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Help needed - B12 Binding Capacity test result

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by seadanc, Sep 20, 2012.

  1. seadanc

    seadanc

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    Hello - I’m struggling to interpret the results / treatment implications for a couple tests my CFS doctor recently ordered. I’ve searched the forums and poked around the internet but, not surprisingly, I remain confused. I’d be super appreciative if some of you learned folks could provide feedback.

    #1…B12 Unsaturated Binding Capacity test. The result came back <300 (reference range 725 – 2045). Unfortunately the doctor didn’t provide a great explanation for what this result indicates and I couldn’t find much discussion elsewhere. Does this result tell me anything about my ability to utilize all forms of supplemented B12? Based on this result the doctor is considering recommending high dose injected methylB12 (up to 25 mg daily).

    Regarding the test itself…the lab required 72 hours without B12 supplements prior to the test – I don’t know if the test protocol assumes the patient would have been using cyanocobalamin supplements. I have been supplementing with 5000mcg sublingual methylB12 and occasional adB12 for the last year. Any idea whether that would have skewed the test results?

    #2…I also got results of a COMT genetic test showing I am heterozygous (Val158/Met158). I’ve come across various postings / commentary that seem to conflict as to whether supplementing with methylB12 and methylfolate are problematic or beneficial. Any thoughts? Also, I can't find much in the way of treatment protocols designed to overcome the COMT enzyme deficiency. Can anyone point me toward treatment discussions?

    As background…I am homozygous 677TT for MTHFR.

    Thanks so much for your input! Dan
     
  2. aquariusgirl

    aquariusgirl Senior Member

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    sorry can't help with interpretation... curious tho about which lab offers the unsaturated binding capacity test...
     
  3. seadanc

    seadanc

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    The blood draw was at a LabCorp facility and from the report it appears that they performed the testing.
     
  4. aquariusgirl

    aquariusgirl Senior Member

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    ok, thanks..
     
  5. aquariusgirl

    aquariusgirl Senior Member

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    Rich is probably your best bet to answer this stuff.. ..I believe he has said that where there is low binding...of B12, you can try and saturate the blood and get it directly into tissues by using large dosages of B12. he favours hydroxocobalamin.. cos he thinks that too much methyl B12, esp. if taken with active folates, can overdrive the methylation cycle resulting in lower production of glutathione. Check his posts on this.

    Do you have liver problems? Cos low binding is seen in people with compromised liver function.. there are prolly other reasons too.

    You could check out amy yasko's forum www.ch3nutrigenomics.com for more on the snps.

    The MTHFR one seems more problematic to me.. because I recall reading that your snp makes you 66% less effective at converting folate from one form to another than regular folks.

    easy to google.... but yeah, low b12, low folate. ....I suspect .you may have arrived at this junction a different route than some/most of us...but a lack of b12 and active folates can throw a monkey wrench in methylation....to state the obvious.
     
  6. richvank

    richvank Senior Member

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    Hi, seadanc.

    AQG has given you some good info, in my opinion.

    Here's a site that gives a good discussion of this test:

    http://www.clinicallabtesting.com/s...c8fefaf5ca76b24e85257934003f0299!OpenDocument

    Basically, it tells you how much more B12 that the transcobalamin and haptocorrin carrier proteins could carry than they are already carrying. (Note that transcobalamin is the new name for transcobalamin II, and haptocorrin is the new name for transcobalamins I and III.)

    In order to interpret this test, one also needs to know what the total blood serum B12 level is, from another measurement. Then, by putting the two together, one can figure out whether there is insufficient B12 in the blood, and if so, whether it is due to a lack of transcobalamin or not.

    Having a low number for the unsaturated binding capacity could mean that you have a lot of B12 in your blood, or it could mean that you don't have enough transcobalamin. So I would say that more information is needed to interpret this.

    If you suspect that you might have ME/CFS, in my opinion a more helpful test panel would be the methylation pathways panel offered by Health Diagnostics and Research Institute. Contact info and an interpretive guide are pasted below. If it turns out that you have a partial methylation cycle block and glutathione depletion, the Simplified Methylation Protocol would likely help you. The most recent version is here:

    http://forums.phoenixrising.me/inde...ation-protocol-august-25-2012-revision.19050/

    I recommend working with a physician when on this type of treatment.

