Summary
High blood pressure is a major cardiovascular risk factor. There is overwhelming evidence that high salt consumption is a major cause of increased blood pressure. There is also a link between high salt consumption and risk of stroke, left ventricular hypertrophy, renal disease, obesity, renal stones and stomach cancer. Reducing salt consumption leads to a decrease in blood pressure and the incidence of cardiovascular disease. There are no deleterious effects associated with reducing salt consumption and it is also very cost-effective. Many organizations and state governments have issued recommendations regarding the suitable amount of salt consumption. In France, the objective is a salt consumption < 8 g/day in men and < 6.5 g/day in women and children. As 80% of consumed salt comes from manufactured products in developed countries, reduction of salt consumption requires the participation of the food industry. The other tool is consumer information and education. Salt consumption has already decreased in France in recent years, but efforts must continue.
Résumé
L’augmentation de la pression artérielle est un facteur de risque cardiovasculaire majeur. Les preuves sont très abondantes d’une relation directe entre consommation de sel et pression artérielle. La consommation de sel est liée aussi au risque d’accident vasculaire cérébral, d’hypertrophie ventriculaire gauche, de maladies rénales, d’obésité, de lithiase rénale et de cancer de l’estomac. La diminution de la consommation de sel est liée à une diminution de la pression artérielle et de l’incidence des maladies cardiovasculaires. Elle n’a pas d’effets délétères. De nombreux pays ont fait des recommandations de diminution de la consommation de sel. En France, l’objectif est une consommation de sel inférieure à 8 g par jour chez les hommes et à 6,5 g par jour chez les femmes et les enfants. Comme, dans les pays occidentaux, 80 % de la consommation de sel provient des produits de l’industrie alimentaire, la réduction de la consommation de sel nécessite la collaboration de celle-ci. L’autre moyen d’action est l’information et l’éducation des consommateurs. La consommation de sel a diminué en France durant ces dernières années, mais les efforts doivent être poursuivis.
Background
For millions of years, terrestrial mammals, including primates, ate very small amounts of salt (0.1–0.5 g/day), as plants contain only trace amounts. Even if a diet includes a large amount of meat, it represents no more than 1–2 g of salt per day. Among the various foods that humans ingest, meat has the highest sodium content (0.6 g of salt per lb). As the average daily consumption of food is 4.7 lb, someone eating only meat would ingest 3.1 g of salt. This is less than the 3.75 g of salt recommended by the American Heart Association. Furthermore, as the average daily consumption of meat is 0.5 lb, the actual amount of salt is much lower. Our ancestors probably ingested far less salt than us. Furthermore, the renin-angiotensin-aldosterone system is very effective at preserving sodium. These two facts suggest that the actual salt requirement is much lower .
Only 5000 years ago, mankind discovered that salt could help to preserve food. Salt thus became highly coveted, acquired an enormous economic value and sovereigns introduced taxes on salt, such as ‘gabelle’ in France. When the refrigerator and the freezer were invented, the need for salt as a preservative vanished, but humans were used to eating salt and the daily amount increased over time, partly because of its use in food seasoning but largely because of highly salted processed foods. The average daily consumption of salt is around 10 g in most countries in the world . Our hunger for salt appears to be growing. In the USA, salt consumption has increased by 55% since the 1970s .
Although the topic is very controversial, there is a huge amount of data supporting the harmful effects of high consumption of salt on health: it increases blood pressure (BP) and thus cardiovascular and renal diseases; it increases the risk of stroke, left ventricular mass and renal diseases independent of its effect on BP; it increases the risk of renal lithiasis, osteoporosis and stomach cancer; and it may also be linked to the severity of asthma .
Salt and sodium are not synonymous. Salt is made up of 60% chloride and 40% sodium. Thus, 1 g of sodium equals 2.5 g of salt. One mmol of sodium equals 23 mg of sodium. For the sake of simplicity, from now on, we will use the term salt.
Salt and blood pressure
‘If too much salt is used for food, the pulse hardens…’ (Huang Ti Nei Ching Su Wen [The Yellow Emperor’s Classic of Internal Medicine], 2698–2598 BC).
A French paper published at the start of the 20th century appears to be the first paper reporting an association between salt consumption and BP in patients with hypertension . Many investigators confirmed this finding, but some did not. A major controversy developed, which is ongoing . There are two main reasons for the controversy. Firstly, about 80% of the salt we consume in developed countries comes from industry-prepared food, so some manufacturers from the salt lobby do not accept the request by many governments and organizations for a reduction in salt consumption; the most active group is the Salt Institute ( www.saltinstitute.org ), a trade organization of salt producers . Secondly, different readers have interpreted the same studies differently ; although some studies are negative, however, the majority support a relationship between salt consumption and BP.
