I found in my notes this townhall/interview that I did with Dave Berg before he retired.

July 16th, 2000


[BERG] Greetings to all and thanks to KEN for asking me to return to the TOWNHALL. Before we get to specific questions, I want to update everyone with new info about coagulation that I garnered at the Scientific Sub Committees (SSC) Meeting (International Society Thrombosis & Hemostasis-ISTH) in Maastricht, Netherlands last month. The more we learn about coag, the more our model stands up and appears to be correct. I even spoke to Prof Vermylen (editor of the ISTH journal 1993-1999) about his model of “Antibody Mediated Thrombosis” (published in 1997) and ask whether his model could apply to Fibrin Deposition as well as a blood clot. After several minutes of silence, he said that it could-yes indeed. He hadn’t thought about that concept before, only that of a full blown clot. I thanked him for his validation.

[BERG] A question that I have always wondered about was “Why don’t CFIDS patients get blood clots routinely?” The answer came from a lecture about new findings on coagulation Factor XIII (thirteen). XIII cross links Soluble Fibrin into INSOLUBLE FIBRIN STRANDS. [The fibrin strands are what hold a scab together after you injure yourself. The red color of the scab is due to the trapped RED CELLS in the scab.] A high level of SFM in the blood is only one SMALL step away from a blood clot. The answer lies in the amount of thrombin needed to activate XIII (one chain) to its active two chain form, XIIIa, which is the active enzyme that forms insoluble fibrin. You need a “THROMBIN BURST” to activate XIII to XIIIa. When there is continuous ongoing LOW LEVEL THROMBIN GENERATION, you generate a lot of SFM, which becomes “Fibrin Deposition”, not a blood clot. Thus, the basis of our model is further substantiated.

[BERG] POP QUIZ TIME ! Did you understand all that technical stuff????? This answer makes it even MORE IMPERATIVE that CFIDS patients learn what their underlying coag protein defect IS. Eventually, all of us will have an accident, trauma or elective surgery. When you have a major wound to the body, you WILL have a THROMBIN BURST. At that time, it will be very important that your physician give you something to prevent a blood clot !!! (low dose heparin or Coumadin). This is a statement to CFIDS patients to be cautious when you need to be.

[Fluffy]What is the significance of CD62P + ADP ?

My test results are as follows for Platelet Activation by Flow: CD62P is 61 which you says indicates an underlying infection along with Platelet Activation Index which is 3+. But CD62P+ADP is 6 which is low. DOes this mean an inactive infection or what ? Could you clarify what this means ?


[BERG] CD62P is a platelet surface marker for a glycoprotein that is normally inside the platelet. When is it expressed on the surface, it means that the platelet is activated. Normal people have values 8, 12, 15%. Because we use 2 Standard Deviation, the Normal Range goes to 27%. If a platelet is already activated (61%), there is LESS to activate: CD62P + ADP = 6 (low). Thus, the3+ Index. My values are 14% & 62%, ie, my platelets have little activation initially, and when you add ADP, they activate a lot (62%), which = NORMAL.

[BERG] Now, there is more to the story than this, HHV6, according to the patent held by the US government, states that HHV6 infects endothelial cells (EC), megakareocytes (platelet producing cells) and neurons (brain). The Platelet Activation Index (PA) test gives us much information. CD62P values that are 25-40%, with normal activation, indicates that the platelets are coming out of the bone marrow activated from the infection. This is a latent infection. When both the CD62P and the PA Index are Positive, this indicates an active infection. I have missed interpreting values at times because both values are normal in patients. I believe that this is because the bone marrow is NOT infected at that time, so around 20% of CFIDS patients may have normal PA values. When patients who have normal or only elevated CD62P values are treated, usually the PA index becomes very positive, which is like the Herxheimer reaction that Ken talks about. It shows activation of the PATHOGEN in reaction to the therapy to kill the pathogen. I hope this answers the question.

[bink]Can diet have a postitive effect on clearing coagulation abnormalities? The “alternative” specialist believes one can thin their blood by eating a particular diet. I believe one based on veganism. Can diet have a postitive effect on coagulation?


