Functional Support for Peptic Ulcers
Peptic ulcers can occur in the stomach (gastric) and upper portion of the small intestine (duodenal) (1). Normally, the epithelial lining of the stomach and duodenal is amply protected from the extreme acidity of gastric juice; however, when the integrity of the protective epithelial lining is compromised or damaged, peptic ulcers may form. Once thought to be the result of high stress and excessive gastric acid output, peptic ulcer disease is now understood to be associated with other factors, the most common of which is the bacterium Helicobacter pylori (H. pylori).
In 1983, H. pylori was discovered to be a major causative factor for peptic ulcer disease (2). In fact, 70% to 100% of people with peptic ulcers have an H. pylori infection (1). This bacterium, which colonizes in the antral and duodenal mucosa of the stomach and small intestine, potentiates oxidative damage to the epithelial lining due to its considerable production of reactive oxygen metabolites (3). The cytopathic toxins released from the bacterium may also inhibit or impair innate protective mucosal secretory mechanisms (3).
Factors Promoting H. pylori Overgrowth
Conventional treatments, which include hydrochloric (HCL) antisecretory drugs and broad-spectrum antibiotics, aim to minimize the irritating effects of gastric acid and eradicate H. pylori. However, anti-secretory drugs generally raise the gastric pH above 3.5, which not only impairs protein digestion and mineral disassociation, but adversely affects the gut microbial flora, promoting overgrowth of H. pylori (1). Additionally, antibiotics kill the resident beneficial and protective bacteria and encourage antibiotic resistance, thus promoting overgrowth of harmful organisms. Therefore, it makes sense to approach this problem from a somewhat different angle, creating an environment that not only eliminates causative factors, supports host defense factors, eradicates the infective agent, and heals the injured tissues.
CAM Support for Peptic Ulcers
Low levels of antioxidants, mainly vitamins C and E, in gastric juice have been associated with the colonization of H. pylori and the progression of ulcer formation (3, 4). In one study, vitamin C has been shown to prevent formation of potentially carcinogenic N-nitrosamines and eliminate oxygen radicals that damage gastric epithelium (3, 4). This and other studies have shows that ascorbic acid is secreted in high amounts in a healthy stomach yet decreases dramatically after H. pylori infection. Though the exact reason for this is unclear, it is hypothesized that the invasion of free radical-producing bacterium may consume the vitamin C present in the mucosa. Furthermore, H. pylori has also been shown to lower systemic availability and absorption of dietary vitamin C, markedly reducing concentration in plasma (3). High-dose vitamin C has been shown to eradicate the bacterium as well as significantly increase its concentration in gastric juice (3).
Vitamin E may play a significant role in mitigating the cellular damage caused by H. pylori cytotoxins. It breaks the chain reaction of lipid perioxidation caused by reactive oxygen species that damage cell membranes in the GI tract (4). Like vitamin C, it can also prevent the formation of N-nitrosamines (an important factor in the development of gastric cancer) and plays an immunomodulatory role by increasing natural killer cells activity (4).
Bovine lactoferrin (blf), when co-administered with antibiotics, has been shown to maximize antibiotic activity, minimize dosage and lessens the side effects of the other commonly used antibiotics (Di Mario, 2006). Moreover, it promotes health-promoting bacteria, such as Bifidobacteria and Lactobacillus species, while inhibiting harmful bacteria (1). Finally, eliminating possible food allergens, which may exacerbate inflammation; increasing fiber; and incorporating cabbage juice, bismuth subcitrate, flavonoids such as catechin, deglycyrrhizinated licorice, and rhubarb (Rheum species) may aid in healing injured tissues (1).
1. Pizzorno, J. E., & Murray, M. T. (2013). Textbook of natural medicine (4th ed.). Philadelphia, PA, United States: Elsevier/Churchill Livingstone.
2. Hildreth, C. J., Lynm, C., & Glass, R. M. (2008). Helicobacter pylori. JAMA, 300(11), 1374-1374. doi:10.1001/jama.300.11.1374
3. Park, J. H., Kim, S. Y., Kim, D. W., Lee, W. G., Rhee, K. H., & Youn, H. S. (2003). Correlation between Helicobacter pylori infection and vitamin C levels in whole blood, plasma, and gastric juice, and the pH of gastric juice in Korean children. Journal of Pediatric Gastroenterology and Nutrition, 37(1), 53-62. Retrieved from http://journals.lww.com/jpgn/Fulltext/2003/07000/Correlation_Between_Helicobacter_pylori_Infection.9.aspx
4. Phull, P. S., Price, A. B., Thorniley, M. S., Green, C. J., & Jacyna, M. R. (1996). Vitamin E concentrations in the human stomach and duodenum--correlation with Helicobacter pylori infection. Gut, 39(1), 31–35. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1383226/
5. Di Mario, F., Aragona, G., Dal Bó, N., Cavallaro, L., Marcon, V., Olivieri, P., . . . & Franzè, A. (2006). Bovine lactoferrin for Helicobacter pylori eradication: An open, randomized, multicentre study. Alimentary Pharmacology & Therapeutics, 23(8), 1235-1240. doi:10.1111/j.1365-2036.2006.02851.x