High BP is a major risk factor for coronary heart disease and both forms of stroke (ischaemic and haemorrhagic): 62% of cerebrovascular disease and 49% of ischaemic heart disease are attributable to suboptimal BP (systolic > 115 mmHg) . The risk of cardiovascular disease increases steadily with BP level, from 115/75 mmHg .
Numerous data have shown convincingly that salt consumption is directly associated with BP. The relationship has been studied extensively in animal experimental models, population studies on restricted salt consumption, epidemiological studies, intervention studies in populations, controlled clinical trials and meta-analyses .
BP can be increased by a salt-rich diet in numerous animal species. Fig. 1 shows the effect of progressively increasing salt in the diet of an experimental group of chimpanzees (5 g/day for 19 weeks, 10 g/day for 3 weeks and 15 g/day for 67 weeks) compared with control chimpanzees . BP increased progressively and at the end of the trial it was on average 33/10 mmHg higher in the experimental group. When additional salt was stopped, BP decreased rapidly.
Several studies in primitive societies with no access to salt have shown that BP was lower than in developed societies and that their BP increased when they migrated to more developed environments .
The Intersalt study is a large cross-sectional study in 10,079 individuals aged 20 to 59 years, in 52 population samples from 32 countries, with a large span of salt consumption (0.5 to 15 g/day) . The 24-hour sodium excretion was significantly related to BP and to an increase in BP with age ( Fig. 2 ). An increase in salt consumption of 6 g/day over 30 years would lead to an increase in systolic BP (SBP) of 9 mmHg. Some studies have shown an inverse relationship between urinary sodium and cardiovascular mortality , but many concerns were raised about the design and analysis of the study (possible underestimation of sodium intake in the low-sodium group, possible differential misclassification bias, residual confounding, overadjustment for factors in the causal pathway, loss to follow-up, missing data, lack of adjustment for multiple testing, reverse causality, generalizability of the cohort and relatively small number of events) .
An overview of population studies suggests that a difference in salt consumption of 6 g/day is associated with an average difference in SBP of 5 mmHg at age 15–19 years and 10 mmHg at age 60–69 years . Diastolic blood pressure (DBP) is reduced by about half as much. The association increases with age and with magnitude of initial BP. It was estimated that a universal reduction in salt consumption by 6 g/day would lead to a 50% reduction in the number of people requiring antihypertensive therapy, a 22% reduction in the number of deaths resulting from stroke and a 16% reduction in the number of deaths from coronary heart disease.
Several intervention studies at population level showed that a decrease in salt consumption led to a decrease in BP. Fig. 3 shows a 13/6 mmHg reduction of BP at 2 years in the Portuguese village that reduced its salt consumption by 42% at 1 year and by 47% at 2 years, compared with a similar village that did not change its salt consumption . A population study in China similarly showed a significant reduction in BP in the intervention group .
Numerous randomized trials have been performed. Two trials tested three rather than just two levels of salt consumption . In the Dietary Approaches to Stop Hypertension (DASH) trial, 412 participants were randomly assigned to eat either a control diet typical of the diet in the USA or the DASH diet, which is rich in vegetables, fruits and low-fat dairy products. Within the assigned diet, participants ate foods with high, intermediate and low levels of salt for 30 consecutive days each, in a random order . Fig. 4 shows a clear dose-response relationship between salt consumption and BP, in both the control diet group and the DASH diet group. Reducing salt consumption from 9 to 6 to 3 g/day reduced SBP by 2.1 mmHg and then by 4.6 mmHg during the control diet and by 1.3 mmHg then 1.7 mmHg during the DASH diet. The DASH diet was associated with a significantly lower SBP at each salt consumption level; the difference was greater with high salt consumption levels than with low ones.
More than 15 meta-analyses (!) and overviews of meta-analyses have studied the relationship between salt consumption and BP in clinical trials and epidemiological studies . A reduction in salt consumption by 6 g/day is associated with a reduction in BP by 7/4 mmHg in hypertensives and 4/2 mmHg in normotensives ( Fig. 5 ) .
Clinical trials have also demonstrated the sustainable BP-lowering effects of restriction of salt consumption in infancy as well as in the elderly, in whom it provides a useful non-pharmacological therapy .
The mechanisms by which salt increases BP are not completely elucidated. The kidneys play an important role. The central nervous system, various neurohumoral factors, various vasoactive substances, the extracellular volume and a direct role for plasma sodium may also be involved .