Revised Simplified Methylation Protocol (August 25, 2012 Revision)

Lotus97

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I take 3 of the 4 precursors you mention above and am considering adding the fourth, but I still take s-acetyl gluthatione because I feel they all do slightly different things. Especially ALA which is good for the brain and chelates mercury out.

Of the all the forms of gluthione I have tried, only IV push and s-acetyl gave me noticeable results. It will be interesting to see what others have to say.
Hmm, some people have problems raising Glutathione too high too quickly such as from an IV push and probably s-acetyl glutathione and liposomal glutathione. Some people can't tolerate glutathione supplementation at all and need to use indirect methods such as methylation. I'm not sure why, but it's been discussed in a lot of threads.

To answer my earlier question about why Rich doesn't have Glutathione in his methylation protocol, here is one of his posts about why methylation is the best way to raise Glutathione.
For a more permanent raising of glutathione, the only thing I have found is to lift the partial methylation cycle block, and the best way to do that is with a methylation protocol, which includes at a minimum a relatively high dosage of B12, by injection or sublingually, together with supplementing an active form of folate (methylfolate or folinic acid, with methylfolate being more effective).

If a person gets B12 alone, I think that they get the benefit of improving the function of the methylmalonate pathway, which feeds more fuel to the mitochondria, producing more ATP and hence more energy to drive the muscles. However, without adding the folate to it, the person does not lift the partial methylation cycle block and does not get the permanent improvement in glutathione level, which gives the longterm improvement in mito function and thus in ATP production and energy.

TMG feeds the alternative BHMT pathway for methylation in the liver and kidneys, and that can give temporary benefit, too, but it does not lift the partial block in methionine synthase, which is the main methylation pathway.
One question I have though is if there is any harm in taking Glutathione in addition to his methylation protocol. I seem to remember reading one of his posts saying that in the initial stages of methylation Glutathione levels actually drop.

Since this thread is about Rich's methylation protocol I don't want to take this off topic, but since I already mentioned these earler I should post a warning about some of the risks ALA and NAC present for those who are mercury toxic. Although these can be effective in boosting glutathione and removing mercury, Alpha Lipoic Acid (ALA), NAC, L-Cysteine, and possibly R-Lipioc Acid can all be double-edged swords in terms of mercury detox so if you suspect you might have a high mercury burden then these should be used with caution. In fact, if you have a high mercury burden then methylation should be approached very cautiously.

As far as Alpha Lipoic Acid goes it is used as a chelator for mercury, but if done incorrectly mercury will not be eliminated and instead be redistributed in the body including possibly the brain or other vital organs. Although I'm not an Andy Cutler follower many people swear by him and he warns against using ALA incorrectly. One thing I disagree with him on is that taking ALA can chelate mercury directly from amalgams. Whether or not this is true, I've taken high doses of Alpha Lipoic Acid (1200mg/day) without any problems. However, if I had done this a few years ago when I was having problems possibly caused by my amalgams it probably would have been dangerous. Besides Andy Cutler, there are plenty of threads on this site and other places such as Curezone that discuss mercury detoxification.

With NAC, L-Cystine, and L-Cysteine Rich cautions the use of it if one is mercury toxic because it could lead to elevated Cysteine levels and also mercury redistribution to the brain.
http://phoenixrising.me/treating-cf...atigue-syndrome-mecfs-by-rich-van-konynenburg
If there is a high level of mercury in the body, such as can occur if glutathione has been low for an extended period of time (months to years) and the person either has silver amalgam fillings in their teeth or they have consumed a significant amount of large, predatory fish, including tuna, then caution should be exercised by limiting the dosages of oral supplements that supply amino acids to the liver for making glutathione. There are two reasons for this:

The first is that mercury can be moved into the brain from other parts of the body by cysteine or N-acetylcysteine if the dosages are too high. Dr. David Quig of Doctors Data Laboratories recommends limiting the dosage of NAC to 300 mg per day and taking it with a high protein diet if heavy metals are elevated.

