Hypercoagulation Theory Viable Explanation for Some CFS & FM Symptoms

[Guest guest]

i was at the acam conference and came across this

resarch, sq heparin was used . i dobut if any

insurance company would pay for it. however if some pt

is interested in this and are in virginia, or maryland

they can contct my office at

dr.jasmine md.

--- Ron wrote:

> Thought this was noteworthy!

> be well!

> ron :}

>

>

> Hypercoagulation Theory Viable Explanation for Some

> CFS & FM Symptoms

> by Berg

> ImmuneSupport.com

>

> 10-03-2001

>

> Editor's Note: The following is a transcript

> discussion with Berg,

> provided exclusively to ImmuneSupport.com.

> Berg is the Director and

> Cofounder with Lois Hill Berg, of HEMEX

> Laboratories. Mr. Berg helped

> develop the Hypercoagulation theory, a proposed

> cause of CFS and FM

> symptoms. He has a M.S. degree in clinical pathology

> and laboratory

> medicine, and has been in practice for 35years. He

> recommends patients

> discuss the following information with their

> physicians.

>

> Berg: We first became involved with research in

> chronic illnesses in 1992.

> At that time, Dr. Couvaras, an infertility

> specialist in Phoenix, AZ,

> and HEMEX, began to research infertility in women.

> We found a

> hypercoagulable state due to a coagulation protein

> defect, existing in women

> that we tested who were infertile and/or had

> recurrent spontaneous

> abortions. In 1996, Dr. Couvaras noted that when he

> put women on low dose

> heparin in order to become pregnant, the CFS/FM

> symptoms, pelvic pain, and

> migraine-like headaches diminished. He asked us,

> " why? " As a result of this

> scientific curiosity, we performed a retrospective

> study on 30 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 AACSF meeting in

> Cambridge.

>

> This study led to a major, multi-center, blinded,

> patient or control study

> with centers in New York, Houston, and Phoenix. When

> the code was broken,

> identifying patients and controls, we were able to

> identify a patient based

> on two or more positive test results out of the five

> assays in the ISAC

> panel. It was the first definitive proof that indeed

> chronic illnesses have

> a basis in the blood system. This was published in

> the international journal

> Blood Coagulation & Fibrinolysis, 1999, 10:435-438.

> In another study

> published in Blood Coagulation & Fibrinolysis, 2000,

> 11:673-678, it was

> determined that Gulf War illness has the same

> mechanism and positive

> findings.

>

> In November 1999, myself and Dr. Joe Brewer (an

> Infectious Disease

> specialist in Kansas City) developed the model of a

> pathogen activating the

> immune and coagulation systems which is now known as

> the Immune System

> Activation of Coagulation or ISAC. The end result is

> increased blood

> viscosity which is due to 1) a regulatory protein

> defect and 2) activation

> of the coagulation system by the pathogen. As the

> blood viscosity increases,

> the blood flow diminishes throughout the body,

> creating anoxia (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 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 microcirculation (capillaries) as

> fibrin or fibrinoid-like

> deposition, blocking oxygen and nutrients to nearby

> 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 of a clinician faces is to figure out

> what pathogens are present

> in the patient, and therefore determine the most

> appropriate therapies

> against these pathogens. The average CFS/FM patient

> has 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 are positive. Someone who may

> be 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

> 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,

> parasites, physical trauma, vaccinations, (anthrax,

> measles, mumps) and/or

> biological warfare agents can also activate or

> poison the immune system.

> This may lead to secondary infections, which 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 eight

> different regulatory proteins of the coagulation

> mechanism in a panel we

> call the HTRP (Hereditary Thrombosis Risk) panel. In

> July 2001, at the

> international meeting of ISTH, we presented data

> that in a retrospective

> study of 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 400+ patients

> have defects in the fibrinolytic system

> (hypofibrinolysis due to elevated

> lipoprotein (a) - Lp(a) and / or PAI1-plasminogen

> activator inhibitor 1).

> Unfortunately, 21% of these patients had a defect in

> both groups. This means

> that not only do they form fibrin easily, but also

> they cannot clean up the

> fibrin deposition generated.

>

> 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 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 deposition. Half of the

> patients

=== message truncated ===

__________________________________________________

[Guest guest]

Subject: Hypercoagulation Theory Viable Explanation for Some CFS & FM

Symptoms

> Hypercoagulation Theory Viable Explanation for Some CFS & FM Symptoms

>

> by Berg

>

> ImmuneSupport.com

>

>

>

> 10-03-2001

>

>

>

> Editor's Note: The following is a transcript discussion with Berg,

>

> provided exclusively to ImmuneSupport.com. Berg is the Director and

>

> Cofounder with Lois Hill Berg, of HEMEX Laboratories. Mr. Berg helped

>

> develop the Hypercoagulation theory, a proposed cause of CFS and FM

>

> symptoms. He has a M.S. degree in clinical pathology and laboratory

>

> medicine, and has been in practice for 35years. He recommends patients

>

> discuss the following information with their physicians.

