Night-time muscle cramping

"JMDO" <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

Two years after double bypass, and am now having severe leg muscle cramping at night. Could this
be a symptom of vascular disease progression?

Yes.

Quoted message said:

I am presently taking aspirin and Zocor to prevent any future blockages.

What about your other risk factors for atherosclerosis?

Humbly,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

JMDO said:

Two years after double bypass, and am now having severe leg muscle cramping at night. Could this
be a symptom of vascular disease progression? I am presently taking aspirin and Zocor to prevent
any future blockages.

Your symptoms could be from spinal stenosis. An MRI of the lumbo-sacral spine would be an
appropriate evaluation.

Lower extremity claudication does not occur during sleep. Well, I suppose it could if you
sleepwalk. 😉

Patrick Blanchard MD
--
SonoScore Winnning against heart attack and stroke sonoscore.comsonoscore.comOpen ↗

"JMDO" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

Two years after double bypass, and am now having severe leg muscle

cramping

Quoted message said:

at night. Could this be a symptom of vascular disease progression? I am presently taking aspirin
and Zocor to prevent any future blockages.

As a matter of fact, last year I had some lower back problems. My doctor informed me that I had
several protruding discs in the lower back area. The pain is now being managed with anti
inflammatory medication.

.

Before getting in bed I lean against the wall and stretch the back of my leg muscles; in addition to
always spending 10 minutes earlier on an exercise cycle, or when weather permits a 20 minute walk
around the neighborhood..

I had a valve implant in 1985; and that valve changed in 2000 along with a quad bypass... I use
Zocor and Asprin (plus other medications); but I must exercise the legs before going to bed to avoid
leg cramps..

Willard(83)

JMDO said:

Two years after double bypass, and am now having severe leg muscle cramping at night. Could this
be a symptom of vascular disease progression? I am presently taking aspirin and Zocor to prevent
any future blockages.

In article <[email hidden]>,

JMDO said:

Two years after double bypass, and am now having severe leg muscle cramping at night. Could this
be a symptom of vascular disease progression? I am presently taking aspirin and Zocor to prevent
any future blockages.

I had always heard that such cramping could be indicative of low potassium (?) levels - mom always
told me to eat a few bananas.

"JMDO" <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

Two years after double bypass, and am now having severe leg muscle cramping at night. Could this
be a symptom of vascular disease progression? I am presently taking aspirin and Zocor to prevent
any future blockages.

John please read through this, and print out and take to your doctor. I do not say this is the
source of your problem, but it is something to consider. I experienced this myself, and was not
taken off statins until terrible damage had happened. I continue to struggle with statin side
effects which have not gone away, have rendered me incapable of working more than little, and
depleted my savings and pension funds to live on while disabled. I too am considered someone who
MUST take statins, but I now refuse to take any cholesteol lowering medication. The new meds out
have not been on the market long enough for me to know what they might and might not do to us. It is
truly a catch 22, and I sympathize with you. But, read the following from a summer issue of Annals
of Internal Medicine. MFG

