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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

[David] Anticoagulants still do not address the problem of THE UNDERLYING

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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