Dave Berg Talk #4

Interview with David Berg

David Berg is the Director and Cofounder, with Lois Hill Berg, of HEMEX Laboratories. Along with Dr. Harold Harrison and several clinical collaborators, they have developed the idea of the hypercoagulation/ immune system activation of coagulation theory in chronic diseases, a proposed cause of Chronic Fatigue Syndrome and Fibromyalgia, and have proposed an appropriate treatment that reduces many related symptoms. Mr. Berg has a M.S. degree in clinical pathology and laboratory medicine, and has been in practice for 35 years. HEMEX Laboratories offers testing and consultative services relating to the diagnosis, treatment, and monitoring of hematological, clotting and/or bleeding disorders.

We first became involved with research in chronic illnesses while we were performing re search regarding hypercoagulability – related infertility in women with one of the local infertility specialists here in Phoenix, AZ. We found that a hypercoagulable state, presumably due to a coagulation protein defect, existed in many women who were infertile and/or who had recurrent spontaneous abortions. Our colleague Dr. Couvaras observed that when he put women on low dose heparin in order to maintain pregnancy, some with CFS/FM-like symptoms, pelvic pain, and migraine-like headaches had amelioration of their symptoms. He asked us “Why?” As a result, we performed a retrospective study on 30 of these obstetric patients with chronic illness symptoms, and determined that all had coagulation system activation. As the hypercoagulability was decreased by heparin injections, the chronic illness symptoms diminished. This was the first clue to the connection between coagulation and chronic illnesses. These findings were published as a poster at the 1998 AACFS meeting in Cambridge, MA.

We subsequently refined our test panel for low level activation of coagulation to include Prothrombin fragment 1+2 (F1+2), thrombin/antithrombin complexes (T/AT) and Platelet Activation by Flow Cytometry assays. Thus, the ISAC or Immune System Activation of Coagulation panel consisting of fibrinogen (FIB), soluble fibrin monomer (SFM), F1+2, T/AT, and PA by Flow was born. With our partner and Medical Director, Dr. Harold Harrison and several clinical collaborators, we then designed and conducted a prospective, multi-center, blinded, case control, associative study of non-obstetric CFS/FM patients and controls, with centers in New York, Houston, and Phoenix. When the code was broken, identifying patients and controls, we were able to identify most of the CFS/FM patients based on having two or more positive test results out of the five assays in the ISAC panel. It was the first definitive evidence that, indeed, chronic illnesses have a demonstrable basis in the blood coagulation system. This study was published in the international journal Blood Coagulation & Fibrinolysis, 1999, 10:435-438. In another associative cohort study published in Blood Coagulation & Fibrinolysis, 2000, 11:673-678, we determined that Gulf War illness has similar findings of low level activation of coagulation.

In November, 1999, Dr. Joe Brewer (an Infectious Disease specialist in Kansas City) and I developed a model of pathogen activation of the immune and coagulation systems. The model proposes that the end result of such pathogenmediated activation is increased blood viscosity due to 1) an underlying coagulation regulatory protein defect, and 2) activation of the coagulation system by the pathogen. As the blood viscosity increases, the diminished blood flow creates hypoxia (lack of oxygen) and nutrient deprivation within various areas of the body. This is like trying to start your car in Wisconsin in the winter with 60- weight engine oil. This model explains the multi-organ symptomatology and also explains why the low dose heparin therapy is effective by increasing blood flow as the blood viscosity decreases. Thus, patients gain relief from their symptoms with this therapy.

The model states that coagulation activation generates thrombin, which converts fibrinogen to soluble fibrin monomer (SFM). Soluble fibrin becomes deposited in the micro-circulation (capillaries) as fibrin or fibrinoid-like deposition, blocking oxygen and nutrients transfer to parenchymal tissues. Many pathogens activate the immune system. These include viruses (such as EBV, CMV, HHV6 & others), bacteria (mycoplasma, chlamydia, borrelia, etc), fungi (such as candida), etc. These pathogens are anaerobes, i.e., they live and reproduce in an oxygen deprived cellular matrix or environment. That’s why fibrin deposition becomes important to the survival of the pathogens because it produces decreased oxygen in cells and tissues. One of the biggest challenges to a clinician is to figure out what pathogens are present in the patient, and therefore the most appropriate therapies against these pathogens. The average CFS/FM patient may have anywhere from one to seven pathogens that need eradication.

