Cholesterol medications lower CoQ10 – Dangerous

Over the past two decades cholesterol medications have exploded on the medical market. They have become some of the most popular prescriptions recommended today. Their sales are in the multi millions.
But, as research continues we are finding out that there are more and more side effects caused by these drugs.
WE have all heard about the liver effects of the statins, and many have heard about or experienced leg cramping. Yet one of the most dangerous complications relates to lowering of coenzyme Q10.
This has been seen in virtually all of this class of medications.
As Q10 is lowered this can decrease contraction of heart muscle, which can lead to or worsen existing heart failure. It is also an important nutrient in maintenance of energy and metabolism.
Some of the latest neurological research describes its significance as an antioxidant that protects brain tissue. Loss of Q10 and Glutathione in the brain may allow rapid degeneration and lead to Parkinson`s disease and Alzheimers disease.
Therapies for Parkinson`s that work extremely well include high dose Q10 (up to 1200 mg) and intravenous Glutathione.
It is now postulated that long term use of cholesterol lowering meds might increase the risk for Parkinson`s.
All the more reason to lower cholesterol naturally with a low carb diet, exercise and correction of vitamin/mineral and hormone deficiency.
Stay tuned,
Atorvastatin Decreases the Coenzyme Q10 Level in the Blood of Patients at Risk for Cardiovascular Disease and Stroke 
Background  Statins (3-hydroxy-3-methylglutaryl coenzymeA reductase inhibitors) are widely used for the treatment ofhypercholesterolemia and coronary heart disease and for theprevention of stroke. There have been various adverse effects,most commonly affecting muscle and ranging from myalgia to rhabdomyolysis.These adverse effects may be due to a coenzyme Q10 (CoQ10) deficiencybecause inhibition of cholesterol biosynthesis also inhibitsthe synthesis of CoQ10.
Objective  To measure CoQ10 levels in blood from hypercholesterolemicsubjects before and after exposure to atorvastatin calcium,80 mg/d, for 14 and 30 days.
Design  Prospective blinded study of the effects of short-termexposure to atorvastatin on blood levels of CoQ10.
Setting  Stroke center at an academic tertiary care hospital.
Patients  We examined a cohort of 34 subjects eligiblefor statin treatment according to National Cholesterol EducationProgram: Adult Treatment Panel III criteria.
Results  The mean ± SD blood concentration of CoQ10was 1.26 ± 0.47 µg/mL at baseline, and decreasedto 0.62 ± 0.39 µg/mL after 30 days of atorvastatintherapy (P<.001). A significant decrease was already detectableafter 14 days of treatment (P<.001).
Conclusions  Even brief exposure to atorvastatin causesa marked decrease in blood CoQ10 concentration. Widespread inhibitionof CoQ10 synthesis could explain the most commonly reportedadverse effects of statins, especially exercise intolerance,myalgia, and myoglobinuria.
Coenzyme Q10 inhibits proliferation of breast cancer cells while stabilizing growth in primary cells in vitro
Coenzyme Q10 (Q10) is an integral component of the mitochondrialinner membrane and serves as an electron carrier in ATP production.Q10 is also a potent scavenger of reactive oxygen species, akey factor in carcinogenesis. Moreover, prior data suggest oralsupplementation is effective in normalizing reduced Q10 serumlevels in cancer patients. We recently demonstrated that Q10induces apoptosis in human melanoma cells and significantlyreduces tumor size in nude mice without any adverse effectsto neonatal fibroblasts (nfib) and keratinocytes (SC-KC).
Takentogether, we hypothesize that Q10 may be an effective anti-tumoragent in breast carcinomas. Given the lipophilic nature of themolecule, in vitro experiments have thus far been difficultto perform. Our laboratory has discovered a novel method tosolubilize Q10 permitting quantitative in vitro experiments.Given the genetic heterogeneity of breast cancer that manifestinto phenotypic diversity, we tested an array of mammary celllines (MCF-7, SK-BR-3, MDA-MB-468, BT-20, ZR-75) each expressingunique mutations. Each cell line was seeded into 6-well tissueculture plates and subjected to a range of Q10 concentrations(0-100µM).