    Best regards,

    Rich



    Methylation Pathways Panel

    This panel will indicate whether a person has a partial methylation cycle block and/or glutathione depletion. I recommend that this panel be run before deciding whether to consider treatment for lifting the methylation cycle block. I am not associated with the lab that offers this panel.

    The panel requires an order from a physician or a chiropractor. The best way to order the panel is by fax, on a clinician’s letterhead.


    Available from:

    Health Diagnostics and Research Institute540 Bordentown Avenue, Suite 2300
    South Amboy, NJ 08879 USA
    Phone: (732) 721-1234
    Fax: (732) 525-3288

    Email: lab@vitdiag.com

    Lab Director: Elizabeth Valentine, M.D.

    Dr. Tapan Audhya, Ph.D., is willing to help clinicians with interpretation of the panel by phone, or you can use the interpretive guide below:


    March 25, 2012
    Interpretation of Results of the Methylation Pathways Panel
    by
    Richard A. Van Konynenburg, Ph.D.
    Independent Researcher


    Disclaimer: The Methylation Pathways Panel is offered by the European Laboratory of Nutrients in the Netherlands and the Health Diagnostics and Research Institute in New Jersey, USA. I am not affiliated with these laboratories, but have been a user of this panel, and have written these suggestions at the request of Tapan Audhya, Ph.D., Director of Research for the Health Diagnostics lab, for the benefit of physicians who may not be familiar with this panel. My suggestions for the interpretation of results of the panel are based on my study of the biochemistry involved, on my own experience with interpreting panel results as part of the analysis of a fairly large number of cases of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) over the past four years, and on discussion of some of the issues with Dr. Audhya. I am a researcher, not a licensed physician. Treatment decisions based on the results of applying this panel and its interpretation to individual cases are the responsibility of the treating physician.

    Application: In addition to being useful in analyzing cases of ME/CFS, this panel can also be usefully applied to cases of autism and other disorders that involve abnormalities in glutathione, methylation and the folate metabolism.

    The panel includes measurement of two forms of glutathione (reduced and oxidized), S-adenosylmethionine (SAMe), S-adenosylhomocysteine (
    SAH), adenosine, and seven folate derivatives.

    According to Dr. Audhya (personal communication), the reference ranges shown on the lab reports for each of these metabolites were 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 (reduced): This is a measurement of the concentration of the
    chemically reduced (active) form of glutathione (abbreviated
    GSH) in the blood
    plasma. The reference range is 3.8 to 5.5 micromoles per liter.


    Glutathione plays many important roles in the biochemistry of the body, including serving as the basis of the antioxidant enzyme system, participating in the detoxication system, and supporting the cell-mediated immune response, all of which exhibit deficits in CFS. The level of GSH in the plasma is likely to be more reflective of tissue intracellular glutathione status than the more commonly and more easily measured red blood cell or (essentially equivalent) whole blood glutathione level, which is about three orders of magnitude greater, because red blood cells are normally net producers of glutathione. Also, knowledge of the level of the reduced form, as distinguished from total (reduced plus oxidized) glutathione, which is more commonly measured, is more diagnostic of the status of glutathione function.

    In order to be able to approximate the in vivo level of reduced glutathione when blood samples must be shipped to a lab, it is necessary to include special enzyme inhibitors in the sample vials, and these are included in the test kit supplied by these two laboratories.

    Most people with chronic fatigue syndrome (PWCs), but not all, are found to have values of GSH that are below the reference range*. This means that they are suffering from glutathione depletion. As they undergo treatment to lift the partial methylation cycle block, this value usually rises into the normal range over a period of a few months. I believe that this is very important, because
    glutathione normally participates in the intracellular metabolism of vitamin B12, and if it is low, a functional deficiency of vitamin B12 results, and insufficient methylcobalamin is produced to support methionine synthase in the methylation cycle. In my view, this is the mechanism that causes the onset of ME/
    CFS. This functional deficiency is not detected in a conventional serum B12 test, but will produce elevated methylmalonate in a urine organic acids test. In my opinion, many of the abnormalities and symptoms in ME/CFS can be traced directly to glutathione depletion.

    Anecdotal evidence suggests that PWCs who do not have glutathione depletion do have abnormalities in the function of one or more of the enzymes that make use of glutathione, i.e. the glutathione peroxidases and/or glutathione transferases. This may be due to genetic polymorphisms or DNA adducts on the genes that code for these enzymes, or in the case of some of the glutathione peroxidases, to a low selenium status.

