The Immune System, Amyloidosis, Atherosclerosis, and Rheumatoid Disease
The Immune System attacks foreign substances and bacteria by phagocytosis and by releasing “antibody” proteins that bind to foreign substances and bacteria and activate immune cells and blood enzymes (the complement cascade) to destroy them.
MSM hyperactivity elevates immune activity, so that elevated immune activity accompanies most forms of disease, but there is no evidence that immune activity causes disease or attacks body tissues. Nevertheless, rheumatoid diseases are often attributed to “autoimmune” activity, if only for lack of a better explanation. Likewise, there is no evidence that immune activity causes or prevents cancer .
All forms of rheumatoid disease are characterized by amyloid protein deposits in affected tissues, including rheumatoid arthritis, Sjogren's disease, systemic lupus Erythematosis, scleroderma, and diabetes. For example, amyloid nodules appear in joint tissues in rheumatoid arthritis. The cause of amyloidosis remains unknown.
The mammalian stress mechanism suggests that amyloid protein results from abnormal insoluble fibrin disintegration. The capillary gate mechanism continuously generates and disintegrates insoluble fibrin to regulate capillary flow resistance. Insoluble fibrin disintegration normally produces harmless "fibrin split products" (FSP). Under certain circumstances fibrillar FSP may undergo abnormal conformational change into harmful amyloid protein that damages organs, tissues, and blood vessels. Amyloidosis is closely associated with atherosclerosis, and may be its underlying cause. Amyloidosis may also explain accelerated capillary senescence.