guinea pig

[wumberlog]

I've come to accept that whether I (or my employer) like it or not, marijuana keeps my MS symptoms manageable
Since I started as a recreational user in college, I was hesitant to trust myself for a long time. But now it's too obvious

After two days of abstaining, my spasms kick in like clockwork. That's been the pattern for about a year.
This sucks. I'm pretty much asymptomatic except for double vision when I use a one-hitter a few times a day. My lungs would probably really appreciate Sativex

I just needed to scream/whine to the universe.

[soul]

Hey Womberlog
I am in full agreement if you follow the Science thats being done in this area
The science agree's with you and I as well as many others
I have been going through hell due to the lack of ..MMJ I am just about ready to except what my Doc has offered me Morphine and become a socially acceptable junkie
soul
Letter abstract

Nature Medicine 13, 492 - 497 (2007)
Published online: 1 April 2007 | doi:10.1038/nm1561

Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB1 on neurons and CB2 on autoreactive T cells

Katarzyna Maresz1,11, Gareth Pryce2,10,11, Eugene D Ponomarev1, Giovanni Marsicano3, J Ludovic Croxford2,4, Leah P Shriver1,5, Catherine Ledent6, Xiaodong Cheng1, Erica J Carrier7, Monica K Mann1,5, Gavin Giovannoni2,10, Roger G Pertwee8, Takashi Yamamura4, Nancy E Buckley9, Cecilia J Hillard7, Beat Lutz3, David Baker2,10,11 & Bonnie N Dittel1,5,11
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The cannabinoid system is immunomodulatory and has been targeted as a treatment for the central nervous system (CNS) autoimmune disease multiple sclerosis. Using an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), we investigated the role of the CB1 and CB2 cannabinoid receptors in regulating CNS autoimmunity. We found that CB1 receptor expression by neurons, but not T cells, was required for cannabinoid-mediated EAE suppression. In contrast, CB2 receptor expression by encephalitogenic T cells was critical for controlling inflammation associated with EAE. CB2-deficient T cells in the CNS during EAE exhibited reduced levels of apoptosis, a higher rate of proliferation and increased production of inflammatory cytokines, resulting in severe clinical disease. Together, our results demonstrate that the cannabinoid system within the CNS plays a critical role in regulating autoimmune inflammation, with the CNS directly suppressing T-cell effector function via the CB2 receptor.