BACKGROUND: The WHO Foundation Collaborating Centre for International Drug Monitoring (Uppsala Monitoring Centre [UMC]) has received many individual case safety reports (ICSRs) associating HMG-CoA reductase inhibitor drug (statin) use with the occurrence of muscle damage, including rhabdomyolysis, and also peripheral neuropathy. A new signal has now appeared of disproportionally high reporting of upper motor neurone lesions.

Researchers are sufficiently worried by new study results that they are planning clinical trials involving thousands of people to examine the possible link between Parkinson’s disease and statins, the world biggest selling drugs, reports Patrick Walter in Chemistry & Industry, the magazine of the SCI.
Suggestions of a statin link are not new, but the results of a recent study linking low LDL cholesterol to Parkinson’s provide the strongest evidence to date that it could be real, because statins work by reducing LDL cholesterol. The study by researchers at University of North Carolina showed that patients with low levels of LDL cholesterol are more than three and a half times more likely to develop Parkinson’s disease than those with higher LDL levels.

When asked whether she was concerned by the new results, study leader Xuemei Huang said: ‘Yes I am very concerned, which is why I am planning a 16000-patient prospective study to examine the possible role of statins.’ Huang was quick to point out, however, that a causal link with statins had not yet been proven. And Yoav Ben-Shlomo, a professor of clinical epidemiology at University of Bristol said that it is also a possibility that LDL cholesterol is a consequence rather than a cause of Parkinson’s.
http://www.physorg.com/news88138832.html

According to my research online, my father’s case was definitely not the only one. My father doesn’t have any family history of ALS and he suffered severe muscular and neural damage right after taking the statin drug, which were rapidlly worsening in the last two years before he passed away.

For those doctors who “confidentally” claim that there is no connection between statin and ALS, SHAME ON THEM! From scientific point of view, if they can’t prove or disprove something, they should make their statement cautiously instead of ignorantly making an assertion based on incomplete facts and evidences.

Why would you call that patient a whore? What do you gain from that?
b

Parkinsonism unmasked by lovastatin.

Muller T, Kuhn W, Pohlau D, P
http://www.go3bj
my husband was diagnosed with Parkinson’s disease 1 1/2 yrs ago( age 59 at the time) after being on Lipitor 10 mgm/day for 4+ yrs. 3 months prior to his diagnosis, my niece and I discovered our respective husbands were exhibiting the same neuro symptoms. we found both had been on lipitor for 4+ yrs. and in surface researching the drug, discovered it depletes the body of coenzyme q10. In simplistic wishful thinking way, my husband discontinued the lipitor and began taking coq10 @ 100 mgm/day. 3 moths later, the neurologist he consulted for the first time made the diagnosis of parkinson’s and stated there were no “traditional” anti parkinson’s drugs for early onset patients, but there was a supplement he could recommend that had shown efficacy in patients with early onset Parkinson’s–that supplement: coenzyme Q10 @ 1200 mgm/day (reported in a study by Clifford Shults, et al in the Annals of Neurology, 2002). we were shocked and no longer felt it simplistic to associate Parkinson’s and statin use. My husband was also an avid exerciser–was a 6 day/week jogger prior to his symptoms development (there is some evidence that those individuals who are/were avid exercisers are more prone to adverse statin effects because of the molecular effects of statins upon muscles)–my niece’s husband was also an avid exciser, jogger, and scratch handicap golfer.
when first diagnosed, my husband asked a friend who is a diagnostic radiologist about PET Scan use to determine if one does have Parkinson’s–when the radiologist asked why he wanted the scan my husband told him that I thought this was all a statin toxicity to which the doc replied that during the past yr he had consulted upon about 2000 patients, and 40 of those were initially diagnosed with ALS (Lou Gehrig disease) that in fact had a statin toxicity. When my husband inquired how he knew to look for statin use in these individuals, the doc replied that his first patient with swallowing and speech difficulty diagnosed as possible ALS was his wife. If one accesses the MDA (muscular dystrophy assoc) web site, there was a feature “ask the expert”–under the heading of ALS, there were 16 questions and answers printed during a 4 month period of time. 4 of those 16 questions or 25% specifically asked if a statin was associated with the onset of ALS in each individual:http://www.mdausa.org/experts/responses.cfm?id=66

Yes, it could easily be coincidence, though could also easily be related instances.

