Sodium is a cation needed to maintain extracellular volume and serum osmolality. Approximately 95% of the total sodium content of the body is found in extracellular fluid, being maintained outside the cell via the sodium/potassium-ATPAdenosine triphosphatease pump. Sodium is also important for maintaining the membrane potential of cells and for active transport of molecules across cell membranes. Absorption of sodium and chloride occurs primarily in the small intestine and is approximately 98% efficient across a wide range of intakes.
Sodium is found in most foods as sodium chloride, generally known as 'salt'. It is also present in the diet as sodium bicarbonate and as monosodium glutamate in processed foods. Sodium is also present in other food additives such as sodium phosphate, sodium carbonate and sodium benzoate. Sodium chloride, however, accounts for approximately 90% of the total sodium excreted in countries like Australia and New Zealand (Fregly 1984, Mattes & Donnelly 1991).
In industrialised countries, the majority of ingested sodium chloride is excreted in the urine, provided that sweating is not excessive (Holbrook et al 1984, Pitts 1974). Absorbed sodium and chloride remain in the extracellular compartments that include plasma and interstitial fluid. There are various systems and hormones that influence sodium balance, including the renin-angiotensin-aldosterone hormone system, the sympathetic nervous system, atrial natriuretic peptide, the kallikrein-kinin system, various intrarenal mechanisms, and other factors that regulate renal and medullary blood flow. In sodium and fluid balance, with minimal sweat losses, the amount of sodium excreted in urine roughly equals intake.
The Intersalt Cooperative Research Group (1988) found that the rate of sodium excretion ranges from less than 0.2 mmol of sodium/day in the Yanomamo Indians of Brazil to 242 mmol/day in Tianjin in China (Intersalt Cooperative Research Group 1988). Estimated intakes in Australia are about 150 mmol/day (Beard et al 1997, Notowidjojo & Truswell 1993). An almost identical figure has been found in New Zealand (Thomson & Colls 1998).
There many healthy populations with estimated intakes of less than 40 mmol/day (Intersalt Cooperative Research Group et al 1988). Survival at extremely low levels such as that of the Yanomamo reflects the ability to conserve sodium by reducing urine and sweat losses. With maximal adaptation, the smallest amount of sodium needed to replace losses is estimated to be no more than 0.18 g/day (8 mmol/day). However, a diet providing this level of sodium intake is unlikely to meet other dietary requirements in countries such as Australia and New Zealand.
Physical activity can potentially affect sodium chloride balance, mostly from increased losses in sweat. People who regularly undertake strenuous activity in the heat can lose substantial amounts of sodium. Loss of sodium in sweat is dependent on overall diet, sodium intake, sweating rate, hydration status and degree of acclimatisation to the heat (Allan & Wilson 1971, Allsopp et al 1998, Brouns 1991). Acclimatisation to the heat decreases the amount of sodium lost in sweat (Sawka & Montain 2002). Exposure to heat without exercise also alters the sodium concentration of sweat.
Other factors that can affect sodium needs include the intake of potassium (Liddle et al 1953) and calcium (Breslau et al 1982, Castenmiller et al 1985, McCarron et al 1981). Administration of potassium salts has been shown to increase urinary sodium excretion and a substantial body of evidence has documented that higher intakes of sodium result in increased urinary excretion of calcium
The major adverse effect of increased sodium chloride intake is elevated blood pressure, a risk factor for cardiovascular and renal diseases. Blood pressure increases progressively in a dose-dependent relationship with sodium chloride excretion across the range seen in populations around the world. There has been a number of meta-analyses of the effect of reduction of sodium on diastolic and systolic blood pressure (Cutler et al 1997, Graudal et al 1998, Midgley et al 1996).
The strongest dose-response evidence comes from clinical trials that specifically examined the effects of at least three levels of sodium intake on blood pressure (Bruun et al 1990, Ferri et al 1996, Fuchs et al 1987, Johnson et al 2001, Kirkendall et al 1976, Luft et al 1979, MacGregor et al 1989, Sacks et al 2001, Sullivan et al 1980). The range of sodium intakes in these studies was 10 mmol/day to 1,500 mmol/day. Several trials included sodium intake levels close to 65 mmol/day and 100 mmol/day.
There is a well-recognised heterogeneity in the blood pressure response to changes in sodium chloride intake. People with hypertension, diabetes and chronic kidney disease and greater age tend to be more sensitive to the blood pressure raising effects of sodium chloride intake. Overweight also appears to increase susceptibility as demonstrated by He et al (1999) in a study of 14,407 participants with a 19-year follow up. In this study, relative risks for stroke and cardiovascular mortality were 1.89 and 1.61, respectively, for an increase in sodium intake of 100 mmol. However, the excess mortality was seen in overweight but not normal weight adults. Given the increasing level of overweight in the community, this is of particular importance. Genetic factors also influence the blood pressure response to sodium chloride. Sodium sensitivity is modifiable with the rise in blood pressure, being less on a diet high in potassium. In non-hypertensive individuals, a reduced sodium intake can decrease the risk of developing hypertension
Indicators that have been used for assessing the need for sodium include sodium balance, serum or plasma sodium concentration, plasma renin activity, elevation in blood pressure, blood lipid concentrations and insulin resistance.
