Peptic Ulcer Disease

Each year approximately half a million people in the United States are newly diagnosed with peptic ulcer disease (PUD), with many more millions of cases likely going undiagnosed.1 PUD is caused by disturbances of the gastrointestinal (GI) mucosa. These disruptions are due to the loss of protective elements and/or damaging insults that result in mucosal erosions, most commonly located in a portion of the small intestine called the duodenum or the stomach. People with PUD commonly complain of epigastric pain (particularly a few hours after meals), bloating, nausea, early satiety, altered bowel habits, and heartburn. Pain is usually improved with food or antacids. PUD may also occur without symptoms, particularly in older adults. Peptic ulcers may cause GI bleeding, which could potentially be life-threatening. Ulcers may rarely perforate leading to intense pain, which is a surgical emergency. Patients with significant weight loss and PUD symptoms should undergo endoscopy to investigate for potential cancer.

The loss of gastrointestinal mucosal integrity is typically multifactorial, with diminished protective elements (due to decreased acid-buffering, reduced immune system functioning, and slowed wound healing) and increased insults (due to infections by Helicobacter pylori bacteria, the use of nonsteroidal antiinflammatory drugs [NSAIDs], increased acidity, and inflammation). Treatment efforts are focused on restoring protective factors and reducing harmful affronts.

Historically, investigators were aware that smoking, stress, NSAIDs, and family history (risk increases 3x with an afflicted first-degree relative)2 contributed to peptic ulcer formation. However, prior to the late 1970s, medicine had limited success in treating PUD until the arrival of two revolutionary developments: the invention of pharmaceuticals that reduced the amount of acid the stomach produced; and the discovery of the Helicobacter pylori bacterium. Besides PUD disease, H. pylori has also been linked to increased rates of gastric cancer, vitamin B12 deficiency, iron deficiency, and low platelets (a condition called ITP, or idiopathic thrombocytopenia).3 Only 10% to 20% of H. pylori-infected individuals develop PUD.4 Thus, current treatment efforts should focus on symptomatic carriers.

Meal timing influences PUD, with skipping breakfast5 and consuming large meals shortly before bedtime shown to increase the risk of PUD.6

Fruit and vegetable intake reduces the risk of developing ulcers. A diet high in plant-based fiber and vitamin A (e.g., carrots, spinach, mango, sweet potatoes, and apricots) helps protect against PUD.7 Flavonoids, compounds found throughout the plant world, have been found to be protective against H. pylori infection and are present in concentrated amounts in citrus, berries, onions, parsley, green tea, red wine, and dark chocolate.8 Sulforaphanes, which are phytochemicals found in vegetables such as Brussels sprouts, broccoli, cabbage, cauliflower, bok choy, turnips, and radishes, are also protective against H. pylori infection.9

Studies have specifically shown that virgin olive oil (30 g daily for 2 weeks) or broccoli sprouts (70 g a day for 8 weeks) have the ability to decrease and potentially eliminate H. pylori.9

Multiple studies have demonstrated that regular physical activity, when compared with a more sedentary lifestyle, is protective against PUD.10,11 One study specifically demonstrated that the risk for duodenal ulcers was 62% less in men who cumulatively walked or ran more than 10 miles per week.

Inadequate sleep is a risk factor for PUD, likely the result of increased stress levels causing immune dysfunction and impaired lifestyle decisions. Maintaining good sleep hygiene is an important component of ulcer avoidance.

Smoking increases rates of PUD up to four times when compared with nonsmokers, likely due to decreased wound healing.10 Accordingly, smoking cessation is essential in addressing PUD.

Alcohol, in large amounts, has been shown to be a risk factor for ulcers, likely as a result of mucosal damage. One study reported that individuals who consumed more than 42 drinks per week had a greater than four-fold increase in the incidence of bleeding ulcers compared with individuals who consumed 1 drink per week or less.12 However, red wine is reported to be protective against H. pylori infection, possibly attributable to the activity of bioactive compounds such as flavonoids.

Certain helpful microorganisms have proven versatile in the treatment of PUD. Probiotics have been shown to reduce ulcer recurrence,13 and individuals with higher intakes of probiotics have correspondingly lower rates of H. pylori infection.

Ascorbic acid (vitamin C) has been shown to have potential for H. pylori eradication; one study demonstrated a 10% eradication rate with 2 weeks of 1000 mg daily.14 A clinical trial has reported zinc accelerates the healing of gastric ulcers up to three times faster than observed with placebo.15

The number of options available to address PUD are quite numerous and at RMRM, we’d be glad to address how some of these remedies apply to your specific case.

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