This Is MS Multiple Sclerosis Community: Knowledge & Support

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Maybe if neuros took the time they spent meeting and being entertained by drug companies, and instead went on the internet and read the most recent PubMed and medical journal articles on Multiple Sclerosis, they might understand.

They do not even know what is going on in the world of doppler technology and 7Tesla MRI. It is up to us. These are not wacky internet theories. This is scientific research...we just care more because our lives and the lives of our loved ones depends on it. And no drug company has asked for our endorsements!
AC
Go Marie!

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Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

One of the bigest issues in the medical world is increasing specialization so that a doctor from one field does not have enough background to understand what is going on in another. They simply refer.

One of the biggest hurdles this has is it is from another field

what about all the crab's it's a shame for all the folks on them

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Had ms for over 19 years now.

I'm a big fan of Dr. Terry Wahls. For those of you who haven't gone to her website (www.terrywahls.com), I highly recommend checking it out. She has SPMS, was generally wheelchair/scooter-bound after doing CRABs, Cellcept, etc., and then came upon a new program to heal herself that seems to be working.

She strongly believes that dysfunction in the mitochondrial respiratory chain is central to the development of disability in MS, and has developed a program to improve mitochondrial function.

The reason I'm posting this in the venous insufficiency thread is that I just ran across an abstract that emphasizes the importance of the mitochondrial respiratory chain in the development of chronic venous insufficiency in the legs.

I think this is a fascinating angle to pursue....

PK said


This thread is huge so rather than say read it all I will tell you that:
Dr Z is doing trials, he is currently doing endovascular surgery to release the strictures in a very few select patients to see IF.....IF.....that helps the course of MS in those people. 4 people from the US are part of the trial out of a hospital in Buffalo. One of them posted on this thread......can't remember his name?

We'll hear more in a few months; Dr Z is going to report his preliminary findings in April on that trial so there should be a paper available after that. I am certain to make that purchase.

I would not make treatment decisions based on anything I read on TIMS, but I'd use that information to have a conversation with my doctor about what it might mean for me.

This work is preliminary and unfinished. It may not help to do surgery as Z is doing, so I would not stop my current plans.

It also may turn out that the best treatment for MS includes suppressives and endovascular surgery.

Remember that long list of inflammatory markers in the MS lesion and in the venous ulcer; perhaps those things NEED to be dampened by something like SCT.......along WITH releasing the vein. Maybe everyone will do revimmune and also see a vascular guy. Perhaps people who had really effective suppression will do the best of all.

No one can say at this point, I'm not a doctor and I sure do want you to talk to your personal doctor, NOT get overly concerned about this as if you have to somehow get on it now; it is not available so we can't!

But if it works it'll be around hopefuly sooner than later!

Hub it looks good I am sure Cheer will be along to add more.......Have you seen the endothellial thread in regimens forum?

Marie - I have seen that thread, thanks. It's a great thread, just like this one. And maybe I should post the info below in that thread, but I'm lazy....

In addition to the abstract that I quoted above, I also want to point out a recent article discussing using glutathione levels as a marker for mitochondrial function.

If, as Dr. Wahls and some researchers suspect, mitchondrial dysfunction is a central feature of MS, then glutathione testing could be extremely helpful in evaluating MS progression (or more optimistically, the healing process).

Cheer -- the article focuses on a breakthrough that occurred at Stanford. Since you're going there in March, I thought you might be interested (if you're persuaded by the line of thought that emphasizes mitochondrial function in MS).

Here's the link:
<shortened url>

I also want to quote a part of the article that's probably hyperbolic, but eye-opening nevertheless:

Thanks, Hub! Interesting stuff. Looks like the mitochondria are the power source for cells, and that they are part of the endothelium. (Boy, do I wish I'd paid more attention in biology!) My research has focused on the endothelium, because that is the lining of the blood vessels, and I've followed the vascular route- including reducing hypercoagulation & inflammation, and hypertension.

Mitochondria are present in every cell of the body except the red blood cells...which is where the 2 theories might split. Mitochondrial disease would certainly explain the fatigue common to MS patients, since it creates a deficit of energy available to the cells. But I have a hard time understanding how mitochondrial disease would create the activation of the immune system we see in MS, when MD is more a disease of "shutting down" of energy and white blood cells. One interesting corrolary is that nitric oxide balance is important to the mitochondria and endothelium.

Looks like mitochondrial disease can be spotted by checking glutathione and antioxidant levels in the blood. In my way of thinking, mitochondrial disease is another way of labeling oxidative stress, which is a huge component in all disease.


This is from the study you posted on the varicose vein treatment...the drug works by stopping oxygen to the endothelial cells and halting venous damage via the mitochondrial respiratory chain. Have to take their word for it!

The treatment protocol for MD doesn't offer much hope...although it's a great program, once again "there is no cure." I'm holding out for something with a cure!

link

Gotta love the development of molecular medicine...will keep my eye on this research. Thanks, Hub!
AC

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

Chlamydia pneumoniae, which has been found in many people with MS brains in many different universities also steals mitochondrial energy, becasue it is an obligate intracellular pathogen. Once it gets in the cell it takes over the mitochondria for its own purposes ie to metabolize, feed etc. It is one of the main circumstantial supports for CPn association with MS in that lack of energy is an important feature and this could account for that.

David Wheldon long ago, roughly '04, outlined a comprehensive list of supplements for MSers that includes several mitochondrial supports like N acetyl cysteine (turns to GSH in the body), AlCAR, which supports mitochondria directly and Coq10.

There is an immense amount of overlap in these varying strategies for supporting the MS body.......in spite of vary different theories as to "why" they work

We cannot tell cause by effect........
Enough on that off topic cmment! see abx for information on that line of thinking if it interests.

Cheer,

First, I want to thank you for the hope you've added to my life with the research you've cited and the analysis you've provided since you've been posting here!

However, I do have a quibble with your comment above. I think that the abstract is saying that when there's hypoxia (not caused by the venotropic drugs), the venotropic drugs prevent endothelial cell activitation, not that the venotropic drugs create the hypoxia.

As for mitochondrial disease being incurable (so far), my understanding is that that's because the MD is caused by a genetic mutation within the mitochondria. So far, no mitochondrial genetic mutation has been definitively found for MS, so maybe there's something else creating the mitochondrial dysfunction in MS that's easier to cure? Marie's theory, for example, explains mitochondrial dysfunction in the absence of mitochondrial genetic mutation, and includes a cure.

Thanks, Hub...yikes...you're right. Your explanation certainly makes more sense than my misreading of the abstract...hypoxia created the endothelial cell activation, the drugs stopped both via mitochondrial respiratory chain. That's what I get for going too fast Hope I didn't come off as dismissive, because there's alot here, and I probably should have studied more before responding.

Also right re: genetic mutations...and that future research could very well find a direct link to MS. And Marie is great to point out the overlap of cpn and MD. Keep it coming!
AC

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

I double what mrhodes40 says, NAC, ALCAR, ALA and Q10 all stimulate nitochondrial function and when taken together their effect is multiplied!

http://www.springerlink.com/content/m20 ... f2126&pi=7

http://www.springerlink.com/content/961 ... f8453&pi=1

http://www.springerlink.com/content/961 ... edeb4&pi=3

http://www.springerlink.com/content/m51 ... f2126&pi=8

http://www.springerlink.com/content/jwx ... 6c96&pi=12

http://www.springerlink.com/content/w73 ... 6c96&pi=14

http://www.springerlink.com/content/j35 ... 6c96&pi=16