1 mmol sodium = 23 mg sodium
1 gram of sodium chloride (salt) contains 390 mg (17 mmol) of sodium
Recommendations by life stage and gender
|0-6 months||120 mg/day||(5.2 mmol)|
|7-12 months||170 mg/day||(7.4 mmol)|
Rationale: The AIAdequate intake for 0-6 months was calculated by multiplying together the average intake of breast milk (0.78 L/day) and the average concentration of sodium of 160 mg/L from the studies of Dewey & Lonnerdal (1983), Gross et al (1980), Keenan et al (1982), Lemons et al (1982), Morriss et al (1986) and Picciano et al (1981). The AIAdequate intake for 7-12 months was extrapolated from that for 0-6 months from a consideration of metabolic body weights and relative energy requirements.
Children & adolescents
|1-3 yr||200-400 mg/day||(9-17 mmol)|
|4-8 yr||300-600 mg/day||(13-26 mmol)|
|9-13 yr||400-800 mg/day||(17-34 mmol)|
|14-18 yr||460-920 mg/day||(20-40 mmol)|
Rationale: There are not enough dose-response data to set an EAREstimated average requirement for children and adolescents, so AIAdequate intakes have been set. There is no reason to expect that the sodium requirement of children ages 1 to 18 years would be fundamentally different from that of adults, given that maturation of kidneys is similar in normal children by 12 months of age (Seikaly & Arant 1992). The AIAdequate intakes for children and adolescents were derived from adult AIAdequate intakes based on relative energy intake.
|Men||460-920 mg/day||(20-40 mmol)|
|Women||460-920 mg/day||(20-40 mmol)|
Rationale: As there are insufficient data from dose-response trials, an EAREstimated average requirement could not be established, and thus a RDIRecommended dietary intake could not be derived. An AIAdequate intake for adults for sodium was set at 460-920 mg/day (20-40 mmol/day) to ensure that basic requirements are met and to allow for adequate intakes of other nutrients. This AIAdequate intake may not apply to highly active individuals, such as endurance athletes or those undertaking highly physical work in hot conditions, who lose large amounts of sweat on a daily basis.
|14-18 yr||460-920 mg/day||(20-40 mmol)|
|19-30 yr||460-920 mg/day||(20-40 mmol)|
|31-50 yr||460-920 mg/day||(20-40 mmol)|
Rationale: During pregnancy there is a small increase in extracellular fluid, but as the AIAdequate intake for women was set generously, there should be no additional requirement in pregnancy.
|14-18 yr||460-920 mg/day||(20-40 mmol)|
|19-30 yr||460-920 mg/day||(20-40 mmol)|
|31-50 yr||460-920 mg/day||(20-40 mmol)|
Rationale: In lactation, there is a small increase in maternal extracellular fluids and some sodium is excreted in breast milk. However, these additional requirements are well within the additional margin added to the adult AIAdequate intake so there are no additional requirements.
Upper Level of Intake
|Age||ULUpper level of intake|
|0-12 months||Not possible to establish. Source of intake should be through breast milk, formula and food only.|
|1-3 yr||1,000 mg/day||(43 mmol)|
|4-8 yr||1,400 mg/day||(60 mmol)|
|9-13 yr||2,000 mg/day||(86 mmol)|
|14-18 yr||2,300 mg/day||(100 mmol)|
|Adults 19+ yr|
|Men||2,300 mg/day||(100 mmol)|
|Women||2,300 mg/day||(100 mmol)|
|All ages||2,300 mg/day||(100 mmol)|
Rationale: The adverse effects of higher levels of sodium intake on blood pressure provide the scientific rationale for setting the ULUpper level of intake. Because the relationship between sodium intake and blood pressure is progressive and continuous, it is difficult to set a ULUpper level of intake precisely. To complicate the analysis, other environmental factors (weight, exercise, potassium intake, overall dietary pattern and alcohol intake) and genetic factors also affect blood pressure. However, there is evidence of a population intake threshold for increased prevalence of hypertension.
