Recently, studies in
in vitro and
in vivo models have shown that intermittent fasting improved the chemotherapeutic response to cisplatin, doxorubicin, cyclophosphamide
70, oxaliplatin
71, sorafenib
72, mitoxantrone
73, gemcitabine
74, etoposide
75, temozolomide
76 and tyrosine kinase inhibitors
77 in models of glioma, neuroblastoma, melanoma, fibrosarcoma and breast cancer, colon cancer, pancreatic cancer, hepatocellular cancer and lung cancer. IF has also been shown to improve the radiosensitivity of glioma
76 and breast cancer
78 in mice. Interestingly, fasting in combination with cytotoxic agents elicited differential responses in normal and cancer cells, a phenomenon known as differential stress resistance (DSR). For DSR, normal cells prioritize maintenance pathways and inactivate growth factor signaling when nutrients are absent. In contrast, cancer cells, due to oncogene activation, do not inhibit stress resistance pathways, thus becoming vulnerable to cytotoxic treatment
70,
75. IF, by reducing the circulating glucose levels, protected mice from doxorubicin toxicity and particularly promoted cardioprotection mediated in part by EGFR1-dependent transcriptional regulation of atrial natriuretic peptide and B-type natriuretic peptide in heart tissue
79. As demonstrated by Tinkum et al.
80, IF also facilitated DNA repair activation mechanisms and preserved small intestinal (SI) stem cell viability as well SI architecture and barrier function after exposure to high-dose etoposide, suggesting that fasting can be applied to reduce side effects and toxicity in patients undergoing chemotherapy.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6257056/