Coenzym Q10


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Co-enzym Q10


Als je regelmatig tijdschriften leest kom je zeer vaak advertenties voor Q10 tegen. Het Co-enzym Q10 zorgt ervoor dat je cellen energie krijgen en is dus zeer belangrijk voor je hart en spieren. Als je ouder wordt neemt dit niveau Q10 ook af. Dit kan zich uiten in vermoeidheid, spierzwakte etc.

Het vervelende echter is dat steeds meer mensen cholesterolremmers slikken en daarmee ook het Q10 niveau nog verder verlagen. Aangezien je hart ook een spier is zul je begrijpen wat er kan gebeuren als dit steeds verder afneemt, een grotere kans op hartfalen en spierproblemen.....

Ik zal zoveel mogelijk artikelen en studies mbt Q10 in kaart brengen en deze pagina dan ook verder uitbouwen.

Ook belangrijk is de mogelijke remming van Alzheimer door Q10.

Verder is er in Amerika recentelijk een labstudie gedaan op prostaatkankercellen, wanneer Q10 werd verlaagd gingen deze cellen groeien en woekeren, nam Q10 toe dan werden de cellen kleiner.

Ron


Co-enzym Q10

Co-enzym Q10 wordt in iedere lichaamscel aangetroffen. De vetoplosbare stof wordt ook wel ubichinon genoemd, wat vrij vertaald zoiets betekent als 'overal aanwezig'. Zonder coenzym Q10 is energievorming in de cel niet mogelijk en sterft de cel. Primair fungeert co-enzym Q10 als co-factor in de oxidatieve fosforylering (celademhaling) in de mitochondriŽn, de cellulaire 'energiecentrales'. Daarnaast is co-enzym Q10 een krachtige antioxidant en radicaalvanger, zorgt het mede voor het soepel houden van cellulaire membranen en voorkomt het lipidenperoxidatie in deze membranen.

http://www.orthokennis.nl/ResearchItem.asp?IDResearch=27


CoŽnzym-Q10 belangrijk bij statinegebruik

Behandeling met de cholesterolverlagende statine, atorvastatine (Lipitor), verslechterde de diastolische functie van de linker hartkamer - het moment waarop de hartspier zich vult met bloed. Deze stoornis is vaak een voorbode van hartfalen op latere leeftijd. Suppletie met coŽnzym-Q10 liet een verbeterde diastole zien bij de patiŽnten bij wie de kwaal was opgetreden (Am J Cardiol 2004; 94:1306-10

http://www.orthoeurope.com/home.php?page=dossiers-statines
uit: Ortho nr.1, 2005


Onderzoekers ontdekken hoe Q10 een rol speelt bij kanker

Onderzoekers van de Miami Leonard M. Miller School of Medicine (Universiteit van Miami) hebben ontdekt welke rol Q10 bij kanker kan spelen. Het blijkt dat Q10 het eiwit Bcl-2 remt. Bij kankercellen zie je dat deze meer Bcl-2 bevatten dan Q10. Stopten de onderzoekers bijvoorbeeld extra Q10 bij prostaatkankercellen dan werden de  Bcl-2 levels verlaagd en werden de tumoren kleiner.

Vorige jaar al ontdekten zij dat Q10 tot celdood kon leiden van kankercellen maar nu blijkt ookt dat Bcl-2 eiwitten dus als soldaten van kankercellen dienen waardoor chemotherapie en bestraling niet aan kunnen slaan. De onderzoekers werken nu aan een creme waarmee ze Q10 makkelijk door de huid heen kunnen transporteren. Er is al grote interesse van onderzoekers en biotech bedrijven voor het uitwerken van deze vinding. Pathfinder management heeft de technologie gelicenseerd.

http://www.med.miami.edu/news/view.asp?id=519


Q10 helpt het hart en tandvlees

Uit diverse onderzoeken blijkt namelijk dat het middel als aanvullende therapie bij kransslagadervernauwing, na een hartinfarct of bij hartfalen een gunstig effect op de aandoening kan hebben. Ook worden gunstige effecten gemeld bij parodontitis (geÔnfecteerd tandvlees). Het zou verder het afweersysteem versterken, reden waarom het ook wordt ingezet bij immuunziekten zoals aids.

http://www.refdag.nl/oud/gezo/980624gezo01.html


Statines en Q10

Arteriosclerose wordt vaak behandeld met lipide (=vet) verlagende middelen, statines bijvoorbeeld werken cholesterol verlagend. De bekendste statines zijn Zocor, Crestor, Lipitor en Selektine. De cholesterolverlagende werking van statines wordt bereikt door de aanmaak van mevalonaat te te blokkeren.

