The term Peptic Ulcer is used to describe a group of ulcerative disorders of the upper gastrointestinal tract. An ulcer is an erosion of the mucous membrane which may be accompanied by inflammation and infection, and may occur at different locations. The major forms of gastrointestinal ulcers are:
Gastric Ulcer: this type of ulcer is found on the lesser curvature of the stomach. Duodenal Ulcer: this type of ulcer usually occurs on the duodenal side of the pyloric region. This is the first part of the small intestine. Excess acid may overflow from the stomach.
Pyloric Ulcer: develop at the point where the muscle ring acts as a valve between the stomach and duodenum.
Peptic Ulcer: is a common name for any of the above. The word ‘peptic’ comes from the enzyme pepsin, which digests protein.
Ulcers average between one-quarter and one-half inch in diameter. They develop when digestive juices produced in the stomach, intestines and digestive glands damage the lining of the stomach or duodenum.
The two important components of digestive juices are hydrochloric acid and the enzyme pepsin. Both substances are critical in the breakdown and digestion of starches, fats, and proteins in food. They play different roles in ulcers.
Pepsin: Pepsin is an enzyme that breaks down proteins in food. Because the stomach and duodenum are also composed of protein, they are susceptible to the actions of pepsin. Pepsin is, therefore, also an important factor in the formation of ulcers.
Fortunately, the body has a defence system to protect the stomach and intestine against these two powerful substances:
The mucus layer: which coats the stomach and duodenum, forms the first line of defense.
Bicarbonate: which the mucus layer secretes, neutralises the digestive acids. Hormone-like substances called prostaglandins help dilate the blood vessels in the stomach, to ensure good blood flow and protect against injury. Prostaglandins are also believed to stimulate bicarbonate and mucus production.
Disrupting any of these defense mechanisms makes the lining of the stomach and intestine susceptible to the actions of acid and pepsin, increasing the risk for ulcers.
Causes of Peptic Ulcer
In 1982 two Australian scientists identified H. pylori as the main cause of stomach ulcers. They showed that inflammation of the stomach, and stomach ulcers, result from an infection of the stomach caused by H. pylori bacteria. This discovery was so important that the researchers were awarded the Nobel Prize in Medicine in 2005. The bacteria appear to trigger ulcers in the following way:
H. pylori’s corkscrew shape enables it to penetrate the mucus layer of the stomach or duodenum so that it can attach itself to the lining. The surfaces of the cells lining the stomach contain a protein, called decay-accelerating factor, which acts as a receptor for the bacterium.
H. pylori survives in the highly acidic environment by producing urease, an enzyme that generates ammonia to neutralise the acid.
H. pylori then produces a number of toxins and factors that can cause inflammation and damage to the stomach and intestinal lining, leading to ulcers in certain individuals.
It also alters certain immune factors that allow it to evade detection by the immune system and cause persistent inflammation – even without invading the mucus membrane.
Even if ulcers do not develop, the bacterium is considered to be a major cause of active chronic inflammation in the stomach (gastritis) and upper part of the small intestine (duodenitis).
H. pylori is also strongly linked to stomach cancer and possibly other non-intestinal problems.
Factors that trigger Ulcers in H. pylori Carriers: Only around 10 to 15 per cent of people who are infected with H. pylori develop peptic ulcer disease. H. pylori infections, particularly in older people, may not always predict whether there are peptic ulcers. Other variables must also be present to actually trigger ulcers. These may include:
Genetic Factors: Some people harbor strains of H. pylori that contain genes that may make the bacteria more dangerous, and increase the risk for ulcers. How important these genetic factors are in the development of ulcers depends on a person’s ethnicity.
Immune Abnormalities: Some experts suggest that certain individuals have abnormalities in their intestinal immune response, which allow the bacteria to injure the lining.