    Glutathione (oxidized): This is a measurement of the concentration
    of the oxidized form of glutathione (abbreviated GSSG) in the blood
    plasma. The reference range is 0.16 to 0.50 micromoles per liter.


    Normally, oxidized glutathione in the cells is recycled back to reduced glutathione by glutathione reductase, an enzyme that requires vitamin B2 and NADPH. If this reaction is overwhelmed by oxidative stress, the cells export excess GSSG to the plasma. In some (but not all) PWCs, GSSG is elevated above the normal
    range, and this represents oxidative stress. It is more common in CFS to see this level in the high-normal range. This value may increase slightly under initial treatment of a partial methylation cycle block.*


    Ratio of Glutatione (reduced) to Glutathione (oxidized): This is not shown explicitly on the panel results, but can be calculated from them. It is a measure of the redox potential in the plasma, and reflects the state of the antioxidant system in the cells. The normal mean value is 14. PWCs often have a value slightly more than half this amount, indicating a state of glutathione depletion and oxidative stress. This ratio has been found to increase during treatment of a partial methylation cycle block, but other types of treatment may be necessary to bring it to normal.*

    S-adenosymethionine (
    RBC): This is a measure of the concentration of S-adenosylmethionine (SAMe) in the red blood cells. The reference range is 221 to 256 micromoles per deciliter.

    SAMe is produced in the methylation cycle and is the main supplier of methyl (CH3) groups for a large number of methylation reactions in the body, including the methylation of DNA and the biosynthesis of creatine, carnitine, phosphatidylcholine, coenzyme Q10, melatonin and epinephrine. This measurement is made in the red blood cells because the level there reflects an average over a longer time and is less vulnerable to fluctuations than is the plasma level of SAMe.

    Most PWCs have values below the reference range, and treatment raises the value.* A low value for SAMe represents a low methylation capacity, and
    in CFS, it usually appears to result from an inhibition or partial block of the enzyme methionine synthase in the methylation cycle. Many of the abnormalities in CFS can be tied to lack of sufficient methylation capacity.

    S-adenosylhomocysteine (RBC): This is a measure of the
    concentration of S-adenosylhomocysteine (SAH) in the red blood cells. The reference range is 38.0 to 49.0 micromoles per deciliter.


    SAH is the product of the many methyltransferase reactions that utilize SAMe as a source of methyl groups. In CFS, its value ranges from below the reference range to above the reference range. Values appear to converge toward the reference range with treatment.

    Sum of
    SAM and SAH: When the sum of SAM and SAH is below about 268
    micromoles per deciliter, it appears to suggest the presence of
    upregulating polymorphisms in the cystathionine beta synthase (CBS)
    enzyme, though this may not be true in every case. For those considering following the Yasko treatment program, this may be useful information.

    Ratio of
    SAM to SAH: A ratio less than about 4.5 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, because they affect the rates of the methyltransferase reactions.


    Adenosine: This is a measure of the concentration of adenosine in the
    blood plasma. The reference range is 16.8 to 21.4 x 10(-8) molar.


    Adenosine is a product of the reaction that converts SAH to homocysteine. It is also exported to the plasma when mitochondria develop a low energy charge, so that ATP drops down to ADP, AMP, and eventually, adenosine. Adenosine in the plasma is normally broken down to inosine by the enzyme adenosine deaminase.

    In some PWCs adenosine is found to be 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 in these patients, and I suspect that 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.

    5-CH3-THF: This is a measure of the concentration of 5L-methyl
    tetrahydrofolate in the blood plasma. The reference range is 8.4 to 72.6 nanomoles per liter.


    This form of folate is present in natural foods, and 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 important form for the methylation cycle. It is also the only form of folate that normally can enter the brain. Its only known reactions are the methionine synthase reaction and reaction with the oxidant peroxynitrite.

    When there is a partial block in methionine synthase, the other forms of folate continue to be converted to 5L-CH3-THF by the so-called “methyl trap” mechanism. Some of the 5L-CH3-THF is broken down by reaction with peroxynitrite, which results from the condition of oxidative stress that is usually concomitant with glutathione depletion.

