Re: Statin - CoQ10 suppression (Arch Neurol, 6/04)

From: Zee (fresh~horses_at_despammed.com)
Date: 09/21/04 

Date: 21 Sep 2004 08:33:48 -0700

John Merlano wrote:
> On Sun, 19 Sep 2004 04:58:44 GMT, Sharon Hope wrote:
>
> Doesn't supplementing with CoQ10 help solve the problem of statins
> preventing the body from making it? Something like 100 mg of CoQ10 in
> softgel form?

There are several studies showing statins deplete coenzyme q10. There
are no double blind randomized studies which show taking CoQ10 will
replenish statin-induced depletion and/or correct damage posited to be
caused by the statin-induced depletion.

Langsjoen and Folkers on Coenzyme Q10 and cardiomyopathy. Also more
recent on www.pubmed.org
http://faculty.washington.edu/ely/coenzq10.html

Zee

>
> > Hardly a surprise finding. The body creates CoQ10 in the
mevalonate
> > pathway. Statins interrupt this pathway upstream of the CoQ10
production.
> > This short-circuiting of the process makes it impossible for the
body to
> > produce this nutrient that is so essential to the mitochondria.
> >
> > Such study findings are roughly equivalent to "when the faucet
turns off,
> > the water flow stops." Necessary to measure the absence of the
water,
> > though, for all those who will doubt it.
> >
> >
> >
> > "ChuckMSRD" <chuckmsrd@aol.com> wrote in message
> > news:20040918065726.15331.00000665@mb-m22.aol.com...
> >> 1: Arch Neurol. 2004 Jun;61(6):889-92. Related Articles, Links
> >>
> >>
> >> Atorvastatin decreases the coenzyme Q10 level in the blood of
patients at
> > risk
> >> for cardiovascular disease and stroke.
> >>
> >> Rundek T, Naini A, Sacco R, Coates K, DiMauro S.
> >>
> >> Department of Neurology, Columbia University College of Physicians
&
> > Surgeons,
> >> New York, NY 10032, USA.
> >>
> >> BACKGROUND: Statins (3-hydroxy-3-methylglutaryl coenzyme A
reductase
> >> inhibitors) are widely used for the treatment of
hypercholesterolemia and
> >> coronary heart disease and for the prevention of stroke. There
have been
> >> various adverse effects, most commonly affecting muscle and
ranging from
> >> myalgia to rhabdomyolysis. These adverse effects may be due to a
coenzyme
> > Q(10)
> >> (CoQ(10)) deficiency because inhibition of cholesterol
biosynthesis also
> >> inhibits the synthesis of CoQ(10). OBJECTIVE: To measure CoQ(10)
levels in
> >> blood from hypercholesterolemic subjects before and after exposure
to
> >> atorvastatin calcium, 80 mg/d, for 14 and 30 days. DESIGN:
Prospective
> > blinded
> >> study of the effects of short-term exposure to atorvastatin on
blood
> > levels of
> >> CoQ(10). SETTING: Stroke center at an academic tertiary care
> > hospital.Patients
> >> We examined a cohort of 34 subjects eligible for statin treatment
> > according to
> >> National Cholesterol Education Program: Adult Treatment Panel III
> > criteria.
> >> RESULTS: The mean +/- SD blood concentration of CoQ(10) was 1.26
+/- 0.47
> > micro
> >> g/mL at baseline, and decreased to 0.62 +/- 0.39 micro g/mL after
30 days
> > of
> >> atorvastatin therapy (P<.001). A significant decrease was already
> > detectable
> >> after 14 days of treatment (P<.001). CONCLUSIONS: Even brief
exposure to
> >> atorvastatin causes a marked decrease in blood CoQ(10)
concentration.
> >> Widespread inhibition of CoQ(10) synthesis could explain the most
commonly
> >> reported adverse effects of statins, especially exercise
intolerance,
> > myalgia,
> >> and myoglobinuria.
> >>
> >> PMID: 15210526 [PubMed - indexed for MEDLINE]

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