Hypercoagulation: Q & A by David Berg/Hemex (LONG)

Discussion in 'Fibromyalgia Main Forum' started by mommysisland, May 13, 2004.

  1. mommysisland

    mommysisland New Member

    I had found this rather obscure Q & A conversation from the CFIDS Yahoo group. I was looking for where I had read David Berg discuss SED rates, and this is it. But it covers much more than that.

    It was posted as an answer to a member's, (who have CFS), questions. It appears to have been from March, 2000.

    The reference at the beginning is to Nicholas Regush's book, "A Virus Within". It is fascinating, and is a medical detective story concerning finding, tracking, studying HHV-6 and how to beat it.

    Okay, here we go:

    support:Welcome David, you have an international audience today - including
    people from Norway and France. We are all looking forwards to you views and
    opinions. Thank you for participating!

    [David] Greetings to all. It's an honor and pleasure to be on line today and
    especially to follow Mr. Regush. His book is excellent and RIGHT ON !. (It's
    funny not being able to see faces that are included in the dialog.) But such
    is the NET. For some time now, I have been frustrated knowing that the
    coagulation part is only half of the problem and that one or more pathogens
    are the other. And that HHV6 has had no know treatment until now. So let's
    begin where Mr. Regush's book ends in October, 1999.

    In November, 1999, at the Infectious Disease Annual Meeting in Philadelphia,
    I saw a poster on HHV6 and spoke with the author, Dr. Joe Brewer of Kansas
    City. Over a four hour plus dinner meeting, we worked out the model that is
    being presented now about a basic coagulation or fibrinolysis regulatory
    protein defect in CFIDS patients as the genetic culprit. Then you add in a
    pathogen (HHV6, CMV, Mycoplasma, Chlamydia pneumonia, etc, or a combination
    of several of these pathogens) and the patient goes down hill rapidly into
    chronic illness due to the pathogen activating the coagulation mechanism.
    This is due to an immune response as well as inflammatory responses to the
    pathogen and probably the pathogen itself activating the coagulation system.
    Anticoagulants (primarily heparin) shut down the Soluble Fibrin generation
    and fibrin deposition on the Endothelial Cell (EC) surfaces. But unless the
    patient can get treatment for the pathogen, the healing response can only
    reach 50% or so.

    My frustration has been HHV6. Dr. Brewer told me about a new colostrum
    derived, highly purified Transfer Factor (TF) that would contain only
    specific IgG and IgM antibodies against CMV and HHV6 (see
    www.immunitytoday.com ). He started testing many of his patients for their
    coag defects and we found such in every patient. Each patient also had
    documented HHV6 infection. Beginning in December, Dr Brewer began treating
    his patients with this new TF. Patient stories are dramatic. We will discuss
    some of them.

    In early December, 1999, at the American Society of Hematology, we met Dr. Konnie Knox. After spending two plus hours discussing theories and therapies, we were all singing the same hymn. So the circle from last week
    to now is complete. The Good Lord has put Lois & I here at the right time, in the right place with the right knowledge and the right people to be able to solve these "Blood Curdling Mysteries" of chronic illnesses, and they
    extend beyond just CFIDS patients.

    WHY is it important to be tested for the coagulation defects? It is VERY
    important, because at some point in time, all CFIDS patients will need
    surgery, be in an accident or traumatic situation and NEED to have
    PROPHYLAXIS to prevent a blood clot, stroke, heart attack or Pulmonary
    Embolism from happening. If you know your protein defect, then proper
    anticoagulant therapy will prevent catastrophic events. I feel very strongly
    about this.

    If you look at the population of America and the patient race distribution
    of CFIDS patients, there are about 5% of bleeders (hemophiliacs or von
    Willebrand Factor deficient patients) and about 5% clotters. Using a bell
    shaped curve, 260 million USA population yields 13 million clotters. 1
    million CFS, 8 million Fibromyalgia, ? Million Multiple Sclerosis, ?
    Recurrent Spontaneous Abortors, etc. Are we close? The protein defects have
    mostly risen from European decent and are mostly white people. Hundreds of
    years ago, when someone cut themselves hunting or preparing food, it was
    advantageous to clot fast (not bleed to death). Life spans were shorter then
    also, so these coagulation or fibrinolysis regulatory protein defects were
    beneficial. Today, with much longer life spans, these defects cause chronic
    illnesses by not controlling the coag response properly. So much for my PhD

    [Fluffy]Are there any non prescription treatments you could recommend and
    what about future treatments ?
    Aspirin supposedly attacks one of the factors involved in coagulation.
    Bromelaine supposedly attacks all 3 of the factors. There are research
    indicating that bromelain increases antibiotic absorbtion. I currently take
    2500 mcu per day with minocin and it seems to help. I did experience a very
    slight headache initially and it seems to help with the brain fog. Any
    comments on this and other possible supplements. Also what is the timeline
    on future treatments ? Please also include anecdotal and personal opinions
    in your comments.

