| Rank |
Pathway / Axis |
Cancer Cells |
Normal Cells |
Label |
Primary Interpretation |
Notes |
| 1 |
Insulin / IGF-1 signaling |
↓ IGF-1 signaling (chronic stress) |
↓ IGF-1 with regenerative priming |
Driver |
Sustained growth factor suppression |
Repeated IGF-1 lowering impairs tumor growth programs |
| 2 |
AMPK → mTOR nutrient sensing |
↓ mTOR; ↑ AMPK (growth inhibition) |
↓ mTOR; ↑ AMPK (maintenance mode) |
Driver |
Prolonged anabolic suppression |
More sustained but less acute than STF |
| 3 |
Autophagy / mitophagy |
↑ autophagy → loss of tumor robustness |
↑ autophagy → rejuvenation |
Driver |
Cellular renewal vs destabilization |
Repeated cycles promote organelle quality control |
| 4 |
Mitochondrial metabolism |
↓ metabolic resilience |
↑ mitochondrial fitness |
Secondary |
Energy efficiency divergence |
Normal cells adapt better across cycles |
| 5 |
Inflammatory signaling (NF-κB / cytokines) |
↓ pro-tumor inflammation |
↓ systemic inflammation |
Secondary |
Anti-inflammatory milieu |
Inflammation reduction contributes to chemopreventive effects |
| 6 |
Reactive oxygen species (ROS) |
↑ ROS (secondary, context-dependent) |
↓ ROS |
Secondary |
Metabolism-linked redox shift |
ROS effects are indirect and less pronounced than STF |
| 7 |
NRF2 antioxidant response |
↔ modest activation |
↑ NRF2 (protective) |
Adaptive |
Stress adaptation |
NRF2 supports normal-cell recovery between cycles |
| 8 |
Cell cycle / regeneration |
↓ proliferation |
↑ regeneration post-cycle |
Phenotypic |
Degrowth vs regeneration |
FMD uniquely promotes regeneration upon refeeding |