The upward national trends in breast cancer incidence have continued and been consistently more marked in postmenopausal than in premenopausal women. The 1970s and 1980s were characterized by an acceleration of the increase in the U.S. postmenopausal breast cancer incidence rate, which has been more marked in women in their later 60s and 70s than in the earlier postmenopausal years. This is also the cohort of women who were too old ever to have taken oral contraceptives. The increase in annual numbers of cases, at least in postmenopausal women, is not completely explained by changes in age at first full-term pregnancy or wholly by increased rates of use of screening mammograms (The Cancer Letter, 1990; Marchant and Sutton, 1990; White et al., 1990). Nor, as yet, is any reason known for the apparently different experiences of younger and older postmenopausal women. Were older women exposed to an additional risk that bypassed younger cohorts? Has the effect of that additional risk yet to appear in younger cohorts? Were the younger cohorts exposed to that risk but protected against its effects by some new experience?
Against this background, the Institute of Medicine's Committee on the Relationship Between Oral Contraceptives and Breast Cancer assessed the role of oral contraceptives in breast cancer etiology. The committee met on three occasions through 1989 and 1990, convening an invitational conference in May 1990 to inform its deliberations. This report of the committee's efforts evaluates ways in which the etiology of breast cancer may relate to the use of oral contraceptives, identifies options for future research on several fronts, and lays out information for clinicians and women considering the use of the pill.
The etiology of breast cancer is unknown. Growth and differentiation of breast tissue are regulated by a large number of factors, including steroid hormones such as estradiol and progesterone. Therefore, it is biologically plausible that exogenously administered steroidal hormones such as those in the pill could have an effect on breast carcinogenesis. On purely theoretical grounds it is impossible to say whether this effect might be adverse or beneficial. Estrogen causes proliferation of breast tissue and would be expected to increase the risk of breast cancer by stimulating growth of stem and intermediate cells (Thomas, 1984). Progestin causes not only alveolar cell growth in the estrogen-primed breast but also differentiation. It is thus unclear whether the net effect would be to increase or decrease breast cancer risk (see Appendix A).