Clinical Manifestations of Hepatitis C
Hepatitis C is a liver-centered viral infection that causes metabolic imbalances in those infected. These imbalances result in clinical manifestations of Hepatitis C, which can be brought into balance (homeostasis) by the dietary administration of specific nutrients at specific levels. These clinical manifestations are:
The HepTech Comprehensive Medical Food involves the administration of distinctive nutrients that Hepatitis C patients require to ameliorate the clinical manifestations of Hepatitis C. Amelioration of these specific clinical manifestations of Hepatitis C decreases levels of activation of the metabolic stimulus (NFkappaB) that triggers the generation and accumulation of scar tissue (fibrosis or cirrhosis) in the spaces of the liver. Click here for more information about fibrosis.
- Hepatitis C causes an increase in the production of free radical reactive oxygen species (ROS) in the mitochondria of cells. The resulting oxidative stress in the cytosol is clinically significant to the pathogenesis of Hepatitis C as well as in the generation and progression of fibrosis in Hepatitis C patients.
- Hepatitis C causes increased levels of inflammation in the cells of the liver. This inflammation is clinically significant to the pathogenesis of Hepatitis C as well as in the progression of fibrosis in Hepatitis C patients.
- Hepatitis C causes oxidative damage to vulnerable cell membranes, including interior organelle membranes. This is manifested by changes in membrane phospholipid profiles, as well as changes in membrane function, fluidity, and integrity. Hepatitis C genotype 3 contributes to steatosis, which is manifested by the abnormal retention of lipids inside the cells of the liver. Steatosis also has metabolic causation, (NAFLD and NASH). Steatosis, regardless of cause, is clinically significant in the pathogenesis of Hepatitis C as well as in the progression of fibrosis in Hepatitis C patients.
The combination of the above clinical manifestations of Hepatitis C:
- Promotes the activation of the gene transcription factor NFkappaB. This activation starts a chain of events that leads the progression of fibrosis or cirrhosis in the liver. Specifically, NFkappaB activation triggers the production of pro-inflammatory peptides and proteins, the activation of stellate cells, their conversion to myofibroblasts, and the secretion and accumulation of collagen (scar tissue) in the spaces of the liver (fibrosis or cirrhosis).