Experiments were performed under physiologicconditions and cells were trypsinized and counted using a Coulter®Particle Counter following incubation. A significant (p<0.05)inhibition of proliferation was observed in a concentrationdependent manner in each of the malignant mammary lines treatedwith Q10 with the exception of ZR-75 cells (Overexpression ofMUC-1). Optimal inhibitions after 72 hours with 100µMQ10 were as follows: MCF7: 52%, SK-BR-3: 44%, MDA-MB-468: 42%,BT-20: 31%, and ZR-75: 1%.
In conclusion, we report herein thatQ10 inhibits the proliferation of the above oncogenic linesexcept that expressing the MUC-1 mutation (ZR-75). Currently,we are testing these lines using JC-1 and Annexin V-PE staining,and microarray analysis. The aforementioned data serve as araionale for the use of Q10 as an adjuvant therapy in breastcancer.
Effects of Coenzyme Q10 in Early Parkinson Disease
Evidence of Slowing of the Functional Decline
Background  Parkinson disease (PD) is a degenerative neurologicaldisorder for which no treatment has been shown to slow the progression.
Objective  To determine whether a range of dosages of coenzymeQ10 is safe and well tolerated and could slow the functionaldecline in PD.
Design  Multicenter, randomized, parallel-group, placebo-controlled,double-blind, dosage-ranging trial.
Setting  Academic movement disorders clinics.
Patients  Eighty subjects with early PD who did not requiretreatment for their disability.
Interventions  Random assignment to placebo or coenzymeQ10 at dosages of 300, 600, or 1200 mg/d.
Main Outcome Measure  The subjects underwent evaluationwith the Unified Parkinson Disease Rating Scale (UPDRS) at thescreening, baseline, and 1-, 4-, 8-, 12-, and 16-month visits.They were followed up for 16 months or until disability requiring treatmentwith levodopa had developed. The primary response variable wasthe change in the total score on the UPDRS from baseline tothe last visit.
Results  The adjusted mean total UPDRS changes were +11.99for the placebo group, +8.81 for the 300-mg/d group, +10.82for the 600-mg/d group, and +6.69 for the 1200-mg/d group. TheP value for the primary analysis, a test for a linear trendbetween the dosage and the mean change in the total UPDRS score,was .09, which met our prespecified criteria for a positivetrend for the trial. A prespecified, secondary analysis wasthe comparison of each treatment group with the placebo group,and the difference between the 1200-mg/d and placebo groupswas significant (P = .04).
Conclusions  Coenzyme Q10 was safe and well tolerated atdosages of up to 1200 mg/d. Less disability developed in subjectsassigned to coenzyme Q10 than in those assigned to placebo,and the benefit was greatest in subjects receiving the highestdosage. Coenzyme Q10 appears to slow the progressive deteriorationof function in PD, but these results need to be confirmed ina larger study
Role of mitochondria in neuronal cell death induced by oxidative stress; neuroprotection by Coenzyme Q10
Neuronal cells depend on mitochondrial oxidative phosphorylation for most of their energy needs and therefore are at a particular risk for oxidative stress. Mitochondria play an important role in energy production and oxidative stress-induced apoptosis. In the present study, we have demonstrated that external oxidative stress induces mitochondrial dysfunction leading to increased ROS generation and ultimately apoptotic cell death in neuronal cells.
Furthermore, we have investigated the role of Coenzyme Q10 as a neuroprotective agent. Coenzyme Q10 is a component of the mitochondrial respiratory chain and a potent anti-oxidant. Our results indicate that total cellular ROS generation was inhibited by Coenzyme Q10. Further, pre-treatment with Coenzyme Q10 maintained mitochondrial membrane potential during oxidative stress and reduced the amount of mitochondrial ROS generation. Our study suggests that water-soluble Coenzyme Q10 acts by stabilizing the mitochondrial membrane when neuronal cells are subjected to oxidative stress. Therefore, Coenzyme Q10 has the potential to be used as a therapeutic intervention for neurodegenerative diseases.