Positivity of two or more tests in the ISAC panel occurs in more than 80% of all patients tested. However, the longer a patient has been ill (many years), the less activation is needed by the pathogens for survival, and therefore fewer tests may be positive. Someone who has been ill for 10 years or more may only have one test positive in the panel. The ISAC panel also works very well for monitoring anticoagulant therapy between 4-6 weeks after therapy has started. It indicates whether or not there is enough heparin being given to the patient, the overall patient improvement and the reaction of the body to the pathogens, such as a Herxheimer-like reaction (relapse from infections or reactivation of pathogens).

In addition to the pathogens that can activate the immune system, metals (e.g. mercury, lead, aluminum), exogenous toxins, chemicals, allergens, physical trauma, vaccinations, and/or biological warfare agents can also activate the immune system. This may lead to secondary infections, which may also trigger coagulation activation. If the coagulation mechanism does not shut down properly, then there is continued thrombin generation and soluble fibrin formation, resulting in increased blood viscosity and decreased blood flow.

When you look for a genetic basis in this model, one can test for seven different regulatory proteins of the coagulation mechanism plus homocysteine in a panel we call the HTRP (Hereditary Thrombosis Risk Panel). In July 2001, at the International Society of Thrombosis and Hemostasis meeting in Paris, we presented data from a retrospective study of over 400 chronically ill patients, 83% had one or more demonstrable coagulation protein defects. Forty percent of the patients had a thrombophilia defect (decreased protein C, decreased protein S, decreased anti-thrombin, APC resistance/factor V Leiden positivity, or increased prothrombin/prothrombin gene mutation positivity). 39% of the patients have defects in the fibrinolytic system (hypofibrinolysis due to elevated lipoprotein (a) – Lp(a) and/or PAI1-plasminogen activator inhibitor-1. 21% of these patients had a defect in both the thrombophilia and hypofibrinolysis marker groups. This means that not only do they form fibrin easily, but also they are compromised in the ability to clean up the fibrin deposition.

Let’s put this in plain English. When a pathogen(s) gains a foothold, especially in the endothelial cells in the blood vessels (as well as other cells), the bug(s) can be protected by the coagulation mechanism of fibrin deposition on top of the infected cells. Half of the patients form fibrin very fast, becoming fibrin(oid) deposition. Half of the patients have an inability to clean up the fibrin, and therefore continue to have oxygen and nutrient starvation of tissues for a long time. For example, if the fibrin deposition occurs in a muscle, it says “ouch,” and you have a tender point as in Fibromyalgia. If it is in the placenta, the placenta is compromised by fibrin deposition and the baby aborts. As blood viscosity increases and blood flow is reduced throughout the body, the patient becomes hypo-this and hypo-that, such as hypothyroid, hypo-HPAaxis, hypo-estrogen, etc. The use of low dose heparin restores blood flow throughout the body and hormones from the endocrine system tend to normalize. Thus, the blood flow issue becomes one of the most important issues of chronic illnesses. Unfortunately there is no easy test to measure blood flow, only the effects of blood flow.

If you consider the movie “Braveheart” (1000 AD) and you went to battle and were wounded, you probably would have bled to death unless you clotted fast. By clotting fast, you saved your own life and passed on this new trait to your children. This hypothesis may explain how these coagulation defects were genetically selected during the last 2000 years in Europe. Life expectancy back then was only 30-40 years. With our life expectancy now of 80+ years, these traits are no longer beneficial, but rather deleterious to our health. It was the Spanish, French, British, Germans, Italians, Scandinavians, etc. (Europeans) that colonized the Americas. This explains why most of the chronically ill patients are white people of European decent. Therefore we have a genetic basis in the coagulation system for chronic illnesses that is very straightforward.

