Database Query Results : diet FMD Fasting Mimicking Diet, ,

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

Scientific Papers found: Click to Expand⟱

1854-

dietFMD,

How Far Are We from Prescribing Fasting as Anticancer Medicine?

Review,

Var,

ChemoSideEff↓, ample nonclinical evidence indicating that fasting can mitigate the toxicity of chemotherapy and/or increase the efficacy of chemotherapy.
ChemoSen↑, Fasting-Induced Increase of the Efficacy of Chemotherapy
IGF-1↓,
IGFBP1↑, biological activity of IGF-1 is further compromised due to increased levels of insulin-like growth factor binding protein 1 (IGFBP1)
adiP↑, increased levels of adiponectin stimulate the fatty acid breakdown.
glyC↓, After depletion of stored glycogen, which occurs usually 24 h after initiation of fasting, the fatty acids serve as the main fuels for most tissues
E-cadherin↑, upregulation of E-cadherin expression via activation of c-Src kinase
MMPs↓, decrease of cytokines, chemokines, metalloproteinases, growth factors
Casp3↑, increase of level of activated caspase-3
ROS↑, it is postulated that the beneficial effects of fasting are ascribed to rapid metabolic and immunological response, triggered by a temporary increase in oxidative free radical production
ATP↓, Glucose deprivation leads to ATP depletion, resulting in ROS accumulation
AMPK↑, Additionally, ROS activate AMPK
mTOR↓, Under conditions of glucose deprivation, AMPK inhibits mTORC1
ROS↑, Beyond glucose deprivation, another mechanism increasing ROS levels is the AA (amino acids) starvation
Glycolysis↓, Indeed, in cancer cells, limited glucose sources impair glycolysis, decrease glycolysis-based NADPH production due to reduced utilization of the pentose phosphate pathway [88,89,90,91],
NADPH↓,
OXPHOS↝, and shift the metabolism from glycolysis to oxidative phosphorylation (OXPHOS) (“anti-Warburg effect”), leading to ROS overload [92,93,94,95].
eff↑, Fasting compared to long-term CR causes a more profound decrease in insulin (90% versus 40%, respectively) and blood glucose (50% versus 25%, respectively).
eff↑, FMD have been demonstrated to result in alterations of the serum levels of IGF-I, IGFBP1, glucose, and ketone bodies reminiscent of those observed in fasting
*RAS↓, A plausible explanation of the differential protective effect of fasting against chemotherapy is the attenuation of the Ras/MAPK and PI3K/Akt pathways downstream of decreased IGF-1 in normal cells
*MAPK↓,
*PI3K↓,
*Akt↓,
eff↑, Starvation combined with cisplatin has been shown in vitro to protect normal cells, promoting complete arrest of cellular proliferation mediated by p53/p21 activation in AMPK-dependent and ATM-independent manner
ROS↑, generation of ROS due to paradoxical activation of the AKT/S6K, partially via the AMPK-mTORC1 energy-sensing pathways malignant cells
Akt↑, cancer cells
Casp3↑, combination of fasting and chemotherapy was in part ascribed to enhanced apoptosis due to activation of caspase 3

5067-

dietFMD,

Fasting-mimicking diet potentiates anti-tumor effects of CDK4/6 inhibitors against breast cancer by suppressing NRAS- and IGF1-mediated mTORC1 signaling

in-vitro,

BC,

mTORC1↓, While fasting-mimicking diet (FMD) enhances the activity of anticancer agents by inhibiting the mTORC1 signaling
IGF-1↓, FMD cooperated with CDK4/6i to suppress the levels of IGF1 and RAS.
RAS↓,

2352-

dietFMD,

Glucose restriction reverses the Warburg effect and modulates PKM2 and mTOR expression in breast cancer cell lines

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

MCF-7

Warburg↓, n this study, we investigated the role of glucose restriction (GR) and mTOR inhibition in reversing the Warburg effect in MDA-MB 231 and MCF-7 breast cancer cell lines
mTOR↓, Glucose restriction contribute to the reduction of the Warburg effect through mTOR inhibition and regulation of PKM2 kinases.
PKM2↓, Glucose restriction contribute to the reduction of the Warburg effect through mTOR inhibition and regulation of PKM2 kinases.

