The Cancer Patient Drowns in the Waves of Homeostatic Disorder

Abstract

Neoplastic cells are formed as a result of reprogramming the gene expression. It is only when these cells are classified as non-local by the normal cells that confrontation occurs, and thus cancer begins as a disease. The tumorogenic degradation of the skeletal muscle plays a highly important role in the pathomechanism of the disease. It transforms a diminishing differentiation into an increasing homeostatic disorder, and is forced to provide energy to the malignant cells. This characterizes the completed form of the pathomechanism. Blocking the pathomechanism is the goal of a therapy that can be realized on two levels: At the level of reprogramming of the gene expression, which initiates the formation of neoplastic cells, a “reprogramming” of the reprogramming of gene expression could be achieved by altering the genomic flow of information. Increased anabolism (corresponding to the nutrient surplus) as well as increased catabolism (corresponding to nutrient) could lead to respective changes of the flows of genomic information. These opposing flows in a patient could be expected to result in interference or a shearing effect. Patients with acromegaly exhibit a 9.25% increased neoplasia prevalence, whilst patients with hyperthyroidism have 8.41% increased neoplasia prevalence. Patients with acromegaly and hyperthyroidism have a lower prevalence of neoplasia of 3.30%, i.e. the chance of these patients not contracting cancer is three times greater than patients with either only acromegaly or only hyperthyroidism. At the level of tumorogenic degradation of skeletal muscle, inhibition of muscle degradation by means of hypertriglyceridemia results in a significant prolongation of the life of carcinoma patients. This is based on the fact that inhibition of muscle degradation occurs after infusion of triglyceride emulsion. In the case of S. sanguinis bacteremia, there may be an interaction between enzymes from S. sanguinis , from the digestive tract and from the tumor. The source of infection determines the inactivation of the tumor enzyme and thus suppresses tumor development.