Commentary: Salt intake, hypertension and risk of cardiovascular disease: an important public health challenge

‘Hence if too much salt is used for food, the pulse hardens ...’ Huang Ti Nei Ching Su Wen, 2698–2598 BC (the Yellow Emperor's classic on internal medicine). Although ancient Chinese medical literature—the Yellow Emperor's classic on internal medicine—reported that a high intake of dietary salt (sodium chloride) might produce a hardened pulse nearly 5000 years ago, the first meaningful scientific evidence for a positive association between salt consumption and level of blood pressure was published by Dahl in 1960.1 Dahl described a remarkable linear relationship between average sodium intake and prevalence of hypertension across five population groups.1 Since then, abundant evidence of a causal association between dietary sodium intake and high blood pressure has emerged from animal experiments and from observational epidemiological studies and randomized controlled clinical trials.2,3 Studies in a variety of laboratory animals have demonstrated that a high dietary intake of salt results in hypertension.4 Recently, Denton et al. reported the findings of a 3-year experiment conducted in 26 chimpanzees with a baseline diet which was very low in sodium and high in potassium content.5 Following a year of baseline observations, salt was added to the diet of 13 animals in increasing amounts (5 g/day for 19 weeks, 10 g/day for 3 weeks, and then 15 g/day for 67 weeks) during an 89-week period of active intervention. Dietary intake of salt remained unaltered in the other 13 control animals. The average level of blood pressure did not change significantly during the intervention phase in the control group. However, in the 13 animals assigned to the active intervention mean systolic blood pressure (SBP) increased by 12 mmHg compared to the corresponding baseline level (P < 0.05) after the first 19 weeks of supplementary salt intake (5 g/day). Following the 39 weeks of supplementation with 10 g/day salt (3 weeks) and 15 g/day salt (36 weeks), mean SBP was increased by 26 mmHg (P < 0.001) and mean diastolic blood pressure (DBP) was increased by 5 mmHg (P > 0.05). Following a further 26 weeks of supplementation with 15 g of salt/day (a total of 84 weeks of supplementation with dietary salt), mean SBP was increased by 33 mmHg (P < 0.001) and DBP was increased by 10 mmHg (P < 0.01). Twenty weeks after the end of the period of salt addition, the animals' average level of blood pressure returned its baseline level. This experiment, conducted in the species that is phylogenetically closest to humans, provides direct evidence in favour of a causal relationship between high salt intake and hypertension.5