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Sodium Intake in Populations: Assessment of Evidence (2013)

Chapter: Appendix F: Presentation of Results - Evidence Tables

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Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
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Appendix F

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.

Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
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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

REFERENCES

Arakawa, K., Y. Matsushita, H. Matsuo, N. Ikeda, M. Iwashita, and K. Kuramoto. 2009. Examination of the efficiency of salt taste preference questionnaire in hypertensive patients—Results from post marketing surveillance of Olmetec (R) tablets and Calblock (R) tablets. Rinsho Iyaku 25:723-734.

Arcand, J., J. Ivanov, A. Sasson, V. Floras, A. Al-Hesayen, E. R. Azevedo, S. Mak, J. P. Allard, and G. E. Newton. 2011. A high-sodium diet is associated with acute decompensated heart failure in ambulatory heart failure patients: A prospective follow-up study. American Journal of Clinical Nutrition 93(2):332-337.

Baune, B. T., Y. Aljeesh, and R. Bender. 2005. Factors of non-compliance with the therapeutic regimen among hypertensive men and women: A case-control study to investigate risk factors of stroke. European Journal of Epidemiology 20(5):411-419.

Chang, H. Y., Y. W. Hu, C. S. Yue, Y. W. Wen, W. T. Yeh, L. S. Hsu, S. Y. Tsai, and W. H. Pan. 2006. Effect of potassium-enriched salt on cardiovascular mortality and medical expenses of elderly men. American Journal of Clinical Nutrition 83(6):1289-1296.

Cohen, H. W., S. M. Hailpern, J. Fang, and M. H. Alderman. 2006. Sodium intake and mortality in the NHANES II follow-up study. American Journal of Medicine 119(3):275. e7-275.e14.

Cohen, H. W., S. M. Hailpern, and M. H. Alderman. 2008. Sodium intake and mortality follow-up in the Third National Health and Nutrition Examination Survey (NHANES III). Journal of General Internal Medicine 23(9):1297-1302.

Cook, N. R., J. A. Cutler, E. Obarzanek, J. E. Buring, K. M. Rexrode, S. K. Kumanyika, L. J. Appel, and P. K. Whelton. 2007. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: Observational follow-up of the trials of hypertension prevention (TOHP). British Medical Journal 334(7599):885-888.

Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
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Cook, N. R., E. Obarzanek, J. A. Cutler, J. E. Buring, K. M. Rexrode, S. K. Kumanyika, L. J. Appel, and P. K. Whelton. 2009. Joint effects of sodium and potassium intake on subsequent cardiovascular disease: The trials of hypertension prevention follow-up study. Archives of Internal Medicine 169(1):32-40.

Costa, A. P. R., R. C. S. de Paula, G. F. Carvalho, J. P. Araújo, J. M. Andrade, O. L. R. de Almeida, E. C. de Faria, W. M. Freitas, O. R. Coelho, J. A. F. Ramires, J. C. Quinaglia e Silva, and A. C. Sposito. 2012. High sodium intake adversely affects oxidative-inflammatory response, cardiac remodelling and mortality after myocardial infarction. Atherosclerosis 222(1):284-291.

Daimon, M., H. Sato, S. Sasaki, S. Toriyama, M. Emi, M. Muramatsu, S. C. Hunt, P. N. Hopkins, S. Karasawa, K. Wada, Y. Jimbu, W. Kameda, S. Susa, T. Oizumi, A. Fukao, I. Kubota, S. Kawata, and T. Kato. 2008. Salt consumption-dependent association of the GNB3 gene polymorphism with type 2 DM. Biochemical & Biophysical Research Communications 374(3):576-580.

Dong, J., Y. Li, Z. Yang, and J. Luo. 2010. Low dietary sodium intake increases the death risk in peritoneal dialysis. Clinical Journal of the American Society of Nephrology 5(2):240-247.

Ekinci, E. I., S. Clarke, M. C. Thomas, J. L. Moran, K. Cheong, R. J. MacIsaac, and G. Jerums. 2011. Dietary salt intake and mortality in patients with type 2 diabetes. Diabetes Care 34(3):703-709.

Gardener, H., T. Rundek, C. B. Wright, M. S. V. Elkind, and R. L. Sacco. 2012. Dietary sodium and risk of stroke in the Northern Manhattan Study. Stroke 43(5):1200-1205.

