A fundamental difference in concept between the altered states of bowel ecology and gastric ecology in the past was that the former was predominantly a "bio-ecosystem" while the latter was essentially a "chemical ecosystem." This concept is rapidly changing; the most visible villain, of course, is the microbe Helicobacter pylori. I have a sense that we will encounter other microbes colonizing the gastric ecosystem in the future as the use of antacids, histamine receptor blockers, nonsteroidal drugs for joint disorders, steroids and other drugs becomes more pervasive.

Gastric acidity — secretion of hydrochloric acid by the stomach lining — is essential for the digestive efficiency of pepsin and for the absorption of minerals such as iron. It is one of the primary host defenses against viral and bacterial infections and against parasitic infestations. Pepsin digestion (and ongoing salivary amylase and other enzyme functions) within the stomach lumen is required for preparing food for digestive-absorptive functions in the small bowel. Normal gastric motility preserves the gastric reservoir function without which undigested foods would readily enter the bowel. A detailed discussion of the patho-physiology of the stomach and derangement of gastric function that leads to gastritis-peptic ulcer continuum as well as to the hypochlorhydria-malabsorption spectrum is outside the scope of this monograph. However, symptom-complexes induced by an altered gastric ecology have become pandemic. Further, bowel ecology disorders frequently cannot be reversed without carefully addressing gastric ecology.

Enzymes are proteins, and are easily injured by accelerated oxidative injury — the root of chronic fatigue. The enzymes of the stomach and intestines are no exception to this. I cite two examples of enzymes that are vulnerable to oxidative injury: H+,K+-ATPase and rhodanese. One type of cell in the stomach lining (parietal cells) in the gastric mucosa secretes hydrochloric acid by a process involving oxidative phosphorylation. This is one of the most astounding phenomena in nature: These cells secrete hydrogen ions at a concentration of about 3 million times that found in blood. So intense is the process that one bicarbonate ion released into the blood as a reciprocal event for secretion of each hydrogen ion causes the alkaline tide in the blood Ph. A key enzyme involved in this proton pump mechanism is the specific enzyme, hydrogen-potassium adenosine triphosphatase (H+,K+-ATPase). Reciprocal bicarbonate release into the blood is mediated by parietal cell carbonic anhydrase.

Rhodanese is a sulfur-transferring enzyme in the surface of cells lining the intestinal surface. It takes cyanide from cyanogenic foods and combines it with thiosulfates to make thiocyanate—a molecule that is necessary for production of acid in the stomach. It is likely that many digestive symptoms in chronic fatigue—especially stomach fullness after small meals—are due to oxidative injury to rhodanese. Thiocyanates are also required for iodine storage as well as for optimal function of ATPase—another essential energy enzyme.

HYPERCHLORHYDRIA AND HYPOCHLORHYDRIA
Hyperchlorhydria — too much acidity — is a gastric maladaptive response to the changes in gastric ecology in chronic fatiguers. Such persons are often given massive quantities of antacids for "regulating" abnormal patterns of gastric acidity — a sad reflection on our capacity for understanding the true nature of these problems. Antacids suppress gastric acidity when it is needed and promote it (through rebound phenomenon) when it is unnecessary. Antacids are a common source of aluminum overload and toxicity. The worst side-effect of antacids, in my judgment, is this: Antacids suppress the symptoms that draw our attention to the underlying abnormalities of the gastric structure and function.

Hypochlorhydria — not enough gastric acid — is much more common among human canaries. Gastric acidity normally declines as we age. Hypochlorhydria is almost a constant feature of atrophic gastritis in the elderly. It is seen with high frequency in patients with recurrent episodes of chronic gastritis. Studies on healthy college students have shown hypochlorhydria to occur following acute viral infections in one-third to one half of volunteers. Hypochlorhydria occurring as a consequence of acute viral infections in otherwise healthy subjects can be expected to resolve spontaneously within a period of a few weeks.