Do Statin Drugs Cause Parkinson's Disease?...

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http://bmj.com/cgi/eletters/325/7369/851

 

Might statins cause Parkinsons?18 October 2002 Richard G Fiddian-Green,

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Cholesterol lowering statins currently being prescribed for patients with

atherosclerosis may reduce mitochondrial coenzyme Q thus potentially

compromising the adequcy of mitochondrial oxidative phosphorylation. An

indequacy of mitochondrial oxidative phosphorylation appears to be the primary

cause of organ dysfunctions and failures, including a wide spectrum of mood and

behavioural disorders, in the critically ill. In which case statins cann be

expected to increase the likelihood of developing organs dysfunctions and

failures in the event of developing an acute illness. Given this report might

statins also be expected to increase the likelihood of developing Parkinson's

and/or even Alzheimer's (1)? If so it might indeed be advisable for patients

taking statins to take coenzyme Q supplements.

1. Hyams DE, Roylance PJ, Kruger K, Bodd E. Do we kill our cardiac patients with

statin therapy? Coenzyme Q10, what do we know? Tidsskr Nor Laegeforen. 1994 Feb

20;114(5):590.

 

Coenzyme Q-10 Repletion20 October 2002 Bill D. Misner Ph.D., C.S.M.T., R & D

E-CAPS Inc. 99205

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Mitochondria cells depend upon electron carrier activity in order to convert

macro-substances into energy-producing Adenosine Triphosphate. Abnormalities may

occur when these substrates are exposed to pathologic-, time- (age), or free

radical- (excess) conditions. Such conditions may deplete the fat-soluble

mitochondrial ubiquitous Q-10 substance faster than the food chain may actively

replenish it, rationally supports a preventative concentrated dose adjunct for

treating Parkinson's Disease persons.

Mitochondrial abnormalities can occur in Steinert's myotonic dystrophy (DM) and

deficiency of coenzyme Q-10 may result due to pathogenic mechanisms associated

with abnormal CTG trinucleotide amplification.[1]. Researchers have reported

developing a system that will detect abnormal patterns of tissue oxygenation in

a well-characterized patient with a deficiency of skeletal muscle coenzyme Q-10

[2]. Administration of coenzyme Q(10) in conjunction with standard medical

therapy has been reported to augment myocardial kinetics, increase cardiac

output, elevate the ischemic threshold, and enhance functional capacity in

patients with congestive heart failure. Coenzyme Q(10) therapy is associated

with significant functional, clinical, and hemodynamic improvements within the

context of an extremely favorable benefit-to-risk ratio. Coenzyme Q(10) enhances

cardiac output by exerting a positive inotropic effect upon the myocardium as

well as mild vasodilatation [3]. Aging as a pleiotropic process involves both

genetic and environmental factors. Recently it has been demonstrated that

dietary constituents may affect senescence. In the present study, adult (3

month-old) mice were fed diets supplemented with ubiquinone (coenzyme Q(10)),

alpha-lipoic acid, melatonin or alpha-tocopherol for a six-month period to

determine if antioxidants may reverse or inhibit the progression of certain age-

associated changes in cerebral mitochondrial electron transport chain (ETS)

enzyme activities. The control consisted of a group of mice maintained on a

basal diet for the same period. The activity of cytochrome c oxidase (Complex

IV) increased with age but melatonin supplementation restored the activity to

levels of 3 month-old animals. The activity of succinate dehydrogenase (Complex

II) showed no age-related changes. However, this enzyme complex was elevated, in

animals supplemented with coenzyme Q(10), alpha-lipoic acid and

alpha-tocopherol, above corresponding values obtained with basal diet.

NADH-ubiquinone oxidoreductase (Complex I) and ubiquinol:ferricytochrome-c

oxidoreductase (Complex III) activities remained unchanged [4].

If environmental or genetic factors are potentiated by time resulting in

depleted levels Coenzyme Q-10, consuming a concentrated dose presents a

rationale means for preventating predicted pathology.

References

[1] Siciliano G, Mancuso M, Tedeschi D, Manca ML, Renna MR, Lombardi V, Rocchi

A, Martelli F, Murri L. Coenzyme Q10, exercise lactate and CTG trinucleotide

expansion in myotonic dystrophy. Brain Res Bull. 2001 Oct- Nov 1;56(3-4):405-10.

