Cholesterol
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According to this study, it looks as though a high LDL ("bad cholesterol") to ubiquinone (another name for CoQ10) ratio is a legitimate risk factor for cardiovascular disease. Statin drugs lower CHOL, and LDL, but also CoQ10. We should keep this in mind.

[4-28}

Coenzyme Q10 and coronary artery disease.

Hanaki Y, Sugiyama S, Ozawa T, Ohno M.

Department of Cardiology, Toyohashi National Hospital.

It has been postulated that oxidatively modified low-density lipoprotein (LDL) contributes to the genesis of atherosclerosis. Ubiquinone has been suggested to be an important physiological lipid-soluble antioxidant and is found in LDL fractions in the blood. We measured plasma level of ubiquinone using high-performance liquid chromatography and plasma levels of total cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides in 245 normal subjects (186 males, 59 females) and in 104 patients (55 males, 49 females) who had coronary artery disease not receiving pravastatin and 29 patients (12 males, 17 females) receiving pravastatin. In the normal subjects, the plasma ubiquinone levels did not vary with age. In the patient groups, the plasma total cholesterol and LDL levels were higher and the plasma ubiquinone level lower than in the normal subject group. The LDL/ubiquinone ratio was higher in the patient groups. We found that ubiquinone level, either alone or when expressed in relation to LDL levels, was significantly lower in the patient groups compared with the normal subject group. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor is thought to prevent atherosclerosis, however, it also inhibits ubiquinone production. The present study revealed that HMG CoA reductase inhibitor decreased plasma cholesterol level, and that it did not improve either the ubiquinone level or the LDL/ubiquinone ratio. From these results, the LDL/ubiquinone ratio is likely to be a risk factor for atherogenesis, and administration of ubiquinone to patients at risk might be needed

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More evidence of how statin drugs deplete all-important CoQ10.

[4-24]

Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study.

Ghirlanda G, Oradei A, Manto A, Lippa S, Uccioli L, Caputo S, Greco AV, Littarru GP.

Institute of Internal Medicine, Catholic University Medical School, Rome, Italy.

Inhibitors of HMG-CoA reductase are new safe and effective cholesterol-lowering agents. Elevation of alanine-amino transferase (ALT) and aspartate-amino transferase (AST) has been described in a few cases and a myopathy with elevation of creatinine kinase (CK) has been reported rarely. The inhibition of HMG-CoA reductase affects also the biosynthesis of ubiquinone (CoQIO). We studied two groups of five healthy volunteers treated with 20 mg/day of pravastatin (Squibb, Italy) or simvastatin (MSD) for a month. Then we treated 30 hypercholesterolemic patients in a double-blind controlled study with pravastatin, simvastatin (20 mg/day), or placebo for 3 months. At the beginning, and 3 months thereafter we measured plasma total cholesterol, CoQIO, ALT, AST, CK, and other parameters (urea, creatinine, uric acid, total bilirubin, gamma GT, total protein). Significant changes in the healthy volunteer group were detected for total cholesterol and CoQIO levels, which underwent about a 40% reduction after the treatment. The same extent of reduction, compared with placebo was measured in hypercholesterolemic patients treated with pravastatin or simvastatin. Our data show that the treatment with HMG-CoA reductase inhibitors lowers both total cholesterol and CoQIO plasma levels in normal volunteers and in hypercholesterolemic patients. CoQIO is essential for the production of energy and also has antioxidative properties. A diminution of CoQIO availability may be the cause of membrane alteration with consequent cellular damage.

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This paper describes why everyone who takes a statin drug--no if's, ands or buts--MUST also then take CoQ10.

Frankly, we cannot understand why all doctors who prescribe them do not tell their patients about this.

It's also good to remember the reason WHY the patient was prescribed a statin: heart disease or diabetes. Both these disease processes produce conditions which deplete, and therefore require supplementation of, CoQ10.

[4-17]

Proc. Natl. Acad. Sci. USA

Vol. 87, pp. 8931-8934, November 1990

Medical Sciences

Lovastatin decreases coenzyme Q levels in humans

(hypercholesterolemia/3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors/ubiquinone/drug side effects)

Karl Folkers*1\ Per Langsjoen*, Richard Willis*, Phillip Richardson*, Li-Jun Xia*, Chun-Qu Ye*,

AND HlROO TAMAGAWA*

'University of Texas at Austin, Austin, TX 78712; and *The Health Center at Tyler, The University of Texas at Tyler, Tyler, TX 75710

Contributed by Karl Folkers, June 20, 1990

ABSTRACT       Lovastatin is clinically used to treat patients with hypercholesterolemia and successfully lowers cholesterol levels. The mechanism of action of lovastatin is inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an enzyme involved in the biosynthesis of cholesterol from acetyl-CoA. Inhibition of this enzyme could also inhibit the intrinsic bio­synthesis of coenzyme Qlo (CoQ10), but there have not been definitive data on whether lovastatin reduces levels of CoQ10 as it does cholesterol. The clinical use of lovastatin is to reduce a risk of cardiac disease, and if lovastatin were to reduce levels of CoQio, this reduction would constitute a new risk of cardiac disease, since it is established that CoQio is indispensable for cardiac function. We have conducted three related protocols to determine whether lovastatin does indeed inhibit the biosyn­thesis of CoQ10. One protocol was done on rats, and is reported in the preceding paper [Willis, R. A., Folkers, K., Tucker, J. L., Ye, C.-Q., Xia, L.-J. & Tamagawa, H. (1990) Proc. Natl. Acad. Sci. USA 87, 8928-8930]. The other two protocols are reported here. One involved patients in a hospital, and the other involved a volunteer who permitted extraordinary mon­itoring of CoQio and cholesterol levels and cardiac function. All data from the three protocols revealed that lovastatin does indeed lower levels of CoQ10. The five hospitalized patients, 43-72 years old, revealed increased cardiac disease from lovastatin, which was life-threatening for patients having class IV cardiomyopathy before lovastatin or after taking lovastatin. Oral administration of CoQ10 increased blood levels of CoQ10 and was generally accompanied by an improvement in cardiac function. Although a successful drug, lovastatin does have side effects, particularly including liver dysfunction, which presum­ably can be caused by the lovastatin-induced deficiency of CoQ10.

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Men and women with congestive heart failure, when given the same dose of carnitine included in CardioFuel, lowered heart rate and water retention, and needed fewer drugs to strengthen the heart. It also improved their lipid profile. Most importantly, they felt better!

[5-28]

Evaluation of the therapeutic efficacy of L-carnitine in congestive heart failure.

Ghidini O, Azzurro M, Vita G, Sartori G.

Reparto Medicina Interna, Ospedale Bussolengo, Verona, Italy.

To evaluate the therapeutic efficacy of L-carnitine in elderly subjects suffering from heart failure, secondary to ischemic and/or hypertensive heart disease, 38 patients (22 men, 16 women) were studied, aged from 65 to 82 years. In addition to traditional therapy (digitalis, diuretics, antiarrhythmic agents) given in all cases, 21 patients received oral L-carnitine on the basis of a randomized protocol in 1-g doses twice daily for 45 days (the other 17 received placebo). In the group treated with L-carnitine, a distinct improvement was observed in both subjective and objective conditions; reduced heart rate, edema and dyspnea, increased diuresis and a marked reduction in daily digitalis consumption. L-carnitine treatment also induced a significant reduction in serum cholesterol and triglyceride levels. No adverse reactions attributable to L-carnitine administration were observed in any of the patients.

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