The second reason is that mercury can block the utilization of cysteine, and if cysteine rises too high, it can act as a neurotoxin. (This last is also the reason L-cysteine is not recommended as a supplement for building glutathione.) It’s a good idea to measure the blood plasma level of cysteine periodically when building glutathione, to make sure it is not rising too high.

If elevated mercury is suspected, it is a good idea to test for mercury and detox it carefully if it is present, with the help of a doctor experienced in doing this.
 
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Hi Jaz and welcome to Phoenix Rising. I'm not too familiar with Fredd's protocol, but I know there are quite a few differences between the two. Whatever you decide to do be aware that are potentially serious risks involved when embarking on any methylation protocol so make sure you start slow and educate yourself about what's involved.
Hi Lotus97 !
i have a question, i am wondering about methylation in general. Is it mostly people with CFS and issues like that who go on the Methylation protocols ? I am suspectinb B12 deficiency and my most bothersome symptom is my spreading numbness which has been going on for about a year but it has been speeding up since 2 months ago and i'm freaking out.
would it be smart to do these protocols even if i don't have CFS or any diagnosed conditions?

thank you
 

adreno

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Hi Lotus97 !
i have a question, i am wondering about methylation in general. Is it mostly people with CFS and issues like that who go on the Methylation protocols ? I am suspectinb B12 deficiency and my most bothersome symptom is my spreading numbness which has been going on for about a year but it has been speeding up since 2 months ago and i'm freaking out.
would it be smart to do these protocols even if i don't have CFS or any diagnosed conditions?

thank you
B12 and methylation in general is essential to nerve health, so I would say yes, this is probably a good idea. You can start with the B12 (perhaps 1mg sublingual) and see how you feel. Then you can add the other supplements later. The most important is definitely B12. If you are not sensitive I would choose methyl B12, as it is more effective in nerve healing compared to other forms. There is certainly no harm in titrating to the doses that Rich suggests, that is around 2mg B12 and 400mcg folate.
 

Lotus97

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B12 and methylation in general is essential to nerve health, so I would say yes, this is probably a good idea. You can start with the B12 (perhaps 1mg sublingual) and see how you feel. Then you can add the other supplements later. The most important is definitely B12. If you are not sensitive I would choose methyl B12, as it is more effective in nerve healing compared to other forms. There is certainly no harm in titrating to the doses that Rich suggests, that is around 2mg B12 and 400mcg folate.
Do you have any idea how much hydroxocobalamin and adenosylcobalamin/dibencozide convert to methyl B12? Rich has said that methylcobalamin could potentially cause problems for those with mercury issues. I wonder though if it's the methylation process in general that causes the issues and not specifically methylcobalamin, but I'll include the quote and let people decide for themselves.
http://forums.phoenixrising.me/index.php?threads/methylb12-how-much-is-too-much.8391/#post-159278
My concern about methylB12 is related only to its possible potential for methylating inorganic mercury that may be in the body, primarily from exposure to mercury vapor, as is released continuously from amalgam fillings in the teeth. Methyl mercury is readily able to cross the blood-brain barrier and enter the brain, where it apparently then reacts with enzymes containing selenium (and to a lesser extent, sulfur) and acts as a neurotoxin, with a residence time in the brain measured in years.

I do not have proof that this will actually occur in humans with the inventories of inorganic mercury that are actually present and the dosages of methyl B12 that are used in treating ME/CFS.

My concern comes from the fact that there are published papers indicating that methyl B12 is able to react and donate a methyl group to inorganic mercury, and in fact, it is one of the only substances in biological systems that is able to do this. The reason is that inorganic mercury exists as a doubly positive mercuric ion (Hg++). In order for a substance to donate a methyl group to it, the substance must be negatively charged. methyl B12 forms a carbanion, which is able to do this.

