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2019 Jan 2
Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Sciences and Odontostomatology, University of Naples Federico II, Naples, Italy
Therapeutic lag in reducing disability progression in relapsing-remitting multiple sclerosis: 8-year follow-up of two randomized add-on trials with atorvastatin.
https://www.ncbi.nlm.nih.gov/pubmed/30623857

Abstract
BACKGROUND:
Current treatments for relapsing remitting multiple sclerosis (RRMS) reduce inflammation, but have a partial or modest effect on disability. This effect may require a much longer follow-up than standard trial design, in particular in RRMS with relatively-preserved functional reserve. We aimed to assess the long-term clinical evolution of RRMS patients exposed to atorvastatin in two trials (ACTIVE and ARIANNA).
METHODS:
We retrospectively looked at 69 participants randomized with atorvastatin or placebo as add-on therapy to interferon-beta for 24 months at a single MS centre. We recorded relapses, 1-point EDSS progression and progression to EDSS 4.0. Cox regression was performed for these three questions. A Poisson regression model was used to evaluate the association between atorvastatin treatment and annualized relapse rate (ARR).
RESULTS:
After 8.4 ± 2.3 (3.7-11.9) years from trial, the use of atorvastatin was associated with reduced risk of 1-point EDSS progression (HR = 0.440; 95%CI = 0.225-0.861; p = 0.017), and of EDSS 4.0 (HR = 0.310; 95%CI = 0.123-0.784; p = 0.013). We found no significant association between atorvastatin and relapses.
DISCUSSION:
These data suggest that a delayed treatment effect may be seen with atorvastatin added to interferon-beta, eight years after entering the clinical trials. Long-term follow-up of trial cohorts should be mandated.

wiki https://en.wikipedia.org/wiki/Atorvastatin

Most drugs have side effects including this one.

Common side effects of atorvastatinm (Lipitor):
Unexplained muscle pain, tenderness, or weakness.
Confusion, memory problems, or other cognitive issues.
Fever, unusual tiredness, and dark-colored urine.
Swelling, weight gain, urinating less than usual or not at all.

Just the kind of side effects someone with MS needs!

Petr,

of course statins have an effect on progression.

see also viewtopic.php?f=1&t=15188&p=256582#p256581

Leo

Elliot:
Effect of statins - I do not know the reasons, but what has a some impact on RS is interesting. (I'm not going to use it.)
Cholesterol level correlate with disability score in patients with relapsing-remitting form of multiple sclerosis. https://www.ncbi.nlm.nih.gov/pubmed/30339921
Lipoprotein markers associated with disability from multiple sclerosis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6242870/

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Leo:
Virus - maybe, but the problem would already be found, I guess
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What changes over time with MS? I do not know. no one knows exactly today. Just theories, stencils .. but the virus does not fit me. But sure, everything is possible.

http://www.neurology.org/content/61/10/ ... nsion.html

"Cholesterol level correlate with disability score in patients with relapsing-remitting form of multiple sclerosis."

While this may be true some or even much of the time, it is not always true. There are certainly people with low cholesterol levels with high levels of disability and some with high cholesterol levels with low levels of disability.

But it is a good theory, none the less.

Petr75 wrote: ↑Sat Feb 02, 2019 1:07 pm Leo:
Virus - maybe, but the problem would already be found, I guess
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What changes over time with MS? I do not know. no one knows exactly today. Just theories, stencils .. but the virus does not fit me. But sure, everything is possible.

http://www.neurology.org/content/61/10/ ... nsion.html

The virus infection and spreading was there all the time and the virus is latent.
The microbiome gets ever worse.
The epigenetic regulation deteriorates over time and cells come to expression.
Herpes viral epitopes that are expressed in cells and immune cells cross react and cause superoxide.
And causes localised oxidative stress (viral/SNP determined)
This explains the scourge of all sort autoimmune diseases.

