180 d |
Readmission for worsening CHF | Normal Na diet associated with significantly reduced readmissions *OR=2.46, CI: 1.84, 3.29, p<0.0001 |
| Intervention Furosemide (250 mg) plus HSS (150 ml) twice daily and fluid intake of 1,000 ml/d Control Furosemide (250 mg) twice a day, without HSS and fluid intake of 1,000 ml/d |
Evaluations by two physicians blinded to the study | 57 mo (mean) Treatment in both groups continued during follow-up |
Mortality Hospitalization time Readmission for worsening CHF |
Intervention vs. control Significant reduction in hospitalization time, readmission rates, and mortality Mortality *12.9 vs. 23.8 percent, p<0.0001 Hospitalization time *3.5 vs. 5.5 days, p≤0.0001 Readmissions *18.5 vs. 34.2 percent, p<0.0001 |
TABLE F-5 Evidence Tables: Congestive Heart Failure Cohort Studies
| Citation | Population Studied | Study Design |
Sample Size |
Sodium Exposure (method and level) |
| Arcand et al., 2011 | Canadian medically stable, ambulatory CHF patients from two outpatient clinics, mean age 60±13 y | Prospective cohort | 123 | Two 3-d food records (1st at study entry, 2nd 6-12 wks later) Records analyzed using ESHA Food Processor SQL vs. 10.1 Validated with 2 urine collections in subgroup Na intake tertiles: T1: ≤1,900 mg/d T2: 2,000-2,700 mg/d T3: ≥2,800 mg/d |
| Lennie et al., 2011 | Chronic CHF patients from outpatient clinics in Kentucky, Georgia, Indiana, and Ohio with LVEF <40% or preserved LVEF ≥40%, on stable doses of medication for 3 mo, average age=62±12 y | Prospective cohort | 302 (203 men; 99 women) |
24-h urine collection UNa excretion levels ≥3,000 mg/d <3,000 mg/d |
| Follow-up Period | Health Outcome | Confounders Adjusted for |
Results |
| 3 y (median) | Mortality or transplantation ADHF events All-cause hospitalization |
Age, sex, caloric intake, LVEF, BMI, furosemide use, β-blockers use |
Higher Na intake associated with mortality, ADHF, and all-cause hospitalization Mortality T3 vs. T1 *HR=3.54, CI: 1.46, 8.62, p=0.005 ADHF T3 vs. T1 *HR=2.55, CI: 1.61, 4.04, p<0.001 All-cause hospitalization T3 vs. T1 *HR=1.39, CI: 1.06, 1.83, p=0.018 |
| 12 mo | Event-free survival | Age, sex, CHF etiology, BMI, ejection fraction, total comorbidity score | Higher UNa excretion levels (≥3,000 mg/d) significantly associated with longer event-free survival NYHA class I/II *HR=0.44, CI: 0.20, 0.97, p=0.040 NYHA class III/IV *HR=2.54, CI: 1.10, 5.83, p=0.028 |
TABLE F-6 Evidence Tables: Kidney Disease Cohort Studies
| Citation | Population Studied | Study Design |
Sample Size |
Sodium Exposure (method and level) |
| Heerspink et al., 2012 | Subjects from the RENAAL (250 centers in 28 countries in the Americas, Asia, and Europe) and IDNT trials 209 centers in the Americas, Australia, Europe, and Israel) (intervention was therapy with angiotensin receptor blockers), 30-70 y, with type 2 diabetic nephropathy, proteinuria (>500 mg/d, RENAAL; >900 mg/d, IDNT), and serum creatinine levels 1.3-3.0 mg/dl (RENAAL) or 1.0-30 mg/dl (IDNT) Randomized to ARB vs. non-RAAS therapy |
Prospective cohort | 1,177 (769 men; 408 women) |
Multiple 24-h urine collections Na intake tertiles based on 24-h Na/ creatinine ratios: T1: <2,783 mg/d T2: 2,783-3,519 mg/d T3: ≥3,519 mg/d |
| McCausland et al., 2012 | Hemodialysis Study subjects (United States), mean age=58±14 y, 44% men, 63% African American, 44% diabetic | Post-hoc analysis of a prospective cohort |
