Atorvastatin Decreases the Coenzyme Q10 Level in the Blood
of Patients at Risk for Cardiovascular Disease and Stroke
Tatjana Rundek, MD; Ali Naini, PhD; Ralph Sacco, MD; Kristen
Coates, MS; Salvatore DiMauro, MD
Arch Neurol. 2004;61:889-892. Vol. 61 No. 6, June 2004
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 Q10 (CoQ10) deficiency because
inhibition of cholesterol biosynthesis also inhibits the
synthesis of CoQ10.
Objective To measure CoQ10 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 CoQ10.
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 CoQ10 was 1.26
± 0.47 µg/mL at baseline, and decreased to 0.62 ± 0.39 µg/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 CoQ10 concentration. Widespread
inhibition of CoQ10 synthesis could explain the most
commonly reported adverse effects of statins, especially
exercise intolerance, myalgia, and myoglobinuria.
From the Department of Neurology, Columbia University
College of Physicians & Surgeons, New York, NY. Dr Sacco has
received honoraria for lecturing and consulting from Pfizer
Inc. Pfizer Inc had no involvement in data analysis or
manuscript preparation.
RELATED ARTICLES IN ARCHIVES OF NEUROLOGY
This Month in Archives of Neurology Arch Neurol. 2004;61:828-
829. FULL TEXT
"Zee" <zwalanga@yahoo.com> wrote in message
news:e5f4a9c2.0406222105.4104895f@posting.google.com...
> Atorvastatin Decreases the Coenzyme Q10 Level in the Blood
> of Patients at Risk for Cardiovascular Disease and Stroke
>
> Tatjana Rundek, MD; Ali Naini, PhD; Ralph Sacco, MD;
> Kristen Coates, MS; Salvatore DiMauro, MD
>
>
> Arch Neurol. 2004;61:889-892. Vol. 61 No. 6, June 2004
>
> 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 Q10 (CoQ10) deficiency because
> inhibition of cholesterol biosynthesis also inhibits the
> synthesis of CoQ10.
>
> Objective To measure CoQ10 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 CoQ10.
>
> 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 CoQ10 was
> 1.26 ± 0.47 µg/mL at baseline, and decreased to 0.62 ±
> 0.39 µg/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 CoQ10 concentration. Widespread
> inhibition of CoQ10 synthesis could explain the most
> commonly reported adverse effects of statins, especially
> exercise intolerance, myalgia, and myoglobinuria.
>
>
> From the Department of Neurology, Columbia University
> College of Physicians & Surgeons, New York, NY. Dr Sacco
> has received honoraria for lecturing and consulting from
> Pfizer Inc. Pfizer Inc had no involvement in data analysis
> or manuscript preparation.
>
>
>
>
>
> RELATED ARTICLES IN ARCHIVES OF NEUROLOGY
>
>
> This Month in Archives of Neurology Arch Neurol. 2004;61:828-
> 829. FULL TEXT
Interesting article. A next step is to see if CoQ10
supplements can reverse that. I wish they had done that.
Bill
> "Zee" <zwalanga@yahoo.com> wrote in message
> news:e5f4a9c2.0406222105.4104895f@posting.google.com...
> > Atorvastatin Decreases the Coenzyme Q10 Level in the
> > Blood of Patients at Risk for Cardiovascular Disease and
> > Stroke
> >
> > Tatjana Rundek, MD; Ali Naini, PhD; Ralph Sacco, MD;
> > Kristen Coates, MS; Salvatore DiMauro, MD
> >
> >
> > Arch Neurol. 2004;61:889-892. Vol. 61 No. 6, June 2004
> >
> > 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 Q10 (CoQ10)
> > deficiency because inhibition of cholesterol
> > biosynthesis also inhibits the synthesis of CoQ10.
> >
> > Objective To measure CoQ10 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 CoQ10.
> >
> > 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 CoQ10 was
> > 1.26 ± 0.47 µg/mL at baseline, and decreased to 0.62 ±
> > 0.39 µg/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 CoQ10 concentration. Widespread
> > inhibition of CoQ10 synthesis could explain the most
> > commonly reported adverse effects of statins, especially
> > exercise intolerance, myalgia, and myoglobinuria.
> >
> >
> > From the Department of Neurology, Columbia University
> > College of Physicians & Surgeons, New York, NY. Dr Sacco
> > has received honoraria for lecturing and consulting from
> > Pfizer Inc. Pfizer Inc had no involvement in data
> > analysis or manuscript preparation.
> >
> >
> >
> >
> >
> > RELATED ARTICLES IN ARCHIVES OF NEUROLOGY
> >
> >
> > This Month in Archives of Neurology Arch Neurol. 2004;61:828-
> > 829. FULL TEXT
>
> Interesting article. A next step is to see if CoQ10
> supplements can reverse that. I wish they had done that.
