Wednesday, May 25, 2011

Coenzyme Q10

Alzheimer & CoQ10

CoenzymeQ10 (CoQ10), a potent antioxidant, may help protect our children's brain from Alzheimer’s.
CoQ10 blocked the type of brain damage that leads to Alzheimer’s disease, say researchers at Johns Hopkins University and Hamdard University in India, who tested CoQ10 on animals with Alzheimer’s-type brain damage.
The Alzheimer’s animals that did not get CoQ10 showed significant loss of cognitive performance. However, animals with Alzheimer’s-like brain damage that got daily supplements of CoQ10 showed no signs of diminished cognitive performance and were just as intellectually competent as animals with no Alzheimer’s damage.
Examinations of the animals’ brains revealed severe neurological dysfunction in those not given CoQ10 and virtually none in animals that took daily oral doses of CoQ10.
In short, the brains of the animals fed CoQ10 remained normal and their learning and memory, as determined by tests, were completely intact.
Researchers explain that ”CoQ10 supplementation improves learning and memory deficits possibly by inhibiting oxidative stress (damage from attacks by free radical chemicals that worsen with age), and improving levels of adenosine triphosphate (ATP). ATP regulates energy production in the cell’s tiny factories (mitochondria). Source: Ishrat T., Behav Brain Res 2006 Apr 16. Epub)

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Ubiquinol, the reduced form of CoQ10, dramatically improves absorption of Co Q 10 compared to supplements of ubiquinone, the unreduced form of CoQ10.


An adult can take up to 1200 mg a day and 2400 mg a day has not caused significant side effects and 20 mg/kg/day for children, according to:  CoQ10 Dosage Considerations
Side Effects

Even though CoQ10 is a supplement and occurs naturally in your body, it doesn't mean that it's side effect free. However, most CoQ10 side effects are mild including nausea, vomiting, upset stomach, heartburn, diarrhea, appetite loss, insomnia, headache, dizziness, irritability, fatigue and flu-like ailments [source: Mayo Clinic]. Some people may experience allergies to increased CoQ10. There have been some reports of rashes and itching.
Other side effects include a lowering of blood sugar within the body. This is particularly a concern for those with diabetes or hypoglycemia [source: Mayo Clinic]. In addition, if you're taking another medicine to regulate blood sugar levels, tell your doctor.
CoQ10 may decrease blood pressure -- which is potentially a great benefit to some, but those with low blood pressure, or those who are already on medication to regulate their blood pressures should exercise caution before embarking on a CoQ10 supplement regimen.


Biofactors. 2010 May-Jun;36(3):229-39.
Enhancement of shortening velocity, power, and acto-myosin crossbridge (CB) kinetics following long-term treatment with propionyl-L-carnitine, coenzyme Q10, and omega-3 fatty acids in BIO TO-2 cardiomyopathic Syrian hamsters papillary muscle.

Vargiu R, Littarru GP, Fraschini M, Perinu A, Tiano L, Capra A, Mancinelli R.

Department of Science Applied to Biosystems, Section of Physiology and Human Nutrition, University of Cagliari, Italy.

Impaired functions of myocardial muscle cells in human and animals, is a primary defect associated with idiopathic dilated cardiomyopathy (DCM). The pathophysiological mechanisms implicated in the DCM are yet to be clarified and an effective therapy is still not available. The BIO TO-2 cardiomyopathic Syrian Hamsters (CMSHs) represent an animal model of idiopathic DCM. The aim of this study was to investigate the effect of long-term treatment (2 months) with propionyl-L-carnitine (PLC), coenzyme Q(10), omega-3 fatty acids and a combination of these three agents (formulation HS12607) on mechanical properties and acto-myosin crossbridges (CBs) kinetics of left ventricular (LV) papillary muscle from control and treated 10 month old BIO TO-2 CMSHs. Isometric and isotonic contractile properties of isolated papillary muscle from control and treated CMSHs were investigated, and acto-myosin CB number, force and kinetics were calculated using Huxley's equations. Mechanical parameter values were higher in treated than in control hamsters, particularly when substances were administered together in a coformulation (HS12607). Compared to control, HS12607-treated papillary muscles showed ....... a significant increase of maximum peak isometric tension (P(o)) (30.06 +/- 4.91 vs. 19.74 +/- 5.00 mN/mm(2)), maximum extent of muscle shortening (0.13 +/- 0.03 vs. 0.07 +/- 0.02 L/L(max)), maximum unloaded shortening velocity (1.18 +/- 0.24 vs. 0.53 +/- 0.13 L/L(max) s(-1)) and maximum peak of power output (5.52 +/- 1.61 vs. 1.58 +/- 0.83). The curvature of the hyperbolic force-velocity relationships did not differ between control and treated hamsters. When compared to controls, acto-myosin CB number increased in treated hamsters [(6.67 +/- 1.91) 10(10)/mm(2) vs. (3.55 +/- 2.08) 10(10)/mm(2)], whereas the unitary force of single CB was similar in control and treated animals. The peak value of the rate constant for CB attachment (f(1)) and detachment (g(2)) was higher in treated animals when compared to control. (93.87 +/- 25.82 vs.47.28 +/- 10.88 s(-1) and 214.40 +/- 44.64 vs. 95.56 +/- 23.49 s(-1), respectively). In conclusion, the present study illustrates that supplementation with PLC, CoQ(10) and omega-3 fatty acids improved motor parameters, energetic, and CB kinetics of BIO TO-2 CMSH papillary muscle indicating that these naturally occurring substances may be a valid adjuvant to conventional therapy in DCM.