Statin-Associated Myopathy with Normal Creatine Kinase Levels TO THE EDITOR: The article by Phillips
and colleagues (1) and the accompanying editorial by Grundy (2) highlight a clinical experience many
of us have had. Are the authors aware of any data, or in their clinical experience have they found
any other noninvasive testing, such as serum aldolase level, that might identify patients who are
experiencing creatine kinase–negative statin myopathy? Mark H. Hyman, MD University of California,
Los Angeles Los Angeles, CA 90025 References
1. Phillips PS, Haas RH, Bannykh S, Hathaway S, Gray NL, Kimura BJ, et al.
Statinassociated myopathy with normal creatine kinase levels. Ann Intern Med. 2002;137:
581-5. [PMID: 12353945]
2. Grundy SM. Can statins cause chronic low-grade myopathy? [Editorial] Ann Intern Med. 2002;137:617-
8. [PMID: 12353951] TO THE EDITOR: We read with interest the article by Phillips and
colleagues (1) and the accompanying editorial (2). One of us (Dr. Torgovnick) developed low-
grade myopathy while receiving statin therapy. Atorvastatin, 5 mg (0.5 tablet), was started
in September 1999. Nonspecific aches and pains were noticed, but no clear weakness was
evident and Dr. Torgovnick continued regular exercise. On several occasions, a burning
sensation beyond what was anticipated developed in the muscles after exercise. Low-grade
myopathy was considered in June 2000, and creatine kinase level was checked. The result,
3.14 _kat/L, was normal (reference range, 0 to 3.34 _kat/L), and atorvastatin therapy was
continued. In early May 2002, 24 hours after exercise, creatine kinase level was checked
and was found to be 4.8 _kat/L. Atorvastatin was withdrawn, and the aches, pains, and
burning sensation gradually resolved. After vigorous exercise, several weeks after
atorvastatin was discontinued, the creatine kinase level was 3.19 _kat/L. On a repeated
test, serum cholesterol level was significantly elevated and pravastatin was introduced.
Symptoms recurred but were tolerated. While Dr. Torgovnick was taking pravastatin, the
creatine kinase level was 4.98 _kat/L shortly after exercise. Phillips and colleagues'
patients ranged in age from 62 to 76 years, and no information was given on their level of
activity or their muscle mass, both of which can affect creatine kinase levels. In the
current author's case, it was clear that something was wrong, but the creatine kinase level
rose only with exercise provocation. The message of the article by Phillips and colleagues
is clear and important. As more patients with this syndrome are identified, perhaps less
invasive evaluation might include the use of exercise provocation to watch for an increase
in creatine kinase level. Alternatively, simple serial measurement of creatine kinase
levels to establish a baseline and subsequent reevaluation after a specified period (or
withdrawal of the agent and a demonstrated decrease in creatine kinase level, particularly
if associated with resolution of symptoms) would be useful. Josh Torgovnick, MD St.
Vincent's Hospital and Medical Center New York, NY 10011 Edward Arsura, MD Salem Veterans
Affairs Medical Center Salem, VA 24153 References
3. Phillips PS, Haas RH, Bannykh S, Hathaway S, Gray NL, Kimura BJ, et al.
Statinassociated myopathy with normal creatine kinase levels. Ann Intern Med. 2002;137:
581-5. [PMID: 12353945]
4. Grundy SM. Can statins cause chronic low-grade myopathy? [Editorial] Ann Intern Med. 2002;137:617-
8. [PMID: 12353951] TO THE EDITOR: Phillips and colleagues (1) nicely documented biopsy-
confirmed myopathy in patients with normal creatine kinase levels in association with
statin therapy. As they mentioned in their discussion, similar features are reported for
coenzyme Q10 deficiency. It is known that 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA)
reductase inhibition by statins influences not only the cholesterol synthesis but also that
of proteins such as farnesylated and geranylgeranylated proteins and ubiquinones such as
coenzyme Q10. Similar to cholesterol synthesis, the primary regulation of coenzyme Q10
biosynthesis is the HMG-CoA reductase reaction, providing its www.annals.org 17 June 2003
Annals of Internal Medicine Volume 138 • Number 12 1007 isoprenyl side chain deriving from
mevalonate. Decreased plasma levels of coenzyme Q10 have been reported in statin-treated
patients (2, 3), and in one of them this decrease was dose related (3). Furthermore, in one
study (4), statin-induced coenzyme Q10 reduction was prevented by exogenous coenzyme Q10
supplementation. On the other hand, similar histopathologic findings of myopathy are well
documented in patients with carnitine deficiency. A 16-week trial of treatment with
lovastatin significantly altered carnitine status in rabbits with decreased tissue levels
of carnitine and increased serum levels of acylcarnitine (5). Use of HMG-CoA reductase
inhibitors leads to increased levels of acyl-CoA and, therefore, to higher requirements of
carnitine for the buffering of acyl-CoA moieties. Assessing the acylcarnitine–free
carnitine ratio before and during therapy with statins might identify the patients who are
most vulnerable to this possible myopathic complication. Although the incidence of statin-
associated myopathy (with abnormal or normal creatine kinase levels) is low, studies on
pathogenic roles of coenzyme Q10 and carnitine are imperative. Finally, well-done clinical
trials addressing the preventive or therapeutic effects of coenzyme Q10 and L-carnitine are
worthy, since millions of people are receiving statins. Emil Toma, MD, DSc, FRCP(C) Maude
Loignon, BSc Hoˆtel-Dieu Hospital Montreal, Quebec H2W 1T8, Canada References
5. Phillips PS, Haas RH, Bannykh S, Hathaway S, Gray NL, Kimura BJ, et al.
Statinassociated myopathy with normal creatine kinase levels. Ann Intern Med. 2002;137:
581-5. [PMID: 12353945]
6. Watts GF, Castelluccio C, Rice-Evans C, Taub NA, Baum H, Quinn PJ. Plasma coenzyme Q
(ubiquinone) concentrations in patients treated with simvastatin. J Clin Pathol. 1993;46:1055-
7. [PMID: 8254097]
7. Mortensen SA, Leth A, Agner E, Rohde M. Dose-related decrease of serum coenzyme Q10 during
treatment with HMG-CoA reductase inhibitors. Mol Aspects Med. 1997;18 Suppl:S137-44.
[PMID: 9266515]
8. Bargossi AM, Grossi G, Fiorella PL, Gaddi A, Di Giulio R, Battino
M. Exogenous CoQ10 supplementation prevents plasma ubiquinone reduction induced by HMGCoA reductase
inhibitors. Mol Aspects Med. 1994;15 Suppl:s187-93. [PMID:
7752830]
7752831. Bhuiyan J, Seccombe DW. The effects of 3-hydroxy-3-methylglutaryl-CoA reductase inhibition
on tissue levels of carnitine and carnitine acyltransferase activity in the rabbit. Lipids.
1996;31:867-70. [PMID: 8869889] TO THE EDITOR: Phillips and colleagues (1) posited that
myopathy with normal creatine kinase levels may occur in patients receiving statin therapy.
Patients with muscular pain or weakness but without elevated enzyme levels pose an
