Aaron E. Miller, MD


October 18, 2013

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Hello. I am Dr. Aaron Miller, Professor of Neurology at the Icahn School of Medicine at Mount Sinai in New York City. I am also Medical Director of the Corinne Goldsmith Dickinson Center for Multiple Sclerosis at Mount Sinai. I am here in Copenhagen and attending the 2013 European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) congress.

I would like to talk about some issues related to risk factors and epidemiologic associations with multiple sclerosis (MS). In the past few years, we have identified what I sometimes refer to as a troika of risk factors -- vitamin D, smoking, and infection with Epstein-Barr virus -- and this meeting has seen its share of additional information on those 3 agents. Alberto Ascherio[1] from Boston reported an analysis from the BENEFIT trial, a trial of interferon beta-1b in patients with clinically isolated syndrome. His group looked at vitamin D levels very early in the course of that study and tried to identify whether they could predict the conversion of clinically isolated syndrome to definite MS. They found that higher levels of vitamin D were associated with a lower risk for conversion to clinically isolated syndrome, and with less MRI activity, fewer lesions, lower lesion load, less brain atrophy, and less clinical progression. This is further evidence that vitamin D may play a role.

Another study[2] looked at the impact of vitamin D levels in patients taking fingolimod. There was a strong trend in that study to suggest that patients who had higher levels of vitamin D had a better response to fingolimod or had lower annualized relapse rates. The evidence continues to mount that vitamin D is related to MS and MS disease activity, although we still don't have an adequate clinical trial to tell us that supplementing patients with vitamin D makes a difference to the course of MS.

Smoking has been a consistently identified risk factor for MS, although with a somewhat lower odds ratio than we saw with vitamin D associations. A more detailed analysis was presented in a paper by Hedstrom and colleagues[3] in which the age at onset of smoking didn't matter. No matter what age you started smoking, your odds ratio for developing MS was higher. The cumulative dose of cigarettes smoked mattered, and this was strikingly true in men, in whom the odds ratio was 3 compared with 1.5 in women. Stopping smoking was beneficial, although it took about 10 years for the odds ratio to return to normal.

A review of the Epstein-Barr story by June Lunemann[4] reaffirmed the fact that clinical infectious mononucleosis is a risk factor for the development of MS, as is a high titer of antibody to the Epstein-Barr nuclear antigen. Some new information related to the epidemiology of MS was presented in a paper from Farez and colleagues[5] that looked at sodium intake. When patients are divided into 3 groups according to sodium intake -- low sodium (< 2 g/day), average sodium (2-4.8 g/day), and high sodium (> 4.8 g/day) -- the lesion load is increased in the high-sodium patients, but even the average-sodium group did worse than the low-sodium group. However, there was no correlation between the serum sodium level and the activity in MS. This adds to other information about metabolic status. At this meeting it was reiterated that a higher body mass index (essentially obesity) is also a risk factor for MS. Dr. Riley Bove,[6] also from the Harvard group, showed evidence that higher levels of adipokines, including leptin, were associated with a greater risk for MS.

We are beginning to mount a profile of epidemiologic factors that are associated with greater risk for the development of MS and, in some cases, greater risk for increased disease activity. It is important to emphasize, however, that all of these are associations. None of them have been demonstrated to be causative in MS, nor do we have data that correcting these conditions is clearly beneficial. Stay tuned for further information to come on all of these factors.


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