Autointoxication chiefly starts in the colon. As Ilya Metchnikoff (1845-1916), the Russian biologist and late director of the Pasleur Institute in Paris, France, put it briefly 'and precisely: "Death lurks in the colon". The naturopath Eric F.W., Powell, N.D., agreed by saying: "The chief area from which the system is poisoned, is the large bowel. Whenever there is constipation, toxic substances will be retained and absorbed into the blood. This self-poisoning gives rise to all kinds of diseases."

The human body metabolizes nutrients in many different ways. Among the intermediaries or end-products, there, can always occur substances which are poisonous and capable of inducing cellular' degeneration and necrosis.

Inside the cell, in its sub-cellular organelles, any molecular deteriorations amplify to become visible 'structural changes. The sub-cellular structures reflect the condition of the molecules.
Unfortunately, the theory of intestinal toxemia and focal intoxication of the colon IS nm generally accepted, at present, although it has not been contradicted by any in-depth investigation. On the other hand, there is plenty of evidence supporting the idea of a connection between the diet and the composition of the bacterial flora hi the intestines, mainly in the colon. This fact has been proven in many animal experiments. Any high-protein diet promotes the proliferance of such proteolytic bacteria, which decompose proteins and their fragments in an abnormal way. These putrefactive bacteria" belong to the category of anaerobic' microorganisms which do not require air or oxygen to maintain their metabolism.

The end-products of their biochemical activities, however, are partly strong toxins. Some of them, such as indole and skatole are responsible for the characteristic smell oft the feces. From experience, it can be said that this smell is the stronger the higher the protein intake. That is particularly obvious in mere carnivores, such as cats. Once the normal balance of the intestinal bacteria is disturbed, the proteolytic bacteria will overgrow, accelerating the putrefactive processes. In all experiments, a reduction of the protein intake in favor of complex carbohydrates instantly stopped putrefaction.

However, high-protein diet is not the only cause, of putrefactive processes in the colon. Any delay in the transfer of the intestinal contents, induced by constipation or intestinal obstruction, also causes an increase in putrefaction. Studies have been performed on animals with a surgically produced intestinal obstruction. Although this "closed intestinal loop" only led to a manifested toxemia in a small number of cases, the experiments showed a significant duplication of pro teolytic bacteria overgrowing the normal intestinal flora. Collecting the produced toxins and injecting them into healthy animals indicated that the liver is not much of a protective organ against these substances. The following compounds have been identified as products of putrefactive bacterlal protein' decomposition.

A) AMMONIA
It is formed in the course of the deamination of amino acids: This product is normally detoxified in the liver which sustains a special chain of biochemical reactions called "urea cycle". Here, ammonia is converted into neutral and readily water-soluble urea. There are now two possibilities for the occurrence of elevated blood-ammonia levels. The urea cycle may be impaired due to some primary liver damage, or the quantity of the produced ammonia exceeds the capacity of the detoxification mechanism. Ammonia is a highly alkaline agent and any abnormal increase in its blood level, a so-called• "hyperammonemia" is prone to cause alkalosis. The symptoms of this condition start with confusion and drowsiness. Elevated ammonia levels also impair the cerebral metabolism leading to hepatic coma. The application of acidifying agents will restore the normal situation by neutralizing the alkali. There are indications that ammonia might even playa part in malignant cellular degeneration.

B) INDOLE
This toxic substance is formed from' the amino acid tryptophan. Certain tryptophan metabolites have been found capable of inducing tumors of the urinary bladder. Under normal conditions, indole is detoxified in the liver by linking it to glucose, a process called "conjugation". The resulting conjugate by the name of "indican" can be readily excreted with the urine. It can be determined as a measure of putrefaction in the GI tract.

C) SKATOLE
Skatole is also a product of bacterial decomposition of tryptophan. The bacterium pseudomonas migula is involved in these processes. The toxic effects of skatole include circulatory depression and functional disorders of the central nervous system• due to its antagonistic action on acetylcholine and potassium. High skatole levels in the blood cause a foul odor of the breath. The cells of the human intestinal walls convert skatole into 6hydroxy-skatole, a substance which damages hemoglobin and lipid-absorbing cells. The appearance of skatole derivatives may be considered an indication of anemia and/or malabsorption syndrome.

D) PUTRESCINE AND CADAVERINE
These two compounds also result from the putrefaction; of tryptophan. They can cause hypotension.

E) HISTAMINE
The last of the important putrefaction products of tryptophan is histamine. High blood levels of this compound can cause headache, nervous depression, cardiac arrhythmia, hypotension, and collapse.

F) HYDROGEN SULFIDE
This gaseous substance is formed in the course of disintegration of sulphur-containing amino acids. It has a very unpleasant odor as known from rotten eggs. Its toxicity equals that of cyanide. The most important effect of hydrogen sulfide is its interference with the cytochrome system, a part of the respiratory chain of enzymes involved in mitochondrial electron transport which is essential to energy production. It can also irritate the mucosae causing congestion and increasing their permeability to contents of the intestines. Hydrogen sulfide may be blamed for "neuro-circulatory myasthenic symptoms", such as weakness, nausea, clammy skin, tachycardia, and cyanosis.

G) NEURlNE
This product is formed from cholin which is contained in a phospholipid by the name of sphingomyelin which occurs in brain, liver, kidneys, and egg yolk. Neurine is particularly poisonous to animals.

H) AMINOETHYL MERCAPTAN
Formed from the amino acid cysteine, this compound has a strong hypotensive effect.

I) TYRAMINE
Tyramine is produced from tyrosine by the action of putrefactive bacteria. Its structure is related to epinephrine, the chief catecholamine hormone of the adrenal medulla. Tyramine has been used as a sympathomimetic drug. Its main effect is blood pressure elevation.

K) PHENOL
This substance is also known under then name of "carbolic acid". It is produced by putrefactive bacteria from the amino acid tyrosine. Phenol is not only a locally corrosive agent but also a systemic toxin. Earlier it was used as an external antiseptic. When absorbed in the system, it causes damage to the mucosae of the G.I. tract as well as to liver and kidney cells. Phenol is not detoxified in the liver but excreted in its free form. Its concentration in the urine is a measure of intestinal putrefaction.

L) CLOSTRIDIUM PERFRINGENSENTEROTOXIN
Clostridium perfringens may also occur among the putrefactive microorganisms in the human colon. Its enterotoxin is highly poisonous.

It should be realized that any chronic intestinal stasis disturbs the natural balance and supports overgrowth of pathological microorganisms which are responsible for putrefactive processes yielding a variety of toxic metabolites. It is also important to take into consideration that an intestinal stasis may exist, even if the number of bowel movements appears normal. Daily bowel movements are no guarantee for complete evacuation of toxic material from the G.I. tract.

The absorption of the toxins which are produced by putrefactive microorganisms does not necessarily depend on pathologically altered mucosae in the GI tract. On the other hand, inflammations of the lower colon or the duodenum have been found to be quite common, even if they remain asymptomatic. Any such inflammation will alter the permeability of the intestinal mucosae promoting toxemia.

Intestinal toxemia is usually accompanied by one or more of the following symptoms:
Fatigue, nervous disorders, GI tract conditions, nutritional deficiencies, dermatoses, hormonal disorders, neurocirculatory disturbances, headaches, arthritis, low back pain, allergies, asthma; eye, ear, nose or throat conditions, cardiac arrhythmia, nodular changes of the female breast tissue, and changes in the thyroid gland.

It must be emphasized that intestinal toxemia doubtlessly plays .a significant role in all processes related to aging and even in the development of malignant growth.