An oral contraceptive is usually a combination of a synthetic estrogen and progestin (i.e., the two major types of female hormones) which women take for 21 days out of a 28 day cycle. These hormones work by suppressing, but not eliminating ovulation, thickening cervical mucus, and by changing the lining of the uterus.
Yes. Concerns were raised in 1972 when it was noted that an oral contraceptive pill containing the artificial hormones mestranol and norethynodrel appeared to cause a case of metastatic breast cancer in a group of six female rhesus monkeys [1]. This was especially worrisome since rhesus monkeys rarely develop breast cancer. Until that time, only three cases of breast cancer in rhesus monkeys were reported. Although some argued that this was simply a "chance finding," concern grew further when it was noted that both beagles and rodents developed breast cancer when exposed to the hormones contained in today's OCPs [sources: 2, 3, 4, 5, 6].
In 1989, Anderson et al [7] published a classic paper regarding the influence of the OCPs on the rate of breast cell division. They found that nulliparous women (ie, women who have not had children) who took OCPs had a significantly higher rate of breast cell division than nulliparous women who did not take them. This was especially important since it is known that in general, cells that divide more rapidly are more vulnerable to carcinogens (ie, cancer producing agents) and thus more likely to become cancerous.
Both pro-life and pro-abortion groups openly admit that OCPs cause early abortions, with the latter doing so publicly in testimony before the Supreme Court in 1989 [8]. Induced abortion before a woman's first-term pregnancy (FFTP) has been noted to increase a woman's risk of breast cancer by 50% [9]. Could an abortion (defined to be the death of the zygote, embryo or fetus after conception has occurred) within the first week after conception have a deleterious effect as concerns breast cancer? The hormonal physiology of early pregnancy is difficult to measure but Stewart et al [10] and Norman et al [11] have shown that estradiol and progesterone levels (ie, the female hormones) start to rise above baseline levels within four days of conception, thus prior to implantation and before hCG levels begin to rise. An early abortion would cause a sudden fall in the levels of these hormones. Could this early "hormonal blow" be playing a role? To this author's knowledge, no one has asked or studied this question.
In 1981, Pike et al [12] found that women who took OCPs for four years before their first term pregnancy had at least a 2.25 fold (125%) increased risk of developing breast cancer before age 32. This startled the research world and led to additional studies, including a very large American trial called the CASH study (ie, Cancer And Steroid Hormone study). In 1993, the CASH study showed that women who took OCPs prior to first term pregnancy and were under 44 years of age had a 40% increased risk in breast cancer, which reached statistically significance in the 35-44 age group [13].
Later in England, Chilvers et al [14] published the results of another large study called the United Kingdom National Study. She showed that young women under the age of 36 who had used oral contraceptives for at least 4 years before their first term pregnancy had at least a 44% increased risk in breast cancer. The last large study was performed in 1995 by Brinton et al [15]. It showed a 42% increased risk for women who used OCPs for more than 6 months prior to having a full term pregnancy.
That is a good question. Major journals and major medical associations (eg, the AMA {American Medical Association}, ACOG {American College of Obstetricians and Gynecologists}, and the AAP {American Academy of Pediatrics}) have failed to stress or properly note this risk. Part of the problem is that because the OCP/breast cancer debate is complicated, most lay people have to rely on what "the experts" tell them.
A good example of this occurred recently in the Oxford study reported in condensed version in The Lancet [16] and in complete form in Contraception [17]. This study was and remains the largest meta-analysis (ie, a synthesis of all the major studies done in a particular field, concluding in an overall risk for the pooled studies) regarding the studies of OCPs and breast cancer. Researchers from around the world studied and combined the data from 54 studies, involving 25 countries and 53,297 women who had breast cancer. It concluded that: "Women who are currently using combined oral contraceptives or have used them in the past 10 years are at a slightly increased risk of having breast cancer diagnosed, although the additional cancers tend to be localized to the breast. There is no evidence of an increase in the risk of having breast cancer diagnosed 10 or more years after cessation of use..." Unfortunately, this study is known more for what it did say, than what it did not say! There were several major weaknesses of the study.
The main weakness was the failure to report any evidence of what the pooled risk of oral contraceptive use before a first term pregnancy was in women less than 45 years old. Another major weakness is that the Oxford study pooled data from studies which looked at women with breast cancer from the early and mid 1970s [17, p56].
A woman's breast is especially sensitive to carcinogenic influence (ie, cancer producing influence) before she has her first child since the breast undergoes a maturing process throughout a woman's first pregnancy. By failing to measure the effect of OCP use before a woman's first term pregnancy (FTP), the Oxford study failed to give data on the one group of women who are most likely to get breast cancer from oral contraceptives, namely, those women who used them before their first term pregnancy (eg, many teenagers and women in their twenties).
The second weakness is that the Oxford study used data from older studies which took some of their data from the mid and early 1970s. This does not leave a long enough latent period. A latent period is the time between exposure to a suspected risk factor (eg, early OCP use) and the cancer which it increases (eg, breast cancer). Often the latent period between a risk factor and a cancer is 15 to 20 years or more (eg, cigarettes and lung cancer). Although women in the US began taking OCPs in the 1960s, they only began taking them for longer periods of time at younger ages in the 1970s. Thus, only studies which include data from the 1980s and 1990s or beyond would allow a long enough latent period to pick up the influence of early OCP use.
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