low normetanephrine levels

Discussion in 'Fibromyalgia Main Forum' started by valliali, Sep 12, 2008.

  1. valliali

    valliali New Member

    Hi all-
    I am newish to the board, I have never posted before. I have been diagnosed with a dysautonomia, but suspect that I have other issues going on. A couple of friends suggested I check out this site for a great wealth of knowledge and support. I am not sure that I have CFS, but it is a definite possibility.
    My dysuatonomia diagnosis really hit a dead end, as my team of doctors don't know much about it. I am seeking an explanation, at this point, to one of the test results I have had returned that I believe holds the key to my issues, if only I can understand it. My doctors all scratched their heads and referred me to someone else at this.
    I have low normetanephrine levels. This was measured through a 24 hour urine catecholamine test. Normetanephrine is the metabolite of norepinephrine. My doctors suspect that since my levels are quite low, this means that a lot of norepinephrine is going into my blood, which causes a lot of the dysautonomic symptoms, like heart issues.
    However, I am looking for an explanation as to why these levels are low, and what this could indicate about what is going on!!!!
    I have recently been turned on to investigating the methylation cycle, which many of you are probably familiar with, since I have read that the enzyme that breaks down norepinephrine into normetanephrine, needs to be methylized in order to function properly.
    So, I am wondering if anyone here has low normetanephrine levels??? And does anyone know why they do???

    I would so greatly appreciate any feedback. Thank you all!!!
  2. valliali

    valliali New Member

    Hi everyone, again. I have noticed that no one has responded to my post, which I expected because I feel like the only person in the world with this issue and I have no idea how to even go about finding out what the cause of this could be. I thought that perhaps many of you would have a similar result, the low normetanephrine levels, if this is due to a blocked methylation cycle.
    I am wondering, then, if many of you have gotten 24 hour urine catecholamine tests, and if so, are they normal???
  3. dirtchick

    dirtchick New Member

    Hi valliali,

    Welcome to the board.

    I am sorry i cant help you with any answers but this will move yor post back to the top of the front page and hopefully get you a response.

    Good luck,
    Barb
  4. pasara

    pasara New Member

    I would suggest you do a search on "dysautonomia" using the search box up top and then selecting to search in "content." When I did this several posts came up that might be interesting to you. You could also search "methylation cycle." I know that A LOT is posted on this regularly.

    I hope someone else can direct you more specifically, but this may get you started. Also, one search might lead to another, such as you might see a member who seems to know a lot about methylation, and you could then post a question specifically to them by starting a new thread with their name in the title to get their attention.

    Good luck!
  5. valliali

    valliali New Member

    thank you guys, for your suggestions! i have researched quite a bit on the methylation cycle, which pointed me to this forum, but it seems that i cannot find anything on low normetanephrine levels. am i the only person in the world with this problem?!?! ah!
  6. findmind

    findmind New Member

    I think you just happened upon something that is common in CFIDS/ME, but not tested for regularly with our doctors.

    Yes, I do think you found a clue as to why a methylation block cycle treatment might help you, but I do not know the protocol well enough to help you.

    You can search above for the "simplified MCB protocol", and try it; I believe it's only 3 supplements in miniscule amounts to start, so a trial could give you more answers, maybe.

    Good luck, I think you've stumbled onto something valuable for your path to healing.

    findmind
  7. greatgran

    greatgran Member

    My levels were high, I had the 24 urine and blood catecholamine test. The doc thought I might have a tumor on my adrenal glands so had a CT Scan wich was normal.

    Then he wanted me to see a psychologist said it was anxiety.

    Do you have anxiety or depression? I was never told why mine was high except for the anxiety, and if I didn't get it under control it would affect my heart.

    This was an Endocr.doctor . I feel mine has something to do with my CFS but not sure. For my anxiety I did try therapy can't say it helped, have been taking xanax for 7 years.

    Did you doctor have any answers? Would this have something to do with your adrenal glands? Oh, did you exercise before the test. I was told by the lab tech, if its low you need to exercise before the test, since mine was high I had to rest 45 min. before they did the test. That is the blood test. This was when I had a repeated test.

