Database Query Results : diet Short Term Fasting, ,

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

Scientific Papers found: Click to Expand⟱

1626-

dietSTF,

dietFMD,

When less may be more: calorie restriction and response to cancer therapy

Review,

Var,

CRM↑,
ChemoSen↑, CR mimetics as adjuvant therapies to enhance the efficacy of chemotherapy, radiation therapy, and novel immunotherapies.
RadioS↑,
eff↑, CR mimetics as adjuvant therapies to enhance the efficacy of chemotherapy, radiation therapy, and novel immunotherapies.
eff↑, Intermittent fasting has been shown to enhance treatment with both chemotherapy and radiation therapy.
IGF-1↓, Exposure to an energy restricted diet results in reduced systemic glucose and growth factors such as IGF-1
TumCG↓, reduction of IGF-1 levels in CR results in decreased tumor growth and progression
AMPK↑, CR also induces activation of AMP-activated protein kinase (AMPK), (working in opposition to IGF-1)
eff↑, Recent research in our lab showed that combining autophagy inhibition with a CR regimen reduced tumor growth more than either treatment alone [20].
ChemoSen↑, Short-term fasting has been shown to improve chemotherapeutic treatment with etoposide [40], mitoxantrone, oxaliplatin [41], cisplatin, cyclophosphamide, and doxorubicin [42] in transgenic and transplant mouse models
RadioS↑, Alternate day fasting has also been shown to improve the radiosensitivity of mammary tumors in mice
ROS↑, improve the radiosensitivity: likely due to enhanced oxidative stress and DNA damage during short-term fasting on cancer cells.
DNAdam↑,
eff↑, fasting-mimicking diet, in which mice are fed the same amount of food as control mice, albeit with a severely reduced caloric density, showed a similar reduction in tumor growth as short-term starvation
HO-1↓, fasting-mimicking diet were associated with increased autophagy in the cancer cells and reduced heme oxygenase-1 (HO-1) in the microenvironment

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,

Rats

*memory↑, Intermittent fasting also prevented memory loss: short-term and special memory loss.
*Aβ↓, the rats in the AD-IMF groups exhibited less β-amyloid deposition than those in the AD-AL
*AST↓, Serum aspartate transaminase (AST) and alanine transaminase (ALT) levels, indexes of liver damage, were not significantly changed by AD but they were greatly lowered by IMF.
*ALAT↓,

3708-

dietSTF,

Fasting as a Therapy in Neurological Disease

*PGC-1α↑, figure 1
*AMPK↑,
*adiP↑,
*glucose↓,
*Insulin↓,
*mTOR↓,
*IL6↓,
*TNF-α↓,
*cognitive↑, or even enhanced—cognitive performance
*Inflam↓, fasting suppresses inflammation, reducing the expression of pro-inflammatory cytokines such as interleukin 6 (IL6) and tumor necrosis factor α (TNFα)
*eff↑, mice fasted on alternate days can eat twice as much on the feeding day, such that their net weekly calorie intake remains similar to mice fed ad libitum; despite the lack of overall calorie restriction, the former still display beneficial metabolic e
*neuroP↑, Fasting can also prevent and treat many neurological disorders in animals;
ChemoSen↑, fasting has been shown to improve the therapeutic responses of a variety of rodent cancer models, including gliomas, to chemotherapy
eff↓, shorter nightly fasts were associated with an increased recurrence of cancer
chemoP↑, fasting before or after chemotherapy decreased chemotherapy-related adverse effects, such as weakness, fatigue, and gastrointestinal upset
*eff↑, implementation of a fasting regimen after a traumatic brain injury confers neuroprotection and improves functional recovery

3709-

dietSTF,

Intermittent Fasting Protects against Alzheimer’s Disease Possible through Restoring Aquaporin-4 Polarity

in-vitro,

AD,

 mouse model of AD

*cognitive↑, results showed that IF ameliorated cognitive dysfunction, prevented brain from Aβ deposition, and restored the AQP4 polarity in a mouse model of AD
*Aβ↓,
*AQPs↓, IF down-regulated the expression of AQP4-M1 and histone deacetylase 3, reduced AQP4-M1/M23 ratio,
*HDAC3↓,

