Abstract
Fasting in disease prevention and treatment has recently become a popular topic, particularly in the context of oncology. Unfortunately, the growing attention paid by the media has created a background of speculations and ambiguous messages.The attitude towards the role of fasting in cancer patients should be very cautious, as the risk of malnutrition/sarcopenia and disinformation may be associated with this approach.Whether the results obtained by fasting in the cellular and animal models can be transferred to cancer patients is still to be ascertained. At the moment, more preclinical studies are required to determine in which cancers, at which stage, and in what combinations fasting, fasting-mimicking diets or caloric restriction mimetics may prove effective.So, despite the “rumors” of marketing and media, nowadays fasting and calorie restriction around CT represent only a promising intuition, which requires proper efforts and time to be validated by evidence-based clinical data.
Highlights
BackgroundFasting for disease prevention and during treatment has recently become a popular topic, in the context of oncology [1]
Most of the available studies regarding fasting or calorie restriction in cancer are still pre-clinical, having been conducted in vitro or in animals
Fasting before chemotherapy (CT) was shown to protect healthy cells from treatment toxicity by reducing the expression of some oncogenes, such as RAS and the Serine/threonine-specific protein kinase (AKT) signaling pathway [2]. This reduction is mediated by the decrease of circulating insulin-like growth factor 1 (IGF-1) and glucose
Summary
Fasting for disease prevention and during treatment has recently become a popular topic, in the context of oncology [1]. Fasting before chemotherapy (CT) was shown to protect healthy cells from treatment toxicity by reducing the expression of some oncogenes, such as RAS and the AKT signaling pathway [2]. This reduction is mediated by the decrease of circulating insulin-like growth factor 1 (IGF-1) and glucose. Starvation and calorie restriction activate other oncogenes in cancer cells, induce autophagy, and decrease cellular growth rates while increasing sensitivity to antimitotic drugs [2]. The molecular mechanisms involved in autophagy following fasting and calorie restriction, represent potentially novel ways of designing more effective anti-cancer treatment strategies [3]. Calorie restriction is able to modulate the tumor microenvironment, by allowing enhanced drug delivery, by reducing substrate availability for cancer cells, and by reducing circulating growth factors and inflammation [5]
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