1,770 | 2-d diet diary assisted calls Restricted cubic spline, knots at 1,500, 2,000, and 2,500 mg/d Na intake quartiles |
| Follow-upPeriod | Health Outcome | Confounders Adjusted for |
Results |
| 30 mo 4-wk intervals until 3 mo, then at 3-mo intervals |
CKD progression (doubling of serum creatinine or incident ESRD) ESRD |
ARBs were significantly more effective at decreasing CKD progression when Na was in the lowest tertile (<2,783 mg/d) CKD progression T1: HR=0.57 CI: 0.39, 0.84 T2: HR=1.00, CI: 0.70, 1.42 T3: HR=1.37, CI: 0.96, 1.96 *p for interaction<0.001 ESRD T1: HR=0.54 CI: 0.34, 0.86 T2: HR=0.82, CI: 0.54, 1.26 T3: HR=1.35, CI: 0.88, 2.07 *p for interaction=0.005 |
|
| 2.1 y (median) | ACM | Age, sex, race (African American vs. non-African American), Hemodialysis Study Kt/V and flux group assignments, post-dialysis weight, sex-by-weight cross-product term access, CHF status, presence absence of diabetes and IHD | Significant association between higher Na intake and increased risk of death (rates not provided) |
| Citation | Population Studied | Study Design |
Sample Size |
Sodium Exposure |
| Thomas et al., 2011 | Finnish, diagnosed with type 1 diabetes diagnosed before 35 y, without ESRD at baseline Mean age=39 y; median duration of diabetes= 20 y |
Prospective cohort | 2,807 | Single 24-h urine collection Na excretion tertiles T1: <2,346 mg/d T2: 2,346-4,301 mg/d T3: >4,301 mg/d |
TABLE F-7 Evidence Tables: Diabetes Cohort Studies
| Citation | Population Studied |
Study Design |
Sample Size |
Sodium Exposure (method and level) |
| Hu et al., 2005 | Finnish, 35-64 y | Prospective cohort | 1,935 (932 men; 1,003 women) |
Self-administered questionnaire that included questions on *Type of food usually consumed *Amount of food consumed *Frequency of consumption of vegetables, fruit, and sausages 24-h urine collectionyy 24-h UNa excretion quartile cutpoints: Men (in 1982 sample) 3,795 mg/d 4,876 mg/d 6,210 mg/d Men (in 1987 sample) 3,496 mg/d 4,646 mg/d 5,819 mg/d Women (in 1982 sample) 2,806 mg/d 3,657 mg/d 4,600 mg/d Women (in 1987 sample) 2,691 mg/d 3,450 mg/d 4,347 mg/d |
| Follow-up Period |
Health Outcome |
Confounders Adjusted for |
Results |
| 18.1 y (mean) |
Type 2 diabetes incidence |
Age, sex, study year, BMI, physical activity, systolic BP, antihypertensive drug treatment, education, smoking, coffee, alcohol, fruit, vegetable, sausage, bread, and sat. fat consumption | Higher Na intake associated with increased risk of type 2 diabetes Q4 vs. Q1 Q1-Q3: HR=1.00 *Q4: HR=2.05, CI: 1.43, 2.96 |
| Citation | Population Studied |
Study Design |
Sample Size |
Sodium Exposure (method and level) |
| Roy and Janal, 2010 | African Americans in New Jersey with type 1 diabetes Mean ages: men, 26.7 y; women, 27.8 y |
Prospective cohort | 469 | Reduced 60-item FFQ (BRIEF87) of the Health Habits and History Questionnaire developed by NCI; administered by a research assistant Recorded average frequency of consumption and serving sizes; nutrient intakes calculated using DietSys version 3.0 and NCI nutrient databases |
| Follow-up Period |
Health Outcome |
Confounders Adjusted for |
Results |
| 6 y | Macular edema (ME) | Baseline age, sex, glycated hemoglobin level, hypertension, proteinuria, blood cholesterol level, socioeconomic status, physical exercise, calories | Baseline Na intake significantly, positively associated with incidence of ME ME *OR=1.43, CI: 1.10, 1.86, p=0.08 |
TABLE F-8 Evidence Tables: Metabolic Syndrome and Diabetes Cross-Sectional Studies