4159-

dietSTF,

2DG,

CRMs,

Meal size and frequency affect neuronal plasticity and vulnerability to disease: cellular and molecular mechanisms

Review,

AD,

*BDNF↑, enhance neuronal plasticity and resistance to oxidative and metabolic insults; they include neurotrophic factors such as brain-derived neurotrophic factor (BDNF), protein chaperones such as heat-shock proteins, and mitochondrial uncoupling proteins
*HSPs↑,
*eff↑, DR can be achieved by administering hormones that suppress appetite (leptin and ciliary neurotrophic factor) or by supplementing the diet with 2-deoxy-d-glucose, which may act as a calorie restriction mimetic

4180-

dietSTF,

Brain-derived neurotrophic factor, but not body weight, correlated with a reduction in depression scale scores in men with metabolic syndrome: a prospective weight-reduction study

Human,

Obesity,

*BDNF↑, Zung SDS only significantly improved in men with increased fasting BDNF levels after a lifestyle intervention.

5065-

dietSTF,

dietFMD,

Nutrition, GH/IGF-I Signaling, and Cancer

Review,

Var,

GH↓, These effects of fasting/FMD on normal and cancer cells are mediated at least in part by the reduction in GH and IGF-I signaling.
IGF-1↓,
glucose↓, In mice, cycles of a 4-day FMD have been shown to lower blood glucose levels by 40 % and IGF-I by 45 % while increasing ketone bodies 9-fold and IGFBP-1, which inhibits IGF-I, by the end of the FMD
IGFBP1↑,
OS↑, FMD cycles adopted twice a month starting in middle age extend health span and longevity, reduce visceral fat and skin lesions, promote hippocampal neurogenesis, rejuvenate the immune system, and delay bone mineral density loss in mice
Imm↑,
neuroP↑,
BMD↑,
Dose↝, FMD is a plant-based caloric-restricted dietary regimen (typically between 300 and 1100 kcal per day) characterized by low proteins, sugars, and relatively high unsaturated fats.
Risk↓, Remarkably, these bi-monthly FMD cycles started in middle age reduce tumor incidence and delay cancer onset.
other↑, The robust epidemiological evidence that high animal protein consumption increases serum IGF-I levels in humans
TumCP↓, For these reasons, the GH/IGF-I axis emerged as a promising target for cancer treatments and prevention aimed at inhibiting cell proliferation by down-regulating IGF-I

5066-

dietSTF,

Intermittent and Periodic Fasting, Hormones, and Cancer Prevention

Review,

Var,

IGF-1↓, Long-term CR is reported to reduce IGF-1 serum levels in rodents by ~30–40%, protecting them against several types of cancers
OS↑, effects of CR in retarding aging, by increasing lifespan by ~35%, reducing the incidence of kidney disorders, chronic pneumonia and tumors [
AntiAge↑,
glucose↓, underline mechanisms could be mediated by the decrease in blood glucose, IGF-1 and insulin levels
Insulin↓,

5068-

dietSTF,

mTOR-autophagy axis regulation by intermittent fasting promotes skeletal muscle growth and differentiation

in-vivo,

Nor,

*glucose↓, Following short-term fasting, blood glucose levels in the sMF and sSF groups were significantly lower than those in the ND group
ROS↑, reactive oxygen species (ROS) levels were significantly higher in the sSF group compared to the sMF and ND groups
LC3B↑, sSF groups exhibited a significant upregulation of LC3B protein levels
p62↓, Conversely, p62 levels (1.00 ± 0.08, 0.58 ± 0.09 & 0.28 ± 0.05, P < 0.01) and the phosphorylation ratio of mTOR (p-mTOR/mTOR) (1.00 ± 0.04, 0.70 ± 0.10 & 0.35 ± 0.03, P < 0.01) were significantly reduced.
p‑mTOR↓,
p‑AMPK↑, IMF group exhibited a significant increase in the LC3B-II/I ratio and the phosphorylation ratio of AMPK (p-AMPK/AMPK)