2152-

dietFMD,

Prolonged Nightly Fasting and Breast Cancer Prognosis

Analysis,

BC,

eff↑, fasting less than 13 hours per night (lower 2 tertiles of nightly fasting distribution) was associated with an increase in the risk of breast cancer recurrence compared with fasting 13 or more hours per night (hazard ratio, 1.36
Dose↓, Nightly fasting less than 13 hours was not associated with a statistically significant higher risk of breast cancer mortality (hazard ratio, 1.21
Risk↓, Prolonging the length of the nightly fasting interval may be a simple, nonpharmacologic strategy for reducing the risk of breast cancer recurrence

1863-

dietFMD,

Chemo,

Effect of fasting on cancer: A narrative review of scientific evidence

Review,

Var,

eff↑, recommend combining prolonged periodic fasting with a standard conventional therapeutic approach to promote cancer‐free survival, treatment efficacy, and reduce side effects in cancer patients.
ChemoSideEff↓, lowered levels of IGF1 and insulin have the potential to protect healthy cells from side effects
ChemoSen↑,
Insulin↓, causes insulin levels to drop and glucagon levels to rise
HDAC↓, Histone deacetylases are inhibited by ketone bodies, which may slow tumor development.
IGF-1↓, FGF21 rises during intermittent fasting, and it plays a vital role in lowering IGF1 levels by inhibiting phosphorylated STAT5 in the liver
STAT5↓,
BG↓, Fasting suppresses glucose, IGF1, insulin, the MAPK pathway, and heme oxygenase 1
MAPK↓,
HO-1↓,
ATG3↑, while increasing many autophagy‐regulating components (Atgs, LC3, Beclin1, p62, Sirt1, and LAMP2).
Beclin-1↑,
p62↑,
SIRT1↑,
LAMP2↑,
OXPHOS↑, Fasting causes cancer cells to release oxidative phosphorylation (OXPHOS) through aerobic glycolysis
ROS↑, which leads to an increase in reactive oxygen species (ROS), p53 activation, DNA damage, and cell death in response to chemotherapy.
P53↑,
DNAdam↑,
TumCD↑,
ATP↑, and causes extracellular ATP accumulation, which inhibits Treg cells and the M2 phenotype while activating CD8+ cytotoxic T cells.
Treg lymp↓,
M2 MC↓,
CD8+↑,
Glycolysis↓, By lowering glucose intake and boosting fatty acid oxidation, fasting can induce a transition from aerobic glycolysis to mitochondrial oxidative phosphorylation in cancerous cells, resulting in increased ROS
GutMicro↑, Fasting has been shown to have a direct impact on the gut microbial community's constitution, function, and interaction with the host, which is the complex and diverse microbial population that lives in the intestine
GutMicro↑, Fasting also reduces the number of potentially harmful Proteobacteria while boosting the levels of Akkermansia muciniphila.
Warburg↓, Fasting generates an anti‐Warburg effect in colon cancer models, which increases oxygen demand but decreases ATP production, indicating an increase in mitochondrial uncoupling.
Dose↝, Those patients fasted for 36 h before treatment and 24 h thereafter, having a total of 350 calories per day. Within 8 days of chemotherapy, no substantial weight loss was recorded, although there was an improvement in quality of life and weariness.

1862-

dietFMD,

Exceptional tumour responses to fasting-mimicking diet combined with standard anticancer therapies: A sub-analysis of the NCT03340935 trial

Trial,

Var,

OS↑, five patients with advanced, poor prognosis solid neoplasms, who achieved complete and long-lasting tumour responses when treated with a combination of cyclic FMD and standard systemic treatments in the context of the NCT03340935 trial.