| Citation | Population Studied | Study Design | Sample Size |
| Daimon et al., 2008 | Japanese subjects in the Takahata study, >35 y | Population-based cross-sectional | 2,956 |
| Rodrigues et al., 2009 | Patients, 25-64 y, who went to the University Hospital in Brazil to undergo clinical and laboratory exams |
Population-based cross-sectional | 1,662 |
| Sodium Exposure (method and level) |
Health Outcome | Confounders Adjusted for |
Results | |
| Brief diet history recall questionnaire to record dietary habits over a 1-month period and measure salt consumption Salt (sodium) intake levels ≥12,440 (5,376) mg/d <12,440 (5,376) mg/d |
Role of genetic polymorphism linked to salt intake in diabetes risk | Age, sex, BMI, serum remnant-like particle cholesterol | Significant association between genetic polymorphism with diabetes in subjects with salt intake <12,440 mg/d (*p=0.032) | |
| 12-h nocturnal urine collection Daily Na intake estimated based on 45% of total daily Na excreted at night |
Metabolic syndrome components (waist circumference, triglycerides level, HDL cholesterol level, glucose level) |
Weight (waist circumference) | No significant association between UNa excretion and metabolic syndrome components when normotensive individuals were stratified by sex and number of metabolic syndrome components (p=0.49 for men, p=0.63 for women) | |
| Citation | Population Studied | Study Design | Sample Size |
| Teramoto et al., 2011 | Participants in the Olmesartan Mega Study to Determine the Relationship between Cardiovascular Endpoints and Blood Pressure Goal Achievement (OMEGA); olmesartan-naïve Japanese adults, 50-79 y diagnosed with hypertension receiving treatment at outpatient clinics | Prospective cohort | 9,585 8,576 at follow-up |
| Sodium Exposure (method and level) |
Health Outcome | Confounders Adjusted for |
Results |
| FFQ, including questions on consumption of high-salt foods Measured as *no intake *1-2/wk *3-5/wk *intake every day Estimated Na intake calculated using formula from Arakawa et al. (2009) Divided into Na intake quartiles (not given) and then 2 score groups *<20 (greater than 75th percentile of intake) *≥20 |
Metabolic syndrome | Age | The highest quartile of Na intake was associated with higher prevalence of metabolic syndrome in men but not in women *p=0.0026 |
TABLE F-9 Evidence Tables: Gastrointestinal Cancer Cohort Studies
| Citation | Population Studied | Study Design |
Sample Size |
Sodium Exposure (method and level) |
| Murata et al., 2010 | Japanese, 40-79 y, without a cancer diagnosis | Population cohort | 6,830 (3,074 men; 3,756 women) |
Self-administered dietary questionnaire to assess usual intake of salted foods (e.g., 1/day, 2-4/week) Classified as "high intake" or "low intake" |
| Follow-up Period |
Health Outcome |
Confounders Adjusted for |
Results |
| 13.9 y | Stomach cancer mortality Rectal cancer mortality Esophageal cancer mortality Colon cancer mortality |
Age, BMI, physical activity, smoking, alcohol, history of diabetes, intake of vegetables, fruit, tea, red meat, processed meat | Higher Na intake associated with increased risk of stomach and rectal cancer in men, but not women High vs. Low intake Stomach cancer *Men: OR=2.05, CI: 1.25, 3.38, p<0.05 Women: OR=1.93, CI: 0.87, 4.88, p=NS Rectal cancer *Men: HR=3.58, CI: 1.08, 11.9, p<0.05 Women: HR=0.40, CI: 0.05, 3.47, p=NS Colon cancer Men: HR=1.43, CI: 0.66, 3.67, P=NS Women: HR=2.21, CI: 0.63, 7.78, p=NS Esophageal cancer Men: HR=1.55, CI: 0.18, 6.39, p=NS Women: HR=1.22, CI: 0.35, 5.43, p=NS |
