Chapter 58 Maldigestion
Introduction
Therapeutic Considerations
Indigestion
The term indigestion is often used by patients to describe a feeling of gaseousness or fullness in the abdomen. It can also be used to describe “heartburn.” In a survey of over 20,000 adults in the United States, the overall prevalence of at least 1 upper gastrointestinal symptom was reported in 45% of those surveyed (based on the preceding 3-month period); symptoms included heartburn, early satiety, loss of appetite, and postprandial fullness (bloating).1 These symptoms of indigestion can be attributed to a great many causes, including not only increased secretion of acid but also decreased secretion of acid and other digestive factors and enzymes.
According to surveys, most people use antacids to relieve symptoms of reflux esophagitis.2 However, reflux esophagitis is most often caused by overeating, not excessive acid production. Other common causes are as follows:
Chronic heartburn may also be a sign of a hiatal hernia. However, although 50% of people older than 50 years have hiatal hernias, only 5% of patients with hiatal hernias actually experience reflux esophagitis. Perhaps the most effective treatment of chronic reflux esophagitis and symptomatic hiatal hernias is to utilize gravity. The standard recommendation is to simply place 4-inch blocks under the bedposts at the head of the patient’s bed. This elevation of the head is very effective in many cases. Another recommendation to heal the esophagus is the use of deglycyrrhizinated licorice.
Enteric-coated peppermint oil has been shown to be very helpful in cases of nonulcer dyspepsia and reflux esophagitis. For more information, see Chapter 105, Mentha piperita (Peppermint).
Hypochlorhydria
In the patient with chronic indigestion, rather than focus on blocking the digestive process with antacids, the natural approach focuses on aiding digestion. Although much is said about hyperacidity conditions, a more common cause of indigestion is a lack of gastric acid secretion. Many symptoms and signs suggest impaired gastric acid secretion, and a number of specific diseases have been associated with insufficient gastric acid output.3–13 They are listed in Boxes 58-1 and 58-2.
BOX 58-1 Common Signs and Symptoms of Low Gastric Acidity
Bloating, belching, burning, and flatulence immediately after meals
A sense of “fullness” after eating
Indigestion, diarrhea, or constipation
Nausea after taking supplements
Weak, peeling, and cracked fingernails
Dilated blood vessels in the cheeks and nose
Several studies have shown that the ability to secrete gastric acid decreases with age.14–16 Some studies found low stomach acidity in more than half of the subjects older than 60 years. The best method of diagnosing a lack of gastric acid is the Heidelberg gastric analysis (see Chapter 18).17 Wright18 suggested that the response to a bicarbonate challenge during Heidelberg gastric analysis, not simply resting pH, was the true test of the functional ability of the stomach to secrete acid.
Because the Heidelberg gastric acid analysis is not widely available, a clinical trial of hydrochloric acid (HCl) supplements can be used as described in Appendix 7.
Etiology
Like peptic ulcer disease, achlorhydria and hypochlorhydria have been linked to the overgrowth of the bacteria H. pylori. Approximately 90% to 100% of patients with duodenal ulcers, 70% of patients with gastric ulcers, and about 50% of people older than 50 years test positive for H. pylori.19 The presence of H. pylori is determined by measuring the level of antibodies to H. pylori in the blood or saliva or by culturing material collected during an endoscopy as well as measuring the breath for urea. A breath test is also available for assessment of current H. pylori activity.
Low gastric output is thought to predispose to H. pylori colonization, and H. pylori colonization increases gastric pH, thereby setting up a positive feedback scenario and increasing the likelihood of colonization of the stomach and duodenum by other organisms.20 Not surprisingly, HCl antisecretory drugs (H2 receptor antagonists and proton pump inhibitors) may actually promote H. pylori overgrowth. Patients with H. pylori experience an exaggerated response in elevations of pH with antisecretory therapy.21 Eradication of H. pylori is associated with a return to normal gastric acidity and pepsinogen ratio.22
Although the typical conventional medicine approach is to focus only on the infective agent, the usual host defense factors are equally or more important. Unfortunately, research has focused on eradicating the organism, and there is little information on protective factors against infectivity. Proposed protective factors against H. pylori-induced intestinal damage are maintaining a low pH and ensuring adequate antioxidant defense mechanisms.23–25 Low levels of vitamin C and vitamin E and other antioxidant factors in the gastric juice appear not only to lead to the progression of H. pylori colonization but also contribute to ulcer formation, because the mechanism by which H. pylori damages the stomach and intestinal mucosa is oxidative.26 Furthermore, antioxidant status and gastric acid output appear to explain the observation that most people infected with H. pylori do not experience peptic ulcer disease or gastric cancer; for more information on natural approaches for eradicating H. pylori, see Chapter 198.
