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autoimmune orthodoxy - by a neuroscientist

Posted: Thu Jul 01, 2010 7:11 am
by sbr487
This was posted by Sharon in general forum -

someone has courage to stand up and question ...

http://www.expert-reviews.com/doi/pdfpl ... /ern.10.69

Posted: Thu Jul 01, 2010 7:56 am
by ozarkcanoer
Thank you for posting this very interesting point of view. It is good that he is questioning the EAE model, the autoimmunity model, and the current drug therapies. I was particularly interested that he says some people claim the 33% effectiveness of the CRABs drugs may only be placebo. Placebo, placebo, placebo !!!! So the benefit of CCSVI Liberation treatment is placebo and not the effectiveness of the MS drugs. And he doesn't even mention CCSVI !!! It is nice to see such a point of view from a non-CCSVI perspective. Research should be focused on other possible causes for MS than the autoimmune EAE model.

This also makes me wonder about where and if there is anyone trying to create a CCSVI mouse model. Surely this would convince scientists. Joan has mentioned somewhere that a scientist at Stanford was attempting to make a mouse model of CCSVI. It is also curious that none of the MS societies' money was granted to a university for research on a mouse model since this seems so obvious to me.

ozarkcanoer

Posted: Thu Jul 01, 2010 8:23 am
by Cece
Mouse model would be basic foundational science of this. Yes, since the NMSS did not want to study treatment, studying mice would have added more to the discourse than some of what they did choose to fund.

It has been said that they may have chosen studies out of a desire to disprove ccsvi, not prove it. Choosing a mouse study would have done little to disprove it, perhaps? With a mouse study you'd have to expect some negative effect to blocking off veins, so it would support the ccsvi theory.

There was a phd student who'd developed a laser to block off venules in rats to look at how it affected the brain. We just need him to step up from venules to jugulars...he's already studying venous outflow.

Posted: Thu Jul 01, 2010 8:32 am
by ozarkcanoer
Cece !! A phd student is trying to create a CCSVI mouse model ! Do you know where ? It is good to know that someone is trying :D.

ozarkcanoer

Posted: Thu Jul 01, 2010 8:32 am
by fernando
History

The history of clinical trials before 1750 is brief.[6][7]
Clinical trials were first introduced in Avicenna's The Canon of Medicine in 1025 AD, in which he laid down rules for the experimental use and testing of drugs and wrote a precise guide for practical experimentation in the process of discovering and proving the effectiveness of medical drugs and substances.[8] He laid out the following rules and principles for testing the effectiveness of new drugs and medications, which still form the basis of modern clinical trials:[9][10][verification needed]

The drug must be free from any extraneous accidental quality.
It must be used on a simple, not a composite, disease.
The drug must be tested with two contrary types of diseases, because sometimes a drug cures one disease by its essential qualities and another by its accidental ones.
The quality of the drug must correspond to the strength of the disease. For example, there are some drugs whose heat is less than the coldness of certain diseases, so that they would have no effect on them.
The time of action must be observed, so that essence and accident are not confused.
The effect of the drug must be seen to occur constantly or in many cases, for if this did not happen, it was an accidental effect.
The experimentation must be done with the human body, for testing a drug on a lion or a horse might not prove anything about its effect on man.

One of the most famous clinical trials was James Lind's demonstration in 1747 that citrus fruits cure scurvy.[11] He compared the effects of various different acidic substances, ranging from vinegar to cider, on groups of afflicted sailors, and found that the group who were given oranges and lemons had largely recovered from scurvy after 6 days.
Frederick Akbar Mahomed (d. 1884), who worked at Guy's Hospital in London,[12] made substantial contributions to the process of clinical trials during his detailed clinical studies, where "he separated chronic nephritis with secondary hypertension from what we now term essential hypertension." He also founded "the Collective Investigation Record for the British Medical Association; this organization collected data from physicians practicing outside the hospital setting and was the precursor of modern collaborative clinical trials."[13]

We know that subjecting humans to potentially harmful experiments is not right, but one thousand years later Avicenna's quote still has some truth in it.

http://en.wikipedia.org/wiki/Clinical_trial

Posted: Thu Jul 01, 2010 9:53 am
by Cece
ozarkcanoer wrote:Cece !! A phd student is trying to create a CCSVI mouse model ! Do you know where ? It is good to know that someone is trying :D.

ozarkcanoer
No, no...the phd student does not even know about CCSVI but developed the laser to block venules and is studying the effect of micro-occlusions on venous outlfow. I'm the one who thinks that it might be possible to take that technology and apply it to a macro-occlusion of the jugular, instead of the micro-occlusion of a venule, in a ccsvi mouse model. I do not know of anyone doing such a thing, and I agree, it ought to have been done yesterday.

here is the link to thread: http://www.thisisms.com/ftopict-11826-laser.html

Posted: Thu Jul 01, 2010 12:04 pm
by 1eye
Before I comment on some of what is in this paper, from my own experience, I'd like to remind that the first thing I heard about Mark Freedman saying to Pablo Zamboni was why don't you tie off a couple of mouse jugulars? I think, and I think Dr. Zamboni thought, that he was being facetious, and not suggesting he develop a mouse model. But he had the right idea.

I noticed in the paper the trial I was on, with Dr. Freedman as lead, was discussed.

"The recent decision to discontinue the dirucotide trial in the huge BioMS and Eli Lilly study is a welcome sign that researchers can no longer accept the therapeutic endeavors based on the autoimmune model [104].