important clinical problem, although the exact incidence of this disorder is not known.
Phillips and colleagues did not discuss a potential mechanism or mechanisms. However, they
reported 3-methylglutaconic aciduria consistent with respiratory chain dysfunction and
pathologic findings similar to those found in coenzyme Q10 deficiency (2). The American
College of Cardiology/American Heart Association/National Heart, Lung, and Blood Institute
clinical advisory states that ubiquinone (coenzyme
Q10) deficiency could be a possible mechanism, although no conclusive data support this hypothesis
(3). The synthesis of coenzyme Q10 in cells involves pathways that are blocked by the statins.
A recent review of statin myopathy (4) discusses this and other topics. Members of the
complementary and alternative medicine community have been advocating the concomitant use of
coenzyme Q10 with statins, although this practice has not been accepted by most mainstream
physicians. Data on whether statins lower coenzyme Q10 levels are contradictory. However,
certain persons with a genetic, biochemical, or other cause of decreased levels of coenzyme Q10
levels in tissue, such as increasing age (5), may experience statininduced decreases in muscle
coenzyme Q10 levels as a cause of the myopathy. Of note, the patients in Phillips and
colleagues' study were 62 to 76 years of age. Do the authors have any information on serum or
muscle coenzyme Q10 levels or coenzyme Q10 use in these patients? I believe the clinical and
pathologic data in Phillips and colleagues' study, coupled with other reports in the peer-
reviewed literature, suggest an etiologic role of coenzyme Q10 deficiency in some patients with
statin-induced myopathy. Although isolated case reports have supported this hypothesis, we need
large randomized, controlled studies studying the concomitant administration of coenzyme Q10
and statins to prevent or treat muscle symptoms, with or without muscle enzyme elevations. Only
then will we be able to address this important controversy. Louis Evan Teichholz, MD Hackensack
University Medical Center Hackensack, NJ 07601 References
1. Phillips PS, Haas RH, Bannykh S, Hathaway S, Gray NL, Kimura BJ, et al.
Statinassociated myopathy with normal creatine kinase levels. Ann Intern Med. 2002;137:
581-5. [PMID: 12353945]
2. Ogasahara S, Engel AG, Frens D, Mack D. Muscle coenzyme Q deficiency in familial
mitochondrial encephalomyopathy. Proc Natl Acad Sci U S A. 1989;86:2379-
3. [PMID: 2928337]
4. Pasternak RC, Smith SC Jr, Bairey-Merz CN, Grundy SM, Cleeman JI, Lenfant C, et al.
ACC/AHA/NHLBI clinical advisory on the use and safety of statins. J Am Coll Cardiol. 2002;40:567-
72. [PMID: 12142128]
5. Baker SK, Tarnopolsky MA. Statin myopathies: pathophysiologic and clinical perspectives.
Clin Invest Med. 2001;24:258-72. [PMID: 11603510]
6. Rosenfeldt FL, Pepe S, Ou R, Mariani JA, Rowland MA, Nagley P, et al. Coenzyme Q10 improves
the tolerance of the senescent myocardium to aerobic and ischemic stress: studies in rats
and in human atrial tissue. Biofactors. 1999;9:291-9. [PMID:
7]IN RESPONSE: Dr. Hyman asks whether other biochemical markers might identify patients with
statin-induced myopathy. Levels of aldolase and myoglobin, which would be released by
disrupted myocyte membranes, have been normal whenever we have tested them in our patients.
We are currently testing other indicators of the metabolic defect associated with this
muscle toxicity (1). Drs. Torgovnick and Arsura inquire about the relation of this toxicity
to exercise. Postexercise creatine kinase level is more sensitive than resting creatine
kinase level in assessing muscle toxicity. The latter is related to membrane disruption but
has not met with much success in assessing statin toxicity (2, 3). We required that all
study patients maintain a consistent exercise and dietary regimen during the 5-month
evaluation. Although all of the creatine kinase evaluations were performed after exercise,
they were not performed late enough (6 to 12 hours later) to make this a sensitive test. We
believe that the preoccupation with muscle membrane abnormalities and Letters 1008 17 June
2003 Annals of Internal Medicine Volume 138 • Number 12 www.annals.org elevation of creatine
kinase levels as indicators of toxicity has delayed the detection of the metabolic toxicity
we described. Other afflictions with similar pathologic characteristics—mitochondrial
myopathies, for example—cause significant abnormalities in muscle function without
disrupting membranes sufficiently to elevate creatine kinase levels. We suspect that further
evaluation of metabolic defects in patients with statin myotoxicity will prove more fruitful
than repeated attempts to evaluate this abnormality from the perspective of muscle membrane
toxicities or rhabdomyolysis. The comments of Dr. Toma and Ms. Loignon and Dr. Teichholz
regarding the possible relationships of carnitine and coenzyme Q10 to statin myotoxicity are
correct. While we found no depression in either serum or muscle carnitine levels in our
patients, measurement of coenzyme Q10 may be more productive. Muscle coenzyme Q10 levels
correlated with toxicity in one of the three patients in our study who underwent muscle
biopsy, both while myopathic and again when toxicity had resolved. We have a report in
preparation that discusses measurement of coenzyme Q10 level in a series of 50 muscle biopsy
specimens from patients under evaluation for statin myotoxicity. The results of that study
should provide further impetus for future trials assessing coenzyme Q10 and carnitine.
Statins are the best therapy available to reduce cardiovascular end points in patients with
atherosclerotic risks. The optimal use of these agents requires a thorough understanding of
their toxicities as well as of their efficacy. We agree that we know too little about the
mechanism and pathophysiology of statin myotoxicity and that further clinical evaluations
and biochemical description are essential. Paul S. Phillips, MD Scripps Mercy Hospital San
Diego, CA 92103 Richard H. Haas, MD University of California, San Diego La Jolla, CA 92093-
0935 References
8. Phillips P, Haas R, Barshop B, Bannykh S, Amjadi D. Utility of abnormal 3-methylglutaconic
aciduria (3MGA) in diagnosing statin associated myopathy. Atheroscler Thromb Vasc Biol
Online Journal. 2002;22:878. Accessed at aha.agora.comaha.agora.comOpen ↗ abstractviewer/av_view.asp.
9. Reust CS, Curry SC, Guidry JR. Lovastatin use and muscle damage in healthy volunteers
undergoing eccentric muscle exercise. West J Med. 1991;154:198-200. [PMID: 2006566]
10. Smit JW, Bar PR, Geerdink RA, Erkelens DW. Heterozygous familial hypercholesterolaemia is
associated with pathological exercise-induced leakage of muscle proteins, which is not
aggravated by simvastatin therapy. Eur J Clin Invest. 1995;25:79-84. [PMID: 7737266]