One natural medicine that may be useful against H. pylori that is not discussed in Chapter 198 is bovine lactoferrin. Lactoferrin exerts broad-spectrum antimicrobial action because it has been shown to be effective in inhibiting the growth of disease-causing protozoa, yeast, bacteria, and viruses. More important than its ability to actually kill organisms is the discovery that lactoferrin prevents the attachment of disease-causing organisms to cells that line the mouth and entire gastrointestinal tract. At the same time, lactoferrin is a powerful booster of health-promoting bacteria like Bifidobacteria and Lactobacillus species. By preventing growth of harmful bacteria while promoting the growth of beneficial Bifidobacteria, lactoferrin assists in the development of proper intestinal flora.
The standard medical treatment of H. pylori infection is a 1- or 2-week course of treatment called triple therapy. It involves taking two antibiotics to kill the bacteria and an acid suppressor drug. On the basis of results of clinical trials, lactoferrin alone or in combination with triple therapy may soon be the treatment of choice. In one study, 151 patients testing positive for H. pylori with indigestion symptoms were given either triple therapy alone or with lactoferrin. H. pylori status assessed 8 weeks after the end of the treatment indicated a 95.9% eradication rate for the group receiving the lactoferrin; the other group had only a 72.5% eradication rate.27 The effective dose of lactoferrin in this application is 300 mg/day.
Pancreatic Insufficiency
The most severe level of exocrine pancreatic insufficiency (EPI) is seen in cystic fibrosis. Next in severity is the EPI associated with the late stages of pancreatitis. These more severe causes of EPI are most often easily recognized, but causes of mild EPI are more insidious and difficult to diagnose. Both physical symptoms and laboratory tests can be used to assess pancreatic function in patients in whom mild EPI is suspected. Common symptoms of EPI are abdominal bloating and discomfort, gas, indigestion, and the passing of undigested food in the stool. For laboratory diagnosis, a comprehensive stool and digestive analysis (discussed in Chapter 27) is quite useful. In addition, the measurement of fecal elastase 1 concentrations using an enzyme-linked immunosorbent assay is an accepted indirect test of the exocrine pancreatic function. It shows higher sensitivity and specificity for EPI than fecal chymotrypsin determination and is comparable to oral pancreatic function tests, such as the pancreolauryl test.28
Pancreatic Enzyme Supplements
Pancreatic enzyme products are an effective treatment for EPI and are widely used. Most commercial preparations are prepared from fresh hog pancreas (i.e., pancreatin) (see Chapter 111 for a full discussion).
Enzyme products are often enteric coated, primarily to protect the more fragile porcine lipase. However, some studies have shown that non–enteric-coated enzyme preparations actually outperform enteric-coated products if they are given before a meal (for digestive purposes) or on an empty stomach (for antiinflammatory effects). In general, there is no significant difference in clinical response to various delivery forms of pancreatin.29
Alternatives to porcine pancreatin include plants (e.g., bromelain, papain, etc.) and enzymes extracted from various microbes or yeast (e.g., Aspergillus oryzae). These enzymes are more resistant to digestive secretions and have a broader range of activity, including pH range (see Chapter 71, Bromelain; and Chapter 106, Microbial Enzyme Preparations). One double-blind, crossover trial in 17 patients with severe EPI and steatorrhea compared the effects of a non–enteric-coated pancreatic enzyme preparation (360,000 lipase U/day), an enteric-coated pancreatic enzyme preparation (100,000 lipase U/day), and a fungal enzyme preparation (75,000 lipase U/ day).30 All three treatment preparations in both groups yielded significant reduction in total daily stool weight and total daily fecal fat excretion compared with controls. It is interesting to point out, however, that the fungal enzyme preparation produced similar benefit at three-fourths the dose of enteric-coated pancreatic enzyme and one-fifth the dose of the non–enteric-coated pancreatic enzyme preparation.
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