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mtDNA -is there possible somatic point mutations from statins?
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PostPosted: Wed May 18, 2005 5:58 pm    Post subject: mtDNA -is there possible somatic point mutations from statins? Reply with quote

mine is a long story beginning june 04 when my niece and i discovered
our respective husbands were exhibiting identical neurological
symptoms. both men had taken only one drug--Lipitor for 4+ yrs. upon
surface researching statins, we found they block the mevalonate pathway
responsible for not only cholestrol, but coq10, dolichols (precursors
for glycoprotein formation--glycosylation), and other isoprenoid
biosynthesis products. my husband stopped lipitor and began taking
coq10 @ 100 mgm/day in a simplistic approach to possible statin
toxicity. 2 months later,both men were diagnosed with parkinson's
disease. my husband was advised that there were no traditional anti PD
drugs for his early onset PD, but that a small study reported in the
ann of neurology 2002, by clifford shults, MD, et.al. showed a
statistically significant decrease in progression of PD symptoms in
early onset Parkinsons utilizing a supplement, and suggested my husband
use the supplement. the supplement: coenzyme Q10--this time in a mega
dose of 1200mgm/day. there are studies documenting decreased coq10
levels in all patients with PD--no mention of statin therapy for these
study patients; there are also documentd decreased coq10 plasma and
platelet levels in patients who are on statin therapy (though not all
studies have shown this effect)--the question becomes does this statin
effect upon the coq10 result in neurodegenerative disease in patients
with a genetic variability predisposing them to one of these diseases?
Is there such an increase in reactive oxygen species because of
interference with the complex I, II and V of the mitochondrial electron
transport train resulting in oxidative stress, and overwhelming death
of neuron cells in structures one's genetic variability predisposes one
to: ie substantia nigra in Pd, upper or lower motorneurones in ALS,
etc.?
Or does this cascade of events(ROS formation, oxidative stress, cell
death) result in mtRNA somatic point mutations--producing Parkinson's
or ALS or alzheimer's?
anecdotally, I have heard from 11 other individuals who feel their
parkinson's or symptoms of parkinson's are due to prior statin
therapy--esp. the lipophilic statins--and also from 3 individuals who
feel their diagnosis of ALS is due to statin therapy. my husband's
neurologist commented on monday taht she has 3 or 4 other patients who
are convinced as I that their parkinson's is directly related to statin
therapy....
the brain is the organ containing the most cholesterol relative to its
size--does lowering cholesterol levels effect the function of the
central nervous system? have pharm companies even looked at that
question?
does anyone have any information that could help us in our quest to
understand what role statins have played in the development of
parkinson's?
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