It is known that the way methylmercury enters fish is that bacteria in aquatic environments use methyl B12 and other similar substances to methylate mercury, and then are eaten and travel up the food chain to the larger fish. Apparently the bacteria methylate the mercury as a means of exporting it to their outer surfaces and so protecting themselves from its toxicity. It can have some toxic effects on fish (see first abstract below) and when people eat fish containing methylmercury, it can be toxic to them, especially if their bodies are low in selenium (see second abstract below). Methylmercury dumped as waste into the ocean in a fishing area was responsible for the Minimata disease disaster in Japan in the late 1950s, and methylmercury used to treat grain seed that was unfortunately later eaten by people caused a disaster in Iraq as well.

There have been experiments in guinea pigs in which it was found that methylation of mercury occurred in their bodies. It is not clear whether this methylation occurred within their own metabolism, or whether it was carried out by bacteria in their gut.

As far as I'm concerned, this is an issue that has not yet been resolved. I'm aware that people with certain polymorphisms will benefit more in terms of helping their methylation cycle by taking methyl B12 rather than hydroxo B12. I know that there are people who are taking dosages of methyl B12 of several milligrams per day, sublingually, and some are reporting benefits. I don't know what their body burdens of inorganic mercury might be. Unfortunately, there is no good way of evaluating it, short of doing autopsies, which isn't very helpful for people who want to keep living for a while!
 

adreno

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Do you have any idea how much hydroxocobalamin and adenosylcobalamin/dibencozide convert to methyl B12? Rich has said that methylcobalamin could potentially cause problems for those with mercury issues. I wonder though if it's the methylation process in general that causes the issues and not specifically methylcobalamin, but I'll include the quote and let people decide for themselves.
http://forums.phoenixrising.me/index.php?threads/methylb12-how-much-is-too-much.8391/#post-159278
I don't know how much is converted. It sounds like Jaz is not ill besides having B12 deficiency and neuropathy, so I wouldn't be too worried about that in his case. But, maybe if someone is worried about this, they might do a metal/mineral test beforehand. I have heard of many compounds being able to move mercury around: methyl B12, NAC, ALA etc. But, is it more than a theoretical concern? Do we know of people who have gotten into trouble over this? As always, we have to weigh the risks against the benefits. The risks of a known, severe B12 deficiency are pretty bad. And if you have neuropathy, your nerves really need the methyl B12.
 

Lotus97

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I don't know how much is converted. It sounds like Jaz is not ill besides having B12 deficiency and neuropathy, so I wouldn't be too worried about that in his case. But, maybe if someone is worried about this, they might do a metal/mineral test beforehand. I have heard of many compounds being able to move mercury around: methyl B12, NAC, ALA etc. But, is it more than a theoretical concern? Do we know of people who have gotten into trouble over this? As always, we have to weigh the risks against the benefits. The risks of a known, severe B12 deficiency are pretty bad. And if you have neuropathy, your nerves really need the methyl B12.
I was asking partially for myself, but there was another person in this thread who also asked the same question. After I had one of my amalgams removed I was taking a high dose of ALA and NAC and a low dose of methyl B12 and methylfolate. I had tolerated all of those fine for at least a year leading up to that (except the methylfolate), but after that they caused me a lot of problems. I'm not sure what to think about Andy Cutler's warnings about ALA. They seem a little extreme, but it can't hurt to be cautious. For methylcobalamin though it did sound like Rich was saying basically the same thing as you that it is mostly theoretical. I don't have a lot of knowledge in this area, but from what I've heard from other people's experiences is that methylation in general can mobilize metals. Here's what Rich says:
lifting the partial block in the methylation cycle more rapidly, which in turn would bring on the renewed function of the detox system more rapidly. Perhaps this would account for the more rapid mobilization of heavy metals that your physician found.
I have another question about methyl B12. Doctors have said my chronic pain is nerve pain. Would methyl B12 help that too? Gabapentin or Lyrica which are supposed to be for nerve pain didn't help at all, but I haven't responded to supplements that affect GABA receptors either although maybe I'm comparing apples and oranges. I don't really understand the mechanisms in which Gabapentin or Lyrica work.
 

