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Coenzyme-A and its role in helping people who suffer from
The problems that many people have with metabolizing fat are often the
result of poor nutrition, which is usually compounded by poisoning from
environmental toxins of the thiols found in our fat-metabolizing cofactors
and enzymes. Coenzyme-A, Acyl Carrier Protein, and Lipoate Acetyl Transferase
are among the more obvious targets for toxic metals and fat-soluble environmental
toxins such as alkyl halides (from chlorinated drinking water) and lipid
epoxides. Coenzyme-A is needed, to metabolize the three major forms of energy
(fat, carbohydrates, and protein). If fat is the energy source that can't
be metabolized due to a shortage or blockage of Coenzyme-A then the fat simply
accumulates. An increase in Coenzyme-A and a reduction in environmental toxins
are essential in correcting this health problem. Consequently, weight gain
is not something that anyone should feel guilty about, since in many cases
it is often just a result of how extensively we have been malnourished and
poisoned.
There are a variety of environmental toxins, including the following:
Plant Toxins (phorbol esters and related compounds capable of producing
epoxides or enol tautomers).
Rancid Fat (polyunsaturated fats poorly stored or contaminated with
peroxidizing metal catalysts).
Toxic Metals (Nickel and Lead being the more common and insidious
in our environment).
Mycotoxins (toxins such as aflatoxin from microbes contaminating our
food and environment).
Toxic herbicides, pesticides and fertilizers.
Chemotherapies, many of which are alkylating agents and/or carcinogenic.
Chemical Warfare Agents (nearly all, including tear gas such as Mace
and HN1).
The body's primary sources of energy are produced at the cellular level by metabolic processes. Coenzyme-A, Acetyl Coenzyme-A, Coenzyme Q10 and Coenzyme 1 (NADH), together with certain B-vitamins and their coenzyme forms are necessary for such energy production during: (1) the tricarboxylic acid cycle (TCA cycle) and (2) the glycolitic cycle. The TCA cycle is responsible for the production of about 90% of the energy the body requires to sustain life.
Coenzyme-A is required to initiate the TCA cycle and the chemical reactions that involve the utilization of Coenzyme Q10 and Coenzyme 1 for the production of energy at the cellular level.
ANALOGY: Coenzyme 1 (NADH/Enada) is the "spark plug" to the TCA cycle of energy production. Coenzyme Q10 (CoQ10) would be considered the "oxygenation" of that process, while Coenzyme-A is the "ignition switch" to the whole process of energy production.
When Coenzyme-A is lacking or blocked, the human body cannot generate energy from the usual sources and may suffer from conditions known by such medical terms as "chronic fatigue syndrome" (CFS). This, in turn, leads to less activity and eventually more weight gain.
Since Coenzyme Q10 and Coenzyme 1 (NADH) cannot be utilized by the human body if Coenzyme-A is lacking or blocked due to nutritional deficiencies or environmental poisoning, one could argue that Coenzyme-A is ultimately more important than Coenzyme Q10 and Coenzyme 1.
In addition, intermediates that accumulate
(when Coenzyme-A is blocked or lacking) poison other systems and lead to
manifestations of other diseases. For example, the body makes Coenzyme-A
from pantothenic acid, adenosine triphosphate (ATP) and cysteine, the latter
being produced through the metabolic intermediate, homocysteine. Homocysteine
accumulates in cancer and heart disease. Half of the heart disease incidence
has been attributed to a deficiency of the vitamins (folic acid and B6) that
help to convert other amino acids into cysteine. A B6 deficiency alone can
prevent homocysteine's conversion into cysteine. Without cysteine, Coenzyme-A
cannot be made. This problem is exacerbated further by any pathological
accumulation of homocysteine that, through its "like" but not quite "cysteine"
chemistry, may interfere with the utilization of cysteine in producing
Coenzyme-A. Thus, we have a ready explanation for "chronic fatigue immune
dysfunction syndrome" (CFIDS).