[2] Wariar R, Gaffke JN, Haller RG, Bertocci LA., A modular NIRS system for

clinical measurement of impaired skeletal muscle oxygenation. J Appl Physiol.

2000 Jan;88(1):315-25.

[3] Sacher HL, Sacher ML, Landau SW, Kersten R, Dooley F, Sacher A, Sacher M,

Dietrick K, Ichkhan K., The clinical and hemodynamic effects of coenzyme Q10 in

congestive cardiomyopathy. Am J Ther. 1997 Feb-Mar;4(2- 3):66-72.

[4] Sharman EH, Bondy SC. Effects of age and dietary antioxidants on cerebral

electron transport chain activity. Neurobiol Aging. 2001 Jul- Aug;22(4):629-34.

Disclosure: The author reports competing interests from the private sector

involved in the formulating supplemental pharmaceutical grade Coenzyme Q-10

specifically for use by athletes competing in extreme endurance exercise events.

 

Coenzyme Q vs levodopa for Parkinson's21 October 2002 Richard G Fiddian-Green,

None

Nonbe

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Levodopa treatments are thought to be the most effective for Parkinson’s disease

but most patients receiving chronic treatment develop motor complications,

specifically motor fluctuations and dyskinesia (1). Levodopa may be toxic to

dopaminergic neurons in vitro depending upon the study circumstances. In

patients the motor complications caused by levodopa appear to be related to the

manner in which the drug is administered. The complications of levodopa are most

likely to be seen after pulsatile stimulation of dopamine receptors by

short-acting dopaminergic agents. Apparently these complications are not caused

by long -acting dopaminergic agents.

This makes sense if the primary defect in Parkinson’s, and other

neurodegenerative disorders such as Alzheimer’s, is a regional and/or systemic

impairment of the adequacy of mitochondrial oxidative phosphorylation (2).

Pulsatile stimulation by short-acting dopaminergic agents are likely to achieve,

for a limited period, higher levels of stimulation of dopamine receptors than

long-acting dopaminergic agents. If the deletarious effects of the levodopa is

due to a compounding of an underlying impairment of the adequacy of

mitochondrial oxidative phosphorylation, then the effect is most likely to be

seen when stimulation of dopamine receptors is greatest. It is under these

circumstances that the demand for energy from ATP hydrolysis is most likely to

exceed the capacity for ATP resynthesis.

Of much greater concern than the motor complications of levodopa is the prospect

of it causing other neurodegenerative disorders such as Alzheimer’s. Coenzyme Q

is more rational therapy for a mitochondrial disorder than levodopa because it

would seem less likely to cause neurodegenerative disorders (3). Other

micronutrients, such as vitamins B12, folic acid, B6, niacin, C, E, iron, and

zinc, that also have the potential to improve mitochondrial function might

enhance the therapetic benefits of coenzyme Q without increasing the risks of

complications (4).

1. Agid Y, Olanow CW, Mizuno Y. Levodopa: why the controversy? Lancet

2002;360:575.

2. Fiddian-Green RG. Might statins cause Parkinsons? bmj.com, 18 Oct 2002

3. Misner BD. Coenzyme Q-10 Repletion bmj.com, 18 Oct 2002

4. Ames BN. Micronutrients prevent cancer and delay aging. Toxicol Lett. 1998

Dec 28;102-103:5-18.

 

Re: Might statins cause Parkinsons?24 October 2002 Bjorn Madsen,

Journalist/medical writer

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It is really quite interesting to observe how strategically discrete the drug

industry has chosen to be, as more and more compromising evidence pops up,

challenging the potential health threat of statin drugs. Statins unquestionably

lower cholesterol. However, there are numerous alternatives to taking this

category of drugs, alternatives that do not cause undesirable side effects. Most

concerning is the fact that the statin manufacturers have neglected to include

in their patient information the very important fact that statin therapy impairs

the liver synthesis of coenzyme Q10, a substance of vital importance to

virtually all bodily functions.

As a journalist and medical writer, I am apalled, though not surprised, to

witness how relevant and critical information gets swept under the carpet for

the sole purpose of maintaining an existing market and avoiding to " rock the

boat " .

More power to those who are able to, and willing to, disclose this ill-mannered

conduct and bring to the surface information that is of benefit to those who

really need to know: the patients.

 

 

 

 

 

 

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