Lifestyle Factors: Although lifestyle factors such as chronic stress, drinking coffee, and smoking were long believed to be primary causes of ulcers, it is now thought that they only increase susceptibility to ulcers in some H. pylori carriers.
Shift work and other causes of interrupted sleep: People who work the night shift have a significantly higher incidence of ulcers than day workers. Researchers suspect that frequent interruptions of sleep may weaken the immune system’s ability to protect against harmful bacterial substances.
When H. pylori was first identified as the major cause of peptic ulcers, it was found in 90 per cent of people with duodenal ulcers and in about 80 per cent of people with gastric ulcers. As more people are being tested and treated for the bacteria, however, the rate of H. pylori- associated ulcers has declined. Currently, H. pylori are found in about 50 per cent of people with peptic ulcer disease.
Some researchers now believe that duodenal ulcers are not caused by H. pylori, but that the presence of the bacteria simply delays healing. This fact, they say, may explain why up to half of acute duodenal perforation cases show no evidence of H. pylori, and why duodenal ulcers can come back even after H. pylori has been eradicated.
Nonsteroidal Anti-Inflammatory Drugs (NSAIDS)
Long-term use of NSAIDs is the second most common cause of ulcers, and the rate of NSAID-caused ulcers is increasing. More than 30 million people take prescription NSAIDs regularly, and more than 30 billion tablets of over-the-counter brands are sold each year in the U.S. alone. The most common NSAIDs are aspirin, ibuprofen (Advil, Motrin), and naproxen (Aleve, Naprosyn), although many others are available.
Patients with NSAID-caused ulcers should stop taking these drugs. However, patients who require these medications on a long-term basis can reduce their risk of ulcers by taking drugs in the proton pump inhibitor (PPI) group, such as omeprazole (Prilosec). A new study shows that famotidine (Pepcid – an H2 blocker) can also protect people who are taking low-dose aspirin for cardiovascular prevention, at least in the short-term.
Certain drugs other than NSAIDs may aggravate ulcers. These include warfarin (Coumadin) – an anticoagulant that increases the risk of bleeding, oral corticosteroids, some chemotherapy drugs, spironolactone and niacin.
Bevacizumab, a drug used to treat colorectal cancer, may increase the risk of GI perforation. Although the benefits of bevacizumab outweigh the risks, GI perforation is very serious. If it occurs, patients must stop taking the drug.
Peptic Ulcers Complications
Most people with severe ulcers experience significant pain and sleeplessness, which can have a dramatic and adverse impact on their quality of life.
Bleeding and Hemorrhage
Peptic ulcers caused by H. pylori or NSAIDs can be very serious if they cause hemorrhage or perforate the stomach or duodenum. Up to 15 per cent of people with ulcers experience some degree of bleeding, which can be life-threatening. Ulcers that form where the small intestine joins the stomach can swell and scar, resulting in a narrowing or closing of the intestinal opening. In such cases, the patient will vomit the entire contents of the stomach, and emergency treatment is necessary.
Complications of peptic ulcers cause an estimated 6,500 deaths each year. These figures, however, do not reflect the high number of deaths associated with NSAID use. Ulcers caused by NSAIDs are more likely to bleed than those caused by H. pylori.
Because there are often no GI symptoms from NSAID ulcers until bleeding begins, doctors cannot predict which patients taking these drugs will develop bleeding. The risk for a poor outcome is highest in people who have had long-term bleeding from NSAIDs, blood clotting disorders, low systolic blood pressure, mental instability, or another serious and unstable medical condition. Populations at greatest risk are the elderly and those with other serious conditions, such as heart problems.
About 25 million people in the U.S. are expected to develop peptic ulcers at some point in their lives. Peptic ulcer disease affects all age groups, but is rare in children. Men have twice the risk of ulcers as women. The risk of duodenal ulcers tends to rise, beginning around age 25, and continues until age 75. The risk of gastric ulcers peaks at ages 55 – 65.