And in the same issue of Annals of Internal Medicine:

Simvastatin TO THE EDITOR: Simvastatin is an antilipemic agent that decreases low-density
lipoprotein cholesterol levels by inhibiting hydroxymethylglutaryl coenzyme A reductase. Statins
have an excellent safety profile (1). However, reports have described a lupus-like hypersensitivity
reaction with late, insidious onset (2– 4). Symptoms include polymyalgia, elevated erythrocyte
sedimentation rate (ESR), positivity for antinuclear antibodies, and potentially life-threatening
pneumonitis. To highlight the diversity of this drug-induced hypersensitivity, we report a case in
which the patient presented with dysphasia. A 74-year-old man with coronary artery disease and
hypertension presented with sudden onset of dysphasia. He was initially thought to have a viral
illness, but symptoms progressed over weeks to the point where he was able to swallow only liquids.
His hematocrit decreased from an initial value of 0.44 to 0.28 with no reticulocyte response or
evidence of hemolysis. Eosinophilia (eosinophils, 38%), ESR of 100 mm/h, and lactate dehydrogenase
level of 320
U/L were noted. Results of endoscopy and esophageal peristalsis studies were normal. Computed
tomography showed borderline splenomegaly with mediastinal and retroperitoneal adenopathy. Bone
marrow biopsy revealed only increased eosinophils. The rheumatoid factor level was normal, and the
patient was strongly positive for antinuclear antibodies. Medications included simvastatin,
fosinopril, aspirin, colchicine, ranitidine, gemfibrozil, digoxin, and atenolol. The patient had
the only drug discontinued, and afterward, the patient's dysphasia resolved in a few days. Lactase
dehydrogenase level and ESR normalized, and hematocrit subsequently improved. Statins are commonly
used, well-tolerated drugs. A few cases of lupus-like hypersensitivity to statins have been
described. Although these reactions are rare, they are difficult to diagnose because they can
occur after several years of treatment. This report highlights the diverse symptoms of this
reaction. For prescribing clinicians, it is very important to bear these unusual, potentially life-
threatening adverse effects in mind. Katarina LeBlanc, MD, PhD Mary T. Brophy, MD, MPH Boston
Veterans Affairs Healthcare System Boston, MA 02130 References
1. Grundy SM. HMG-CoA reductase inhibitors for treatment of hypercholesterolemia. N Engl J
Med. 1988;319:24-33. [PMID: 3288867]
2. Hill C, Zeitz C, Kirkham B. Dermatomyositis with lung involvement in a patient treated with
simvastatin [Letter]. Aust N Z J Med. 1995;25:745-6. [PMID: 8770347]
3. De Groot RE, Willems LN, Dijkman JH. Interstitial lung disease with pleural effusion caused
by simvastin. J Intern Med. 1996;239:361-3. [PMID:
4]
5. Liebhaber MI, Wright RS, Gelberg HJ, Dyer Z, Kupperman JL. Polymyalgia, hypersensitivity
pneumonitis and other reactions in patients receiving HMG-CoA reductase inhibitors: a
report of ten cases. Chest. 1999;115:886-9. [PMID:
6]

