diet FMD Fasting Mimicking Diet / Akt 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


Akt, PKB-Protein kinase B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Akt1 is involved in cellular survival pathways, by inhibiting apoptotic processes; Akt2 is an important signaling molecule in the insulin signaling pathway. It is required to induce glucose transport.

Inhibitors:
-Curcumin: downregulate AKT phosphorylation and signaling.
-Resveratrol
-Quercetin: inhibit the PI3K/AKT pathway.
-Epigallocatechin Gallate (EGCG)
-Luteolin and Apigenin: inhibit AKT phosphorylation


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↑,
1860- dietFMD,  Chemo,    Fasting-mimicking diet blocks triple-negative breast cancer and cancer stem cell escape
- in-vitro, BC, SUM159 - in-vitro, BC, 4T1
PI3K↑, Akt↑, mTOR↑, CDK4↑, CDK6↑, hyperG↓, TumCG↓, TumVol↓, Casp3↑, BG↓, eff↑, eff∅, PKA↓, KLF5↓, p‑GSK‐3β↑, Nanog↓, OCT4↓, KLF2↓, eff↑, ROS↑, BIM↑, ASK1↑, PI3K↑, Akt↑, mTOR↑, CDK1↓, CDK4↑, CDK6↑, eff↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

hyperG↓, 1,   OXPHOS↝, 1,   ROS↑, 4,  

Metal & Cofactor Biology ⓘ

KLF5↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis ⓘ

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

Cell Death ⓘ

Akt↑, 3,   ASK1↑, 1,   BIM↑, 1,   Casp3↑, 3,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK4↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

p‑GSK‐3β↑, 1,   IGF-1↓, 1,   IGFBP1↑, 1,   mTOR↓, 1,   mTOR↑, 2,   Nanog↓, 1,   OCT4↓, 1,   PI3K↑, 2,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   KLF2↓, 1,   MMPs↓, 1,   PKA↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↑, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 6,   eff∅, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,  

Functional Outcomes ⓘ

ChemoSideEff↓, 1,   TumVol↓, 1,  
Total Targets: 36

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: Akt, PKB-Protein kinase B
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#:4  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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