Geleijnse, J. M., J. C. M. Witteman, T. Stijnen, M. W. Kloos, A. Hofman, and D. E. Grobbee. 2007. Sodium and potassium intake and risk of cardiovascular events and all-cause mortality: The Rotterdam Study. European Journal of Epidemiology 22(11):763-770.

Heerspink, H. J. L., F. A. Holtkamp, H. H. Parving, G. J. Navis, J. B. Lewis, E. Ritz, P. A. De Graeff, and D. De Zeeuw. 2012. Moderation of dietary sodium potentiates the renal and cardiovascular protective effects of angiotensin receptor blockers. Kidney International 82(3):330-337.

Hu, G., P. Jousilahti, M. Peltonen, J. Lindstrom, and J. Tuomilehto. 2005. Urinary sodium and potassium excretion and the risk of type 2 diabetes: A prospective study in Finland. Diabetologia 48(8):1477-1483.

Jafar, T. H. 2006. Blood pressure, diabetes, and increased dietary salt associated with stroke— results from a community-based study in Pakistan. Journal of Human Hypertension 20(1):83-85.

Kono, Y., S. Yamada, K. Kamisaka, A. Araki, Y. Fujioka, K. Yasui, Y. Hasegawa, and Y. Koike. 2011. Recurrence risk after noncardioembolic mild ischemic stroke in a Japanese population. Cerebrovascular Diseases 31(4):365-372.

Larsson, S. C., M. J. Virtanen, M. Mars, S. Männistö, P. Pietinen, D. Albanes, and J. Virtamo. 2008. Magnesium, calcium, potassium, and sodium intakes and risk of stroke in male smokers. Archives of Internal Medicine 168(5):459-465.

Lazarević, K., A. Nagorni, D. Bogdanović, N. Rančić, L. Stošić, and S. Milutinović. 2011. Dietary micronutrients and gastric cancer: Hospital based study. Central European Journal of Medicine 6(6):783-787.

Lee, S. A., D. Kang, K. N. Shim, J. W. Choe, W. S. Hong, and H. Choi. 2003. Effect of diet and Helicobacter pylori infection to the risk of early gastric cancer. Journal of Epidemiology 13(3):162-168.

Lennie, T. A., E. K. Song, J. R. Wu, M. L. Chung, S. B. Dunbar, S. J. Pressler, and D. K. Moser. 2011. Three gram sodium intake is associated with longer event-free survival only in patients with advanced heart failure. Journal of Cardiac Failure 17(4):325-330.

Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

McCausland, F. R., S. S. Waikar, and S. M. Brunelli. 2012. Increased dietary sodium is independently associated with greater mortality among prevalent hemodialysis patients. Kidney International 82(2):204-211.

Murata, A., Y. Fujino, T. M. Pham, T. Kubo, T. Mizoue, N. Tokui, S. Matsuda, and T. Yoshimura. 2010. Prospective cohort study evaluating the relationship between salted food intake and gastrointestinal tract cancer mortality in Japan. Asia Pacific Journal of Clinical Nutrition 19(4):564-571.

Nagata, C., N. Takatsuka, N. Shimizu, and H. Shimizu. 2004. Sodium intake and risk of death from stroke in Japanese men and women. Stroke 35(7):1543-1547.

O’Donnell, M. J., S. Yusuf, A. Mente, P. Gao, J. F. Mann, K. Teo, M. McQueen, P. Sleight, A. M. Sharma, A. Dans, J. Probstfield, and R. E. Schmieder. 2011. Urinary sodium and potassium excretion and risk of cardiovascular events. Journal of the American Medical Association 306(20):2229-2238.

Parrinello, G., P. Di Pasquale, G. Licata, D. Torres, M. Giammanco, S. Fasullo, M. Mezzero, and S. Paterna. 2009. Long-term effects of dietary sodium intake on cytokines and neurohormonal activation in patients with recently compensated congestive heart failure. Journal of Cardiac Failure 15(10):864-873.

Paterna, S., P. Gaspare, S. Fasullo, F. M. Sarullo, and P. Di Pasquale. 2008. Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: Is sodium an old enemy or a new friend? Clinical Science 114(3):221-230.

