diet FMD Fasting Mimicking Diet / GutMicro 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


GutMicro, Gut Microbiota: Click to Expand ⟱
Source:
Type:
Gut microbiome may affect responses to numerous forms of cancer therapy.
The gut microbiota plays a multifaceted role in cancer biology, influencing tumor development, progression, and patient prognosis. Dysbiosis and specific microbial populations have been linked to various cancers, with implications for patient outcomes. While the relationship between gut microbiota and cancer prognosis is an active area of research, it holds promise for the development of microbiome-based biomarkers and therapeutic strategies in oncology.


Scientific Papers found: Click to Expand⟱
1863- dietFMD,  Chemo,    Effect of fasting on cancer: A narrative review of scientific evidence
- Review, Var, NA
eff↑, ChemoSideEff↓, ChemoSen↑, Insulin↓, HDAC↓, IGF-1↓, STAT5↓, BG↓, MAPK↓, HO-1↓, ATG3↑, Beclin-1↑, p62↑, SIRT1↑, LAMP2↑, OXPHOS↑, ROS↑, P53↑, DNAdam↑, TumCD↑, ATP↑, Treg lymp↓, M2 MC↓, CD8+↑, Glycolysis↓, GutMicro↑, GutMicro↑, Warburg↓, Dose↝,
1856- dietFMD,  immuno,    Targeting the Gut Microbiome to Improve Immunotherapy Outcomes: A Review
- Review, Var, NA
GutMicro↑,
1850- dietFMD,    Fasting-mimicking diet remodels gut microbiota and suppresses colorectal cancer progression
- in-vivo, CRC, NA
TumCP↑, angioG↓, CD8+↑, GutMicro↑, eff↑,
1844- dietFMD,    Unlocking the Potential: Caloric Restriction, Caloric Restriction Mimetics, and Their Impact on Cancer Prevention and Treatment
- Review, NA, NA
Risk↓, AMPK↑, Akt↓, mTOR↓, SIRT1↑, Hif1a↓, NRF2↓, SOD↑, ROS↑, IGF-1↓, p‑Akt↓, PI3K↑, GutMicro↑, OS↑, eff↝, ROS↑, TumCCA↑, *DNArepair↑, DNAdam↑,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

HO-1↓, 1,   NRF2↓, 1,   OXPHOS↑, 1,   ROS↑, 3,   SOD↑, 1,  

Mitochondria & Bioenergetics

ATP↑, 1,   Insulin↓, 1,  

Core Metabolism/Glycolysis

AMPK↑, 1,   Glycolysis↓, 1,   SIRT1↑, 2,   Warburg↓, 1,  

Cell Death

Akt↓, 1,   p‑Akt↓, 1,   MAPK↓, 1,   TumCD↑, 1,  

Autophagy & Lysosomes

ATG3↑, 1,   Beclin-1↑, 1,   LAMP2↑, 1,   p62↑, 1,  

DNA Damage & Repair

DNAdam↑, 2,   P53↑, 1,  

Cell Cycle & Senescence

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

HDAC↓, 1,   IGF-1↓, 2,   mTOR↓, 1,   PI3K↑, 1,   STAT5↓, 1,  

Migration

Treg lymp↓, 1,   TumCP↑, 1,  

Angiogenesis & Vasculature

angioG↓, 1,   Hif1a↓, 1,  

Immune & Inflammatory Signaling

M2 MC↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 1,   Dose↝, 1,   eff↑, 2,   eff↝, 1,  

Clinical Biomarkers

BG↓, 1,   GutMicro↑, 5,  

Functional Outcomes

ChemoSideEff↓, 1,   OS↑, 1,   Risk↓, 1,  

Infection & Microbiome

CD8+↑, 2,  
Total Targets: 42

Pathway results for Effect on Normal Cells:


DNA Damage & Repair

DNArepair↑, 1,  
Total Targets: 1

Scientific Paper Hit Count for: GutMicro, Gut Microbiota
4 diet FMD Fasting Mimicking Diet
1 Chemotherapy
1 immunotherapy
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#:350  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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