Gastric ulcers are ulcerations that occur in the mucosal lining of the stomach while duodenal ulcers occur in the mucosa of the duodenum. The annual cost associated with gastric ulcers (peptic ulcer disease) is estimated to be $6 billion in the U.S. while gastric cancer kills over 700,000 people per year globally. H. pylori is considered by many researchers to be the primary cause of peptic and duodenal ulcers and gastric cancer.
“Helicobacter pylori (H. pylori) infection underlies gastric ulcer disease, gastric cancer and duodenal ulcer disease. The disease expression reflects the pattern and extent of gastritis/gastric atrophy (i.e., duodenal ulcer with non-atrophic (gastritis) and gastric ulcer and gastric cancer with atrophic gastritis).”
“The association between H. pylori infection and chronic gastritis, peptic ulcer disease, gastric cancer, and lymphoma has been well established.”
As you can see, the literature supports the significant risk of developing gastric (peptic) ulcers, duodenal ulcers and gastric cancer secondary to H. pylori infection. In fact, the literature supports a progression of stomach disease that results from H. pylori infection that starts with gastritis (inflammation of the stomach lining), which often occurs without symptoms, and progresses to gastric and/or duodenal ulcers and finally to gastric cancer.
“H. pylori infection causes chronic gastritis, which is asymptomatic in the majority of carriers but is considered a major risk factor for the development of gastric and duodenal ulcers and the two gastric malignancies (cancers).”
“Infection with H. pylori causes chronic inflammation and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer.”
Duodenal and gastric ulcers are common and serious diseases but occur in only a minority of people infected with H. pylori. It is estimated that approximately 50% of the world’s population is infected with H. pylori yet only a small percentage of this population (10-15%) develop these stomach disorders.[243,245] Why is this?
Factors that Affect Outcome of H. Pylori Infection
The pathogenicity of H. pylori depends on the interaction of bacterial virulence, the host, genetic and environmental factors. An important factor that affects the outcome of H. pylori infection includes the host response to the infection, particularly the extent and severity of gastric inflammation and the amount of acid secreted by parietal (gastric) cells.
“Pathogenesis is dependent upon inflammation, a Th-1 acquired immune response and hormonal changes including hypergastrinemia (excess gastrin production). Host genetic polymorphisms that lead to high-level pro-inflammatory cytokine release in response to infection increase cancer risk.”
H. pylori can elevate acid secretion in people who develop duodenal ulcers or decrease acid production in those who develop gastritis, gastric ulcers or stomach cancer. This occurs through gastric atrophy (loss of gastric cells) secondary to H. pylori infection. In people who do not develop these diseases, acid secretion is largely unchanged. Dietary and environmental factors also play a role. A diet high in salt and lacking in antioxidants promotes low acid secretion with gastritis. Cigarette smoking strongly predisposes to both duodenal ulcer and gastric cancer. Stress may also play a role in the development of peptic ulcers.
The use of non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, or aspirin (ASA), is an established significant risk factor in the development of gastric ulcers.
“Helicobacter pylori (H. pylori) infection, NSAID or low dose aspirin (ASA) use independently and significantly increases the risk for the development of peptic ulcer disease.”
“Based on the diagnosis of H. pylori as a single causative factor in 44.1% of our patients while that of NSAIDs/ASA in 9.2% of cases, H. pylori infection and NSAID/ASA usage seem to represent independent synergistic risk factors for uncomplicated peptic ulcers.”
Before the discovery of H. pylori it was known that patients with duodenal ulcers (in the small intestine) secrete about twice as much acid as controls because they have twice as many gastric parietal cells. Duodenal ulcers can be healed, but not cured, by suppression of acid secretion by medications. Excess acid secretion in duodenal ulcer disease is virtually always due to H. pylori infection because secretion returns to normal after the infection is eradicated. Therefore, eradication of H. pylori is the most efficient treatment approach to duodenal ulcers when H. pylori infection is present. This can be done with antibiotics (conventional approach) or herbal antibiotics (functional medicine approach). The herbal approach is very effective in treating and eliminating H. pylori infection and decreases risk of destroying beneficial gut flora.[251-253] Conventional treatment has been associated with high recurrence rate of infection and risk of complications.
“Antibiotics treatment for H. pylori has been such a controversial issue that it is still not well established as to who should be treated. The high ‘recurrence rate’, potential long term complications, and socioeconomic usefulness of the bactericidal treatment have been disputed.”
H. pylori infection in the stomach predisposes to gastritis and gastric ulcer, but patients who develop this condition have decreased acid secretion (hypochlorhydria) due to inflammation of the gastric lining. Therefore, supplementation with HCl and betaine is important in these conditions in order to minimize the risks associated with hypochlorhydria as discussed above. As in hypersecretion of gastric acid conditions, eradication of H. pylori is the most efficient treatment approach to gastric ulcers when H. pylori infection is present. This can be done with antibiotics (conventional approach) or herbal antibiotics (functional medicine approach). Again, the herbal approach is very effective in treating and eliminating H. pylori infection and decreases risk of destroying beneficial gut flora.[251-253]
Mucosal resistance refers to the ability of the mucosal stomach lining to resist inflammation secondary to infection or medications. Mucosal resistance is an important factor in risk of developing gastritis or gastric ulcer secondary to H. pylori infection. But what are the predisposing factors that decrease mucosal resistance? We know that smoking and non-steroidal anti-inflammatory drugs (NSAIDs) are known to be important predisposing factors. However, dietary influence has been getting increasing attention in the literature.[255-257]
An important factor that could be contributing to mucosal resistance is the presence or absence of protective substances in the diet which protect the mucosa. Studies show that the geographical differences in the prevalence of duodenal ulcers indicate that protective lipids in the staple diets (certain phospholipids and sterols) can protect the mucosa against H. pylori.[255,256] These dietary variations could also account for the appearance of duodenal ulcers at the beginning of the twentieth century which coincided with the introduction of roller milling resulting in the increasing refinement of wheat, maize, and rice and the removal of these protective lipids.