The model of reduced blood flow from increased blood viscosity due to activation of coagulation accompanied by a coagulation protein defect gives a scientific basis for a contribution to the pathophysiology of chronic illness. It also gives a measurable or quantifiable, objective aspect to testing the blood of patients with these diseases. It is no longer “all in your head”, but rather in your “blood.” It’s not rocket science, but a simple, logical explanation for what’s going on in many chronically ill patients.

HEMEX Laboratories provides testing services and consultative interpretations to clinicians and physicians throughout the United States. For more information, technical reprints, and/or patient information, please see their website at www. hemex.com


The following is a brief summary of the work of David Berg of Hemex Laboratory in Phoenix, Arizona, linking an immune activated hypercoagulation mechanism to a wide range of chronic conditions.

Immune System Activation of Coagulation ( I S A C ) :Chronic Illnesses Due to a Coagulation Protein Defect

Infertility (Recurrent Fetal Loss), TIA, Osteonecrosis of the Jaw, Chronic Fatigue Syndrome/Fibromyalgia (CFS/FM), Crohn’s Disease, IBD, Multiple Sclerosis, Sjogren’s Syndrome, Lyme Disease.

The Model – A Paradigm Shift

The model proposes that a majority of individuals diagnosed with chronic illnesses, based on clinical criteria, may be potentially classified as “Anti Phospholipid Antibody Syndrome” (APS) with the endothelial cell (EC) as the disease target. These patients have a hypercoagulable state demonstrated by increased markers of coagulation activation and increased blood viscosity due to the generation of Soluble Fibrin Monomer (SFM). The CFS/FM process may be triggered by a variety of pathogens (CMV, HHV6, Mycoplasma, Ch1, pneumonia, etc.), resulting in pathogen-mediated immune activation that induces antibodies which cross-react with BC protective proteins B2GP1 & Annexin V. These antibodies dislodge the protective proteins from EC surfaces, exposing PhosphatidylSerine (PS) on the EC surfaces in capillary beds. Pathogens induce inflammatory responses which include cytokine modulation of EC to down-regulate the antithrombotic environment (Thrombomodulin, tPA) in favor of prothrombotic expression of Tissue Factor (TF). TF and PS exposure allows binding of the coagulation tenase and prothrombinase complexes to EC surfaces.

This results in thrombin generation leading to SFM formation. SFM dimerizes easily, increasing blood viscosity and precipitating out on EC surfaces as fibrin(old) deposition, creating local ischemia and pathology, blocking nutrient and oxygen delivery in the microcirculation. A hereditary defect in a coagulation regulatory protein, such as protein C, protein S, Factor VL, prothrombin gene mutation, PAI-1, Lp(a), or elevated homocysteine is predispositional in greater than 755 of patients. Because this hypercoaguability does not result in an immediate thrombosis (100% occlusion), but rather in fibrin deposition (50-95%), we suggest that an appropriate name for this antiphospholipid antibody process to be Immune System Activation of Coagulation (ISAX) syndrome. This model provides an explanation for the therapeutic benefits reported with low dose anticoagulant therapy (heparin or warfarin) in the majority of chronically ill patients.

People are not chronically ill unless there is a coagulation regulatory protein defect as seen in Thrombophilia or Hypofibrinolysis.

Hemex Protocol and Dave Berg

This is the parent page of the material still surviving about the Hemex protocol before it was purchased at the retirement of David Berg


 March 24, 2000

Heparin Time Line:

Day 1           30 Days        60 Days       90 Days      120 Days      150 Days      180 Days

Transfer Factor Time Line:

30 Days       60 Days        90 Days     120 Days

Antibiotics Time Line:

30 Days       60 Days        90 Days

Bromelain Time Line:For patients that have high Lp(a) or high PAI-1 values (500-1000mg/day).