5069-

dietSTF,

The Role of Intermittent Fasting in the Activation of Autophagy Processes in the Context of Cancer Diseases

Review,

Var,

Risk↓, IF has shown potential for reducing cancer risk and enhancing therapeutic efficacy by sensitizing tumor cells to chemotherapy and radiotherapy.
ChemoSen↑, intermittent fasting (IF) may enhance the effectiveness of chemotherapy and targeted therapies by activating autophagy. IF enhances the effectiveness of chemotherapy, including drugs such as cisplatin, cyclophosphamide, and doxorubicin
RadioS↑, disease stabilization, improved response to radiotherapy patients with glioma
*Dose↝, 16:8—16 h of fasting with an 8 h eating window;
*Dose↝, 5:2—consuming a standard number of calories for 5 days and reducing intake to 25% of daily requirements for 2 days;
*Dose↝, Eat–Stop–Eat—complete fasting for 24–48 h.
*LDL↓, IF during Ramadan (approximately 18 h of fasting for 29–30 days) reduces LDL cholesterol levels and increases HDL cholesterol in women, as well as reducing inflammatory markers such as CRP and TNF-α
*CRP↓,
*TNF-α↓,
TumAuto↓, Intermittent fasting activates autophagy as an adaptive mechanism to nutrient deprivation, which may modulate tumor development and treatment
GLUT1↓, fasting reduces the expression of glucose transporters GLUT1/2, which slow down cancer metabolism and increase the susceptibility of cancer cells to oxidative stress
GLUT2↓,
glucose↓, studies on cell and animal models have shown that intermittent fasting reduces glucose and insulin-like growth factor (IGF-1) levels [103], as well as insulin [104,105], resulting in the inhibition of the mTOR kinase pathway (PI3K/Akt/mTOR), suppress
IGF-1↓,
Insulin↓,
mTOR↓,
mTORC1↓, suppression of mTORC1 [22], and activation of AMPK through increased ADP/ATP ratio in cells, which supports autophagy and induces apoptosis
AMPK↑,
Warburg↓, Moreover, IF counteracts the Warburg effect by promoting oxidative phosphorylation, leading to an increase in the production of reactive oxygen species (ROS) and enhanced oxidative stress in cancer cells [106,108], causing DNA damage and the activati
OXPHOS↑,
ROS↑,
DNAdam↑,
JAK1↓, fasting reduces the production of adenosine by cancer cells, inhibiting the activation of the JAK1/STAT pathway, thereby reducing cancer cell proliferation
STAT↓,
TumCP↓,
QoL↑, reduction in IGF-1 levels, improved quality of life patients with multiple cancer types

5070-

dietSTF,

A review of fasting effects on the response of cancer to chemotherapy

Review,

Var,

chemoP↑, Studies suggest that fasting before or during chemotherapy may induce differential stress resistance, reducing the adverse effects of chemotherapy and enhancing the efficacy of drugs.
ChemoSen↑,
*DNArepair↑, (1) repairing DNA damage in normal tissues (but not tumor cells);
*Apoptosis↓, preventing apoptosis-mediated damage to normal cells;
*CD8+↑, depleting regulatory T cells and improving the stimulation of CD8 cells;
UPR↑, accumulating unfolded proteins and protecting cancer cells from immune surveillance
eff↝, discuss how ‘fasting-mimicking diet’ as a modified form of fasting enables patients to eat a low calorie, low protein, and low sugar diet while achieving similar metabolic outcomes of fasting.
TumAuto↑, upregulating autophagy flux as a protection against damage to organelles and some cancer cells;

5071-

dietSTF,

Unraveling the impact of intermittent fasting in cancer prevention, mitigation, and treatment: A narrative review