1861-

dietFMD,

Chemo,

Fasting induces anti-Warburg effect that increases respiration but reduces ATP-synthesis to promote apoptosis in colon cancer models

in-vitro,

Colon,

CT26

in-vivo,

NA,

selectivity↑, Short-term-starvation (STS) was shown to protect normal cells and organs but to sensitize different cancer cell types to chemotherapy
ChemoSen↑, STS potentiated the effects of OXP on the suppression of colon carcinoma growth and glucose uptake in both in vitro and in vivo models.
BG↓, glucose and amino acid deficiency conditions imposed by STS promote an anti-Warburg effect
AminoA↓,
Warburg↓,
OCR↑, characterized by increased oxygen consumption but failure to generate ATP, resulting in oxidative damage and apoptosis.
ATP↓,
ROS↑, a significant increase in O2consumption rate (OCR), indicative of an increased oxidative metabolism, was observed
Apoptosis↑,
GlucoseCon↓, STS was as effective as oxaliplatin (OXP) in reducing the average tumor glucose consumption
PI3K↓, STS and in particular STS+OXP down-regulated the expression of PI3K
PTEN↑, and up-regulated PTEN expression
GLUT1↓, STS induced a profound reduction in GLUT1 , GLUT2 , HKII , PFK1, PK
GLUT2↓,
HK2↓,
PFK1↓,
PKA↓,
ATP:AMP↓, Accordingly, the ATP/AMP ratio, a good indicator of cellular energy charge, was dramatically reduced by the two STS settings
Glycolysis↓, results strongly support the effect of STS on reducing glycolysis and lactate production and increasing respiration at Complexes I-IV resulting in superoxide production/oxidative stress but in reduced ATP generation.
lactateProd↓,

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↑, FMD activates PI3K-AKT, mTOR, and CDK4/6 as survival/growth pathways, which can be targeted by drugs to promote tumor regression.
Akt↑,
mTOR↑,
CDK4↑,
CDK6↑,
hyperG↓, FMD cycles also prevent hyperglycemia and other toxicities caused by these drugs.
TumCG↓, cycles of FMD significantly slowed down tumor growth, reduced tumor size, and caused an increased expression of intratumor Caspase3
TumVol↓,
Casp3↑,
BG↓, confirming our hypothesis that lowering intracellular glucose levels (through reduced extracellular levels or reduced uptake) reduces CSC survival
eff↑, 2DG potentiated the effect of FMD both in terms of delaying tumor progression and in decreasing the number of mammospheres derived by tumor masses,
eff∅, metformin did not show any additive or synergistic antitumor effect when combined with the FMD, thus suggesting that FMD and metformin have redundant effects on blood glucose levels
PKA↓, We have previously shown that prolonged fasting reduces the activity of protein kinase A (PKA) in different types of normal cells
KLF5↓, PKA inhibition resulted in the downregulation of KLF5, a potential therapeutic target for TNBC
p‑GSK‐3β↑, (GSK3β) phosphorylation
Nanog↓, stemness-associated genes NANOG and OCT4, and KLF2 and TBX3,
OCT4↓,
KLF2↓,
eff↑, Combining FMD cycles with PI3K/AKT/mTOR inhibitors results in long-term animal survival and reduces treatment-induced side effects
ROS↑, FMD resulted in an increased expression of pro-apoptotic molecules, such as BIM, and ASK1, a critical cellular stress sensor frequently activated by ROS, whose production was previously shown to be increased by the FMD
BIM↑,
ASK1↑,
PI3K↑, FMD cycles upregulate PI3K-AKT and mTOR pathways and downregulate CCNB-CDK1 while upregulating CCND-CDK4/6 signaling axes
Akt↑,
mTOR↑,
CDK1↓,
CDK4↑,
CDK6↑,
eff↑, combining STS with pictilisib, ipatasertib, and rapamycin, selective inhibitors for PI3K, AKT, and mTOR, respectively, resulted in enhanced cancer cell death and reduction of mammosphere numbers in SUM159 cells

1859-

dietFMD,

Chemo,

Fasting-Mimicking Diet Reduces HO-1 to Promote T Cell-Mediated Tumor Cytotoxicity

in-vitro,

BC,

4T1

in-vivo,

Melanoma,

B16-BL6

mice

CLP↑, combination of chemotherapy and a fasting-mimicking diet (FMD) increases the levels of bone marrow common lymphoid progenitor cells (CLP) and cytotoxic CD8+ tumor-infiltrating lymphocytes (TILs), leading to a major delay in breast cancer and melanoma
CD8+↑,
TumCG↓,
HO-1↓, In breast tumors, this effect is partially mediated by the down-regulation of the stress-responsive enzyme heme oxygenase-1 (HO-1)
TILs↑, FMD in combination with doxorubicin (DXR) promotes accumulation of tumor-infiltrating lymphocytes (TILs) in the tumor bed

