The scientific literature relating sodium intake to blood pressure is extensive and dates back more than 100 years. High blood pressure, or hypertension, means that your blood is pumping harder than normal through your arteries. This condition is a risk factor in many illnesses, such as heart attack and stroke. The risk of stroke rises with every increment of diastolic pressure above 70mmHg. Hypertension is common but often without any noticeable symptoms. This means most people don't even realise they have it. Too much salt in the diet has been linked to high blood pressure. The extent to which sodium restriction lowers blood pressure is generally agreed to depend on age, initial blood pressure and degree of over weight - it is greater with age, in the more overweight and at higher blood pressures. Also, the effect of sodium restriction may not be seen for at least 5 weeks. Sodium restriction may not lower blood pressure further if blood pressure is within the nomal range. The exact mechanism is unclear, but it is thought that the excess salt increases the blood's fluid volume.

It is believed that genetic factors are also involved. About 90 per cent of Australians will experience some rise in blood pressure by the age of 65 to 69. Most doctors recommend a low salt diet if you have high blood pressure; however, the most effective dietary treatment for hypertension is weight loss. A meta-analysis of 56 trials concluded (Midgley et al JAMA 1996; 275: 1590-97) "dietary sodium restriction for older hypertensive individuals might be considered, but the evidence in the normotensive population does not support current recommendations for universal dietary sodium restriction".
This does not mean, however, that the RDI for soidum can be safely ignored.

Much of the genetic predisposition to hypertension seems to reside in renal function. It is usual to lose 50% of functioning nephrons between ages 40-70; declining renal function accelerates the rise in blood pressure with age.  Expansion of the extracellular fluid (ECF) begins at sodium (Na) intakes within the recommended dietary intake of 40-100mmol/d OR <2500mg/day - many Australians have double this amount.

The kidney's work constantly to remove this effect, but constant replenishment of excess salt at every meal keeps the EFC permenantly expanded. The EFC contracts by about 10% (or 1.5 litres of water in a person weighing 70kg) within a few days of adopting a low salt diet.  This is enough to have considerable clinical significance in all conditions associated with oedema, such as idiopathic oedema, premenstrual syndrome, travel oedema, carpel tunnel syndrome and Meniere's syndrome.

Essential hypertension is attributed to an interaction between genetic predisposition and one or more of six main environmental factors:

1. excess body weight 
2. inactivity
3. excess alcohol (causes up to 20% of hypertension in Australia)
4. excess sodium (many Australians have double the recommended intake
5. inadequate potassium, calcium and magnesium
6. psychological factors.

Food Intake, mediterranean diet and olive oil

A study from Greece (Psaltopoulou et al) examined whether the Mediterranean diet, as an entity, and olive oil, in particular, reduce arterial blood pressure. The study was based on the Greek arm of the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Of the Greek participants, 20 343 had never received a diagnosis of hypertension and were included in an analysis in which systolic and diastolic blood pressure were statistically regressed with possible predictors of blood pressure, including a 10-point score that reflects adherence to the Mediterranean diet and, alternatively, the score's individual components and olive oil. The statistical analysis showed that adherence to the Mediterranean diet, and olive oil intake, per se, is associated with lower blood pressure.

Sodium (Na)

Some authors assume that only ‘sodium sensitive’ people need to avoid salt. Salt sensitive persons (perhaps 1 in 2-3 adults) tend to retain excess sodium (above 3000mg daily) instead of excreting it. Such persons are more likely to develop hypertension and would benefit the most from sodium restriction. If there is a family history of hypertension, then that person is probably sensitive to salt – but there is no way of knowing for sure.

If a proportion of the population can safely ignore the RDI for sodium, it is not yet possible to identify sodium sensitive people with certainty. However, analyses of the sodium blood pressure relationship in the 10,079 participants in the Intersalt study, showed that even those without hypertension (n=8344) yielded significant positive associations similar in size to those of the entire cohort, indicating that a measurable degree of sodium sensitivity is widespread, and not restricted to hypertensives. In any case, young people who feel inclined to ignore the RDI should note that there is very good evidence that Na sensitivity increases with age.