| Citation | Population Studied | Study Design |
Sample Size |
Sodium Exposure (method and level) |
| Shikata et al., 2006 | Japanese, ≥40 y, with no history of gastrectomy or gastric cancer Mean ages: 57.3 y (men), 58.7 y (women) |
Prospective cohort | 2, 467 (1,023 men; 1,444 women) |
70-item self-administered FFQ over the last year Nutritional intake was calculated using the 4th revision of the Standard Tables of Food Composition in Japan Adjusted for energy intake with Willet and Stamper method Salt (sodium) intake quartiles: Q1: <10,000 (4,000) mg/d Q2: 10,000 (4,000)-12,900 (5,160) mg/d Q3: 13,000 (5,200)-15,900 (6,360) mg/d Q4: ≥16,000 (6,400) mg/d |
| Sjödahl et al., 2008 | Norwegian (mean age at baseline: 49 y) | Population-based, prospective cohort |
73,133 (35,955 men; 37,178 women) |
FFQ: average frequency of dietary intake of salted foods (never or <1/mo, 1-2/mo, up to 1/wk, up to 2/wk, more than 2/wk) with no list of foods to select Assessed frequency of intake of salted foods and sprinkling extra salt on food, and then calculated a summary score of salt intake |
| Follow-up Period |
Health Outcome |
Confounders Adjusted for |
Results |
| 14 y | Gastric cancer | Age, sex, H. pylori infection, atrophic gastritis, medical history of peptic ulcer, family history of cancer, BMI, diabetes, cholesterol, physical activity, alcohol, smoking, intake of total energy, protein, carbohydrate, dietary fiber, and vitamins B1, B2, C |
Positive association between dietary salt and gastric cancer compared to Q1 *Q2: HR=2.12, CI: 1.08, 4.17, p<0.05 Q3: HR=1.88, CI: 0.91, 3.89, NS *Q4: HR=2.67, CI: 1.36, 5.24, p<0.01 Significant association between gastric cancer and atrophic gastritis + H. pylori infection *HR=2.87, CI: 1.14, 7.24, p<0.05 |
| 15.4 y | Gastric adenocarcin- oma |
Age, gender, smoking status, alcohol use, physical activity, occupation level | No statistically significant association between levels of intake of salted foods and risk of gastric adenocarcinoma Intake of salted foods p for trend=0.39 Sprinkling extra salt on food p for trend=0.56 Summary score of salt intake p for trend=0.87 |
| Citation | Population Studied | Study Design |
Sample Size |
Sodium Exposure (method and level) |
| Takachi et al., 2010 | Japanese subjects in the 2 cohorts of the Japan Public Health Center-based Prospective Study 4059 y (cohort I) and 40-69 y (cohort II) | Prospective cohort | 77,500 (35,730 men; 41,770 women) |
138-item FFQ Na intake calculated using the Standardized Tables of Food Composition, 5th edition revised Validated with 24-h UNa excretion in subsamples Na intake quintiles (median): Q1: 3,084 mg/d Q2: 4,005 mg/d Q3: 4,709 mg/d Q4: 5,503 mg/d Q5: 6,844 mg/d |
| Follow-up Period |
Health Outcome |
Confounders Adjusted for |
Results |
| 10 y (cohort I) 7 y (cohort II) |
Total cancer Gastric cancer Colorectal cancer |
Sex, age, BMI, cancer smoking status, alcohol consumption, physical Gastric activity, quintiles of cancer energy, K, and Ca |
Higher Na consumption not associated with increased risk of cancer Total cancer Q1: HR=1.00 Q2: HR=1.02, CI: 0.93, 1.13 Q3: HR=1.07, CI: 0.96, 1.18 Q4: HR=1.01, CI: 0.91, 1.12 Q5: HR=1.04, CI: 0.93, 1.16 p for trend=0.61 Gastric cancer Q1: HR=1.00 Q2: HR=1.05, CI: 0.84, 1.31 Q3: HR=1.06, CI: 0.84, 1.34 Q4: HR=1.05, CI: 0.83, 1.34 Q5: HR=1.07, CI: 0.83, 1.38 p for trend=0.64 Colorectal cancer Q1: HR=1.00 Q2: HR=1.05, CI: 0.84, 1.33 Q3: HR=1.08, CI: 0.85, 1.37 Q4: HR=1.08, CI: 0.84, 1.37 Q5: HR=1.10, CI: 0.85, 1.42 p for trend=0.51 |