Mevalonaat is de voorloper van cholesterol, coŽnzym Q10 en selenoproteÔnen.

Door mevalonaat, via een remming op HMG-CoA (3-hydroxy-3-methyl-glutaryl coŽnzym A - voorloper van mevalonaat), te blokkeren (de HMG-CoA reductase) wordt inderdaad minder cholesterol aangemaakt. Dit is ook meetbaar.

Nadeel is dat dan ook de aanmaak van geslachtshormonen, galzouten en vitamine D geremd wordt omdat deze worden gemaakt uit cholesterol.

Door mevalonaat te blokkeren wordt ook de aanmaak van het coŽnzym Q10 geblokkeert. Q10 is onder andere nodig voor de aanmaak van energie in de hartspiercellen. Door het slikken van statines wordt deze aanmaak met 40% onderdrukt. Het hart kan zijn werk niet meer doen (energietekort) en een chronisch hartfalen kan daarvan het gevolg zijn.

http://www.kruidenvrouwtje.nl/zozitdat/arteriosclerose.htm


CoŽnzym Q10 en glutathionrepletie pijlers in orthomoleculaire aanpak Parkinson

In de Orthomoleculaire Koerier, nummer 97 van december 2002, staat op pagina 10 een kort redactioneel over nieuwe bevindingen met coŽnzym Q10 (CoQ10) bij de behandeling van de ziekte van Parkinson. (Shults et al. Arch. Neurol. 2002; 59: 1541-1550). In dit artikel wordt ingegaan op de achtergronden van de ziekte, die zich met name toespitsten op de ontregeling van de functie van mitochondriŽn en de rol van oxidatieve stress. In het licht daarvan worden de resultaten uit het onderzoek van Shults et al. besproken en wordt ingegaan op de hoge doseringen CoQ10, die in het onderzoek zijn gebruikt.

http://www.timpani.nl/download.asp?file=content/artikelq10.doc


Internationaal


Serious side-effects related to statins

The International Coenzyme Q10 Association is a group of scientists and medical professionals with a research focus on coenzyme Q10, which plays a crucial role in cellular ATP production. It has been demonstrated that HMG-CoA reductase inhibitors, also known as statins, block the biosynthesis of coenzyme Q10 and of dolichol, besides the well known effect on cholesterol synthesis. Several studies have shown that administration of different kinds of statins can lead to a parallel decrease of coenzyme Q10 and cholesterol in plasma. Animal studies have also demonstrated a tissue depletion in the course of statin treatment which was particularly evident in aged animals. We can reasonably hypothesize that in some conditions where other CoQ10 impoverishing situations exist, treatment with statins may seriously impair plasma and possibly tissue levels of coenzyme Q10. A physiological decline in tissue CoQ10 has for instance been implicated in ageing which would make the elderly more susceptible to statin-induced CoQ10 depletion.

http://www.coenzymeq10.it/issues/issues.html


Introduction to Q10

Coenzyme Q10 (CoQ 10) or ubiquinone is essentially a vitamin or vitamin-like substance. Disagreements on nomenclature notwithstanding, vitamins are defined as organic compounds essential in minute amounts for normal body function acting as coenzymes or precursors to coenzymes. They are present naturally in foods and sometimes are also synthesized in the body. CoQ10 likewise is found in small amounts in a wide variety of foods and is synthesized in all tissues. The biosynthesis of CoQ10 from the amino acid tyrosine is a multistage process requiring at least eight vitamins and several trace elements. Coenzymes are cofactors upon which the comparatively large and complex enzymes absolutely depend for their function. Coenzyme Q10 is the coenzyme for at least three mitochondrial enzymes (complexes I, II and III) as well as enzymes in other parts of the cell. Mitochondrial enzymes of the oxidative phosphorylation pathway are essential for the production of the high-energy phosphate, adenosine triphosphate (ATP), upon which all cellular functions depend.

http://faculty.washington.edu/~ely/coenzq10.html


Coenzyme Q10

ROBERT ALAN BONAKDAR, M.D., and ERMINIA GUARNERI, M.D.
Scripps Center for Integrative Medicine, La Jolla, California

Coenzyme Q10 is a vitamin-like substance used in the treatment of a variety of disorders primarily related to suboptimal cellular energy metabolism and oxidative injury. Studies supporting the efficacy of coenzyme Q10 appear most promising for neurodegenerative disorders such as Parkinson's disease and certain encephalomyopathies for which coenzyme Q10 has gained orphan drug status. Results in other areas of research, including treatment of congestive heart failure and diabetes, appear to be contradictory or need further clarification before proceeding with recommendations. Coenzyme Q10 appears to be a safe supplement with minimal side effects and low drug interaction potential.

http://www.aafp.org/afp/20050915/1065.html


Coenzyme Q10 improves blood pressure and glycaemic control: a controlled trial in subjects with type 2 diabetes.

