ALTERED STATES OF GASTRIC ECOLOGY

[Guest guest]

ALTERED STATES OF GASTRIC ECOLOGY

 

Altered gastric ecology is one of the dominant chronic disorders of

our time. Most — though not all — chronic fatiguers develop problems

of indigestion and upper abdominal discomfort after variable periods

of fatigue.

 

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.

 

For suspected or documented gastric hypoacidity, my own clinical

preference is to avoid the use of acid-containing products such as

betaine hydrochloride.

 

Such products often carry the risk of inducing excessive acidity.

 

The use of herbal digestives is much more desirable. Patients must

be prepared for a slow restorative approach, as is done for other

patients managed with nondrug management protocols of molecular

medicine.

 

Digestive enzymes administered with or soon after meals

significantly expedite restoration of gastric ecology.

 

http://majidali.com/Bowel%20I%20Altered%20States%20of%20Gastric%

20Ecology.htm

_________________

 

JoAnn Guest

mrsjoguest

DietaryTipsForHBP

http://www.geocities.com/mrsjoguest