Paterna, S., G. Parrinello, S. Cannizzaro, S. Fasullo, D. Torres, F. M. Sarullo, and P. Di Pasquale. 2009. Medium term effects of different dosage of diuretic, sodium, and fluid administration on neurohormonal and clinical outcome in patients with recently compensated heart failure. American Journal of Cardiology 103(1):93-102.

Paterna, S., S. Fasullo, G. Parrinello, S. Cannizzaro, I. Basile, G. Vitrano, G. Terrazzino, G. Maringhini, F. Ganci, S. Scalzo, F. M. Sarullo, G. Cice, and P. Di Pasquale. 2011. Short-term effects of hypertonic saline solution in acute heart failure and long-term effects of a moderate sodium restriction in patients with compensated heart failure with New York Heart Association class III (class C) (SMAC-HF study). American Journal of the Medical Sciences 342(1):27-37.

Peleteiro, B., C. Lopes, C. Figueiredo, and N. Lunet. 2011. Salt intake and gastric cancer risk according to Helicobacter pylori infection, smoking, tumour site and histological type. British Journal of Cancer 104(1):198-207.

Pelucchi, C., I. Tramacere, P. Bertuccio, A. Tavani, E. Negri, and C. La Vecchia. 2009. Dietary intake of selected micronutrients and gastric cancer risk: An Italian case-control study. Annals of Oncology 20(1):160-165.

Rodrigues, S. L., M. P. Baldo, R. de Sa Cunha, R. V. Andreao, M. Del Carmen Bisi Molina, C. P. Goncalves, E. M. Dantas, and J. G. Mill. 2009. Salt excretion in normotensive individuals with metabolic syndrome: A population-based study. Hypertension Research— Clinical & Experimental 32(10):906-910.

Roy, M. S., and M. N. Janal. 2010. High caloric and sodium intakes as risk factors for progression of retinopathy in type 1 diabetes mellitus. Archives of Ophthalmology 128(1):33-39.

Shikata, K., Y. Kiyohara, M. Kubo, K. Yonemoto, T. Ninomiya, T. Shirota, Y. Tanizaki, Y. Doi, K. Tanaka, Y. Oishi, T. Matsumoto, and M. Iida. 2006. A prospective study of dietary salt intake and gastric cancer incidence in a defined Japanese population: The Hisayama study. International Journal of Cancer 119(1):196-201.

Sjödahl, K., C. Jia, L. Vatten, T. Nilsen, K. Hveem, and J. Lagergren. 2008. Salt and gastric adenocarcinoma: A population-based cohort study in Norway. Cancer Epidemiology Biomarkers and Prevention 17(8):1997-2001.

Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

Stolarz-Skrzypek, K., T. Kuznetsova, L. Thijs, V. Tikhonoff, J. Seidlerová, T. Richart, Y. Jin, A. Olszanecka, S. Malyutina, E. Casiglia, J. Filipovský, K. Kawecka-Jaszcz, Y. Nikitin, and J. A. Staessen. 2011. Fatal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion. Journal of the American Medical Association 305(17):1777-1785.

Strumylaite, L., J. Zickute, J. Dudzevicius, and L. Dregval. 2006. Salt-preserved foods and risk of gastric cancer. Medicina 42(2):164-170.

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Teramoto, T., R. Kawamori, S. Miyazaki, and S. Teramukai. 2011. Sodium intake in men and potassium intake in women determine the prevalence of metabolic syndrome in Japanese hypertensive patients: OMEGA Study. Hypertension Research 34(8):957-962.

Thomas, M. C., J. Moran, C. Forsblom, V. Harjutsalo, L. Thorn, A. Ahola, J. Wadén, N. Tolonen, M. Saraheimo, D. Gordin, and P. H. Groop. 2011. The association between dietary sodium intake, ESRD, and all-cause mortality in patients with type 1 diabetes. Diabetes Care 34(4):861-866.

Tikellis, C., R. J. Pickering, D. Tsorotes, V. Harjutsalo, L. Thorn, A. Ahola, J. Waden, N. Tolonen, M. Saraheimo, D. Gordin, C. Forsblom, P. H. Groop, M. E. Cooper, J. Moran, and M. C. Thomas. 2013. Association of dietary sodium intake with atherogenesis in experimental diabetes and with cardiovascular disease in patients with type 1 diabetes. Clinical Science 124(10):617-626.