Hodgson JM, Watts GF, Playford DA, Burke V, Croft KD.

University of Western Australia Department of Medicine and HeartSearch, Royal Perth Hospital, Perth, Western Australia, Australia.

OBJECTIVE: Our objective was to assess effects of dietary supplementation with coenzyme Q10 (CoQ) on blood pressure and glycaemic control in subjects with type 2 diabetes, and to consider oxidative stress as a potential mechanism for any effects.

CONCLUSIONS: These results show that CoQ supplementation may improve blood pressure and long-term glycaemic control in subjects with type 2 diabetes, but these improvements were not associated with reduced oxidative stress, as assessed by F2-isoprostanes. SPONSORSHIP: This study was supported by a grant from the NH&MRC, Australia.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve
&db=pubmed&dopt=Abstract&list_uids=12428181


Coenzyme Q10 and diabetic endotheliopathy: oxidative stress and the 'recoupling hypothesis'.

Chew GT, Watts GF. School of Medicine and Pharmacology, University of Western Australia, Royal Perth Hospital Unit, GPO Box X2213, Perth, Western Australia, Australia 6847.

Increased oxidative stress in diabetes mellitus may underlie the development of endothelial cell dysfunction by decreasing the availability of nitric oxide (NO) as well as by activating pro-inflammatory pathways. In the arterial wall, redox imbalance and oxidation of tetrahydrobiopterin (BH4) uncouples endothelial nitric oxide synthase (eNOS). This results in decreased production and increased consumption of NO, and generation of free radicals, such as superoxide and peroxynitrite. In the mitochondria, increased redox potential uncouples oxidative phosphorylation, resulting in inhibition of electron transport and increased transfer of electrons to molecular oxygen to form superoxide and other oxidant radicals. Coenzyme Q10 (CoQ), a potent antioxidant and a critical intermediate of the electron transport chain, may improve endothelial dysfunction by 'recoupling' eNOS and mitochondrial oxidative phosphorylation. CoQ supplementation may also act synergistically with anti-atherogenic agents, such as fibrates and statins, to improve endotheliopathy in diabetes.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=
Retrieve&db=pubmed&dopt=Abstract&list_uids=15256611


Coenzyme Q10: A Review of Essential Functions and Clinical Trials

Several clinical trials and case series have provided evidence, supporting the use of CoQ10 in the prevention and treatment of various disorders related to oxidative stress. It has been shown that CoQ10’s antioxidant properties and central role in mitochondrial oxidative phosphorylation make it useful as adjunct therapy for cardiovascular diseases such as CHF, hypertension, stable angina, drug-induced cardiotoxicity, and ventricular arrhythmia, and non-cardiac conditions including cancer, periodontal disease, compromised immune systems, COPD, and muscular dystrophy. Therefore, healthcare professionals are advocating its use as a supplement.

http://www.uspharmacist.com/oldformat.asp?
url=newlook/files/comp/acfaa8.htm


Study Suggests Coenzyme Q10 Slows Functional Decline in Parkinson's Disease

Overview Results of the first placebo-controlled, multicenter clinical trial of the compound coenzyme Q10 suggest that it can slow disease progression in patients with early-stage Parkinson's disease (PD). While the results must be confirmed in a larger study, they provide hope that this compound may ultimately provide a new way of treating PD.

Results of the first placebo-controlled, multicenter clinical trial of the compound coenzyme Q10 suggest that it can slow disease progression in patients with early-stage Parkinson's disease (PD). While the results must be confirmed in a larger study, they provide hope that this compound may ultimately provide a new way of treating PD.

The phase II study, led by Clifford Shults, M.D., of the University of California, San Diego (UCSD) School of Medicine, looked at a total of 80 PD patients at 10 centers across the country to determine if coenzyme Q10 is safe and if it can slow the rate of functional decline. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS) and appears in the October 15, 2002, issue of the Archives of Neurology . 1

"This trial suggested that coenzyme Q10 can slow the rate of deterioration in Parkinson's disease," says Dr. Shults. "However, before the compound is used widely, the results need to be confirmed in a larger group of patients."

PD is a chronic, progressive neurological disease that affects about 500,000 people in the United States. It results from the loss of brain cells that produce the neurotransmitter dopamine and causes tremor, stiffness of the limbs and trunk, impaired balance and coordination, and slowing of movements. Patients also sometimes develop other symptoms, including difficulty swallowing, disturbed sleep, and emotional problems. PD usually affects people over the age of 50, but it can affect younger people as well. While levodopa and other drugs can ease the symptoms of PD, none of the current treatments has been shown to slow the course of the disease.

