repost --why we take serrapeptase---fyi----

[Guest guest]

PART 1

http://www.springboard4health.com/notebook/health_hypercoagulation_il

l.html

Read these related articles:

Hypercoagulation Linked to Chronic Fatigue, Fibromyalgia, MS,

Infertility, Chronic Illness - PART 2

Hypercoagulation & Heparin - A Second Look.

Interview with Berg

Berg is the Director and Cofounder, with Lois Hill Berg, of

HEMEX Laboratories. Along with Dr. Harold on 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 on 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