SODIUM

Function and Essentiality Sodium (Na) is the principal cation in extracellular fluid where it exists in its ionised state. Its physiological roles include the maintenance of (i) extracellular fluid (ECF) volume which is closely related to total body Na content, (ii) extracellular fluid oncotic pressure, (iii) acid base balance, (iv) electrophysiological phenomena in muscle and nerves and (v) the generation of transmembrane gradients which enable the energy dependent uptake of nutrients (eg amino acids and hexoses) by cells including those of the intestinal mucosa and renal tubules.


Metabolism

An adult male weighing 65 to 70 kg has a total body Na of 4 mol (92 g); of this 500 mmol (11.5 g) is in the intracellular fluid at an activity concentration of 2 mmol/L (46 mg/L), 1500 mmol (34.5 g) is sequestered in bone and 2,000 mmol (46 g) is in the ECF. Intestinal Na absorption is virtually complete and occurs in the distal small intestine and colon. Its concentration in the ECF of 135-145 mmol/L (3.1-3.3 g/L) is maintained by renal excretion and conservation. The kidneys filter 25 mol (575 g) of Na daily; since daily dietary intakes (50-200 mmol; 1.15-4.6 g) approximate only 0.2-0.8 per cent of this amount, almost all of this filtered Na needs to be reabsorbed. Renal Na reabsorption is highly efficient and adaptable. In pregnancy the glomerular filtration rate and the corresponding filtered load of Na can be doubled.

Regulation of the Na content of ECF is closely related to the systemic control of ECF volume. If the body Na burden is increased, water is also retained and the ECF volume increases; conversely, if the body Na burden falls the ECF volume decreases. Regulation of these changes in ECF volume is mediated by sensors of pressure and distension which are located in the cardiac atria and right ventricle, the pulmonary vasculature, the carotid arteries and the aortic arch. The nerve pathways from these sensors end in the medulla and hypothalamus of the brain. When ECF or blood volume falls retention is stimulated, sympathetic activity increases, stimulation of nerves supplying the afferent renal arterioles induces vasoconstriction, and a redistribution of renal blood flow which by reducing gomerular filtration increases Na and water retention. Additionally stimulation of nerves to the juxtaglomerular apparatus increases renin production leading to an increase in circulating angiotensin II, adrenal medullary secretion of noradrenalin and adrenaline and pituitary release of adrenocorticotrophin (ACTH) and antidiuretic hormone (ADH). ACTH and angiotension 11 induce adrenal cortical secretion of aldosterone and other mineralocorticoids which stimulate Na retention and potassium loss by the kidneys and distal bowel. Increased secretion of ADH promotes water reabsorption from the renal distal tubules.

Several factors increase renal Na excretion. These natriuretic factors include a specific natriuretic hormone, and vasodilators, parathormone, pros- taglandins and kinins. Some of these may act on the renal vasculature, others may have direct effects on renal tubular reabsorption; atrial natriuretic polypeptide may affect both processes.

In infants and old people Na and fluid homeostasis are less efficient. Neonates are less able to conserve Na than are adults, and the ECF volume does not reach the adult proportion of body weight until about one year of age. Glomerular filtration in children is less variable then in adults, but tubular Na reabsorption is as efficient. Thus although children's ability to excrete excessive Na loads is limited, they are able to respond to deprivation by reducing urinary Na loss almost to zero. In the elderly the onset of renal responses to altered Na intakes, in particular reduced intakes, is slow although such adaptation is ultimately achieved. Since the elderly may be on inadvertently or thera- peutically restricted Na intakes they may become Na depleted, and thus susceptible to anorexia and confusion which could further compromise their general nutrient intake thereby creating a disadvantageous cycle.


Requirements

Healthy adults maintain balance on intakes as low as 3-20 mmol/d (69-460 mg/d) (1,2) and some healthy populations have daily intakes of less than 40 mmol (920 Mg) (3,4). The role of higher Na intakes in the pathogenesis of hypertension has generated much interest, but the evidence supporting this or indicating the relative importance of Na intakes is unclear (5). High body mass index (BMI) (obesity), alcohol and smoking are important contributory factors to the development of hypertension (4). In adolescents obesity may increase the sensitivity of blood pressure to dietary Na intake (6). The lower Na intakes of 'less developed communities' with lower blood pressure than those seen in developed societies with increased incidences of hypertension may reflect different lifestyles rather than a causal relationship between Na intake and increased blood pressure, although more recent evidence is in favour of the latter (7).

