In my last post, many studies cited proteins being altered.

Fibromyalgia pain may be “microclots” et al

I asked ChatGpt to list the proteins involved. The answer matched my memories (and saves time digging up citations)

Coagulation, also known as blood clotting, is a complex physiological process that involves a series of protein interactions. The main proteins associated with coagulation are part of the clotting cascade, which can be divided into two pathways: the intrinsic pathway and the extrinsic pathway. These pathways eventually converge to activate a common pathway leading to the formation of a stable blood clot. Here are some key proteins involved in these pathways:

Intrinsic Pathway:

1. Factor XII (Hageman Factor): It initiates the intrinsic pathway by becoming activated upon contact with exposed subendothelial surfaces.
2. Factor XI (Plasma Thromboplastin Antecedent): Activated by factor XIIa, it then activates factor IX.
3. Factor IX (Christmas Factor): Activated by factor XIa, it forms a complex with factor VIIIa and calcium ions to activate factor X.
4. Factor VIII (Antihemophilic Factor A): This protein, along with von Willebrand factor, is involved in stabilizing factor IX and preventing its premature degradation.
5. Factor X (Stuart-Prower Factor): Activated by the factor IXa-factor VIIIa complex, it is a critical point where the intrinsic and extrinsic pathways converge.

Extrinsic Pathway:

1. Tissue Factor (Factor III): Released from damaged tissues, it combines with activated factor VII to initiate the extrinsic pathway.
2. Factor VII (Proconvertin): Activated by tissue factor, it forms a complex with tissue factor to activate factor X.

Common Pathway:

1. Factor X (Stuart-Prower Factor): Activated by both intrinsic and extrinsic pathways, it forms a complex with factor V to convert prothrombin (Factor II) to thrombin.
2. Factor V (Labile Factor): Forms a complex with factor X to accelerate the conversion of prothrombin to thrombin.
3. Thrombin (Factor IIa): Generated from prothrombin, thrombin is a central enzyme in coagulation. It converts fibrinogen to fibrin, activates factor XIII, and also plays a role in platelet activation.
4. Fibrinogen (Factor I): Thrombin cleaves fibrinogen to form fibrin monomers, which then polymerize to create a fibrin mesh that stabilizes the blood clot.
5. Factor XIII (Fibrin-Stabilizing Factor): Activated by thrombin, it crosslinks fibrin strands, contributing to the stability of the clot.

This cascade of protein interactions ultimately leads to the formation of a stable fibrin clot that helps prevent excessive bleeding at the site of injury. It’s important to note that coagulation is a tightly regulated process, and any imbalance can lead to bleeding disorders (if clotting is impaired) or thrombotic disorders (if clotting is excessive).

From Coagulation Cascade

For FM, ME/CFS and Long COVID — different enzymes!

The amount of each protein is often determined by a person’s DNA. For example, I have a Prothrombin G20210A defect A.K.A. Factor II mutation since that is what it impacts. A person may have multiple DNA coagulation defects. The typical impact of a defect is to create a bottleneck in the normal process resulting in micro-clots, sticky blood and other manifestations. For myself, there are several documented fibrinolytic substances (dissolvers of fibrin) which I use periodically. It works for my defect (it may not for other defects).

The usual problems are:

• Getting DNA testing, many labs and MDs will only test some items: “When testing is indicated, we only screen for the G20210A variant and not for the other rare F2 variants listed above.”[src]
• The best general treatment is low molecular weight heparin (Lovenox is one brand) – why, because it usually has all of the proteins in it — thus an absence is compensated. The downside is that if you have a surplus of one protein it may make things worse — i.e. bleeding risk.