I have amassed a huge # of studies and articles related to statins and effects upon the body–one could study forever the effects of blocking the mevalonate pathway to isoprenylated proteins by statins–and thus interfering with the production of selenoproteins or glutathione synthase or a myraid of other compounds. the importance of these compounds within the neurological system is incredible to learn (glutathione, a vital antioxidant within the neuro system is found to be depleted in Parkinson’s patients–as is coenzyme q10–regardless of whether they have ever taken a statin–most researchers feel the coq10 depeletion is part of the disese process, related to mitochondrial dysfunction). and medicine cavalierly interferes with the production of these compounds with a drug to decrease cholesterol IN BASICALLY WELL INDIVIDUALS for “primary prevention”—–I am currently trying to piece together a coherent “citizen’s petition to the FDA” to mandate post marketing studies to determine if statins have a causal relationship to parkinson’s disease.

I think Lipitor caused Parkinson’s in my husband and my niece’s husband. Since their diagnoses, i have had a friend whose husband is 50 diagnosed with Parkinson’s who had been on lipitor for 2+ yrs….I have also been in contact with a woman who was diagnosed with ALS and continued to consult new physicians until one did extensive EMG testing and changed her diagnosis to “statin toxicity”. last i heard from her, she had not improved, but her condition had stabilized for which she was thankful.
we are in hopes many of the neurological effects can be reversed, though there is NO help from the medical community since there is no acknowledgment this neurological condition could be related to lipitor. and it may all be coincidental–though without some study, even an epidemiological one–to determine is there is a possible relationship, we will never know, there will be No therapies developed to address damage done by statins, and just guess work therapies on our parts.

perhaps it is a genetic variation coupled with an environmental agent–in this case Lipitor–which triggered these cases of neurodegenerative diseases–the following is certainly important to consider: (from a press release)
Genetic variations in three enzymes that detoxify insecticides and nerve gas agents as well as metabolize cholesterol-lowering statin drugs may be a risk factor for developing sporadic amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease), and possibly responsible for a reported twofold increased risk of ALS in Gulf War veterans…

The genes for human paraoxanases (PON 1, PON 2 and PON 3), which are located on chromosome 7q21.3, code for the production of detoxifying enzymes involved in the metabolism of a variety of drugs, organophosphate insecticides, such as parathion, diazinon and chlorpyrifos, and nerve gas agents such as sarin…

PON gene cluster variants have previously been associated with other neurodegenerative and vascular disorders, including Alzheimer’s disease, Parkinson’s disease,(from a study led Teepu Siddique, M.D., and colleagues at Northwestern University,Siddique is Les Turner ALS Foundation/Herbert C. Wenske Professor, Davee Department of Neurology and Clinical Neurosciences, professor of cell and molecular biology and director of the Neuromuscular Disorders Program at Northwestern University Feinberg School of Medicine.)

I have now been in contact with other individuals who feel they or their loved ones’ neurodegenerative diseases are related to statin use. if this is a genetic variant, given the millions of people taking a statin today, there could be an enormous # who are effected in this way by this class of drugs.
so dr. kevin, any of your patients exhibiting neurological symptoms on a statin? I think the process that results in Parkinson’s from statins also produces ALS and alzheimer’s. the next time one of your semi elderly patients develops alzheimer’s who is also aking a statin, ask yourself if this line of inquiry is worth undertaking.
In the meantime, all the physicians reading this, please consider the possibility that statins ARE capable of causing irreparable, devastating harm to some people–and that the #’s involved may be much more than the 2% side effects reported by the pharm industry…..alas, who would dare to study this relationship????
Der Nervenarzt
Publisher: Springer-Verlag Heidelberg
ISSN: 0028-2804 (Paper) 1433-0407 (Online)
DOI: 10.1007/s00115-002-1445-6
Issue: Volume 74, Number 2
Date: February 2003
Pages: 115 – 122
Fibrat-/Statin-Myopathie

J. Finsterer A1

A1 Neurologische Abteilung,KA Rudolfstiftung,Wien
Letter in response with case study of statin-unmasked Parkinsons
“To the excellent review about the development of
myopathies following long-term medication of cholesterol
level decreasing fibrates and statins, there should be
considered additional differential diagnostic possibilities.

Because of the similar clinical symptomatology with muscle
aches and increased stiffness, the diagnosis of statin-
induced aggravated Parkinson Disease Syndrome should
be discussed. The development of such muscular side
effects is seen more with statins than with fibrates.
The case report in Table 1 indicates the history of a 60 year
old patient with statin-induced Parkinson Syndrome
occurring over a long time.

On the other hand, with central effective statins, a possible
neuro-protective effect in neuro-degenerative diseases has
been considered, especially in dementia. But long term use
of statins, especially Lovastatin, leads to the reduction of
coenzyme Q10 and can cause damage of the mitochondrial
breathing chain. Co Q-10 is an electron receptor in the
mitochondrial complexes 1 and 2 and very effective
absorber of radicals. This antigen substance increases the
complex 1 activity. Co-Q10 shows a certain therapeutic
effect with encephalomyopathy where there is a lack of
various enzyme functions of the breathing chain.

