Nutrition and breast cancer risk: Can an effect via insulin resistance be demonstrated?

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Abstract
It is postulated that the metabolic/endocrine concomitants of insulin resistance resulting from high animal fat intake and weight gain after the age of 30 could be contributing to the increasing incidence of postmenopausal breast cancer and recent changes in its biologic characteristics. Case/control studies have shown that hyperinsulinaemia and abdominal obesity, which are recognized as markers of insulin resistance, are risk markers for postmenopausal breast cancer also. Excess weight gain linked to high dietary intake of saturated fat is thought to be a major cause of insulin resistance. The hypothesis is compatible with the "breast tissue age" model for breast cancer risk. Biological evidence suggests that the concomitants of insulin resistance may stimulate growth activity in existing breast cancer also. The hypothesis that nutritional factors which favour hyperinsulinaemia may also favour breast cancer growth can be tested. Restriction of dietary fat and high intake of fibre and complex carbohydrate have been shown to normalise insulin levels in a proportion of subjects with hyperinsulinaemia. Restriction of dietary fat intake has also been shown to reduce bioavailable oestrogen levels in healthy postmenopausal women. A randomised trial of a low fat, high fibre, high complex carbohydrate regimen is proposed as adjuvant treatment following primary surgery in postmenopausal women with early breast cancer. A cancer preventive or delaying ability can be assessed by comparing the incidence of contralateral second breast cancer and the metastasis rate in the diet and control groups. Insulin levels, abdominal obesity, and body mass should be monitored although normalisation of insulin levels need not necessarily involve decrease in body mass.