Tsugane, S., S. Sasazuki, M. Kobayashi, and S. Sasaki. 2004. Salt and salted food intake and subsequent risk of gastric cancer among middle-aged Japanese men and women. British Journal of Cancer 90(1):128-134.

Umesawa, M., H. Iso, C. Date, A. Yamamoto, H. Toyoshima, Y. Watanabe, S. Kikuchi, A. Koizumi, T. Kondo, Y. Inaba, N. Tanabe, and A. Tamakoshi. 2008. Relations between dietary sodium and potassium intakes and mortality from cardiovascular disease: The Japan Collaborative Cohort study for evaluation of cancer risks. American Journal of Clinical Nutrition 88(1):195-202.

van den Brandt, P. A., A. A. M. Botterweck, and R. A. Goldbohm. 2003. Salt intake, cured meat consumption, refrigerator use and stomach cancer incidence: A prospective cohort study (Netherlands). Cancer Causes and Control 14(5):427-438.

Yang, Q., T. Liu, E. V. Kuklina, W. D. Flanders, Y. Hong, C. Gillespie, M. H. Chang, M. Gwinn, N. Dowling, M. J. Khoury, and F. B. Hu. 2011. Sodium and potassium intake and mortality among US adults: Prospective data from the Third National Health and Nutrition Examination Survey. Archives of Internal Medicine 171(13):1183-1191.

Zhang, Z., and X. Zhang. 2011. Salt taste preference, sodium intake and gastric cancer in China. Asian Pacific Journal of Cancer Prevention 12(5):1207-1210.

Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
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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

Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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.

Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

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)
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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)
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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)
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
Follow-up
Period
Health Outcome Confounders
Adjusted for
Results
10 y (median) ESRD Age, sex, duration of diabetes, presence/severity of CKD, presence of established CVD, systolic BP UNa excretion significantly associated with ESRD (*p<0.001)

T1 had the highest cumulative incidence of ESRD
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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)
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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












Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

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"
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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)
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×

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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
Citation Population studied Study Design Sample Size
(case/control)
Zhang and
Zhang, 2011
Cases: Japanese men and women diagnosed with gastric cancer, 40-75 y

Controls: Japanese men and women, 35-77 y
Population-based case-control 235 cases
410 controls












Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
×
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
Suggested Citation:"Appendix F: Presentation of Results - Evidence Tables." Institute of Medicine. 2013. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press. doi: 10.17226/18311.
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Despite efforts over the past several decades to reduce sodium intake in the United States, adults still consume an average of 3,400 mg of sodium every day. A number of scientific bodies and professional health organizations, including the American Heart Association, the American Medical Association, and the American Public Health Association, support reducing dietary sodium intake. These organizations support a common goal to reduce daily sodium intake to less than 2,300 milligrams and further reduce intake to 1,500 mg among persons who are 51 years of age and older and those of any age who are African-American or have hypertension, diabetes, or chronic kidney disease.

A substantial body of evidence supports these efforts to reduce sodium intake. This evidence links excessive dietary sodium to high blood pressure, a surrogate marker for cardiovascular disease (CVD), stroke, and cardiac-related mortality. However, concerns have been raised that a low sodium intake may adversely affect certain risk factors, including blood lipids and insulin resistance, and thus potentially increase risk of heart disease and stroke. In fact, several recent reports have challenged sodium reduction in the population as a strategy to reduce this risk.

Sodium Intake in Populations recognizes the limitations of the available evidence, and explains that there is no consistent evidence to support an association between sodium intake and either a beneficial or adverse effect on most direct health outcomes other than some CVD outcomes (including stroke and CVD mortality) and all-cause mortality. Some evidence suggested that decreasing sodium intake could possibly reduce the risk of gastric cancer. However, the evidence was too limited to conclude the converse—that higher sodium intake could possibly increase the risk of gastric cancer. Interpreting these findings was particularly challenging because most studies were conducted outside the United States in populations consuming much higher levels of sodium than those consumed in this country. Sodium Intake in Populations is a summary of the findings and conclusions on evidence for associations between sodium intake and risk of CVD-related events and mortality.

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