Mark:Here is the trial data again. As you can see he used conventional meds along with oral ala.
He also used a mast cell stabilizer and butytate in the enemas.
If I remember correctly butyrate enemas by themselves don't work all that well.
Regardless of what he used in the enemas, I don't believe you can find a human trial with close
to 100% remission,ever.
As you can see if I keep all this info in one thread I can find it again.
It was not a placebo controlled trial,so the medical community will say gee that's great, it needs more work.
here is the patent aging,while rereading it seems that glutathione peroxidase more important that catalase.
Patent goes into somewhat more detail on certain aspects.
Guess will have to reread my references on GPx again, so I know for sure what is going on,hopefully.
Not finding much that I have referenced for GPx perhaps it is buried in papers.
Here is the patent give more detail on the human trial.
A degradation profile for H2O2 has been established in human Jurkat T cells. This study determined that glutathione peroxidase activity is responsible for 91% of H2O2 consumption while catalase only contributes a minor role at 9% (Boveris and Cadenas, 2000
On a populational level, ethnic variation of glutathione peroxidase has been recorded with individuals of Jewish or Mediterranean origin exhibiting lower activities (The Metabolic and Molecular Basis of Inherited Disease, 2001, 8th ed., p. 4650). A two to four fold increase in incidence and prevalence of ulcerative colitis has also been reported for these ethnic groups (Roth et al., 1989).
Dam going to have to lay off of the VO.
Alcohol inhibits glutathione peroxidase; a crucial enzyme that neutralizes H2O2, and depletes mitochondrial glutathione (Hoek et al., 2002). Glutathione is not synthesized within mitochondria and must be transported from the cytoplasm into the mitochondria through the mitochondrial membranes. Alcohol interferes with the active transport of glutathione into the mitochondria (Maher, 1997). This leads to mitochondrial depletion of glutathione and H2O2 accumulation. Depleted glutathione and increased H2O2 levels enhance the risk of entering the induction phase of ulcerative colitis. Thus, the methods of the invention contemplate modification of patient intake of alcohol and alcoholic beverages
As far as taking vitamins/supplements in concert, I normally would agree, but I am somewhat wary of B6.
So taking B complex would also have B6.
Been trying to figure out B6 for a long time whether it is a problem or not.
Here is something indicating the need for it.
My old B6 thread.
I have taken B complex in the past, also multi vitamins and minerals, actually believe they make me somewhat
Tunnel: I am not against conventional meds,even though my son lost his colon,which soured me on all the meds
at the time.
I don't go to GI docs so I can get no meds.
If I can go into remission with a sample size N=1, there is hope for everyone.
Well here is one I think I have posted before much made in the kidney.
glutathione peroxidase GPx /eGpx
jumping around a bit here while searching one of my old threads
it seems that the bacteria in colon ulcers can make more hydrogen peroxide than immune cells or at least quite a bit. This also would tie in with the rate of cell death higher than the regeneration rate.
So another reason for FMT and why it might work
Post Edited (Old Mike) : 5/12/2015 8:51:41 AM (GMT-6)