The investigators believe coenzyme Q10 works by improving the function of mitochondria, the "powerhouses" that produce energy in cells. Coenzyme Q10 is an important link in the chain of chemical reactions that produces this energy. It also is a potent antioxidant - a chemical that "mops up" potentially harmful chemicals generated during normal metabolism. Previous studies carried out by Dr. Shults, Richard Haas, M.D., of UCSD and Flint Beal, M.D., of Cornell University have shown that coenzyme Q10 levels in mitochondria from PD patients are reduced and that mitochondrial function in these patients is impaired. Animal studies have shown that coenzyme Q10 can protect the area of the brain that is damaged in PD. Dr. Shults and colleagues also conducted a pilot study with PD patients which showed that consumption of up to 800 mg/day of coenzyme Q10 was well-tolerated and significantly increased the level of coenzyme Q10 in the blood.

All of the patients who took part in the new study had the three primary features of PD - tremor, stiffness, and slowed movements - and had been diagnosed with the disease within 5 years of the time they were enrolled. After an initial screening and baseline blood tests, the patients were randomly divided into four groups. Three of the groups received coenzyme Q10 at three different doses (300 mg/day, 600 mg/day, and 1,200 mg/day), along with vitamin E, while a fourth group received a matching placebo that contained vitamin E alone. Each participant received a clinical evaluation 1 month later and every 4 months for a total of 16 months or until the investigator determined that the patient needed treatment with levodopa. None of the participants or the study investigators knew which treatment each patient had received until the study ended.

The investigators found that most side effects of coenzyme Q10 were mild, and none of the patients required a reduction of their dose. The percentage of people receiving coenzyme Q10 who reported side effects was not significantly different from that of the placebo group. During the study period, the group that received the largest dose of coenzyme Q10 (1,200 mg/day) had 44 percent less decline in mental function, motor (movement) function, and ability to carry out activities of daily living, such as feeding or dressing themselves. The greatest effect was on activities of daily living. The groups that received 300 mg/day and 600 mg/day developed slightly less disability than the placebo group, but the effects were less than those in the group that received the highest dosage of coenzyme Q10 .

The groups that received coenzyme Q10 also had significant increases in the level of coenzyme Q10 in their blood and a significant increase in energy-producing reactions within their mitochondria.

The results of this study suggest that doses of coenzyme Q10 as high as 1,200 mg/day are safe and may be more effective than lower doses, says Dr. Shults. The findings are consistent with those of a recently published study of patients with early Huntington's disease - another degenerative neurological disorder - that showed slightly less functional decline in groups that received 600 mg/day of coenzyme Q10 .

The new study also used an efficient phase II clinical trial design - developed by biostatistician David Oakes, Ph.D., of the University of Rochester, and other study investigators - which should be useful for testing other drugs that might slow the progression of PD, says Dr. Shults. The design allowed the researchers to study the effects of three doses plus a placebo in less than 3 years, and to obtain useful data about the compound's effectiveness.

Dr. Shults and his colleagues strongly caution patients against taking coenzyme Q10 until a larger, definitive trial can be conducted. Because coenzyme Q10 is classified as a dietary supplement, it is not regulated by the U.S. Food and Drug Administration. The versions of the supplement sold in stores may differ, they may not contain potentially beneficial amounts of the compound, and taking coenzyme Q10 over a number of years may be costly, says Dr. Shults. In addition, the current study included only a small number of patients, and the findings may not extend to people in later stages of PD or to those who are at risk but have not been diagnosed with the disorder, he notes. Finally, if many people begin taking coenzyme Q10 because of these early results, it might make it impossible for investigators to find enough patients to carry out definitive studies of the compound's effectiveness and the proper dosages, since patients must not be taking any treatments in order to be considered for enrollment in a definitive trial.

The investigators are now planning a larger clinical trial that will examine the effects of 1,200 mg/day of coenzyme Q10 , and possibly a higher dose as well, in a larger number of patients.

The NINDS is a component of the National Institutes of Health in Bethesda, Maryland, and is the nation's primary supporter of biomedical research on the brain and nervous system.

1 Shults CW, Oakes D, Kieburtz K, Beal F, Haas R, Plumb S, Juncos JL, Nutt J, Shoulson I, Carter J, Kompoliti K, Perlmutter JS, Reich S, Stern M, Watts RL, Kurlan R, Molho E, Harrison M, Lew M, and the Parkinson Study Group. "Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline." Archives of Neurology , October 2002, Vol. 59, No. 10, pp. 1541-1550.