adreno

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I have another question about methyl B12. Doctors have said my chronic pain is nerve pain. Would methyl B12 help that too? Gabapentin or Lyrica which are supposed to be for nerve pain didn't help at all, but I haven't responded to supplements that affect GABA receptors either although maybe I'm comparing apples and oranges. I don't really understand the mechanisms in which Gabapentin or Lyrica work.
Hm. Gabapentin and Lyrica block ion channels, leading to less excitation of the nerves. This should normally help with pain. I am not sure why this doesn't in your case.

Pain is normally mediated through NMDA receptors - glutamate. So high glutamate levels would cause pain. Again, the meds should help with hyperstimulation and release of glutamate. Inflammation can be another source of pain. Maybe you have high inflammation levels. Just my 2 cents.
 

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Lotus97

Personally, I've found that Methylcobalamin has worked best for nearly all my pain, be it nerve, joint, even psychic pain. It's just slow to work.

I did try Lyrica for a time... it helped a little, but there were the side effects. I tried to talk the doctor into giving me morphine. She said no. ( mean ol' nanny)

Now, I can present myself to her with no more need for pain meds., at least.

Potassium is good for other types of pain, muscular,etc. It's good for moods too.
 

Lotus97

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I found one of Rich's most recent posts (August 15, 2012) on Glutathione supplementation in relation Methylation. The post is dated 10 days before this thread was created so I assume it was Rich's final opinion on it.
I encouraged people to boost gltutathione directly from about 1999 through 2004. It gave temporary help to some, but was not a permanent way to raise glutathione. In late 2004 I read the work of S.Jill James et al. in autism. They found that glutathione was also low in autism, but that it could be raised by lifting the partial methylation cycle block that is upstream of glutathione synthesis in the sulfur metabolism. I encouraged people with ME/CFS to try this, since the biochemistry in autism and ME/CFS are quite similar. It turned out to work for most people who tried it. The simplified methylation protocol is designed to lift this partial block.

Since this treatment seems to lower glutathione initially, and this is likely responsible for the excitotoxicity that many people experience initially on this protocol, more recently I have suggested adding something to support glutathione initially, either liposomal glutathione or acetylglutathione. I've also suggested trying L-cystine (not to be confused with L-cysteine) to suppport glutathione in the brain. This should not be done if a high body burden of mercury is suspected, since it may move mercury into the brain. I haven't received much feedback on these approaches yet.

There are other things that people have taken to lower excitotoxicity. They have included GABA, theanine, magnesium, taurine, progesterone cream, valerian, grape seed extract, and pycnogenol. Some people report that one or another of these has helped them.
 

Lotus97

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Since there was only a short mention of potassium supplementation in this thread I thought I'd post one of Rich's more in-depth posts about potassium. There are plenty of threads about potassium which can provide more info on how to go about supplementing potassium.

Potassium deficiency is an important issue to watch for and to correct when a person is doing one of the methylation protocols for ME/CFS.

Freddd is the one who first brought this to our attention, I think because it showed up so strongly with his protocol, which includes relatively high dosages of B12 and folate, compared to what is suggested in the simplified methylation protocol.

It made sense to me from the standpoint of the biochemistry of ME/CFS when he first mentioned it, though I hadn't thought of it before. Here's why:

In 2001, Burnet et al in Australia reported measuring the whole-body potassium content of people with CFS compared to healthy normals. This is possible by using a whole-body gamma ray counter, because all potassium, including that in our bodies, contains a small amount of the natural radioactive isotope, potassium-40, which emits an energetic gamma ray. (This potassium isotope has a very long half-life, and is thought to have been present since the formation of the earth, several billion years ago. It has been decaying ever since, but there is still enough to measure because of its long half-life.) Since the current concentration of potassium-40 in potassium is known, it is possible to calculate the total potassium in the body using this measurement.

