Dr. Ron’s Research Review – November 22, 2017

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This week’s research review focuses on Vitamin C and gastritis

The relationship of ascorbic acid and gastritis and peptic ulcer and its complications was extensively studied during the 1930s through the 1950s. Much of this extensive literature has been effectively "lost." Ascorbic acid deficiency was associated with all forms of gastritis (e.g., autoimmune, chemical, and infectious) due in varying degrees to insufficient intake, increased metabolic requirements, and destruction within the GI tract. Occasionally, looking back can help plot the way forward. (Aditi and Graham, 2012)
A population-based double-blind randomised controlled trial in a Japanese population with atrophic gastritis in an area of high stomach cancer incidence was conducted between 1995 and 2000. Daily doses of 50 or 500 mg vitamin C were given, and 120 and 124 participants completed the 5-year study, respectively. Although serum ascorbic acid was higher in the high-dosage group (1.73 (sd 0.46) mug/l) than in the low-dosage group (1.49 (sd 0.29) mug/l, P < 0.001), at the end of the study, no significant difference was observed for CRP between the low- and high-dosage groups (0.39 (95 % CI 0.04, 4.19) mg/l and 0.38 (95 % CI 0.03, 4.31) mg/l, respectively; P = 0.63) or for SAA between the low- and high-dosage groups (3.94 (95 % CI 1.04, 14.84) mug/ml and 3.85 (95 % CI 0.99, 14.92) mug/ml, respectively; P = 0.61). Vitamin C supplementation may not have a strong effect on reducing infections in individuals with atrophic gastritis. (Ma et al., 2012)
A study evaluated the effect of acid-suppressive therapy and vitamin C on H. pylori-associated gastritis. Forty patients with reflux esophagitis were divided into three groups by the status of H. pylori and therapy: group A (n=15), H. pylori (+) and omeprazole 20 mg; group B (n=15), H. pylori (+) and omeprazole 20 mg + vitamin C 1200 mg; and group C (n=10), H. pylori (-) and omeprazole 20 mg. In all three groups, the mucosal interleukin (IL)-8 contents, H. pylori colonization density, neutrophil infiltration in the corpus, and serum gastrin were evaluated at entry and 2 weeks after starting therapy; in group B, serum vitamin C levels were also measured. In group A, the IL-8 contents and the degree of neutrophil infiltration during therapy exceeded those at entry, whereas in groups B and C, these values did not change significantly with treatment. Helicobacter pylori colonization density during therapy was similar to that at entry in all three groups. The serum gastrin (in all groups) and vitamin C levels (in group B) during therapy exceeded those at entry. Potent acid suppression worsens H. pylori-associated corpus gastritis, although such worsening gastritis may be inhibited by vitamin C. (Yoshinaga et al., 2001)

Dr. Ron


Articles

 

Vitamin C, gastritis, and gastric disease: a historical review and update
            (Aditi and Graham, 2012) Download
The discovery of Helicobacter pylori as the cause of gastritis and peptic ulcers ushered in the modern era of research into gastritis and into acid-peptic diseases and rekindled interest in the role of ascorbic acid in the pathophysiology and treatment of gastritis and peptic ulcer disease. Here, we review historic and modern studies on ascorbic acid and gastric diseases with an emphasis on H. pylori gastritis and its sequelae. The relationship of ascorbic acid and gastritis and peptic ulcer and its complications was extensively studied during the 1930s through the 1950s. Much of this extensive literature has been effectively "lost." Ascorbic acid deficiency was associated with all forms of gastritis (e.g., autoimmune, chemical, and infectious) due in varying degrees to insufficient intake, increased metabolic requirements, and destruction within the GI tract. Importantly, gastritis-associated abnormalities in gastric ascorbic acid metabolism are reversed by H. pylori-eradication and potentially worsened by proton pump inhibitor therapy. Diets rich in naturally occurring ascorbic acid are associated with protection of the gastric corpus from atrophy and a reduction in the incidence of gastric cancer possibly through the ability of ascorbic acid to reduce oxidative damage to the gastric mucosa by scavenging carcinogenic N-nitroso compounds and free radicals and attenuating the H. pylori-induced inflammatory cascade. Ascorbic acid supplementation was possibly associated with a decreased incidence of bleeding from peptic ulcer disease. Pharmacologic doses of ascorbic acid also may improve the effectiveness of H. pylori-eradication therapy. Occasionally, looking back can help plot the way forward.

Vitamin C supplementation in relation to inflammation in individuals with atrophic gastritis: a randomised controlled trial in Japan
            (Ma et al., 2012) Download
Evidence has shown that both C-reactive protein (CRP) and serum amyloid component A (SAA) are increased in individuals with gastritis and stomach cancer. Controlling the level of these biomarkers by inhibiting the gastric infection with high doses of ascorbic acid may reduce the risk of carcinogenesis. A population-based double-blind randomised controlled trial in a Japanese population with atrophic gastritis in an area of high stomach cancer incidence was conducted between 1995 and 2000. Daily doses of 50 or 500 mg vitamin C were given, and 120 and 124 participants completed the 5-year study, respectively. Although serum ascorbic acid was higher in the high-dosage group (1.73 (sd 0.46) mug/l) than in the low-dosage group (1.49 (sd 0.29) mug/l, P < 0.001), at the end of the study, no significant difference was observed for CRP between the low- and high-dosage groups (0.39 (95 % CI 0.04, 4.19) mg/l and 0.38 (95 % CI 0.03, 4.31) mg/l, respectively; P = 0.63) or for SAA between the low- and high-dosage groups (3.94 (95 % CI 1.04, 14.84) mug/ml and 3.85 (95 % CI 0.99, 14.92) mug/ml, respectively; P = 0.61). Vitamin C supplementation may not have a strong effect on reducing infections in individuals with atrophic gastritis.

Vitamin C inhibits corpus gastritis in Helicobacter pylori-infected patients during acid-suppressive therapy
            (Yoshinaga et al., 2001) Download
BACKGROUND: Previous studies have shown that gastric acid suppression worsens corpus gastritis in Helicobacter pylori (H. pylori)-positive patients. We evaluated the effect of acid-suppressive therapy and vitamin C on H. pylori-associated gastritis. METHODS: Forty patients with reflux esophagitis were divided into three groups by the status of H. pylori and therapy: group A (n=15), H. pylori (+) and omeprazole 20 mg; group B (n=15), H. pylori (+) and omeprazole 20 mg + vitamin C 1200 mg; and group C (n=10), H. pylori (-) and omeprazole 20 mg. In all three groups, the mucosal interleukin (IL)-8 contents, H. pylori colonization density, neutrophil infiltration in the corpus, and serum gastrin were evaluated at entry and 2 weeks after starting therapy; in group B, serum vitamin C levels were also measured. RESULTS: In group A, the IL-8 contents and the degree of neutrophil infiltration during therapy exceeded those at entry, whereas in groups B and C, these values did not change significantly with treatment. Helicobacter pylori colonization density during therapy was similar to that at entry in all three groups. The serum gastrin (in all groups) and vitamin C levels (in group B) during therapy exceeded those at entry. CONCLUSIONS: Potent acid suppression worsens H. pylori-associated corpus gastritis, although such worsening gastritis may be inhibited by vitamin C.

References

Aditi, A. and D. Y. Graham (2012), ‘Vitamin C, gastritis, and gastric disease: a historical review and update’, Dig Dis Sci, 57 (10), 2504-15. PubMed: 22543844
Ma, E., et al. (2012), ‘Vitamin C supplementation in relation to inflammation in individuals with atrophic gastritis: a randomised controlled trial in Japan’, Br J Nutr, 1-7. PubMed: 23167953
Yoshinaga, M., et al. (2001), ‘Vitamin C inhibits corpus gastritis in Helicobacter pylori-infected patients during acid-suppressive therapy’, J Gastroenterol Hepatol, 16 (11), 1206-10. PubMed: 11903736