    Sorry, I have no feedback for you hope you find some answers.

    God Bless,
    greatgran

    p.s. This probably didn't help at all but my norepinephrine levels were very high are they the same as normetanephrine?



  8. valliali

    valliali New Member

    coming up with a new title for every reply is hard!! :)

    thank you all for your responses. to clarify, normetanephrine is the metabolite of norepinephrine. when NE is produced in the adrenal glands, most of it is immediately metabolized, then the remainder goes off into the blood to do its job. so i have very low levels of the metabolite, which leads my doc and i to believe that a lot of NE is going into the blood, which explains many of my symptoms (i have been diagnosed with autonomic dysfunction-though questionable- and inappropriate sinus tachycardia).
    i have learned that NE is metabolized by an enzyme called COMT, which becomes affective by the methylation cycle. hence, me thinking i may be having problems with my methylation cycle.
    i have other unusual symptoms that do not seem to fit in with dysautonomia at all, like swollen lymph nodes and curling and sore fingers. my doctor had suggested chronic fatigue syndrome, but said he didn't know anything about it and didn't feel comfortable diagnosing me.
    i'm not sure it's what is going on either, but it seems that many CFS suffers also have methylation cycle blocks. but i would assume that if this is what is going on in my case, as well as many of yours, then there would be more people with similar findings.
    however, it is a very good point that perhaps many people have not been tested for this but would have it.
    gran, my norepinephrine levels were low-normal but i suffer from a lot of anxiety and panic attacks. i think it is because i am not metabolizing the norepinephrine so a lot of it is being dumped into my blood. but i am new to this, and don't know. i know that high levels of NE are a sign of a pheochromocytoma, a tumor on the adrenal gland, but we have ruled that out for me.
    i was prescribed xanax, but i don't really like it. though i don't know what's worse - that or panic attacks! my panic attacks are very much physiological, i would like to try therapy but am quite positive it won't be doing the trick. i don't feel mentally anxious, in fact i am a very relaxed person, but my body constantly feels on edge.
  9. ellikers

    ellikers New Member

    Have you tried googling "low normetanephrine levels"?? That should give you a lot more general and specific resources on it than we could here.

    My thoughts are that you could have more than one imbalance if one neurotransmitter/hormone is being affects ...

  10. valliali

    valliali New Member

    oh yes, i have definitely googled, and yahoo'd and pubmed'd... there is hardly anything about this, which makes me feel like a freak!
    i have read many publications on the enzyme responsible for making normetanephrine, and many of the publications indicate that cfs sufferers have polymorphisms with this enzyme. so it seems like if the enzyme isn't functioning properly, especially with cfs, then there should be other people with low normetanephrine levels??
    perhaps many of you have not had 24 hour urine catecholamine testing?
  11. spacee

    spacee Member

    I agree I think the test holds a valuable key. Your team of docs know how to do the testing but not what to do with it.
    I was just telling a woman yesterday that I had a "little illness" haha..just trying to downplay it. But that my doc didn't understand it and that I had to do the research for it..

    The methyl. protocol would seem like an possible place to start. Have you joined the Yahoo CFS Yasko Experimental Group?
    Should you do the protocol that it a way to ask questtions to the reactions that arise.

    I wish you luck with this. One of the things we do here, is try things, try things, try things. It is good to try to get to the root of the cause, I think.

    Spacee
  12. marcomaestrini

    marcomaestrini New Member

    Hi . I'm new to this sight. I wanted to get a hold of you because I to have low normetanephrine levels and have bad dysautonomia. Was seeing if any doctor figured it out for you. They don't say any thing about it. They tell me don't worry.I have had thousand blood test and finally this one came back really low. Hope to hear from you. I know you haven't posted since 2008.
  13. richvank

    richvank New Member

    Hi, valliali.

