Indirect support for this hypothesis comes from observational studies of Helicobacter pylori infection. Specifically, seropositivity for H. pylori was directly related to gastric cancer mortality (Eurogast Study Group, 1993), and the prevalence of H. pylori has been associated with the intake of salty foods (Tsugane et al., 1994).

Evidence in laboratory animals indicates that high intakes of salt may increase the incidence of gastric cancer when animals are exposed to various carcinogens (Cohen and Roe, 1997). It has been suggested that salt exerts an enhancing effect on both the initiation and promotion steps of gastric carcinogenesis (Takahashi and Hasegawa, 1986). The evidence in humans is less clear because the source of available data is limited to epidemiological studies.

A number of cross-sectional studies have been conducted to evaluate the association between salt intake and risk of gastric cancer. A significant positive association was observed between sodium or salt intake (or sodium excretion) and incidence of gastric cancer in most (Bernstein and Henderson, 1985; Kneller et al., 1992; La Vecchia et al., 1997; Lee et al., 1995; Montes et al., 1985; Palli et al., 2001; Tsubono et al., 1997; Tsugane et al., 1991), but not all (Honjo et al., 1994; Ikeda et al., 1988) of these studies. More recently, the Intersalt study correlated gastric cancer mortality with sodium intake from 24 countries (Joossens et al., 1996). Multiple regression analysis of these data yielded a significant positive correlation (p < 0.001) of urinary sodium excretion with evidence of a threshold. Specifically, there was no increased incidence of cancer mortality below 117 mmol (2.7 g)/day in men and 91 mmol (2.1 g)/day in women. The RR for gastric cancer as determined from case-control studies ranged from 1.4 to 6.7 with higher intakes of salt (Boeing et al., 1991; Coggon et al., 1989; Graham et al., 1990; Hoshiyama and Sasaba, 1992; Lee et al., 1995; Nazario et al., 1993; Tuyns, 1983; You et al., 1988).

In the one available prospective study, salt intake was significantly and directly associated in a dose-response fashion with gastric cancer in men, but not in women (Tsugane et al., 2004).

Data Selection. The model for establishing Tolerable Upper Intake Levels (ULs) (see Chapter 3) depends upon being able to identify a hazard or adverse effect associated with consumption of a nutrient at levels above an individual’s requirement for the nutri-