methyl B12 spray

[ukxmrv]

Thanks Rich and Fred for talking here. The rest of us can stand in awe as your two greats minds work through these important theories that will benefit us all.

 

[Freddd]

Hi, justy.

I can give you my perspective on the protocols, but I know that freddd has different views. I'll try to represent his thinking here, too, since he hasn't been around for a while, and I don't know if he will post.

In my hypothesis for ME/CFS, which is called the GD-MCB or glutathione depletion--methylation cycle block hypothesis, the key issue is that the enzyme methionine synthase, which joins the methylation cycle and the folate metabolism, is partially blocked. This was originally discovered in autism, but has been proven by lab testing to be true in ME/CFS as well. So the treatments that had been helping in autism were found to work for ME/CFS, also.

There are several of these methylation-type treatments in use now by various practitioners as well as a large number of PWME's/PWC's and autism patients. The key aspect of all of them is that they combine high-dosage B12, given sublingually or by injection, with at least RDA-level dosages of folate, usually one or both of the active folates, 5-methyl tetrahydrofolate and folinic acd, but in one protocol (Dr. Alan Vinitsky's) very high dosages of sublingual folic acid are used instead. The various protocols also include some other supplements, but the combination of B12 and folate are the common denominator. Taking B12 by itself, without folate, has been somewhat helpful to some people with ME/CFS, but to really get benefit, it's necessary to combine it with folate. That has been the breakthrough based on the methylation cycle block, which was discovered first in autism.

freddd himself has reported to this forum that he has inherited an inborn error of metabolism (a genetic mutation) in the intracellular B12 processing enzymes. This type of mutation is reported to be rare. freddd's cells are apparently not able to utilize hydroxocobalamin to make the two active coenzyme forms of B12 that they need (methylcobalamin and adenosylcobalamin). However, freddd has found that if he supplements both sublingually in large dosages, and also takes 5-methyl tetrahydrofolate (Metafolin) and some additional cofactor supplements, he can overcome this genetic problem and correct his symptoms. He has reported that there are actually many other people who respond the same way he does to the various supplements.

I have favored starting with hydroxocobalamin as the B12 form, and moving to methylcobalamin if there is no response. In my experience, most PWME's/PWC's do respond to hydroxocobalamin. In theory, methylcobalamin can methylate mercury and make it easier for it to move into the brain, so if a high body burden of mercury is known or suspected, I suggest starting with a low dosage of methylcobalamin and working up if it is tolerated.

freddd, on the other hand, reports that hydroxocobalamin does not work for him, or for many other people, and that methylcobalamin and adenosylcobalamin are the ones to use.
It hasn't been clear to me whether the people freddd has mentioned actually have ME/CFS, since his earlier experience was with people who suffered from absolute B12 deficiency, which is not the same as ME/CFS. In ME/CFS, there is usually a functional deficiency of B12, rather than an absolute deficiency.

Another difference between what I have suggested and freddd's approach is in the response to increased symptoms on the treatment. I have recommended that the dosages be decreased until the symptoms are tolerable. freddd, on the other hand, has favored maintaining or even increasing the dosages, in order to "push through" the symptoms.
Various people have reported different experiences with this. Some have confirmed freddd's views, by eventually feeling better, though their symptoms increased quite a bit initially. Others have said that they could not tolerate freddd's approach, and some have decided to use the lower dosages, as I have suggested.

At this point, I don't think it's clear which approach is best, and it may differ for different people. Unfortunately, there have not been any controlled clinical studies comparing these different protocols, so all we have to go on is biochemical theory and anecdotal reports from a few people.

I hope this is helpful.

Best regards,

Rich

Hi Rich,


freddd himself has reported to this forum that he has inherited an inborn error of metabolism (a genetic mutation) in the intracellular B12 processing enzymes.

It's not absolute as cyanocbl and folic acid did prevent my MCV from going above 100. So it also made a just barely noticeable difference on my burning beef-red tongue. So the conversion is limited but not absolute or it would have been noticed as an infant and I probably would not have survived in 1948. Of course it left a couple of hundred other symptoms free to develop and worsen. So my keyhole is smaller than some and larger than others. It is still a keyhole.


It hasn't been clear to me whether the people freddd has mentioned actually have ME/CFS, since his earlier experience was with people who suffered from absolute B12 deficiency, which is not the same as ME/CFS. In ME/CFS, there is usually a functional deficiency of B12, rather than an absolute deficiency.

