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PostPosted: Mon Aug 30, 2010 2:43 pm 
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Anyone have some guesses?

http://www.businessweek.com/lifestyle/c ... 42570.html


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PostPosted: Mon Aug 30, 2010 2:59 pm 
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Interesting study, scorp. This paragraph made the most sense to me--

Quote:
The other intriguing issue is that while new lesions are likely to appear in the spring and summer, that doesn't mean a causal agent is operating at that time. It could be something going on prior to those seasons that takes a longer time to manifest. In the fall and winter, there is less exposure to ultraviolet light, so there's less vitamin D. Also, in the fall and winter, there is greater exposure to viral infections. Or, maybe it's dietary. People may eat different things in different seasons," LaRocca said.


My hunch is that lower vit D, more exposure to colds and flus, eating fattier foods, and just general less movement/exercise during the winter months leads to more endothelial dysfunction -and this shows up as lesions in spring/summer. But who knows? Jeff was dx with MS in the spring of '07 w/lots of shiny new lesions. How about everyone else?
cheer

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS


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PostPosted: Tue Aug 31, 2010 12:45 am 
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I take Extra thingies to lower Gamma Interferon levels in the fall, winter and very early spring.

The Gamma Interferon connection is well known and well documented.

I have noticed that the effects (lesions and symptoms) do not occur immediately but seem to show up in my case in the Jan/Feb/March time frame.

jackD


Neurology. 2002 Apr 9;58(7):1077-80.

Seasonal variation in immune measurements and MRI markers of disease activity in MS.

Killestein J, Rep MH, Meilof JF, Adèr HJ, Uitdehaag BM, Barkhof F, van Lier RA, Polman CH.

Department of Neurology, VU Medical Center, Amsterdam, The Netherlands. J.Killstein@vumc.edu

Abstract
BACKGROUND: The exact mechanisms by which T cells contribute to MS progression are not known. Recently, the results of cross-sectional studies suggested seasonal variation of both interferon (IFN)-gamma production and the number of active MRI lesions in MS.

OBJECTIVE: To investigate whether seasonal fluctuations of IFN-gamma and active MRI lesions could be confirmed and whether any correlations could be detected.

METHODS: Data were analyzed from a group of 28 MS patients in whom detailed longitudinal monitoring of both immune function and MRI measurements had taken place.

RESULTS: Significant seasonal variation was observed in T-cell activation as measured by the ability of T cells to secrete the pro-inflammatory cytokines tumor necrosis factor-alpha and IFN-gamma. Maximum values were found in samples obtained during autumn. Even though clear fluctuations were observed, no significant seasonal variation could be detected in the number of active MRI lesions. Fluctuations of in vitro IFN-gamma secretion correlated weakly with changes in active MRI lesions.

CONCLUSIONS: The finding of seasonal variation of immune function in serially MRI-monitored MS patients suggests an environmental role in T-cell activation.

PMID: 11940696 [PubMed - indexed for MEDLINE]


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