    Low normetanephrine together with low-normal norepinephrine suggests that the rate of synthesis of norepinephrine might be low. This could be caused by a slow conversion of dopamine to norepineprhine, or it might be caused by an earlier problem in the catecholamine synthesis pathway, causing dopamine also to be low. Do you have data on your dopamine level, and if so, is it normal? If it is, then the dopamine beta-hydroxylase reaction that converts dopamine to norepinephrine could be running slow. This reaction requires vitamin C and copper. If your dopamine level is also low, then the problem is likely earlier in this pathway.

    As you may know, the catecholamines are synthesized from phenylalanine and tyrosine, which are amino acids that come from proteins in food. Phenylalanine is considered an essential amino acid. Its conversion to tyrosine requires tetrahydrobiopterin (BH4) and iron. If there is a methylation cycle partial block, this will also affect the folate metabolism, which in turn will impact the biopterin cycle and cause low BH4.

    Tyrosine is converted to DOPA by the tyrosine hydroxylase reaction, which also requires BH4 and iron. DOPA is converted to dopamine by the DOPA decarboxylase reaction., which requires P5P, the active form of vitamin B6. Vitamin B2 is required to convert B6 to its active form.

    Deficiencies in the amino acid precursors or the essential nutrients that are needed can slow these reactions.

    A partial methylation cycle block can cause lots of problems with the neurotransmitter metabolism, both in the synthesis and the breakdown of the neurotransmitters.

    I would suggest that you ask your physician (or chiropractor) to order the Health Diagnostics and Research Institute methylation pathways panel. This will tell you how your methylation cycle, folate metabolism and glutathione are doing. Contact information and interpretive comments are pasted below. If you have a partial methylation cycle block, non-drug treatment is available. There are several methylation protocols now in use. The one I have suggested is also pasted below. This has helped about two-thirds of those who have a partial methylation cycle block. This has included some people with dysautonomia diagnoses as well as many with ME/CFS diagnoses. I am currently recommending that this protocol be tried for three months, and if it is not producing positive results by that time, it would be a good idea to do some testing to find out why. Some people do better with methyl B12 and adenosyl B12 than with hydroxo B12. If the treatment is working, we have seen benefits continuing out to a year.

    I hope this is helpful.

    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 Institute
    540 Bordentown Avenue, Suite 2300
    South Amboy, NJ 08879
    USA
    Phone: (732) 721-1234
    Fax: (732) 525-3288

    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:


    May 19, 2011


    Interpretation of Results of the Methylation Pathways Panel

    by
    Richard A. Van Konynenburg, Ph.D.
    Independent Researcher
    (richvank@aol.com)


    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.*

    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, 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 be converging 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, 5L-CH3-THF drains from the cells into the blood plasma by the so-called “methyl trap” mechanism. As other forms of folate are converted to 5L-CH3-MTF, this mechanism depletes the cells of folates in general.

    Many PWCs have a low value of 5L-CH3-MTF, consistent with a partial block in the methylation cycle. Most methylation treatment protocols include supplementation with 5L-CH3-MTF, which is sold over-the-counter as Metafolin, FolaPro, or MethylMate B (trademarks), 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.

    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 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.

    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/www.mecfs-vic.org.au/files/Article-2009VanKonynenburg-TrtMethylStudy.pdf)


    March 30. 2011

    SIMPLIFIED TREATMENT APPROACH
    FOR LIFTING THE METHYLATION CYCLE BLOCK
    IN CHRONIC FATIGUE SYNDROME—March 30, 2011 Revision
    Rich Van Konynenburg. Ph.D.
    (Based on the full treatment program
    developed by Amy Yasko, Ph.D., N.D.
    which is used primarily in treating autism [1])

    SUPPLEMENTS

    1. General Vitamin Neurological Health Formula [2]: Start with ¼ tablet and increase dosage as tolerated to 2 tablets daily
    2. Hydroxy B12 Mega Drops [3]: 2 drops under the tongue daily
    3. MethylMate B [4]: 3 drops under the tongue daily
    4. Folinic acid [5]: ¼ capsule daily
    5. Phosphatidyl Serine Complex [6]: 1 softgel capsule daily (or lecithin, see below)