Peptic ulcers are less common than they once were. Research suggests that ulcer rates have even declined in areas where there is widespread H. pylori infection. The increased use of proton pump inhibitor (PPI) drugs may be responsible for this trend.
Who is at risk for Ulcers from H. Pylori?
Although H. pylori infection is common, ulcers in children are very rare, and only a small percentage of infected adults develop ulcers. Some known risk factors include smoking, alcohol use, having a relative with peptic ulcers, being male, and having the cytotoxin-associated gene A (CagA). Experts do not know of any single factor or group of factors that can determine which infected patients are most likely to develop ulcers.
Peptic ulcers are always suspected in patients with persistent dyspepsia (bloating, belching, and abdominal pain). Symptoms of dyspepsia occur in 20 – 25 per cent of people who live in industrialised nations, but only about 15 – 25 per cent of those with dyspepsia actually have ulcers. A number of steps are needed to accurately diagnose ulcers.
Medical and Family History
The doctor will ask for a thorough report of a patient’s dyspepsia and other important symptoms, such as weight loss or fatigue, present and past medication use (especially chronic NSAID use), family members with ulcers, and drinking and smoking habits.
Ruling out other disorders
In addition to peptic ulcers, a number of conditions, notably gastro esophageal reflux disease (GERD) and irritable bowel syndrome, cause dyspepsia. Often, however, no cause can be determined. In such cases, the symptoms are referred to collectively as functional dyspepsia.
Peptic ulcer symptoms, particularly abdominal pain and chest pain, may resemble those of other conditions, such as gallstones or a heart attack. Certain features may help to distinguish these different conditions. However, symptoms often overlap, and it is impossible to make a diagnosis based on symptoms alone. A number of tests are needed.
Misdiagnosis of Peptic Ulcer
The following disorders may be confused with peptic ulcers:
GERD: About half of patients with GERD also have dyspepsia. With GERD or other problems in the esophagus, the main symptom is usually heartburn, a burning pain that radiates up to the throat. It typically develops after meals and is relieved by antacids. The patient may have difficulty swallowing and may experience regurgitation or acid reflux. Elderly patients with GERD are less likely to have these symptoms, but instead may experience appetite loss, weight loss, anemia, vomiting, or dysphagia (difficult or painful swallowing).
Heart Events: Cardiac pain, such as angina or a heart attack, is more likely to occur with exercise and may radiate to the neck, jaw, or arms. In addition, patients typically have distinct risk factors for heart disease, such as a family history, smoking, high blood pressure, obesity or high cholesterol.
Gallstones: The primary symptom in gallstones is typically a steady gripping or gnawing pain on the right side under the rib cage, which can be quite severe and can radiate to the upper back. Some patients experience pain behind the breast bone. The pain often occurs after a fatty or heavy meal, but gallstones almost never cause dyspepsia.
Irritable Bowel Syndrome: Irritable bowel syndrome can cause dyspepsia, nausea and vomiting, bloating, and abdominal pain. It occurs more often in women than in men.
Dyspepsia may also occur with gastritis, stomach cancer, or as a side effect of certain drugs, including NSAIDs, antibiotics, iron, corticosteroids, theophylline, and calcium blockers.
Noninvasive tests for gastrointestinal (GI) bleeding
The doctor will order tests to detect bleeding. These may include a rectal exam, complete blood count, and fecal occult blood test (FOBT). The FOBT tests for hidden (occult) blood in stools. Typically, the patient is asked to supply up to six stool specimens in a specially prepared package. A small quantity of feces is smeared on treated paper, which reacts to hydrogen peroxide. If blood is present, the paper turns blue.
Traditional radiology tests have not yet proven valuable for diagnosing ulcers.
Tests to detect H. Pylori
Simple blood, breath, and stool tests can now detect H. pylori with a fairly high degree of accuracy. It is not entirely clear, however, which individuals should be screened for H. pylori.