1858-

dietFMD,

Chemo,

Effect of short-term fasting on the cisplatin activity in human oral squamous cell carcinoma cell line HN5 and chemotherapy side effects

in-vitro,

HNSCC,

HN5

Apoptosis↑, This study revealed that short-term fasting chemotherapy significantly improved HNSCC cell line apoptosis and necrosis.
necrosis↑,

1857-

dietFMD,

Fasting cycles retard growth of tumors and sensitize a range of cancer cell types to chemotherapy

in-vitro,

BC,

4T1

in-vivo,

NA,

mouse

TumCG↓, Cycles of starvation were as effective as chemotherapeutic agents in delaying progression of different tumors and increased the effectiveness of these drugs against melanoma, glioma, and breast cancer cells
ChemoSen↑,
OS↑, In mouse models of neuroblastoma, fasting cycles plus chemotherapy drugs—but not either treatment alone—resulted in long-term cancer-free survival.

1856-

dietFMD,

immuno,

Targeting the Gut Microbiome to Improve Immunotherapy Outcomes: A Review

Review,

Var,

GutMicro↑, Dietary patterns like the Mediterranean diet, caloric restriction modifications, and specific nutritional components show promise in influencing the tumor microenvironment and gut microbiome for better treatment outcomes

1855-

dietFMD,

Impact of modified short-term fasting and its combination with a fasting supportive diet during chemotherapy on the incidence and severity of chemotherapy-induced toxicities in cancer patients - a controlled cross-over pilot study

Trial,

NA,

ChemoSideEff↓, total toxicities’ score were significantly reduced. reported significantly fewer chemotherapy-induced side effects, including asthenia, fatigue and gastrointestinal problems such as vomiting and diarrhoea
QoL↑, We also observed significantly fewer chemotherapy postponements post-mSTF, reflecting improved tolerance of chemotherapy
IGF-1↓, On average, Insulin [− 169.4 ± 44.1; 95% CI -257.1 – (− 81.8); P < 0.001] and Insulin-like growth factor 1 levels [− 33.3 ± 5.4; 95% CI -44.1 – (− 22.5); P < 0.001] dropped significantly during fasting.
Insulin↓,

1853-

dietFMD,

Impact of Fasting on Patients With Cancer: An Integrative Review

Review,

Var,

*toxicity∅, Data suggest overall good compliance, no malnutrition, minimal side effects. No significant changes were identified to suggest increased harm.
QoL∅, unchanged quality of life (QOL),
eff↑, improved endocrine parameters
eff↝, mixed results for cancer outcomes
ChemoSideEff↓, decreasing chemotherapy-related side effects
TumCG↓, limiting tumor growth
Dose↑, When fasting is used as an adjunct to chemotherapy, a minimum fasting period of at least 48 hours is currently recommended for nutritional interventions in order to achieve a measurable metabolic response at the cellular level
toxicity↝, The increased risk for poor outcomes associated with malnutrition, weight loss, and cachexia poses an obvious safety concern for patients with cancer who participate in calorie-restricted fasting
eff↑, short-term fasting involving water-only or limited daily calorie consumption for less than a week has the potential to achieve positive metabolic changes while avoiding malnutrition and significant weight loss
IGF-1↑, statistically significant decrease in IGF-1 among participants compliant with fasting compared with regular diet during the middle of therapy
*OXPHOS↑, Healthy cells also use mitochondrial oxidative phosphorylation for metabolism while cancer cells use aerobic glycolysis, also known as the Warburg effect
BG↓, statistically significant decrease in glucose among participants compliant with fasting compared with controls
Insulin↓, statistically significant decrease in insulin among participants compliant with fasting compared with regular diet before the first cycle of chemotherapy (p = .001), as well as during the middle of therapy
RadioS↑, A complete or partial radiographic response was also noted more often among fasting participants compared with normal diet participants

1852-

dietFMD,

Chemo,

Starvation Based Differential Chemotherapy:  A Novel Approach for Cancer Treatment