    (supplement website removed by Prohealth moderator)


    The fourth supplement comes in capsules that contain 800 mcg. It will be necessary to open the capsules, dump the powder onto a flat surface, and separate it into quarters using a knife to obtain the daily dose. The powder can be taken orally with water, with or without food.
    These supplements can make some patients sleepy, so in those cases they take them at bedtime. In general, they can be taken at any time of day, with or without food.
    Phosphatidyl serine can lower cortisol levels. Patients who already have low evening cortisol levels may wish to substitute lecithin [7] (at one softgel daily) for supplement number 5 above. Lecithin is also available from http://www.holisticheal.com.
    For those allergic to soy, lecithin from other sources is available.
    GO SLOWLY. As the methylation cycle block is lifted, toxins are mobilized and processed by the body, and this can lead to an exacerbation of symptoms. IF THIS HAPPENS, try smaller doses, every other day. SLOWLY work up to the full dosages.
    Although this treatment approach consists only of nonprescription nutritional supplements, a few patients have reported adverse effects while on it. Therefore, it is necessary that patients be supervised by physicians while receiving this treatment.

    [1] Yasko, Amy, Autism, Pathways to Recovery, Neurological Research Institute, 2009, available from http://www.holisticheal.com or Amazon.
    [2] General Vitamin Neurological Health Formula is formulated and supplied by Holistic Health Consultants LLC.
    [3] Hydroxy B12 Mega Drops is a liquid form of hydroxocobalamin (B12), supplied by Holistic Health Consultants. 2 drops is a dosage of 2,000 mcg.
    [4] MethylMate B is a liquid form of (6s)-methyltetrahydrofolate supplied by Holistic Health Consultants, based on Extrafolate S, a trademark of Gnosis S.P.A. 3 drops is a dosage of 210 mcg.
    [5] Folinic acid is 5-formyltetrahydrofolate. ¼ capsule is a dosage of 200 mcg.
    [5] Phosphatidyl Serine Complex is a product of Vitamin Discount Center. 1 softgel is a dosage of 500 mg.
    [7] Lecithin is a combination of phospholipids without phosphatidylserine. One softgel is a dosage of 1,200 mg.
















    [This Message was Edited on 07/12/2011]
  14. richvank

    richvank New Member

    Hi, valliali.

    Based on the combination of symptoms you have reported, I think it is very likely that you do have ME/CFS. The anxiety and "on edge" feeling, in particular, suggests that you are suffering from excitotoxicity. This is a common feature of ME/CFS, and is caused by overactivity of the NMDA receptors on neurons in the brain. According to my hypothesis, this in turn is caused by glutathione depletion in the astrocytes in the brain. One of the functions normally performed by the astrocytes is to sweep glutamate (the main excitatory neurotransmitter in the brain) out of the synapses between neurons. When glutathione is low, the mitochondria in these cells is not able to produce ATP as fast as they should, and that causes the astrocytes not to be able to import glutamate and convert it to glutamine for recycle to the neurons as fast as they should. The result is that the glutamate level stays too high in the synapses, and it continues to interact with the NMDA receptors, causing the neurons to fire too often. This amounts to excitotoxicity, and it can damage the neurons over time.

    Panic attacks are usually caused by elevated epinephrine. These are also common in ME/CFS. Usually the HPA axis is dysfunctional in ME/CFS, and this causes problems with the diurnal cortisol variation. Have you had your 24-hour cortisol variation measured, with saliva testing? When cortisol goes too low, epinephrine is used to compensate, but high levels of it can produce panic attacks. Low cortisol can cause low blood sugar. If this happens during sleep, the sympathetic nervous system can call for elevated epineprhine production to bring the sugar level up, to save the brain, and that can result in a panic attack, waking the person up.

    The lymph node involvement would also be consistent with ME/CFS.

    Again, I would suggest running the methylation pathways panel.

    Best regards,

    Rich
  15. Alyssa-Admin

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