>
> Bill
Re: Atorvastatin Decreases the Coenzyme Q10 Level in
the Blood of Patients at Risk for Cardiovascular
Disease and Stroke
Tatjana Rundek, MD; Ali Naini, PhD; Ralph Sacco, MD; Kristen
Coates, MS; Salvatore DiMauro, MD Arch Neurol. 2004;61:889-
892. http://archneur.ama- (http://archneur.ama-/)
assn.org/cgi/content/abstract/61/6/889
Is Pfizer doing studies for a combo drug: Lipitor with
coenzyme
q10...? Is it now in Pfizer's interests to do such studies?
Why wasn't this done five-10 years ago. Now, when Pfizer
is getting hit by Crestor, Zocor is going OTC and
Lipitor approaches losing patent—now *they* need it so
now they do it.
Will taking a combo pill mitigate adverse effects caused by
statin induced coenzyme q10 depletion? We don't know.
Will taking coenzyme q10 orally treat and/or cure statin
induced illness and disability in those already injured? We
don't know.
Will Pfizer be taking it to the bank?
"Dr Sacco has received honoraria for lecturing and
consulting from Pfizer Inc."
July 8, 2002
http://www.redflagsweekly.com/features/2002_july08P.html STATIN-
INDUCED CARDIOMYOPATHY INTRODUCTION TO THE CITIZEN'S
PETITION ON STATINS By Peter H. Langsjoen, MD
The medical profession has, after more than 30 years of
excellent propaganda, successfully created the wholly
iatrogenic - "pseudo-disease" dubbed "hypercholesterolemia"
and the associated malady "cholesterol neurosis". After
decades of dismal failure to cure this "disease" of numbers
with low fat diets and a host of cholesterol lowering drugs,
the medical profession stumbled upon the magic bullet, the
cure for this dreaded artificial disease - statins (HMG-CoA
reductase inhibitors).
First released on the US market in 1987, statins have
rapidly grown into one of the most widely prescribed class
of drugs in history. Statins do three things:
1. They block the body's ability to make cholesterol, thus
lowering the blood level of cholesterol, thereby curing
cholesterol neurosis. Doctors and patients equally
neurotic have immediate gratification. The "evil" high
cholesterol has been dramatically lowered and the future
is bright and promising. So far...so good.
2. Unrelated to their cholesterol lowering, statins have
been found to have anti-inflammatory, plaque-
stabilizing properties which have a slight benefit in
coronary heart disease.
3. Statins kill people - lots of people - and they wound
many, many more. All patients taking statins become
depleted in Coenzyme Q10 (CoQ10), eventually - those
patients who start with a relatively low CoQ10 levels
(the elderly and patients with heart failure) begin to
manifest signs/symptoms of CoQ10 deficiency relatively
rapidly - in 6 to 12 months. Younger, healthier people
who's only "illness" is the non-illness
"hypercholesterolemia" can tolerate statins for several
years before getting into trouble with fatigue, muscle
weakness and soreness (usually with normal muscle enzyme
CPK tests) and most ominously - heart failure.
In my practice of 17 years in Tyler, Texas, I have seen
a frightening increase in heart failure secondary to
statin usage, "statin cardiomyopathy". Over the past
five years, statins have become more potent, are being
prescribed in higher doses, and are being used with
reckless abandon in the elderly and in patients with
"normal" cholesterol levels.
We are in the midst of a CHF epidemic in the US with a
dramatic increase over the past decade. Are we causing this
epidemic through our zealous use of statins? In large part I
think the answer is yes. We are now in a position to witness
the unfolding of the greatest medical tragedy of all time -
never before in history has the medical establishment
knowingly (Merck & Co., Inc. has two 1990 patents combining
CoQ10 with statins to prevent CoQ10 depletion and attendant
side effects) created a life threatening nutrient deficiency
in millions of otherwise healthy people, only to then sit
back with arrogance and horrific irresponsibility and watch
to see what happens
- as I see two to three new statin cardiomyopathies per week
in my practice, I cannot help but view my once great
profession with a mixture of sorrow and contempt.
Statin-induced CoQ10 depletion is the topic of a recent
petition to the FDA requesting that this drug/nutrient
interaction be identified in a black box warning as part of
statin package insert information. A comprehensive review of
animal and human trials addressing this issue has been
submitted to the FDA as a supporting document. We, of
course, do not expect any response from the FDA, but 10
years from now when the full extent of statin toxicity
becomes painfully evident, at least we can, in good
conscience, know that we tried and who knows, sometimes
small sparks may spread in dry grass.
Cholesterol Drugs And The Depletion Of Coenzyme Q10: A
Review Of Human And Animal Data. By Peter H. Langsjoen, MD
Citizen Petition: Needed - A Change In The Labeling Of All
Statin Drugs
Did you see any improvement in your symptoms after taking
CoQ10 supplements or do you know of others who have statin
side effects who have?
Thanks.
Bill
