Elevated b12 blood test

Thank you for your response. Just to clarify, I don’t eat any meat or anything made with chiken or beef base in soups, gravies or whatever. As I get older I become less “militant” with myself about it. I imagine my supplements may have some sort of animal content. The b12 in my multiple is methylcobalamin but I don’t think it matters according to your response. But if the b12 is inactive, why is it checked? Or is it just inactive for people with MHTFR.

I will order the Homocystenex as you suggested. You mentioned I should do a 30 minute consultation for my son. My Dr. is doing other blood work and when all that comes in I will call. I want to have as much info as possible when we talk. In the meantime can you recommend which supplement should replace the Deplin? Is Deplin a natural form of Folate?

Thanks again

Dr. Ben,

I just learned about you from a friend and am grateful for your work and information!

You said: If your son has other mutations in the CBS, MAO A or COMT genes, Deplin can really backfire.

I am COMT homozygous X2 (yasko’s testin), MOA A homozygous and CBS heterzygous (A360A). Hetero for both MTHFr mutations.

I recently experimented with higher (than 400-800 mcg) doses of metafolin up to 2800mcg and felt like my head was going to explode, anxiety and irritbility were unreal. Felt like I was going to pass out (very unstable) and no other way to pu it, like my brain might explode. It took several days at this dose for this to happen.

Can you explain your statement above and also about glutamates … I can’t remember exactly what I read in your “files” here but some comment about glutamates and use of metafolin? When tested in past both ammonia and glutamates were high. Pre methylation protocol (yasko).

I also have high serum b12 as well as high serum folate.

Are you aware of the Methylation Panel from Health Diagnostics which measures red blood cell l-5 methyltetrahydrofolate?

http://planetthrive.com/2009/06/glutathione-depletion%E2%80%94methylation-cycle-block-hypothesis-the-customized-approach/

from an addendum comment:

The panel consists of measurement of two forms of glutathione (reduced and oxidized), adenosine, S-adenosylmethionine (SAM) , S-adenosylhomocysteine (SAH), and seven folic acid derivatives or vitamers.

According to Dr. Audhya, the reference ranges for each of these metabolites was derived from measurements on at least 120 healthy male and female volunteer medical students from ages 20 to 40, non- smoking, and with no known chronic diseases. The reference ranges extend to plus and minus two standard deviations from the mean of these measurements.

Glutathione: This is a measurement of the concentration of the reduced (active) form of glutathione (abbreviated GSH) in the blood plasma. From what I’ve seen, most people with chronic fatigue syndrome (PWCs) have values below the reference range. This means that they are suffering from glutathione depletion. As they undergo the simplified treatment approach to lift the methylation cycle block, this value usually rises into the normal range over a period of months. I believe that this is very important, because if glutathione is low, vitamin B12 is likely unprotected and reacts with toxins that build up in the absence of sufficient glutathione to take them out. Vitamin B12 is thus “hijacked,” and not enough of it is able to convert to methylcobalamin, which is what the methylation cycle needs in order to function normally. Also, many of the abnormalities and symptoms in CFS can be traced to glutathione depletion.

Glutathione (oxidized): This is a measurement of the concentration of the oxidized form of glutathione (abbreviated GSSG) in the blood plasma. In many (but not all) PWCs, it is elevated above the normal range, and this represents oxidative stress.

Adenosine: This is a measure of the concentration of adenosine in the blood plasma. Adenosine is a product of the reaction that converts SAH to homocysteine. In some PWCs it is high, in some it is low, and in some it is in the reference range. I don’t yet understand what controls the adenosine level, and I suspect there is more than one factor involved. In most PWCs who started with abnormal values, the adenosine level appears to be moving into the reference range with methylation cycle treatment, but more data are needed.

S-adenosymethionine (RBC) (SAM): This is a measure of the concentration of SAM in the red blood cells. Most PWCs have values below the reference range, and treatment raises the value. S-adenosylmethionine is the main supplier of methyl groups in the body, and many biochemical reactions depend on it for their methyl groups. A low value for SAM represents low methylation capacity, and in CFS, it appears to result from a partial block at the enzyme methionine synthase. Many of the abnormalities in CFS can be tied to lack of sufficient methyation capacity.

S-adenosylhomocysteine (RBC) (SAH): This is a measure of the concentration of SAH in the red blood cells. In CFS, its value ranges from below the reference range, to within the reference range, to above the reference range. Values appear to be converging toward the reference range with treatment. SAH is the product of reactions in which SAM donates methyl groups to other molecules.

Sum of SAM and SAH: When the sum of SAM and SAH is below 268 micromoles per deciliter, it appears to suggest the presence of upregulating polymorphisms in the cystathione beta synthase (CBS) enzyme, though this may not be true in every case.

Ratio of SAM to SAH: A ratio less than about 4.5 also represents low methylation capacity. Both the concentration of SAM and the ratio of concentrations of SAM to SAH are important in determining the methylation capacity.

5-CH3-THF: This is a measure of the concentration of 5-methyl tetrahydrofolate in the blood plasma. It is normally the most abundant form of folate in the blood plasma. It is the form that serves as a reactant for the enzyme methionine synthase, and is thus the most important form for the methylation cycle. Many PWCs have a low value, consistent with a partial block in the methylation cycle.

(Vitamin Diagnostics is now called Health Diagnostics)

Thank you!

Robin,
Mutations in the NOS (Nitric oxide synthase)system cause problems with detoxification of ammonia. Were you tested for the NOS mutation?

Carlos,

I believe there are other reasons that serum B12 levels can become elevated. One is if a person consumes substances that have analogue forms of B12 in them. E.g. spirulina, chlorella, seaweeds. The analogue form of cobalamin is not usable by the human body and will not reduce MMA.

See http://www.veganhealth.org/b12/plant

The other reason is if a person takes an oral supplement of cyanocobalamin or maybe even hydroxycobalamin but has a polymorphism that keeps the body from being able to metabolize these inactive forms.