Dysfunction of various parts of the mitochondrial breathing
chain is also considered in the pathophysiological
mechaism of idiopathic Parkinson’s disease. Treatment
with Co-Q10 in patients who are not treated with Dopamine
for Parkinson patients, caused less disease symptomatology
and progression than patients treated with placebo, though
placebo treatment can cause stimulation of dopaminergic
neurotransmission. Therefore, the long-term treatment with
Co-Q10 possibly is neuroprotective in idiopathic morbid
Parkinson, though new evidence shows it appears to cause
mild symptomatic effect.

Under these circumstances treatment with prophylactic
medication of Co-Q10 which has been well tolerated in
doses up to 1200mgm in patients with neurodegenerative
diseases should be considered for statin myopathy or statin-
induced Parkinson syndrome in addition to discontinuation
of the cholesterol decreasing medication.

The Table 1 summarizes a patient with Parkinson
syndrome.

1996: start of therapy with Fluvastatin 40 mg.

1997: increasing weakness with shoulder and hip pain on the
right

1999: diagnosis of right sided Parkinson syndrome of
akinetic dominance type. Careful induction of Pergolid with
daily doses of 3 mg and Salagen 7.5 mgm

2000: complaints about increasing edema development in
legs, loss of hair, start of a potas.sium sparing diuretic and
increasing of Pergolid medication from 4.5 mg in June 2000
to 6 mgm in December.

March 2001: discontinuation of Fluvastatin, continuation of
Pergolid 6 mg

June 2001: reduction of Pergolid to 4 mgm

Sept 2001 Pergolid 3 mgm. Improvement of edema

December 2001 discontinuation of Pergolid and diuretics

March, 2002 discontinuation of Salagen”

Dr. Th. T. Muller

1.Finsterer J (2003) Fibrat-/Statin-Myopathie. Nervenarzt
:115-122

2.Müller T, Kuhn W, Pohlau D, Przuntek H (1995) Parkinsonism
unmasked
by lovastatin. Ann Neurol 37:685-686

3.Simons M, Schwarzler F, Lutjohann D, von Bergmann K, Beyreuther K,
Dichgans J et al. (2002) Treatment with simvastatin in
normocholesterolemic patients with Alzheimer’s disease: A 26-week
randomized, placebo-controlled, double- blind trial. Ann Neurol
52:346-350

4.Folkers K, Langsjoen P, Willis R, Richardson P, Xia LJ, Ye CQ et al.
(1990) Lovastatin decreases coenzyme Q levels in humans. Proc Natl Acad

Sci U S A 87:8931-8934

5.Shults CW, Haas RH, Pas.sov D, Beal MF (1997) Coenzyme Q10 levels
correlate with the activities of complexes I and II/III in mitochondria

from parkinsonian and nonparkinsonian subjects. Ann Neurol 42:261-264

6.Rotig A, Appelkvist EL, Geromel V, Chretien D, Kadhom N, Edery P et
al. (2000) Quinone-responsive multiple respiratory-chain dysfunction
due to widespread coenzyme Q10 deficiency. Lancet 356:391-395

7.Schapira AH, Mann VM, Cooper JM, Krige D, Jenner PJ, Marsden CD
(1992) Mitochondrial function in Parkinson’s disease. The Royal Kings
and Queens Parkinson’s Disease Research Group. Ann Neurol 32
Suppl:S116-S124

8.Chan A, Reichmann H, Kogel A, Beck A, Gold R (1998) Metabolic changes

in patients with mitochondrial myopathies and effects of coenzyme Q10
therapy. J Neurol 245:681-685

9.Haas RH, Nasirian F, Nakano K, Ward D, Pay M, Hill R et al. (1995)
Low platelet mitochondrial complex I and complex II/III activity in
early untreated Parkinson’s disease. Ann Neurol 37:714-722

10.Shults CW, Oakes D, Kieburtz K, Beal MF, Haas R, Plumb S et al.
(2002) Effects of coenzyme q10 in early Parkinson disease: evidence of
slowing of the functional decline. Arch Neurol 59:1541-1550

11.Fuente-Fernandez R, Stoessl AJ (2002) The biochemical bases for
reward. Implications for the placebo effect. Eval Health Prof
25:387-398

12.Müller T, Buttner T, Kuhn W (2003) A mild benefit of Coenzyme Q
10
supplementation in patients with Parkinson’s disease. J Neural Transm
: (P 57) XIIï€

13.Feigin A, Kieburtz K, Como P, Hickey C, Claude K, Abwender D et al.
(1996) As.sessment of coenzyme Q10 tolerability in Huntington’s
disease.
Mov Disord 11:321-323

# posted by Anonymous : 4:09 PM