| Citation | Population Studied | Study Design |
Sample Size |
Sodium Exposure (method and level) |
| Tsugane et al., 2004 | Japanese, 40-59 y, without a self-reported serious illness (cancer, cerebrovascular disease, MI, chronic liver disease) Individuals were from 14 administrative districts supervised by 4 regional public health centers |
Population-based prospective cohort |
39,065 (18,684 men; 20,381 women) |
Self-administered 27-item FFQ assessing weekly intake Na intake calculated using the Standardized Tables of Food Composition (Science and Technology Agency, 1982) Individuals with extreme energy intakes were excluded (upper and lower 2.5%) Validated with 28-day dietary record Na intake quintiles by median: Q1: 2,900 mg/day Q2: 4,800 mg/day Q3: 6,100 mg/day Q4: 7,500 mg/day Q5: 9,900 mg/day |
| Follow-up Period |
Health Outcome |
Confounders Adjusted for |
Results |
| 12 y | Gastric cancer | Age, smoking, fruit and non-green-yellow vegetable intake | High salted foods were strongly associated with gastric cancer in men Men Q1: RR=1.00 Q2: RR=1.74, CI: 1.14, 2.66 Q3: RR=1.96, CI: 1.30, 2.97 Q4: RR=2.30, CI: 1.53, 3.46 Q5: RR=2.23, CI: 1.48, 3.35 *p for trend<0.001 Women Q1: RR=1.00 Q2: RR=0.86, CI: 0.47, 1.56 Q3: RR=0.96, CI: 0.54, 1.72 Q4: RR=0.58, CI: 0.30, 1.12 Q5: RR=1.32, CI: 0.76, 2.28 p for trend=0.48 Further stratification by study location diminished the association |
| Citation | Population Studied | Study Design |
Sample Size |
Sodium Exposure (method and level) |
| van den Brandt et al., 2003 | Dutch, 55-69 y, excluding those with stomach cancer at baseline | Prospective cohort | 120,852 (58,279 men; 62,573 women) |
Semiquantitative 150-item FFQ (dietary salt intake, salty food intake, added salt) Dietary Na calculated using computerized Dutch food composition table and validated against 9 dietary records Na intake adjusted for energy intake Na intake quintiles by median: Q1: 1,640 mg/d Q2: 2,040 mg/d Q3: 2,280 mg/d Q4: 2,600 mg/d Q5: 3,240 mg/d |
| Follow-up Period |
Health Outcome |
Confounders Adjusted for |
Results |
| 6.3 y | Stomach cancer | Energy, age, sex, education level, self-reported stomach disorders, family history of stomach cancer, smoking status | No relationship between energy-adjusted salt intake quintiles and stomach cancer Q1 vs. Q5 Positive, nonsignificant associations were found for bacon (RR=1.33; CI 1.03, 1.71) and other sliced cold meats (RR=1.29; CI: 0.96, 1.72, p for trend=0.07) |
TABLE F-10 Evidence Tables: Gastrointestinal Cancer Case-Control Studies
| Citation | Population studied | Study Design | Sample Size (case/control) |
| Lazarevic et al., 2011 | Cases: Serbian, 45-85 y, diagnosed with gastric adenocarcinoma Controls: Serbians matched by age, sex, and residence |
Hospital-based case-control | 102 cases 204 controls |
| Lee et al., 2003 | Cases: Korean men and women diagnosed with gastric cancer and without H. pylori infection Controls: Korean men and women |
Hospital-based case-control | 69 cases 199 controls |
| Peleteiro et al., 2011 | Cases: Portuguese, diagnosed with gastric cancer Controls: Portuguese, 18-92 y |
Hospital-based case-control | 422 cases 649 controls |
| Sodium Exposure (method and level) |
