In part 1 we looked at the provenance of the Abortion-Breast Cancer (ABC) hypothesis and demonstrated, pretty conclusively, that its main proponents are religious zealots who are motivated to promote this hypothesis by their religious/moral objections to induced abortion.
As we move on to look at the science behind this hypothesis the key thing to bear in mind is the observation made by Polly Newcomb*, a cancer researcher at the Fred Hutchinson Cancer Research Center in Seattle back in 2003:
“Circumspection, unfortunately, is what you have to do to practice epidemiology,” says Polly Newcomb, a researcher at the Fred Hutchinson Cancer Research Center in Seattle. “That’s something Brind is incapable of doing. He has such a strong prior belief in the association [between abortion and cancer] that he just can’t evaluate the data critically.”
*Newcomb is, nine years on from that comment, Program Head of the Fred Hutchinson Center’s Cancer Prevention programme.
Joel Brind and Angela Lanfranchi, like Priscilla Coleman and David Reardon in relation to abortion and mental health, have a pronounced tendency to grossly overstate the nature and extent of the evidence which they see as supporting their hypothesis that inducted abortion is linked to an increase risk of breast cancer, a fact which quickly become apparent when you look at their published work with a critical eye.
In order to understand the ABC hypothesis properly we need to start by looking at what is currently known about the relationship between pregnancy and breast cancer, and this has ben usefully summarised as follows by the US National Cancer Institute:
Is there a relationship between pregnancy and breast cancer risk?
Studies have shown that a woman’s risk of developing breast cancer is related to her exposure to hormones that are produced by her ovaries (endogenous estrogen and progesterone). Reproductive factors that increase the duration and/or levels of exposure to ovarian hormones, which stimulate cell growth, have been associated with an increase in breast cancer risk. These factors include early onset of menstruation, late onset of menopause, later age at first pregnancy, and never having given birth.
Pregnancy and breastfeeding both reduce a woman’s lifetime number of menstrual cycles, and thus her cumulative exposure to endogenous hormones. In addition, pregnancy and breastfeeding have direct effects on breast cells, causing them to differentiate, or mature, so they can produce milk. Some researchers hypothesize that these differentiated cells are more resistant to becoming transformed into cancer cells than cells that have not undergone differentiation.
So, there is pretty good evidence that pregnancy and breastfeeding can reduce womens’ overall risk of developing breast cancer but some uncertainty as to the exact mechanisms that underpin this phenomenon, hence the statement that some researchers hypothesize that these differentiated cells are more resistant to becoming transformed into cancer cells. The question of whether these biological changes in breast cells, which are called ‘lobules’, have a definite preventative effect is still an open field of research and yet, in Lanfranchi’s latest ‘paper’ she makes the following unequivocal assertion:
Developmental biology concerning the breast changes that occur with puberty and with a normal pregnancy further supports the theory of an independent link between induced abortion and breast cancer.
Immature, cancer-vulnerable Type 1 and 2 lobules mature to cancer-resistant Type 4 lobules after 32 weeks of pregnancy. After weaning, Type 4 lobules regress to Type 3 lobules which have permanent genetic changes that protect against the development of cancer within these Type 3 lobules.
Compare that rather bald statement to the two most recent papers on lobular type/architecture I could track down on PubMed –
Ramakhrishan et al (2004)  failed to find an association between lobular architecture and breast cancer in a relatively small scale study of biopsy tissue samples (n=284) but did find that the lobular architecture of the breast was influenced by the menstrual cycle:
Lobule type was not associated with menstrual phase classified by dates; however, when menstrual phase was classified using breast morphological characteristics, type I lobules were more abundant in follicular phase and type II in the luteal phase (p < 0.001).
And concluded that:
…we did not observe a relationship between lobular architecture and breast cancer susceptibility when using smaller breast samples usually available in epidemiological studies, but these data highlight the need for menstrual phase stratification in future investigations.
However Baer et al (2009) , a nested case control study of benign breast disease and breast cancer, found that:
…women with predominant type 1 and no type 3 lobules had a reduction in breast cancer risk compared to women with all other lobule types, even after adjustment for histologic category of BBD. Some decrease in risk was observed for all categories of BBD, although the stratified analyses were limited by small numbers of cases and controls. These results suggest that having a larger proportion of type 1 lobules and no type 3 lobules may be protective against the development of breast cancer among women who have had BBD, regardless of their histologic category. Therefore, evaluation of lobule type in the background breast tissue of women who have had a benign breast biopsy may provide additional information about their subsequent risk of breast cancer.
