Even after starting a thread about it and reading some information elsewhere I still don't understand the Methyl Trap/Folate Trap very well. I'm not even sure how much is theoretical, but if you're increasing folate wouldn't you also need to increase B12? Or do you have an alternate theory?
Hi Lotus,
Let's look at how the MeCbl is actually used. Somewhere, there is a methylation diagram already posted here that assumes starting with MeCbl and there are ones out on the web. Choosing the right diagram of circles and arrows makes all the difference. Now in the diagrams showing starting with HyCbl, they show a "side diagram", involving l-methylfolate, SAM-e, etc that in the process of passing a methyl group around forms MeCbl where it is needed for the transaction. Generally it is said that MeCbl forms SAM-e and that SAM-e is the "universal methylator". Now looking at where there is MeCbl in the first place there is no need to borrow a methylgroup to pass around. These methylgroups come from all sorts of sources of origin. So MeCbl appears to act as a catalyst and emerges unchanged from the homocysteine and DNA transactions. Same thing happens in the mitochondria, the AdoCbl isn't used up but it acts as a catalyst. The b12s are used up by being oxidized by all sorts of toxins.
So the MeCbl acts as a catalyst, and as long there is sufficient other methylgroups available it is excreted unchanged. It is a weak methyl source, only 1.4% by mass. In theory if everybody has enough and a fully functioning body a person only needs to replace the daily losses of perhaps 5-10mcg via normal oxidation by toxins. Cyanide can destroy many grams of MeCbl, HyCbl and AdoCbl. It doesn't appear to get used up in the normal process of things. However, AdoCbl doing inflammation control appears to be used up in that mode, oxidized.
If you look at the amount of actual methyl groups TMG and choline are heavy duty sources. People take 500 or 1000mg of TMG which has a couple of methyl groups available in a smaller molecule. These other sources supply thousands to millions of times as much actual methyl (CH4) as MeCbl.
So having 100mcg B12 in diffusion distribution in the blood is sufficient for all normal healing needs because it isn't used up in that mode. Sometimes HyCbl can slip into that recycling process. B12 level is much more a matter of tissue penetration before the kidneys knock it down too much. This is especially apparent in the CNS for trying to trigger physical damage SACD type healing. A study using doses of 120mcg and 1500mcg found that people healed with both but healed more extensively and faster with more 1500mcg which was large enough to get 100mcg into serum while the 120mcg oral dose could not cause that diffusion healing. Other studies have shown that oral doses of 125mcg are barely enough to saturate the active distribution system. It isn't a more or less linear response. It is more like discontinuities, sudden thresholds and steep knees in the graphs.
I still don't understand the Methyl Trap/Folate Trap very well. I'm not even sure how much is theoretical
The methyltrap "hypothesis" was proposed in the 1960s. At the time MeCbl and AdoCbl, if available at all were $1000/10mg-vial by 1970 or thereabouts. It was more valuable per mcg than anything else on Earth at the time. Very expensive and not something you can run a lot of studies with because of costs.
Basically things point at it over and over and over. The real work is now going on to understand that. With l-methylfolate and MeCbl etc easily available to study without breaking the bank, now they are trying. Up until my glutathione (precursor) disaster there was no quick and easy way to experimentally produce methyltrap. Some chemotherapy drugs do and perhaps that is one reason they can make people so sick with all those familiar things like brainfog, mood changes, skin changes, nausea, IBS, etc. I have a friend who had a drug ointment treatment of her skin for pre-cancerous skin changes. Within a few days she had what looked like full blown methyltrap. It took 3 or 4 days of 8000mcg a day of Metafolin and 6000mcg of MeCbl sublingual to back that off to at least not a total emotional wreck. The doctor was surprised she absorbed so much topically as to give her the chemotherapy side effects including chemo brain (brainfog). On the second round she was already taking the Metafolin and MeCbl and had no problems at all. It was an astonishing difference to see, no mood or cognitive changes at all.
There are lots of studies that approach methyltrap from the microscopic level. There are none that I know of approach from a "what are the symptoms?" and "what reverses it ?". Rich very carefully explained it if you can find his original post in a reply to me. He also was aware of the sudden onset of the more severe symptoms that about half or more of us have done and made very clear that something different was happening from the "partial methylation block" and used them to make a distinction. I talked about if for years as "falling over an edge" pushed by just about any stressor after being in a "depleted methylator" state. It is only now with having a model of induced methyltrap can it be shown just how suddenly and extreme onset is and how quickly it can be broken out of, can we point at it and say "THIS IS METHYLTRAP". It's like that Vince Lombardi moment of "Gentlemen, This is a football". Anybody reading these materials can now make a better stab at recognizing methyltrap than anybody who hasn't.
In reading studies, reading between the lines is often far more important than the conclusions they are willing to pin their reputations on. In B12 and folate research, people dropping out for side effects or even what side effects they have can tell a whole lot if startup is understood.
Understanding the paradoxical folate-b12 symptoms swapping that can happen in all sorts of paradoxical ways in methyltrap helps illuminate it.
I think that at last we have a pragmatic handle on it. One of the things that is abundantly clear is that there is no linear proportionate relationship between the amount of MeCbl needed for healing as compared to L-methylfolate. Anything based on the assumption that there is such a linear relationship doesn't work in the expected manner. MeCbl doesn't drive healing, it makes it possible. AdoCbl doesn't drive energy production, it just has to be in place for it to occur.
This is where the pragmatic descriptions of the various forms of paradoxical folate deficiency/insufficiency, methyltrap, and crossover points and partial ATP block all come together in pragmatic terms, symptoms (as best I can so far), how to trigger it and how to exit it all come together.
You and I and all the rest here are sitting at the bleeding edge of knowledge. The system bled me dry for 50 years without ever understanding or fixing the problem. Its taken 5 years with Rich's help to reach these understandings after 30+ years of preparation. I came HERE because Rich was here and ready to discuss and had ideas that fit in near perfectly with what I had already realized
I find that the methyltrap is easily demonstrated and reversed. However, onset can be brutal and getting out of it is can be rough going.
