Douglas Kell Phd & Etheresia Pretorius Phd did great research on mechanisms of leaky gut leading to dormant bacteria accumulating in the blood. Then when there is iron overload, or damage to liver cells (especially liver cells), but can occur with damage to other cells, there is increased free iron in the blood. LPS and free iron make the blood more thrombotic. Liver releases acute phase reactants including fibrinogen, factor 8, von Willebrand factor (all 3 are clotting factors) because can trap a bacteria inside a blood clot. Liver also releases hep-cidin (made in liver-kills bacteria) which blocks ferro-portin (iron-door) on duodenocytes (duodenum, small bowel, lining cells that absorb iron). Just as LPS and free iron predispose the fibrinogen protein to become more likely to clot; they make beta amyloid protein more likely to transform from alpha helix to beta pleated sheet. Alpha helices are coiled like cylinders. Beta pleated sheets are flat; more stackable. Beta sheets can stack up into polymers of beta amyloid. The bigger the molecule, the more likely it is insoluble. Proteins are only functional when they are soluble. Big insoluble protein aggregates can have mass effect on adjacent cells; this mass effect can cause adjacent beta amyloid protein to also precipitate (become insoluble). This provides a mechanism for how a protein (a PRION) can propagate disease.
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Mitochondria News for Athletes
