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Statin Therapy Inhibits Remyelination in the Central Nervous System

Statin Therapy Inhibits Remyelination in the Central Nervous System

http://ajp.amjpathol.org/cgi/content....2009.080947v1

Am J Pathol. 2009 Apr 6.
Statin Therapy Inhibits Remyelination in the Central Nervous System. Miron VE, Zehntner SP, Kuhlmann T, Ludwin SK, Owens T, Kennedy TE, Bedell BJ, Antel JP.
Our findings suggest that simvastatin inhibits central nervous system remyelination by blocking progenitor differentiation, indicating the need to monitor effects of systemic immunotherapies that can access the central nervous system on brain tissue-repair processes.
__________________

In plainer English (which I needed myself to understand the seriousness of this report)

http://bloodbrainbarrierblog.blogspo...elination.html

Quote:

This not only suggests that relapsing/remitting MS patients should be carefully monitored while taking simvastatin (if they should be taking it at all in the first place), but that long-term treatment with simvastatin could have profound effects on the CNS. This should definitely temper the enthusiasm expressed by the American Academy of Pediatrics last year for giving statins to children as young as eight years old.

Great -- I have been taking it for several years. It has lowered my cholesterol.

Quote:

Originally Posted by olsen (Post 493932)

http://ajp.amjpathol.org/cgi/content....2009.080947v1

Am J Pathol. 2009 Apr 6.
Statin Therapy Inhibits Remyelination in the Central Nervous System. Miron VE, Zehntner SP, Kuhlmann T, Ludwin SK, Owens T, Kennedy TE, Bedell BJ, Antel JP.
Our findings suggest that simvastatin inhibits central nervous system remyelination by blocking progenitor differentiation, indicating the need to monitor effects of systemic immunotherapies that can access the central nervous system on brain tissue-repair processes.

WOW-thanks for the info. I started taking Zocor-then the generic simvastatin years ago when "they" started saying it could help with fighting ms. Now, after reading this info, I want to stop. VERY frustrating:mad: I guess I should call my pcp :confused: Doggone it. As I understand Tysabri, which I've been on for 2 1/2yrs, works by stopping the attack of T-cells which gives your body a chance to repair itself; if by taking simvastatin I have reduced or halted that repair I am not a happy camper.
Linda

My father's been on statins for quite a long time now, and constantly complains about them because of the side effects they can cause. He swears by CoQ10.

Thanks for the information, I'll have to share it with Dad (who has heart troubles, not MS, but it'll be a common point of interest for us).

Thanks for the link, but please read!

Hi--I'm glad our humble little blog is generating discussion, but I feel (based on some comments I've read) that I need to emphasize the following:

I am NOT a physician (I'm a scientist), and NOTHING I write on the BBB Blog should in any way be construed as medical advice. PLEASE do not make any changes to the medications you are taking without consulting your physician first.

Many thanks, and best wishes,
Brian Hawkins, PhD

[QUOTE=mrsD;493965]In plainer English (which I needed myself to understand the seriousness of this report)

Quote:

Originally Posted by BBBBlog (Post 495209)

Quote:

Originally Posted by mrsD (Post 493965)

In plainer English (which I needed myself to understand the seriousness of this report)

I think we all understand your concern, Brian.
Everyone here mostly checks with their doctor.
What is concerning about the newest statin information for the readers of the MS forum, is that high dose statins were touted by the drug companies as a TREATMENT for MS. And it looks like this is not going to work or be good for them.
If you cruise around, you'll find olsen and myself putting up all the data coming out about statins, not just the positive ones, we get in the general media.
I think doctors have been kept in the dark about the damage potential statins have, and therefore cannot answer questions adequately when patients ask them. Providing that data here gives them a chance to print it out and take it with them to the doctor. In that case it is a roundabout way of providing CME for those doctors!

And I agree with you...that the newest attempt to suggest use of statins for children is deporable! It is right up there with atypical antipsychotics for toddlers! (and we know where that has gone)

We have a warning on every page of these forums to consult your doctor, before trying any suggestions that appear here.
And I always put up carefully checked medical information, to support my posts as well.

Thanks for chiming in.

WHAT!?:mad:

Stupid drugs with their stupid side effects. I need to read up on more alternative meds for MS. Homeopathic, I think it's called.

My first neuro put me on simvistatin shortly after I was dx. My level was 223, whereas 2 years prior it was at 175. When I quizzed him on how the jump occurred with no real change in my diet, he said the demyelazation (or however it's spelled) dumps the fat stripped off the nerves as cholesterol into our bloodstream.

I haven't been doing any real research of my own on MS lately. That stops today because;

I am the MonSter that MS fears.

Wait. I realize I'm overreacting. But does the body really replace that stuff that's been stripped off? If so, how could this disease even exist?

I have so much reading to do.

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?

Quote:

Originally Posted by MooseasaurusRex (Post 496775)

WHAT!?:mad:

Wait. I realize I'm overreacting. But does the body really replace that stuff that's been stripped off? If so, how could this disease even exist?

I have so much reading to do.

Just wanted to share that yes, the body can replace myelin. Except in examples like MS. And yes, Moose can retract his hot-headedness and knee jerk reaction and do the research needed.

But don't tell anyone.

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.

Quote:

Originally Posted by barb02 (Post 496891)

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.

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

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

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