    [David] The ISAC Panel contains a test called the Platelet Activation Index.
    What we have learned is that this is really showing us whether or not there
    is an infection in the patient. If the CD62P alone is elevated, then this
    indicates an UNDERLYING INFECTION. When both are elevated and the PA Index
    is 1-3+, then this indicates an ACTIVE INFECTION. My guess is that HHV6 has
    infected the bone marrow (as it can!) and is inside the platelets when they
    leave the bone marrow for the blood stream. Because the immune system "sees"
    infected cells, Immunoglobulins (IgG or IgM) attach to the platelets,
    causing the alpha granules to partially release and CD62P gets transferred
    from the inside of the platelet to the outer membrane. This accounts for the
    elevated CD62P value in the assay. The higher the CD62P value, the greater
    the infection. Aspirin is NOT going to be effective against infected cells,
    and this is what we have seen in general, that ASA does not make the patient
    feel much better.

    [David] I am in the process of forming my opinion on Bromelain. Elly (in
    Wash DC) told me about this last fall, but I did not understand her. Several
    months ago I did a literature review on Bromelain and was amazed at the
    scientific articles related to Bromelain. Bromelain, from pineapples and
    totally natural, seems to help FIBRINOLYSIS. There are no studies to
    actually prove this, but it is STRONGLY suggested in literature that it does
    activate fibrinolysis. Since no docs or researchers will touch using tPA or
    Urokinase (drugs that activate fibrinolysis in vivo) in CFIDS patients,
    Bromelain seems to be just the ticket. And it is all natural. Many anecdotal
    responses that I have received, confirm that it helps in patients that have
    elevated inhibitors of fibrinolysis - Lp(a) or PAI-1 - as their underlying
    genetic defect. So, Bromelain helps increase fibrinolysis. As for it
    inhibiting platelets or the coagulation cascade, nothing in literature
    suggests that it does such. I may have overlooked something, so if anyone
    has a reference to the contrary, please send it to me. Thanks.

    [David] As for minocin, I have no knowledge of its properties or use, except
    that others report good results using it.

    [David] As for Bromelain enhancing antibiotic adsorption, I believe it would
    work like this. By increasing fibrinolysis, any fibrin on the endothelial
    cell (EC) surfaces (the cells that line the capillaries or very small blood
    vessels in the body) would be mostly removed, and that would make the
    antibiotics more effective at getting into the infected EC. Since Bromelain
    is a digestive aid, then more might be absorbed through the GI track as
    another possibility.

    [David] As for a time line for therapeutic agents, we just posted one on our
    web site Friday. It uses heparin for 6 months, adds Bromelain at the
    beginning for 4-6 months for patients that have a increased Lp(a) or PAI-1.
    The time line starts with Transfer Factor after 30 days of heparin for 2-3
    months. Also, antibiotics are started after 30 days of heparin. Using
    heparin for 30 days first (plus bromelain if indicated), gives the body time
    to shut down the coagulation mechanism during the first 30 days and allow
    the fibrinolytic system to clean up part of the fibrin deposition on the EC
    surfaces. This makes the Transfer Factor (TF) and antibiotic use MUCH more
    effective. The patient continues to use heparin for another 2 months, just
    in case. If there are still a few pathogens left after these therapies, they
    will attempt to reactivate the coagulation cascade again, to generate
    Soluble Fibrin &/or fibrin deposition. So by continuing heparin, this will
    prevent cascade reactivation and the immune system will be able to clean up
    the remaining pathogens. From information given to me by patients on this
    new TF, I think we NOW have a treatment protocol that will get patients ALL
    the way back to good health. This was a long winded answer, but the question
    was a good one to answer and gives much of the information about these

    [Bob R.]Time Frame of Treatment
    David, I have been on Lovenox 30 mg for almost 4 months. I received an
    dramatic improvement in IBS symptoms, brain fog improved, fatigue improved
    somewhat however nothing dramatic. Two weeks ago I switched over to standard
    heparin and have started to feel a little better. In short , if possible at
    this point, have you had any experience with patients recovering very slowly
    for lets say a year time period. Or do you notice immediate improvement with
    your patients over a very short time frame?