Burnet et al. found that the CFS patients who had predominately fatigue but not muscle pain were low in whole-body potassium by more than 10% compared to normal. They also measured the plasma level in the blood serum, and that was found to be normal.

It is known that at least 95% of the potassium in the human body is inside cells. Potassium is the most abundant positive ion inside all cells. So the measurements of Burnet et al. mean that the CFS patients they studied were significantly low in intracellular potassium.

The observation of low intracellular potassium in the presence of normal serum potassium means that there is a problem with the membrane ion pumps that normally pump potassium in (and sodium out) of the cells. These pumps require ATP for their energy supply, and that implies that the mitochondria are not able to supply enough ATP.

We have other evidence now for mitochondrial dysfunction in ME/CFS, so this fits together very well. In the GD-MCB hypothesis, the mito dysfunction is a result of glutathione depletion and a partial methylation cycle block.

O.K., this part was important to explain, because it means that there is no "cushion" in terms of potassium supply in these PWCs.

Now, another thing to note is that it is likely that PWCs have a smaller total number of cells than normal. The reason is that measurements have shown a higher rate of die-off of cells (early apoptosis) in CFS, and also an abnormal arrest in the S phase and the G2/M boundary of the cell cycle (Vojdani et al., 1997). What this means is that the cells are dying off early, and are not being replaced as fast as normal.

According to the GD-MCB hypothesis, the early apoptosis occurs because of damage to the cells by oxidative stress resulting from glutathione depletion.
The arrest of the cell cycle occurs at the stages where the DNA is supposed to be replicated and the cell is supposed to divide, to form two cells. Something is hindering the DNA replication. What is it?

According to the GD-MCB hypothesis, this is caused by the inability of the cells to produce new DNA at a normal rate, which in turn is caused by depletion of the folates in the cells. This in turn is caused by the partial block of the methionine synthase reaction, coupled with the methyl trap mechanism and the catabolism of methylfolate by peroxynitrite, which is elevated because of glutathione depletion.

O.K., so now we have a situation in which the PWC has fewer total cells than normal, and the cells that the PWC does have are lower in potassium than normal.

Now, enter a methylation protocol, which incorporates at least B12 and methylfolate. The effect of this will be to increase the rate of the methionine synthase reaction. One of the effects of this will be to convert methylfolate into tetrahydrofolate more rapidly, and the latter is then converted to other forms of folate, including those needed to make purines and thymidine, which are necessary for making new DNA.

All of a sudden, the cells now have enough DNA to overcome the arrest of the cell cycle, and their rate of cell division goes up, making new cells more rapidly.

These new cells require potassium, and their membrane pumps start pumping it in from the blood plasma. Unfortunately, since the existing cells, which contain 95% of the body's potassium inventory, are already low in potassium, there is no cushion or buffer for the blood plasma potassium level, and if it is not augmented by increased potassium intake from the diet or supplements, the PWC's blood plasma potassium level drops, resulting in hypokalemia. This is hazardous, because it can have detrimental effects on the heartbeat and on other vital processes in the body, such as the use of muscles for breathing.

So that, in my opinion, is why it is important to watch the potassium level when on methylation treatment.

I think this is especially important if large dosages (several milligrams per day) of methylfolate and sublingual or injected methyl B12 are used, because this takes control of the rate of the methionine synthase reaction away from the cells and overdrives the methylation cycle. One result of this is that the folate levels rise rapidly, and cell division also rises rapidly. Under these circumstances, the normal supply of potassium from the diet may not be sufficient to supply the extra potassium that is needed. This is one reason why I do not favor taking high dosages of methylfolate and methyl B12 together by a person who has ME/CFS, but if a person chooses to do this, it is important that they monitor their blood potassium level and augment it as needed.

Note that over-the-counter potassium supplements are limited to 99 mg per pill. The reason for this is that if too much potassium is concentrated in one place in the digestive system, it can damage the wall of the digestive system.
It is preferable to take the potassium in the form of high-potassium foods or juices, or solutions of potassium salts, as tolerated.

