diet FMD Fasting Mimicking Diet / glyC Cancer Research Results

dietFMD, diet FMD Fasting Mimicking Diet: Click to Expand ⟱
Features:
5-day diet to mimic fasting without fasting.
FMDs are caloric-restricted plant–based diets containing low proteins, low sugar and high fats which represent a more feasible and safer option to water-only fasting.
Fasting modality                         Approx CRIS
--------------------------------------   ----------
Time-restricted eating (12–16 h)          –3 to –4
Early time-restricted eating (eTRE)        –4
Intermittent fasting (24 h 1–2x/week)     –4
Periodic fasting / FMD                    –4 to –5*
Calorie restriction (chronic)             –3 (risk tradeoffs)

Compare STF(short term Fasting) to FMD
IGF-1 / insulin suppression (core driver)
| Aspect            | STF                 | FMD      |
| ----------------- | ------------------- | -------- |
| Depth             | **Very deep**       | Moderate |
| Speed             | **Rapid (24–48 h)** | Gradual  |
| Tumor stress      | **High**            | Medium   |
| Normal protection | High                | High     |
Fasting-Mimicking Diet (FMD; ~5-day low-protein, low-calorie cycle) Cancer vs Normal Cell Effects
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


glyC, glycogen: Click to Expand ⟱
Source:
Type:
Glycogen
• Many tumors, especially under hypoxic or nutrient-deprived conditions, reprogram their metabolism to store glycogen as an energy reserve.

• Increased glycogen accumulation can serve as a survival mechanism that helps cancer cells endure metabolic stress, which, in turn, may be associated with more aggressive behavior.

• Prognosis:
– In certain cancers (e.g., certain glioblastomas, pancreatic cancers), high intratumoral glycogen content has been associated with adaptation to hypoxia and resistance to therapy.
– Such adaptations often correlate with a poorer prognosis, as the glycogen reservoir helps support tumor progression under adverse conditions.
Frequently increased (accumulated) in tumors exposed to hypoxia, nutrient deprivation, or intermittent perfusion.

Glycogen accumulation in cancer marks a stress-adapted metabolic state. It functions as an internal energy and redox buffer that enables tumors to survive hypoxia and treatment-induced shocks.


Scientific Papers found: Click to Expand⟱
1854- dietFMD,    How Far Are We from Prescribing Fasting as Anticancer Medicine?
- Review, Var, NA
ChemoSideEff↓, ChemoSen↑, IGF-1↓, IGFBP1↑, adiP↑, glyC↓, E-cadherin↑, MMPs↓, Casp3↑, ROS↑, ATP↓, AMPK↑, mTOR↓, ROS↑, Glycolysis↓, NADPH↓, OXPHOS↝, eff↑, eff↑, *RAS↓, *MAPK↓, *PI3K↓, *Akt↓, eff↑, ROS↑, Akt↑, Casp3↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

OXPHOS↝, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis ⓘ

adiP↑, 1,   AMPK↑, 1,   glyC↓, 1,   Glycolysis↓, 1,   NADPH↓, 1,  

Cell Death ⓘ

Akt↑, 1,   Casp3↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1↓, 1,   IGFBP1↑, 1,   mTOR↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   MMPs↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 3,  

Functional Outcomes ⓘ

ChemoSideEff↓, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

Akt↓, 1,   MAPK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,   RAS↓, 1,  
Total Targets: 4

Scientific Paper Hit Count for: glyC, glycogen
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:79  Target#:1192  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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