Day 1            30 Days       60 Days        90 Days      120 Days

Heparin Protocol:

See instruction sheet of Dr. Couvaras. (This sheet is not available online.  Contact David Berg at 800-999-2568 or by email for more information about this sheet).
For a 150# slender patient, use 4000units, sq, BID.  If insurance will pay for LMWH (Lovenox), use 30 mg. in AM.
For a >150 # overweight patient, use 5000 units, sq, BID.  If insurance will pay for LMWH (Lovenox), use 30 mg. in the morning and 15 mg. at night.
It is suggested that heparin be continued for a time period after discontinuation of other therapies in order to prevent any remaining pathogens from activating the coagulation mechanism and starting the fibrin deposition cycle again.

Transfer Factor:

Transfer Factor (from colostrum) is available from several sources. The source that we have patient data using this protocol is Immunity Today, LLC.  The dosage suggested by the company is 3 capsules per day. The cost is $270 for a 1 month supply. TF is more effective if started after heparin has been used for a period of time to allow some cleanup of fibrin deposition from endothelial cell surfaces in the capillaries.


Antibiotics, such as Doxycyline, may be used if there are known pathogens such as Mycoplasma or Chlamydia pneumonia. Each clinician must make the decision to use or not to use antibiotics based on their knowledge of their patient.


Bromelain may be used as an activator of fibrinolysis, especially in patients that have high Lp(a) or high PAI-1 values (which blocks fibrinolysis). A possible dosage is 500 to 1000 mg/day. There is no data that states that bromelain helps in these patients, but several journal articles suggest that bromelain does enhance fibrinolysis. Since bromelain is a natural substance from pineapples, it is an alternative to using tPA or Urokinase as fibrinolysis activators in patients.

1.  This protocol should be used only  under direction and supervision of the patient’s physician. This suggested protocol has been developed by an Infectious Disease specialist and HEMEX Laboratories, Inc.  In no way should a patient treat him/herself.  HEMEX is in no way responsible for patient care. All drug precautions should be noted and followed. Questions can be addressed todberg@hemex.com.

All information and graphics are © HEMEX Laboratories, Inc. unless otherwise noted. No part of this website or the information contained with individual documents may be redistributed or reposted without the express consent of HEMEX Laboratories, Inc.

Dave Berg – CFS Radio Program 1999-08-29

CFS Radio Program
August 29th, 1999
Roger G. Mazlen, M.D., Host
Dr. David Berg

Dr. Mazlen
I’m excited to tell you that we have a very important guest today, live from Phoenix, AZ, Dr. David Berg. David is Director of Hemex Laboratories. He has a graduate degree in clinical pathology. He’s been a medical technologist for 36 years and along with his wife he started the HEMEX company in 1983 and has had about 16 years of specialty coagulation experience and has published over 12 major peer reviewed articles. He’s going to tell you about his exciting new findings in the field of Chronic Fatigue Syndrome and Fibromyalgia Syndrome and as well as it’s bearing on a lot of other clinical problems including infectious diseases. Welcome, David, we’re delighted to have you with us today. I’d like to start out, because we have a lot to go over, by having you, from your standpoint, develop the history of this research as it started out.

