Authors
Breast cancer, which continues to rob the world of approximately half a million women per year, is surprisingly poorly understood.Despite application of all the tools of epidemiology: ecological studies, migrant studies, case-control and cohort studies, and measurement of multiple exposures at various times of life, we still cannot advise women on how to protect themselves or their daughters from breast cancer.The disease has a familial and a hormonal component, but current knowledge of these components does not adequately explain breast-cancer risk.In the search for strategies to prevent this devastating disease, potential food-borne exposures have been studied in both animal models and in women.These include studies of the relationship of the macronutrients (fat, and alcohol, as well as total energy intake), studies of antioxidant micronutrients, studies of body fat and oestrogen levels, and studies of specific foods (such as cruciferous vegetables and soyabean products).Even substances carried by food, such as the pesticide dichloro-diphenyltrichlorethane (DDT), have received and continue to receive scrutiny.The present paper will attempt to summarize current knowledge and belief in the area of these food-borne exposures. DIETARY FAT, ENERGY INTAKES AND BREAST CANCERThe involvement of dietary fat as a risk factor for breast cancer remains controversial.There seems to be a strong and consistent relationship between per capita average total fat disappearance and breast-cancer incidence, when assessed in international ecological studies (Prentice & Sheppard, 1989).However, results of case-control and cohort studies in which diet was assessed by food-frequency questionnaire are inconsistent.The controversy surrounding this has focused in part on colinearity with energy intakes (Palmgren, 1993).Particularly after adjustment for energy intakes, the independent effect of total dietary fat intakes appears to be minimal if existent at all (Hulka, 1989).The importance of fat intake to breast cancer needs to be examined both in its role as a contributor of energy, and in its potential for influencing risk independent of an energy effect.Non-energy-adjusted models ask whether absolute intakes of fat contribute to breast cancer, either through an association with energy intakes or otherwise.Energy-adjusted models ask something much more subtle: to what extent does the amount of fat consumed, beyond that expected of a woman at her reported energy intake level, relate to breastcancer risk, when fat is exchanged isoenergetically for other nutrients?Some animals, such as rats, do appear to adjust their energy intake to the nutrient density of their feed (Braden & Carroll, 1986).Hamsters, on the other hand, will substantially increase body weight if fed on a fat-rich diet ad libitum (Birt et al. 1989).Human subjects are unfortunately more like hamsters: in free-living human populations, as with caged hamsters, dietary fat is rarely exchanged isoenergetically for other macronutrients.Instead, people consuming more fat tend to consume more total energy and become fatter (Astrup ef al. 1995).Therefore, the public health importance of the contribution of fat to total energy intakes remains strong, even if the effect is through total energy intake.
Loading...
Kohlmeier et al. (1997) studied this question.
Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context: