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Letters to Red Flags
Letters 2005-11-07 RFD edited http://www.redflagsdaily.com/letters/letters8.htm
Subject: Statins And The Onset Of Neurodegenerative Diseases
I am interested in sharing and obtaining information relating statins,
especially the lipophilic ones, to the onset of neurodegenerative diseases —
Parkinson's, ALS and Alzheimer's. I know of three males (ages 50, 58 and 60)
who were diagnosed with Parkinson's disease within two weeks of one another.
The primary commonality was that all three had been on lipitor for several
years. It could be a coincidence. Yet, in surface researching lipitor, we
found that it depletes the body of coenzyme Q10 — as well as several other
factors vitally important to metabolic functioning. In a simplistic
approach, one of the men stopped the lipitor and began taking coenzyme Q10
at a dose of 100 milligrams a day. Two months later, upon consulting with
the neurologist who made the diagnosis of Parkinson's, we learned that there
were no drugs recommended for early onset Parkinson's, but there is
a supplement — coenzyme Q10 in a megadose of 1,200 milligrams a day. It
seems a study — published in Archives of Neurology in 2002 by C. W.
Shults et al — has shown the efficacy of this megadose in decreasing
progression of the disease in Parkinson’s patients.
Even more compelling is sound scientific evidence that interfering with the
body's production of coenzyme Q10 can lead to, or at least worsen,
Parkinson's.
1) There is evidence that both serum and platelet coenzyme Q10 levels are
lower than normal in all Parkinson’s patients who have been tested. Recent
theory is that lowered coenzyme Q10 is part of the process of Parkinson's
disease, directly related to mitochondrial dysfunction.
(2) Statins deplete the body of coenzyme Q10 by blocking the mevalonate
pathway. HMG-CoA reductase inhibitors lower cholesterol by blocking this
pathway to its production; unfortunately, this is also the pathway to the
production of coenzyme Q10 and dolichols (precursors to glycoproteins and
stabilizers of lipid membranes of cells). There are studies showing the use
of statins results in lower than normal serum and platelet levels of
Coenzyme Q10.
Current theory concerning the three major neurodegenerative diseases —
Parkinson's, Alzheimer's, and ALS — is that they share the same molecular
pathophysiology. The areas affected determine the disease that develops.
Mitochondrial dysfunction and oxidative stress are thought to be the
molecular level dysfunctions of all three diseases. Coenzyme Q10 is a
critical element of the mitochondrial electron transport chain, especially
for the metabolic system responsible for generating more than 96 percent of
all ATP produced within the body. The heart, nerves and muscles require a
high level of coenzyme Q10. A form of this coenzyme, ubiquinone, plays a
major role in maintaining membrane integrity of nerves so nerve conduction
can occur. This coenzyme is also a major antioxidant within the
mitochondria, "neutralizing" reactive oxygen species. (These species account
for the oxidative stress within the cells, leading to apoptosis of cells.)
There are two case presentations in the literature reporting individuals who
developed Parkinson's, which the authors directly attribute to statin
therapy.
(Reference: Mueller, T., Kuhn, W., et.al. "Parkinsonism Unmasked by
Lovastatin". Annals of Neurology volume 37, number 5, May 1995.)
A report of one individual who developed Parkinson's while on a statin,
discontinued the statin and recovered from the symptoms of Parkinson’s
appears in a letter to the German medical journal Der Nervenarzt,
volume 74, number 2.
Statins are the biggest selling drug in the world today. Pfizer made more
than $14 billion last year on lipitor alone. With exposure through the media
of the potential association, the Food and Drug Administration may be forced
to mandate phase IV studies to determine statistically whether there exists
a probable relationship between statins and neurodegenerative diseases.
Further studies to determine the damage wrought, and modalities of therapy,
could then be undertaken.
These instances may be representations of genetic variability interacting
with an environmental factor (a statin) to produce a disease. However, this
occurs rarely. Given the millions of individuals who are on this class of
drug, and the newest recommendations for additional millions, who "should"
be placed on the drugs, the numbers affected by neurodegenerative diseases
could be enormous. And it will all be attributed to our "aging" population.
Who notices when someone who is 78 years old and taking a statin develops
Alzheimer's? Or someone who is 61 and taking a statin develops Parkinson’s
disease? Or ALS?
Madelyn Levy,
Cincinnati, Ohio, U.S.A.