Berg's comments on the genetic link of hypercoagulation

[Guest guest]

This is from 2001. But in a nut shell he found that 83% of us had

one or more coagulation defects. Of those 40% (there's our #) had

thrombophilia defects. 39% had defects in the fibrinolytic system

due to elevated lipoprotien. Of those 21% had defects in both

groups.

" 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. "

This came from another report:

Conclusions: These data support the general hypothesis of concerted

genetic contribution(s) ofcoagulation protein abnormalities to

CFS/FM and are consistent with family histories. The pooled CFS/FM

and related chronic illnesses are associated with increased rates of

abnormalities for all markers except APCR. CFS patients with normal

HTRP results may warrant testing forrarer inheritable

thrombopathies. Genetic testing to identify the type of procoagulant

defect may be warranted as effective interventions to prevent or

treat CFS/FM become available. 1) Oral Presentation,

7thInternational Biennial Conference on Chronic Fatigue Syndrome,

Oct, 2004, Madison, WI, USA – In Press

http://www.hemex.com/pdf/hhh%20aacfs%20web%20presentation.pdf

This part does show a date of 2004. There was much more info to wade

through, but I don't have time right now. Alot of stuff though about

genetic and acquired hypercoagulaton.