Apoptosis = Programmed Cell Death of Damaged Cells

We want damaged cells to die off, protecting the rest of the cells from getting hurt.

Cancer cells grow and grow and continue to make more cancer cells (tumors). Cancer apoptosis, the killing off of these damaged cells. 


Cancer continues to grow especially when it  gets blood supplied to the growing cancer tumor.  Angiogenesis is when the tumor has blood supplied to it.


 then they move to other parts of the body (metastasize). 

What will damage and weaken cells?

Cells that have been attacked by cancer causers (mutations from carcinogens),

Stressed out cells (free radical attack and oxidative stress)

What helps our bodies get rid of damaged cells?  How can we help our damaged cells to do Apoptosis = programed cell death?

Antioxidants are awesome!  Antioxidants help protect our stressed cells from free radical attack.  Vitamins A (B-carotene, Vitamins C and E are excellent!

Short-term (24 hours) or intermittent fasting twice to three times per year in consultation with a doctor or dietitian.






2.1.4 Pathway of apoptosis

As mentioned earlier, the mechanism of apoptosis involves an energy-dependent cascade of molecular events. Apoptotic cell death machinery includes the mitochondria-dependent (intrinsic) pathway and death receptor-dependent (extrinsic) pathway. The intrinsic pathway arises from intracellular signals like cellular stress and DNA damage and relies on the release of proteins from the intermembrane space of mitochondria. However, the extrinsic pathway is activated through the binding of extracellular ligands to death receptors at the cell surface that trigger the multiprotein complex formation known as death-inducing signaling complex (DISC). These two mitochondria- and death receptor-mediated pathways are interconnected and the molecules in one pathway can affect another pathway [3233].

2.1.5 The intrinsic mitochondrial pathway

As its name implies, the intrinsic pathway is activated in response to internal stimuli such as hypoxia, severe DNA damage and oxidative stress and mitochondria play a critical role throughout this apoptosis signaling pathway [3435].