This is from another Townhall meeting that I did with Dave Berg back in 2000. I followed his protocol concurrent with Cecil Jadin’s protocol for pathogens and went into full remission for 11 years. Both Berg and Jadin cites that relapse can happen, but with an ability to reduce the risk.

March 26th, 2000

[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 ). 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 thesis.

[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%.

[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 women.)

[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 often?

[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 mos.?!?!

[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? 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 pursuing 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 panel/ If so, what are they?

[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 others.

[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 of a tech that might run these assays once a week or month in other laboratories.

[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 testing?
[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 choice.

[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 thinning 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. 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 #####. 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 crossoverstudies? 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 coag. 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.

[Nelly]:Rickettsia and hypercoag, the CFIDS missing link ? Infections of the Rickettsia type have an affinity for the endothelium. Could these particular organisms (or close relatives like Coxiella Burnetii) CAUSE the hypercoagulation cascade you are describing ? Can the vicious circle hypercoag/infection be broken or do the people affected need to be on blood thinning medication forever ?

[David] As I have stated in other questions, the underlying infective pathogen(s) must be treated for a good recovery. Any of the organisms can trigger the inflammatory and immune systems, which in turn triggers the coagulation system. Once the pathogen(s) are treated, stay on anticoagulation therapy for another several months to prevent a few organisms from becoming overwhelming again (see question 1 for additional information).

[wanda ]:Common CFS and atypical CFS–differences in hypercoagulability Are you aware of the subsets of CFS and, if so, how do they differ with regard to blood disorder conditions?

[David] Regarding subsets of CFIDS, see question 15 for Thrombophilia or Hypofibrinolysis sub groups. We don’t get much feedback from clinicians in terms of patients, other than they are doing better or basically no change. I would like more information, but we don’t have staff or time to process such information.

[Larry]:Labs, anticoagulation treatment appropriate here? Homocysteine, serum 9.3 UMOL/L (ref 0.0-9.0) Coagulation: Fibrinogen 260 MG/DL (ref
200-400) Protein S, Antigenic 105% (ref 70 or greater) Plasminogen, Functional 104% (ref 70-143) ERS 9 MM/HR (ref 0-15) Coagulatin INR 0.88 (ref .8-1.10) Prothrombin time 9.1 seconds (ref 8.8-11.8( Cardiolipin AB IGM 36 MPL Units (ref 20-80 medium positive) Anti Thrombin, Functional 132% (ref 80-120) Protein C, Antigenic 88% (ref 70 or greater)

[David] I don’t usually discuss patient information, other than to the patient directly. However, these lab data do have several interesting points. See Q 11 for fibrinogen. This reference range is exactly what is discussed in #11. Again, “Activity” assays are better than the “Antigen” assays because you may have a normal “antigen” level (amount of protein) with a not so functioning protein (decreased “activity”). What is missing in this workup is the Factor II level (screening for the Prothrombin Gene mutation), Lp(a), PAI-1 and Heparin Cofactor II levels. Lp(a) and PAI-1 increases (hypofibrinolysis) account for 53% of the defects we found in patients in our 1999 data base. Another concept that is seen in Larry’s labs is that the AntiThrombin is ELEVATED. When there is a genetic defect (none has been demonstrated in Larry at this time), Protein C, Protein S
or AntiThrombin will be increased in these patients as the body is trying to shut down the hypercoagulability due to the defective protein. We have seen this in around 30-40% of our patients that have such a defect and we are submitting a manuscript on this in the near future. So, Larry, get the rest of the testing done by a qualified laboratory.

[Patricia]:Funding Research A question from My Husband & Brother, Have you been helped with funding this besides out of your own personal monies and donations from The National CFIDS Foundation. Have you received any financial help or inqueries from the CDC,NIH and or any part of medical gov’t branches?

[David] The only funding that HEMEX has received for our research has been $4000 from Gail Kansky and her association and $1000 from Dr. David Bell, when we were working on the original prospective studies in early 1999. HEMEX has paid the bills on over $45,000 of work in this research. We have not received any other donations except for less than $ 200.00 from sales of video tapes of previous lectures. There is a VERY REAL NEED for a foundation or such that HEMEX can bill for work done on sick patients that cannot afford to have the lab testing performed. We are not in a financial place that we can do the testing for free. If monies were available, then I know many patients could be tested from the requests that we have received to do free testing. These assays (specific antibodies) are expensive for us to purchase. We have lowered several of the fee schedule prices as we have become more efficient in some assays. But our direct costs are still very high. If anyone knows of such a foundation or grant, please let me know.

[CARLSON] One of our members has a question for Dr. Berg. She is not on-line, so I am asking this for her. She is currently receiving intravenous infusions of gamma globulin about every 3 weeks to one month. I don’t know how many grams she is getting, however. Her question is: would it do her any good to get the coag test since the gamma thins the blood? How long would it affect the blood after it is given? Could she get an accurate result with the coag test under these circumstances?

[David] Gamma Globulin: Patient testing is relevant most of the time, except within 4-5 days of 1 liter of IV saline or solutions which are used at times for therapy. We want to see what the patient is like in a basal state if possible. If the gamma globulin helps in the therapy, then have the coag labs drawn a day or so before the next therapy. This will be the closest to a baseline condition. The ISAC panel is also good for monitoring therapy, especially after 1 month of heparin. We look for the SFM to be in the normal range and the fibrinogen to drop from the first draw. We also look to see if the platelets are showing signs of reactivation. The F1+2 should be going down and the T/ATs should be increasing in the normal range. By looking at 2 data points, we can fine tune therapies if needed.


[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 ( ), 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. My goal in this process of answering these questions was to get information to patients and researchers that is easy to understand. These answers may seem simplistic by design. I do NOT want to understate the COMPLEXITIES of these disease processes. There are numerous interactions that are not understood yet. As Dr. Triplett says: “There are many issues we don’t understand. It’s like a detective story, where people try to piece together the pieces of the puzzle. We’re getting part of the puzzle put together, but we still have a big enough segment that we can’t explain about thrombosis. So the story will continue to evolve, and the answers will become more complex.” Dr. Triplett proposed the model that we have expanded about Thrombophilia or Hypofibrinolysis defects in 1997. I have attempted to give a model that in its simplicity is understandable and logical. Remember that the elephant can be described by many parts. It is dependent on what part is being examined at the time.