Objective: The incidence of breast cancer in the Western world runs parallel to that of the major components of the insulin resistance syndrome--hyperinsulinaemia, dyslipidaemia, hypertension and atherosclerosis. Evidence is reviewed that the growth of breast cancer is favoured by specific dietary fatty acids, visceral fat accumulation and inadequate physical exercise, all of which are thought to interact in favouring the development of the insulin resistance syndrome.
Design: Clinical, epidemiological and experimental studies linking breast cancer risk with evidence of insulin resistance and its concomitants, were searched for in the MEDLINE database since 1985.
Results: Clinical and epidemiological evidence suggests that both breast cancer and the metabolic disorders comprising the insulin resistance syndrome are polygenic and multifactorial in origin. Experimental evidence suggests that hyperinsulinaemia and its concomitants can increase the promotion of mammary carcinogenesis and the mechanism is likely to involve increased bioactivity of insulin-like growth factor 1 (IGF-1). Case-control and cohort studies have shown that higher serum levels of IGF-1 are associated with increased breast cancer risk. Pharmacological agents which lower IGF-1 concentrations are under clinical trial for breast cancer prevention.
Conclusions: Nutritional and lifestyle modifications that improve insulin sensitivity may not only decrease a tendency to atherosclerosis but also reduce breast cancer risk in women. In addition to a reduced fat intake, the dietary regimen might involve a reduced n-6/n-3 ratio of polyunsaturated fatty acids and should be associated with avoidance of obesity and regular physical exercise. Interventions to decrease breast cancer risk in first-degree relatives of breast cancer patients need to begin at an early age.