For adults, a ULUpper level of intake of 2,300 mg/day (100 mmol/day) is set on the basis of population studies showing low levels of hypertension (less than 2%) and no other observed adverse effects in communities with intakes below this level. The ULUpper level of intake was also based on experimental studies such as the DASHDietary approaches to stop hypertension-sodium trial that showed an additional systolic blood pressure reduction of 4.6 mmHg (p < 0.001) at intakes of 1,500 mg/day (65 mmol/day) compared to 2,500 mg/day (107 mmol/day) in people on the control diet. In this study, decreasing sodium intake by approximately 920 mg/day (40 mmol/day) caused a greater lowering of blood pressure when the starting sodium intake was at the intermediate level than when it was at a higher intake similar to the Australian/New Zealand average of about 6g/day. A NOAELNo observed adverse effect level of 2,300 mg/day (100 mmol) was therefore adopted. However, this NOAELNo observed adverse effect level was adopted in recognition of the fact that the considerable number of older and overweight people in the Australian and New Zealand population who have pre-existing hypertension will derive additional benefit from lowering intakes to 1,600mg/day (70 mmol). This level of 1,600 mg has thus been set as a Suggested Dietary Target for chronic disease prevention in line with WHOWorld Health Organization of the United Nations recommendations (WHOWorld Health Organization of the United Nations 2000) (see also 'Chronic disease' section).
A UF of 1 was applied as, by definition, there is no convincing evidence of harm in the general population at levels of intake of 100 mmol or less. There are no data to suggest increased susceptibility in pregnancy or lactation, so the ULUpper level of intake is set at the same level as for adult women.
For infants, a ULUpper level of intake could not be established because of insufficient data documenting the adverse effects of chronic over-consumption of sodium in this age group. The ULUpper level of intake for children was extrapolated from the adult ULUpper level of intake on an energy intake basis as numerous observational studies have documented that blood pressure tracks with age from childhood into the adult years (Bao et al 1995, Dekkers et al 2002, Gillman et al 1993, Van Lenthe et al 1994).
Allan JR, Wilson CG. Influence of acclimatization on sweat sodium concentration. J Appl Physiol 1971;30:708-12.
Allsopp AJ, Sutherland R, Wood P, Wootton SA. The effect of sodium balance on sweat sodium secretion and plasma aldosterone concentration. EurJ Applied Physiol 1998;78:516-21.
Bao W, Threefoot SA, Srinivasan SR, Berenson GS. Essential hypertension predicted by tracking of elevated blood pressure from childhood to adulthood; the Bogalusa heart study. Am J Hypertens 1995;8:657-65.
Beard TC, Woodward DR, Ball P, Hornsby H, von Witt RJ, Dwyer T. The Hobart salt study 1995: few meet national sodium intake data. Med J Aust 1997;166:404-7.
Breslau NA, McGuire JL, Zerwekh JE, Pak CYC. The role of dietary sodium on renal excretion and intestinal absorption of calcium and on vitamin D metabolism. J Clin Endocrinol Metab 1982;55:369-73.
Brouns F. Heat-sweat-dehydration-rehydration: A praxis oriented approach. J Sports Sci 1991; 9:143-52.
Bruun NE, Skott P, Nielsen MD, Rasmussen S, Schutten HJ, Leth A, Pedersen
Giese J. Normal renal tubular response to changes of sodium intake in hypertensive man. J Hypertens 1990;8:219-27.
Castenmiller JJM, Mensink RP, van der Heijden L, Kouwenhoven T, Hautvast J, de Leeuw PW, Schaafsma G. The effect of dietary sodium on urinary calcium and potassium excretion in normotensive men with different calcium intakes. Am J Clin Nutr 1985;41:52-60.
Cutler JA, Follmann D, Allender PS. Randomised trials of sodium reduction: an overview. Am J Clin Nutr 1997:65:643S-651S.
Dekkers DC, Sneider H, Van Den Oord EJ, Treiber FA. Moderators of blood pressure development from childhood to adulthood: a 10-year longitudinal study. J Pediatr 2002;141:770-9.
Dewey KG, Lonnerdal B. Milk and nutrient intake of breast-fed infants from 1 to 6 months: Relation to growth and fatness. J Pediatr Gastroenterol Nutr 1983;2:497-506.
Ferri C, Bellini C, Carlomagno A, Desideri G, Santucci A. Active kallikrein response to changes in sodium-chloride intake in essential hypertensive patients. J Am Soc Nephrol 1996;7:443-53.
Fregly MJ. Sodium and Potassium. In: Nutrition Reviews' Present Knowledge in Nutrition, 5th ed. Washington, DC: The Nutrition Foundation, 1984. Pp 439-58.
Fuchs FD, Wannmacher CM, Wannmacher L, Guimaraes FS, Rosito GA, Gastaldo G, Hoeffel CP, Wagner EM. Effect of sodium intake on blood pressure, serum levels and renal excretion of sodium and potassium in normotensives with and without familial predisposition to hypertension. Brazilian J Med Biol Res 1987;20:25-34.
Gillman MW, Cook NR, Rosner B, Evans DA, Keough ME, Taylor JO, Hennekens CH. Identifying children at high risk for the development of essential hypertension. J Pediatr 1993;122:837-46.