    Many PWCs have a low value of 5L-CH3-THF, consistent with a partial block in the methylation cycle. Most methylation treatment protocols include supplementation with 5L-CH3-THF, which is sold over-the-counter as Metafolin, FolaPro, or MethylMate B (trademarks), as well as the newer Quatrefolic (trademark) and in the prescription “medical foods” supplied by PamLab, including Deplin, CerefolinNAC and Metanx. There are some others on the market that include both racemic forms (5L and 5R) of this folate.

    When methylation treatment is used, the level of 5-CH3-THF rises in nearly every PWC. If the concentration of 5-CH3-THF is within the reference range, but either SAM or the ratio of SAM to SAH is below the reference values, it suggests that there is a partial methylation cycle block and that it is caused by inavailability of sufficient bioactive B12, rather than inavailability of sufficient folate. A urine organic acids panel will show elevated methylmalonate if there is a functional deficiency of B12. I have seen this combination frequently, and I think it demonstrates that the functional deficiency of B12 is the immediate root cause of most cases of partial methylation cycle block. Usually glutathione is low in these cases, which is consistent with such a functional deficiency. As the activity of the methylation cycle becomes more normal, the demand for 5-CH3-THF will likely increase, so including it in the treatment protocol, even if not initially low, will likely be beneficial.

    10-Formyl-THF: This is a measure of the concentration of 10-formyl
    tetrahydrofolate in the blood plasma. The reference range is 1.5 to 8.2 nanomoles per liter.


    This form of folate is involved in reactions to form purines, which form part of RNA and DNA as well as ATP. It is usually on the low side in PWCs, likely as a result of the methyl trap mechanism mentioned above. This deficiency is likely the reason for some elevation of mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) often seen in PWCs. This deficit may also impact replacement of cells lining the gut, as well as white blood cells.

    Rarely, 10-formyl-THF is found to be much higher than the normal reference range. If this is found, the patient should be examined for cancer, since cancer cells upregulate this form of folate in order to make purines more rapidly to support their rapid cell division.

    5-Formyl-THF: This is a measure of the concentration of 5-formyl
    tetrahydrofolate (also called folinic acid) in the blood plasma. The reference range is 1.2 to 11.7 nanomoles per liter.


    This form is not used directly as a substrate in one-carbon transfer reactions, but it can be converted into other forms of folate, and may serve as a buffer form of folate. Most but not all PWCs have a value on the low side. It is one of the
    supplements in some methylation protocols. It can be converted to 5L-CH3-THF in the body by a series of three reactions, one of which requires NADPH, and it may also help to supply other forms of folate to the cells until the methionine synthase reaction comes up to more normal activity.

    THF: This is a measure of the concentration of tetrahydrofolate in
    the blood plasma. The reference range is 0.6 to 6.8 nanomoles per liter.


    This is the fundamental chemically reduced form of folate from which several other reduced folate forms are synthesized, and thus serves as the “hub” of the folate metabolism. THF is also a product of the methionine synthase reaction, and participates in the reaction that converts formiminoglutamate (figlu) into glutamate in the metabolism of histidine. If figlu is found to be elevated in a urine organic acids panel, it usually indicates that THF is low. In PWCs it is lower than the mean normal value of 3.7 nanomoles per liter in most but not all PWCs.

    Folic acid: This is a measure of the concentration of folic acid in
    the blood plasma. The reference range is 8.9 to 24.6 nanomoles per liter.


    Folic acid is a synthetic form of folate, not found in nature. It is added to food grains in the U.S. and some other countries in order to lower the incidence of neural tube birth defects, including spina bifida. It is the oxidized form of folate, and therefore has a long shelf life and is the most common commercial folate supplement. It is normally converted into THF by two sequential reactions catalyzed by dihydrofolate reductase (DHFR), using NADPH as the reductant. However, some people are not able to carry out this reaction well for genetic reasons, and PWCs may be depleted in NADPH, so folic acid is not the best supplemental form of folate for these people.

    Low values suggest folic acid deficiency in the current diet. High values, especially in the presence of low values for THF, may be associated with inability to convert folic acid into reduced folate readily, such as because of a genetic polymorphism in the DHFR enzyme. They may also be due to high supplementation of folic acid.

    Folinic acid (WB): This is a measure of the concentration of folinic acid in the whole blood. The reference range is 9.0 to 35.5 nanomoles per liter.


    See comments on 5-formyl-THF above. Whole blood folinic acid usually tracks with the plasma 5-formyl-THF concentration. They are the same substance.

    Folic acid (
    RBC): This is a measure of the concentration of folic acid in the red blood cells. The reference range is 400 to 1500 nanomoles per liter.