Health Outcome | Confounders Adjusted for |
Results |
| 98-item FFQ National food composition tables and USDA food composition tables Na intake tertiles (no ranges or median provided) |
Gastric cancer | Association of Na intake with gastric cancer in men: T2 vs. T1 *OR=4.66, CI: 0.28, 19.96, p=0.000 T3 vs. T1 *OR=6.22, CI: 1.99, 7.86, p=0.000 |
|
| Person-to-person interview conducted using semiquantitative 161-item FFQ No Na intake levels provided; frequency of consumption of various foods Semiquantitative 82 item FFQ T1: <3,067.5 mg/d T2: 3,067.53,960.1 mg/d T3: >,3960.1 mg/d |
Gastric cancer Gastric cancer |
Age, sex, family history, duration of education, smoking, drinking, H. pylori infection Age, sex, education, smoking, H. pylori infection, total energy intake |
Increase in early gastric cancer risk positively and significantly associated with increased intake of salt-fermented fish (*HR=2.4, CI: 1.0, 5.7) and kimchi (*HR=1.9, CI: 1.3, 2.8) Risk of gastric cancer associated with highest salt exposure (T3 vs. T1): *OR=2.01, CI: 1.16, 3.46 |
| Citation | Population studied | Study Design | Sample Size (case/control) |
| Pelucchi et al., 2009 | Cases: Italian men and women, 22-80 y, with confirmed stomach cancer Controls: Italian men and women, 22-80 y, frequency matched by age and sex |
Hospital-based case-control | 230 cases 547 controls |
| Strumylaite et al., 2006 | Cases: Lithuanian with newly diagnosed gastric cancer, 22-86 y Controls: Lithuanian individually matched by gender and age ±5 y |
Hospital-based case-control | 379 cases 1,137 controls |
| Sodium Exposure (method and level) |
Health Outcome | Confounders Adjusted for |
Results |
| 78-item FFQ grouped into 6 sections (milk/hot beverages, bread/ cereal dishes, meat/main dishes, vegetables, fruit, sweets/ desserts/soft drinks) Na intake computed using an Italian food composition database (with other sources when needed) Na intake quartiles (not provided) |
Gastric cancer | Education, period of interview, BMI, smoking, family history of stomach cancer in first-degree relatives, total energy intake | Gastric cancer was associated with Na intake compared to Q1: Q2: OR=2.22, CI: 1.27, 3.88 Q3: OR=2.56, CI: 1.41, 4.63 Q4: OR=2.46, CI: 1.22, 4.95 *p for trend=0.02 |
| Self-administered structured questionnaire about dietary habits (56 diet items) based on the Aichi Cancer Center Questionnaire No Na intake levels provided | Gastric cancer | Smoking, alcohol consumption, family history of cancer, education level, residence, other dietary habits (e.g., speed of eating), other dietary habits, smoking, alcohol consumption, family history of cancer, education level, residence | Increased risk of gastric cancer associated with: Use of additional salt: *OR=2.98, CI: 2.15, 4.15, p for trend<0.001 Liking salty foods: *OR=3.88 CI: 1.98, 7.60, p for trend<0.001 Putting additional salt on prepared meal: *OR=2.98 CI: 2.15, 4.15, p for trend<0.001 |
| Sodium Exposure (method and level) |
Health Outcome | Confounders Adjusted for |
Results |
| 98-item FFQ Daily Na intake calculated by national food composition tables and the USDA food composition tables Na intake tertiles T1: <3,000 mg/d T2: 3,000-5,000 mg/d T3: >5,000 mg/d |
Gastric cancer | Age, sex, education level, smoking, alcohol intake, H. pylori infection |
Na intake was associated with an increased risk of gastric cancer: T1: OR=1.00 T2: OR=1.95, CI: 1.23, 3.03, p=0.012 T3: OR=3.78, CI: 1.74, 5.44, p=0.12 |