Furthermore, data from the US NHANES study has shown that salt intake in the absence of high blood pressure could increase the risk of death from heart disease in people who are overweight. In those who were not overweight, salt intake did not appear to be associated with heart disease risk (He et al. JAMA 1999; 282 (21): 2027-34).

A meta-analysis of 56 trials concluded (Midgley et al JAMA 1996; 275: 1590-97) “dietary Na restriction for older hypertensive individuals might be considered, but the evidence in the normotensive population does not support current recommendations for universal dietary sodium restriction”. It is surprising how many health professionals think this means that the RDI can now be safely ignored.

The RDI is a compromise between what may be ideal and what is likely to be feasible, therefore lowering the RDI is intended to prevent the rise of blood pressure with age. The RDI stands even if it is useless as a treatment for hypertension, or if it fails to reverse any smaller rise that may have occurred with age. Prevention and treatment (reversal) are separate issues, indeed they probably involve different mechanisms.

The RDI for Na is not only cheaper than drugs, it is available in normotensives. About half of all strokes occur at ‘normal’ blood pressure levels where drug treatment is not indicated, and the risk of stroke rises with every increment of diastolic pressure above 70mmHg. It can be extrapolated from epidemiological data that even the most aggressive program of drug treatment for established hypertension would be unable to prevent more than half of the strokes. An essential component of any program for stroke prevention would therefore be the adoption of  the RDI for sodium by the whole population, including normotensives (Beard MJA 1987: 147: 29-38)

Better controlled studies have confirmed that, after a period of drug treatment for hypertension, drugs can often be withdrawn for a variable period. The drug-free period can be prolonged if habitual sodium intake is reduced and this has been confirmed in the elderly as well. A reduction that still leaves people well above the RDI for Na may have no measurable effect, for instance a drop from 165 mmol/d to 115 mmol/d was shown to be ineffective (Morgan et al., Cardiology in the Elderly 1994; 2: 119-25).

Both in experimental animals and humans an increase in urinary sodium excretion causes an obligatory increase in urinary calcium excretion, and the current epidemic of osteoporosis has been attributed partly to the salt content of the Western diet. A high calcium intake would also be expected to reduce this effect, but there is a tendency for calcium absorption to be impaired with advancing age, and this makes the RDI for sodium even more desirable for older Australians than for young people.

Potassium

The RDI for potassium of 50-140 mmol/d exceeds the range for sodium (40-100mmol/d). This seems appropriate because human evolution adapted us to a diet low in sodium and high in potassium (Na:K molar ratio <1). A reversed ratio from an excess of Na is  phylogenetically recent. Potassium the predominant intracellular cation in unsalted foods of both animal and vegetable origin. Apart from silverbeet, celery and a few seafoods which may be contaminated with seawater, most foods are low in sodium.

When the diet has a Na:K molar ratio >1, supplementary potassium reduces blood pressure, but patients whose blood pressure has already responded to a reduction in Na intake to the range of the RDI derive no additional benefit from a potassium supplement.

Rats still have a higher blood pressure at a higher absolute sodium intake, even with enough supplementary potassium to maintain the Na:K ratio.

The optimum Na:K ratio is only speculative at present.  There is no direct evidence that the boundary between danger and safety lies exactly at a ratio of 1.0. Some foods naturally high in sodium with a Na:K ratio >1 includes silverbeet (Na 195mg/100g, K 260mg/100g molar Na/K1.27).

Meanwhile it is hard to escape the conclusion that the minimal goal should be Na;K >=1 (preventing inversion) as currently recommended.  This ratio is arbitrary, but probably a desirable goal.

See also Fact Sheet on Salt

Last Updated: July 2005s