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Methylation Stopped working

Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by paul80, Jun 8, 2012.

  1. paul80

    paul80

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    On tuesday after 12 days of great results on the methylation treatment, it just suddenly stopped working. My whole body feels so weak, i can hardly do anything. I've had to go on anti-depressants because i can't cope. i'm still carrying on with the treatment but it just seems to having no effect at all now, i don't understand, i didn't change anything.
     
  2. place

    place Be Strong!

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    Paul I ran into problems when my energy was high but my muscles felt drained. Caretine fixed that. What are your taking maybe I can problem shoot with you? Also tell me the amounts and when you take them. Also B2 helped a lot, plus potassium, you may need SAM-e?
     
  3. paul80

    paul80

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    Hi place, I wrote what i'm taking at the bottom of this page: http://forums.phoenixrising.me/index.php?threads/b-12-the-hidden-story.142/page-129

    I am taking acytel carintine but i ordered fumerate so i can try that soon. I already have sam-e but i haven't tried it yet, i just noticed on the box it says not to take with SSRI, i just started antidepressants so i guess i can't this now. i could try b2 and potassium though.

    Thanks.
     
  4. place

    place Be Strong!

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    I don't have to look at your list. But will this afternoon and write back. I just wanted to get this message to you as soon as possible

    Take the potassium, now if you can. For me, that solved the following within half hour; depression, body pain, flue like symptoms, anxiety, low energy, afternoon fatigue, negative thoughts on any subject even on really happy subjects. Really take 5 pills (.99) with some water. I really can't stress it enough! The daily amount of potassium is 4800, so taking 500, is nothing but it will turn things around.
     
  5. place

    place Be Strong!

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    I know others will have ideas to but my (unlicensed medical) thoughts are:

    1) I don't like multi anything, you can't control each supplement and document the changes. I did the calculations of myhills multi, even if you take 5, your nowhere near same level of the potassium you need. But I guess it won't kill you to keep taking it until it runs out. But anyone of those ingredients could cause an issue.... Moreover, you are relying on some else opinion on what your body needs verse your body telling you what you need.

    2) I note your extra potassium and magnesium 200mg potassium 200mg magnesium, for me I do Magnesium: 400 x twice a day and Potassium up to 3000 per day

    3) L- carnetine- I take 2000. I think 1000 is standard protocol. two pills in the morning and 2 in the afternoon. Don't take it to late at night or it will keep you up. Within 24hrs, I had functionality in my muscles and after 1 week, I felt strong (was a gymnast, so I know what strong feels like). Love this stuff.

    4) B2- I was having some eye floaters and other symptoms- I started taking B2- it helped a great deal, even for some of the emotional stuff.

    Final words: potassium, potassium potassium

    Good luck
     
    arx likes this.
  6. Freddd

    Freddd Senior Member

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    Hi Paul,

    This often happens when one or more things run out. What are you taking, all details and anything at all changed recently?
     
  7. kurt

    kurt Senior Member

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    USA.Earth
    Paul, this has happened to me when I ran out of d-Ribose but kept on the methylation protocol. So that makes me wonder whether you are needing d-Ribose?

    I read your list of supplements, some others that I have found essential are missing. That includes Ester-C, Magnesium (I prefer Chloride form), and higher dose B6 (the B multi does not have enough of several of the Bs for some people, some need more B2 or B5 also). But the d-Ribose seems critical to keeping my energy up. Also Goji helps (any form).
     
    Allyson likes this.
  8. paul80

    paul80

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    Thanks for the suggestions guys. you give me some hope. I need to experiment more like you have.

    I have d-ribose but haven't been taking it. How much did you need to take Kurt? I'll give the others a try when i get them.

    Fred i didn't change anything. the list of what I've been taking is at the bottom of the page i linked.
     
  9. Freddd

    Freddd Senior Member

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    Hi Paul,

    I started with the basics, the vitamins, minerals, omega3, lecithin, and a few misc items. Then when I added mb12 I leared about potassium quickly. Each time I ran out of steam I foeund something else that revved up healing again; adb12, SAM-e, l-carnitine fumarate, increased zinc fro 15mg to 65 mg/day, Metafolin. Some things made no difference. Others have reported magnesium, vit D, Vit C, Vit A, d-ribose, B2, p5p,TMG and so on. For some, it was the active froms that helped, Metafolin instead of folic/folinic acid, p5p instead of b6, mb12 and adb12 instead of cyanocbl or hydroxycbl. Almost anything essential, and even some ot the things considered "not essential" could be what holds things up. So I do lots and lots of mini-trials to see what made a difference. In many cases it takes tge correct combination and sequence. So if a person tries SAM-e before mb12 and Metafolin, it has a huge effect but if tried after mb12 and metafolin which generate SAM-e, it may not have any effect or very little. So SAM-e acts as a surrogate for mb12 in methylation but NOT as mb12 for other effects. Carnitine may make no difference at all if the person is deficient of adb12 and conversely, adb12 may have no effect if very deficient of carnitine. A person can be very deficient of adb12 while taking mb12, cyanocbl and hydroxycbl and a person may be very deficient of mb12 despite taking adb12, hydroxycbl or cyanocbl. Even the brand of some things makes a big differnce, such as mb12, adb12 and carnitine.
     
    taniaaust1 likes this.
  10. Hoops

    Hoops

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    Hi Fred

    I seem to be in a similar situation where my body has run out of something but I don't know what it is, could you help me out ? Paul - hope you don't mind me jumping onto this thread ?