    [David] I BELIEVE that most (>80%, if not ALL) CFIDS patients have an
    underlying infective pathogen (HHV6, CMV, Mycoplasma, Chlamydia pneumonia,
    etc, or a combination of several of these pathogens). Anticoagulants stops
    the coagulation component but does nothing against the underlying pathogen.
    Thus the need for antibiotics, antivirals, Transfer Factor, etc. You need
    BOTH heparin and some treatment against the pathogens. That's why patients
    on heparin ONLY get about 50-70% well and not 100%.< /P>

    [Fluffy]Could food sensitivity of ME/CFIDS people be related to coagulated
    blood ?
    ME/CFIDS are prone to food sensitivity. Calcium is suppose to promote blood
    coagulation so foods like milk, cheese may seem like they could promote
    blood coagulation and have negative consequences for people with coagulation
    problems. Are there any foods which seem to promote blood coagulation ?
    Please also include anecdotal and personal opinions.

    [David] Most of the peripheral problems of the CFID patients (HPA axis,
    headaches, brain fog, IBS, and allergies) are caused by poor blood flow due
    to thick blood (hyper viscous blood). When heparin is used to "thin out the
    blood", this decreases the high blood viscosity by shutting down Soluble
    Fibrin Monomer generation. When viscosity returns to normal, these
    peripheral problems lessen or go away completely. We have seen these allergy
    problems (complete with increased eosinophils on blood smears) from our
    early days of infertility testing 7 years ago. The allergies decreased
    significantly in these patients as they use heparin throughout their
    successful pregnancies. (To date, we have already had over 400 successful
    first time deliveries of normal healthy children in previously infertile

    [Kru Heller]What other non prescription treatments can be used for treating
    thick blood.
    Aspirin and Bromelain were mentioned above. I have also heard of the use of
    Vit. E, Garlic, Pycnogenol and Ginko. What amounts should be used? and how

    [David] Remember the ACE of Hearts! Use Beta Carotine (15mg or 25000 IU) at
    NIGHT time,1gm Vit C am & pm, and 400IU Vit E pm (A,C,E for a healthy heart)
    . 60 mg Ginko am & pm, and Glucosamine (500mg)/Chondroitin (400mg) am & pm
    and 81mg ASA at night. The Ginko & Glucosamine/Chondroitin have very mild
    anticoagulant effects as well as aspirin as an antiplatelet. Since these are
    VERY mild in their anticoagulant effect, it would take many months to notice
    any improvement in CFIDS as an anticoagulant using these. That is why I
    strongly recommend the heparin protocol for immediate therapy. The
    B-Carotine increases tPA release from ECs over a 12 hour period, so take at
    night when PAI-1 routinely goes up at night. Everyone has an opinion on
    supplements. All I can say is to find the right combination for you.

    [Sean L]Different blood thinners
    Dear Mr. Berg, When you use heparin to treat CFIDS, do you think it is
    purely its blood thinning properties that help, or are it's other properties
    (such as it's antiviral properties) part of the picture. I ask because when
    I talk to people who have tried different blood thinners they seem get quite
    different reactions to each. Heparin seems to get the best response,
    Coumadin the weakest and Lovenox somewhere in between. Thank you for all
    your hard work in this area. Best regards, Sean (Lovenox 30mg/day for 3
    months, slight +'ve response, soon to switch to heparin to see if there is a
    difference in response).

    [David] Coumadin is only an anticoagulant. It works by decreasing Factors
    II, VII, IX & X and Protein C and Protein S in the blood. The negative about
    coumadin is that any green foods that contain Vit K counteracts the coumadin
    effect, so you have to be very careful about diet, even if you are on low
    dose coumadin(<2.5mg/day). Heparin is an anticoagulant (anti Factor X and
    II), anti-inflammatory, antiplatelet, vasodilator, increases NO production
    and other beneficial side effects. It is normally occurring on the surface
    of ECs as heparans or heparan sulfate. It is a large molecule and the
    heparin solutions contain many different sizes, from low molecular weights
    of 2000-10,000 to high molecular weights up to 25,000. There are two sources
    for heparin: bovine and porcine. Porcine is less allergenic and the
    recommended type. Low molecular weight heparins (LMWH), such as Lovenox, is
    made up of heparins form 2000-9000 size (frequently around 4-6000 size). I
    like the regular heparin because it is inexpensive compared to Lovenox and
    seems to work the best.