Candidates for Screening: Some doctors currently test for H. pylori only in individuals with dyspepsia who also have high-risk conditions, such as: symptoms of ulcers, such as weight loss, anemia or indications of bleeding.
History of active ulcers
Risk factors for stomach cancer or other complications from ulcers
Smokers and those who experience regular and persistent pain on an empty stomach may also be good candidates for screening tests. Some doctors argue that testing for H. pylori may be beneficial for patients with dyspepsia who are regular NSAID users. In fact, given the possible risk for stomach cancer in H. pylori-infected people with dyspepsia, some experts now recommend that any patient with dyspepsia lasting longer than 4 weeks should have a blood test for H. pylori. This is a subject of considerable debate, however.
Tests for Diagnosing H. Pylori: The following tests are used to diagnose H. pylori infection. Testing may also be done after treatment to ensure that the bacteria have been completely eliminated.
Breath Test: A simple test called the carbon isotope-urea breath test (UBT) can identify up to 99 per cent of people who have H. pylori. Up to 2 weeks before the test, the patient must stop taking any antibiotics, bismuth-containing medications such as Pepto-Bismol, and proton pump inhibitors (PPIs). As part of the test, the patient swallows a special substance containing urea (a waste product the body produces as it breaks down protein) that has been treated with carbon atoms. If H. pylori are present, the bacteria convert the urea into carbon dioxide, which is detected and recorded in the patient’s exhaled breath after 10 minutes. This test can also be used to confirm that H. pylori have been fully treated.
Blood Tests: Blood tests are used to measure antibodies to H. pylori, and the results are available in minutes. Diagnostic accuracy is reported to be 80 – 90 per cent. One such important test is called enzyme-linked immunosorbent assay (ELISA). An ELISA test of the urine is also showing promise for diagnosing H. pylori in children.
Stool Test: A test to detect the genetic fingerprints of H. pylori in the feces appears to be as accurate as the breath test for initially detecting the bacteria, and for detecting recurrences after antibiotic therapy. This test can also be used to confirm that the H. pylori infection has been fully treated.
The most accurate way to identify the presence of H. pylori is by taking a tissue biopsy from the lining of the stomach. The only way to do this is with endoscopy. It is an invasive procedure, but it is the most accurate test. However, many patients are treated for H. pylori based on the three noninvasive tests listed above.
Endoscopy is a procedure used to evaluate the esophagus, stomach and duodenum using an endoscope – a long, thin tube equipped with a tiny video camera. When combined with a biopsy, endoscopy is the most accurate procedure for detecting the presence of peptic ulcers, bleeding, and stomach cancer, or for confirming the presence of H. pylori.
Appropriate Candidates for Endoscopy: Because endoscopy is invasive and expensive, it is unsuitable for screening everyone with dyspepsia. Most individuals with these symptoms are managed effectively without endoscopy. Endoscopy is usually reserved for patients with dyspepsia who also have risk factors for ulcers, stomach cancer, or both. Risk factors include the following:
“Alarm” symptoms (unexplained weight loss, gastrointestinal bleeding, vomiting, difficulty swallowing, or anemia). Patients with these symptoms generally have an endoscopy before treatment.
Over age 55 (when the risk for stomach cancer increases)
Failure to respond to medical treatment of H. pylori, if present
Experts disagree about whether endoscopy should be performed on all patients who do not respond to initial medication, unless there is evidence or suspicion of bleeding or serious complications, because it does not appear to add any useful information about treatment choices. There is also some debate about whether patients under age 45 who have persistent dyspepsia but no alarm symptoms should have an endoscopy.
Upper GI Series
An upper GI series was the standard method for diagnosing peptic ulcers until endoscopy and tests for detecting H. pylori were introduced. In an upper GI series, the patient drinks a solution containing barium. X-rays are then taken, which may reveal inflammation, active ulcer craters, or deformities and scarring due to previous ulcers. Endoscopy is more accurate, although it is also more invasive and expensive.
