diet FMD Fasting Mimicking Diet / hyperG 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


hyperG, hyperglycemia: Click to Expand ⟱
Source:
Type:
Hyperglycemia is defined as elevated blood glucose levels and may result from diabetes mellitus, insulin resistance, or stress-induced metabolic changes.

– Elevated glucose levels provide abundant energy resources, potentially facilitating rapid tumor cell division and growth.
– Some cancers upregulate glucose transporters (such as GLUT1) to utilize the increased availability of glucose.

Oxidative Stress and DNA Damage:
– Hyperglycemia is associated with the production of reactive oxygen species (ROS) and advanced glycation end-products (AGEs).
– Both ROS and AGEs can lead to DNA damage, genomic instability, and alterations in cell signaling pathways that promote tumor progression.

– Studies have linked hyperglycemia with increased tumor aggressiveness in several cancer types, including breast, colorectal, and pancreatic cancers.
– Patients with hyperglycemia may experience more rapid disease progression and a higher likelihood of metastasis.
– In some cases, elevated glucose levels have been associated with chemotherapy resistance and decreased sensitivity to radiation therapy.

– Effective control of blood sugar through dietary interventions, medications (e.g., insulin, metformin), and lifestyle modifications may beneficially impact cancer outcomes.
– Regular monitoring of blood glucose and hemoglobin A1c (HbA1c) can inform oncologists about potential metabolic challenges during cancer treatment.
Scientific Papers found: Click to Expand⟱
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 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 ⓘ

hyperG↓, 1,   ROS↑, 1,  

Metal & Cofactor Biology ⓘ

KLF5↓, 1,  

Cell Death ⓘ

Akt↑, 2,   ASK1↑, 1,   BIM↑, 1,   Casp3↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK4↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

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

Migration ⓘ

KLF2↓, 1,   PKA↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↑, 2,  

Drug Metabolism & Resistance ⓘ

eff↑, 3,   eff∅, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,  

Functional Outcomes ⓘ

TumVol↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: hyperG, hyperglycemia
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#:1167  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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