About half of the people have had a diagnosis of FMS or CFS or both. However, there is no difference between symptoms overall of those diagnosed with those or a dozen other diagnoses. Let's see, I had diagnoses of polyneuropathy, peripheral neuropathy, idiopathic neuropathy, FMS, CFS, chronic pain, depression, IBS, brisk reflexes, and myofacial pain syndrome (most worthless diagnosis I ever had), neurological degeneration for unknown cause and a bunch of others that didn't work out either. I and most people were NEVER diagnosed with any kind of b12 deficiency, absolute or functional. Such a distinction is pure bunkum when it comes down to it. A 20 year long functional deficiency in the mitochondria of the brain eventually damages the brain and appears to cause Parkinson's. Let's get real. If a person is having any of the 300 deficiency symptoms, most of them functional, but also causing damage beyond repair in the long run, does it matter that they never have any of the 5 or 10 signs of "absolute" deficiency? The sooner they catch it and repair it, whether you want to call it "absolute" or functional, the less damage will occur and the faster they will heal. Dithering around with hydroxycbl allows 200 or so of the 300 functional symptoms that cause damage to continue on their merry way eventually causing damage.

Maintenance of ill health because of a bogus definition? How quaint.

Another difference between what I have suggested and freddd's approach is in the response to increased symptoms on the treatment. I have recommended that the dosages be decreased until the symptoms are tolerable. freddd, on the other hand, has favored maintaining or even increasing the dosages, in order to "push through" the symptoms.

Since the startup responses give every appearance of being dose related with each doubling of dose increasing such response by about 50%, and the responses maintained at intensity until equilibrium is reached at which point they fall off rapidly in a very few days as opposed to going on apparently indefinitely at a dose that never reaches equilibrium or does so very slowly, and I have experienced both states, total discomfort is usually substantially less by increasing the dose until it makes no additional difference. Then equilibrium is reached very rapidly. As most of the startup responses appear to be an aritifact of the mitochondria and nervous system coming back to normal, and it appears to take an "over" response to cause the "thermostat to reset", it does not appear to reset until that "over" is maintained. For me, having been so ill for 17 years, I interpreted every change as leading to normalization and for me and those who continue through, we get well. Typically sufficient healing occurs in the first year to allow exercise and rehabilitation to proceed. That does not happen for the people who back off over and over. In fact in many cases the magnitude of the fluctuations appear to worsen considerably and fear and anxiety increase in anticipation. Methylb12 works directly on intensifying the neurological functioning and that gives the appearance of all sorts of intensified symptoms which revert to normal if given a chance. It's like there is 100 miles to walk but you are carried 5 miles further back each day so to make progress one has to walk more than 5 miles. How much more determines how quickly one makes it through and less than 5 miles per day never makes it through.

Even on the active protocol it takes years and rehabilitation exercise to get all the way recovered. That is far quicker than on hydroxycbl which leaves more symptoms in place than it affects.

Let's have a 3 day series of 5k road races or other aerobic equivalent with matched pairs with CFS/FMS to start I am confident that a team can be prepared in 2-3 years with the active b12 protocol. Do you think that is so with hydroxycbl? I say the same people 3 days in a row because that is a suitably impossible task for anybody with FMS/CFS and quite possible for those without physical injuries to achieve, working up to jogging 3 miles a day. Or we could make it very technological and do it on tilting treadmills or whatever. I used to jog 5 miles a day 5 days a week for 20 years until one day I woke up and couldn't walk to the bathroom. I had been skiing a couple of days before. I had trouble walking 500 feet once a week at the worst. It took me two years to work up to that 500 ft without the active b12s.

I'm sure we could find sponsors. It might be a good gimmick for raising money for research. We could have a team representing each protocol for as many protocol-sponsors that would like to enter.

 

[Freddd]

Hi Rich,

The path to "absolute b12 deficiency" diagnosis is littered with the damaged bodies of those merely having "functional b12 deficiencies". This is the outcome of 50+ years of research using cyanocbl and hydroxycbl and the lack of knowledge about how light affects mb12 and adenosylb12. A country such as the UK using hydroxycbl and a country such as the USA using cyanocbl each have different lists of symptoms that are characteristic of b12 deficiency. There is a feedback loop at work here. "B12 deficiency" is being defined by what symptoms the specific vitamer used affects. There are problems with the tests. Serum level can remain relatively constant as adb12 and mb12 leak from tissues into the bloodstream, sometimes attached to various transport proteins, TC1, TC2, TC3 (HTC1, HTC2, HTC3 with cobalamin attached) and sometimes not. Only a couple of mcg in serum in any way brings the serum up to "normal" levels and it can remain "normal" while almost all the b12 in the body leaches out. Further, inactive cobalamins are also counted. For me cyanocobalamin worked obviously on several signs/symptoms, MCV<100 and related blood details and beef-red burning tongue came off of maximum burn just a little. My nervous system, peripheral and central were deteriorating from functional deficiencies; schwann cells were no longer doing their job and I had distal dieback of nerves, demyelination of the spinal cord, sensory changes in entire body, mood and personality changes, sensory changes, multi sensory hallucinations. My epithelial tissues were breaking down all over my body (skin, digestive system, lungs, bladder, mouth), I had a number of indications of endothelial breakdown, terrrible headaches, muscles deteriorating and terribly sore and burning and tight, uncontrollable spasms helped by Dilantin along with neurological pain. My blood wasn't right, my immune system didn't work right, my mitochondria didn't work right in muscles or neurons. Not a system in my body worked correctly and all were progressively breaking down but I NEVER had any "absolute b12 deficiency". Most people who become sick for decades and have hundreds of symptoms and are disabled and even die from it never are diagnosed with or even have "absolute b12 deficiency".