Review,

Var,

ChemoSideEff↓, Ten volunteers with different types of cancers were starved for 48–140 hours before chemotherapy and five–56 hours after. Overall, all patients showed decreased side effects of chemotherapy.
*toxicity↓, A case report showed that short-term starvation of up to five days followed by chemotherapy is not only safe and feasible, but also helps to ameliorate chemotherapy related side-effects.3
mTOR↓, reduction in mTOR activity
IGF-1↓, Studies reveal that starvation reduces levels of IGF-1 significantly. Short-term starvation of 72 hours reduces circulating IGF-1 by 70%
IGFBP1↑, and increases the level of IGF binding protein (IGFBP-1) an IGF-1 inhibitor, by 11-fold
BG↓, glucose levels were reduced by 41%
ROS↑, Increased metabolic rate as a result of DR causes increased ROS production

1851-

dietFMD,

Chemo,

Starvation-dependent differential stress resistance protects normal but not cancer cells against high-dose chemotherapy

in-vitro,

GBM,

LN229

in-vitro,

neuroblastoma,

SH-SY5Y

selectivity↑, Short-term starved S. cerevisiae or cells lacking proto-oncogene homologs were up to 1,000 times better protected against oxidative stress or chemotherapy drugs than cells expressing the oncogene homolog Ras2
selectivity↑, Finally, short-term starvation provided complete protection to mice but not to injected neuroblastoma cells against a high dose of the chemotherapy drug/pro-oxidant etoposide
ROS↑, promote oxidative stress and DNA damage
DNAdam↑,
BG↓, blood glucose level for both mice and humans is ≈1.0 g/liter but can reach 0.5 g/liter after starvation.

1850-

dietFMD,

Fasting-mimicking diet remodels gut microbiota and suppresses colorectal cancer progression

in-vivo,

CRC,

mice

TumCP↑, FMD cycles effectively suppressed colorectal cancer growth, reduced cell proliferation and angiogenesis, increased tumor-infiltration lymphocytes especially CD8+T cells
angioG↓,
CD8+↑,
GutMicro↑, FMD stimulated protective gut microbiota, especially Lactobacillus.
eff↑, Additionally, FMD synthesizing with anti-PD-1 therapy effectively inhibited CRC progression.

1849-

dietFMD,

The emerging role of fasting-mimicking diets in cancer treatment

Review,

Var,

TumCG↓, Accumulating evidence suggests that FMDs attenuate tumor growth by altering the energy metabolism of cancer cells
toxicity∅, FMD reduces risk factors and markers for aging, cardiovascular disease, diabetes, and cancer without serious adverse effects in healthy adults.
BG↓, dramatic downregulation of blood glucose
IGF-1↓, prolonged fasting downregulated IGF-1
mTOR↓, inhibits cellular mTOR activity.
M2 MC↓, In addition, alternate-day fasting inhibited colorectal cancer growth by suppressing adenosine-induced M2 macrophage polarization in the tumor microenvironment
eff↑, large prospective cohort study of breast cancer patients, a longer nightly fasting duration was associated with a decreased risk of breast cancer recurrence, so the FMD may also be beneficial after the eradication of the initial tumo
ChemoSen↑, Combining fasting cycles with chemotherapeutic agents markedly prevented the progression of subcutaneous breast cancer, melanoma, and glioma in mouse models
QoL↑, Fasting for 60 hours seemed to improve the patients' fatigue and quality of life during chemotherapy
RadioS↑, In response to stress, cancer cells engage antioxidant and DNA repair mechanisms in an energy-demanding manner, facilitating cancer cell survival. Thus, restriction of the energy supply would improve the antitumor activity of radiotherapy.
selectivity↑, Recently, short-term starvation was shown to increase the DNA damage induced by a single exposure to high-dose radiation in metastatic cancer cell lines, whereas healthy cells were not affected by starvation medium

1848-

dietFMD,

Chemo,

Fasting mimicking diet as an adjunct to neoadjuvant chemotherapy for breast cancer in the multicentre randomized phase 2 DIRECT trial

Trial,

BC,

ChemoSideEff↓, Short-term fasting protects tumor-bearing mice against the toxic effects of chemotherapy while enhancing therapeutic efficacy
ChemoSen↑,
eff↑, FMD significantly reinforces the effects of neoadjuvant chemotherapy on the radiological and pathological tumor response in patients with HER2 negative early breast cancer.

