Multiple sclerosis is almost universally labeled an “autoimmune disease.” Yet after decades of research, there is still no proof that MS is the result of autoimmunity.
Several papers by Drs. Abhijit Chaudhuri and Peter Behan [1,2] discuss problems with the conventional explanation:
- Unlike other diseases which are known to have an autoimmune component (rheumatoid arthritis, systemic lupus erythematosus, and myasthenia gravis), MS has no specific immunological marker. This after 60 years of search for such a marker.
- The standard animal model for MS, experimental allergic encephalomyelitis (EAE), is generated by inducing autoimmunity against myelin basic protein in mice. However, EAE symptoms do not closely resemble those of MS; rather, EAE mice look like humans with a different disease — acute disseminated encephalomyelitis (ADEM). Some differences: EAE and ADEM lack the characteristic large plaques radiating from a central focus seen in the brains of MS patients. EAE and ADEM both feature destruction of endothelial cells lining blood vessels, a pattern not seen in MS.
- The autoimmune model does not explain the neurodegeneration and loss of brain matter in the brains of MS patients; the observation that widespread neuronal loss is present even at the earliest clinical stage of the disease; the absence or slight infiltration of lymphocytes in MS plaques; the role of vitamin D in MS prevention; and the general failure of immunotherapies.
Whether MS is an autoimmune disease has implications for treatment. Autoimmune diseases are commonly treated by immunosuppression. But if MS is an infectious disease, immunosuppression would be a terrible mistake.
After 60 years of research, the autoimmune model has failed to produce a single effective treatment for MS. Drugs have been found that improve mice with EAE, but none does much to help MS patients. Chaudhuri and Behan note:
The two most widely prescribed therapies for MS (interferon and glatiramer acetate) have no effect on the progressive forms of the disease (primary or secondary MS), although relapse rates may be reduced by about one third in some patients. A response rate of one third is considered to be a powerful placebo effect in treatment trials. 
The continued dominance of the autoimmune paradigm in MS research calls to mind Einstein’s definition of insanity.
Meanwhile, other work has established that at least some cases of MS are infectious in origin, and can be cured with antibiotic and dietary therapies. That will be the subject of tomorrow’s post.
 Chaudhuri A, Behan PO. Multiple sclerosis: looking beyond autoimmunity. J R Soc Med. 2005 Jul;98(7):303-6. http://pmid.us/15994589.
 Chaudhuri A, Behan PO. Multiple sclerosis is not an autoimmune disease. Arch Neurol. 2004 Oct;61(10):1610-2. http://pmid.us/15477520.