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17 years of a ME/CFS dx, and it is Lyme, Bartonella and Babesia not ME/CFS

Discussion in 'Lyme Disease and Co-Infections' started by katieann, Jul 8, 2011.

  1. Timaca

    Timaca Senior Member

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    Dufresne~ You could also consider getting tested at SUNY if you would like to do further Lyme testing: http://www.path.sunysb.edu/labsvs/ticklab.htm As you noticed, some people think Igenex is the best Lyme lab, others think it gives too many false positives.

    I've been tested numerous times at Igenex and also at several other labs. I also know 2 people who were CDC positive from Igenex who were totally healthy. Another person had a lot of positive bands at Igenex but she didn't have Lyme, she had Brucellosis. I would not ignore your positive tests from Igenex but I would possibly consider being tested at another lab for Lyme, and also consider getting tested for viruses. See: http://chronicfatigue.stanford.edu/ Do your homework and a lot of testing to figure out what is most likely causing your illness and then treat that.

    Best, Timaca
     
  2. Tristen

    Tristen Senior Member

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    Certain viruses such as HSV, and EBV can cause false positives which is another good reason to consider the whole picture including both lab results and clinical presentation, as interpreted by a good LLMD. Responsiveness to meds can be quite diagnostic as well.
     
  3. Dufresne

    Dufresne almost there...

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    Thanks for the info Timaca and Tristen.

    Back in 2006 I had some testing done.

    EBV
    VCA - IgG (E:A) - reactive
    EA - IgG <1:40
    EBNA _ IgG (E:A)

    So at the time I'd been exposed to EBV but there wasn't evidence of a current infection. I also apparently had testing for mycoplasma and Lyme, and although I don't have a specific negative report as I do for EBV (which puzzles me somewhat), the doctor said I was negative. A couple years later I tried doxicycline and experienced significant herx. However after further research and deliberation I decided to not pursue the regimen. What led me to getting tested recently was a visit with a naturopath in Toronto, a follower of Dr Klinghardt, who showed me all sorts of intracellular bacteria under the dark field microscope.

    Now there's a lot more to it clinically but I think I qualify for Lyme. I can get an ELISA done here in Quebec and have it covered. Would the result of that give me a good idea of the integrity of the Igenex test? How likely is it that ELISA come's up negative with a confirmed case?
     
  4. Timaca

    Timaca Senior Member

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  5. Crappy

    Crappy Senior Member

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    I am just wondering what the latest; best protocol is for treating Lyme? I have had it for years, and go to an LLMD. I have not had much luck getting rid of it, and have kind of resolved to living with it. I would sure like to kill it if it's possible though.
     
  6. aiden424

    aiden424

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    I got sick in 1986. Was diagnosed in 1988 with CFS. About 6 years ago I had the Lyme western blot IGG and IGM at IGeneX and was very positive on both IGG and IGM. Later was positive to Bart too. Treated for years and have gotten some better but not close to where I was before I got sick. So I think I have Lyme but I think I also have something else that the doctors are missing. Also I am so drug sensitive to everything that it makes treating anything next to impossible.

    So for me Lyme was a piece of the puzzle but I'm still missing some of the pieces.
     
  7. richvank

    richvank Senior Member

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    Hi aiden and the group.

    I think it's possible that a partial methylation cycle block can be hindering the effectiveness of treatment for Lyme disease. The vicious circle mechanism associated with this partial block can be expected to inhibit the effectiveness of the immune system, and it's necessary for the immune system to be operating properly in order to get control of infections.

    Some of the Lyme docs are testing for the partial methyation cycle block now, and I've heard from one of them that treating this turned out to be the remaining thing that certain of his patients needed to recover.

    Contact info for this test panel and a guide to interpreting the results are pasted below.

    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 clinicians 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 the guide below can be used for interpretation:


    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/w...Article-2009VanKonynenburg-TrtMethylStudy.pdf)
     
  8. justinreilly

    justinreilly Stop the IoM & P2P! Adopt CCC!

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    Katieann,

    I have considered trying to get an accurate Lyme test. I have had ME for 8 years. In the beginning I had some joint pain, only in my knees, but I think it was mostly from skiing. After I stopped skiing, because i was sick, it went away in a few months and i have had no joint pain, but always a lot of muscle pain. Do you think it's worth doing one of the good Lyme tests for me? If you don't mind, pls PM me so i don't miss it. thanks!

    I read Cure Unknown and was shocked at the insurance-connected 'experts' who screwed over the Lyme patients with their 'expert guidelines' which CDC of course adopted. It was even more blatant than what CDC etc have done to ME patients! The PoS CDC test is a kindergarten level effort. It is totally outrageous that they push that nearly useless test and the useless interpretation guidelines! CDC is killing millions of Americans.
     
  9. svetoslav80

    svetoslav80 Senior Member

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    I cannot agree that "a negative result doesn't mean much". If you:
    - know that 4 months have passed from the eventual tick byte, but not more than 1-2 years
    - know that you are not immunosuppressed
    - have not recently taken antibiotics
    - have not recently taken anti-inflammatory drugs

    ,then there's a really big chance that your negative ELISA test is accurate, and you don't have lyme.
     
  10. Lotus97

    Lotus97 Senior Member

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    What sort of methods are recommended for dealing with neurotoxins associated with die-off? (or any neurotoxins for that matter). I'm already dealing with brain fog (which might be partially be caused by Lyme) and I definitely don't want to make it worse.
     
  11. Wayne

    Wayne Senior Member

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    Hi Lotus97,

    I'm getting ready to retire for the evening, but I wanted to respond at least briefly first. There's actually quite a number of things I've read about or experienced that are helpful for detoxification. I'll try to get back tomorrow and expound a bit. If I don't, you may want to do a search for clay foot baths (under my username), which I've found to be helpful. Also, I've heard of one man who struggled with Lyme detoxification until he added enough iodine to help detoxify. -- Just a very broad subject.

    Best, Wayne
     
  12. Lotus97

    Lotus97 Senior Member

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    I've read that Smilax/Sarsaparilla and Benicar can be helpful for die-off symptoms. Has anyone used either of these? I'm not sure I want to go on Benicar because weight gain is one of the possible side effects and I just started another med that can potentially cause weight gain, but I thought I'd mention it in case someone else wants to try it.
     
  13. cigana

    cigana Senior Member

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    Hi Justin,
    I wouldn't base the likeleness of Lyme being a problem on yours symptoms (joint pain). I have symptoms that I wouldn't think match with Lyme and yet KDM has diagnosed me with chronic Lyme.
    My symptoms are: fatigue (inc. PE), lack of sleep, exhaustion, memory problems, depression.
    I live in the city and did not expect Lyme at all.
    You may need many tests too before you come up positive. I think KDM just continually tests patients because he sees it so frequently.
     
  14. Lotus97

    Lotus97 Senior Member

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    Joint pain can be a symptom of Lyme, but it can also be from a lot of other things.
     

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