    [David] There is hope for 2001 to get rid of the needle when an oral heparin
    from Emisphere Technologies will be available. I've asked about
    compassionate use for 2000, but Emisphere will not release any until the
    current Phase III trials are finished and the product is approved by the
    FDA. Our work on this technology over the last 2 years indicates that the
    product really does work!!!

    [David] Anticoagulants still do not address the problem of THE UNDERLYING
    PATHOGENS (HHV6) !!!.

    [Sean L]Plavix
    Recently Prof. Al Cocchetto told me that some GWS sufferers where doing well
    on a potent new platelet activation inhibtor called Plavix. Do you have any
    opinions on the use of this drug for CFIDS/FMS/GWS? Best regards, Sean.

    [David] YES. Most of the GWI patients have platelet activation from sources
    other than infection. So these patients react well to Plavix. CFS patients
    have infected bone marrows, so ASA or Plavix doesn't solve this type of
    activation. (See Fluffy's question for an extended answer)

    [Kuby]Sed Rates
    How often do you find an Myalgic Encephalopathy patient with a sed rate
    below 3 who does not have a coagulaton problem and how often does a patient
    with a sed rate of above 5 encounter coagulation?

    [David] We are writing a new journal article addressing the Normal Range of
    Sed Rates (ESRs). <5 test values are indicative of a hypercoagulable state.
    The only time this is not true is a cancer called Multiple Myeloma where
    there is a lot of extra protein produced by the cancer cells. In either
    case, because of the Soluble Fibrin or extra proteins, the RBCs cannot
    settle out of the plasma and thus you have rates of 0-4. The lower the Sed
    Rate, the more SFM and the more hypercoagulable the patient is !.

    [KenL] Whey - an Alternative to Transfer Factor?
    Non-denatured wheys, like Immunopro, appear to function in a manner similar
    to Transfer factor - but is significantly cheaper. Do you have any comments
    or have you investigated this type of product?

    [David] Both are from Cow's Milk. Both are extracts from the milk. Both have
    "flu like symptoms" / Herxheimer reactions reported at the start of use. It
    is an interesting concept and worthy of study. But I do not have knowledge
    to clearly answer this question at this time.

    [DebbieSinKC] new protocol time lines
    i don't understand the time lines - is it saying transfer factor for only 3

    [David] We will change our chart to DAYS on the time line instead of MONTHS
    to make it clearer. Thanks for the comment. {Editor note: Already done}

    [karen]:If blood work results from a "standard work-up " are normal, can?you
    still justify ordering the ISAC panel?l.
    I am very interested in getting the Isac panel but my doctors hesitate
    because they say there is no indication of blood abnormality in standard lab
    work that would justify persuing this avenue. Could standard work up be
    normal and ISAC panel still be positive. If so, could you explain this so
    that I could refer my doctor to your explanation? Are there patterns in
    normal blood work that correlate with positive ISAC oanel/ If so, what are
    [karen]:If my doctor ordered a hyperocagulability panel from another lab,
    would this have to be duplicated at Hemex to get the
    My physcian was somewhat interested in the earlier information I brought to
    him on your work and wrote out a script for a hypercoagulability profile but
    did not specify Hemex or Isac panel. I did not get the test done because I
    suspect I need the specific Hemex tests but I have not yet discussed this
    with him. Can you comment on these issues in a way that will help me
    communicate with and educate my doctor to be sure Im getting a good
    evaluation regarding usefulness and specificity of tests? Im sick and ndot
    much of a biologist so this would be very helpful to me and probably to
    [David] Good questions and ones that I have not answered before. "Standard
    coagulation workup" would NOT show any abnormalities unless the aPTT was
    BELOW the normal range, which indicates a hypercoag condition, but docs are
    not taught this information. The ISAC panel is like 10 - 20 times as
    sensitive as the standard screening tests.