That definition becomes a reason for "denial of service" or "controlling utilization" (group health plan jargon). You don't have "b12 deficiency", no doc I have ever heard and I've heard a lot, has ever mentioned the word "absolute" in that diagnosis. Most don't appear to know enough that there might even be that distinction. They think "pernicious anemia", not deteriorating everything. The stance of the AMA management is that "b12 deficiency is not cost effective to screen for" so just wait ... Again the official stance is that it afflicts at most 1-3% of population no matter what studies suggest that it may be 25% of population and 50% over age 60, depending upon what symptoms one includes in the definition which depends upon which forms of cobalamin are used and whether Metafolin is used or not.

A definition of deficiency that depends on which choices of 4 possibilities of cobalamin and which of 3 forms of Folate one uses doesn't change the reality that the people with the 200 or so symptoms outside of the official CYCBL/HYCBL /FOLIC-ACID based definitions and way outside the test based (uMMA. Hcy, serum cobalamin, bound cobalamin for "absolute deficiency") definitions are still sick and can't ever get well on the official but inactive vitamins. And of course does one use the 160pg/ml of The UK and USA or the 550pg/ml of Japan to define the relative level of "absolute" lowness.

And of course there us the newer conundrum, low CSF/CNS levels of whichever cobalamin. So for MS for which "b12 deficiency" must be ruled out yet has clearly demonstrable CSF/CNS cobalamin deficiency with elevated CSF HCY levels suggesting methylb12 is low and Parkinson's with low CSF/CNS cobalamin levels with increased CSF MMA suggesting specifically adenosylb12. Then of course there is CSF/CNS cobalamin deficiency(s) in CFS/FMS. So how does that reconcile with "ruling out b12 deficiency". How does that reconcile with "absolute" vs "functional" b12 deficiencies if the CSF level is measured and is an indicator of "absolute deficiency".


If a cell doesn't have the b12 or folate in it that it needs to function yet the serum has "normal" amounts the person is still deficient. The best test of all is a "trial". According to much research, the only real test of b12 deficiency is if the person responds to b12. Hycbl and Cycbl are not sacred cows. There is no innate rightness that response only to them should identify "real deficiency". The universe of all responsive symptoms and signs to all types of folates and cobalamins needs to be the defining set, not some small subset of those. It's a pity that the standards of practice define b12 deficiency and b12 therapy at the level yielding the worst possible results and yet doing something. Calling neuropathies "conversion disorder" and prescribing psychiatric medications is no favor to the patient and doesn't heal them.

Doctors call their patients names and/or kick them out of their practices after being forced to look at these conundrums. Only a few are willing to look and treat accordingly. I am most fortunate to find an internist willing to treat me for health results rather than make me stay sick with "normal" test results.

When test results are not predictive of effectiveness of the substance, such as a whole ranges of tests based on cycbl/hycbl/folic-acid that are not predictive of mb12/adb12/mfolate results, a different approach is needed. In the kingdom of the blind it can be dangerous to talk about "seeing".

If you read my post with symptoms counts by decade you can see how things changed. I can break it down by year of sudden changes and what changed each time. I am in the best health of my life, now at 62. To ignore that because of test results seems rather bizarre to me. To stay in ill health and/or die to protect theories based on much less active vitamers and their holy test results appears ridiculous to me. My doc is pleased that I have done so well, for the first time in my life.

 

[justy]

A very interesting and lively discussion.
Im more confused than ever and worried that just taking a vitamin could make me worse. My health has deteriorated since i stopped the MB12 spray, but the horrible anxiety and palpitations etc have also gone. I seem to be stuck in a quandry of indecision re which approach to take - lifting the methylation block or Fredds protocol. They also seem to have quite a lot of similarities.
Still confused.

