Re: Kaiser "cholesterol clinic" experience

Alice Faber wrote:
In article <4d91fa60$0$19838$882e7ee2@xxxxxxxxxxxxxxx>,
"GysdeJongh" <JonghSevenHundredElevenAtPlanet.nl> wrote:

Ellen K. wrote:
"Susan" <susan@xxxxxxxxxxxx> wrote in message
news:8vcob2F3ccU4@xxxxxxxxxxxxxxxxxxxxx
x-no-archive: yes

On 3/28/2011 8:15 PM, Ellen K. wrote:

My response was not that neuropathy can't be a side effect of
simvastatin, rather that contrary to Susan's assertion it is not
listed as such in the official documentation.


I never said it was listed there, did I?


Yes, you did. You said if I had read the documentation provided by
the drug company I would have seen it.

I said it was well known and common.

But if your doctor goes by the official documentation, your doctor
won't know it.


Not only the documentation provided by the drug company, but also
the documentation provided by the national institute of health does
not mention neuropathy as a side effect of simvastatin. Do you
really expect a professional physician to make recommendations
based on something some unknown individual happens to post on the
internet?

here is a free review :
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849981/?tool=pubmed
Am J Cardiovasc Drugs. 2008;8(6):373-418. doi:
10.2165/0129784-200808060-00004.
Statin adverse effects : a review of the literature and evidence for
a mitochondrial mechanism.

Snipped to focus on one specific sentence in the abstract:

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.

Are they actually suggesting that diabetics are at greater risk than
the general population for suffering side effects from statins?

it is a (free) review, so it contains lots of references and tables with summary of all the large trials they could find back in 2008. have a look :)

They do suggest that the statin effect is related to mitochondrial function and that diabetics and the other above mentioned are at greater risk.

The metabolic syndrome, diabetes and recently neuropathy might be related to mitochondrial function. The new theory is that neuropathy results from damaged mitochondria that can not sufficient fast be replaced because it takes month for them to travel down into the long axons :

Ann Neurol. 2011 Jan;69(1):100-10. doi: 10.1002/ana.22150. Epub 2010 Nov 8.
Mitochondrial dysfunction in distal axons contributes to human immunodeficiency virus sensory neuropathy.

Abstract
OBJECTIVE: Accumulation of mitochondrial DNA (mtDNA) damage has been associated with aging and abnormal oxidative metabolism. We hypothesized that in human immunodeficiency virus-associated sensory neuropathy (HIV-SN), damaged mtDNA accumulates in distal nerve segments, and that a spatial pattern of mitochondrial dysfunction contributes to the distal degeneration of sensory nerve fibers.

METHODS: We measured levels of common deletion mutations in mtDNA and expression levels of mitochondrial respiratory chain complexes of matched proximal and distal nerve specimens from patients with and without HIV-SN. In mitochondria isolated from peripheral nerves of simian immunodeficiency virus (SIV)-infected macaques, a model of HIV-SN, we measured mitochondrial function and generation of reactive oxygen species.

RESULTS: We identified increased levels of mtDNA common deletion mutation in postmortem sural nerves of patients with HIV-SN as compared to uninfected patients or HIV patients without sensory neuropathy. Furthermore, we found that common deletion mutation in mtDNA was more prevalent in distal sural nerves compared to dorsal root ganglia. In a primate model of HIV-SN, freshly isolated mitochondria from sural nerves of macaques infected with a neurovirulent strain of SIV showed impaired mitochondrial function compared to mitochondria from proximal nerve segments.

INTERPRETATION: Our findings suggest that mtDNA damage accumulates in distal mitochondria of long axons, especially in patients with HIV-SN, and that this may lead to reduced mitochondrial function in distal nerves relative to proximal segments. Although our findings are based on HIV-SN, if confirmed in other neuropathies, these observations could explain the length-dependent nature of most axonal peripheral neuropathies.

PMID: 21280080

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