Considerations for Supplementing with Coenzyme Q<sub>10</sub> During Statin Therapy

Levy, Hedva Barenholtz; Kohlhaas, Heather K

doi:10.1345/aph.1g409

Cited by 29 publications

(26 citation statements)

References 31 publications

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“…Chronic inhibition of HMG-CoA reductase can lead to decreased levels of numerous non-sterol metabolites that are essential for cell viability (Levy and Kohlhaas, 2006). Furthermore, recent clinical studies suggest that the use of high doses of statins may lead to an increased risk of developing type II diabetes.…”

Section: Isoprenoids Fpps/ggpps and Neurodegeneration—the Current Hypmentioning

confidence: 99%

Human isoprenoid synthase enzymes as therapeutic targets

et al. 2014

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In the human body, the complex biochemical network known as the mevalonate pathway is responsible for the biosynthesis of all isoprenoids, which consists of a vast array of metabolites that are vital for proper cellular functions. Two key isoprenoids, farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP) are responsible for the post-translational prenylation of small GTP-binding proteins, and serve as the biosynthetic precursors to numerous other biomolecules. The down-stream metabolite of FPP and GGPP is squalene, the precursor to steroids, bile acids, lipoproteins, and vitamin D. In the past, interest in prenyl synthase inhibitors focused mainly on the role of the FPP in lytic bone diseases. More recently pre-clinical and clinical studies have strongly implicated high levels of protein prenylation in a plethora of human diseases, including non-skeletal cancers, the progression of neurodegenerative diseases and cardiovascular diseases. In this review, we focus mainly on the potential therapeutic value of down-regulating the biosynthesis of FPP, GGPP, and squalene. We summarize the most recent drug discovery efforts and the structural data available that support the current on-going studies.

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Section: Isoprenoids Fpps/ggpps and Neurodegeneration—the Current Hypmentioning

confidence: 99%

Human isoprenoid synthase enzymes as therapeutic targets

et al. 2014

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“…However, the results of our studies and other authorities contradict this hypothesis [3,12]. Apart from inhibition of cholesterol (CH) biosynthesis, statins block the synthesis of the major antioxidant compound ubiquinone (ubiphenol) Q 10 [10] protecting plasma low-density lipoproteins (LDL) from atherogenic oxidative modification. Statins also block the synthesis of selenoproteins (e.g., Se-containing glutathione peroxidase utilizing lipid hydroperoxides) [12].…”

mentioning

confidence: 54%

Effect of β-hydroxy-β-methylglutaryl coenzyme a reductase inhibitors and antioxidant vitamins on free radical lipid oxidation in rat liver

et al. 2007

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We studied the effects of two inhibitors of beta-hydroxy-beta-methylglutaryl coenzyme A reductase, simvastatin and lovastatin, on the lag phase of ascorbate-dependent lipid oxidation in rat liver. Oxidizability of liver biological membranes significantly increased in intact animals and rats with induced hypercholesterolemia after peroral administration of these statins. The lag phase of ascorbate-dependent lipid oxidation in liver biomembranes decreased by 2.1 times in hypercholesterolemic rats. In animals of the lovastatin group this parameter decreased by 4.4 times compared to the control. In intact rats receiving simvastatin, the lag phase of oxidation in biomembranes from the liver decreased practically by 2 times. At the same time, in animals receiving simvastatin in combination with antioxidant vitamins (vitamins E and C, provitamin A) and selenium, the period of induction of oxidation increased by 3.3 times. Our results indicate that beta-hydroxy-beta-methylglutaryl coenzyme A reductase inhibitors produce a prooxidant effect on the liver, which can be prevented by administration of antioxidant agents.