“The evidence from animal models shows that certain dietary phospholipids and phytosterols have a protective action against gastroduodenal ulceration, both singly and in combination. This supports the protective role of staple diets in areas of low duodenal ulcer prevalence and may prove to be of importance in the prevention and treatment of duodenal ulceration and management of recurrent ulcers. A combination of phospholipids and phytosterols could also play an important role in protection against ulceration due to NSAIDs.”
The protective activity appears to be related to specific phospholipid, sterol and sterol ester fractions. In the phospholipid fraction, phosphatidylcholine (lethicin) and phosphatidyl ethanolamine (cephalin) appear to be protective. In the sterol fraction, β-sitosterol, stigmasterol, and an unidentified isomer of β-sitosterol appear to have protective activity.
PPIs, such as omeprazole and H2-receptor blockers, such as cimetidine, remain the standard treatment of gastric and duodenal ulcers. These acid suppressing medications have various side effects as discussed in the article Adverse Effects of PPIs. When H. pylori is present, the standard treatment is triple-antibiotic therapy to eradicate the pathogen. However, there are various adverse effects associated with this therapy, including microbial resistance, a high recurrence rate and potential long-term complications, including elimination of beneficial GI flora.
Clinical Management of Gastric and Duodenal Ulcers in Functional Medicine
There are numerous published studies showing the gastroprotective and anti-ulcer properties of herbal compounds against damage induced by NSAIDs, H. pylori and alcohol causing ulcer formation, primarily by supporting gastric mucosal proliferation and inhibition of gastric acid secretion.[259-270] Some of these compounds have also been shown to have anti-H. pylori effects as well. [255,256,259,270] In addition, many natural compounds, including certain probiotics, have been found to be useful as adjuncts to standard antibiotic therapy against H. pylori to reduce side-effects of these drugs and decrease the need for additional medications. [271-274]
“…numerous studies have demonstrated that herbal medicines can effectively treat gastric ulcer in humans and various animal models via divergent mechanisms. Studies have demonstrated that the efficacy of herbal medicines is comparable or superior to that of drugs such as omeprazole or cimetidine in humans and animal models, and herbal medicines display fewer adverse effects. The mechanisms by which herbal medicines benefit gastric ulcer include stimulation of mucous cell proliferation, anti-oxidation, and inhibition of gastric acid secretion and H(+)/K(+)-ATPase activity. Some herbal medicines also exhibit antimicrobial properties. Utilization of herbal medicines could be a valuable alternative to treat gastric ulcer in humans effectively, with few adverse effects.”
Summary of Gastric and Duodenal Ulcers and Treatment Options
H. pylori is the most common cause of gastric and duodenal ulcers. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) are another common cause. Duodenal and gastric ulcers are common and serious diseases but occur in only a minority of people infected with H. pylori. It is estimated that approximately 50% of the world’s population is infected with H. pylori yet only a small percentage of this population develop these stomach disorders, therefore there are other important factors that influence the progression of H. pylori infection. Mucosal resistance is an important factor in the risk of developing gastritis or gastric ulcer secondary to H. pylori infection. In addition to NSAID use and smoking, dietary factors appear to be important predisposing factors in mucosal resistance. The evidence from animal models shows that certain dietary phospholipids and phytosterols have a protective action against gastroduodenal ulceration. A combination of phospholipids and phytosterols could play an important role in protection against ulceration.
H. pylori can elevate acid secretion in people who develop duodenal ulcers or decrease acid production in those who develop gastritis, gastric ulcers or stomach cancer. PPIs, such as omeprazole and H2-receptor blockers, such as cimetidine, remain the standard treatment of gastric and duodenal ulcers. These acid suppressing medications have various side effects as discussed above (see Adverse Effects of PPIs). Eradication of H. pylori is the most efficient treatment approach to gastric and duodenal ulcers when H. pylori infection is present. H. pylori can be eliminated effectively with both conventional antibiotic therapy and herbal antibiotic therapy. There are various adverse effects associated with conventional antibiotic therapy, including microbial resistance, a high recurrence rate and potential long-term complications.
There are several advantages to the use of herbal medicine in treating H. pylori, including decreased risk of adverse effects associated with conventional antibiotics. Numerous studies have demonstrated that herbal medicines can effectively treat gastric ulcer via divergent mechanisms and some of these compounds have been shown to have anti-H. pylori effects. Studies have demonstrated that the efficacy of herbal medicines is comparable or superior to that of acid-suppressing drugs such as omeprazole or cimetidine and herbal medicines display fewer adverse effects. In addition, many plant compounds, phospholipids and certain probiotics have been found to be useful adjuncts to standard antibiotic therapy against H. pylori and in the treatment of ulcers.
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