PMID: 20533397


Panminerva Med. 2010 Jun;52(2 Suppl 1):21-5.
Investigation of Pycnogenol® (pine bark) in combination with coenzymeQ10 in heart failure patients (NYHA II/III).

Belcaro G, Cesarone MR, Dugall M, Hosoi M, Ippolito E, Bavera P, Grossi MG.

Irvine3 Labs, Department Biomedical Sciences, Chieti-Pescara University, Pescara, Italy.

AIM: In this study we investigated benefits of a Pycnogenol - coenzyme Q10 combination (PycnoQ10) taken as an adjunct to medical treatment in stable heart failure patients. The aim of this single-blinded, 12-week observational study was to provide functional parameters such as exercise capacity, ejection fraction and distal edema.

METHODS: The essential element for inclusion was a stable level of heart failure within the past three months and stable NYHA class II or III (6 months). The heart failure management was in accordance with AHA guidelines for "best treatment." The treatment and control groups were comparable at baseline. The mean age of the PycnoQ10-treated patients was 61.3+/-7.1 years and 62.1+/-3.7 in the control group. All patients were taking medication and most patients (>75%) used three or more drugs for heart failure treatment. There were two dropouts in the PycnoQ10 treatment group and 6 in the control group (5 NYHA III patients).

RESULTS: Nine PycnoQ10 treated patients (out of 32) and 3 (out of 21) taking placebo improved NYHA class. Systolic and diastolic pressure as well as heart rate and respiratory rate were significantly lowered with PycnoQ10 as compared to the control group (P<0.05). No significant changes were observed in controls. Heart ejection fraction increased by 22.4% in the treatment group (P<0.05) versus 4.0% in controls. Walking distance on treadmill increased 3.3-fold in PycnoQ10 treated patients (P<0.05) but marginally improved in the control group. Distal edema decreased significantly in PycnoQ10 treated patients and only slightly in controls.

CONCLUSION: The association of Pycnogenol and CoQ10 may offer an important therapeutic option with a very good tolerability that improves heart failure management without side effects.

PMID: 20657530

Med Hypotheses. 2010 Aug;75(2):141-7. Epub 2010 Jan 18.
Practical prevention of cardiac remodeling and atrial fibrillation with full-spectrum antioxidant therapy and ancillary strategies.

McCarty MF.

NutriGuard Research, 1051 Hermes Ave., Encinitas, CA 92024, USA.

A wealth of research data points to increased oxidative stress as a key driver of the cardiac remodeling triggered by chronic pressure overload, loss of functional myocardial tissue, or atrial fibrillation. Oxidative stress is a mediator of the cardiomyocyte hypertrophy and apoptosis, the cardiac fibrosis, and the deficits in cardiac function which typify this syndrome, and may play a role in initiating and sustaining atrial fibrillation. Nox2- and Nox4-dependent NADPH oxidase activity appears to be a major source of this oxidative stress, and oxidants can induce conformational changes in xanthine dehydrogenase, nitric oxide synthase, and the mitochondrial respiratory chain which increase their capacity to generate superoxide as well. Consistent with these insights, various synthetic antioxidants have been shown to suppress cardiac remodeling in rodents subjected to myocardial infarction, aortic constriction, or rapid atrial pacing. It may prove feasible to achieve comparable benefits in humans through use of a "full-spectrum antioxidant therapy" (FSAT) that features a complementary array of natural antioxidants. Spirulina is a rich source of phycocyanobilin, a derivative and homolog of biliverdin that appears to mimic the potent inhibitory impact of biliverdin and free bilirubin on NADPH oxidase activity. Mega-doses of folate can markedly increase intracellular levels of tetrahydrofolates which have potent and versatile radical-scavenging activities - including efficient quenching of peroxynitrite-derived radicals Supplemental coenzyme Q10, already shown to improve heart function in clinical congestive failure, can provide important antioxidant protection to mitochondria. Phase 2 inducer nutraceuticals such as lipoic acid, administered in conjunction with N-acetylcysteine, have the potential to blunt the impact of oxidative stress by boosting myocardial levels of glutathione. While taurine can function as an antioxidant for myeloperoxidase-derived radicals, its positive inotropic effect on the failing heart seems more likely to reflect an effect on intracellular calcium dynamics. These measures could aid control of cardiac modeling less directly by lowering elevated blood pressure, or by aiding the perfusion of ischemic cardiac regions through an improvement in coronary endothelial function. Since nitric oxide functions physiologically to oppose cardiomyocyte hypertrophy and cardiac fibrosis, and is also a key regulator of blood pressure and endothelial function, cocoa flavanols - which provoke endothelial release of nitric oxide - might usefully complement the antioxidant measures recommended here.
Copyright 2010 Elsevier Ltd. All rights reserved.

PMID: 20083360


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