Abstract
Background: The process by which salt affects the gastric precancerous process has not been adequately studied in humans. Methods: We investigated the effects of salt on gastric inflammation, epithelial damage, the density of Helicobacter pylori infection, and gastric epithelial cell proliferation, all of which may be mediators between salt and gastric precancerous/cancerous lesions. These potential mediators were measured using gastric biopsies as: (a) the density of polymorphonuclear and mononuclear cells (gastric inflammation), (b) mucus depletion (gastric epithelial damage), and (c) the severity of H. pylori infection. Salt intake was measured with spot urine samples (using urinary sodium/creatinine ratios), self-reported frequency of adding salt to food, and as total added salt. Results: The average sodium/creatinine ratio (at baseline and post-treatment at five months) was associated with increased epithelial damage over the 12-year follow-up period among those with a greater severity of chronic inflammation and among those with continued H. pylori infection after treatment at five months. This association was stronger when both severe gastric inflammation and H. pylori infection were present at five months (ß: 1.112, 95% CI: 0.377, 1.848). Conclusion: In humans, salt was associated with an increase in epithelial damage in stomachs with more severe previous H. pylori-induced chronic inflammation.
Highlights
Gastric cancer is the third leading cause of cancer deaths worldwide [1,2]
We investigated the association between salt intake and gastric precancerous progression
We observed that the sodium/creatinine ratio was associated with a small increase in the change in gastric inflammation over the 12-year follow-up period, with a greater change among those infected with H. pylori infection at the five-month follow-up (Table 1)
Summary
There has been a steady decline in the incidence and mortality of gastric cancer since the first half of the 20th century This decline correlated with the increased use of refrigeration and decreased use of traditional methods of food preservation, such as salting [6]. This led researchers to hypothesize that the decline in the incidence and mortality of gastric cancer may have occurred due to a decreased intake of salt-preserved foods and that salt may be involved in the etiology of gastric cancer [6]. Salt intake was measured with spot urine samples (using urinary sodium/creatinine ratios), self-reported frequency of adding salt to food, and as total added salt
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