Hi aprilk1859, this information on epo and PGE1 is correct, and I think PGE1 is a good thing. However, this is correct in the context of general biochemistry, not CFS, and I am unsure of the information regarding MS specifically. We often arachidonic acid deficient, and that will drive increased synthesis (Le Chatelier's principle). However against this we frequently have reduced delta 5 and delta 6 desaturase activity. This decreases arachidonic acid synthesis. One of the things that will happen on the methylation protocol is the inhibition on arachidonic acid synthesis will be decreased as glutathione levels rise (this includes lipoic acid, nebulized GSH, liposomal GSH and NAC therapies as well). So unless the inflammatory factors causing increased arachidonic acid usage improve as well, evening primrose oil will drive arachidonic acid metabolism. Ironically it is those in whom the glutathione levels are the worst (and these will typically be highly salicylate intolerant) who will respond best to evening primrose oil, but only for a while.
I asked a number of researchers back in about 2000 why PGE1 has not been tried directly, rather than epo. It is available as a drug because it has been used to treat circulation and gangrene issues. This would bypass any risk that the epo could be converted to rapidly metabolized arachidonic acid. To my knowledge this has never been tested.
Barry Sears found that increasing DGLA gives a temporary benefit re anti-inflammatory activity, but in the long run it fails. The enzymes responsible are under dynamic control, and strongly affected by many factors.
This is an area begging for more research but almost nobody trying to get grants to research this area has got the funding they need. To my knowledge this area of research in CFS goes back to around 1988!
I think the post arachidonic acid anti-inflammatory is PGI2, but its been so long since I researched this so I could be wrong. It is also a vasodilator and blood thinner.
Bye
Alex
PS This paper indicates that short chain omega 6s are preferentially directed at series two eicosanoids:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1222686/
I have not checked this enough to be sure of other sources, it looks like this area is either contraversial or that evening primrose oil is more likely to make series two prostaglandins.
This abstract is a one liner but it matches some of the things Barry Sears has said over the years:
http://www.ncbi.nlm.nih.gov/pubmed/6092876
Essemtially this an hypothesis that immunodeficiency syndromes can be caused by a failure in series one PG synthesis. It might be worth reading the full paper but I havent seen it yet.
In my own case I tried evening primrose oil for years, but it accelerated my crash cycle. This was in the mid 90s. It helped initially then made me much sicker over time. That is not to say it can't help, only that it is problematic.
However, in the next paper Sjogrens syndrome is improved by omega 6 fats, although they also used omega-3 fats. Note the short chain faits that were used - the longer the process to create arachidonic acid, the lower the amount that will be converted, especially since the enzymes are often compromized in CFS and ME (note that alcohol also inhibits these enzymes, its not just oxidative stress and low gluatathione levels).
http://www.iovs.org/content/46/12/4474.full
So it is possible that epo will help those people who have dry eyes and are salicylate intolerant, but the dosage would need to be tightly controllled.
This is just my opinion and analysis, I could be wrong.
