Coenzyme-A and its role in helping people who suffer from
Obesity, CFS, MD, Malnutrition and Toxic Poisoning

by Nickolaos D. Skouras, PhD.

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:

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:

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  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.