Source: http://www.ninds.nih.gov


CoQ10 may protect against Alzheimer’s

Increasing intake of coenzyme Q10 may ward off the threat of Alzheimer’s disease, if the results of an animal study can be applied to humans. The body's manufacture of CoQ10 begins to drop after the age of about 20, leading to its investigation in age-related disease. It has been shown to help prevent Parkinson's and is also thought to prevent skin ageing

http://www.nutraingredients.com/news/ng.asp?
n=67263-coq-alzheimer-s-antioxidant


Effects of Coenzyme Q10 in Early Parkinson Disease

Coenzyme Q10 was safe and well tolerated at dosages of up to 1200 mg/d. Less disability developed in subjects assigned to coenzyme Q10 than in those assigned to placebo, and the benefit was greatest in subjects receiving the highest dosage. Coenzyme Q10 appears to slow the progressive deterioration of function in PD, but these results need to be confirmed in a larger study.

http://archneur.ama-assn.org/cgi/content/abstract/59/10/1541


Meer studies


Open label trial of coenzyme Q10 as a migraine preventive.

Rozen TD, Oshinsky ML, Gebeline CA, Bradley KC, Young WB, Shechter AL, Silberstein SD.

Jefferson Headache Center/Thomas Jefferson University, Philadelphia, Pennsylvania, USA. RozenT@ccf.org

The objective was to assess the efficacy of coenzyme Q10 as a preventive treatment for migraine headaches. From this open label investigation coenzyme Q10 appears to be a good migraine preventive. Placebo-controlled trials are now necessary to determine the true efficacy of coenzyme Q10 in migraine prevention.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&
db=PubMed&list_uids=11972582&dopt=Abstract


An open, pilot study to evaluate the potential benefits of coenzyme Q10 combined with Ginkgo biloba extract in fibromyalgia syndrome.

Lister RE.  Phylax Ltd, Beaconsfield, UK. bobphylax@cs.com

An open, uncontrolled study was undertaken to measure the subjective effects of coenzyme Q10 combined with a Ginkgo biloba extract in volunteer subjects with clinically diagnosed fibromyalgia syndrome.

A progressive improvement in the quality-of-life scores was observed over the study period and at the end, the scores showed a significant difference from those at the start. This was matched by an improvement in self-rating with 64% claiming to be better and only 9% claiming to feel worse. Adverse effects were minor. A controlled study is now planned.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve
&db=PubMed&list_uids=12025528&dopt=Abstract


Statins and chronic heart failure: do we need a large-scale outcome trial?

The potential adverse effects of statins in CHF include reduction in levels of coenzyme Q10 (which may further exacerbate oxidative stress in CHF) and loss of the protection that lipoproteins may provide through binding and detoxifying endotoxins entering the circulation via the gut. In support of these possibilities are epidemiologic data linking a lower serum cholesterol with a poorer prognosis in CHF. These uncertainties indicate the need for a definitive outcome trial to assess the efficacy and safety of statins in CHF, despite their current widespread, nonevidence based use in this population.

http://content.onlinejacc.org/cgi/content/abstract/39/10/1567?
maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=q10&
andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=
relevance&resourcetype=HWCIT


 

Coenzyme Q10: Absorption, tissue uptake, metabolism and pharmacokinetics.

Bhagavan HN, Chopra RK. Tishcon Corporation, 30 New York Avenue, Westbury, NY, 11590, USA.

Available data on the absorption, metabolism and pharmacokinetics of coenzyme Q10 (CoQ10) are reviewed in this paper. CoQ10 has a fundamental role in cellular bioenergetics. CoQ10 is also an important antioxidant. Because of its hydrophobicity and large molecular weight, absorption of dietary CoQ10 is slow and limited. In the case of dietary supplements, solubilized CoQ10 formulations show enhanced bioavailability. The T(max) is around 6 h, with an elimination half-life of about 33 h. The reference intervals for plasma CoQ10 range from 0.40 to 1.91 micromol/l in healthy adults. With CoQ10 supplements there is reasonable correlation between increase in plasma CoQ10 and ingested dose up to a certain point. Animal data show that CoQ10 in large doses is taken up by all tissues including heart and brain mitochondria. This has implications for therapeutic applications in human diseases, and there is evidence for its beneficial effect in cardiovascular and neurodegenerative diseases. CoQ10 has an excellent safety record.

Free Radic Res. 2006 May;40(5):445-53.


Supplemental conditionally essential nutrients in cardiovascular disease therapy.