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“…The only randomised controlled clinical trials investigating this area showed contrasting results and further well-performed clinical trials are needed to investigate whether CoQ 10 can be used to support statin therapy. Although several studies have shown that plasma CoQ 10 levels are decreased after statin therapy, existing evidence also suggests that skeletal muscle CoQ 10 levels are not affected or even increased after statins (113,115,116) .…”

Section: Effects Of Combination Therapy With Coenzyme Q 10 and Statinsmentioning

confidence: 99%

Support of drug therapy using functional foods and dietary supplements: focus on statin therapy

et al. 2010

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Functional foods and dietary supplements might have a role in supporting drug therapy. These products may (1) have an additive effect to the effect that a drug has in reducing risk factors associated with certain conditions, (2) contribute to improve risk factors associated with the condition, other than the risk factor that the drug is dealing with, or (3) reduce drug-associated side effects, for example, by restoring depleted compounds or by reducing the necessary dose of the drug. Possible advantages compared with a multidrug therapy are lower drug costs, fewer side effects and increased adherence. In the present review we have focused on the support of statin therapy using functional foods or dietary supplements containing plant sterols and/or stanols, soluble dietary fibre, n-3 PUFA or coenzyme Q 10 . We conclude that there is substantial evidence that adding plant sterols and/or stanols to statin therapy further reduces total and LDL-cholesterol by roughly 6 and 10 %, respectively. Adding n-3 PUFA to statin therapy leads to a significant reduction in plasma TAG of at least 15 %. Data are insufficient and not conclusive to recommend the use of soluble fibre or coenzyme Q 10 in patients on statin therapy and more randomised controlled trials towards these combinations are warranted. Aside from the possible beneficial effects from functional foods or dietary supplements on drug therapy, it is important to examine possible (negative) effects from the combination in the long term, for example, in post-marketing surveillance studies. Moreover, it is important to monitor whether the functional foods and dietary supplements are taken in the recommended amounts to induce significant effects. Combination therapy: Dyslipidaemia: Statins: Functional foodsThe world market for functional foods (FF) and dietary supplements (DS) is expanding rapidly. In 2010 FF are expected to represent 5 % of the total global food market (1) and the market for DS is estimated at more than $60 billion worldwide (2) . In general, the target population of FF or DS is healthy individuals with slightly elevated risk factors or some physical discomfort. However, due to the fast growing market of FF or DS and the accompanying strong advertising and marketing, also patients on medication may be stimulated to use FF or DS. This may have several consequences for the quality of drug treatment as stated by de Jong et al. with the example of the combined intake of plant sterols and/or stanols and statins (3) . Whereas they addressed the additive effect of plant sterols and/or stanols on reducing LDL-cholesterol values in patients on statin treatment, their main focus was the possible negative aspects of the combination, such as unfavourable effects on patient adherence with drug treatment and increasing the potential for food-drug interactions.In the present review we will focus on the possible beneficial effects that FF or DS may have on drug therapy. Because of the large number of subjects treated suboptimally with statins (hydroxymethylglutaryl Co...

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Considerations for Supplementing with Coenzyme Q₁₀ During Statin Therapy

Abstract: Routine CoQ10 supplementation for all patients taking statins to prevent myotoxicity is not recommended. However, certain subpopulations might be at risk and warrant further study.

Cited by 29 publications

References 31 publications

Human isoprenoid synthase enzymes as therapeutic targets

Human isoprenoid synthase enzymes as therapeutic targets

Effect of β-hydroxy-β-methylglutaryl coenzyme a reductase inhibitors and antioxidant vitamins on free radical lipid oxidation in rat liver

Support of drug therapy using functional foods and dietary supplements: focus on statin therapy

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Considerations for Supplementing with Coenzyme Q10 During Statin Therapy

Abstract: Routine CoQ10 supplementation for all patients taking statins to prevent myotoxicity is not recommended. However, certain subpopulations might be at risk and warrant further study.

Cited by 29 publications

References 31 publications

Human isoprenoid synthase enzymes as therapeutic targets

Human isoprenoid synthase enzymes as therapeutic targets

Effect of β-hydroxy-β-methylglutaryl coenzyme a reductase inhibitors and antioxidant vitamins on free radical lipid oxidation in rat liver

Support of drug therapy using functional foods and dietary supplements: focus on statin therapy

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Product

Resources

About

Considerations for Supplementing with Coenzyme Q₁₀ During Statin Therapy