[BERG] YES, BUT…..Diet is a very slow process to anticoagulate a patient. Instead of relief in a matter of a few days, dietary changes may take MONTHS to achieve the same effect. If a patient has IBD (irritable bowel disease) from the illness, diet may not do anything, since the IBD may not allow for proper adsorption of nutrients from the gut. The IBD is primarily caused by thick blood (increased SFM), with the decreased blood flow not providing the proper nourishment to the gut itself. ISCHEMIA is defined as lack of oxygen and nutrients to a given area. If the bowel itself becomes ischemic, it will sluff it contents. So, you end up with IBD from increased SFM. In this case, only exogenous anticoagulation will help in a timely manner. A healthy diet is always something desirable for all. Just think when you have had a delicious heavy meal with lots of fats and you can feel those arteries clogging up from the chylomicra floating in the plasma. AH, those good old days !

[BERG] Antibiotics kill the good bacteria in the gut that make Vit K for us. Therefore, antibiotic therapy can produce a mild anticoagulated state, similar to using low dose Coumadin. But many patients have reported that Coumadin does not work very well on them, so they go back to low dose heparin.

[James Roberton]Chiari, cervical spinal stenosis and thick blood

Do you believe that some people are unnecessarily having surgery to relieve symptoms that are actually the result of thick blood and swelling of the CNS? Is there any evidence to support this idea?


[BERG] This question is a difficult question to answer: the chicken and the egg question. If the blood viscosity goes up from the increased SFM, it is possible to cause brain swelling. The only way to answer this question would be to take a study group and do surgery on half and give heparin to the other half and compare the results. My personal thinking is I would rather try the heparin approach first, and if it did not solve the problem, then consider the surgical intervention.

[Cindi Anderson]SED Rate Definition

When you talk about low SED rates? Are you speaking of them measured as ESR?


[BERG] The ESR (erythrocyte sedimentation rate – red blood cell sed rate) is called SED RATE for short. We are close to having enough data to publish that the normal range for SED RATES should start above 3 or 4. Values below this are correlated with high SFM values. As the Soluble Fibrin Monomer (SFM) goes up in the plasma, these molecules form dimers (2 stuck together). This physically blocks the RBCs from settling out of the plasma, thus a low sed rate. The only other clinical condition to demonstrate low values involves paraproteins in the plasma such as in a cancer patient.

[Cindi Anderson]Influences on testing for Coagulation

I have been trying to get an answer to this question from your clinic. What medications would make the results from your tests not valid? For example, I was taking Niacin to reduce Lp(a). Would this affect the hypercoagulation tests and if so how long should I not take the Niacin before taking the tests? What about antibiotics, gamma globulin, Catapres. These are things I take; I think a general answer covering all types of medications would be useful to people.


[BERG] The ISAC panel answers the question “what is my current state of activation of the coagulation system”. There is really only one therapy that can give erroneous answers, and that is an IV of 500 mls or more prior to having the blood drawn for the testing. If a patient has any type of IV within 5 days of the blood draw, this can result in negative or normal answers, which may not be representative of the patient. Aspirin, in high doses, might lessen the platelet activation, but if there is an HHV6 infection, the CD62P should still be positive. My suggestion is to continue with what you are taking now, other than an IV or aspirin, because we want to know how well those current medications are working or not working. We also use the ISAC panel as repeat testing one month or so on heparin to see the beneficial changes it has. This also answers the question “is this enough heparin or not?”. We use the one month testing to adjust therapy in most patients, as well as looking for the reactivation of the pathogen(s) [herxheimer reaction] in the patient. Occasionally, the physician will order the ISAC late in therapy to look for complete normalization of the test values.

[BERG] As for the HTRP (Hereditary Thrombosis Risk Panel – risk factors), most of these protein levels do NOT change much during life. They are genetically controlled. So as long as your physician knows what you are taking at the time of the blood draw, these values can easily be interpreted. If you know you have a high Lp(a), for example, stay on the niacin and see what the value really is (is the therapy really working?). As for Bromelain, this aids in the process of cleaning up the blood vessels, just as heparin aids in shutting down the SFM generation. Neither effect the protein levels. They are exogenous components.