Best regards,

Rich
 

ahmo

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Unless you have a food sensitivity to lecithin, there's no reason not to take lecithin since it's pretty cheap (unless you get the liquid phospholipids). As Rich said, they even have a sunflower based lecithin for those sensitive to soy. I just wanted to make it clear I wasn't telling people not to take lecithin.
My self-testing strongly rejects it. It's Nutricology's Lipo-Phos Forte. I took the advice from heartfixer, but as soon as I ordered it, had misgivings. No GMO statement, so presumably made of GMO soy. thanks.
 

Lotus97

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In addition to phospholipids, there are other supplements for mitochodrial support. They include coenzyme q10/ubiquinol, carnitine, alpha lipoic acid/R-lipoic, PQQ, and Shilajit/Fulvic Acid. Caution should used with lipoic acid if one suspects mercury toxicity because it can mobilize the mercury. Also Shilajit/Fulvic Acid has been used for metal toxicity, but if used improperly it can also cause problems for those with metal toxicity. It's recommend to use Shilajit/Fulvic Acid with non-chlorinated water because the chlorine can interact with it. Also, all of these supplements can be overstimulating so it's recommended to start at a low dose (maybe even half a capsule for some of them) and only add one thing at a time. These should probably be added only after a person has been doing methylation for a period of time since methylation can also be overstimulating and it's important to gauge how well the methylation supplements are working before adding anything new. Improving mitochondrial function can increase ATP and Glutathione production. Of course, methylation itself also increases ATP and Glutathione among other things. Although I'm not suggesting to buy from iHerb, a search using "mitochondria" or "mitochondrial" can provide some other supplements used for mitochondria support and also provide information from customer reviews to find out how well they work and also potential side effects.
 

Lotus97

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My self-testing strongly rejects it. It's Nutricology's Lipo-Phos Forte. I took the advice from heartfixer, but as soon as I ordered it, had misgivings. No GMO statement, so presumably made of GMO soy. thanks.
I just checked the ingredients of that Fish Oil Phospholipids product and it does have sunflower lecithin. Somehow I thought it was natural phospholipids like Krill Oil. I deleted my posts to avoid any confusion.
 

Lotus97

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After some failed attempts at methylation I decided to start again. I'm taking 100 mcg folinic acid, 100 mcg methylfolate, 1000 mcg hydroxocobalamin, 250 mcg adenosylcobalamin, and various cofactors. I'm also taking around 500 mg of Niacin to prevent me from overmethylating. I was wondering if anyone knows how long I should wait before I increase the dosage. Thanks.
 

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Hi Lotus,

Why the adenoB12? I understand the combination with mB12 but not with hB12, would you be so kind to explain?

How long to wait. Three or seven days, according to Ben Jenkins of mthfr.net. In his latest videos he's advising seven days, as far as I know.
But negative effects of methylfolate may even turn up after a week, he said. (When starting some have an incredible first week, "happy, interacting and alert. Then the second week comes and they switch to wanting to hide in a room by themselves or literally throw dishes across the room out of anger. Or they may become bed ridden from muscle aches, intense headaches or joint pain".)

If you want to be safe: take at least seven days before increasing.
 

Lotus97

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Hi Lotus,

Why the adenoB12? I understand the combination with mB12 but not with hB12, would you be so kind to explain?

How long to wait. Three or seven days, according to Ben Jenkins of mthfr.net. In his latest videos he's advising seven days, as far as I know.
But negative effects of methylfolate may even turn up after a week, he said. (When starting some have an incredible first week, "happy, interacting and alert. Then the second week comes and they switch to wanting to hide in a room by themselves or literally throw dishes across the room out of anger. Or they may become bed ridden from muscle aches, intense headaches or joint pain".)