    I'm a 40 yo male, had CFS and a range of fairly standard B12 deficiency symptoms for 3 years. I've been on the active protocol almost 4 weeks . After several weeks of improving energy and other symptoms I'm having to start sleeping during the day again, energy seems to be going backwards, and I have started to feel depressed - moderate but not severe. Ten days ago I started getting very noticeable angular cheilitis, as well as intermittent diarrhea, so using the decision tree I increased Metafolin all the way up to 16,000 mcg / day but the cheilitis has not cleared up yet.

    I'm currently taking:

    3,000 mcg Jarrow mb12
    16,000 mcg Metafolin
    2 x dibencozide
    3,000 - 4,000 mg potassium (in addition to food)
    2 x Thorne Research B-complex #5
    50 mg zinc picolinate
    400mg magnesium (amino acid chelate)
    1,000 mg L-carnitine fumarate
    400 IU Vitamin E mixed tocopherols
    100 mg B2
    2,400 mg Omega 3 fish oil
    1,200 mg sunflower lecithin
    2,000 mg C
    2,000 mg D3
    37.5 mcg liothyronine (T3 thyroid medication)

    I have been feeling angry and agitated at times too so I have just stopped the LCF, I thought I would give it a break and then re-start more slowly. In retrospect I think I may have added too many things in too early.

    If the max dose of Metafolin doesn't heal the cheilitis does that mean I should reduce the mb12 to slow the whole process down ? I have had severe mouth ulcers and skin peeling around my finger tips for many years but only discovered recently this was related to folate.

    Does a fairly sudden onset of depression give any clue to what's going on ?

    Any help most appreciated ....
     
  11. Rand56

    Rand56 Senior Member

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    hi paul80

    Just a word of caution for you, and I don't know if you'd have the same reaction as I did when I was adding in B2..but it made my depression worse. MAO is dependent on riboflavin for it's activity. Could be a reason why I felt worse on it. Nothing worse than getting more depressed when you have depression. If I were you, and if you were going to try the B2, I'd go super slow on it to see how you react to it. Just my 2 cents from my own experience.
     
  12. place

    place Be Strong!

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    Hoops- Couple things I ran into or needed. It may not apply because I never ran out of energy. I did have to take B2 with out my B mulit.

    1)I got sick last week with the flue. It was slow coming on about 6 days. During that time I could not sleep and I got cold sores and cheilitis. So you might have something coming on that is wearing down your immune system. Also, years ago, I found Olive leaf extract got rid of my cheilitis. I take one pill a day. OLE is know as an anti-viral.

    2) You may have some food/ substance issues. I found out I was allergic to yeast when I too a b- complex. Most B's are made out of yeast. Soy gives me sinus issues, corn make's my skin itch and if I have to much wheat I start to feel sick over the course of several days.

    3) You could up your mb12 you take 3mg, I think it tops out at 20mg. I take 10mg.

    4) Could try TMG.

    Hopefully others will have the answer!
     
  13. Freddd

    Freddd Senior Member

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    Hi Hoops,

    With the high amount of Metafolin I would expect that you have a paradoxical folate deficiency reaction to veggie folate. In that case for me the timing was critical for the folate to be effective. I have to take 4000mcg with each meal and 2400mcg three times daily without food to hold it consistantly at bay. Also, Thorne research #5 has folic acid in it which ciould further block the Metafolin. I had to get rid of all folic acid to even have a chance.

    Also,the if the Dibencozide is COuntry Life, that is MORE folic aicd. Also, you may only need the Dibencozide once or twice a week unless it is a titration sthat shoowed you need more.

    The carnitine needs to be taken on an empty stomach. This is often something not done.





    DISCLAIMER

    I am a self taught systems analyst and consultant working in group healthcare since 1979, full time in group healthcare since 1985. I am not credentialed, certified or licensed to do anything besides drive a car. I have been disabled by the disease processes being discussed and affecting neurology in a multitude of ways for 10 years and impaired in a variety of ways and levels for 54 years before that. Everything I say is my opinion, synthesis, understanding or otherwise of my own creation except direct attributed quotes. Approximate paraphrases are also my interpretation of what I have read. All of this is at best my data analysis, understanding, synthesis and hypotheses and not to be construed as medical advice. I am not responsible for anything you do with any information provided in any way. Anything you do is your own responsibility and at your own risk. There are no published peer reviewed studies backing up my opinions or statements, except the incidental ones quoted or implicit in my synthesis or understanding, and then only in so far any reading of such papers may confer. Your interpretations, actions and variations of what I say are strictly at your own risk.
     
