Coenzyme Q-10 (Ubiquinone)
8/98 Dr. David Martin

DOSAGE: Recommended dosages from the literature. In Japan all "cardiac" patients receive 10 mg tid for the rest of their lives. Therapeutic trial - 8 weeks

Angina Pectoris:

50 mg tid

CHF mild:

30 mg daily

CHF severe:

30 mg tid

Cardiomyopathy:

50 mg bid

Mitral Valve Prolapse:

Children 2 mg/Kg/d

Hypertension:

30 mg bid

Protectant in myocardial ischemia/reperfusion:

5 mumol/L in cardioplegia solution

 

TOXIC DOSE: nkn

 

SIDE EFFECTS:

essentially none

< 1%

epigastric discomfort

0.39%

loss of appetite

0.23%

nausea

0.16%

diarrhea

0.11%

 

PHARMACOKINETICS: ukn -- absorption probably 80%. Diet source -- meat (beef heart) greatest amount. Animal meat contains Q-6 to Q-10 which is converted in the body to Q-10 -- probably inefficiently. Probably most effective taken q 8 hours.

Clinical effects seen in 6 to 8 weeks. If blood levels of Q-10 normal, the supplementation with Q-10 will usually have no effect. Base dosage on outcome on re-evaluation every 2 months until optimal dose is determined.

 

DRUG INTERACTIONS:

Lovastatin -- depletes Q-10 and Vit. E

Beta-blockers -- depletes Q-10

Corisol -- lowers serum levels of Q-10

SUPPLIED: 11/97 Co Q-10

10 mg approx. .14 per tab.

30 mg approx. .30 per tab.

50 mg approx. .35 per tab.

DISCUSSION: Coenzyme Q-10 (ubiquinone) is found in every cell in the body. It is found in the cytosol and in the mitochondria. It is essential for energy metabolism for the Kreb's cycle as succinate dehydrogenase Co-Q-10 reductase and to regenerate ATP. The coenzyme portion requires calcium, magnesium, zinc and some vitamins. In patients with hypomagnesium, etc. Q-10 supplements will probably be ineffective until "cofactors" are replenished.

Age, disease and drugs decrease the body's ability to synthesize Q-10 resulting in deficiency, it also decreases cardiac and liver function and response to stress. 50 to 75% of patients with cardiovascular disease have been reported to be deficient in Q-10. Since the heart is almost entirely dependent on mitochondrial phosphorylation for energy, the empirical supplementation of Q-10 in these patients is probably beneficial.

Medical studies have shown Q-10 therapy resulted in 53% decrease in anginal episodes, increase exercise tolerance to pain and ST-segment depression, 50% improvement in the NYHA classification for CHF with improvement in ejection fraction.

It is possible that Q-10 can prevent the negative effects of beta-blocker therapy without reducing the benefits of beta-blockers on myocardial oxygen consumption.

If clinical improvement is seen in 8 to 12 weeks, I suggest life-long supplementation, as stopping supplements will probably result to relapse to the former level of function.

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