Statin Therapy Inhibits Remyelination in the Central Nervous System

Becky21 · 04-18-2009, 01:48 AM

Statins lowered my cholesterol dramatically within 6 weeks to a normal rate last year. However, I was the "one in a million" as the drug mfgs. claim, who develop muscle wasting and nerve damage in my thighs.

I don't for one minute believe than this is a one in a million chance. I was on intramuscular Avonex shots at the time I started taking stains and it attacked the weak muscle area I was injecting in both thighs.

I had to stop both Avonex and statins and am now taking Niacin to try to get my cholesterol under control. The damage to my thighs is permanent a year later and I have been Neurontin 3 times a day for the pain.

My Cardiologists said that I will never be put back on statin drugs. My Neuro said no more DMD's because of the nerve damage.

It has been very difficult and a very painful experience for me.

mrsD · 04-18-2009, 01:48 PM

Quote:

Originally Posted by barb02

For now, I plan on staying on simivastatin, but do plan on asking my neuro his thoughts about the article. My dosage is fairly low, and it has helped reduce my cholesterol. It is just one study -- correct?

No, not just one study... in fact there are many many:

Quote:

ScienceDaily: Your source for the latest research news and science breakthroughs -- updated daily
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Statins' Adverse Effects Documented

ScienceDaily (Jan. 29, 2009) — A paper co-authored by Beatrice Golomb, MD, PhD, associate professor of medicine at the University of California, San Diego School of Medicine and director of UC San Diego's Statin Study group cites nearly 900 studies on the adverse effects of HMG-CoA reductase inhibitors (statins), a class of drugs widely used to treat high cholesterol.

The result is a review paper, currently published in the online edition of American Journal of Cardiovascular Drugs, that provides the most complete picture to date of reported side effects of statins, showing the state of evidence for each. The paper also helps explain why certain individuals have an increased risk for such adverse effects.

"Muscle problems are the best known of statin drugs' adverse side effects," said Golomb. "But cognitive problems and peripheral neuropathy, or pain or numbness in the extremities like fingers and toes, are also widely reported." A spectrum of other problems, ranging from blood glucose elevations to tendon problems, can also occur as side effects from statins.

The paper cites clear evidence that higher statin doses or more powerful statins – those with a stronger ability to lower cholesterol – as well as certain genetic conditions, are linked to greater risk of developing side effects.

"Physician awareness of such side effects is reportedly low," Golomb said. "Being vigilant for adverse effects in their patients is necessary in order for doctors to provide informed treatment decisions and improved patient care."

The paper also summarizes powerful evidence that statin-induced injury to the function of the body's energy-producing cells, called mitochondria, underlies many of the adverse effects that occur to patients taking statin drugs.

from http://www.sciencedaily.com/releases...0127090735.htm

The mitochondrial damage remains for me one of the most
serious so far:
This is the abstract for the same paper:

Quote:

Am J Cardiovasc Drugs. 2008;8(6):373-418. doi: 10.2165/0129784-200808060-00004.Links
Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism.
Golomb BA, Evans MA.

Department of Medicine, University of California, San Diego, California 92093-0995, USA. bgolomb@ucsd.edu

HMG-CoA reductase inhibitors (statins) are a widely used class of drug, and like all medications, have potential for adverse effects (AEs). Here we review the statin AE literature, first focusing on muscle AEs as the most reported problem both in the literature and by patients. Evidence regarding the statin muscle AE mechanism, dose effect, drug interactions, and genetic predisposition is examined. We hypothesize, and provide evidence, that the demonstrated mitochondrial mechanisms for muscle AEs have implications to other nonmuscle AEs in patients treated with statins. In meta-analyses of randomized controlled trials (RCTs), muscle AEs are more frequent with statins than with placebo. A number of manifestations of muscle AEs have been reported, with rhabdomyolysis the most feared. AEs are dose dependent, and risk is amplified by drug interactions that functionally increase statin potency, often through inhibition of the cytochrome P450 3A4 system. An array of additional risk factors for statin AEs are those that amplify (or reflect) mitochondrial or metabolic vulnerability, such as metabolic syndrome factors, thyroid disease, and genetic mutations linked to mitochondrial dysfunction. Converging evidence supports a mitochondrial foundation for muscle AEs associated with statins, and both theoretical and empirical considerations suggest that mitochondrial dysfunction may also underlie many nonmuscle statin AEs. Evidence from RCTs and studies of other designs indicates existence of additional statin-associated AEs, such as cognitive loss, neuropathy, pancreatic and hepatic dysfunction, and sexual dysfunction. Physician awareness of statin AEs is reportedly low even for the AEs most widely reported by patients. Awareness and vigilance for AEs should be maintained to enable informed treatment decisions, treatment modification if appropriate, improved quality of patient care, and reduced patient morbidity.

PMID: 19159124 [PubMed - indexed for MEDLINE]

from: http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

We are seeing more and more negative papers on statins now, since their patents are almost over. Once they are expired there will be much more information released.
This is a typical situation that happens with all drugs. And as drug companies are discovered in their ways of slanting things to their favor only then do we get some truth. The mito information is about 2-3 yrs old. Once they lose the patent=exclusive right to market, all the negative hidden things become exposed.

barb02 · 04-18-2009, 05:52 PM

I was referring to one study suggesting that it may hinder the remyelination process.

mrsD · 04-18-2009, 06:29 PM

Here is another:

Quote:

Exp Neurol. 2009 Jan;215(1):41-7. Epub 2008 Sep 27.Click here to read Links
Simvastatin induces cell death in a mouse cerebellar slice culture (CSC) model of developmental myelination.
Xiang Z, Reeves SA.

CNS Signaling Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USA.

Statins (inhibitors of HMG-CoA reductase) have shown promise in treating multiple sclerosis (MS). However, their effect on oligodendrocyte remyelination of demyelinated axons has not been clarified. Since developmental myelination shares many features with the remyelination process, we investigated the effect of lipophilic simvastatin on developmental myelination in organotypic cerebellar slice cultures (CSC). In this study, we first characterized developmental myelination in CSC from postnatal day (P)5 and P10 mice that express enhanced green fluorescence protein (eGFP) in oligodendrocyte-lineage cells. We then examined the effect of simvastatin on three developmental myelination stages: early myelination (P5 CSC, 2DIV), late myelination (P10 CSC, 2DIV) and full myelination (P10 CSC, 10DIV). We found that treatment with simvastatin (0.1 microM) for 6 days decreased the survival of Purkinje cells and oligodendrocytes drastically during the early myelination stage, while moderately during the late and full myelination stages. Oligodendrocytes are more resistant than Purkinje cells. The toxic effect of simvastatin could be rescued by the product of HMG-CoA reductase mevalonate but not low-density lipoprotein (LDL). Additionally, this toxic effect is independent of isoprenylation since farnesyl pyrophosphate (Fpp) but not geranylgeranyl pyrophosphate (GGpp) provided partial rescue. Our findings therefore suggest that inhibition of cholesterol synthesis is detrimental to neuronal tissue.

PMID: 18929563 [PubMed - indexed for MEDLINE]

from http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

barb02 · 04-18-2009, 07:31 PM

Thanks! I will print this one out for my neuro also.

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