Kendler BS.Dept. of Biology, CMSV Campus, Manhattan College, Riverdale, NY 10471, USA. barry.kendler@mountsaintvincent.edu

Conditionally essential nutrients (CENs) are organic compounds that are ordinarily produced by the body in amounts sufficient to meet its physiological requirements. However, in disorders, such as cardiovascular disease (CVD), and in other physiologically stressful conditions, their biosynthesis may be inadequate. Under these circumstances, CENs become essential nutrients, comparable to vitamins. The CENs of primary importance in CVD, based on the quantity and quality of human clinical studies, are l-arginine, l-carnitine, propionyl-l-carnitine, and coenzyme Q10. Controlled studies of these CENs are reviewed in depth. Taurine is a CEN of secondary importance caused by a limited human database. Other putative CENs include alpha-lipoic acid, betaine, chondroitin sulfate, glutamine, and d-ribose, each of which is mentioned in passing. Collectively, CENs have demonstrated favorable clinical effects in CVDs, including chronic heart failure, myocardial infarction, angina pectoris, and in CVD risk factors, such as hypertension, hyperlipidemia, and lipoprotein(a). Limited research has pointed to possible benefits in CVD therapy accruing from supplementation with several CENs in combination. Additional controlled clinical studies of CENs in CVD are urgently needed. In view of the efficacy and safety of appropriate supplementation with CENs, it is strongly suggested that healthcare professionals become knowledgeable of these potentially important additions to the CVD therapeutic armamentarium.

J Cardiovasc Nurs. 2006 Jan-Feb;21(1):9-16.


Myocardial dysfunction in mitochondrial diabetes treated with Coenzyme Q10.

Salles JE, Moises VA, Almeida DR, Chacra AR, Moises RS. Division of Endocrinology, Department of Medicine, Federal University of Sao Paulo, Rua Botucatu, 740 0434-970, Sao Paulo, SP, Brazil.

Maternally-inherited diabetes and deafness (MIDD) has been related to an A to G transition in the mitochondrial tRNA Leu (UUR) gene at the base pair 3243. Although some previous articles have reported that this mutation may be a cause of cardiomyopathy in diabetes, the degree of cardiac involvement and a specific treatment has not been established. Here, we reported a case of a patient with MIDD who developed congestive heart failure and the therapeutic usefulness of Coenzyme Q10 (CoQ10). In our patient, after the introduction of Coenzyme Q10 150mg/day, there was a gradual improvement on left ventricular function evaluated by echocardiography. The fractional shortening (FS) and ejection fraction (EF) increased from 26 to 34% and from 49 to 64%, respectively. No side effects were noted. Three months after CoQ10 discontinuation, the parameters of systolic function evaluated by echocardiography decreased, suggesting that CoQ10 had a beneficial effect. Identification of diabetes and cardiomyopathy due to mitochondrial gene mutation may have therapeutic implications and Coenzyme Q10 is a possible adjunctive treatment in such patients.

Diabetes Res Clin Pract. 2006 Apr;72(1):100-3. Epub 2005 Oct 25.


Clinical aspects of coenzyme Q10: an update.

Littarru GP, Tiano L. Institute of Biochemistry, Polytechnic University of Marche, Via Ranieri, Ancona, Italy. g.littarru@univpm.it

PURPOSE OF REVIEW: Coenzyme Q10 is administered for an ever-widening range of disorders, therefore it is timely to illustrate the latest findings with special emphasis on areas in which this therapeutic approach is completely new. These findings also give further insight into the biochemical mechanisms underlying clinical involvement of coenzyme Q10. RECENT FINDINGS: Cardiovascular properties of coenzyme Q10 have been further addressed, namely regarding myocardial protection during cardiac surgery, end-stage heart failure, pediatric cardiomyopathy and in cardiopulmonary resuscitation. The vascular aspects of coenzyme Q10 addressing the important field of endothelial function are briefly examined. The controversial issue of the statin/coenzyme Q10 relationship has been investigated in preliminary studies in which the two substances were administered simultaneously. Work on different neurological diseases, involving mitochondrial dysfunction and oxidative stress, highlights some of the neuroprotective mechanisms of coenzyme Q10. A 4-year follow-up on 10 Friedreich's Ataxia patients treated with coenzyme Q10 and vitamin E showed a substantial improvement in cardiac and skeletal muscle bioenergetics and heart function. Mitochondrial dysfunction likely plays a role in the pathophysiology of migraine as well as age-related macular degeneration and a therapy including coenzyme Q10 produced significant improvement. Finally, the effect of coenzyme Q10 was evaluated in the treatment of asthenozoospermia. SUMMARY: The latest findings highlight the beneficial role of coenzyme Q10 as coadjuvant in the treatment of syndromes, characterized by impaired mitochondrial bioenergetics and increased oxidative stress, which have a high social impact. Besides their clinical significance, these data give further insight into the biochemical mechanisms of coenzyme Q10 activity.

