Hypercoagulation hypothesis

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history

Dr. David Berg and Dr. Joseph Brewer developed a theory in the late 1990s that the symptoms of chronic fatigue syndrome are caused by one or more active infections that the immune system is unable to effectively fight due to genetic variations related to coagulation.

Their model proposes that a pathogen activates the coagulation system in genetically vulnerable individuals, that is those with one or more protein defects relating to coagulation.

Berg co-founded Hemex Laboratories

History[edit | edit source]

Dr. Berg first became interested in hypercoagulation while researching hypercoagulation-related infertility. A colleague of Dr. Berg's observed that women with CFS and Fibromyalgia-like symptoms, when given low-dose heparin in order to maintain their pregnancies, found their symptoms improve.

Theory[edit | edit source]

Mechanism[edit | edit source]

One or more anaerobic viral, bacterial, and/or fungal pathogens activates coagulation pathways. Fibrin deposits decrease oxygen in tissues, creating a more hospitable environment for these pathogens.[1]

In his research, Berg found that a large proportion of patients had a tendency to either quickly form fibrin deposits, others to clean up fibrin, while still others had defects in both. Increased blood viscosity results in a chronic lack of oxygen and nutrients to a variety of body systems with effects on the muscles, brain, HPA axis and endocrine system.

Testing[edit | edit source]

Berg developed a test called the Immune System Activation of Coagulation panel (ISAC) to test for fibrinogen (FIB), soluble fibrin monomer (SFM), Prothrombin fragment 1+2 (F1+2), thrombin/antithrombin complexes (T/AT) and Platelet Activation by Flow Cytometry.

Berg also uses the Hereditary Thrombosis Risk Panel (HTRP), which tests for thrombosis and fibrinolytic defects. Potential thrombin defects include decreased protein C, decreased protein S, decreased anti-thrombin, APC resistance/factor V Leiden positivity, or increased prothrombin/prothrombin gene mutation positivity. Fibrinolytic defects include elevated lipoprotein a (Lp(a)) and plasminogen activator inhibitor-1. [2]

Proposed treatment[edit | edit source]

Treatment focuses on decreasing coagulation through the use anti-coagulants such as heparin or warfarin and treating the individual patient's infections.[3]

Proposed non-prescription anti-coagulants include enzymes such as serrapeptase, nattokinase and lumbrokinase.[4]

Evidence[edit | edit source]

Berg and his colleagues found evidence of hypercoagulation in CFS, Fibromyalgia, and Gulf War Illness patients using their testing methods.[5][6] Another study using different methods found no evidence of hypercoagulation.[7]

Learn more[edit | edit source]

See also[edit | edit source]

References[edit | edit source]