Treatment of Peptic Ulcers
Deciding which treatment is best for patients with symptoms of dyspepsia or peptic ulcer disease depends on a number of factors. An endoscopy to identify any ulcers and test for H. pylori probably gives the best guidance for treatment. However, dyspepsia is such a common reason for a doctor’s visit that many people are treated initially based on their symptoms and blood or breath H. pylori test results. This approach (called test and treat) is considered an appropriate option for most patients. Patients who do not have any evidence of bleeding or other alarm symptoms, and who are over age 55 should have an endoscopy performed first.
Approach to patients who are not taking NSAIDS
If an endoscopy is performed soon after the patient first visits a doctor for symptoms, treatment is based on the results of the endoscopy:
If an ulcer is seen and the patient is infected with H. pylori, treatment for the infection is started, followed by 4 to 8 weeks of treatment with a proton pump inhibitor. Most patients will improve with this treatment.
If an ulcer is seen but H. pylori is not present, patients are usually treated with proton pump inhibitors for 8 weeks.
If no ulcer is seen and the patient is not infected with H. pylori, the first treatment attempt will usually be with proton pump inhibitors. These patients do not need antibiotics to treat H. pylori. Other possible causes of their symptoms should also be considered.
As mentioned above, most patients who do not have risk factors for additional complications are treated without first having an endoscopy. The decision of which treatment to use is based on the types of symptoms patients have, and on the results of their H. pylori blood or breath tests.
Patients who are not infected with H. pylori are given a diagnosis of functional (non-ulcer) dyspepsia. These patients are most commonly given 4 to 8 weeks of a proton pump inhibitor. If this dose is not effective, occasionally doubling the dose will relieve symptoms. If there is still no symptom relief, patients may have an endoscopy. However, it is unlikely that an ulcer is present. In this group of patients, symptoms may not fully improve.
Patients who test positive for H. pylori infection will receive an antibiotic regimen that eradicates H. pylori. Those who have an ulcer are more likely to respond to such treatment. Unfortunately, because an endoscopy is not performed before treatment in the test and treat strategy, patients who do not have an ulcer are also treated with antibiotics. Even if they are positive for H. pylori, these patients are less likely to have a full response.
When the test and treat approach is used, those who do not respond to treatment, or whose symptoms return relatively quickly, will often need an upper endoscopy.
There is considerable debate about whether to test for H. pylori and treat infected patients who have dyspepsia but no clear evidence of ulcers. Increased risk for gastroesophageal reflux disease (GERD). A number of studies suggest that H. pylori in the intestinal tract protects against GERD, which in severe cases can be a risk factor for cancer of the esophagus. Eliminating H. pylori may also have other adverse effects.
Overuse of antibiotics: There is concern that using antibiotics when there is no clear evidence of ulcers will lead to unnecessary antibiotic prescriptions and increase the risk for side effects. Overuse may also contribute to a growing public health problem – the emergence of antibiotic-resistant bacteria.
Because the number of people infected with H. pylori is declining in the United States, and therefore the number of people being helped by this approach is declining, the test and treat approach is becoming expensive.
Antibiotic and Combination Drug Regimens for the Treatment of H. Pylori
Reported cure rates for H. pylori range from 70 – 90 per cent after antibiotic treatment. The standard treatment regimen uses two antibiotics and a PPI:
PPIs: These drugs include omeprazole (Prilosec), lansoprazole (Prevacid), esomeprazole (Nexium), and rabeprazole (Aciphex). PPIs are important for all types of peptic ulcers, and are a critical partner in antibiotic regimens. They reduce acidity in the intestinal tract, and increase the ability of antibiotics to destroy H. pylori.
Antibiotics: The standard antibiotics are clarithromycin (Biaxin) and amoxicillin. Some doctors substitute the antibiotic metronidazole (Flagyl) for either clarithromycin or amoxicillin.
