Sodium

BACKGROUND

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-ATPase 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 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.