“As a follow-up to the MS Society’s ‘MS Prevention Meeting‘. I was asked to step in at short notice for Max Parmar and talk on prevention trials. I simply presented the conclusions from the NMSS task force meeting in 2011. Interestingly, Gary Cutter’s Big Data study got the most interest. It was suggested look at the doing a pilot study to test the feasibility of doing a ‘Big Data’ prevention study. I am up for this and will contact Gary Cutter to see if he is still interested in taking this forward.”
The big questions I posted earlier this week are still pertinent and I have added a few more:
- How do we stop the population smoking, or at least people who are at high-risk of getting MS from smoking?
- How does smoking increase the risk of getting MS?
- Is it vitamin D deficiency, or lack of sunlight exposure, the risk factor for developing MS and other autoimmune diseases? Is low vD levels simply a surrogate of low sunlight exposure and it is the latter that is the risk factor?
- How do we design a vitamin D prevention trial? Should we focus on the general population or high-risk groups (1st and 2nd generation family members of MSers)? What dose of vD should we use or do we need to supplement to a target (e.g. >100nmol/L)? Is it ethical to do a placebo controlled trial? Could we use 400IU of vD (the current RDA) as the comparator? What about the timing of vD supplementation; should it be started in utero, childhood, adolescence or early adulthood? Can we simply supplement the population and look at disease trends?
- Should we be partnering with other disease groups; for example the type 1 diabetes community? If we use type 1 diabetes as a surrogate prevention trials will report out decades earlier than with MS.
- EBV; how good are the current EBV vaccines? Do we need new vaccines? Is it safe to prevent the population from acquiring EBV? EBV is one of our most co-evolved viruses, it is part of our metagenome. Preventing people getting EBV may have consequences. What role does EBV play at the population level? I suspect it may play a role in immunological memory and that stopping the general population from being infected with the virus will have consequences.
- Would simply preventing people getting infectious mononucleosis (IM) be sufficient to lower the risk of developing MS? Is the EBV-IM MS link simply an association and not causal? In other words the observation that people who develop IM are at increased risk of MS may simply indicate that these people have something wrong with their immune systems that also happens to predispose them to getting MS. I don’t buy into this latter argument, but it is out there, nevertheless.
- Should we developing a treatment for IM? Will treating IM successfully lower their risk of someone getting MS? What happens to the immune system post-IM that predisposed people to getting MS?
- Is there a link between vD and EBV?
- What about EBV itself? Is there a mutant EBV variant that causes MS and/or other autoimmune diseases?
As you can see there remain more questions than answers. What I do know is that we need to act now if we don’t want the next generation of MSers to look back at us and ask ‘why didn’t you do something about it?‘