“All things are subject to interpretation; whichever interpretation prevails at a given time is a function of power, not truth.” – Frederich Nietzsche
Thrombin is the “universal enzyme of extracellular energy transduction.” It utilizes ATP to energize all extracellular enzymes and cell activities involved with embryological development, physiology, pathology, and stress, including hemodynamic physiology, hormone release, nervous activity, tissue maintenance, and tissue repair.
The MSM continuously generates thrombin in all tissues to energize tissue maintenance. It elevates thrombin to energize tissue repair. It restores thrombin to maintenance levels as tissue repair nears completion.
Like intracellular ATPase, extracellular thrombin activity requires ATP and Ca+. Parathyroid glands maintain Ca+ within a narrow range to optimize thrombin activity. Drugs and chemicals that elevate Ca+ exaggerate thrombin activity, and vice-versa. For example, magnesium Sulphate treats eclampsia by displacing Ca+ and inhibiting thrombin activity.
All cells thus far tested have PAR (thrombin receptors) on their outer surface that determine how they react to thrombin elevations. Four different types of PAR have been discovered thus far. Individual cell types have characteristic PAR types and numbers that determine how the cell reacts to thrombin elevations. Like sails on tiny ships, these can be reconfigured by the cell to alter cell reactions to thrombin during embryological development, tissue repair, and malignancy.
Ordinarily thrombin elevations energize cellular activities and inhibit apoptosis while thrombin starvation initiates apoptosis in fibroblasts, but cells react to thrombin differently at different times and in different contexts. Thrombin can energize apoptosis, inhibit apoptosis, or be toxic to the cell. Additional research is needed to clarify thrombin effects, as present understanding relies on invitro studies that may not apply to living organisms.
The following thrombin effects of thrombin reflect its universal role in extracellular ATP energy utilization:
• Chemotaxis of platelets, osteocytes, white blood cells, and other tissue repair cells
• Mitosis (cell multiplication)
• Metabolism (cell energy consumption and heat production)
• Muscle contraction
• Angiogenesis (capillary proliferation)
• Platelet activation, chemotaxis, and thromboxane release
• Proliferation, spreading and gap formation in the vascular endothelium
• Chemokine, cytokine, interleukin, bradykinins, caspase, and prostaglandin release
• Bone, muscle, collagen, and immune protein production by osteocytes, myocytes, fibroblasts, and immune cells
• Conversion of fibrinogen to soluble fibrin
• Conversion of fibrillar soluble fibrin to three-dimensional insoluble fibrin
• Stabilization of insoluble fibrin via “Thrombin-Activated Fibrinolysis Inhibitor” (TAFI)
• Inflammation, which loosens cell connections to facilitate chemotaxis
• Astrocyte and glial cell proliferation in brain tissue
• Gelsolin activation, which digests harmful actin in blood
• Complement cascade activity
• T-cell activation
• Blast transformation in lymphocytes
• Macrophage phagocytic activity
• Plasma (immune) cell and neutrophil activation
• “Tumor Necrosis Factor” release from microglial cells
• Tumor growth, malignancy, and fibrosis
• Apoptosis inhibition
• Intracellular gap formation in the vascular endothelium