After BMI and alcohol consumption have been allowed for, a relationship does exist between urinary Na excretion (assumed to be a marker of intake) and increasing blood pressure with age (4). However this correlation was not as strong as that found either between urinary potassium (K) excretion or urinary Na:K excretion ratios with increasing blood pressure. Although restricted Na intakes reduce blood pressure in individuals with established hypertension, they do not do so reliably in those with normal blood pressure. It has been calculated that a reduction of daily Na intake from 170 mmol to 70 mmol (3.9 to 1.6 g) might reduce systolic blood pressure by 2.2 mm Hg and diastolic pressure by 0.1 mm Hg, but recent evidence suggests this may be a considerable underestimate (7). The Panel accepted the possibility that public health benefits such as reduced cardiovascular disease mortality might arise from such a change, but other interventions such as reduction of obesity, increased potassium, reduced energy intakes, altered quantity and quality of fat intake and reduced alcohol consumption may also have at least as great an impact on such diseases. The Panel cautioned against any trend towards increase Na inta es. The Panel further agreed that current Na intakes were needlessly high, and decided to set DRVs on the basis of the balance of risks and benefits which might practically be expected to occur, given the prevailing socio-cultural environment.

The determination of a potentially toxic threshold for Na intake is also difficult. The possibility of a genetic susceptibility to Na related hypertension in perhaps 10 per cent of the population is of some concern. This association with elevated diastolic and systolic blood pressures may be apparent at intakes of 140-205 mmol/d (3.2-4.7 g/d).

Adults On these bases it is not possible to derive an EAR for Na but the Panel suggests that the LRNI for adults is set at 25 mmol/d (575 mg/d) with an RNI of 70 mmol/d (1600 mg). The Panel were unable to offer guidance on high consumption though noted that usual intakes are in excess of 140 mmol/d (3.22 g/d). The Panel saw no physiological advantage in exceeding this intake and considered that it would not be appropriate to increase these intakes further.

Infants and children The LRNIs have been estimated by calculating the daily increments in total body Na content (140 mmol/L of ECF and 2 mmol/L of intracellular fluid) allowing for the declining proportion with age of ECF in body masS (8) with an allowance for dermal, faecal and some urinary losses. The LRNI in infants up to 6 months approximates to calculated intakes for breastfed infants in whom, on the basis of 850 ml milk consumed daily and a Na content of 7 mmol/L, intakes up to 3 months of age are 1.4 mmol/kg/d and 0.9 mmol/kg/d at 4-6 months of age.

Environmental effects Sodium requirements may be increased with unaccustomed hard exercise or exposure to high ambient temperatures. In such circumstances daily sweat losses may increase acutely from 2-4 mmol (46-92 mg) to 350 mmol (8.0 g). However adaptation provides a more dilute sweat resulting in a daily loss of 30 mmol (690 mg), and a need for a continuing intake above the range proposed is not established, although in the short term additional Na (salt) may be required.

Intakes Daily Na intakes are 2-10 g (90-440 mmol). In the UK mean daily urinary Na excretion has been estimated as 187 mmol (4.3 g) and 131 mmol (3.0 g) in men and women respectively with a urinary Na/K ratio of more than two (9). In the Dietary and Nutritional Survey of British Adults mean Na intakes, excluding discretionary salt, were 3,376 and 2,351 mg/d (147 and 102 mmol/d) in men and women respectively, while mean 24 hour urinary excretion was 173 mmol (3979 mg) and 132 mmol (3036 mg) respectively (1O). A wide range of daily urinary Na excretion of 18-150 mg (0.8-6.6 mmol) has been noted in normal children.


References


1 Simpson F 0. Sodium intake, body sodium and sodium excretion. Lancet 1988; 2: 25-28.

2 Luft F C. Sodium, chloride and potassium. In: Brown M, ed. Present Knowledge in Nutrition 6th Ed. Washington DC: International Life Sciences Institute Nutrition Foundation, 1990; 233-240.

3 GIieberman L. Blood pressure and dietary salt in human populations. Ecol Fd Nutr 1973; 2: 143-156.

4 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: 319-328.

5 Swales J D. Salt saga continued. Br Med J 1988; 297: 307-308.

6 Rocchini A P, Key J, Bondie D et al. The effect of weight loss on the sensitivity of blood pressure to sodium in obese adolescents. New Engl J Med 1989; 321: 580-585.

7 Law M R, Frost C D, Wald N J. By how much does dietary salt reduction lower blood pressure? Br Med J 1991; 302: 811-815, 815-818, 819-824.

8 Friis-Hanson B. Body weight compartments in children: changes during growth and related changes in body composition. Pediat 1961; 28: 169-181.

9 Sanchez-Castillo C P, Warrender S, Whitehead T P, James W P T. An assessment of the sources of dietary salt in a British population. Clin Sci 1987; 72: 95-102.

10 Gregory J, Foster K, Tyler H, Wiseman M. The Dietary and Nutritional Survey of British Adults. London: HMSO, 1990.