To a degree this rather seems to contradict Lanfranchi’s blunt characterisation of type 1 lobules as ‘cancer vulnerable’ – at the very least it suggests that if lobular type and architecture are a factor in determining breast cancer risk then the relationship may easily be much more complicated that Lanfranchi suggests.
Baer’s paper also includes the following statement, which serve to put the current status of this whole research area into its proper perspective:
The types of lobules and the stages of lobular development have been well-characterized in animal models, and there is substantial experimental evidence in rodents indicating that the degree of lobular development may be an important determinant of breast cancer risk; however, there are very limited data on this subject in humans. To our knowledge, only one previous epidemiologic study has formally examined the association between lobule type and breast cancer risk; that study found no association between predominant lobule type and breast cancer risk.
The ‘one previous epidemiologic study’ that Baer refers to is Ramakrishnan et al (2004).
To read Lanfranchi’s account of this hypothesis, which runs to a full three pages in even the edited extract of her ‘paper’, you’d be forgiven for thinking that it had been proven beyond all reasonable scientific doubt when, in reality, almost all the data comes from animal studies, not least studies conducted by Jose and Irma Russo on rats.
When Joel Brind tries to link abortion and breast cancer, he starts with Jose and Irma Russo’s research. In 1978 the husband-and-wife team took 49 female rats and divided them into groups: rats that had carried a pregnancy to term and delivered offspring, rats that had been given abortions, and rats that had not mated. Then they exposed the animals to a chemical that is known to give female rats cancer: 7,12-dimethylbenz(a)anthracene. One of the 18 rats that had given birth developed a malignancy, seven of the nine rats that had abortions developed malignancies, and 15 of the 22 virgins developed malignancies.
Writing in The American Journal of Pathology in August 1980, the Russos concluded that a full pregnancy appeared to give female rats protection against a known carcinogen. They pointed out that female rats are born with terminal end buds: bulbous groups of cells at the tips of their mammary ducts that are prone to cancer. As pregnancy progresses, those cells differentiate into more mature structures called alveolar buds and lobules to prepare for nursing. The Russos drew parallels between rats and humans: Like rats, pregnant women undergo hormonal changes that stimulate the growth and subsequent specialization of breast cells into lactating cells. “Abortion would interrupt this process,” they added, “leaving in the gland undifferentiated structures like those observed in the rat mammary gland, which could render the gland again susceptible to carcinogenesis.”
As to the relevance of this evidence to humans, Gil Mor, director of the reproductive immunology unit at the Yale University School of Medicine, dealt with this in no uncertain terms:
“Humans are not rats.” Humans and rats are fundamentally different organisms, he says, pointing out that rats don’t even have breasts and, therefore, “there is no breast cancer in rats. We [use] the rat to understand basic biological process. Period. Basic biological processes.” In short, Mor says the Russos are on solid ground studying the basic processes of mammary-gland differentiation in rats. But when they or someone like Brind tries to extrapolate those processes to humans, the terrain gets wobbly.
This is hardly surprising when you understand that the nearest common ancestor of humans and rats is estimated to have lived somewhere around 70-100 million years ago during the Cretaceous Era living alongside the Tyrannosaurs and Velociraptors.
That said, what we have here is a scientifically plausible hypothesis which is certainly capable of explaining, at the very least in part, why pregnancy and breastfeeding lower womens’ risk of developing breast cancer but, as yet, nothing like enough evidence to validate this hypothesis – and even the evidence we do have to date is equivocal in relation to breast cancer. The question is, therefore, how does this relate to abortion and/or demonstrate a link between abortion and an allegedly increased risk of breast cancer?
To state the obvious first, if carrying a pregnancy to term (and breastfeeding) has the effect of reducing the risk the developing breast cancer then , at the very least, a women who aborts a pregnancy will lose those benefits. However, if this is all there is to it then that would leave women who have abortions in no worse a position vis-a-vis their risk of breast cancer than women of the same age who have never been pregnant.