It was very large, and we were only one of the sites. I applaud the decision to terminate it. I wonder if anyone made money by short-selling.

I did not know that interferon trials were so close to being only explainable by the placebo effect. I have, on this site, said I think placebo is nonsense. I still believe that. I was on placebo in that trial. I did not know it. It didn't help me one iota. In fact, one of the shortcomings of that trial was its inability to detect my progression. By the time I had my next dose, I was in a wheelchair. I had a heart attack instead, featuring three (arterial) stents. The testing was partly by private MRI. That is one reason I am incensed that I cannot even get CCSVI treatment by paying for it.

Posted: Thu Jul 01, 2010 5:44 pm
by Cece
1eye wrote:I did not know that interferon trials were so close to being only explainable by the placebo effect.
One good thing about this: the bar is extremely low for what CCSVI treatment has to achieve in terms of reduction of the rate of progression, let alone actual improvements, for it to beat out everything currently on the market.

Posted: Fri Jul 02, 2010 12:33 am
by cah
Cece wrote:
1eye wrote:I did not know that interferon trials were so close to being only explainable by the placebo effect.
One good thing about this: the bar is extremely low for what CCSVI treatment has to achieve in terms of reduction of the rate of progression, let alone actual improvements, for it to beat out everything currently on the market.
Sorry, I can't really see how this is a good thing...

I think this article does not really contribute to the CCSVI theory, but the CCSVI theory contributes to this article. Even if the CCSVI theory would be disproven (I don't think so), it will, no it does HUGELY help to think in other directions as the "autoimmune orthodoxy". And this in itself is a good thing.

Bottom line is, even those CCSVI sceptics who aren't single-minded must already admit today that MS is anything, but not autoimmune.

Posted: Fri Jul 02, 2010 2:35 am
by TMrox
There are quite a few articles explaining why MS is NOT an autoimmune disorder. An abnormal immune reaction is observed but that does not necesarily mean it is autoimmune. See:
http://www.direct-ms.org/pdf/Immunology ... immune.pdf

and this 2010 article which states, "MS as autoimmune disease: this is the most popular theory, although the disease does not fulfill all the criteria for a definite autoimmune disease."
http://www.ncbi.nlm.nih.gov/pubmed/19932200

See here Zamboni explaining the theory of how CCSVI might contribute to that abnormal immune reaction seen in MS:

http://hosted.mediasite.com/mediasite/V ... ebb41a8ba6

Posted: Fri Jul 02, 2010 11:51 am
by Cece
cah wrote:
Cece wrote:
1eye wrote:I did not know that interferon trials were so close to being only explainable by the placebo effect.
One good thing about this: the bar is extremely low for what CCSVI treatment has to achieve in terms of reduction of the rate of progression, let alone actual improvements, for it to beat out everything currently on the market.
Sorry, I can't really see how this is a good thing...
My thought is that, in order to become standard of care, you have to prove that the treatment is better than other treatments out there.

Although thinking that over it doesn't really apply between ccsvi treatment and drugs because they are adjunctive, you can do both, so it's not a one-over-the-other. Still if the CCSVI results come in lower than what we'd expect, perhaps as DrS suggested because inexperienced doctors are starting randomized trials without first getting familiar with the procedure and their first attempts are included in with the data, it really won't need as much for ccsvi treatment to be far superior than anything currently on the market.

Posted: Thu Jul 08, 2010 1:35 am
by sbr487
I am resurrecting this threat hoping to get answer to the following -

assuming that MS is autoimmune and issue really starts somewhere in our immune system, is there some study/explanation as to why BBB also goes haywire? are these two isolated events (too much of a coincidence I think)

Posted: Thu Jul 08, 2010 4:25 am
by costumenastional
TMrox wrote:There are quite a few articles explaining why MS is NOT an autoimmune disorder. An abnormal immune reaction is observed but that does not necesarily mean it is autoimmune. See:
http://www.direct-ms.org/pdf/Immunology ... immune.pdf

and this 2010 article which states, "MS as autoimmune disease: this is the most popular theory, although the disease does not fulfill all the criteria for a definite autoimmune disease."
http://www.ncbi.nlm.nih.gov/pubmed/19932200

See here Zamboni explaining the theory of how CCSVI might contribute to that abnormal immune reaction seen in MS:

http://hosted.mediasite.com/mediasite/V ... ebb41a8ba6
thanks for that TMrox.

Posted: Thu Jul 08, 2010 5:28 am
by cheerleader
sbr487 wrote:I am resurrecting this threat hoping to get answer to the following -

assuming that MS is autoimmune and issue really starts somewhere in our immune system, is there some study/explanation as to why BBB also goes haywire? are these two isolated events (too much of a coincidence I think)
The immune system is also activated in stroke and dementia, and white matter lesions and oligoclonal banding are seen in neurovascular diseases that are created by hypoxic/ischemic insult or plasmic deposition in brain tissue. Why did doctors assume that MS is autoimmune? Stroke isn't autoimmune....maybe "autoimmune" just means we have no idea why.
cheer

Posted: Thu Jul 08, 2010 5:43 am
by TMrox
I agree with Cheer,

My condition Transverse Myelitis (TM) can be caused by a bunch of viruses, vaccines and autoimmune disorders.

However in 40-50% of TM patients a cause cannot be identified so they are referred as Idiopathic transverse myelitis, where the autoimmune system is thought to be involved. Meaning put everythign that we don't know in that black box 'autoimmune'.