Significant radiation exposure at certain times in a woman’s life has been shown to increase the risk of subsequent breast cancer. The initial studies relating to this risk were performed after the atomic bomb was used in Hiroshima and Nagasaki, Japan. Subsequent to the bombings, survivors who were in adolescence or early adulthood at the time of the bombing were noted to have an increased risk of breast cancer.
In contrast, women over the age of 40 at exposure had a decrease in the incidence of subsequent breast cancer. These findings suggest that breast tissue exposed to radiation during particularly active periods of growth is most sensitive to radiation exposure.
The decreased incidence in women nearing menopause most likely occurred because of an induction of premature menopause in this population.
More recent studies of radiation exposure and subsequent breast cancer risk have corroborated the early findings. In a study of patients undergoing fluoroscopic examinations for tuberculosis treatment during adolescence, the risk of breast cancer was double that of the general population. The statistics for increased risk in women having undergone mantle radiation therapy for the treatment of lymphoma during adolescence and early adulthood are even more staggering.
In one review performed at Stanford University, the relative risk of breast cancer development was 136 for women irradiated prior to the age of 15. Even women who underwent radiation between the ages of 20 and 30 had relative risks of breast cancer ranging from 7-19. Thus, all women who receive radiation therapy during adolescence and early adulthood should be considered to carry an increase risk for breast cancer.
Breast cancer occurs with a greater frequency in countries in which the intake of dietary fat is higher. Additionally, women who move from environments in which there is a low dietary fat consumption to areas with higher dietary fat consumption eventually increase their risk for breast cancer development. These findings have led to the assumption that dietary fat intake must be a significant risk factor for the development of breast cancer.
Despite these findings, case-control studies in which dietary habits of women with breast cancer are compared to those of women without a history of breast cancer have not been able to show a direct relationship between dietary fat consumption and the subsequent risk of breast cancer. Further studies evaluating this relationship are ongoing. It appears that, if dietary fat contributes in any way to breast cancer risk, it is likely to be through its role in altering hormonal regulation.
The relationship of alcohol intake to subsequent risk of breast cancer is less controversial. Almost every study that has investigated this relationship has demonstrated a dose-related increase in breast cancer risk. Even in women drinking approximately one drink per day, the risk of breast cancer is slightly elevated when compared to that of nondrinkers. With increasing alcohol intake (two to five drinks per day), the risk of breast cancer may double.
The effect of antioxidants and vitamins on breast cancer risk is currently of considerable interest. While it is believed that cruciferous vegetables and fruits may play a role in protection from breast cancer risk, studies investigating high-dose vitamin and antioxidant intake have not demonstrated significant reductions in breast cancer risk with their use. Thus, the appropriate role for these agents continues to be controversial.
Alexandra S. Heerdt
Breast cancer detection demonstration project: five-year summary report. CA 2003
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