Autointoxication chiefly starts in the colon. As Ilya Metchnikoff (1845-1916),
the Russian biologist and late director of the Pasteur 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 not 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 in the intestines, mainly in the colon.
This fact has been proven in many animal experiments. Any high-protein diet
promotes the proliferation 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 of the feces. From experience, it can be said
that the stronger the smell, 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 proteolytic 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 bacterial 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 play a 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 G.I. 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 similar to 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 the 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 G.I.
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, G.I. 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.