  14. richvank

    richvank Senior Member

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    Hi, Hoops.

    If the trial and error approach does not pay off for you, I suggest running some tests to see what is going on. The most helpful are the Health Diagnostics methylation pathways panel and the Metametrix 40 plasma amino acids panel. The first requires an order from a physician or a chiropractor, and costs $295. Contact info is below. The second can be obtained without a doctor's order from www.directlabs.com.


    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)














     
  15. Hoops

    Hoops

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    Thanks Rich - I will order the methylation pathways panel. The Metametrix 40 amino acids panel is a fairly big investment ($1,000+, including shipping). I assume you think the quality of the information it provides is worth the cost ?

    Through several years of CFS I haven't had much of a problem with depression, but it has hit me fairly hard a few weeks after starting the active protocol. From reading people's experiences on the forum there seems to be so many possible causes of depression and ideas on how to address it, that I have no idea where to start. Do you think the Health Diagnostics neurotransmitter test panel would be worth doing ? Or would the methylation and amino acids test panels provide enough information to go on ?

    Thanks again for your help ....
     
  16. adreno

    adreno 3% neanderthal

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    Tundras of Europa
    This is not likely to tell you why you are depressed. Peripheral levels of neurotransmitters (which the test measures) are different from CNS levels (which is where it matters). Also, neurotransmitter levels are dependent upon location in the brain, so even measuring overall CNS levels (which requires a lumbar puncture) wouldn't tell you much.
     
  17. Hoops

    Hoops

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    Brisbane, Australia
    Thanks Fred. The Dibencozide is Source Naturals, and I am currently eating very limited vegetables. The Thorne B-Complex #5 has 100mcg folic acid in it - I use this because I live in Australia and I can't get any of the folic/folinic acid- free B-complex's delivered to Australia. I guess my only other option is to take all the B vitamins separately, which I was hoping to avoid since I am already taking 40 tablets per day. Could 100-200 mcg folic acid neutralise 16,000 mcg of Metafolin ?

    Could paradoxical folate deficiency itself cause a fairly sudden onset of depression (i.e. within 2 weeks) ? I haven't had any major depression problems until now.

    Thanks again for your continued help ....
     
  18. Hoops

    Hoops

    Messages:
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    Brisbane, Australia
    Ok thanks Place - will give that a go.
    Regards ...
     
  19. paul80

    paul80

    Messages:
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    Update. Each day i carried on with the methylation treatment, the energy in my muscles became worse and worse until i was struggling to walk and could barely hold my head up when sitting. That is the worst i've ever been with m.e. At that point i had to stop all supplements and since then i've been recovering each day since.

    I was really disappointed because for 12 days i thought i was being cured, but at this point i feel more positive that something actually finally worked, if only for a short time.

    I don't know what happened but it felt to me like my glutathione was boosted very fast for the first 12 days then it started to go down and kept plunging. Now what would cause it to do this? Could the dose have been to high?

    if i used an inactive form of b12 would this allow my body to convert only as much to active b12 as i need (assuming my body can) and thus avoid the glutathione dropping?

    Also i am considering the test Rich recommends, although money is very tight. I'm just wondering if it is really worth it. What important information can it tell me?
    I mean it's obvious my glutathione is low otherwise i wouldn't have had such an amazing initial reaction to the treatment would i?
    If it could give me more detail about the supplements to take and dosages it could be worth it though.
     
  20. Freddd

    Freddd Senior Member

    Messages:
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    954
    Salt Lake City
    Hi Hopps,

    Could 100-200 mcg folic acid neutralise 16,000 mcg of Metafolin ?

    I don't think it could by itself. However, in combination with veggie folate who have a paradoxical response to folinic acid it could. I find that if I take my 16,200 mcg of Metafolin daily in a carefully tested pattern, it is enough.



    Could paradoxical folate deficiency itself cause a fairly sudden onset of depression (i.e. within 2 weeks) ? I haven't had any major depression problems until now.

    Yes, among other things. In those having a limbic response of anxiety > fear > panic on the rising level of mb12, adb12, LCF and anger > >rage> depression on the declining side of the same nutrients, serum level of these things can casue very powerful emotional changes in minutes to hours. I have found that spreading the nutrients out, same dose per day, gets rid of a lot of the serum change artifacts if done very carefully.

    Also, the balance between mb12-adb12-LCF can influence depression. Depression in all has been affected by SAM-e, mb12, adb12, LCF, Metafolin, zinc, vit D, D-ribose and some others.
     

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