Increasing Oxidation via Chemicals,Radiation,toxins, heavy metals is other then the best ever
- Conventional Cancer treatments kill cancer cells by increasing oxidation and including apoptosis
- Damaged Apoptosis control mechanisms,such as the p53 gene, allow therapy-resistant cells to emerge and multiply
The ideal redox therapy would do both
- an antioxidant that repairs apoptosis controls
- a pro oxidant that signals DNA initiation of apoptosis in damaged cancer cells
oxidizes NADH to NAD thus helping to restore aerobic function
- Oxidative stress/injury and oxygen under-utilization cause progressive anaerobic shift
- Sustained cellular injury leads to excessive inflammatory cytokines which eventually change cellular behavior
- Damaged cells (that sustain aerobic metabolism) normally respond to the oxidative signal with mitochondria-coordinated apoptosis
- Excessive DNA damage and mutations with shift to glycolytic metabolism results in loss of p53 control of apoptosis
- oxidation/inflammation promotes uncontrolled cellular proliferation
- injured multi-cellular tissues undergo malignant transformation and regress back to the selfish cell - single cell survival behaviors
- Cancer stabilizes in anaerobic metabolism,angiogenesis, with aggressive cellular proliferation, metastases, and body wasting
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Preventing and treating cancer with progesterone.
Cell division, when it is part of the body's continuous renewal and adaptation, isn't a source of mutations or degeneration, but when it is induced by the mediators of inflammation produced in response to injury, it leads to inherited changes, loss of differentiated function, and eventually to genetic instability.
When cell division is so disturbed that the number of chromosomes becomes abnormal, the instability of these cells decreases their ability to survive, but when the causes of the inflammation persist, they will continue to be replaced by other abnormal cells. The toxic products of dying cells can reach a point at which the debris can't be removed, adding to the injury and inflammation. The damaged bystander cells spread their influence through a cancer field, injuring more cells.
- Conventional Cancer treatments kill cancer cells by increasing oxidation and including apoptosis
- Damaged Apoptosis control mechanisms,such as the p53 gene, allow therapy-resistant cells to emerge and multiply
The ideal redox therapy would do both
- an antioxidant that repairs apoptosis controls
- a pro oxidant that signals DNA initiation of apoptosis in damaged cancer cells
oxidizes NADH to NAD thus helping to restore aerobic function
- Oxidative stress/injury and oxygen under-utilization cause progressive anaerobic shift
- Sustained cellular injury leads to excessive inflammatory cytokines which eventually change cellular behavior
- Damaged cells (that sustain aerobic metabolism) normally respond to the oxidative signal with mitochondria-coordinated apoptosis
- Excessive DNA damage and mutations with shift to glycolytic metabolism results in loss of p53 control of apoptosis
- oxidation/inflammation promotes uncontrolled cellular proliferation
- injured multi-cellular tissues undergo malignant transformation and regress back to the selfish cell - single cell survival behaviors
- Cancer stabilizes in anaerobic metabolism,angiogenesis, with aggressive cellular proliferation, metastases, and body wasting
=======================
Preventing and treating cancer with progesterone.
Cell division, when it is part of the body's continuous renewal and adaptation, isn't a source of mutations or degeneration, but when it is induced by the mediators of inflammation produced in response to injury, it leads to inherited changes, loss of differentiated function, and eventually to genetic instability.
When cell division is so disturbed that the number of chromosomes becomes abnormal, the instability of these cells decreases their ability to survive, but when the causes of the inflammation persist, they will continue to be replaced by other abnormal cells. The toxic products of dying cells can reach a point at which the debris can't be removed, adding to the injury and inflammation. The damaged bystander cells spread their influence through a cancer field, injuring more cells.