    [David] Most laboratories report a normal range for Fibrinogen of 200-400 or
    higher. The real range should be 200-300. Ours goes up to 315mg/dl. Most
    labs don't want to deal with minor elevations in results, so they increase
    the acceptable range a little. That is why patients with activated coag
    systems have minor fibrinogen elevations which are very significant to us
    but not to the physicians who routinely see higher normal ranges. The
    Prothrombin Fragment 1+2 test indicates that thrombin has been generated
    when this test is increased. This excess thrombin should be removed by
    AntiThrombin, which will give increased T/AT Complexes. There are probably
    12 labs around the country that can do these two tests, so they would not be
    included in the standard screening. The Soluble Fibrin Monomer (SFM) test
    indicates that the thrombin has converted fibrinogen to SFM when this test
    goes up. SFM is the culprit for FIBRIN DEPOSITION and increasing BLOOD
    VISCOSITY. There are probably only 5 labs around the country that can do
    this assay. As for the Platelet Activation test, this is our proprietary
    assay. We have learned so much from using this assay. If time permits later
    this year, we will submit our findings and methodology to a peer reviewed
    lab journal for publication.

    [David] As to the hypercoag panel or Hereditary Thrombosis Risk Panel
    (HTRP), there are several labs that offer the routine tests in these panels.
    Certainly Antithrombin III (AT), Protein C, Protein S, APC Resistance can be
    done elsewhere. You should always ask for the "ACTIVITY" assay of these
    proteins. Do not let the lab substitute the "ANTIGEN" assay as it is not as
    sensitive as the activity assays. Remember that <50% of the patient defects
    are in this group (HEMEX 1999 stats = 47% in 300+ patients). Homocysteine
    is run routinely in many labs. The other 3 assays are more specialized.
    Factor II level or the Prothrombin Gene Mutation is rarely performed but
    positive in about 20-25% of patients. Lp(a) and PAI-1 defects have been
    found in 53% of our 1999 patient data base. These tests would be performed
    in maybe 12 labs around the country. So, all in all, send your blood to
    laboratories that specialize in this type of testing. Our technologists do
    these assays daily and are very competent in what they do, instead of a tech
    that might run these assays once a week or month in other labatories.

    [Patti]:Started heparin 1 1/2 weeks ago.
    So far I haven't noticed any benefit from heparin (except warm toes :). I
    have had reallyl bad headaches. Could the headaches be related to the
    heparin? Also - I have really high PAI levels but allergic to bromelain and
    garlic. Would niacin be an effective way to reduce PAI? Also - do different
    labs have different norms for fibrinogen levels? I saw a result from a
    different lab that said a fibrinogen level of 400 was within "normal" range?
    [David] See my previous answer on fibrinogens. High PAI or Lp(a) patients
    are the hardest to treat. If you can't use bromelain, then niacin may be the
    next choice. Niacin is hard on the liver. Consult with your physician on
    this. There is a time release formula that is less toxic and hard on the
    body. I tried niacin myself, but I couldn't handle the vasodilitation
    (flushing effect). Give yourself time on the heparin. It takes much longer
    to see beneficial effects when a patient has a high PAI-1 or Lp(a),
    sometimes 2-3 months.

    [Patricia]:Blood Tests
    Dr.Berg Thank you for joining us today. Are there any blood tests you would
    reccommend to our Drs. for us to have in conjunction with Hemex's blood
    [Patricia]:EBV & or HHV6a,b
    Have you noticed patients with high titers or counts with EBV reactivation
    and or HHV6a or b ?
    [David] With the time line that we have proposed, knowing that one is
    positive for CMV, EBV, or HHV6 may be academic. It may cost less to go
    through the therapy of TF and antibiotics than getting these viral test
    performed. I do not know the cost or time to run these tests. Personally, I
    would want to know the data, so I would get tested. It is an individual

    [Kru]:I'm interested in sub groups of CFS
    Are you noticing anything about sub groups or sub sets of people that have
    CFS in relation to when blood thining works and when it doesn't? Or anything
    else about sub sets for that matter.
    [David] The two subgroups that we see are the genetic defects in Thrombin
    regulation (THROMBOPHILIA) or Fibrinolysis regulation (HYPOFIBRINOLYSIS).
    HYPOFIB patients are definitely harder to treat, since the process to clean
    up the vessels is inhibited by high values of Lp(a) or PAI-1. It may take
    2-3 months for these patients compared to 2-3 weeks for thrombophilia
    patients to get to equivalent points in relief.