Patients typically take this combination treatment for at least 14 days. Many studies, however, suggest that a 7-day treatment may work just as well.
Follow-Up: Follow-up testing for the bacteria should be done no sooner than 4 weeks after therapy is completed. Test results before that time may not be accurate.
In most cases, drug treatment relieves ulcer symptoms. However, symptom relief does not always indicate treatment success, just as persistent dyspepsia does not necessarily mean that treatment has failed. Heartburn and other GERD symptoms can get worse and require acid-suppressing medication.
Treatment of NSAID-induced ulcers
If patients are diagnosed with NSAID-caused ulcers or bleeding, they should:
Get tested for H. pylori and, if they are infected, take antibiotics. Possibly use a PPI. Studies suggest that these medications lower the risk for NSAID-caused ulcers, although they do not completely prevent them.
Healing Existing Ulcers: A number of drugs are used to treat NSAID-caused ulcers. PPIs – omeprazole (Prilosec), lansoprazole (Prevacid), or esomeprazole (Nexium) –are used most often. Other drugs that may be useful include H2 blockers, such as famotidine (Pepcid AC), cimetidine (Tagamet), and ranitidine (Zantac). Sucralfate is another drug used to heal ulcers and reduce the stomach upset caused by NSAIDs.
People with chronic pain may try a number of other medications to minimise the risk of ulcers associated with NSAIDs.
When a patient comes to the hospital with bleeding ulcers, endoscopy is usually performed. This procedure is critical for the diagnosis, determination of treatment options, and treatment of bleeding ulcers.
In high-risk patients or those with evidence of bleeding, options include watchful waiting with medical treatments or surgery. The first critical steps for massive bleeding are to stabilise the patient and support vital functions with fluid replacement and possibly blood transfusions. People on NSAIDs should stop taking these drugs, if possible.
Depending on the intensity of the bleeding, patients can be released from the hospital within a day or kept in the hospital for up to 3 days after endoscopy. Bleeding stops spontaneously in about 70 – 80 per cent of patients, but about 30 per cent of patients who come to the hospital for bleeding ulcers need surgery. Endoscopy is the surgical procedure most often used for treating bleeding ulcers and patients at high-risk for re-bleeding. It is usually combined with medications, such as epinephrine and intravenous proton pump inhibitors.
Between 10 – 20 per cent of patients require more invasive procedures for bleeding, such as major abdominal surgery.
Major Abdominal Surgery
Major abdominal surgery for bleeding ulcers is now generally performed only when endoscopy fails or is not appropriate. Certain emergencies may require surgical repair, such as when an ulcer perforates the wall of the stomach or intestine, causing sudden intense pain and life-threatening infection.
Surgical Approaches: The standard major surgical approach (called open surgery) uses a wide abdominal incision and standard surgical instruments. Laparoscopic techniques use small abdominal incisions, through which inserted tubes are that contain miniature cameras and instruments. Laparoscopic techniques are increasingly being used for perforated ulcers. Research finds that laparoscopic surgery for a perforated peptic ulcer is comparable in safety with open surgery, and results in less pain after the procedure.
Major Surgical Procedures: There are a number of surgical procedures aimed at providing long-term relief of ulcer complications. These include:
Vagotomy, in which the vagus nerve is cut to interrupt messages from the brain that stimulate acid secretion in the stomach. This surgery may impair stomach emptying. A recent variation that cuts only parts of the nerve may reduce this complication.
Antrectomy: in which the lower part of the stomach is removed. This part of the stomach manufactures the hormone responsible for stimulating digestive juices.
Pyloroplasty: which enlarges the opening into the small intestine so that stomach contents can pass into it more easily.
Antrectomy and pyloroplasty are usually performed with vagotomy.
The following drugs are sometimes used to treat peptic ulcers caused by either NSAIDs or H. pylori.
