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| 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
Fasting Type vs Effectiveness
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
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 |
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| Oxidative phosphorylation (or phosphorylation) is the fourth and final step in cellular respiration. Alterations in phosphorylation pathways result in serious outcomes in cancer. Many signalling pathways including Tyrosine kinase, MAP kinase, Cadherin-catenin complex, Cyclin-dependent kinase etc. are major players of the cell cycle and deregulation in their phosphorylation-dephosphorylation cascade has been shown to be manifested in the form of various types of cancers. Many tumors exhibit a well-known metabolic shift known as the Warburg effect, where glycolysis is favored over OxPhos even in the presence of oxygen. However, this is not universal. Many cancers, including certain subpopulations like cancer stem cells, still rely on OXPHOS for energy production, biosynthesis, and survival. – In several cancers, especially during metastasis or in tumors with high metabolic plasticity, OxPhos can remain active or even be upregulated to meet energy demands. In some cancers, high OxPhos activity correlates with aggressive features, resistance to standard therapies, and poor outcomes, particularly when tumor cells exploit mitochondrial metabolism for survival and metastasis. – Conversely, low OxPhos activity can be associated with a reliance on glycolysis, which is also linked with rapid tumor growth and certain adverse prognostic features. Inhibiting oxidative phosphorylation is not a universal strategy against all cancers. Targeting OXPHOS can potentially disrupt the metabolic flexibility of cancer cells, leading to their death or making them more susceptible to other treatments. Since normal cells also rely on OXPHOS, inhibitors must be carefully targeted to avoid significant toxicity to healthy tissues. Not all tumors are the same. Some may be more glycolytic, while others depend more on mitochondrial metabolism. Therefore, metabolic profiling of tumors is crucial before adopting this strategy. Inhibiting OXPHOS is being explored in combination with other treatments (such as chemo- or immunotherapies) to improve efficacy and overcome resistance. In cancer cells, metabolic reprogramming is a hallmark where cells often rely on glycolysis (known as the Warburg effect); however, many cancer types also depend on OXPHOS for energy production and survival. Targeting OXPHOS(using inhibitor) to increase the production of reactive oxygen species (ROS) can selectively induce oxidative stress and cell death in cancer cells. -One side effect of increased OXPHOS is the production of reactive oxygen species (ROS). -Many cancer cells therefore simultaneously upregulate antioxidant systems to mitigate the damaging effects of elevated ROS. -Increase in oxidative phosphorylation can inhibit cancer growth. |
| 5069- | dietSTF, | The Role of Intermittent Fasting in the Activation of Autophagy Processes in the Context of Cancer Diseases |
| - | Review, | Var, | NA |
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
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