So far as the relationship between age, pregnancy and breast cancer goes, the risk of a woman developing breast cancer later in life is halved if has her first baby before the age of 20 compared to a woman who delays her first pregnancy until she is over 30 years of age, and women who delay their first pregnancy until their 30s have a slightly higher risk of developing breast cancer than women who have never been pregnant. This is not, however, the whole story as – in general terms, women’s risk of developing breast cancer is linked to the duration and/or level of their exposure to ovarian hormones, which stimulate cell growth, and as such pregnancy itself is associated with a short-term increase in the risk of developing breast cancer:
Women who have recently given birth have a short-term increase in risk that declines after about 10 years. The reason for this temporary increase is not known, but some researchers believe that it may be due to the effect of high levels of hormones on microscopic cancers or to the rapid growth of breast cells during pregnancy. – National Cancer Institute.
Uniparous women were at higher risk of breast cancer than nulliparous women for up to 15 years after childbirth and at lower risk thereafter. The excess risk was most pronounced among women who were older at the time of their first delivery (odds ratio 5 years after delivery among women 35 years old at first delivery, 1.26; 95 percent confidence interval, 1.10 to 1.44). Women who had two pregnancies had a less striking increase in risk.
Pregnancy has a dual effect on the risk of breast cancer: it transiently increases the risk after childbirth but reduces the risk in later years. In women with two pregnancies, the short-term adverse effect is masked by the long-term protection imparted by the first pregnancy. A plausible biologic interpretation is that pregnancy increases the short-term risk of breast cancer by stimulating the growth of cells that have undergone the early stages of malignant transformation but that it confers long-term protection by inducing the differentiation of normal mammary stem cells that have the potential for neoplastic change. – Lambe et al (1994) 
This being the case it can be argued that women who do have termination, of a first pregnancy in particular, may be subject to the same short-term increase in breast cancer risk as other women, who carry their pregnancy to term, but lose out on the long term reduction in risk associated with carrying a first pregnancy to term – all depending, of course, on the age at which that first pregnancy occurs and assuming that it is, indeed, the first pregnancy that is terminated, which is certainly not always the case. Lambe et al also found that women who have two children have, overall, a lower transient risk of developing breast cancer that women who carry only one child to term across all age groups other than for women who’s second delivery occurs after the age of 35.The relationship between age, pregnancy and breast cancer risk is a complex one, for more complex that proponents of the ABC hypothesis will tend to admit when pushing the claim of the link between abortion and breast cancer, although this is briefly acknowledged in Lanfranchi’s ‘paper ‘ in arguing that her hypothesis is consistent with other evidence of the relationship between women’s reproductive history and breast cancer risk.
Even if we accept the hypothesis that abortion may expose women to the same kind of increased transient risk of developing breast cancer as a full-term pregnancy while depriving them, to some degree, of the long term benefits of an early full-term pregnancy this is not, in any real sense, evidence of a straightforward causal link between abortion and breast cancer, not least because the evidence clearly indicates that the transient increase in breast cancer risk is associated not with abortion but with pregnancy. It’s also clear from the complex nature of the relationship between pregnancy and breast cancer risk that any increase – or decrease – in risk associated with an individual reproductive event, whether this is a full-term pregnancy, an abortion or, in some cases, a miscarriage – particularly a miscarriage in the second trimester – can be mediated by other reproductive events making it difficult, if not impossible, to adequately estimate the degree of long-term risk to which an individual woman may be subject.
Even without examining the epidemiological evidence relating to abortion and breast cancer, it is apparent that Lanfranchi and Brind’s strong claims of a specific link between abortion and breast cancer sit on very shaky ground when one takes into consideration the complex but well evidenced links between pregnancy and breast cancer.
That said, if a link between abortion and breast cancer does exist then it should be evident in the epidemiological evidence, which is what we’ll be looking in part 3.
1. Ramakrishnan R, Gann PH, Wiley EL, Khurana KK, Khan SA. (2004). Normal breast lobular architecture in breast biopsy samples from breast cancer cases and benign disease controls. Breast Cancer Research and Treatment. 86(3):259-68.
2. Baer, H. J., Collins, L. C., Connolly, J. L., Colditz, G. A., Schnitt, S. J. and Tamimi, R. M. (2009), Lobule type and subsequent breast cancer risk: Results from the Nurses’ Health Studies. Cancer, 115: 1404–1411. doi: 10.1002/cncr.24167
3. Lambe M, Hsieh C, Trichopoulos D, Ekbom A, Pavia M, Adami HO. (1994) Transient increase in the risk of breast cancer after giving birth. New England Journal of Medicine. 331(1):5–9.
10 thoughts on “Debunking the Abortion-Breast Cancer Hypothesis – pt2.”
Thanks for all your hard work on this.
Just wanted to ask when you anticipated posting part three and if that would conclude this series as am looking to link to it all once complete.