Dr. Berg
We’ve been in really a very exciting time in the last one year because the culmination of many years of work has come to fruition. And a lot of that started back in about 1994 when the infertility doctor here in town by the name of Dr. John Couvaras asked the question of me “I think infertility is a hypercoagulable state, can you prove it?” So using tests that were available to us back then to look at hypercoagulability I told him what to order and 4 months later he brought back these results on a series of patients that we had no idea that he was running these. And we looked at these results and said “Why are all these women in DIC?” He said, “They’re not in DIC, they’re normal women, they’re just infertile.” So we started developing ideas and concepts why these women would have such a hypercoagulability and that fall there was an international meeting on Antiphospholipid antibodies syndrome and we looked at a lot of the new information then, and then in 1995 a good friend of yours, Dr. Jacob Rand, produced a beautiful paper on Annexin V previously called placental anticoagulant protein I and in that paper he described a lot of how Annexin V is a protective protein and without it we become hypercoagulable. The following year in 1996, at the International APS meeting there was a tremendous understanding of how antiphospholipid antibodies syndrome really contributes to hypercoagulability when you have this underlying disease. Another significant finding in 1996 was the fact that a new protein called Beta II Glycoprotein I came on the scene and the question was, what is this function, what does this protein do? So if we move forward to 1997 that was a very good year, as the song says. Dr. Rand published a new paper, “Pregnancy Lost and Antiphospholipid Antibody Syndrome” and by that point in time we had had 150 successful pregnancies. These are first time pregnancies with women from 35 to 45 years of age and they had been on heparin throughout their entire pregnancy and so we published a paper monitoring heparin by the use of a new method called Soluble Fibrin Monomer. That same year, Dr. Couvaras made the observation to us that many of his women had Chronic Fatigue type symptoms as well as infertility, that is migraines, irritable bowel syndrome, pelvic pain and when he put them on heparin these symptoms went away. So, we were presenting a paper at the Temple University Meeting, Coagulation Update in 1998 and looking at this pregnancy loss, and I mentioned at the end of the program that we had seen this thing in Fibromyalgia and Chronic Fatigue patients and the director of that meeting, Dr. James Dey suggested that we do a retrospective study and even pulled out an abstract form for us for the American Association of Chronic Fatigue Syndrome. So we went back and looked at from between April and October, 21 cases that would be considered truly Chronic Fatigue patients and in that process, how did they improve?, what were their improvements like or was it a placebo effect?, and out of 21 patients, 19 had moderate to very good improvement and the other 2 at least had some improvement. So, this led us to the AACFS meeting and at that meeting Dr. David Bell from upstate New York presented a paper on using saline in these Chronic Fatigue patients for improvement and we said, this is an underlying hypercoag state, if we used anticoagulants it would probably be even better. So using Dr. Bell as one of our consultants, early this year we started a blinded, prospective study and we were able to enroll 54 patients and 23 controls from his site and a site in Houston and a couple of sites here in Phoenix and the real question was, could we separate the patients from the controls and, in fact, we did and using a panel Immune System Activation of Coagulation (ISAC) we were, in fact, able to separate patients by having 2 positive tests out of the 5 with a very significant p value of < .001 for the statisticians out there, and so now we know can identify these patients and the hypercoagulable state using these new markers of coagulation activation and so what that leaves us with is with a model that the culprit really is thick blood, or hyperviscous blood, that we have reduced blood flow in these patients because of the hyperviscosity, the thick blood, and that causes it to appear that the red cell mass is low because it’s just not flowing properly and this is a hypercoagulable state. Soluble fibrin being the main entity in this. So, why do we have a hypercoagulable state? As with the infertility patient, my basic belief, at this point in time, is that 90% or better of all the Chronic Fatiguers, Fibromyalgia, infertility patients, I may go out on a limb with Multiple Sclerosis here, all have a genetic predisposition for hypercoagulability.

Dr. Mazlen
We’re going to go into that. You’ve said quite a lot and we’re going to be talking shortly about the model you’ve developed which is equally important to explain how this works in the individual. I just wanted to congratulate you on what you’ve done so far. It’s extremely important to our Chronic Fatigue Syndrome and Fibromyalgia community but it goes beyond that. We’re going to go back to these genetic findings and the model. We want to hear about this model that you’ve developed David.