Patrick Blanchard MD said:

JMDO said:

Two years after double bypass, and am now having severe leg muscle cramping at night. Could this
be a symptom of vascular disease progression? I am presently taking aspirin and Zocor to prevent
any future blockages.

Your symptoms could be from spinal stenosis. An MRI of the lumbo-sacral spine would be an
appropriate evaluation.

Lower extremity claudication does not occur during sleep. Well, I suppose it could if you
sleepwalk. 😉

Actually, lower extremity ischemia can occur at rest in severe cases. When it does, it typically
occurs when one is lying down which causes perfusion pressure to the lower legs and feet decreases
(loss of gravitational assist).

Humbly,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

Willard <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

Before getting in bed I lean against the wall and stretch the back of my leg muscles; in addition
to always spending 10 minutes earlier on an exercise cycle, or when weather permits a 20 minute
walk around the neighborhood..

I had a valve implant in 1985; and that valve changed in 2000 along with a quad bypass... I use
Zocor and Asprin (plus other medications); but I must exercise the legs before going to bed to
avoid leg cramps..

Willard(83)

JMDO said:

Two years after double bypass, and am now having severe leg muscle cramping at night. Could this
be a symptom of vascular disease progression? I am presently taking aspirin and Zocor to prevent
any future blockages.

Having experienced muslce cramping first at night, then anytime, along with muscle pain, weakness
and atropy on pravastatin, atorvastatin, cerivastatin and simvastatin, I think your problem is
caused by STATINS. Do a search on www.rxlist.com for the side effects of your particular statin, and
lipitor as well just to see that another statin does similar or same. Eventually no amount of
exercise, stretching, heat, ice or pain meds will look after this, and you risk permanent damage. I
am two years off Baycol and not yet fully recovered, and I am better than most. Statins cause
mitochondrial damage. Go to www.impostertrial.com, the site of Dr. S. Phillips of Scripps Mercy
Hospital's studies on statin myopathy. Read through BOTH patient site and physician site. Also do a
google on Dr. P. Langsjoen AND cardiomyopathy, and see what you may be doing to your heart muscle if
you take statins, which deplete the body's store of coenzyme Q10, an essential enzyme for cell
function. Depletion of this enzyme may not be replenished by taking coenzyme q10 orally. Then go to
www.spacedoc.org for a run down of how statins can affect memory, thinking, learning, language and
reading, cause transient global amnesia (which I experienced on lipitor, baycol and zocor) and
aphasia. Take all this to your doctor, and if he or she puts you down, get another. Right? Patrick
and Andrew?

It seems to me I heard somewhere that Owen Lowe wrote in article
<[email hidden]>:

Quoted message said:

In article <[email hidden]>, "JMDO" <[email hidden]> wrote:

Quoted message said:

Quoted message said:

Two years after double bypass, and am now having severe leg muscle cramping at night. Could this
be a symptom of vascular disease progression? I am presently taking aspirin and Zocor to prevent
any future blockages.

Quoted message said:

I had always heard that such cramping could be indicative of low potassium (?) levels - mom always
told me to eat a few bananas.

Some people, including my wife, get fair relief from drinking tonic water that contains quinine. My
wife sips it from time to time as a preventative, but more often takes it stops an attack of cramps.

Of course if John's cramps are related to his disease or his medications quinine may not be helpful.
--
Don [email hidden]

MD/PhD said:

Patrick Blanchard MD said:

JMDO said:

Two years after double bypass, and am now having severe leg muscle cramping at night. Could
this be a symptom of vascular disease progression? I

am

Quoted message said:

presently taking aspirin and Zocor to prevent any future blockages.

Your symptoms could be from spinal stenosis. An MRI of the lumbo-sacral spine would be an
appropriate evaluation.

Lower extremity claudication does not occur during sleep. Well, I suppose it could if you
sleepwalk. 😉

Actually, lower extremity ischemia can occur at rest in severe cases. When it does, it typically
occurs when one is lying down which causes perfusion pressure to the lower legs and feet decreases
(loss of gravitational assist).

Humbly,

Andrew

--
Dr. Andrew B. Chung, MD/PhD Board-Certified Cardiologist heartmdphd.comheartmdphd.comOpen ↗

I would suppose that ambulation during the day would preceed this gentlman's nocturnal pain, but you
have a nice point.

