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| The genetic risk for premenopausal breast cancer is much greater. 14,15 Studies have shown that Jewish Ashkenazi women are at high risk for mutations in the BRCA 2 gene.16 |
| Dietary Factors |
| Dietary fat intake. In some studies, overall fat intake has shown a modest increase in risk, but fried food and refined fat (hydrogenated and transfatty acids) continues to demonstrate a much stronger and more conculsive risk factor. Obesity, particularly in women with upper-body fat, is a significant risk factor.17,18 |
| Vegetable intake. Studies have demonstrated a strong inverse relationship between vegetable consumption and breast cancer,19 i.e., the fewer the vegetables in the diet, the higher the breast cancer risk. |
| Cooked meat mutagens. Heterocyclic amines (HCAs), a food derived mutagen found in ''blackened'' or overcooked meat, has long been shown to induce breast cancer in rodents. Recent studies, however, have demonstrated a strong association between eating overcooked meats and breast cancer in human subjects.20,21 |
| Alcohol. Studies have demonstrated an increased risk factor for breast cancer, even at moderate levels of consumption.22,23 |
| Exogenous Hormones |
| Hormone replacement therapy. Current findings support a causal relationship between use of estrogens and progestins and breast cancer incidence in postmenopausal women. Further, these hormones may actually promote the late stages of carcinogenesis among postmenopausal women and facilitate the proliferation of malignant cells.24 |
| Oral contraceptive use. Oral contraceptives affect the proportions of estrogen and proliferating cells that occur during natural menstrual cycles. These changes are interrupted by oral contraceptives and result in a greater suppression of estrogen and a longer period of high proliferation during the menstrual cycle, both factors linked to increased risk of breast cancer.25 |
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