[BERG] As for the positivity we see in the ISAC panel, we just submitted an abstract for the AACFS meeting next January, in Seattle, where we looked at 400+ patient results. 79% of the patients had positive (2 or more tests) ISAC panel results. Another 19% had one test positive. This equals 98% positivity in patients. When analyzing the data further, I have come to the conclusion that as the pathogen(s) gets a large, comfortable area which is infected with lots of fibrin deposition, the less active the pathogen needs to be. Thus, in patients who have been ill for more than 10 years or so, the less likely they will test positive for 2 or more tests. HOWEVER, when given heparin and/or Transfer Factor and/or antibiotics, as the fibrin layer is cleaned up, these pathogen(s) reactivate the coag system in an effort to make fibrin again. This is why on repeat ISAC testing at one month, we see MORE positivity than we may have seen on baseline testing. In regards to the HTRP panel, around 75% of all patients have a demonstrable defect of risk factor in this panel of 8 proteins. I think it highly likely that if we tested for 4-8 minor regulatory proteins, we would find a defect in over 90% of all patients. Part of this conclusion isreached because in patients with no defect found, there is still an increase in Protein C, Protein S &/or AntiThrombin in an effort to shut down the hypercoagulable state ! This panel also gives us much more information than just protein defects.

[JJWalker]Hormones and Coagulation

How would the lack of particular homones that patients with M.E. are known to be absent, such as ADH and or Oxytocin, effect blood coagulation.


[BERG] I can only answer this question as a general statement. If the blood viscosity goes way up (very low sed rate), then the blood flow throughout the body is greatly decreased. This includes blood flow through the endocrine glands from which the hormones are produced, such as all the publications on the HPA axis and decreased hormone levels. If you were to study a group of patients with low HPA hormone levels baseline, then give them 30 days of heparin and retest those patients, I bet that the hormone levels would normalize. The exception to this would be that, if there is reduced blood flow for a very long time to an endocrine gland, the gland itself might be in failure. This would cause continued low hormone levels for a long time.
[BERG] Speaking of thick blood, there are many studies about reduced BLOOD VOLUME. I think we finally have an answer to this also. In looking at microscopic blood samples, we have now seen actual SFM fibers precipitate out on the slides. These are single strands, not cross linked strands as in a clot. This is also what the model predicts. Since this is correlated with high SFM levels in the plasma on these patients, we can say that the levels on the slide are high also. The additional effect seen on the slide is the remarkedly high ROULEUX FORMATION of the RBCs (red blood cells). This looks like a stack of coins, if you can imagine such. Since rouleux formation is NOT normal, it is possible to conclude that the increased SFM is responsible for holding the RBCs together in chains of 3-10 cells long. Since this is what is observed at 1000 power and 8000 power under the microscope, then it is possible that this is happening in the body. If so, then the oxygen delivery will be greatly reduced because the cells stick together and oxygen cannot escape, ie, hypotention. If you are looking at blood volume based on RBCs, then a group of RBCs stuck together would act as one cell, not 3, 8 or 10, etc. Thus you could conclude that there is a low blood volume. This will be interesting experiment to repeat a patient with “low blood volume” after a short period of time on heparin. The blood volume would probably correct, since the cells would not be stuck together by the SFM.

[BERG] I don’t want to appear as a know-it-all, but there are logical answers for most of the problems seen in CFIDS symptoms. We just have to look for answers to these complex questions, and most answers come from RHEOLOGY (Blood Flow) and are base on the laws of physics. So if you increase the viscosity (SFM) you create different results in CFIDS patients than seen in people with normal blood viscosity. This may also be involved in the question of alkaline blood pH in patients verses and normal acidic values found in healthy people.

[BERG] I have to go back to the statement I made 2 years ago. 30% of the proteins in the blood plasma (liquid portion) are involved in the regulation and maintenance of the coagulation system. Understanding this, it is no wonder that so many defects can appear if there is a coag problem. And we are all born with about 40 defects in our human genome (which causes us to be different from each other). Thus, around 5% of the population have bleeding defects (hemophilias, von Willebrand disease, XI defects, etc) and 5% have clotting defects, which can lead to chronic illnesses when the coag system is not controlled properly.