--
~~~ Patrick Blanchard, M.D., A.B.F.P. Board Certified in Family Practice
familydoctor.orgblanchardOpen ↗ ~~~ SonoScore Winning against heart attack and stroke
sonoscore.comsonoscore.comOpen ↗

mfg said:

Willard <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

Before getting in bed I lean against the wall and stretch the back of my leg muscles; in
addition to always spending 10 minutes earlier on an exercise cycle, or when weather permits a
20 minute walk around the neighborhood..

I had a valve implant in 1985; and that valve changed in 2000 along with a quad bypass... I use
Zocor and Asprin (plus other medications); but I must exercise the legs before going to bed to
avoid leg cramps..

Willard(83)

JMDO said:

Two years after double bypass, and am now having severe leg muscle cramping at night. Could
this be a symptom of vascular disease progression? I am presently taking aspirin and Zocor to
prevent any future blockages.

Having experienced muslce cramping first at night, then anytime, along with muscle pain, weakness
and atropy on pravastatin, atorvastatin, cerivastatin and simvastatin, I think your problem is
caused by STATINS. Do a search on www.rxlist.com for the side effects of your particular statin,
and lipitor as well just to see that another statin does similar or same. Eventually no amount of
exercise, stretching, heat, ice or pain meds will look after this, and you risk permanent damage.
I am two years off Baycol and not yet fully recovered, and I am better than most. Statins cause
mitochondrial damage. Go to www.impostertrial.com, the site of Dr. S. Phillips of Scripps Mercy
Hospital's studies on statin myopathy. Read through BOTH patient site and physician site. Also do
a google on Dr. P. Langsjoen AND cardiomyopathy, and see what you may be doing to your heart
muscle if you take statins, which deplete the body's store of coenzyme Q10, an essential enzyme
for cell function. Depletion of this enzyme may not be replenished by taking coenzyme q10 orally.
Then go to www.spacedoc.org for a run down of how statins can affect memory, thinking, learning,
language and reading, cause transient global amnesia (which I experienced on lipitor, baycol and
zocor) and aphasia. Take all this to your doctor, and if he or she puts you down, get another.
Right? Patrick and Andrew?

Sure. There is no utility in a doctor that won't hear your views.

Humbly,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

(mfg) said:

Go to www.impostertrial.com, the site of Dr. S. Phillips of Scripps Mercy Hospital's studies on
statin myopathy. Read through BOTH patient site and physician site.

Interesting site. Especially:

"Cholesterol lowering therapy with HMGCoA reductase inhibitors (statins) convincingly reduces death
and myocardial infarction among patients with coronary heart disease. Application of the National
Cholesterol Education Program’s ATP III guidelines could lead to as many as 36 million patients
receiving this therapy in the United States.

The remarkable success and proliferation of statin therapy is largely due to the absence of
significant toxicity occurring in more than 50,000 patients included in randomized controlled trials
of statins over the last 16 years. Statins are regularly declared 'safer than aspirin' based on this
phenomenal safety record. Myopathy defined as unexplained muscle pain or weakness accompanied by a
muscle enzyme level in the blood greater than 10 times normal, occurred in only one case per 10,000
person years among subjects randomized to statin treatment in the 4S and Heart Protection Study
trials. An identical incidence has been calculated when statins are used in the community at large.
Despite this very low incidence of serious muscle toxicity, many patients in these trials have had
minor muscle complaints. However, these minor muscle complaints occur with the same frequency among
patients randomized to placebo or no therapy as on statins.

Statins are easier to take than any of the previous cholesterol therapies. They generally reduce
cholesterol levels by more than 20%. Statins have been demonstrated to have many beneficial effects
in addition to reducing the cholesterol levels. They improve the health of the inner lining of our
arteries, the endothelium. This makes our blood vessels more healthy. They have been shown to reduce
the formation of clots which can cause heart attacks, strokes and lung problems. When clots have
already formed, statins help them to dissolve. Statins reduce the tendency for platelets, the
blood's sticky, clotting cells to aggregate. This probably also helps them to prevent disorders
associated with thrombus or clots. These drugs reduce the body's inflammatory reactions and make the
plaques which form on arteries from atherosclerosis less likely to rupture and cause heart attacks.
In some large trials statins have seemed to prevent diabetes. Statins may reduce the rate of bone
loss or osteoporosis as we age. This can result in less bone pain and fewer fractures in patients on
statins. Small studies have demonstrated less leakage of protein into the urine in patients on
statins as well as less harmful thickening of the heart muscle. These phenomenal improvements occur
in many diverse areas of health far removed from the cholesterol disorders for which these drugs
were originally prescribed. When physicians at national meetings have suggested in jest that statins
be placed in the water supply, it is because very few bad results have ever been reported on these
therapies."

[email hidden] wrote in message news:<[email hidden]>...

Quoted message said:

(mfg) said:

Go to www.impostertrial.com, the site of Dr. S. Phillips of Scripps Mercy Hospital's studies on
statin myopathy. Read through BOTH patient site and physician site.

Interesting site. Especially:

"Cholesterol lowering therapy with HMGCoA reductase inhibitors (statins) convincingly reduces
death and myocardial infarction among patients with coronary heart disease. Application of the
National Cholesterol Education Program?s ATP III guidelines could lead to as many as 36 million
patients receiving this therapy in the United States.

And the date of this study was what? Since 2000, when questions arose about statins side-effects,
and then 2001, after baycol was recalled, much more has become known about what statins do and don't
do. I'm afraid the latest studies, and Dr. Phillips, don't come down on the side of blanket
approval, or condemnation. Who did this study? Who paid them? Was it a pharma or industry study?
That is not unbiased. The National Cholesterol Education program consists of several cardiologists
who are consultants to the pharmas who produce the drugs they laud. It is important to look at all
the work, and ask, where did this study come from, who paid for it. And to look at newer studies
which are coming out with much information culled since after-market lab rats like me were nearly
killed by statins. Information known to the pharmas, and cardiologists such as those who are on the
National Cholesterol Education Program consultant board was suppressed.

I am posting here to try and show those who will not be properly informed by their doctors that
there is something else to consider. Have you read for example, the Baycol trial transcripts, the
url I posted earlier this week on medical ghostwriting, where the writer says he was told what to
write, and the LATimes stories on the corruption in the National Institutes of Health?

The site is not propaganda, it is a balanced look at what cholesterol lowering therapy does and does
not, particularly statins and myopathy. Did you read any of that? What is your assessement after
reading through the site completely? Do you, have you, taken statins? Did you have side effects?

Thank you for the giving me the opportunity to more broadly present my findings. MFG

[email hidden] wrote in message news:<[email hidden]>...

Quoted message said:

On 15 Dec 2003 13:10:41 -0800, [email hidden] (mfg) wrote:

Listener please tell me, how many is 2 per cent of 35 million? Or 5 per cent?

I have read conservative estimates that 35 million people are taking statins. So if 2 per cent of
those taking statins have side effects (Pfizer choses 2 per cent. Some clinicians estimate
greater than 10 per cent, but never mind we son't quibble)....how many people is that with statin
side effects?

I can't figure this out. Since taking statins I have lost my ability to do maths computations.
(Muldoon et al in the book "Neuropsychology of Cardiovascular disease" on the memory loss, transient
global amnesia, aphasia, etc observed in study participants while on statins.)

2 per cent of 35 million.

I think you'll be able to figure it out. MFG

[email hidden] wrote in message news:<[email hidden]>...

Quoted message said:

(mfg) said:

Go to www.impostertrial.com, the site of Dr. S. Phillips of Scripps Mercy Hospital's studies on
statin myopathy. Read through BOTH patient site and physician site.

Interesting site. Especially:

"Cholesterol lowering therapy with HMGCoA reductase inhibitors (statins) convincingly reduces
death and myocardial infarction among patients with coronary heart disease. Application of the
National Cholesterol Education Program?s ATP III guidelines could lead to as many as 36 million
patients receiving this therapy in the United States.

Listener I do not find the paragraphs as you have copied them here for us, in your post above. I am
not including your whole post in mine, for space reasons, but I am sure readers here will read what
you have set it out, above. Please give me the url for the place on Dr. Phillip's site that you
found this study as you have copied it. I would like to see it in context.

I'm glad you posted it because it lends us some new insight into how drugs are marketed. Dr.
Jacques Genest, a Montreal cardiologist, is one of the authors, or writers, of the Canadian
heart guidelines, which are based on the American guidelines (to which you have referred in your
above post.)

Dr. Jacues Genest is the person who made the comment about "statins in the drinking water" which is