Malnourished and/or poisoned individuals cannot convert dietary lipids from
animals and plants into human fat compositions. In essence, we are trying
to build and maintain the lipid-containing myelin sheaths that surround and
protect our nerve fibers with, say, cow "parts". This probably contributes
to pathological situations in which there is an established autoimmune component,
such as in multiple sclerosis. An environmental poisoning of the immune system
while "cow parts" (antigens) are being used in human structures clearly can
contribute to autoimmunity. In other words, a confused and poorly targeted
immune system, especially when one's lipid membranes are in disrepair or
of an improper composition, may be the underlying cause of some autoimmune
and neurodegenerative diseases. Again, obesity could be a result of dangerous
metabolic imbalances (brought on by malnutrition and environmental poisonings)
that can lead to rheumatoid conditions, Parkinson's, Alzheimer's, and other
autoimmune, immunodeficiency, and infectious diseases.
Having a lot of accumulated fat deposits to process to find or create the
right "parts" for nerve maintenance, certainly does not help the body to
cope with these diseases, so weight control should help obese individuals
with any signs of these diseases. At the same time, too little fat in the
diet, such as that provided by reduced-fat and fat-free foods, may be similarly
problematic in neurodegenerative diseases. When they take the fat out of
our food, what happens to the essential fatty acids, fat-soluble vitamins
and fat-soluble antioxidants? They're either gone or, hopefully, at least
some of them are put back into capsules to sell to us separately. Without
supplementation on a fat-free diet, it is not a matter of the "right parts"
being available for nerve maintenance; there are no "parts".
Muscular dystrophy (MD) has a tentative link to obesity since it has been
associated with deficiencies of vitamin E and of selenium, both of which
are implicated metabolically in protecting lipids and therefore thiol compounds
from undesirable oxidations and chemical modifications. Since vitamin E is
fat-soluble, dietary intakes may be inadequate to prevent the detrimental
effects of lipid epoxidation, especially in those obese individuals on fat-free
or starvation diets. Dietary supplements including a good antioxidant mix
are indicated under these circumstances. Hence, moderation and nutritional
supplementation are essential for any safe weight "control" program; we must
supplement with vitamins, enzymes, minerals and other nutrients, eat well
(focus on "quality" not quantity), exercise, and avoid environmental toxins
to lose weight safely.
Any steps taken to improve nutrition, avoid toxins, and exercise or at least
work up a sweat (sweating is one way our body gets rid of nickel, lead and
other toxic metals) should help to fortify your defenses against both,
environmental and infectious assaults. Also, it is important to make sure
that your body has a constant supply of the nutrients it requires to produce
Coenzyme-A because Coenzyme-A is expended by the metabolic processes of the
body and constantly needs replenishing. At this time, Coenzyme-A is not
commercially available in the form of a one compound synthetic dietary
supplement. Further, it is doubtful that a compound of Coenzyme-A would be
an effective dietary supplement because the digestive process would break
such a compound back down into its components before it entered the bloodstream.
Coenzyme-A is not manufactured during the digestive process, it is manufactured
in the cells of the body! This is why the products offered by Coenzyme-A
Technologies are based upon a balanced combination of components that are
used by the cells of the body to manufacture and utilize Coenzyme-A.
In summary, good nutrition, Coenzyme-A, vitamin, and mineral supplementation,
exercise, and environmental awareness are your best prescription for restoring
proper immune responses, for minimizing health costs, and for providing the
best "health insurance" for long life.
References:
1. Knight, G. D., Ph.D.; A Waist is a terrible thing to mind; Medical Hypothesis 1998.
2. Leung, L. H., M.D.; Pantothenic Acid as a Weight Reducing Agent: Fasting Without Hunger, Weakness and Ketosis; Medical Hypothesis 1995; 44, 403, 405.
3. Abiko Y.; Metabolism of Coenzyme-A; New York Academic Press, Third Edition 1975; 7:1-25.
4. Robishaw, J. D. & Neely, J. R.; Coenzyme A Metabolism; American Journal of Physiology 1985; 248: El- E9.
5. Krebs, H. A.; The Regulation of Release of Ketone Bodies by the Liver; Advanced Enzyme Reaction 1966; 4: 339-354.
The statements contained in this article have not been evaluated
by the U.S. Food & Drug Administration (FDA).
The products discussed are not intended to diagnose, treat, cure, or prevent
any disease.
© 1999-2007 Coenzyme-A Tech. Inc. All rights reserved.
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