[JJWalker]Athletes and overtraining

I read that a doctor at UGA found that many ME patients who were overtraining had coagulation problems. How does overtraining contribute to hypercoagulation and is this a different subset than the rest?

[BERG] I’m sorry, but I cannot answer this question. Overtraining causes what TYPE
of coag problems? I don’t have enough information on this question to answer it.

[Fluffy]How would Bromelaine effect the ISAC test ?

I was taking that and wonder whether any of the test results would be invalid. I did stop taking it about 36 hours before taking the heriditary part of the test.


[BERG] I do not have much knowledge on Bromelain. What I have read in the scientific literature is that it helps with the activation of fibrinolysis, like tPA does. The literature does NOT state how it might activate fibrinolysis, but if there is a chance that it can, then it should be used by patients who have either a high Lp(a) or PAI-1 protein. As to standardization of the various manufactures, this is information I do not have either. I was told by a knowledgable person that one should take 400 mg, 3 times a day, ie, between 1000 and 1500mg a day. If someone has all the conversion factors and knows what is the best dosing, please email me with the information. Thanks.

[BERG] I am pleased to announce that we have had the first 2 patient trails of using tPA in an outpatient IV setting on patients with very high Lp(a) values. The first patient’s comments were that he felt better, the tingling in his hands and legs disappeared and the mental fog dissipated. Not too shabby ! Similar results were seen in the second patient. This is a VERY EXPENSIVE therapy, $1500 for the drug alone. But in patients with high Lp(a) or PAI-1, this may be “just what the doctor ordered”. As we get more experience with this, we will let patients know.


[private] Are there any special considerations for patients who test positive for >parasites, yeast and/or Mycoplasma?? (For example, should any of these be treated before treating coagulation problems)

[BERG] This is a good question to drive home the idea that the PATHOGEN(S) are half of the problem with coag defects being the other half. Whether the underlying problem is HHV6, CMV, EBV, Chlamydia Pneumonia, Mycoplasma, Rikettsia, Lymes Disease, Candida, etc., the pathogens MUST be treated. ALL of these activate the coag mechanism, because it is part of the host defense mechanism. It is when a patient has a regulatory defect that the disease turns into chronic illness. Anticoagulants (heparin & Coumadin) shut down the ability of the pathogen to generate fibrin. So the pathogen is left in a vulnerable state. Thus combined therapies, anticoagulants, antibiotics, antifungals, transfer factor, Ultraviolet blood irradiation, IV peroxide, and perhaps even IV high dose vitamin C therapy, may all have there place. It is up to the clinician to decide the best therapy. My personal experience of seeing positive ISAC values turn negative with TF is the first time I have ever seen anything touch HHV6. Treatment of the pathogens can be concurrent therapy, or anticoagulants can be started first. Using heparin to help clean up the capillaries before therapy makes many of these therapies more effective. I also advocate staying on heparin for 1-2 months after the pathogen therapies is completed because if there are any pathogens left, they cannot generate fibrin with the heparin present. This also gives the body the extra time to wipe out the remaining pathogens naturally.


My 21yr old daughter has had SED rates of 2 and 5 over recent years. Her ISAC panel was all within range, however. The Hereditarty Panel showed a borderline 66 on Protein S activity and a 10.8 for Homocysteine. Is this enough evidence of a hypercoaglable state and need to proceed with your protocol?
[BERG] As stated before, low sed rates indicate a hypercoagulable state at that point in time. Borderline Protein S deficiency is a very real problem. When the body is stressed beyond normal, the Protein S dropps even lower (C4b Binding Protein is the carrier protein and when it increases, it binds up the free Protein S). Homocysteine usually reflects dietary problems. If B12, Folate & B6 doesn’t correct the value, then there are 2 genetic enzyme deficiencies that should be tested. This is a great question in that some patients are borderline on their testing. Does this prove anything??? I suggest that because the low dose heparin therapy is NOT dangerous, give it a try for 4 weeks. If the patient feels better, GREAT. If the patient gets worse, check the ISAC again to see if you have activated the coag system from a pathogen (herxheimer reaction). This is the case in over 90% of the patients. Patients DO NOT react to heparin (less than 1%). Heparin is in all of us and as we age, the loss of the ability to make heparin may be the biggest part of the aging process. Patients who have reactions are usually reactions from the pathogens.

