Association between Dietary Salt Intake and Progression in the Gastric Precancerous Process

Abstract

Gastric cancer is the third leading cause of cancer mortality worldwide. Studies investigating the effect of salt on gastric cancer have mainly used self-reported measures, which are not as accurate as sodium/creatinine ratios because individuals may not know the amount of salt in their food. Using data from a prospective cohort study, we investigated the effect of salt intake on progression to gastric precancerous lesions. Salt intake was estimated by urinary sodium/creatinine ratios, self-reported frequencies of adding salt to food, and total added table salt. We repeated the analyses among groups with and without Helicobacter pylori infection. We did not observe a positive association between salt intake, measured by urinary sodium/creatinine ratio, and overall progression in the gastric precancerous process (adjusted risk ratio (RR): 0.94; 95% confidence interval (CI) 0.76–1.15). We did observe an association between salt intake and increased risk for progression to dysplasia or gastric cancer overall (adjusted risk ratio (RR): 1.32; 95% confidence interval (CI): 0.96–1.81), especially among those who continued to have H. pylori infection at the five-month follow-up (adjusted RR: 1.53; 95% CI: 1.12–2.09), and among those who had persistent H. pylori infection over 12 years (adjusted RR: 1.49; 95% CI: 1.09–2.05). Salt intake may increase the risk of gastric dysplasia or gastric cancer in individuals with H. pylori infection.

Estimation of salt intake from spot urine may assist the risk assessment of gastric cancer

“…In the study, H. pylori infection was not evaluated and could not be excluded as a confounding factor. Thapa et al (14) showed that salt intake estimated by urinary sodium/creatinine ratio is associated with progression of GC or dysplasia in patients with persistent H. pylori infection at a risk ratio of 1.49. This result was originally intended for patients who were positive for H. pylori, and H. pylori-uninfected patients were not included.…”

Linking gut microbiota with human diseases

“…Production of low gastric acid makes an ideal environment for some nitrogen reducing bacteria that convert nitrates or nitrites from the saliva and dietary substrates further produce carcinogenic N-nitroso compound which causes damage to DNA and methylation of epithelial cells promotes carcinogenesis of the stomach. High dietary salt intake promotes gastric carcinogenesis [85]. Epidemiological reports showed that a high intake of salt is related to the incidence of H. pylori infection.…”

“…[85]. The two fundamental components which induce gastric cancer are Cytotoxin-Associated Gene A (CagA) and Vacuolating Cytotoxin A (VacA)[77].…”

Outcome of public consultations on the Scientific Opinions of the EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA) on Dietary Reference Values for sodium and chloride

“…• H. pylori is present in half of world's population and its prevalence increases with age (25-60% in Europe, Muhammad, 2012); it persistently colonizes the human stomach despite a robust immune response (Algood, 2006). • Increasing evidence (Wang, X 2008;Yassibas, 2012;Epplein, 2014), including prospective studies (Shikata, 2006;Thapa, 2019), indicates that in presence of persistent colonization of H. pylori, high salt intake can exert synergistic effects in promoting gastric carcinogenesis. Considering the high prevalence of H. pylori infection in Europe, the biological relevance for the general healthy population, and the biological plausibility of the combined effect of salt intake and H. pylori (Gaddy, 2013), we consider that there is a need of further well conducted studies on this topic.…”