    The red blood cells import folic acid when they are initially being formed, but during most of their lifetime, they do not normally import, export, or use it. They simply serve as reservoirs for it, giving it up when they are broken down.

    Many PWCs have low values of this parameter. This can be caused by a low folic acid status in the diet over the previous few months, since the population of RBCs at any time has ages ranging from zero to about four months. However, in CFS it can also be caused by oxidative damage to the cell membranes, which allows folic acid to leak out of the cells. Dr. Audhya reports that treatment with omega-3 fatty acids has been found to raise this value over time in one cohort.

    If anyone finds errors in the above suggestions, I would appreciate being notified at richvank@aol.com.

    * Nathan, N., and Van Konynenburg, R.A., Treatment Study of Methylation Cycle Support in Patients with Chronic Fatigue Syndrome and Fibromyalgia, poster paper, 9th International IACFS/ME Conference, Reno, Nevada, March 12-15, 2009. (http://www.mecfs-vic.org.au/sites/w...Article-2009VanKonynenburg-TrtMethylStudy.pdf)












     
  7. seadanc

    seadanc

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    I'm very appreciative of the info and advice!

    Sounds like it would have been important to have a serum B12 test at the same time. I wonder if my serum B12 levels were high even though I stopped supplementing for the required 72 hours before the test. (I had been supplementing with methylB12 and some adB12.) Maybe the carrier proteins were already maxed out?

    The doctor also ordered a methylmalonic acid test. I'm awaiting the results although I'm not sure if that will help to draw conclusions about B12 status.

    I will push the doctor to order the Methylation Pathways Panel - it would be great to get some insight into how the pathways are actually functioning.

    Thanks again, Dan
     
  8. pg600rr

    pg600rr

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    I know this is an old thread but was hoping to revive it, I too tested for low B12 binding capacity, B12 serum which was done at the same time was 512....so in normal range...not sure what the two together mean? I have A1298C, but still waiting on my other 23andMe SNP's.... any insight would be great...I am thinking about starting hyroxy b12 since it seems safer than methyl for those who dont have the other SNP's yet...
     
  9. Lynn_M

    Lynn_M Senior Member

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    pg600rr,

    The B12 serum test is kind of a garbage test. It measures both active and inactive B12 - I think those are transcobolamin and haptocorrin, respectively.

    Hydroxy B12 still needs to get converted to methyl B12 for your body to use it. Hydroxy might be "safer", but it might also be less effective for you. If you start on methyl B12, if you have "reactions", you could always switch to hydroxy. Whereas if you start with hydroxy, it would be harder to know the absence of it doing you any good.
     
    Last edited: Dec 12, 2015
  10. pg600rr

    pg600rr

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    Thanks so much. So given my very low b12 binding capacity test is there a follow up I can have my doc do to flesh out say transcol I, transcol II, etc. levels?

    I've been very sick for a long time and they e been chasing Lyme. Just don't want to miss anything. All my symptoms line up with b vitamin issues to a T but my serum B12 has always been mid range so it was dismissed. However with the low b12 binding capacity I'm now thinking it needs to be revisited.

    Was just reading a paper outlying a genetic defect where low b12 binding capacity is a common finding, along with normal serum b12 BUT transcol II actually ends up being very low causing problems.
     
  11. Freddd

    Freddd Senior Member

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    Just a few things to comment. If a person is taking a MeCbl sublingual enough active b12 is in the body and distributed by diffusion where and when it is needed. An ordinary blood draw with exposure to light makes it impossible to tell what the unbound b12 type might actually be because light causes a breakdown of MeCbl, CyCbl and AdoCbl to an equilibrium reaction of HyCbl <> H2OCbl. There is a fully opaque draw kit available if it is important to do type of B12 analysis but it is rarely done or needed and very expensive. The HTC2 protects the attached cobalamin from all sorts of assaults. It also delivers B12 on a rationed basis, those same "internal triage levels" we have been talking about.

    I posted some while back a ZONES OF B12 HEALING or something like that. B12 limited to only the HTC bound b12 rarely causes widespread healing because it is almost always the "most limiting factor". As soon as one has 100mcg + in the serum healing can really take off. Just to be clear, a general serum level of 500 pg/ml indicates that there is a total of 2.5mcg of b12 in 5 liters of blood. 100mcg on serum gives 20,000pg/ml serum level but the kidneys get rid of it quickly, 75% in 1 hour often. Unbound b12 is essentially 100% gone in 3 days which is why symptoms restart after 3 days without supplemental B12. Limiting B12 to bound B12 only slows down healing so much that anybody like me with a lot of damage will never catch up.