Curr Opin Clin Nutr Metab Care. 2005 Nov;8(6):641-6.


The effect of micronutrient supplementation on quality-of-life and left ventricular function in elderly patients with chronic heart failure.

Witte KK, Nikitin NP, Parker AC, von Haehling S, Volk HD, Anker SD, Clark AL, Cleland JG.

Department of Academic Cardiology, Castle Hill Hospital, Castle Road, Cottingham, Hull HU16 5JQ, UK. klauswitte@hotmail.com

AIMS: Chronic heart failure (CHF) is a common and leading cause of death in industrialized countries. The potential benefits of micronutrient supplementation in CHF are extensive. Therefore, we examined the influence of long-term multiple micronutrient supplementation on left ventricular (LV) function, levels of pro-inflammatory cytokines, and quality-of-life (QoL) in elderly patients with CHF. METHODS AND RESULTS: Thirty CHF patients [age 75.4 (0.7), mean (SEM), LV ejection fraction (LVEF) < or =35%] were randomized to receive capsules containing a combination of high-dose micronutrients (calcium, magnesium, zinc, copper, selenium, vitamin A, thiamine, riboflavin, vitamin B(6), folate, vitamin B(12), vitamin C, vitamin E, vitamin D, and Coenzyme Q10) or placebo for 9 months in a double-blind fashion. All subjects were on stable optimal medical therapy for at least 3 months before enrolment. At randomization and at study end, tumour necrosis factor-alpha and its soluble receptors TNFR-1 and TNFR-2 were measured and six-minute walk test and QoL were assessed. Cardiac magnetic resonance scanning was performed to evaluate cardiac dimensions and LVEF. Two patients died during follow-up. The remaining patients (14 randomized to placebo and 14 to micronutrients) were well matched for LV function, symptoms, and exercise capacity. At the end of the follow-up period, LV volumes were reduced in the intervention group with no change in the placebo group [-13.1 (17.1)% vs. +3.8 (10.0)%; P<0.05]. LVEF increased by 5.3+/-1.4% in the intervention group and was unchanged in the placebo group (P<0.05). Patients taking micronutrients also had a significant improvement in QoL score between enrolment and study end [+9.5 (1.6)%; P<0.05], whereas those taking placebo had a slight deterioration [-1.1 (0.8)%; P=0.12]. Six-minute walk test and inflammatory cytokine levels remained unchanged in both groups. CONCLUSION: Long-term multiple micronutrient supplementation can improve LV volumes and LVEF and QoL scores in elderly patients with heart failure due to LV systolic dysfunction.

Eur Heart J. 2005 Nov;26(21):2238-44. Epub 2005 Aug 4.


The role of coenzyme Q10 in heart failure.

Weant KA, Smith KM.

University of Kentucky Chandler Medical Center, Lexington, KY 40536-0293, USA.

OBJECTIVE: To review the clinical data demonstrating the safety and efficacy of coenzyme Q10 (CoQ10) in heart failure (HF). DATA SOURCES: Pertinent literature was identified through MEDLINE (1966-January 2005) using the search terms coenzyme Q10, heart failure, antioxidants, and oxidative stress. Only articles written in the English language and evaluating human subjects were used. DATA SYNTHESIS: HF impairs the ability of the heart to maintain its normal cardiac output. Following an initial insult, cardiac remodeling ensues, resulting in left ventricular dilation and hypertrophy. Oxidative stress is also increased, while CoQ10 levels are decreased in patients with HF. This has led to the hypothesis that CoQ10, an antioxidant, may decrease oxidative stress, impair remodeling, and improve cardiac function. CONCLUSIONS: Large, well-designed studies on this topic are lacking. The limited data from well-designed trials indicate there may be some minor benefits with CoQ10 therapy in ejection fraction and end diastolic volume. CoQ10 therapy has been shown to be relatively safe with a low incidence of adverse effects.

Ann Pharmacother. 2005 Sep;39(9):1522-6. Epub 2005 Jul 26.


Coenzyme q10 for prevention of anthracycline-induced cardiotoxicity.