1847-

dietFMD,

VitC,

Synergistic effect of fasting-mimicking diet and vitamin C against KRAS mutated cancers

in-vitro,

PC,

PANC1

vitamin C (≥0.3 mM)

TumCG↓, Fasting-mimicking diets delay tumor progression
ChemoSen↑, sensitize a wide range of tumors to chemotherapy
eff↑, vitamin C anticancer activity is limited by the up-regulation of the stress-inducible protein heme-oxygenase-1. The fasting-mimicking diet selectivity reverses vitamin C-induced up-regulation of heme-oxygenase-1
HO-1↓, FMD reverses the effect of vitamin C on HO-1(downregulating HO-1)
Ferritin↓,
Iron↑, consequently increasing reactive iron, oxygen species, and cell death
ROS↑, Vitamin C’s pro-oxidant action is strictly dependent on metal-ion redox chemistry. In particular, free iron was shown to be a key player in vitamin C-induced cytotoxic effects
TumCD↑,
IGF-1↓, effects on the insulin-like growth factor 1 (IGF-1)
eff↓, When cancer cells were grown under STS conditions before and during treatment, vitamin C-mediated toxicity was strongly enhanced
eff↓, Conversely, KRAS-wild-type CRC (SW48, HT29), prostate cancer (PC-3), ovarian cancer (COV362) cell lines and a normal colon cell line (CCD841CoN) were resistant to vitamin C when used both as a single agent and in combination with STS

1846-

dietFMD,

VitC,

A fasting-mimicking diet and vitamin C: turning anti-aging strategies against cancer

Study,

Var,

TumCG↓, FMDs delay tumor progression
ChemoSen↑, potentiate chemotherapy efficacy
ChemoSideEff↓, while protecting healthy tissues from chemo-associated side effects in different cancer models
ROS↑, presence of metals, and particularly iron, high dose of vitamin C exerts a pro-oxidant action by generating hydrogen peroxide and hydroxyl radicals via Fenton chemistry
Fenton↑,
H2O2↑,
eff↑, we show that FMD cycles potentiate high-dose vitamin C anti-cancer effects in a range of cancer types
HO-1↓, KRAS-mutant cancer cells respond to vitamin C treatment by up-regulating HO-1, and consequently limiting vitamin C pro-oxidant action. FMD is able to revert HO-1 up-regulation
DNAdam↑, increase in free reactive iron and oxygen species causing DNA damage and cell death
eff↑, we found that the nontoxic FMD + vitamin C combination therapy is as effective as oxaliplatin + vitamin C in delaying tumor progression while the triple FMD, vitamin C and chemotherapy combination treatment is the most effective.

1845-

dietFMD,

Fasting and fasting mimicking diets in cancer prevention and therapy

Review,

Var,

eff↑, Unlike chronic dietary restrictions or water-only fasting, FMDs represent safer and less challenging options for cancer patients.
selectivity↑, FMD cycles increase protection in healthy cells while sensitizing cancer cells to various therapies,
ChemoSen↑, FMD cycles enhance the efficacy of a range of drugs targeting different cancers in mice by stimulating antitumor immunity.

1844-

dietFMD,

Unlocking the Potential: Caloric Restriction, Caloric Restriction Mimetics, and Their Impact on Cancer Prevention and Treatment

Review,

NA,

Risk↓, CRMs were well tolerated, and metformin and aspirin showed the most promising effect in reducing cancer risk in a selected group of patients.
AMPK↑, the increased AMP levels activate AMPK
Akt↓, This activation results in the inhibition of AKT and mTOR pathways
mTOR↓,
SIRT1↑, energy deficit also activates the SIRT pathways, which downregulates HIF1α, and the Nrf2 pathway
Hif1a↓,
NRF2↓,
SOD↑, enhances antioxidant defenses (e.g., superoxide dismutase SOD1 and SOD2)
ROS↑, Additionally, in prostate cancer (PC) [55] and triple-negative breast cancer (TNBC) [56] cell lines glucose restriction (GR) has been shown to trigger an increase in ROS, leading to cell death.
IGF-1↓, CR decreases poor prognosis markers such as IGF1, pAKT, and PI3K
p‑Akt↓,
PI3K↑,
GutMicro↑, induces changes in the gut microbiome linked to anti-tumor effects
OS↑, Incorporating a nutraceutical regimen like CR or KD with CT has reduced tumor growth and relapse and improved the survival rate
eff↝, type of dietary intervention, with FMD being the first option, followed by KD and CR last. FMD has been considered the most cost-effective and applicable because it does not completely restrict food intake.
ROS↑, findings consistently indicating that dietary restrictions render highly proliferative tumor cells more susceptible to oxidative damage
TumCCA↑, CR has been reported to induce cell cycle arrest in the G0/G1 phases , enabling cells to undergo DNA repair more efficiently and diminishing DNA damage by CRT
*DNArepair↑,
DNAdam↑, In contrast, tumoral cells, which have an altered cell cycle, are unable to repair DNA, leading to cell death

