Hypothesis: I'm Full Of It

We don't really understand how the interferons work. We have some pretty good ideas, but they don't work for everyone. One hypothesis is that they work by increasing production of a protein that facilitates the death of melin-reactive immune cells (the cells that destroy myelin) and prevents inflammation. If those cells aren't destroyed, you get MS. Simple, eh?

How do you test the hypothesis? You check the blood of people on the interferons for that protein. Presence of that protein is a good thing. Lack of it means the interferons probably aren't working for you.

Whose blood you might ask? Mine for one. Starting next month, I'll be enrolled in another study through the MS clinic in Halifax and have my blood tested at regular intervals to see if the protein is present. My hypothesis, based on the researcher's, is that I'm full of it.

The whole point of this particular study is to be able to predict, based on blood studies, who will benefit from receiving interferons (Betaseron, Avonex). As it stands now, docs are encouraging everyone to get on a treatment as soon as possible. The sooner you are on treatment, the better your long term outcome: fewer attacks means less permanent damage and less disability. For some people, that means trying one drug after another, which takes precious time and may possibly result in more attacks and greater disability. So if we know right off the bat that the interferons won't work for you because you lack a certain protein or ability to make that protein, the docs can move onto another non-interferon treatment sooner.

Scientific progress is slow, I know. But it is plodding along.

S.