>

>

>

> Berg: We first became involved with research in chronic illnesses in 1992.

>

> At that time, Dr. Couvaras, an infertility specialist in Phoenix, AZ,

>

> and HEMEX, began to research infertility in women. We found a

>

> hypercoagulable state due to a coagulation protein defect, existing in

women

>

> that we tested who were infertile and/or had recurrent spontaneous

>

> abortions. In 1996, Dr. Couvaras noted that when he put women on low dose

>

> heparin in order to become pregnant, the CFS/FM symptoms, pelvic pain, and

>

> migraine-like headaches diminished. He asked us, " why? " As a result of

this

>

> scientific curiosity, we performed a retrospective study on 30 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 AACSF meeting in Cambridge.

>

>

>

> This study led to a major, multi-center, blinded, patient or control study

>

> with centers in New York, Houston, and Phoenix. When the code was broken,

>

> identifying patients and controls, we were able to identify a patient

based

>

> on two or more positive test results out of the five assays in the ISAC

>

> panel. It was the first definitive proof that indeed chronic illnesses

have

>

> a basis in the blood system. This was published in the international

journal

>

> Blood Coagulation & Fibrinolysis, 1999, 10:435-438. In another study

>

> published in Blood Coagulation & Fibrinolysis, 2000, 11:673-678, it was

>

> determined that Gulf War illness has the same mechanism and positive

>

> findings.

>

>

>

> In November 1999, myself and Dr. Joe Brewer (an Infectious Disease

>

> specialist in Kansas City) developed the model of a pathogen activating

the

>

> immune and coagulation systems which is now known as the Immune System

>

> Activation of Coagulation or ISAC. The end result is increased blood

>

> viscosity which is due to 1) a regulatory protein defect and 2) activation

>

> of the coagulation system by the pathogen. As the blood viscosity

increases,

>

> the blood flow diminishes throughout the body, creating anoxia (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 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 microcirculation (capillaries) as fibrin or

fibrinoid-like

>

> deposition, blocking oxygen and nutrients to nearby 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 of a clinician faces is to figure out what pathogens are

present

>

> in the patient, and therefore determine the most appropriate therapies

>

> against these pathogens. The average CFS/FM patient has 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 are positive. Someone who may be 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 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,

>

> parasites, physical trauma, vaccinations, (anthrax, measles, mumps) and/or

>

> biological warfare agents can also activate or poison the immune system.

>

> This may lead to secondary infections, which 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 eight

>

> different regulatory proteins of the coagulation mechanism in a panel we

>

> call the HTRP (Hereditary Thrombosis Risk) panel. In July 2001, at the

>

> international meeting of ISTH, we presented data that in a retrospective

>

> study of 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 400+

patients

>

> have defects in the fibrinolytic system (hypofibrinolysis due to elevated

>

> lipoprotein (a) - Lp(a) and / or PAI1-plasminogen activator inhibitor 1).

>

> Unfortunately, 21% of these patients had a defect in both groups. This

means

>

> that not only do they form fibrin easily, but also they cannot clean up

the

>

> fibrin deposition generated.

>

>

>

> 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 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 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 baby starves, the baby

>

> dies, 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-HPA axis, hypo-estrogen, etc. Restoring the

blood

>

> flow by 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, " and you went to battle during the

>

> middle ages, 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 explains how these coagulation

defects

>

> occurred over 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 from a

>

> coagulation protein defect gives a scientific basis for chronic illness.

It

>

> also gives a measurable or quantifiable aspect to testing a patient's

blood

>

> for 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 chronically ill patients.

>

>

>

> HEMEX Laboratories offers testing and consultative services relating to

the

>

> diagnosis, treatment, and monitoring of hematological, clotting and/or

>

> bleeding disorders. HEMEX provides services and interpretations to

>

> clinicians and physicians throughout the United States. For more

>

> information, technical reprints, & /or patient information, please see

their

>

> website at www.hemex.com.

[Guest guest]

This is super interesting and could be an explanation for things like

painful feet, hands, and brain fog, all extremity areas of the body

where blood flow is slowest, very interesting indeed

In @y..., " Patty " <fdp@l...> wrote:

>

> Subject: Hypercoagulation Theory Viable Explanation for Some CFS &

FM

> Symptoms

>

>

>

> > Hypercoagulation Theory Viable Explanation for Some CFS & FM

Symptoms

> >

> > by Berg

> >

> > ImmuneSupport.com

> >

> >

> >

> > 10-03-2001

> >

> >

> >

> > Editor's Note: The following is a transcript discussion with

Berg,

> >

> > provided exclusively to ImmuneSupport.com. Berg is the

Director and

> >

> > Cofounder with Lois Hill Berg, of HEMEX Laboratories. Mr. Berg

helped

> >

> > develop the Hypercoagulation theory, a proposed cause of CFS and

FM

> >

> > symptoms. He has a M.S. degree in clinical pathology and

laboratory

> >

> > medicine, and has been in practice for 35years. He recommends

patients

> >

> > discuss the following information with their physicians.