Graudal NA, Galloe AM, Garred P. Effects of sodium restriction on blood pressure, renin, aldosterone, catecholamines, cholesterols and triglyceride: a meta-analysis. JAMA 1998;279:1383-91.
Gross SJ, David RJ, Bauman L, Tomarelli RM. Nutritional composition of milk produced by mothers delivering preterm. J Pediatr 1980;96:641-4.
He J, Ogden LG, Vupputuri S, Bazzano LALinoleic acid, Loria C, Whelton PK. Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults. JAMA 1999;282:2027-34.
Holbrook JT, Patterson KY, Bodner JE, Douglas LW, Veillon C, Kelsay JL, Mertz W, Smith JC. Sodium and potassium intake and balance in adults consuming self-selected diets. Am J Clin Nutr 1984;40:786-93.
Intersalt Cooperative Research Group. Intersalt: An international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Br Med J 1988; 297:319-28.
Keenan BS, Buzek SW, Garza C, Potts E, Nichols BL. Diurnal and longitudinal variations in human milk sodium and potassium: Implication for nutrition and physiology. Am J Clin Nutr 1982;35:527-34.
Kirkendall WM, Conner EW, Abboud F, Rastogi SP, Anderson TA, Fry M. The effect of dietary sodium chloride on blood pressure, body fluids, electrolytes, renal function, and serum lipids of normotensive man. J Lab Clin Med 1976;87:418-34.
Lemons JA, Moye L, Hall D, Simmons M. Differences in the composition of preterm and term human milk during early lactation. Pediatr Res 1982;16:113-7.
Liddle GW, Bennett LL, Forsham D. The prevention of ACTH-induced sodium retention by the use of potassium salts: A quantitative study. J Clin Invest 1953; 32:1197-207.
Luft FC, Rankin LI, Bloch R, Grim CE, Weyman AE, Murray RH, Weinberger MH. Plasma and urinary norepinephrine values at extremes of sodium intake in normal man. Hypertension 1979;1:261-6.
Mattes RD, Donnelly D. Relative contributions of dietary sodium sources. J Am Coll Nutr 1991;10:383-93.
McCarron DA, Rankin LI, Bennett WM, Krutzik S, McClung MR, Luft F. Urinary calcium excretion at extremes of sodium intake in normal man. Am J Nephrol 1981;1:84-90.
MacGregor GA, Markandu ND, Sagnella GA, Singer DRJ, Cappuccio FP. Double-blind study of three sodium intakes and long-term effects of sodium restriction in essential hypertension. Lancet 1989; 2:1244-7.
Midgely JP, Matthew AG, Greenwood CMT, Logan AG. Effects of reduced dietary sodium
on blood pressure: a metaanalysis of randomised control trials. JAMA 1996:275:
Morriss FH, Brewer ED, Spedale SB, Riddle L, Temple DM, Caprioli RM, West, MS. Relationship of human milk pH during course of lactation to concentrations of citrate and fatty acids. Pediatrics 1986;78:458-64.
Notowidjojo L, Truswell AS. Urinary sodium and potassium in a sample of healthy adults in Sydney, Australia. Asia Pac J Clin Nutr 1993;2:25-33.
Picciano MF, Calkins EJ, Garrick JR, Deering RH. Milk and mineral intakes of breastfed infants. Acta Paediatr Scand 1981;70:189-94.
Pitts RF. Physiology of the Kidney and Body Fluids. 3rd ed. Chicago, IL: Year Book Medical Publishers Inc, 1974.
Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, ObarzanekE, Conlin PR, Miller ER, Simons-Morton DG, Karanja N, Lin PH. Effects of blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASHDietary approaches to stop hypertension) diet. N Engl J Med 2001:344:3-10.
Sawka MN, Montain SJ. Fluid and electrolyte balance: Effects on thermoregulation and exercise in the heat. In: Bowman BA, Russell RM, eds. Present Knowledge in Nutrition, Eighth Edition. Washington, DC: ILSI Press, 2001. Pp 115-24.
Seikaly MG, Arant BS. Development of renal hemodynamics: Glomerular filtration and renal blood flow. Clin Perinatol 1992;19:1-13.
Sullivan JM, Ratts TE, Taylor JC, Kraus DH, Barton BR, Patrick DR, Reed SW. Hemodynamic effects of dietary sodium in man. Hypertension 1980;2:506-14.
Thomson CD, Colls AJ. Twenty-four hour urinary sodium excretion in seven hundred residents of Otago and Waikato. A report prepared for the Ministry of Health. Dunedin: University of Otago, 1998.
Van Lenthe FJ, Kemper HCG, Twisk JWR. Tracking of blood pressure in children and youth. Am J Hum Biol 1994;6:389-99.