    [Patti]:Injection questions
    I ice my injection sites, but sometimes I get large bruises (2-3 inches in
    diameter) and other times I get small ones (~1/2 inch). Is there anything to
    be worried about with the large bruises? The injection sites on my stomach
    look much worse than the ones on my leg (very red), does this mean anything?
    How long should I wait until I "revisit" and area for injection? Can the top
    side of the leg be used for injection? About stomach injections, should you
    go above the waist AND below? How high above the waist? What can you do to
    make bruises go away faster?
    [David] I don't have any good answer to these questions. Beth, our long term
    patient, has much experience on this. Contact her at pbdrechsel@m....
    Beth's husband asked me about UBS! "What?" I asked. He responded - "the Ugly
    Belly Syndrome" !!!!I We all laughed. This is a small price for improved
    health. I am looking forward to 2001 when Emisphere has oral heparin
    available, because it will allow scientific study whereas today we don't
    have much. If you give heparin as an injection, it will bruise. What can we
    use as a PLACEBO for controlled crossover studies? The oral heparin will
    allow these crossover studies where the patient will not know if it is
    heparin or placebo. WE NEED THESE SCIENTIFIC STUDIES."

    [Ruth]:dosage requirements
    Why does your suggested protocol have a 30mg Lov. morning shot and a 15mg
    evening shot. Are you stating that the half-life of Lovenox is up to 24 hrs?
    Or, is it thought that less dosage is needed during sleep intervals?
    [David] LMW Heparin dosing is based on a body height & weight calculation.
    If the person is average height & weight, then 30 mg/day in the AM is a good
    prophylaxis level. If the person is over weight moderately or more, then a
    second dose at 15 mg given at night may be needed for the extra body weight.
    Heparin is a fat soluble product and a full dose may not make it into the
    blood stream if there is a lot of adipose tissue. Thus a second reduced dose
    injection for some patients.

    [James Roberton]:Are you familiar with the work of Professor Kakkar of the
    Thrombosis Research Unit in Europe?
    Are you aware of any other research correlating with your findings?
    Professor Kakkar's team research on PWME has found poor blood circulation,
    reducing oxygen supply to the brain and muscles. The production of the
    normal blood thinning enzyme TPA is also reduced, as well of that of certain
    blood clotting proteins. Prof Kakkar advocates thermo regulatory
    hydrotherapy (TRHT), cold baths to the rest of us, as a treatment in CFS/ME
    to improve circulation and stimulate the endocrine and immune systems. What
    is your opinion on this?
    [David] Last summer, Prof Kakkar called me from England and we chatted for
    some time. He told me that we had our manuscript accepted just before they
    were to submit theirs. Such is science. Anyway, there are only a handful of
    laboratories around the world that have capabilities to run these assays
    properly. His is one of them. Regarding his TRHT (cold baths) therapy, I am
    not familiar with the protocol to improve circulation as you state. It still
    seems to me that if a patient wants to improve their health quickly, rather
    than slowly over time, prescribed anticoagulants is the fastest way to
    improve it, not over the counter items or cold treatment.

    [DebbieSinKC]:blood thinning and TF
    should those of us who started the TF (formula 560) without the blood
    thinning stop now, and do a month of bromelain? this is all so confusing . .
    . i have so many questions . . .
    [David] NO. Follow your physician's instructions. Our recommended protocols
    are just that - recommendations. Your physician has responsibility for you
    as his patient, not us. In regards to Dr. Brewer's protocol, don't change
    it! Follow it. If he wants to modify it, it is his prerogative to do such,
    not yours or mine. We (HEMEX) are consultants to the patient's physician.

    [JamesD.]:Coagulable State Fluctuations
    I notice my blood becomes thicker, I get dizzy and faint more easily, bruise
    all over, and can't have blood drawn when I seem to be in an activated state
    of infection or partial, short relapse condition. Do you see the symptoms of
    coagulable blood fluctuate with infectious activities in many of your
    patients. What does such a fluctuation imply?
    [David] Active infections activate the coagulation mechanism. These relapses
    are the pathogen's way of creating an environment that the bug wants,
    usually an anaerobic environment. So it is natural to have increased SFM
    which increases blood viscosity and makes it difficult to draw a blood
    sample. Active infections also cause inflammatory reactions, which again
    triggers the coagulation mechanism. As the active infection becomes more
    dormant, there should be less SFM in the plasma. We have seen this repeated
    cycle in patients many times, from relapses several days apart to several
    weeks apart. It all depends on what the underlying pathogen is or are if
    there are multiple infections. I believe that HHV6 is the biggest player and
    should be treated accordingly.

