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Fasting and fasting-mimicking diets for chemotherapy augmentation

The increasingly older population in most developed countries will likely experience aging-related chronic diseases such as diabetes, metabolic syndrome, heart and lung diseases, osteoporosis, arthritis, dementia, and/or cancer. Genetic and environmental factors, but also lifestyle choices including physical activity and dietary habits, play essential roles in disease onset and progression. Sixty-five percent of Americans diagnosed with cancer now survive more than 5 years, making the need for informed lifestyle choices particularly important to successfully complete their treatment, increase the recovery from the cytotoxic therapy options, and improve cancer-free survival. This review will discuss the findings on the use of prolonged fasting, as well as fasting-mimicking diets to augment cancer treatment. Preclinical studies in rodents strongly support the implementation of these dietary interventions and a small number of clinical trials begin to provide encouraging results for cancer patients and cancer survivors.

Keywords: Cancer, Chemotherapy, Fasting, Fasting-mimicking diet
“Periodic water-only fasting (PF) consists of total food abstinence for several days, in mouse models generally 48–72 h, without limiting hydration. Benefits of PF in preclinical studies include weight loss (during the fasting period but regained after refeeding), improved insulin sensitivity, autophagy activation, cell renewal, and anticancer effects, but safety and compliance concerns may be responsible for the limited contribution of PF to standard medical practice [, , , ]. The differences between IF and PF in mice include the duration and/or frequency: IF cycles usually last up to 24 h and are separated by 24 h of food intake (caloric intake may be higher on the refeeding days to compensate for the reduced calories on the fast days). PF instead lasts 2 or more days and is followed by 1 week of normal food intake to regain normal weight []. Owing to this difference, the molecular changes of a variety of growth factors (including IGF-1) and metabolic markers (such as ketone bodies, serum glucose, etc.) differ significantly in their response.”
Published inAllgemein

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