Dr. Berg
The question is, when two people are exposed to the same pathogen attack, such as CMV, HHV6, mycoplasma, chlamydia pneumonia, the question is why does one recover and the other one become chronically ill and our belief is that one that becomes chronically ill does not control the thrombin generation or the coagulation cascade properly as the person that recovers does. So, we’ve got a genetic predisposition. In our blood, if we take a ml of blood, half of that blood is our red cells, white cells and platelets. The other half is plasma containing all the protein. 30% of all those proteins in the plasma regulate the coagulation mechanism. And each one of us is born with about 40 mutations in our genetic makeup in the human genome. If we have one mutation in that plasma protein then we have an inability to control thrombin generation properly and there are risks of two different groups of potential genetic defects for us and those that don’t control thrombin properly might have an anti-thrombin defect, Protein C, Protein S, Factor V Leiden, there’s a new pro-thrombin gene mutation now, Thrombomodulin Heparin Co-factor II and most sick patients, I believe, fall into the second category, which is hypofibrinolysis, the inability to clean up the blood vessel walls once fibrin is formed and those defects are high plasminogen activator inhibitor or PAI-i, Lipoprotein-a, tissue plasminogen activator and plasminogen itself. So the model simply says that somebody has a genetic predisposition, they in fact get this illness, they form antibodies to whatever their invading pathogen is, the immunoglobulins knock off the protective proteins on the endothelial cell’s surface and those protective proteins are Beta II Glycoprotein I and Annexin V. This exposes phosphatidyl serine in the capillaries to the flowing blood and that allows the coag proteins to bind and so all of a sudden we’re generating thrombin in the small vessels in the capillaries throughout the body. So, if we take a muscle and pull it down to a ligament or a tendon and wrap that with the fascia, that fascia is only 5 or 6 cells thick, that’s where the capillary blood flow is and so if you coat the insides of that capillary with fibrin, not a blood clot, but fibrin, then nutrients and oxygen does not pass through to that ligament or tendon on the other side and all of a sudden it says “Ouch” and we’ve got a trigger point, a defined trigger point as in Fibromyalgia. The same thing holds true in the placenta. The baby can’t get oxygen or nutrients, the baby starves, the baby dies, the baby aborts. We have chronic, recurrent, miscarriages.

Dr. Mazlen
I have to interrupt you to just clarify one thing. Does fibrin deposition on vessel walls or what we call the endothelial lining, it can also trap infectious agents. Isn’t that correct?

Dr. Berg
You bet it can. One of the major findings is that some of these pathogens actually have the ability to generate fibrin around them so that they grow in what we call an anaerobic environment such as mycoplasma which is an anaerobe. And so by having fibrin around it, it doesn’t get oxygen and it also hides the pathogen from the immune system. And this is how cancer cells get started. Undifferentiated cells grow fibrin around them and that gives a physical support to grow on as well hiding it from the immune system.

Dr. Mazlen
That leads us into treatment. What would you like to cover?

Dr. Berg
Well, maybe one of the best things to do would be to read you a couple of testimonials and I know that’s not scientific but this is typical of what you expect from the thrombophilia defects, the people that have the too much thrombin generation. This is from a patient that actually has gone so far as to have had a couple of TIA’s as a consequence of her hypercoagulable state and she writes:

“I swam three laps and then worked in my yard with loafers. Oh am I going to pay for it tomorrow but only with sore muscles that haven’t been used in so long. Today, when I came in the house I gave in to my urge that I’ve had for the last 2 days to go skipping down the hall. I did it 3 times. How funny I looked. Like a little kid just learning to balance and learning to skip. Now I have to retrain my muscles but my mind still remembers how. That little girl in me got the biggest kick out of skipping again and it’s been years.”

This is a typical comment when someone has started on heparin, and this patient had been on heparin for 6 days, they start feeling better right away. The people with the hypofibrinolysis problems, we shut down the thrombin generation with the heparin but we don’t really clean up the capillaries and that’s one of the big problems. The other one, is our long term patient that we’ve been working with for a year and a half now and she writes:

“It’s been the easiest year physically that I’ve had in a long time. And because of feeling better I’ve experienced a new joy in life.”

