This Is MS Multiple Sclerosis Community: Knowledge & Support

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]

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 .

ozarkcanoer

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...

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

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)