> >

> >

> >

> > Berg: We first became involved with research in chronic illnesses

in 1992.

> >

> > At that time, Dr. Couvaras, an infertility specialist in

Phoenix, AZ,

> >

> > and HEMEX, began to research infertility in women. We found a

> >

> > hypercoagulable state due to a coagulation protein defect,

existing in

> women

> >

> > that we tested who were infertile and/or had recurrent spontaneous

> >

> > abortions. In 1996, Dr. Couvaras noted that when he put women on

low dose

> >

> > heparin in order to become pregnant, the CFS/FM symptoms, pelvic

pain, and

> >

> > migraine-like headaches diminished. He asked us, " why? " As a

result of

> this

> >

> > scientific curiosity, we performed a retrospective study on 30

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 AACSF meeting in Cambridge.

> >

> >

> >

> > This study led to a major, multi-center, blinded, patient or

control study

> >

> > with centers in New York, Houston, and Phoenix. When the code was

broken,

> >

> > identifying patients and controls, we were able to identify a

patient

> based

> >

> > on two or more positive test results out of the five assays in

the ISAC

> >

> > panel. It was the first definitive proof that indeed chronic

illnesses

> have

> >

> > a basis in the blood system. This was published in the

international

> journal

> >

> > Blood Coagulation & Fibrinolysis, 1999, 10:435-438. In another

study

> >

> > published in Blood Coagulation & Fibrinolysis, 2000, 11:673-678,

it was

> >

> > determined that Gulf War illness has the same mechanism and

positive

> >

> > findings.

> >

> >

> >

> > In November 1999, myself and Dr. Joe Brewer (an Infectious Disease

> >

> > specialist in Kansas City) developed the model of a pathogen

activating

> the

> >

> > immune and coagulation systems which is now known as the Immune

System

> >

> > Activation of Coagulation or ISAC. The end result is increased

blood

> >

> > viscosity which is due to 1) a regulatory protein defect and 2)

activation

> >

> > of the coagulation system by the pathogen. As the blood viscosity

> increases,

> >

> > the blood flow diminishes throughout the body, creating anoxia

(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 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 microcirculation (capillaries) as fibrin or

> fibrinoid-like

> >

> > deposition, blocking oxygen and nutrients to nearby 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 of a clinician faces is to figure out what pathogens

are

> present

> >

> > in the patient, and therefore determine the most appropriate

therapies

> >

> > against these pathogens. The average CFS/FM patient has 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 are positive. Someone who may be 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 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,

> >

> > parasites, physical trauma, vaccinations, (anthrax, measles,

mumps) and/or

> >

> > biological warfare agents can also activate or poison the immune

system.

> >

> > This may lead to secondary infections, which 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

eight

> >

> > different regulatory proteins of the coagulation mechanism in a

panel we

> >

> > call the HTRP (Hereditary Thrombosis Risk) panel. In July 2001,

at the

> >

> > international meeting of ISTH, we presented data that in a

retrospective

> >

> > study of 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 400+

> patients

> >

> > have defects in the fibrinolytic system (hypofibrinolysis due to

elevated

> >

> > lipoprotein (a) - Lp(a) and / or PAI1-plasminogen activator

inhibitor 1).

> >

> > Unfortunately, 21% of these patients had a defect in both groups.

This

> means

> >

> > that not only do they form fibrin easily, but also they cannot

clean up

> the

> >

> > fibrin deposition generated.

> >

> >

> >

> > 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 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 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 baby starves,

the baby

> >

> > dies, 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-HPA axis, hypo-estrogen, etc. Restoring

the

> blood

> >

> > flow by 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, " and you went to battle

during the

> >

> > middle ages, 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 explains how these

coagulation

> defects

> >

> > occurred over 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

from a

> >

> > coagulation protein defect gives a scientific basis for chronic

illness.

> It

> >

> > also gives a measurable or quantifiable aspect to testing a

patient's

> blood

> >

> > for 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 chronically ill patients.

> >

> >

> >

> > HEMEX Laboratories offers testing and consultative services

relating to

> the

> >

> > diagnosis, treatment, and monitoring of hematological, clotting

and/or

> >

> > bleeding disorders. HEMEX provides services and interpretations to

> >

> > clinicians and physicians throughout the United States. For more

> >

> > information, technical reprints, & /or patient information, please

see

> their

> >

> > website at www.hemex.com.