in your above post. He made this commment in a story to the Calgary Herald, in spring of 2002,
while he attended a pharma sponsored cardiology conference at Lake Louise. The conference
sponsoring pharma, coincidentally, makes a statin.

Now then, we have whoever wrote the study you have posted, presumably a member of the American
guideline writers, quoting one of the Canadian guideline writers, one of his own, so to speak, as
evidence of why we should all be on statins.

This is what I find I Dr. Phillip's website. I'm sure you will correct me, and show me where on his
site, are the paragraphs as you have set them out.

Ds. Phillips on statin-induced myopathy: "The recent withdrawal of cerivastatin from the market has
highlighted both our ignorance and the need for post-marketing surveillance of these therapies."

impostertrial.comphysician.htmOpen ↗

What is Known about Statin Associated Myopathy with Normal CK?

Success and Proliferation of Statins

Cholesterol lowering therapy with HMGCoA reductase inhibitors (statins) convincingly reduces death
and myocardial infarction among patients with coronary heart disease Application of the National
Cholesterol Education Program's ATP III guidelines could lead to as many as 36 million patients
receiving this therapy in the United States.

The remarkable success and proliferation of statin therapy is largely due to the absence of
significant toxicity occurring in more than 50,000 patients included in randomized controlled trials
of statins over the last 16 years. Myopathy' defined as unexplained muscle pain or weakness
accompanied by a CK greater than 10 times normal, occurred in only one case per 10,000 person years
among subjects randomized to statin treatment in the 4S and Heart Protection Study trials. An
identical incidence has been calculated when statins are used in the community at large. Despite
this very low incidence of serious muscle toxicity, many patients in these trials have had minor
muscle complaints. However, these minor muscle complaints occur with the same frequency among
patients randomized to placebo. Consequently, it is generally believed that patients whose CK levels
remain normal are not having a reaction to these drugs, despite complaints of muscle symptoms.
Nonetheless, both minor and major muscle toxicities related to statin therapy are not well
understood and have been poorly studied. The recent withdrawal of cerivastatin from the market has
highlighted both our ignorance and the need for post-marketing surveillance of these therapies.
Several lines of evidence suggest that there are common minor myopathic toxicities in addition to
the rare rhabdomyolytic reactions to these drugs."

And then he goes on to discuss other aspects of statin-induced myopathy. MFG

(mfg) said:

[email hidden] wrote in message news:<[email hidden]>...

Quoted message said:

(mfg) said:

Go to www.impostertrial.com, the site of Dr. S. Phillips of Scripps Mercy Hospital's studies on
statin myopathy. Read through BOTH patient site and physician site.

Interesting site. Especially:

"Cholesterol lowering therapy with HMGCoA reductase inhibitors (statins) convincingly reduces
death and myocardial infarction among patients with coronary heart disease. Application of the
National Cholesterol Education Program?s ATP III guidelines could lead to as many as 36 million
patients receiving this therapy in the United States.

And the date of this study was what? Since 2000, when questions arose about statins side-effects,
and then 2001, after baycol was recalled, much more has become known about what statins do and
don't do. I'm afraid the latest studies, and Dr. Phillips, don't come down on the side of blanket
approval, or condemnation. Who did this study? Who paid them? Was it a pharma or industry study?
That is not unbiased. The National Cholesterol Education program consists of several cardiologists
who are consultants to the pharmas who produce the drugs they laud. It is important to look at all
the work, and ask, where did this study come from, who paid for it. And to look at newer studies
which are coming out with much information culled since after-market lab rats like me were nearly
killed by statins. Information known to the pharmas, and cardiologists such as those who are on the
National Cholesterol Education Program consultant board was suppressed.

I am posting here to try and show those who will not be properly informed by their doctors that
there is something else to consider. Have you read for example, the Baycol trial transcripts, the
url I posted earlier this week on medical ghostwriting, where the writer says he was told what to
write, and the LATimes stories on the corruption in the National Institutes of Health?

The site is not propaganda, it is a balanced look at what cholesterol lowering therapy does
and does not, particularly statins and myopathy. Did you read any of that? What is your
assessement after reading through the site completely? Do you, have you, taken statins? Did
you have side effects?

Thank you for the giving me the opportunity to more broadly present my findings. MFG

Huh? Are you questioning what I posted? Or just upset that I chose to post something POSTIVE
regarding Statins? Really, I don't understand. Afterall, this was YOUR link!

Yes, I read through the whole site.

Findings? What are you talking about. Are you a doctor...a scientist...a researcher...? Corruption
at NIH - I'm SHOCKED! Of course it's really a sad commentary, if true, but what institution doesn't
have some level of corruption?

Hey, I'm not arguing that statins don't have side-effects. ALL medications have side-effects of one
sort of another, from mild to severe. I'm just not as anti-statin as you seem to be.

Yes, I've taken a statin (Pravachol) since 1995. Ready?: Last month I told my primary doctor that I
was experience some mild, intermittent leg calf soreness when I awoke in the morning. As it happened
I had just had bloodwork done and my liver enzymes were slightly elevated. My doctor had me stop
Pravachol immediately. I go back in February for more bloodwork and a followup. No big deal.

Does this experience make me want to yell FIRE - stay away from statins!? No.

My assesment? Some people have no side effects from statins. Some people have mild side effects from
statins. Some people have severe side effects from statins. As YOUR link stated, many studies have
shown the positive effectiveness of statins. Side effects do not negate that. (Unless you believe
that ALL positive statin studies are bogus - or some sort of conspiracy!)

(mfg) said:

[email hidden] wrote in message news:<[email hidden]>...

Quoted message said:

On 15 Dec 2003 13:10:41 -0800, [email hidden] (mfg) wrote:

Listener please tell me, how many is 2 per cent of 35 million? Or 5 per cent?

I have read conservative estimates that 35 million people are taking statins. So if 2 per cent of
those taking statins have side effects (Pfizer choses 2 per cent. Some clinicians estimate
greater than 10 per cent, but never mind we son't quibble)....how many people is that with statin
side effects?

I can't figure this out. Since taking statins I have lost my ability to do maths computations.
(Muldoon et al in the book "Neuropsychology of Cardiovascular disease" on the memory loss,
transient global amnesia, aphasia, etc observed in study participants while on statins.)

2 per cent of 35 million.

I think you'll be able to figure it out. MFG

As I said on my other reply - yes, I understand there are side effects whether it's one person or
700,000 people. And these side effects can possibly range from mild to severe. And there are also
can be many people who do not experience side effects. But does the possibility or actuality of side
effects (discounting death, obviously) negate the positive nature of a drug? Especially, when so
many studies have shown such?

No.

(mfg) said:

[email hidden] wrote in message news:<[email hidden]>...

Quoted message said:

(mfg) said:

Go to www.impostertrial.com, the site of Dr. S. Phillips of Scripps Mercy Hospital's studies on
statin myopathy. Read through BOTH patient site and physician site.

Interesting site. Especially:

"Cholesterol lowering therapy with HMGCoA reductase inhibitors (statins) convincingly reduces
death and myocardial infarction among patients with coronary heart disease. Application of the
National Cholesterol Education Program?s ATP III guidelines could lead to as many as 36 million
patients receiving this therapy in the United States.

Listener I do not find the paragraphs as you have copied them here for us, in your post above. I am
not including your whole post in mine, for space reasons, but I am sure readers here will read what
you have set it out, above. Please give me the url for the place on Dr. Phillip's site that you
found this study as you have copied it. I would like to see it in context.

I'm glad you posted it because it lends us some new insight into how drugs are marketed. Dr.
Jacques Genest, a Montreal cardiologist, is one of the authors, or writers, of the Canadian
heart guidelines, which are based on the American guidelines (to which you have referred in your
above post.)

Dr. Jacues Genest is the person who made the comment about "statins in the drinking water" which is
in your above post. He made this commment in a story to the Calgary Herald, in spring of 2002,
while he attended a pharma sponsored cardiology conference at Lake Louise. The conference
sponsoring pharma, coincidentally, makes a statin.

Now then, we have whoever wrote the study you have posted, presumably a member of the American
guideline writers, quoting one of the Canadian guideline writers, one of his own, so to speak, as
evidence of why we should all be on statins.

This is what I find I Dr. Phillip's website. I'm sure you will correct me, and show me where on his
site, are the paragraphs as you have set them out.

Dr. Phillips on statin-induced myopathy: "The recent withdrawal of cerivastatin from the market has
highlighted both our ignorance and the need for post-marketing surveillance of these
therapies."