Many antacids are available without a prescription, and they are the first drugs recommended to relieve heartburn and mild dyspepsia. Antacids are not effective for preventing or healing ulcers, but they can help in the following ways:
They neutralise stomach acid with various combinations of three basic compounds – magnesium, calcium, or aluminum.
They may protect the stomach by increasing bicarbonate and mucus secretion. (Bicarbonate is an acid-buffering substance.)
It is generally believed that liquid antacids work faster and are more potent than tablets, although some evidence suggests that both forms work equally well.
Basic salts used in antacids
There are three basic salts used in antacids:
Magnesium: Magnesium compounds are available in the form of magnesium carbonate, magnesium trisilicate, and, most commonly, magnesium hydroxide (Milk of Magnesia). The major side effect of these magnesium compounds is diarrhea.
Calcium: Calcium carbonate (Tums, Titralac, and Alka-2) is a potent and rapid-acting antacid, but it can cause constipation. There have been rare cases of hypercalcemia (elevated levels of calcium in the blood) in people taking calcium carbonate for long periods of time. Hypercalcemia can lead to kidney failure.
Aluminum: The most common side effect of antacids containing aluminum compounds (Amphogel, Alternagel) is constipation. Maalox and Mylanta are combinations of aluminum and magnesium, which balance the side effects of diarrhea and constipation. People who take large amounts of antacids containing aluminum may be at risk for calcium loss and osteoporosis. Long-term use also increases the risk of kidney stones. People who have recently experienced GI bleeding should not use aluminum compounds.
Interactions with Other Drugs: Antacids can reduce the absorption of a number of drugs. Conversely, some antacids increase the potency of certain drugs. The interactions can be avoided by taking other drugs 1 hour before or 3 hours after taking the antacid.
Prevention of Ulcer
Lifestyle Changes: In the past, it was common practice to tell people with peptic ulcers to consume small, frequent amounts of bland foods. Exhaustive research conducted since that time has shown that a bland diet is not effective in reducing the incidence or recurrence of ulcers, and that eating numerous small meals throughout the day is no more effective than eating three meals a day. Large amounts of food should still be avoided, because stretching the stomach can result in painful symptoms.
Fruits and Vegetables: The good news is that a diet rich in fibre may cut the risk of developing ulcers in half and speed the healing of existing ulcers. Fibre found in fruits and vegetables is particularly protective; vitamin A contained in many of these foods may increase the benefit.
Milk: Milk actually encourages the production of acid in the stomach, although moderate amounts (2 – 3 cups a day) appear to do no harm. Certain probiotics, which are “good” bacteria added to yogurt and other fermented milk drinks, may protect the gastrointestinal system.
Coffee and Carbonated Beverages: Coffee (both caffeinated and decaffeinated), soft drinks, and fruit juices with citric acid increase stomach acid production. Although no studies have proven that any of these drinks contribute to ulcers, consuming more than 3 cups of coffee per day may increase susceptibility to H. pylori infection.
Spices and Peppers: Studies conducted on spices and peppers have yielded conflicting results. The rule of thumb is to use these substances moderately, and to avoid them if they irritate the stomach.
Garlic: Some studies suggest that high amounts of garlic may have some protective properties against stomach ulcer, although a recent study concluded that garlic offered no benefits against H. pylori and, in large amounts, can cause considerable GI distress.
Olive Oil: Studies from Spain have shown that phenolic compounds in virgin olive oil may be effective against eight strains of H. pylori, three of which are antibiotic-resistant.
Vitamins: Although no vitamins have been shown to protect against ulcers, H. pylori appears to impair the absorption of vitamin C, which may play a role in the higher risk of stomach ulcer.
Exercise: Some evidence suggests that exercise may help reduce the risk for ulcers in some people.
Stress Relief: Stress relief programmes have not been shown to promote ulcer healing, but they may have other health benefits.
Report compiled by Temitope Obayendo with additional information from MedicineNet.com and http://au.lifestyle.yahoo.com