Conklin KA. Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-1778, USA. kconklin@mednet.ucla.edu

Preclinical and clinical studies suggest that anthracycline-induced cardiotoxicity can be prevented by administering coenzyme Q10 during cancer chemotherapy that includes drugs such as doxorubicin and daunorubicin. Studies further suggest that coenzyme Q10 does not interfere with the antineoplastic action of anthracyclines and might even enhance their anticancer effects. Preventing cardiotoxicity might allow for escalation of the anthracycline dose, which would further enhance the anticancer effects. Based on clinical investigation, although limited, a cumulative dose of doxorubicin of up to 900 mg/m2, and possibly higher, can be administered safely during chemotherapy as long as coenzyme Q10 is administered concurrently. The etiology of the dose-limiting cardiomyopathy that is induced by anthracyclines can be explained by irreversible damage to heart cell mitochondria, which differ from mitochondria of other cells in that they possess a unique enzyme on the inner mitochondrial membrane. This enzyme reduces anthracyclines to their semiquinones, resulting in severe oxidative stress, disruption of mitochondrial energetics, and irreversible damage to mitochondrial DNA. Damage to mitochondrial DNA blocks the regenerative capability of the organelle and ultimately leads to apoptosis or necrosis of myocytes. Coenzyme Q10, an essential component of the electron transport system and a potent intracellular antioxidant, appears to prevent damage to the mitochondria of the heart, thus preventing the development of anthracycline-induced cardiomyopathy.

Integr Cancer Ther. 2005 Jun;4(2):110-30.


Potential role of ubiquinone (coenzyme Q10) in pediatric cardiomyopathy.

Bhagavan HN, Chopra RK. Nutrition Science Department, Tishcon Corporation, 30 New York Avenue, P.O. Box 331, Westbury, NY 11590, USA. hemmin@msn.com

Pediatric cardiomyopathy (PCM) represents a group of rare and heterogeneous disorders that often results in death. While there is a large body of literature on adult cardiomyopathy, all of the information is not necessarily relevant to children with PCM. About 40% of children who present with symptomatic cardiomyopathy are reported to receive a heart transplant or die within the first two years of life. In spite of some of the advances in the management of PCM, the data shows that the time to transplantation or death has not improved during the past 35 years. Coenzyme Q10 is a vitamin-like nutrient that has a fundamental role in mitochondrial function, especially as it relates to the production of energy (ATP) and also as an antioxidant. Based upon the biochemical rationale and a large body of data on patients with adult cardiomyopathy, heart failure, and mitochondrial diseases with heart involvement, a role for coenzyme Q10 therapy in PCM patients is indicated, and preliminary results are promising. Additional studies on the potential usefulness of coenzyme Q10 supplementation as an adjunct to conventional therapy in PCM, particularly in children with dilated cardiomyopathy, are therefore warranted.

Clin Nutr. 2005 Jun;24(3):331-8.


Antioxidant treatment of patients with Friedreich ataxia: four-year follow-up.

Hart PE, Lodi R, Rajagopalan B, Bradley JL, Crilley JG, Turner C, Blamire AM, Manners D, Styles P, Schapira AH, Cooper JM.

University Department of Clinical Neurosciences, Royal Free and University College Medical School, London, England.

BACKGROUND: Decreased mitochondrial respiratory chain function and increased oxidative stress have been implicated in the pathogenesis of Friedreich ataxia (FRDA), raising the possibility that energy enhancement and antioxidant therapies may be an effective treatment. OBJECTIVE: To evaluate the long-term efficacy of a combined antioxidant and mitochondrial enhancement therapy on the bioenergetics and clinical course of FRDA. DESIGN: Open-labeled pilot trial over 47 months.Patients Seventy-seven patients with clinical and genetically defined FRDA.Intervention A combined coenzyme Q(10) (400 mg/d) and vitamin E (2100 IU/d) therapy of 10 patients with FRDA over 47 months. MAIN OUTCOME MEASURES: Clinical assessment using echocardiography and the International Cooperative Ataxia Rating Scale and cardiac and skeletal muscle bioenergetics as assessed using phosphorus P 31 magnetic resonance spectroscopy. RESULTS: There was a significant improvement in cardiac and skeletal muscle bioenergetics that was maintained throughout the 47 months of therapy. Echocardiographic data revealed significantly increased fractional shortening at the 35- and 47-month time points. Comparison with cross-sectional data from 77 patients with FRDA indicated the changes in total International Cooperative Ataxia Rating Scale and kinetic scores over the trial period were better than predicted for 7 patients, but the posture and gait and hand dexterity scores progressed as predicted. CONCLUSION: This therapy resulted in sustained improvement in mitochondrial energy synthesis that was associated with a slowing of the progression of certain clinical features and a significant improvement in cardiac function.

Arch Neurol. 2005 Apr;62(4):621-6.


Meer links

http://www.lef.org/prod_hp/abstracts/php-ab099a.html

http://www.coenzymeq10.it/literature/literature.html

http://www.natuurlijkerwijs.com/
overige_voedingsstoffen.htm#coenzym_q_10

http://www.soe.nl/ord/resQ10.htm


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