diet Short Term Fasting / ALAT Cancer Research Results

dietSTF, diet Short Term Fasting: Click to Expand ⟱
Features:
Short-term fasting (STF) 48 to 72 h before chemotherapy appears to be more effective than intermittent fasting. Preliminary data show that STF is safe but challenging in cancer patients receiving chemotherapy.

Short-Term Fasting (STF; ~24–72 h water / very low calorie fast) Cancer vs Normal Cell Effects
Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Insulin / IGF-1 signaling ↓ IGF-1 survival signaling (stress) ↓ IGF-1 with adaptive protection Driver Differential stress resistance (DSR) Cancer cells fail to adapt to acute IGF-1 withdrawal; normal cells enter protective mode
2 AMPK → mTOR nutrient sensing ↑ AMPK; ↓ mTOR (growth crisis) ↑ AMPK; ↓ mTOR (protective quiescence) Driver Catabolic enforcement Rapid mTOR suppression removes anabolic support from tumors
3 Autophagy (ATG program) ↑ autophagy → metabolic exhaustion ↑ autophagy → cytoprotection Driver Catabolic stress vs survival recycling Autophagy is protective in normal cells but destabilizing in cancer cells
4 Mitochondrial metabolism / flexibility ↓ metabolic flexibility; ↓ ATP resilience ↑ mitochondrial efficiency Secondary Energy crisis vs optimization Tumors struggle to switch fuels; normal cells adapt
5 Reactive oxygen species (ROS) ↑ ROS (secondary to energy stress) ↓ ROS Secondary Metabolic redox divergence ROS increase is indirect, arising from metabolic collapse
6 NRF2 antioxidant response ↔ or insufficient activation ↑ NRF2 (protective) Adaptive Stress buffering in normal cells Normal cells activate antioxidant defenses; tumors often cannot
7 Cell cycle / proliferation ↓ proliferation / ↑ arrest ↓ proliferation (protective quiescence) Phenotypic Growth suppression Cell-cycle slowdown reflects upstream nutrient deprivation
8 Therapy sensitivity (chemo / RT) ↑ sensitivity ↓ toxicity Phenotypic Differential stress sensitization STF selectively sensitizes tumors while protecting normal tissue