 

[Freddd]

A very interesting and lively discussion.
Im more confused than ever and worried that just taking a vitamin could make me worse. My health has deteriorated since i stopped the MB12 spray, but the horrible anxiety and palpitations etc have also gone. I seem to be stuck in a quandry of indecision re which approach to take - lifting the methylation block or Fredds protocol. They also seem to have quite a lot of similarities.
Still confused.

Hi Justy,

My health has deteriorated since i stopped the MB12 spray

That appears to say it all. Symptoms start returning within 12 -72 hours since the last dose for most people with these kinds of deficiencies and keep worsening indefinitely. They become very noticable when one sees what and how fast mb12 affects things. Heart palpitations are a common characteristic of b12 deficiency which also requires cofactors. I have to take B-right twice a day not to have return of palpitations which I had during 50 years of deficiency.

Methylb12 rapidly starts healing in a much more widespread manner than hydroxycbl. This is easily demonstrated just by the causing of hypokalemia which is very common with methylb12 which is why I strongly suggest potassium and why it is rare with hydroxycbl, which does not start rapid widespread healing.

lifting the methylation block or Fredds protocol.


The active b12 protocol will lift the methylation block faster than the much more limited protocol and a whole lot more. It isn't an "or" situation. It's a "lift the block" AND heal massively. The methylb12 protocol will produce more and faster healing for more symptoms for more people than any hydroxcbl protocol. The startup effects are from that very starting of some 600 processes that were not working before. Methylation is one of those things. This is one of the cases where starting the adb12 a day or three before the mb12 might help. Also, the less time you wait to do the mb12 again, the less severe the startup effects. If you wait a full week before trying it that will cause more lost ground to make up for.

 

[justy]

Thanks for ther clarity, Fredd. I am also taking a special mineral mix which has 1000mcg B12 per dose and im taking 3 doses a day. It doesnt say what type of B12 it is. Is it ok to take this and the methyl and the adb12.?

Heart palpitations - mine went away when i STOPPED the mb12, not the other way around. I seem to have gotr rid of mine by cutting out wheat and sugar, but being on the MB12 made them come back very severely.
Thanks again for your time.

 

[alex1968]

Hi Justy,

I use B12 methyl liquid, I also have hydro injections, I get a lot more from the liquid than the injections, I can live without the injections but not the liquid. I buy my stuff from a place called metabolics in the uk the B12 I buy is this http://www.metabolics.com/store/natural+healthcare/product/meth0100t/ it comes in a blue bottle so that light does not affect it as much as in a clear bottle. Each drop from the bottle contains 1.3mg of B12 methyl which I do single drops under my tongue every 2-3 hours. I take the view that because it is water soluble a little fairly often is better than 1-2 large doses. You cant really over do it with B12, from the little I know too much will just mean you will pee out the excess.


good luck with it.

 

[Freddd]

Thanks for ther clarity, Fredd. I am also taking a special mineral mix which has 1000mcg B12 per dose and im taking 3 doses a day. It doesnt say what type of B12 it is. Is it ok to take this and the methyl and the adb12.?

Heart palpitations - mine went away when i STOPPED the mb12, not the other way around. I seem to have gotr rid of mine by cutting out wheat and sugar, but being on the MB12 made them come back very severely.
Thanks again for your time.

Hi Justy,

In my case, and quite possibly in yours, as regards the heart palpitations, they may be casued by an induced deficiency of one or more of the other b-vitamins or minerals since starting methylb12 puts a big strain on the nutritional resources. Mb12 is just one of the deficiencies associated with them. Heart palpitations are also a sign of hypokalemia, low potassium, which I have been warning about. This low potassium can be induced within days of starting mb12 and can be dangerous. This is the most probably dangerous reaction to starting mb12 and cofactors that most people are likely to have.

In the USA when "B12" alone is specified, often one can find out by looking on the ingredients list and finding cyanocobalamin. However, since cyanocobalamin is officially "B12" when it isn';t specified it is cyanocobalamin. Whether it can be a problem or not when taking active b12s I honestly don't know. There is some research that supports the idea that inactive cobalamins of multiple varieties can block active b12 from being utilized. However, in the situation where one is taking enough active b12 to be available by diffusion I wouldn't expect it to be a big problem. If you have/had significant startup and are maintaining healing I wouldn't think that it interferes much. If you are unable to get healing going it is a possibility that there is a problem. A week on then a week off and on and off through a couple of repetitions would probably be sufficient to show what is going on since unbound cobalamins are cleared so rapidly by the kidneys and cyanocbl is the preferred kidney clearance form according to some research. It is what the body produces after using other forms of cobalamin to detoxify cyanide.