I find it a bit odd that you apparently snipped my entire response...oh, well.

Anyway....here's the url for the website YOU orginally posted:

impostertrial.comvirtues.htmOpen ↗

This article and comments by Dr. Phillips aside, I still stand by what I said.

[email hidden] wrote in message news:<[email hidden]>...

Quoted message said:

(mfg) said:

[email hidden] wrote in message news:<[email hidden]>...

Quoted message said:

On 15 Dec 2003 13:10:41 -0800, [email hidden] (mfg) wrote:

> Go to www.impostertrial.com, the site of Dr. S. Phillips of Scripps Mercy Hospital's studies
> on statin myopathy. Read through BOTH patient site and physician site.

Interesting site. Especially:

"Cholesterol lowering therapy with HMGCoA reductase inhibitors (statins) convincingly reduces
death and myocardial infarction among patients with coronary heart disease. Application of the
National Cholesterol Education Program?s ATP III guidelines could lead to as many as 36 million
patients receiving this therapy in the United States.

Huh? Are you questioning what I posted?

Listener I cannot find what you have posted. Will you please give me the url from Dr. Phillips'
website which has exactly what you have posted? What I find is different. The first couple (2)
paragraphs are the same, then it differs. I have the ocular damage that the dogs in the baycol trial
had (before Bayer went back to the FDA, requested and got permission to replace the dogs with an
animal which would not react that way) and my vision is still impaired. I am not finding the article
as you have posted it, so think I must have overlooked it somewhere. What is the url, from Dr.
Phillips' website? MFG

Here is what I find. It does not match what you have posted:

"Cholesterol lowering therapy with HMGCoA reductase inhibitors (statins) convincingly reduces death
and myocardial infarction among patients with coronary heart disease Application of the National
Cholesterol Education Program's ATP III guidelines could lead to as many as 36 million patients
receiving this therapy in the United States.

The remarkable success and proliferation of statin therapy is largely due to the absence of
significant toxicity occurring in more than 50,000 patients included in randomized controlled trials
of statins over the last 16 years. Myopathy' defined as unexplained muscle pain or weakness
accompanied by a CK greater than 10 times normal, occurred in only one case per 10,000 person years
among subjects randomized to statin treatment in the 4S and Heart Protection Study trials. An
identical incidence has been calculated when statins are used in the community at large. Despite
this very low incidence of serious muscle toxicity, many patients in these trials have had minor
muscle complaints. However, these minor muscle complaints occur with the same frequency among
patients randomized to placebo. Consequently, it is generally believed that patients whose CK levels
remain normal are not having a reaction to these drugs, despite complaints of muscle symptoms.
Nonetheless, both minor and major muscle toxicities related to statin therapy are not well
understood and have been poorly studied. The recent withdrawal of cerivastatin from the market has
highlighted both our ignorance and the need for post-marketing surveillance of these therapies.
Several lines of evidence suggest that there are common minor myopathic toxicities in addition to
the rare rhabdomyolytic reactions to these drugs."

Evidence for Statin Toxicity without Rhabdomyolysis from Trials

When statin therapy is used in larger than conventional doses, the incidence of both rhabdomyolysis
and of minor muscle complaints increases. While the incidence of muscle complaints with normal CK
in patients participating in statin trials has been similar in the treated and placebo groups there
is a tendency to increased minor muscle complaints and to rhabdomyolysis at higher dosages of
statin. In the EXCEL trial in which patients were treated with low (40 mg) or high (80 mg) dose
lovastatin, the group that received 80 mg daily demonstrated a trend to more muscle complaints than
the placebo group
(9.3% of 1352 high dose patients vs. 7.5% of 1352 low dose patients and 7.5% of placebo patients).
Similarly while simvastatin 80 mg daily was associated with only 2.3% myalgias with normal CK,
myalgias occurred in 5.7% of patients receiving a 160-mg daily preparation. This increase in
minor muscle complaints and the occurrence of rhabdomyolysis caused Merck to withdraw plans to
market the larger dose of simvastatin.

Evidence for Statin Toxicity without Rhabdomyolysis from Laboratory Models

Cell culture studies and animal models of statin toxicity have repeatedly demonstrated that
histochemical and biochemical toxicity develops at doses well below those which cause rhabdomyolysis
or CK enzyme leakage. In myocyte cell culture, statin toxicity causing morphological abnormalities,
decreased protein synthesis and decreased ATP levels occurs at doses lower than those required to
produce enzyme leakage or CK elevations. In a rabbit model, muscle toxicity and myotonia are not
always associated with elevated CK. There is thus evidence that muscle toxicity occurs at statin
dosages well below those required to cause rhabdomyolysis and it is reasonable that the muscle
complaints of some patients on statins with normal serum CK might represent a toxicity below the
threshold needed to trigger CK elevation.

Evidence for Statin Toxicity without Rhabdomyolysis from Case Reports

Despite the remarkable safety record of statins in clinical trials, there are a number of small
studies and credible case reports describing myopathic complaints in patients on statins with
normal CK levels. One of our co-investigators described 15 patients from a single cholesterol
clinic with muscle stiffness and tenderness that had normal CK tests. Muscle biopsies in these
patients revealed ragged red fibers consistent with mitochondrial myopathy. Others have described
patients with reproducible muscle pain on statins despite normal CK. Isoprostane levels are
elevated in some patients with muscle aches on statins despite normal CK suggesting an oxidation
injury to the muscle.

Despite the success of these therapies, several lines of evidence suggest that there may indeed be a
poorly studied minor muscle toxicity related to statin use. Our preliminary work suggests that
certain patients with muscle complaints on statins are indeed suffering from myotoxicity despite
normal CK levels. In a brief report published in the Annals of Internal Medicine, October 1, 2002,
we present four such patients. These patients were repeatedly able to identify blinded statin
therapy due to their symptoms. They had measurable weakness while on statins which reversed on
placebo. Biopsies of these patients while toxic on statins revealed similar histopathology
indicating myopathy due to mitochondrial dysfunction. The IMPOSTER (Is Myopathy Part Of Statin
ThERapy?) Trial is a double blinded placebo controlled crossover evaluation designed to clarify the
clinical description of statin myopathy with normal CK.

[Back]

How to Evaluate Patients with Muscle Symptoms on Statins?

We have been evaluating patients in both the IMPOSTER trial and in consultative practices since
1998. Certain patterns of symptoms seem to reliably predict the patients with the most severe
myopathy on muscle biopsy. These patients usually complain of muscle aching in the quadriceps,
gluteals and biceps femoris. They describe burning pain in these muscle groups during exercise such
as mounting stairs. Some patients complain of weakness particularly of the hip musculature. They
often complain of progressive inability to rise from a low chair a bed or from squatting position.
The most myopathic patients have noted increased dyspnea on exertion while on statins.

When we analyzed preliminary data from the IMPOSTER trial, patients who correctly identified blinded
statin therapy had significant weakness on standardized muscle testing including: hip abduction
measured by Nicholas Manual Muscle Tester™, standing time from a low chair, and stair stepping.

Many of the myopathic patients had felt markedly improved when they stopped their statin therapy for
two weeks before entry into the trial.

While our findings are preliminary, we have developed a pathway for evaluating patients who feel
that their muscle aches are due to statin therapy. We evaluate patients who need statin for
secondary prevention or are diabetic somewhat differently from those who are receiving statins as
primary prevention. This evaluation starts with administration of a myopathy patient questionnaire
to search for alternate causes of myopathy. Next we measure CK, sedimentation rate (ESR) and thyroid-
stimulating hormone (TSH). If the CK is elevated we search for alternate explanations such as
exercise or hypothyroidism. If no alternative presents itself we retest the CK off statins for 6
weeks. In a patient requiring statin for secondary prevention whose CK remains elevated we proceed
directly to percutaneous muscle biopsy. If the CK returns to normal we consider the patient to have
a likely reaction to statins and choose alternaitve cholesterol lowering therapies. Patients with
normal CK, ESR and TSH are divided into those with typical symptoms and those atypical symptoms. In
patients with atypical symptoms we generally search for alternative explanations for their symptoms.
In patients with typical symptoms we stop statin therapy for 2 weeks. If their symptoms resolve and
they were receiving statins for primary prevention we recommend alternate lipid lowering therapies.
If their symptoms resolve and they require statins for secondary prevention a higher level of
evidence is sometimes required. In a patient with typical myopathic symptoms that improve off
statins for whom statin therapy is an indispensable part of their risk modification program a
percutaneous biopsy may be necessary to decide whether statin should be stopped. These patients are
placed back on statins and biopsied after they have been on therapy for at least 6 weeks.