[RUTH]Platelet activation by Flow and chronic, active infection and Lovenox usage

My last test results were:

  • CD62 P was 10
  • CD62 P + ADP 36
  • and Plt Act Index 1+

Is this an active infection state? My need for Lovenox is continuing to diminish and is now down to 15mg a day. Would that indicate active infection to you or would you say that I am better maintaining the chronic DIC? Thank you David for all your work

[BERG] You have pointed out the third possibility with the PA Index, that of a normal CD62P and a Positive Index. This is easy to answer in that we see this type of activation in PEOPLE who have bad coronary or carotid arteries or veins (vericose veins). It is due to a restriction in the size of the vessel which speed up the blood flow through the constriction, just as water speeds up if you put some bolders in the stream and narrow the channel. This is MECHANICAL activation of platelets due to a stenosis. These patients need 81mg of Aspirin daily to minimize this effect.
[BERG] I don’t know if you have had a repeat ISAC or not. If you have children, then vericose veins are a real probability. If you are still concerned about this, call me. Since you are doing much better and the Lovenox doseage is less, that’s GREAT !

[ ]Any further ideas for non-responders

For people who do not respond to well heparin alone and who do not have hypofibrinolysis, do you have any new suggestions beyond adding Tranfer factor, and antibiotics?
[BERG] As I have said in other answers, patients should not have reactions to heparin. It is the pathogens that are causing the reactions. This question sounds like the pathogens are NOT yet identified in the patient. What about parasites or fungal infections. You must get rid of the pathogen to get well.

[BERG] We ARE seeing success in many patients now. Our long term patient, Beth, is probably back to 90% of her original life style. That’s GREAT ! She is an example of hypofibrinolysis and HHV6 and it has taken over 4 months of TF therapy to get rid of the HHV6.

[BERG] In closing, there is some information that I want to share with you about one other protein that fits into this puzzle. Dr Urnovitz Berkeley, CA) has discovered chromosome rearrangement on chromosome 22q11 [*], especially in Gulf War illness. This may also be the basis of chemical sensitivity patient problems. This is the location for the production of Heparin Cofactor II. This is one of 4-8 minor regulatory coagultion proteins involved with control of thrombin generation. Several of the patients tested have had low levels of this protein. [BERG] When thrombin is generated, AntiThrombin (AT) grabs the excess thrombin in the plasma. There are 2 binding sites on the thrombin molecule, exocite I & II. AntiThrombin binds to exocite I on the thrombin molecule forming T/AT complexes. When there is fibrin (SFM) present, thrombin binds to SFM via exocite I and AntiThrombin cannot bind and down regulate the thrombin. Thrombin bound to fibrin remains active for a short period of time, causing more thrombin generation. This is how a blood clot forms quickly (within a few minutes). Heparin Cofactor II binds to exocite II, and thus, it can down regulate thrombin even when it is bound to fibrin (SFM). This is the backup mechanism for AT. So, if there is a defect in chromosome 22q11, this could explain some of the lack of control and excess SFM generation in patients who do not have a demonstrable risk factor in the HTRP.
[BERG] Thanks again to Ken for inviting me back to the TOWNHALL. I continue to give thanks to the good Lord for giving us the ability to solve these “Blood Curdling Mysteries”. Additionally, thanks to all who have sent me literature that you have found pertinent to coag and these disease processes. Your tireless reviews of web sites, literature banks and news is very appreciated. One person just does NOT have the time to gather all this information. At least with your help, I am able to add important findings to the disease model and processes, which gives benefit to all patients. KEEP THOSE CARDS AND LETTERS COMING, FOLKS !!! I am still way behind in answering some email and phone calls. Please be patient or email me again.(D Berg has since retired)