Fasting Type vs Effectiveness
Fasting Type Definition Primary Metabolic / Signaling Effects Cancer-Relevant Mechanisms Evidence Base Relative Effectiveness*
Caloric Restriction (CR) Chronic daily reduction in total caloric intake (typically 20–40%) without malnutrition. ↓ insulin, ↓ IGF-1, ↓ mTOR, ↑ AMPK, ↑ autophagy Reduces growth signaling; improves metabolic milieu; may slow tumor initiation/growth in models. Extensive animal data; observational human data. Moderate–High
Caloric Restriction Mimetic (CRM) Non-fasting interventions that mimic CR signaling without major calorie reduction. ↓ mTOR, ↑ AMPK, ↑ autophagy; altered acetyl-CoA/epigenetic tone (context-dependent) Replicates key CR pathways while preserving nutrition; potential synergy with therapy (context-specific). Strong mechanistic + preclinical; growing human data. Moderate–High
Intermittent Fasting (IF) Regular cycles of fasting and feeding (e.g., 16:8, 18:6, 20:4). Periodic ↓ insulin/IGF-1; ↑ fat oxidation; mild ketosis (variable) Metabolic stress on tumor cells; improved insulin sensitivity; may modulate inflammation. Good animal data; emerging human data. Moderate
Alternate-Day Fasting (ADF) Alternating 24 h fasting with 24 h ad libitum feeding. Strong oscillations in insulin/glucose/ketones; improved metabolic switching Enhanced metabolic flexibility; may promote normal-cell stress resistance. Animal data strong; limited oncology-specific human data. Moderate–High
Short-Term Fasting (STF) Complete or near-complete fasting for ~24–72 h (often around therapy). Sharp ↓ IGF-1; ↓ glucose; ↑ ketones; ↑ autophagy Differential stress resistance (normal-cell protection) and potential tumor sensitization (context-specific). Strong preclinical; small human trials. High
Fasting-Mimicking Diet (FMD) Low-calorie, low-protein, low-sugar diet for 3–5 days designed to simulate fasting. ↓ IGF-1; ↓ mTOR; ↑ autophagy; partial ketosis Similar benefits to STF with improved tolerability; may enhance therapy response in some contexts. Strong animal; increasing human interventional data. High
Protein Restriction (PR) Reduction in total protein or specific amino acids (e.g., methionine restriction). ↓ IGF-1; ↓ mTORC1; altered amino-acid sensing Targets amino-acid dependencies and growth signaling; may synergize with selected therapies. Strong mechanistic; animal + early human data. Moderate–High
Ketogenic / Very-Low-Carb Diet Diet inducing sustained ketosis without fasting (variable protein content). ↓ glucose; ↓ insulin; ↑ ketones May constrain glycolysis-dependent tumors; effects are heterogeneous by cancer type and context. Mixed animal data; heterogeneous human data. Low–Moderate
Time-Restricted Feeding (TRF) Fixed daily eating window (typically 6–12 h), emphasizing circadian alignment. Circadian stabilization; modest ↓ insulin exposure; partial metabolic switching Improves metabolic control; limited deep autophagy unless fasting is long (≥18–20 h). Early-stage; indirect oncology evidence. Low–Moderate
Water-Only Prolonged Fasting Extended complete fasting (>72 h). Deep ketosis; strong autophagy; high physiological stress Potentially strong tumor stress but higher risk and limited controlled oncology study. Limited / heterogeneous; safety considerations significant. Uncertain / Not Rated 
Notes on Effectiveness Ratings
-High: Consistent preclinical efficacy + mechanistic clarity + early human interventional support
-Moderate–High: Strong biology with partial human validation
-Moderate: Solid rationale but limited oncology-specific human data
-Low–Moderate: Indirect or context-dependent effects
-Uncertain: Insufficient or high-risk evidence base
TRF Pattern Feeding Window Fasting Duration Metabolic Depth Cancer-Relevant Effects
14:10 TRF 10 h eating / 14 h fast 14 h Mild Improves insulin sensitivity; typically minimal autophagy.
16:8 TRF 8 h eating / 16 h fast 16 h Mild–Moderate Reduces daily insulin/IGF-1 exposure; partial metabolic switching.
18:6 TRF 6 h eating / 18 h fast 18 h Moderate Greater fat oxidation; autophagy initiation more likely (variable).
20:4 TRF 4 h eating / 20 h fast 20 h Moderate–High Lower insulin for longer; early ketosis in some individuals; more “fasting-like.”
22:2 TRF 2 h eating / 22 h fast 22 h High (borderline IF) Strong circadian + metabolic stress; limited tolerability for many. 
Circadian Timing (Critical for Cancer Relevance)
Early TRF (eTRF)
-Feeding window: ~07:00–15:00 or 08:00–16:00
-Superior reductions in insulin, glucose AUC, and IGF-1 signaling
-Aligns with PER/CRY, BMAL1, CLOCK oscillations
-More favorable for cancer-relevant metabolic control
Late TRF
-Feeding window: ~12:00–20:00 or later
-Weaker insulin and IGF-1 suppression
-Circadian misalignment may blunt benefits


ALAT, ALT, alanine aminotransferase: Click to Expand ⟱
Source:
Type: enzyme
(or ALT) -Used to be called serum glutamic-pyruvic transaminase (SGPT)
Most common in the liver.
An enzyme your body needs to break down proteins into energy.
It plays a crucial role in amino acid metabolism and is often measured in blood tests to assess liver function.
The catabolism of alanine by alanine aminotransferase 2 (ALT2) to pyruvate, was critical for the survival of non-small cell lung carcinoma (NSCLC) cells during glucose starvation. After knockdown of ALT2, cells were significantly more sensitive to glucose withdrawal compared to wildtype cells, which were rescued when supplemented with pyruvate.
Alanine aminotransferase (ALT) expression is highly elevated in the serum of patients with hepatocellular carcinoma.
A common example of dietary cancer therapy is the ketogenic diet, providing a fat-rich, low carbohydrate diet. The rationale is to reduce circulating glucose levels and induce ketosis.
Used as a clinical biomarker for Liver function.


Scientific Papers found: Click to Expand⟱
3707- dietSTF,    Intermittent fasting protects against the deterioration of cognitive function, energy metabolism and dyslipidemia in Alzheimer’s disease-induced estrogen deficient rats
- in-vivo, AD, NA
*memory↑, *Aβ↓, *AST↓, *ALAT↓,

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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,  
Total Targets: 5

Scientific Paper Hit Count for: ALAT, ALT, alanine aminotransferase
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#:226  Target#:554  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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