Cappuccio, Francesco PFrancesco PCappuccioSever, Peter SPeter SSever2019-06-272019-10-262019-05-01Journal of Human Hypertension, 2019, 33 (5), pp.345-3480950-9240http://hdl.handle.net/10044/1/70914High salt (salt is sodium chloride – 2.5 g of salt contain 1 g of sodium) intake is a major determinant of blood pressure (BP) in individuals and populations [1]. A reduction of salt intake leads to a reduction in BP and is associated with a reduction in the incidence of cardiovascular disease (CVD) [1,2,3]. However, in the past few years, some epidemiological studies suggested the presence of a J-shaped association between salt (sodium) consumption and CVD [4,5,6,7,8,9]. These results sparked both scientific and media interest and opened a debate on the wisdom of pursuing population-wide salt reduction policies to reduce CVD, as currently recommended by most national and international health organizations, including the World Health Organization (WHO) [10]. Systematic appraisal of these studies identified a variety of pitfalls, suggesting that their results were based on flawed methodologies [11, 12]. The present scientific statement aims to briefly discuss only one such flaw, the use of biased methods of assessing salt consumption, and the consequences of using such biased estimates of exposure (salt intake) when assessing both individual salt intake (for associations with CVD) and population salt consumption (to evaluate population salt reduction programmes).© 2019 Springer-Verlag. The final publication is available at Springer via https://doi.org/10.1038/s41371-019-0203-1.Science & TechnologyLife Sciences & BiomedicinePeripheral Vascular DiseaseCardiovascular System & CardiologyURINARY SODIUM-EXCRETIONPOTASSIUM EXCRETIONCARDIOVASCULAR-DISEASEMORTALITYRISKJournal Articlehttps://www.dx.doi.org/10.1038/s41371-019-0203-11476-5527