Abstract
In a large international ecological study, comparing urinary sodium excretion and stomach cancer mortality in 39 countries, Joossens et al (1996) concluded that ‘Salt intake, measured as 24-hour urine sodium excretion, is likely the rate-limiting factor of stomach cancer mortality at the population level'. On the basis of human observational and animal experimental data, as well as mechanistic plausibility, the 2003 report from the joint World Health Organization/Food and Agriculture Organization Expert Consultation (WHO/FAO) concluded that salt-preserved food and salt ‘probably' increase the risk of gastric cancer (WHO/FAO, 2003). In fact, there is substantial evidence that the risk of gastric cancer is increased by high intakes of some traditionally preserved salted foods, especially meats and pickles, and with salt per se (Palli, 2000; Tsugane, 2005). The World Cancer Research Fund (WCRF) report (2007) concluded that ‘salt is a probable cause of stomach cancer', and that there is robust evidence for the mechanisms operating in humans. In the UK, the Committee on Medical Aspects of Food Policy (COMA) panel on Dietary Reference Values (Department of Health, 1991) advised that sodium (Na) intakes should be maintained below 3.2 g (or 8.0 g of salt) per day and set the reference nutrient intake (RNI) for men and women at 1.6 g of sodium (or 4.0 g of salt) per day. Following this, COMA's Cardiovascular Review Group recommended that salt intake should be gradually reduced further to a daily average of 6 g (Department of Health, 1994). This recommendation was also accepted in the food and health action plan ‘Choosing a better diet' (Department of Health, 2005). In this section, we consider the population-attributable fraction of stomach cancer associated with an intake of salt >6 g per day.
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