    As long as a person is taking MeCbl (daily) and AdoCbl binding capacity is irrelevant and can be essentially zero and a person can still heal. I take 10mg MeCbl by subcutaneous injection 3 times each day and may have the most expensive urine of anybody here. However, before it is excreted I get enough diffused into my brain and cord to keep them functional and me alive.

    5ml of semen has the same amount of TC2 as 1000ml of blood, if the man has enough B12 available in his body.
     
  12. Lynn_M

    Lynn_M Senior Member

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    pg600rr,

    If your symptoms point to B12 deficiency issues, then I would trust that more than a serum B12 test. Your low B12 binding capacity probably means your B12 is mostly in the inactive form, but I don't know enough about that test to really comment. Freddd has previously cited a study where even patients with supposedly normal serum B12 levels greatly benefited from B12 supplementation.

    If you feel you it's imperative to have a test result showing you are low in B12, then a MMA test (methylmalonic acid) is much more trustworthy than a serum B12 test. It shows how well the B12 in your body is functioning, because the body needs B12 to get rid of MMA, and high MMA values indicate low B12. The urine rather than plasma MMA test is best, and is available as a standalone test or as part of an OAT test.

    Another good test is the Spectracell Micronutrient Test, where they measure the levels within the lymphocytes of 35 different nutritional components, including B12. It reflects the last 3 months of nutrient status. See here. Either a doctor or patients themselves can order this test.

    Do you have mutations in your FUT2, CUBN, TCN1, TCN2, or MUT genes? These have been all shown to influence VitB12 levels in European ancestry patients. Tests don't always accurately reflect the status or function of nutrients.

    If it was me, I wouldn't be concerned with trying to flesh out the various transcobalamin levels, which probably isn't possible other than in a research lab, I would just start taking B12, either hydroxyl or methyl, and adenosyl. I don't like the sublingual form because when I took it Freddd's suggested way, by parking it under my upper lip for an hour or so, I wound up with my teeth getting eroded form the acid in the sublingual forms. I use the transdermal form that is available from B12oils.com, available as meB12/adenoB12 or hydroxyB12/adenoB12. Greg, the biochemist who developed it, says it is as effective as sublingual B12. You don't need a Rx, so you don't need to convince your doctor that you are low in B12.

    My Spectracell micronutrient test showed I was deficient only in B12 and total antioxidant function. After using the B12oil for 6 months, my MMA was well within the 1 sd range. I haven't retested the Spectracell.
     
    Last edited: Dec 12, 2015
    ScottTriGuy likes this.
  13. Little Bluestem

    Little Bluestem All Good Things Must Come to an End

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    If you are not able to get the Australian B12 oils, there is a thread here on various ways to do transdermal B12.
     
  14. pg600rr

    pg600rr

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    Thanks Freddd, so I am not gonna lie, I dont totally understand everything in the above post, but I think the gist of what you are saying is that even if one has some sort of transcobalmin deficiency (whether it be mild, partial, hereditary, etc.) it doesnt really matter, as long as they are properly supplementing with B12, either via methyl, adeno, or hydroxy, subling or injection.

    This is important to me as I have been quite sick for 4 years with a number of symptoms all linked to B12 deficiency, yet my docs never explored it given my "normal" serum b12 levels. I think the one time my serum MMA was tested it was normal as well, though homocysteine was a tad high at like 11 or something.

    I am not under any illusion that this is my whole problem or will solve all my issues but I am now wondering if it is a part of the puzzle, given that the transcobalmin test clearly shows the biological b12 in cells is probably low, even though serum is showing 'okay' levels.

    I am still waiting on the remainder of my 23 and me report but lets say there are COMT mutations, should I avoid the methly b12 and stay solely with Hyrdroxy
     
  15. Lynn_M

    Lynn_M Senior Member

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    pg600r,

    I've done some reading on the B12 unsaturated binding capacity. According to a book excerpt quoted at this website, "Measurement of unsaturated B12 binding capacity is rarely undertaken and is only available in reference laboratories. (Details of the method were given in the 9th edition of this book.) It is mainly of use for detection of transcobalamin I deficiency as a cause for very low serum B12 with no clinical features of cobalamin deficiency. It is also required for diagnosing the rare TCII deficiency." Check out the website.

