Hyaluronidase, from wound healing to cancer.
An explanation is proposed as to how the total amount of cells normally are in a cellular equilibrium which results from an energetic equilibrium. When a group of cells is damaged the body can restore this disturbance by the fight and flight reaction-a mechanism in which the circulating body energy is redistributed and in which all body cells are involved cooperatively. An unfavourable side-effect of this mechanism is a diminished uptake of nutrients from the gastro-intestinal tract. Therefore in chronic irritation, cachexia and a decreased resistance to all forms of insult occurs. The energetic equilibrium becomes severely disturbed. Differentiation from a morula cell to a ripe cell is proposed to be an expression of a decreased nutrient supply to the morula. The predominant mechanism for cellular survival is a change from a demand on nutrient supply to a demand on the specialisation of the cell function. The role of the nutrient supply - regulated by hyaluronidase synthesis - then becomes subsidiary to this specific function. It is proposed that cancer originates because of chronic irritation. As a result of the secondary chronic redistribution of body energy in the direction of the irritated area, these cells are chronically hypernourished and then dedifferentiate again in the direction of the morula cell. As a consequence of the reactive mechanism, the cachexia which is so typical of cancer, then occurs. From theoretical considerations, it is predictable that cancer may be effectively treated by two basic manipulations of the energetic equilibrium: firstly by chronically decreasing the nutrient supply to the cancer cells, thereby stimulating differentiation again, and secondly by restoring the energetic equilibrium. In practice this involves supplementation of hyaluronidase together with hyperalimentation.
D002454:Cell Differentiation; D004734:Energy Metabolism; D006801:Humans; D006821:Hyaluronoglucosaminidase / Q000378:metabolism*; D007109:Immunity; D008938:Mitosis; D008954:Models, Biological; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000201:enzymology* / Q000209:etiology / Q000628:therapy; D014945:Wound Healing
D006821:Hyaluronoglucosaminidase