    [Annie]:Autonomic Nervous System and hypercoagulable state
    Is there any connection between multiple systems dysautonomia and
    hypercoagulable blood? Thank you.
    [David] In patients where there is no demonstrable pathogen, there is still
    a trigger to activate the coagulation mechanism, whether it is stress,
    trauma, accident, surgery, pregnancy, undetected pathogen, etc. The BASIC
    PREMISE is that the patient has a genetic protein defect !. People develop
    blood clots for many unknown reasons. We still have much to learn and this
    is a multi-system interactive process.

    [NancyMcFadden]:th1 (cell mediated /th2 (humoral) imbalance, relation to
    Last year i was tested by immunosciences lab, and my (th2) humoral immunity
    was definitely dominant over my cell mediated immunity (th1). in addition,
    my helper/ suppressor ratio (of cd4 cells) was high, which shows an immune
    activation state. have you found hypercoagulation seems to correspond to a
    th1/th2 imbalance and to a high helper/suppressor ratio? I know Nancy Klimas
    spoke about th1/th2 imbalance being common in cfids, last year in
    Connecticut, I heard it on tape.... if this correlates, then my doctor will
    be easily convinced to run these tests, so i appreciate your answer. Thanks!
    Nancy McFadden, Nashville TN
    [David] The problem with HHV6 as pointed out by Mr. Regush is that this
    virus is capable of altering many systems, including the immune system. I
    have had many patients reiterate the same comments as your question. If I
    were the patient, I would ask my physician to test me for both a pathogen
    and coag screens, including HHV6, Mycoplasma, Chlamydia, ISAC, HTRP and the
    B2GPI panels. Once I knew what the defects are and the triggering pathogens,
    treat all of it. The coag problem is only half of the problem.

    [DebbieSinKC]:treating pets
    any ideas on how much bromelain or other blood thinners (NO ASPIRIN - i
    think it's poison to them) for our cats/dogs/birds. then how much TF? maybe
    i should just print off the HEMEX human protocol and ask the vet if it's
    alright to dose them, and how much . . . i don't want to take up limited
    time with this LOL - but in case many others are interested, thought i'd
    ask. we have 3 cats, one (maybe two) i'm sure has something similar to
    cfs/me/fm. i've never mentioned this to vet (think she might think i'm
    nuts), the cats always pass annual check ups. only way i can think of to get
    this stuff down a cat is mixing it in baby food.
    [David] I know that pets can be effected by these pathogens and need to be
    treated. Your question is a good question, but I am not a VET, and I have no
    knowledge of small animal systems as a vet will. Ask your vet to look at
    these materials and then ask for a recommendation.

    There are an ADDITIONAL 4-6 more answers coming... tomorrow
    [David] I trust that the combined information from last week and this week
    makes sense and is logical. The coag Paradigm Shift is that we should now
    treat patients with fibrin deposition as we treat patients who have had a
    blood clot. The new protocol on our web site (www.hemex.com) [which will be
    modified tomorrow], should help most CFIDS patients get back to almost
    complete health for under $3000, including lab testing, TF, antibiotics and
    physician charges. There will always be the coag protein defect in the
    patients, but once the infection is treated completely, then the protein
    defect can be monitored over time. When a relapse occurs, use heparin to
    control the infection quickly before becoming a CFIDS patients again.
    Remember, the longer one has been ill, the longer it may take to get rid of
    the HHV6.

    To the audience, please accept my apology for the technical snafu on Sunday.
    I would like to participate again in the Town Hall if you have more
    questions, and I promise, no technical snafus.

    TO BETTER HEALTH. David Berg

    Okay, who got all the way through that?? I'd have cleaned it up, but I'd be here all night.:)

    Hugs to all,

  2. mommysisland

    mommysisland New Member

  3. suttles

    suttles New Member

  4. Johnniebear

    Johnniebear New Member

    I might add that Dave Berg's thinking has changed some since he gave this interview & I think he now prefers lumbrokinase or nattokinase over the Bromelain.


    ANNXYZ New Member

    for this excellent info!