PMID: 11535871

Issn Print: 0959-8278

Publication Date: 2001/08/01


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Oral contraceptives, cancer and vascular disease

C La Vecchia

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Several new data sources have contributed towards a better understanding of the oral contraceptive (OC) and cancer issue. With reference to breast cancer, it is now established that there is a moderate excess risk among current OC users, which tends to level off in the few years after stopping use. Most data have been included in the Collaborative reanalysis of individual data on 53 297 women with breast cancer and over 100 000 controls (Collaborative Group on Hormonal Factors and Breast Cancer, 1996), and subsequent studies have added little to this overall evidence (WHO–IARC, 1999). A historical cohort study suggested that the risk of breast cancer related to OC use may be elevated in women with family history of breast cancer (Grabrick et al., 2000). However, the relative risk (RR) of 3.3 was based on 16 cases only, while the estimate of 1.06 for ever OC use of the Collaborative Group on Hormonal Factors and Breast Cancer (1996) was based on 454 cases.
With reference to the well-known protection of OC use on endometrial carcinogenesis, additional information from a Swedish case–control study including 709 cases (Weiderpass et al., 1999) suggested that the protection is consistent across type of OC use (i.e. OC potency).
Further data on ovarian cancer indicate that the protection on ovarian carcinogenesis is long lasting, and may well be observed 15–20 years after stopping use (Beral et al., 1999; La Vecchia and Franceschi, 1999; WHO–IARC, 1999). A reanalysis of the data of the Centers for Disease Control Cancer and Steroid Hormone (CASH) Study (1987) suggested that OC with high progestin potency conferred a twofold greater protection against ovarian cancer compared with low progestin pills (Schildkraut et al., 2001).
The general assumption is that OCs affect ovarian cancer risk by reducing the lifetime number of ovulations. Repeated cycles of ovulation cause recurrent damage to the ovarian epithelium; this may eventually result in genetic changes that can lead to cancer. However, this explanation is not conclusive. Little information is available on progestin-only contraceptives, but the few available data tend to show that women who take these pills are at reduced risk of ovarian cancer as well (WHO–IARC, 1999). Many women on progestin-only pills continue to have ovulatory cycles. Moreover, OC use has a disproportionately greater protective effect than can be attributed solely to ovulation suppression (La Vecchia et al., 1983), and treatment with progestins results in an increased rate of apoptosis in the ovarian epithelium (Rodriguez et al., 1998). Thus, apoptosis may be a relevant factor in the protective role of OC on ovarian carcinogenesis.
A new open issue concerns a potential protective effect of combined OC use against the risk of colorectal cancer. Several studies have suggested an inverse relation between use of combined OC and the risk of colorectal cancer. In order to obtain summary quantitative estimates, a meta-analysis of published data was conducted (Fernandez et al., 2001). Articles considered were epidemiological studies on colorectal cancer published as full papers in English up to June 2000, and including quantitative information on OC use. The pooled RR of colorectal cancer for ever OC use from eight case–control studies was 0.81 (95% confidence interval (CI) 0.69–0.94), and the pooled estimate from four cohort studies was 0.84 (95% CI 0.72–0.97). The pooled estimate from all studies combined was 0.82 (95% CI 0.74–0.92), in the absence of apparent heterogeneity (Figure 1). Duration of use was not associated with a further decrease in risk, but there was some indication that the apparent protection was stronger for women who had used OCs more recently (RR 0.46; 95% CI 0.30–0.71).

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