Have just been reading something that could be relevant to why this happens for you OM but it is by Amy Yasko so I wouldn't call it hard science.
The proposal is that arginine needs BH4 to support its conversion. In the Yasko lecture she says that the cycle goes - purines to GTP to H2NTP and at this point if there is not enough BH4 and the body is in an inflammatory state, rather than move into the urea cycle the H2NTP is converted to neopterin which elevates an ongoing inflammatory immune response.
I am presuming that this is speculation though because if it was that purines are associated with ongoing overactive immune system when BH4 is lacking, given all the work into overactive immune systems, you'd think that would have been discovered alongside the research into gout? I would hate to have to give up my sardines in oil (high purine) which are giving me Omega 3 and calcium!
However, just to confuse things further, a quick Google shows that it is recently discovered that fecal neopterin is a marker for active IBD! (but a marker is reactive not proactive so not necessarily relevant for this theory)
www.ncbi.nlm.nih.gov/pubmed/23269308However, I haven't yet found what Yasko based the opinion on that H2NTP converts to neopterin in the absence of BH4 - need that to support the theory
but low BH4 will certainly make NO toxic from what I have read, i.e. here
atvb.ahajournals.org/content/24/3/413.full.pdf[quote]Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a key signaling molecule in vascular homeostasis. Loss of NO bioavailability due to reduced synthesis and increased scavenging by reactive oxygen species is a cardinal feature of endothelial dysfunction in vascular disease states. The pteridine cofactor tetrahydrobiopterin (BH4) has emerged as a critical determinant of eNOS activity: when BH4 availability is limiting, eNOS no longer produces NO but instead generates superoxide. In vascular disease states, there is oxidative degradation of BH4 by reactive oxygen species. However, augmentation of BH4 concentrations in vascular disease by pharmacological supplementation, by enhancement of its rate of de novo biosynthesis or by measures to reduce its oxidation, has been shown in experimental studies to enhance NO bioavailability. Thus, BH4 represents a potential therapeutic target in the
regulation of eNOS function in vascular diseaseAbove reminds that loss/lack of vascular pattern in colon is common finding in UC.
Makes me wonder if it is worth trying to get hold of some BH4 to see what happens. I don't know though, could be playing with fire. The more I read about
these genetic polymorphisms I see how they seem to deal with each other in the body - thus, it is not so simple for those of us lacking in MTHR to just supplement methylfolate, as several of us have found, we get ill, because I suppose other genetic changes have already taken place to try and deal internally with the errors.
Now editing above to add this research I just found...
www.ncbi.nlm.nih.gov/pubmed/23912334 Thus, pharmacologic modulation of BH4 with currently available drugs may provide a mechanism for alleviating some forms of colitis and potentially minimizing the potential for colorectal cancer in patients with colitis. And editing to add again - just reading on forums that Royal Jelly is thought to be a pre-cursor of BH4 - the SCD of course uses lots of good quality, Royal Jelly containing honey.
Post Edited (London Lurker) : 3/25/2014 6:02:22 AM (GMT-6)