1843-

dietFMD,

BTZ,

Cyclic Fasting–Mimicking Diet Plus Bortezomib and Rituximab Is an Effective Treatment for Chronic Lymphocytic Leukemia

in-vivo,

CLL,

mouse

AntiTum↓, Cyclic fasting–mimicking diet (FMD) is an experimental nutritional intervention with potent antitumor activity in preclinical models of solid malignancies.
Apoptosis↑, murine CLL models had mild cytotoxic effects, which resulted in apoptosis activation mediated in part by lowered insulin and IGF1 concentrations.
IGF-1↓,
eff↑, In CLL cells, fasting conditions promoted an increase in proteasome activity that served as a starvation escape pathway. Pharmacologic inhibition of this escape mechanism with the proteasome inhibitor bortezomib resulted in a strong enhancement
OS↑, combining cyclic fasting/FMD with bortezomib and rituximab, an anti-CD20 antibody, delayed CLL progression and resulted in significant prolongation of mouse survival
eff↑, recent clinical reports have shown that combining cyclic FMD with chemotherapy, endocrine therapies, or immunotherapy improves tumor responses in patients with early-stage neoplasms

1842-

dietFMD,

Safety and Feasibility of Fasting-Mimicking Diet and Effects on Nutritional Status and Circulating Metabolic and Inflammatory Factors in Cancer Patients Undergoing Active Treatment

Trial,

Var,

Strength∅, The patients’ weight and handgrip remained stable, the phase angle and fat-free mass increased
Weight∅,
IGF-1↓, FMD reduced the serum c-peptide, IGF1, IGFBP3 and leptin levels
IGFBP3↑,
IGFBP1↑, while increasing IGFBP1
eff↑, these modifications persisted for weeks beyond the FMD period.

1841-

dietFMD,

Fasting-Mimicking Diet Is Safe and Reshapes Metabolism and Antitumor Immunity in Patients with Cancer

Trial,

Var,

BG↓, In 101 patients, the FMD was safe, feasible, and resulted in a consistent decrease of blood glucose and growth factor concentration
AntiCan↑, mediate fasting/FMD anticancer effects in preclinical experiments
IFN-γ↑, enrichment of IFNγ
eff↑, Cyclic FMD Is Safe in Combination with Standard Anticancer Treatments
Dose↝, five-day FMD followed by 16 to 23 days of refeeding
CD14↓, end of five-day FMD, we found a significant decrease of total monocytes (CD14+)
IGF-1↓, Preclinical evidence in tumor-bearing mice suggests that fasting/FMD-induced reduction of blood glucose and insulin/IGF1 concentration
IGFR↓, induced reduction of serum IGF1 levels is associated with the downregulation of total and activated IGF1R at the tumor level
CD8+↑, where five-day fasting/FMD in patients with breast cancer increased total and activated intratumor CD8+ T cells, aDCs, NK cells, and Tem cells,
NK cell↑,

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

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

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 28

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 4,
Total Targets: 118

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

OXPHOS↑, 1,

Cell Death ⓘ

Akt↓, 1, MAPK↓, 1,

DNA Damage & Repair ⓘ

DNArepair↑, 1,

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1, RAS↓, 1,

Functional Outcomes ⓘ

toxicity↓, 1, toxicity∅, 1,
Total Targets: 8

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#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Database Query Results : diet FMD Fasting Mimicking Diet, ,

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Cell Death ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Functional Outcomes ⓘ

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