If you want to be safe: take at least seven days before increasing.
I'm taking the adb12 because it's in a sublingual b complex by Source Naturals I bought. I'm only taking 1/4 of a tablet twice a day so I'm not sure I'm really getting enough of the other b vitamins even though some of the other ones are in coenzymated forms too. I've considered scrapping that idea and just taking hb12.

My last methylation attempt I was taking both adb12 and hb12. It was going ok, but then upped the dose of each. I'm not exactly sure what the dosage was after I increased it, but maybe around 2000 mcg hb12 and 500-1000 mcg adb12. There might have been some days where I took more hb12 and less adb12, but I'm pretty sure I never went above 2000 of the hb12. I think I might have decreased the adb12 once I increased the hb12, but I don't remember. I wasn't taking any folate except that I was getting around 300 mcg from my food. Then I decided to add folinic acid first before methylfolate, but I misread Rich's instructions and was taking 800 mcg instead of 200 mcg. I did that for about 5 days and then stopped. Then I gradually stopped the B12 too. The overstimulation eventually died down, but didn't go away completely. I think this is because my adrenals are really screwed up now. Then I got really depressed so I decided to start methylation again because I was thinking it would help. Actually, when I got up this morning I took folate, B12, and a little glutathione and I felt really good after that. I am aware that the effects of methylation stack up as the days go on which is why I'm being cautious about increasing the dose.

I thought the methylfolate was the main thing to cause problems which is why I was waiting to add it. My first attempt at methylation I was only taking methylfolate. I wasn't taking any B12 unless you count 200 mcg methylcobalamin taken orally. My first "attempt" actually wasn't really and attempt. I had never heard of methylation before. The reason I was taking those was because I was taking Jarrow's B Right b complex. I took it for over a year and then they added methylfolate to the formula. By sheer coincidence I started taking the B Right with methylfolate a few days after my tooth with an amalgam cracked. I don't know if that's why I reacted so strongly to the methylfolate or if I'm just sensitive or both. It took a month or two of extreme overstimulation and heart palpitations and only after discovering Phoenix Rising and reading about methylation did I figure out what was going on. I remember reading one of Rich's posts saying that for some people a toothpick of methylfolate is enough to blow them away. After I stopped methylfolate I got really tired, but my mood was good. I eventually started methylation again after a few weeks because I assumed I needed to do it based on my reaction to methylfolate. I tried methylcobalamin first and I got overstimulated right away. I then read a quote by Rich saying that methylcobalamin could methylate inorganic mercury so I stopped. Otherwise I might have tried taking 1/4 tablet or something.
 

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Lotus97;
I agree that too many methyl groups can cause overstimulation, even inflammation in certain people.( They do have a degree of toxicity, in excess.)
I've been having to reduce the amount of methyl donors I've been consuming, even MB12.
Many people are sensitive to methyl donors, ( genetic polymorphisms), and respond better to Hydroxocobalamin.
 

Lotus97

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Lotus97;
I agree that too many methyl groups can cause overstimulation, even inflammation in certain people.( They do have a degree of toxicity, in excess.)
I've been having to reduce the amount of methyl donors I've been consuming, even MB12.
Many people are sensitive to methyl donors, ( genetic polymorphisms), and respond better to Hydroxocobalamin.
I think part of my problem is that I'm taking a lot of supplements related to methylation, but I'm taking them for reasons other than methylation. I think I need the other supplements as much as the B12 and folate so I guess I'll just be careful with those.
 

Lotus97

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As I mentioned earlier, I'm getting at least 300 mcg of reduced folate from my food in addition to the supplemental folinic acid and methylfolate I'm taking. Someone told me that only meat has methylfolate so I thought I was only getting an extra 30-50 mcg of methylfolate and the rest was folinic acid. According to Rich, it turns out that methylfolate is in some of the other foods I'm eating. Perhaps meat has only methylfolate while other foods have a combination of folinic acid and methylfolate.
The main folates found in vegetables are 5L-methyl tetrahydrofolate and folinic acid, both of which are readily used in the bodies of most people.