    I'm wondering if you are interpreting the meaning of the B12 unsaturated binding capacity test correctly. If you have a low capacity, it means the carrier protein that B12 binds to is full-up and can't carry around much more B12. It's like a wheelbarrow and dirt. Using the metaphor of B12 as dirt, a low capacity means the wheelbarrow is pretty full of dirt and you can't put much more dirt in it. Now if you had been taking supplemental B12 regularly before the test, even with the 3-day break from B12 they recommend before the test, it wouldn't be surprising for your capacity to be low. When Dr. Ben Lynch had a patient with a low capacity test result, he had him get off all B12 supplementation for 2 weeks. When retested, his B12 unsaturated binding capacity test was normal.

    Dr. Ben Lynch explains more about the test in this short podcast. It sounds like he wouldn't consider a low B12 unsat. binding capacity and mid-range serum B12 to be at all concerning.
     
  16. Sea

    Sea Senior Member

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    The other unknown variable is the size of the wheelbarrow. There can be a deficiency of the carrier protein, which has the same result on this test as an abundance of B12.

    These are not B12, they are the proteins which carry or transport B12
     
  17. pg600rr

    pg600rr

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    Thanks. I wasn't on any supplementation at the time of the test. I've actually never been on any b vitamin or multivitamin supplementation thto out hour all this.

    From the reading I've done on it, it sounds like the UBBC represents a deficiency in carriers, which essentially means you have enough serum b12 floating around but probably not enough of it getting into the cells. The mystery is whether it's a TCI/III deficiency or a TCII which would seem more serious.

    The aymptoms I've been dealing with past 4 years include nausea, bloating, extreme weight loss pretty much muscle as I was in great shape prior, brain fog, POTS, low bp, muscle aches, chills w/o fever, mild anemia, very easy brushing with prolonged heal time, feelings of muscle tightness, and a few others.

    My diagnosis was Lyme disease but this makes me wonder if it is incorrect or if there is another piece to the puzzle. If the UBBC is reflecting even a mildly low TCII it would seem to point towards not enough b12 in the cells them self.

    If the wheelbarrow was full to use the reference above, reflected by UBBC being low, I would expect serum b12 to be especially high, not 400 or even 500. But I might be understanding exactly how the process works incorrectly.

    All I know is that the research papers on true hereditary TCII deficiency all show normal serum b12 and low UBBC as lab findings. Scientists have also started finding that true Heridatary TCII isn't the only possible issue, and that there can be 'mild' deficiency or partial, still causing issues.

    The other interesting thing in my case is that my mother has a number of issues including spinal issues and has very low b12 tested many years ago. She also had low bp issues and passing out issues in here 20's. She's been getting b12 shots for a very long time monthly, they helped a bit in the beginning but not much any more. Point being b12 deficiency issues seem to run on my mothers side in some capacity, whether it relates to genetics who knows.
     
  18. Lynn_M

    Lynn_M Senior Member

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    Sea,
    Thank you for your corrections. I hesitated in writing those terms, and my bad memory and incomplete understanding won out.
     
  19. pg600rr

    pg600rr

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    So I just went back and listened to Ben Lynch's podcast on UBBC/binding capacity. It sounds like the above is correct i.e., the wheel barrel theory, if and only if, one is supplementing with B12 at the time of the UBBC test and their B12 serum levels are elevated.

    However, if one is not supplementing at the time and serum is normal, and UBBC comes back low, it is an accurate assessment.. v. the false positive that Lynch describes.

    I just sent him a message for further clarification but thats what he describe in the last minute or two of the podcast. Doubt he'll reply but ya never know.

    In any event, given that I have never supplemented with any b12, I am going to give it a shot and keep an eye on UBBC levels in regard, it'll be interesting to see if it rises, and then falls again once I get my serum levels up out of range...

    Also, my 23 and ME will be done in about 7-10 days, will be interesting to see if I have either of the TCN1 or TCN2 synps
     
  20. Sea

    Sea Senior Member

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    NSW Australia
    It will be interesting, but may not be conclusive. 23andme don't test anywhere near all of the relevant snps so you can't use it to rule out an issue. A positive result on the snps they do test would give you an answer though.
     
    Valentijn likes this.

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