I have been hearing a lot lately about lipitor causing leg pain. I have been on it 80mg for 10 years. I have been having unexplained muscle pain in my legs. Going off lipitor hasn't helped in a couple of weeks. Early days yet, but my doc says there are other statins I can try. I need it because I have 3 heart stents. Maybe the stuff they are working on in Las Vegas...

1eye wrote: ↑Wed Feb 06, 2019 5:53 pm I have been hearing a lot lately about lipitor causing leg pain. I have been on it 80mg for 10 years. I have been having unexplained muscle pain in my legs. Going off lipitor hasn't helped in a couple of weeks. Early days yet, but my doc says there are other statins I can try. I need it because I have 3 heart stents. Maybe the stuff they are working on in Las Vegas...

I have a family member who lowered their LDL by 29 points just through diet and increased walking. The dietary changes were simple, e.g., eating more salads and vegetables, some at every dinner.

That won't work for me. Apparently I was on a high dose of lipitor because of my 3 heart stents.

i've just learned that lipitor / atorvastatin is 'atorvastatin calcium'.
that made me think of calcium magnesium balance. so far though, i can find no research looking at the long term effects of lipitor at any dose on calcium and magnesium levels or ratios in serum. nothing on any effects of long term statin use on magnesium status.

magnesium is included here however:

Coping with statin side effects
Some people experience muscle aches or muscle cramps, but trying these tips may help.
https://www.health.harvard.edu/heart-he ... de-effects
To minimize muscle cramps, doctors often recommend doing stretching exercises, wearing compression stockings, avoiding high-heeled shoes, keeping the arms and legs warm, and taking magnesium supplements.

i also like that they even make the stents out of magnesium now, too

Temporary scaffolding of coronary arteries with bioabsorbable magnesium stents: a prospective, non-randomised multicentre trial
https://www.sciencedirect.com/science/a ... 3607608538

This study shows that biodegradable magnesium stents can achieve an immediate angiographic result similar to the result of other metal stents and can be safely degraded after 4 months. Modifications of stent characteristics with prolonged degradation and drug elution are currently in development.

Maybe it's biodegradable because your body wants to absorb it!

precisely!

• Drug-Eluting Bioabsorbable Magnesium Stent (2004)
  "In this article, we describe the first biodegradable stent based on a magnesium alloy that allows controlled corrosion with release to the vessel wall and the blood stream of a natural body component such as magnesium with beneficial antithrombotic, antiarrhythmic, and antiproliferative properties."

2020 Oct 24
Department of Vascular Surgery, The Second Hospital of Hebei Medical University, Hebei, China
The combined treatment of NAD + and atorvastatin ameliorates the development of experimental autoimmune encephalomyelitis in C57BL/6 mice
https://pubmed.ncbi.nlm.nih.gov/33176238/

Abstract

Multiple sclerosis (MS) is a demyelinating and degenerating disorder of the central nervous system impacting many patients worldwide. Due to the complex pathogenesis of MS, drugs to treat MS often show partial effectiveness. Earlier experiments have demonstrated that both atorvastatin and nicotinamide adenine dinucleotide (NAD+) may ameliorate experimental autoimmune encephalomyelitis (EAE), which is known as a classical model of MS, via different protective mechanisms. Since combination therapy can exhibit more beneficial effects than monotherapy, we observed the protective effects of combined treatment of atorvastatin and NAD+ in EAE mice. Our results showed that the combined treatment of these two drugs at half of their optimal dosages had synergistic effect to alleviate the severity of EAE in mice than treatment with each alone. The combined treatment of EAE mice with atorvastatin plus NAD+ relieved the clinical signs and histologic changes, increased the proportion of Treg cells, attenuated IL-17 production, reduced proinflammatory cytokine secretion of Th17 cells, and increased cytokine secretion of Treg cells. In addition, the combined treatment also diminished phosphorylation of both P38 MAPK and ERK, while elevated SIRT1 expression. Taken together, these data suggested that combined treatment with NAD+ and atorvastatin could attenuate the progression of EAE by synergistic immune regulation.