Breast Cancer - Looking at lifestyle

A 1995 study from the NCI suggested that, according to the data available, approximately half of US breast cancer cases may not be attributable to the recognized risk factors such as later age at first birth, nulliparity, and family history of breast cancer. The study recommended that intensive research attention be paid to other potential factors, such as weight gain, diet, and occupational or environmental influences. Despite a great deal of interest and investigation, however, the role of modifiable risk factors such as dietary fat, exercise, and alcohol consumption continue to provoke interest, controversy, and confusion.

A study from the Canadian Diet and Breast Cancer Prevention Study Group found that, after 2 years, areas of dense mammary tissue (a radiographic marker suggestive of neoplasia) were found to shrink among patients following a low fat, high-carbohydrate diet. In an Italian study, increased intake of unsaturated fatty acids and raw vegetables appeared to be protective. However, a recent analysis from the Nurses’ Health Study, which has followed a cohort of 88,795 women since 1976 for the development of cancer and heart disease, found no evidence of a correlation between dietary fat intake and breast cancer risk. The authors of this most recent analysis stated, “In contrast to the predominant hypotheses, we saw no increased risk of breast cancer with increased intake of animal fat, polyunsaturated fat, saturated, or trans-unsaturated fat in models in which fat intake replaced carbohydrate intake…. Also contrary to the predominant hypothesis, we found an increased risk of breast cancer associated with omega-3 fat from fish.” The study concluded that decisions about dietary fat should focus primarily on the potential effects on heart disease.

A meta-analysis published recently by another group of investigators highlighted the fact that the relationship between dietary fat, estrogen, and breast cancer is far more complicated than was formerly realized. In this analysis, serum estradiol levels from 13 dietary fat intervention studies were consistently lower among women whose fat intake was limited to less than 20% of total calorie intake. In discussing their findings, the investigators noted that fiber intake typically increases when fat intake is limited, and that the types of fiber consumed, whether from grain, legume, vegetable, or fruit sources, could exert complex influences on estradiol levels. These investigators also noted that lowering of fat intake often is accompanied by a reduction in body weight; excess fatty tissue has consistently been shown to be associated with elevations of estrogen levels.

An association also has been reported between increased breast cancer risk and consumption of red meat cooked at high temperatures, such as occurs during grilling and barbecuing. As part of the Iowa Women’s Health Study, women with breast cancer and a group of controls were asked about their preferences on degree of doneness for meat. Those who ate well-done hamburger, beef steak, and bacon had a 4.62 times higher risk than the women who indicated preferences for rare or medium-cooked meat.

Alcohol intake also has been shown to elevate estrogens in postmenopausal women. One study evaluating the effects of acute alcohol ingestion (0.7 g/kg) on blood levels of plasma estradiol and estrone found elevations of 300% among women taking HRT compared with those not taking supplemental estrogen. Because moderate alcohol use appears to exert other health benefits, however, authorities do not recommend total avoidance. Furthermore, a cohort study within the Nurses’ Health Study suggested that increased folate intake may help counteract the negative effects of excess alcohol intake.

Because so many questions remain and so few answers have come from the conventional medical community, many women now are looking at alternative approaches such as dietary supplementation with soy and green tea. Others are asking questions about environmental issues such as the effects of pesticides and carcinogens and the need for screening for genetic abnormalities (see “Genetics and the price of fear,” below). “Races for the cure” are being held across the country.

Clearer messages on how to prevent breast cancer should be available in the coming years, but for now, authorities agree, the safest advice for all women is to do regular breast self-examinations and undergo screening mammography at appropriate intervals. Overall healthy lifestyle also is important, and not only for older women. Some authorities now suggest that diet during puberty and adolescence may influence breast cancer risk later in life.

Postmenopausal women who are not at risk for thromboembolic disorders, particularly those with strong family histories of breast cancer and those who, for any reason, are especially concerned about the disease, now have the option of taking tamoxifen or entering the STAR trial, too. Those considering treatment with raloxifene to prevent osteoporosis may consider the possibility that raloxifene also decreases cancer risk. They must, however, be cognizant of the uncertainties involved and, with the help of their physicians, make a careful risk-benefit analysis of this intervention in the context of their overall long-term health.


1. Fisher B, Costantino JP, Wickerham DL, et al. Tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. J Natl Cancer Inst. 1998;90:1371-1388.

2. Cummings SR, Eckert S, Krueger KA, et al. The effect of raloxifene on risk of breast cancer in postmenopausal women: results from the MORE randomized trial. JAMA. 1999;281:2189-2197.

3. Altman LK. Drug slashes breast cancer risk, study shows. The New York Times. June 16, 1999:A,27.

4. Powles T, Eeles R, Ashley S, et al. Interim analysis of the incidence of breast cancer in the Royal Marsden Hospital tamoxifen randomised chemoprevention trial. Lancet. 1998;352:98-101.

5. Veronesi U, Maisonneuve P, Costa A, et al. Prevention of breast cancer with tamoxifen: preliminary findings from the Italian randomised trial among hysterectomised women. Lancet. 1998;352:93-97.

6. Pritchard KI. Is tamoxifen effective in prevention of breast cancer? [commentary]. Lancet. 1998;352:80-81.

7. Chlebowski RT, Collyar DE, Somerfield MR, et al. American Society of Clinical Oncology technology assessment on breast cancer risk reduction strategies: tamoxifen and raloxifene. J Clin Oncol. 1999;17:1939-1955.

8. Madigan MP, Ziegler RG, Benichou J, et al. Proportion of breast cancer cases in the United States explained by well-established risk factors. J Natl Cancer Inst. 1995;87:87:1681-1685.

9. Boyd NF, Greenberg C, Lockwood G, et al. Effects at two years of a low-fat, high-carbohydrate diet on radiologic features of the breast: results from a randomized trial. J Natl Cancer Inst. 1997;89:488-496.

10. Franceschi S, Favero A, Decarli A, et al. Intake of macronutrients and risk of breast cancer. Lancet. 1996;347:1351-1356.

11. Holmes MD, Hunter DJ, Colditz GA, et al. Association of dietary intake of fat and fatty acids with risk of breast cancer. JAMA. 1999;281:914-920.

12. Wu AH, Pike MC, Stram DO. Meta-analysis: dietary fat intake, serum estrogen levels, and the risk of breast cancer. J Natl Cancer Inst. 1999;91:529-534.

By Trudy L. Bush, PhD, Steven R. Cummings, MD, and Clifford A. Hudis, MD

Provided by ArmMed Media