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Berg 3-23-00
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Speaker: David E Berg
March 26th, 2000 12PM (Noon) PST, 3PM EST
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!
Greetings to all. It’s an honor and pleasure to be on line today and especially
to follow Mr. Regush. His book is excellent and RIGHT ON !. (It’s funny not
being able to see faces that are included in the dialog.) But such is the NET.
For some time now, I have been frustrated knowing that the coagulation part
is only half of the problem and that one or more pathogens are the other.
And that HHV6 has had no know treatment until now. So let’s begin where
Mr. Regush’s book ends in October, 1999.
In November, 1999, at the Infectious Disease Annual Meeting in
Philadelphia, I saw a poster on HHV6 and spoke with the author, Dr. Joe
Brewer of Kansas City. Over a four hour plus dinner meeting, we worked out
the model that is being presented now about a basic coagulation or
fibrinolysis regulatory protein defect in CFIDS patients as the genetic culprit.
Then you add in a pathogen (HHV6, CMV, Mycoplasma, Chlamydia
pneumonia, etc, or a combination of several of these pathogens) and the
patient goes down hill rapidly into chronic illness due to the pathogen
activating the coagulation mechanism. This is due to an immune response
as well as inflammatory responses to the pathogen and probably the
pathogen itself activating the coagulation system. Anticoagulants (primarily
heparin) shut down the Soluble Fibrin generation and fibrin deposition on the
Endothelial Cell (EC) surfaces. But unless the patient can get treatment for
the pathogen, the healing response can only reach 50% or so.
My frustration has been HHV6. Dr. Brewer told me about a new colostrum
derived, highly purified Transfer Factor (TF) that would contain only specific
IgG and IgM antibodies against CMV and HHV6 (see
www.immunitytoday.com ). He started testing many of his patients for their
coag defects and we found such in every patient. Each patient also had
documented HHV6 infection. Beginning in December, Dr Brewer began
treating his patients with this new TF. Patient stories are dramatic. We will
discuss some of them.
In early December, 1999, at the American Society of Hematology, we met
Dr. Konnie Knox. After spending two plus hours discussing theories and
therapies, we were all singing the same hymn. So the circle from last week
to now is complete. The Good Lord has put Lois & I here at the right time, in
the right place with the right knowledge and the right people to be able to
solve these “Blood Curdling Mysteries” of chronic illnesses, and they extend
beyond just CFIDS patients.
WHY is it important to be tested for the coagulation defects? It is VERY
important, because at some point in time, all CFIDS patients will need
surgery, be in an accident or traumatic situation and NEED to have
PROPHYLAXIS to prevent a blood clot, stroke, heart attack or Pulmonary
Embolism from happening. If you know your protein defect, then proper
anticoagulant therapy will prevent catastrophic events. I feel very strongly
about this.
If you look at the population of America and the patient race distribution of
CFIDS patients, there are about 5% of bleeders (hemophiliacs or von
Willebrand Factor deficient patients) and about 5% clotters. Using a bell
shaped curve, 260 million USA population yields 13 million clotters. 1 million
CFS, 8 million Fibromyalgia, ? Million Multiple Sclerosis, ? Recurrent
Spontaneous Abortors, etc. Are we close? The protein defects have mostly
risen from European decent and are mostly white people. Hundreds of years
ago, when someone cut themselves hunting or preparing food, it was
advantageous to clot fast (not bleed to death). Life spans were shorter then
also, so these coagulation or fibrinolysis regulatory protein defects were
beneficial. Today, with much longer life spans, these defects cause chronic
illnesses by not controlling the coag response properly. So much for my PhD
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.
1.
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.
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.
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.
As for minocin, I have no knowledge of its properties or use, except
that others report good results using it.
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.
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 processes.
[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?
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>
2.[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.
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.)
3.[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?
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 goes up 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).
Coumadin is only an anticoagulant. It works by decreasing Factors II,
VII, IX & X and Protein C and Protein S. 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.
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!!!
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.
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)
6.
[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?
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 !.< /P >
7.
[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?
I do not have knowledge to answer this question at this time. It is an
interesting concept.
8.
[DebbieSinKC]new protocol time lines
i don't understand the time lines - is it saying transfer factor for only 3
mos.?!?!
We will change our chart to DAYS on the time line instead of MONTHS
to make it clearer. Thanks for the comment.
9.
[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 they?
10.
[karen]:If my doctor ordered a hyperocagulability
panel from another lab, would this have to be
11.
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.
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. 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.
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.
[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?
See my previous answer on fibrinogens. High PAI or Lp(a) values are
the hardest to treat. If you can't use bromelain, then niacin is 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.
12.
[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?
13.
[Patricia]:EBV & or HHV6a,b
Have you noticed patients with high titers or counts with EBV
reactivation and or HHV6a or b ?
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.
14.
[Kru]:I'm interested in sub groups of CFS
Are you noticing anything about sub groups or sub sets of
15.
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.
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?
I don't have any good answer to these questions. Beth, our long term
patient, has much experience on this. Contact her at
pbdrechsel@msm.com .
16.
SUMMARY:
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 ( http://www.hemex.com/cfs/ ), 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. T
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