![]() ![]() ![]() These reviews have, however, tended to focus on specific conditions, e.g. Insulin resistance coincides with an increased risk of cancer in a variety of conditions, including aging, physical inactivity, obesity, central body fat distribution, Type 2 diabetes, hyperglycaemia, the metabolic syndrome, liver disease, subclinical inflammation, acromegaly, a high-glycaemic-index diet and a high-saturated-fat diet, and there is extensively reviewed evidence linking measures associated with insulin resistance with the subsequent development of cancer or pre-cancerous changes. The possibility that some of the effects of hyperinsulinaemia might then augment pro-carcinogenic changes associated with disturbances in these factors emphasizes how, rather than being a single causative factor, insulin resistance may be most usefully viewed as one strand in a network of interacting disturbances that promote the development and progression of cancer. Several factors can independently modify both cancer risk and insulin resistance, including subclinical inflammation and obesity. Hyperinsulinaemia may also induce other changes, particularly in the IGF (insulin-like growth factor) system, that could promote cell proliferation and survival. ![]() There are, however, theoretical mechanisms by which hyperinsulinaemia could amplify such growth-promoting effects as insulin may have, as well as the growth-promoting effects of other, more potent, growth factors. Access content during the Covid-19 pandemicĮxperimental, epidemiological and clinical evidence implicates insulin resistance and its accompanying hyperinsulinaemia in the development of cancer, but the relative importance of these disturbances in cancer remains unclear. ![]()
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