The anabolic signals by insulin or IGF-I can promote tumour development by inhibiting apoptosis, and by stimulating cell proliferation. There is dynamic change in gene expression in response to nutritional availability.  Caloric restriction enhances apoptosis of preneoplastic cells.   Insulin Resistance Status characterized by hyperinsulinemia is associated with an excessive increased risk for a number of malignancies.   An increasing clinical, biological and epidemiological evidence sustain that Insulin-IGFs System has been implicated in breast, prostate, pediatric, colon-recto and gynecological cancers, including sarcomas, epithelial cancers, multiple myeloma and melanoma. Chronic hyperinsulinaemia may be a cause of cancers of the colon, pancreas, endometrium, breast, prostate, ovarium, and lung, and may predispose to melanoma development, reducing the hormone vitamin D  anticancerigen properties.

Caloric Restriction is a powerful protective therapy in Cancer. Prevention has been known for some time: “Mechanism of the increased cancer risk reflects the consequences of the hyperinsulinaemia”. Thus, increased glucose uptake activates known oncogenic pathways to induce malignant phenotype and promotes oncogenesis. Accumulative evidence demonstrated a causal role of higher fasting insulin levels in the etiology of cancer risk.  Increased levels of endogenous hormones -like insulin- can result in genomic damage.  Overeating and an unhealthy diet may incur an excessive intake of nutrients and potential carcinogens.  Insulin activate the same signalling pathways as some of the most recurrent mutations in human cancer.  Adult height was associated with risk of several cancer sites because Insulin excess. On the contrary, the oncogenic process doesn´t occur during the aging in the Insulin- IGF-1 deficiency:  A carbohydrate-restricted diet will slow cancer growth in patients by decreasing the secretion and circulating levels of insulin.

 

Keywords: Insulin, Chronic hyperinsulinaemia, Cancer