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Ubiquinone is one of the two most important essential nutrients (the other being ascorbic acid). These two molecules, along with other essential nutrients, have been rejected as unpatentable and unprofitable by certain "authorities" and interests, according to expose's by Pauling and others.[1,2] This has been one of the most lethal errors of modern medicine because no cell, organ, function, remedy, etc, can avoid failure unless essential nutrients, especially these two, are optimal. Supplementation of both is mandatory: for ascorbate, lifelong (since humans can't synthesize it); for ubiquinone, increasingly with age. In this update, to facilitate study of ubiquinone, we seek to assemble in one place vital information that is not widely known.


Negative "Studies." A very few negative "studies" from the early 1990's up to present have reported lack of beneficial effects of ubiquinone for congestive heart failure (CHF). Fundamentally, these negative studies have been criticized as cases of too little ubiquinone, for too short a time and too late in the course of CHF in the trial patients. Correct treatment should include the essential nutrients (ubiquinone, vitamin E, and ascorbic acid) and no statins. Self-appointed "experts" who have no experience in treating CHF correctly have praised these few negative "studies" while ignoring the vastly greater literature cited above including the large scale trials demonstrating the positive aspects of ubiquinone. Could the negative studies have been "designed" to produce failures? Is this action designed to oppose acceptance of the low cost (unprofitable), non-toxic (endogenous), versatile ubiquinone modality. Certainly the investigators and extollers of these negative "trials" appear to be totally oblivious of the fundamental physiology of ubiquinone requiring its constant replacement at 500 mg/day by synthesis from exogenous substrate or by supplementation.

Positive Studies. Clinical observations of cardiologists who have had extensive experience with the use of ubiquinone (such as Peter Langsjoen) find dramatic improvements in heart function in CHF patients treated with ubiquinone prior to the development of irreversible damage. While the optimal dose of ubiquinone in the treatment of congestive heart failure is not established, it has become clear over the past 15 years, that 100 mg per day (the dose used in some of the negative studies) is suboptimal for the majority of patients. A higher dose of ubiquinone for a longer period of time has demonstrated highly significant benefit in many previously published trials. An extensive review of ubiquinone use for cardiovascular disease (CVD) in 34 controlled clinical trials and several open-label and long-term studies has recently been published.42

2006-07-23 08:04:48 · answer #1 · answered by spiritwalker 6 · 0 0

Ubiquinone is an important part of the cycle that produces energy in each cell. Also known as Coenzyme-Q, it could be very hepful for people taking Statins for cholesterol. Statins can weaken heart muscle, and Co-Q 10, as it is also called, can offset some of that effect.

2006-07-23 09:03:22 · answer #2 · answered by ED S 1 · 0 0

History
Coenzyme Q was first discovered in 1957 by professor F. L. Crane and colleagues at the University of Wisconsin Enzyme Institute. In 1958, its chemical structure was reported by Dr. D.E. Wolf and a research group at Merck Laboratories led by Dr. Karl Folkers.

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Chemical properties
The oxidized structure of CoQ, or Q, is given here:



The various kinds of Coenzyme Q can be distinguished by the number of isoprenoid side chains they have. The most common CoQ in human mitochondria is Q10. The image above has three isoprenoid units and would be called Q3.

If Coenzyme Q is reduced by one equivalent, the following structure results, a ubisemiquinone, and is denoted QH. Note the free radical on one of the ring oxygens (either oxygen may become a free radical, in this case the top oxygen is shown as such).



If Coenzyme Q is reduced by two equivalents, the compound becomes a ubiquinol, denoted QH2:



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Biochemical role
CoQ is found in the membranes of endoplasmic reticulum, peroxisomes, lysosomes, vesicles and notably the inner membrane of the mitochondrion where it is an important part of the electron transport chain; there it passes reducing equivalents to acceptors such as Coenzyme Q - cytochrome c reductase:

CoQH2+ 2 Fe+3-cytochrome c → CoQ + 2 Fe+2-cytochrome c
In bacteria CoQ is involved in direct electron transfer towards oxygen:

CoQH2 + O2 → CoQ + H2O

CoQ is also essential in the formation of the apoptosome along with other adapter proteins. The loss of trophic factors activates pro-apoptotic enzymes, causing the breakdown of mitochondria.

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Supplementation
Because of its ability to transfer electrons and therefore act as an antioxidant, Coenzyme Q has become a valued dietary supplement.

Young people are able to make Q10 from the lower numbered ubiquinones such as Q6 or Q8. The sick and elderly may not be able to make enough, thus Q10 becomes a vitamin later in life and in illness.

Supplementation of Coenzyme Q10 has been found to have a beneficial effect on the condition of some sufferers of migraine headaches, and is a common component of the "mito cocktail" used to treat mitochondrial disorders and other metabolic disorders. It is also being investigated as a treatment for cancer, and as relief from cancer treatment side effects.

Recent studies have shown that the antioxidant properties of Coenzyme Q10 benefit the body and the brain. Some of these studies indicate that Coenzyme Q10 protects the brain from neurodegenerative disease such as Parkinsons and also from the damaging side effects of a transient ischemic attack (stroke) in the brain.

Another recent study shows a survival benefit after cardiac arrest if coenzyme Q10 is administered in addition to commencing active cooling (to 32–34 degrees Celsius).

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Synthesis and its inhibition by statins and beta blockers
The isoprene sidechain of Coenzyme Q10 is synthesized from acetyl CoA by a series of enzymatic reactions, while the benzoquinone portion is synthesized from amino acids.

Coenzyme Q10 shares a common biosynthetic pathway with cholesterol. Isopentenyl pyrophosphate and its isomer, dimethylallyl pyrophosphate, are linked alternatingly in polyprenyl chains, which are also called isoprenes. The 15-carbon isoprene chain is farnesyl pyrophosphate, which is a precursor to cholesterol, while the 50-carbon isoprene chain forms the sidechain of coenzyme Q10.

The synthesis of an intermediary precursor of Coenzyme Q10, mevalonate, is inhibited by some beta blockers, blood pressure lowering medication [1], and statins, a class of cholesterol lowering drugs [2]. Statins can reduce serum levels of coenzyme Q10 by up to 40% [3]. Some research suggests the logical option of supplementation with coenzyme Q10 as a routine adjunct to any treatment which may reduce endogenous production of coenzyme Q10, based on a balance of likely benefit against very small risk. [4][5]


Please check out this website http://en.wikipedia.org/wiki/Ubiquinone
so you can see the tables. I wasn't able to paste them. Good luck and I hope this helps. :)

2006-07-23 09:42:35 · answer #3 · answered by pinkribbons&walking4boobies 4 · 0 0

A more common term is Coenzyme Q10 and it is used for heart problems and is also a base for skin care products. See these sites for more information.

2006-07-23 08:11:40 · answer #4 · answered by # one 6 · 0 0

Look here - http://en.wikipedia.org/wiki/Ubiquinone

2006-07-23 08:04:01 · answer #5 · answered by jasenlee 3 · 0 0

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