Just when we thought we had it right -- i.e, that estrogens are among the primary causes of breast cancer -- along comes a new study seeming to disavow this "truth." And not just any study: the respected Women's Health Initiative study, underwritten by the National Institutes of Health and published in the Journal of the American Medical Association. Among the study's 10,000-plus post-menopausal women, those randomly assigned to take conjugated equine estrogens (CEE, as Premarin) had a definite trend toward a reduction -- yes, a reduction -- in the incidence of breast cancers, as compared to the group on placebo. This trend, so-called because the reduction was not quite statistically significant, was especially pronounced in cancers deemed "invasive" and "ductal," while the rate of occurrence of the less-dangerous "in situ" type was similar in both groups. (The women in this study were able to take estrogen alone because they had previously had a hysterectomy. In women with a uterus, administration of estrogen without the protective effect of concomitant progesterone is a major risk factor for excessive growth of uterine tissue and can promote uterine cancer.)
The results of this study conflict with the previously published Women's Health Initiative study of women taking both estrogen and progesterone, that showed a significant increase in their risk of breast cancer. Why the discrepancy? If, as we thought, estrogen is one of the main culprits in the production of breast cancer, why should using estrogen alone not cause it, while taking the combination of estrogen and progesterone does? One of the current study authors had two ideas as to possible answers: Dr. Marcia Stefanick of Stanford Prevention Research Center mused that perhaps the CEE/Premarin, being a mixture of estrogens, might contain both cancer-causing and cancer-protective agents. Alternatively, she noted, most of the women in the study were fat, and since, after menopause, fat is a main source of estrogen, perhaps the women were already making so much that the estrogen in the pills did not add to their risk.
These theories need to be tested with new randomized, controlled trials: this topic is too important to be left to speculation, even educated guesswork from someone as esteemed as Dr. Stefanick. If exogenous estrogens (pills, as opposed to estrogens our bodies make) don't make a major contribution to breast cancer, how would we explain the efficacy of anti-estrogen drugs, especially the new aromatase inhibitors, in treating and even preventing breast cancer?
Gilbert Ross, M.D., is Executive and Medical Director of the American Council on Science and Health (ACSH.org, HealthFactsAndFears.com).
