This Is MS Multiple Sclerosis Community: Knowledge & Support

Robbie, this is going to be as big a change in the status quo as when Marshall and Warren proved that stomach ulcers were caused by helico bacter pylori:

The two trials which found improvement in MS using antibiotics are the US one (S. Sriram, C. Stratton and co-workers) and the Canadian one (L. Metz and co-workers). The US trial is particularly compelling because it showed objective halting of the rate of loss of grey matter. As far as I am aware the only trial which found no improvement is that of Woessner et al. [Woessner R, Grauer MT, Frese A, Bethke F, Ginger T, Hans A, Treib J. Long-term Antibiotic Treatment with Roxithromycin in Patients with Multiple Sclerosis. Infection. 2006 Dec;34(6):342-4.] This last is badly flawed in that it used intermittent monotherapy with a macrolide, likely inducing persistence in the organism without eradicating it. An excellent discussion of the problems of treatment of chronic chlamydial infectionsi can be found here [Villareal C, Whittum-Hudson JA, Hudson AP. Persistent Chlamydiae and chronic arthritis. Arthritis Res. 2002;4(1):5-9.] This is a highly recommended article, and the full text is available in pdf format. The authors ponder whether eradication of chronic chlamydial infection is possible. Fortunately, it is; Chuck Stratton and colleagues found ways to address all forms of the organism simultaneously, and have demonstrated this in tissue culture and animal studies. It's a brilliant insight, and it works in humans, too.

Are double blind studies necessary? Not strictly in progressive MS where the natural history is toward inexorable deterioration. Halting that deterioration is of itself completely unprecedented. Double blind studies are something of a shibboleth. They are often used to make a big noise about tiny statistical differences. They are likely to be difficult to recruit for; if you had a wife or daughter with rapidly progressive disease you'd want her treated, wouldn't you, rather than risk her languishing on a placebo arm. Of course, the situation is rather different in mild relapsing-remitting disease.

Acceptance of MS being primarily an infection is difficult, not because of the evidence, which is both abundant and difficult to refute, but because of the difficulty of effecting a paradigm change. All the eggs are in the autoimmune basket.

1) Which white blood cells are the ones that are implicated in the theoretical pathology of Cpn in MS?

2) Has anyone done a statistical study of folks who have Cpn v/s don't have Cpn and compared the rates of illnesses in the two groups?

3) Given the strong likelihood that your average neuro is professionally restricted from acting on this, which kind of doctor is best to approach with this idea and what should we ask for? How do we present this desire to be tested?

Naypay, you really do sound like an accountant.

If you really want to find something out, you investigate

Most of the population has antibodies to cpn by the time they're fifty, so whether it's 'interesting' or not doesn't really matter. Start with NAC. If you feel flu-like when you take it, you are reacting to cpn kill-off.