FunkOdyssey
Senior Member
- Messages
- 144
Mainstream autism doctors are coming around to XMRV and contributing useful perspectives:
More Evidence TNF-alpha Allows Viral Persistence
This suggests that rather than some vague voodoo explanation that B12 is hijacked by toxins, the real culprit behind the decreased methionine synthase activity in our condition is elevated TNF-alpha.
Not to imply that B12/folate do not work to stimulate methionine synthase activity, because they clearly seem to, but this information suggests an alternate approach may exist: TNF-a inhibition. This can be done in a safe/moderate fashion (unlike anti-TNF antibody drugs) using pentoxifylline and various supplements.
More Evidence TNF-alpha Allows Viral Persistence
Dr. Jeff Bradstreet MD on 3/21/2011 said:This comment came on one of my think tank blogs from researcher and professor Dick Deth:
“Viruses such as XMRV are suppressed by methylation, and the enzyme methionine synthase is a master controller of methylation. We observed very powerful and rapid inhibition of methionine synthase (MS) transcription by TNF-alpha (>90% decrease of MS mRNA). An examination of the promoter region of methionine synthase revealed a consensus site for NF-kappa-B binding which overlaps the normally promotional AP-1 site. Thus we can hypothesize that TNF-alpha decreases methylation activity via NF-kappa-B. This decrease will augment viral persistence and replication. Notably, MS is very sensitive to oxidative stress, implying that oxidative stress, initiated by any number of provocations, would increase susceptibility to viral infection. Persistent viral infection could in turn prolong/delay recovery from oxidative stress, leading to a persistent oxidative stress and persistent v (a self-reinforcing relationship). In other words we normally recover from an oxidative stress-producing event, but the presence of a viral infection can turn this into a chronic condition…”
This is exactly what we are observing in numerous conditions including XMRV, Autism and ME/CFS. The good news is these conditions can be treated.
This suggests that rather than some vague voodoo explanation that B12 is hijacked by toxins, the real culprit behind the decreased methionine synthase activity in our condition is elevated TNF-alpha.
Not to imply that B12/folate do not work to stimulate methionine synthase activity, because they clearly seem to, but this information suggests an alternate approach may exist: TNF-a inhibition. This can be done in a safe/moderate fashion (unlike anti-TNF antibody drugs) using pentoxifylline and various supplements.