Some information about Q10.You can take this together with 200 mg magnesium citrate.
CoQ10 and the Heart
CoQ10 was discovered in 1957-relatively late as vitamins discoveries go-by Frederick Crane, Ph.D., now at Purdue University in Indiana. Four years later, Peter D. Mitchell, Ph.D., of the University of Edinburgh, figured out how CoQ10 produces energy at the cellular level and, in 1978, won the Nobel Prize for chemistry for this discovery.
By the mid-1960s, Japanese researchers recognized that CoQ10 concentrated in the myocardium, or heart muscle. Its role in the heart makes sense: the heart, one of the body's most energetic organs, beats approximately 100,000 times a day and 36 million times a year, and depends on CoQ10 for "bioenergetics." In the early 1980s, Folkers, director of the Institute for Biochemical Research at the University of Texas, and the late Per H. Langsjoen, M.D. (Peter's father), conducted the first study of CoQ10 in the treatment of cardiomyopathy, a form of progressive heart failure.
The findings were astounding. In a well-controlled study, 19 patients who were expected to die from heart failure rebounded with an "extraordinary clinical improvement," according to Folkers and Langsjoen's report in the Proceedings of the National Academy of Sciences of the USA (June 1985;82:4240-4).
Case studies demonstrate the dramatic effect of CoQ10. In Biochemical and Biophysical Research Communications (Jan 15, 1993;182:247-53), Folkers described a 43-year-old man suffering from cardiomyopathy. After being given CoQ10, his enlarged heart became smaller (indicating it was working more efficiently), and he was able to resume an "extremely active athletic lifestyle." The heart function of another patient, a 50-year-old man with very severe cardiomyopathy, returned after he took CoQ10, and he has since had "no limitations of activity."
Numerous other studies have confirmed the role of CoQ10 in treating heart failure, which is otherwise treated with drugs (such as beta blockers and ACE inhibitors)-or with a heart transplant. A sampling:
• Sixty-five cardiologists treating 806 patients for heart failure or ischemic heart disease indicated "significant" benefits from CoQ10. (Langsjoen, PH, Klinische Wochenschrift, 1988;66:583-90.)
• Twenty-five hundred heart failure patients at 173 Italian medical centers were given 50 to 150 mg CoQ10 daily for three months. Eighty percent of the patients had some type of improvement. (Clinical Investigator, Aug. 1993;71S:145-9)
• A 12-month double-blind study compared 319 patients taking CoQ10 with 322 taking a placebo. CoQ10 reduced complications of heart failure as well as the need for hospitalization. (Clinical Investigator, Aug. 1993;71S:134-6).
The best Q 10 you can buy is Ubiquinol and not Ubiquinone.
Compared with conventional ubiquinone CoQ10, ubiquinol was shown to absorb into the bloodstream up to eight times better, reduce fatique 90%, and slow aging in middle-aged mice 40% better.
About the carnitine,
Several experimental studies have shown that levocarnitine reduces myocardial injury after ischemia and reperfusion by counteracting the toxic effect of high levels of free fatty acids, which occur in ischemia, and by improving carbohydrate metabolism. In addition to increasing the rate of fatty acid transport into mitochondria, levocarnitine reduces the intramitochondrial ratio of acetyl-CoA to free CoA, thus stimulating the activity of pyruvate dehydrogenase and increasing the oxidation of pyruvate. Supplementation of the myocardium with levocarnitine results in an increased tissue carnitine content, a prevention of the loss of high-energy phosphate stores, ischemic injury, and improved heart recovery on reperfusion. Clinically, levocarnitine has been shown to have anti-ischemic properties. In small short-term studies, levocarnitine acts as an antianginal agent that reduces ST segment depression and left ventricular end-diastolic pressure. These short-term studies also show that levocarnitine releases the lactate of coronary artery disease patients subjected to either exercise testing or atrial pacing. These cardioprotective effects have been confirmed during aortocoronary bypass grafting and acute myocardial infarction. In a randomized multicenter trial performed on 472 patients, levocarnitine treatment (9 g/day by intravenous infusion for 5 initial days and 6 g/day orally for the next 12 months), when initiated early after acute myocardial infarction, attenuated left ventricular dilatation and prevented ventricular remodeling. In treated patients, there was a trend towards a reduction in the combined incidence of death and CHF after discharge. Levocarnitine could improve ischemia and reperfusion by (1) preventing the accumulation of long-chain acyl-CoA, which facilitates the production of free radicals by damaged mitochondria; (2) improving repair mechanisms for oxidative-induced damage to membrane phospholipids; (3) inhibiting malignancy arrhythmias because of accumulation within the myocardium of long-chain acyl-CoA; and (4) reducing the ischemia-induced apoptosis and the consequent remodeling of the left ventricle. Propionyl-l-carnitine is a carnitine derivative that has a high affinity for muscular carnitine transferase, and it increases cellular carnitine content, thereby allowing free fatty acid transport into the mitochondria. Moreover, propionyl-l-carnitine stimulates a better efficiency of the Krebs cycle during hypoxia by providing it with a very easily usable substrate, propionate, which is rapidly transformed into succinate without energy consumption (anaplerotic pathway). Alone, propionate cannot be administered to patients in view of its toxicity. The results of phase-2 studies in chronic heart failure patients showed that long-term oral treatment with propionyl-l-carnitine improves maximum exercise duration and maximum oxygen consumption over placebo and indicated a specific propionyl-l-carnitine effect on peripheral muscle metabolism. A multicenter trial on 537 patients showed that propionyl-l-carnitine improves exercise capacity in patients with heart failure, but preserved cardiac function.
I really don`t believe that changes the brand gives you any trouble, I never heard of this before.
D-Ribose is a part of the protocol, but not everyone is using this,
D-Ribose improves diastolic function and quality of life in congestive heart failure patients: a prospective feasibility study.Omran H, Illien S, MacCarter D, St Cyr J, Luderitz B.
Department of Medicine-Cardiology, University of Bonn, Sigmund-Freud-Street 25, D-53105, Bonn, Germany. firstname.lastname@example.org
Patients with chronic coronary heart disease often suffer from congestive heart failure (CHF) despite multiple drug therapies. D-Ribose has been shown in animal models to improve cardiac energy metabolism and function following ischaemia. This was a prospective, double blind, randomized, crossover design study, to assess the effect of oral D-ribose supplementation on cardiac hemodynamics and quality of life in 15 patients with chronic coronary artery disease and CHF. The study consisted of two treatment periods of 3 weeks, during which either oral D-ribose or placebo was administered followed by a 1-week wash out period, and then administration of the other supplement. Assessment of myocardial functional parameters by echocardiography, quality of life using the SF-36 questionnaire and functional capacity using cycle ergometer testing was performed. The administration of D-ribose resulted in an enhancement of atrial contribution to left ventricular filling (40+/-11 vs. 45+/-9%, P=0.02), a smaller left atrial dimension (54+/-20 vs. 47+/-18 ml, P=0.02) and a shortened E wave deceleration (235+/-64 vs. 196+/-42, P=0.002) by echocardiography. Further, D-ribose also demonstrated a significant improvement of the patient's quality of life (417+/-118 vs. 467+/-128, P< or =0.01). In comparison, placebo did not result in any significant echocardiographic changes or in quality of life. This feasibility study in patients with coronary artery disease in CHF revealed the beneficial effects of D-ribose by improving diastolic functional parameters and enhancing quality of life.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum