diet FMD Fasting Mimicking Diet / M2 MC 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


M2 MC, M2 macrophage conversion: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
M2 macrophages (M2 MC) are a subtype of macrophages that are generally associated with anti-inflammatory responses, tissue repair, and the promotion of tumor growth.
Strategies to reprogram M2 macrophages into a more pro-inflammatory M1 phenotype or to inhibit their function are being explored in cancer therapies.
M2 macrophages can play a dual role, promotion/suspression.
M2 macrophages are a subtype of macrophages that are generally associated with anti-inflammatory responses, tissue repair, and the promotion of tumor growth. The conversion of macrophages from the M1 (pro-inflammatory) to the M2 (anti-inflammatory) phenotype is a critical process in the tumor microenvironment and has significant implications for cancer progression.

M2 macrophages are generally considered protumorigenic. They secrete various cytokines and growth factors that promote tumor cell proliferation, angiogenesis, and tissue remodeling. Additionally, they can suppress the activity of cytotoxic T cells and natural killer (NK) cells, further aiding tumor immune evasion.
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↝,
1849- dietFMD,    The emerging role of fasting-mimicking diets in cancer treatment
- Review, Var, NA
TumCG↓, toxicity∅, BG↓, IGF-1↓, mTOR↓, M2 MC↓, eff↑, ChemoSen↑, QoL↑, RadioS↑, selectivity↑,

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 ⓘ

HO-1↓, 1,   OXPHOS↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   Insulin↓, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   SIRT1↑, 1,   Warburg↓, 1,  

Cell Death ⓘ

MAPK↓, 1,   TumCD↑, 1,  

Autophagy & Lysosomes ⓘ

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

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   IGF-1↓, 2,   mTOR↓, 1,   STAT5↓, 1,   TumCG↓, 1,  

Migration ⓘ

Treg lymp↓, 1,  

Immune & Inflammatory Signaling ⓘ

M2 MC↓, 2,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

BG↓, 2,   GutMicro↑, 2,  

Functional Outcomes ⓘ

ChemoSideEff↓, 1,   QoL↑, 1,   toxicity∅, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 34

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: M2 MC, M2 macrophage conversion
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#:177  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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