By taking the Pill, you expose breast tissue to higher than normal amounts of oestrogen. The Pill works by maintaining high levels of oestrogen in the body in order to prevent the ovaries from releasing eggs. The first oral contraceptives contained high doses of mestranol (ethinyloestradiol methyl ether) a relatively weak synthetic oestrogen and a synthetic progesterone or progestogen. In the late 1970s, scientists developed a "second generation" Pill, one that delivered lower doses of ethinyl oestradiol, a highly potent synthetic oestrogen. Because the doses of oestrogen and progestogen are lower in the second generation Pill than in the first, it is hailed as being safer. However, several factors indicate just the opposite.
The type of oestrogen used in the first generation Pill is half as potent as the type used in the second generation Pill. Also, unlike ethinyl oestradiol, mestranol does not bind to oestrogen receptors in the breast.
Most women who used the first generation Pill did so for a relatively short time, usually starting in their 20s. Women using the second generation Pill tend to do so for longer, sometimes starting in their teens and continuing to menopause, thus putting breast tissue under constant hormone stimulation. Most studies that have been performed on the Pill were based on the first generation form. Most women in the 1980s and 1990s use the second generation Pill.
In 1995, a National Cancer Institute study found that a few months' use of oral contraceptives could increase the risk of breast cancer by 30 per cent; a more than twofold risk was found with 10 years of use or longer (J Nat Cancer Inst, 1995; 87: 827-35). Eleven published studies have shown an increased risk of breast cancer with the Pill; a 1990 analysis of 32 studies revealed a "statistically positive trend" in the risk of premenopausal breast cancer for women exposed to OCs for longer duration (Cancer, 1990; 2253-63). The main risk was among women who'd used the Pill for at least four years before their first full term pregnancy. And progestogen only forms of third generation pills also show a 30 per cent increased risk (New Eng J Med, 1986; 315: 405-11).
According to reviews pooling earlier studies, hormone replacement therapy is responsible for up to 8 per cent of all postmenopausal breast cancers in the United States (Am J Epidemiology; 1991; 134: 1396-1401). A series of well controlled human studies and reviews conducted over the last two decades clearly shows that extended use and high dosages of HRT increase the risk of breast cancer by about 30 to 70 per cent. This statistic means that a 70 year old woman on HRT may increase her chances of breast cancer from one in 14 to up to one in five and even higher still if she has a family history of breast cancer. In 1995, the Harvard Nurses's Health Study confirmed these statistics, adding that prolonged use (over five years) has a particularly significant impact on health (New Eng J Med, 1995; 332: 1589-93). (For further details of specific studies, see the WDDTY Guide to the Menopause).
Dietary fat contains a wide range of contaminants pesticides, industrial pollutants and sex hormones known to cause breast cancer and/or to have oestrogenlike effects (pseudo-oestrogens). Several contaminants, including the pesticide atrazine, have both carcinogenic and oestrogenic effects, which makes them particularly dangerous. Once in your system, these contaminants tend to accumulate and concentrate in body and breast fat at levels thousands of times greater than in food, thus putting the breast at special risk.