Diet and carcinogenesis

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Abstract
Gastric cancer (Gc) is generally conceived as having a multifactorial origin. Different genetic factors, soil, nutritional and socioeconomic factors have all been mentioned in the literature as possible causes. Further research on the causation of Gc has, in fact, been hampered by the large number of hypotheses. A strong geographic association between gastric cancer and stroke mortality was found by chance in 1964; this association could be spurious, but the quantitative analysis of the data showed similar relationships both between countries and within countries (e.g., in countries as different as the US and Japan), a very unlikely situation if due to chance. The same quantitative relationship was maintained using multiple regression analysis of stroke mortality. All this was observed for each sex separately and for both sexes combined. The working hypothesis was set forth in 1965 that salt intake was the predominant linking factor for both types of mortality. Stroke would then be influenced by the relationship between salt and blood pressure; Gc would result from the delaying and caustic properties of a hypertonic stomach content. The latter condition could produce atrophic gastritis, a common problem in Japan, Chile and Columbia. Atrophic gastritis favors the synthesis of endogenous nitrites and, henceforth, of nitroso‐carcinogens. The salt hypothesis can give an explanation for the geographical and time behavior of Gc and stroke mortality and for the socioeconomic gradient of both diseases. Gc mortality can also be used to provide a rough estimate of the salt intake in a given country and year. The salt hypothesis was tested in Belgium through a deliberate attempt to lower the salt intake of the population. The observed decreases in Gc and stroke mortality were consistent with the measured decrease in salt excretion. Further research is urgently needed through the monitoring of 24‐hour salt and creatinine excretion in different countries and over many years.