Review,

Var,

Review,

AD,

Risk↓, Intermittent fasting (IF) has emerged as a potential adjunctive strategy in cancer prevention, mitigation, and treatment.
TumCMig↓,
IGF-1↓, IF may reduce cancer risk, including its effects on insulin-like growth factor 1 suppression, autophagy induction, and chronic inflammation reduction.
TumAuto↑,
Inflam↓, IF has been shown to reduce chronic inflammation,13,40 a risk factor for various cancers
ChemoSen↑, we discuss IF’s potential to enhance the efficacy of conventional cancer therapies by sensitizing cancer cells, promoting apoptosis, and reducing treatment-related side effects.
Apoptosis↑,
chemoP↑, IF has shown potential in protecting healthy tissues during chemotherapy.
*glucose↓, Fasting has been shown to enhance metabolic health by improving insulin sensitivity, lowering blood sugar levels, and reducing the risk of type 2 diabetes.
*AntiDiabetic↑,
*cardioP↑, Recent studies support the cardioprotective effect of IF by reducing cholesterol levels, lowering blood pressure, and improving cardiovascular health
*LDL↓,
*BP↓,
*neuroP↑, IF may reduce the risk of neurodegenerative diseases, enhance cognitive function, and improve memory
*cognitive↑,
*memory↑,
*OS↑, some studies have suggested that IF may extend lifespan and improve overall health
*QoL↑,
Imm↑, In the context of cancer prevention, IF may directly affect the function of immune cells, reducing their production of inflammatory cytokines and promoting a more anti-inflammatory environment.5
TumCG↓, Evidence suggests that FMDs can effectively slow tumor growth by altering cancer cell metabolism, enhance the efficacy of traditional cancer therapies by reducing side effects, and potentially bolster antitumor immune surveillance
ChemoSideEff↓, IF may also help alleviate common side effects such as fatigue, nausea, and weight loss associated with cancer treatments
QoL↑, Results showed that chemotherapy-induced QoL decline was significantly less pronounced during fasting periods compared to non-fasting periods

597-

VitC,

dietSTF,

GlucDep,

The Result of Vitamin C Treatment of Patients with Cancer: Conditions Influencing the Effectiveness

other↝, action as an electron donor
H2O2↑, ascorbate readily undergoes pH-dependent autoxidation creating hydrogen peroxide (H2O2).
ROS↑, high concentration is pro-oxidant (IV 25–30 mmol/L are safely achieved)

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Mitochondria & Bioenergetics ⓘ

Insulin↓, 1, PGC-1α↑, 1,

Core Metabolism/Glycolysis ⓘ

adiP↑, 1, ALAT↓, 1, AMPK↑, 1, glucose↓, 3, LDL↓, 2,

Cell Death ⓘ

Apoptosis↓, 1,

Protein Folding & ER Stress ⓘ

HSPs↑, 1,

DNA Damage & Repair ⓘ

DNArepair↑, 1,

Proliferation, Differentiation & Cell State ⓘ

HDAC3↓, 1, mTOR↓, 1,

Barriers & Transport ⓘ

AQPs↓, 1,

Immune & Inflammatory Signaling ⓘ

CRP↓, 1, IL6↓, 1, Inflam↓, 1, TNF-α↓, 2,

Synaptic & Neurotransmission ⓘ

BDNF↑, 2,

Protein Aggregation ⓘ

Aβ↓, 2,

Drug Metabolism & Resistance ⓘ

Dose↝, 3, eff↑, 3,

Clinical Biomarkers ⓘ

ALAT↓, 1, AST↓, 1, BP↓, 1, CRP↓, 1, IL6↓, 1,

Functional Outcomes ⓘ

AntiDiabetic↑, 1, cardioP↑, 1, cognitive↑, 3, memory↑, 2, neuroP↑, 2, OS↑, 1, QoL↑, 1,

Infection & Microbiome ⓘ

CD8+↑, 1,
Total Targets: 34

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
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  -different cell line effects
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  -if effect was for normal or cancerous cells

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Database Query Results : diet Short Term Fasting, ,

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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