And this is not without her ups and downs. We changed her from heparin to coumadin and she went downhill from there. And then after 4 months of the coumadin, she said, “enough of this, let’s go back to the heparin,” and now she’s doing very well. Heparins offer 4 distinct benefits over coumadin and a couple of those are that heparin is an anti-platelet and part of this syndrome is that you have very active platelets in over half of the patients. Heparin is a vasodilator, it increases nitric oxide in the endothelial cell and heparin is an antimicrobial, an antiviral, so by shutting down the pathogen’s ability to create fibrin around it, the immune system sees it, so there’s many more benefits that heparin can give us than what coumadin can.

Dr. Mazlen
And in low doses it’s relatively safe if you follow it, obviously, along with your physician and health care person.

Dr. Berg
Absolutely. In the hospital a person that has a blood clot and is given heparin normally gets like 24,000 units in a day, 1000 units an hour, so we’re using 5,000 units twice a day as an injection, so that’s 10,000 units. That’s not eve half what you would be getting in the hospital, so the safety issue is very, very good.

Dr. Mazlen
I know, I’ve had personal experience with heparin in the past after surgery so I know it’s easy to administer and easy to monitor which is of great benefit. We’re going to take one quick question. Drew, have you got a question?

I wanted to say first to Dr. Berg that I’m very grateful. I’ve had Chronic Fatigue for 15 years and your research and findings offer hope to not just myself but I think all of us who have been struggling with this condition for so long and we’re looking for that ray of hope and this seems very promising. I wanted to ask just very quickly as a sufferer, what tests should I go out to have and should I start on the heparin or is it necessary to have multiple tests before I begin heparin?

Dr. Berg
Excellent question. We offer what’s an ISAC panel and we’re looking at these 5 markers to see how activated the patient and it’s important to know if the platelets are activated because in addition to anticoagulants you may need an anti-platelet drug like 81 mg of aspirin a day. And the other thing is that we need to have the hereditary thrombosis risk panel which is 8 different proteins, and this is the extensive part, and these proteins then tell us where the genetic defect is. Dr. David Bell who participated with us in the blinded study started 4 patients on heparin and the first one did very well and the other three did not and I suspect, by genetic predisposition, that those 3 that didn’t respond have the hypofibrinolysis and that’s where our research is taking us now. We need a good sized research grant to develop a protocol for this 40% of all the Chronic Fatiguers, which I believe is a fairly close number, we need to be able to give these people a low dose or quarter dose of TPA or something to get systemic fibrinolysis to clean out the vessels, then the anticoagulants will hold the patient from generating more fibrin and the patient will respond very well.

Dr. Mazlen
Thank you very much Drew for calling. You can get in touch with Dr. Berg at 800-999-CLOT.

Dr. Berg
Now, these tests are not cheap and it costs about $900 to work up a patient and I realize that that’s a problem with many patients and that’s why we’re looking for research money–my wife and I have funded most of this so far– to handle the people that can’t pay or insurance doesn’t pay much to make up the difference.

Dr. Mazlen
David, you have some acknowledgments, I’m going to let you make them now.

Dr. Berg
First off, our model is based on a 1997 model out of the dental world and Dr. Doug Triplet (sp?) of Munsey, Indiana, has given me much input from that and that’s basically osteonecrosis of the jaw where the bone dissolves and the simple treatment for this is that the patients get coumadin, 5 mg and the bone starts growing again. In other words, another example of hypercoagulability that responds to anitcoagulants. My main thank you needs to go to Prof. Al Cocchetto in your area in Artport, New York who’s been my sidekick in all of this development. Al has been a great mind and a great resource for getting me information that I’ve needed for publications, vital references and really a wonderful mind to banter ideas back and forth as we developed our model and most importantly and last, I want to thank Gail Kansky of the National CFIDS Foundation and her very generous $5,000 contribution that was given to us to help pay for part of the reagents in our studies.

Dr. Mazlen
All right, and I’m going to ask you to give your email address so that people can write to you.

Dr. Berg
Our website is http://www.hemex.com and my email address is dberg@hemex.com. I get 10 to 20 emails a day so if I don’t answer you right away please be patient.


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