The Abortion-Breast Cancer Link: The Biology (Part Four of Four)


By Joel Brind, Ph.D.

Joel Brind, Ph.D.

In the three previous installments of this series, I documented the epidemiological evidence for the abortion-breast cancer (ABC) link, and the ongoing wall of denial from the official purveyors of public health information, including the National Cancer Institute (NCI). In this final installment, I’ll go over the basic, underlying biology of how and why abortion interferes with normal breast development and breast health, thus leading to a higher risk of breast cancer later in life for women who have chosen abortion.

Everyone knows that a woman’s breasts, as part of the reproductive system, do not develop until puberty. But most people — even doctors — do not know that the breasts really do not develop substantially even at puberty: they essentially just grow in size. What that means is that from the time of puberty, a girl has a lot more breast tissue capable of growing — and capable of becoming cancerous — than she had before puberty. Thus does puberty open what breast cancer researchers call the “susceptibility window.”

The susceptibility window — when potentially cancer-causing mutations can collect in vulnerable breast lobule cells — only closes when a woman has her first full-term pregnancy. It is in fact at about 32 weeks of a normal pregnancy that most of the primitive, growing cells of the breast become differentiated into cells that can actually produce milk.

Why are these mature cells resistant to becoming cancerous? Because their ability to proliferate has been turned off. That explains not only the epidemiological evidence showing abortion’s link to future breast cancer risk, but also the fact that a live birth before 32 weeks gestation also increases risk; the effect on the mother of “terminating” a normal pregnancy is the same, regardless of the fate of the child.

A little more detailed look at what happens to the breasts during pregnancy clearly shows two major ways in which abortion raises the risk of future breast cancer.

The future milk-producing structures in the breast that multiply during puberty are called Type 1 and Type 2 lobules. It is Type 1 and Type 2 lobules where almost all breast cancers start. Microscopically, these lobules look rather like trees in winter, with the branches bare except for small buds. After puberty but before first pregnancy, almost 100 percent of the lobules are Type 1 and 2 — to emphasize again, where almost all breast cancers begin.

When a woman becomes pregnant, the hormones estrogen and progesterone surge and cause a massive growth spurt in the breasts, doubling the size of the lobular tissue by mid-pregnancy (20 weeks gestation). But by 32 weeks gestation, only about 20 percent of the lobules are still cancer-vulnerable Type 1 and 2. Most have matured to Type 4 and can produce colostrum (milk).

Putting all this together in terms of breast cancer risk, we can see that putting off childbirth until a woman is older results in a greater likelihood of getting breast cancer, because the susceptibility window is open much longer. This fact has been well established, ever since a definitive, international multi-center study commissioned by the World Health Organization (WHO) was published in 1970.

Moreover, it is widely known to be responsible for most of the difference between the high rate of breast cancer incidence among women in North America and Europe — who typically wait until they are in their late 20′s or 30′s to start having children — and the much lower breast cancer incidence rates among women in Asia and Africa. Thus there is no controversy about the fact that the longer a woman waits to start having children, the higher her future risk of breast cancer. Importantly, by delaying the closing of the susceptibility window, abortion abrogates the protective effect of full-term pregnancy.

But abortion does more damage than merely postponing first childbirth, nullifying the protective impact that comes because immature and cancer-prone breast tissue have matured. The surging estrogen and progesterone of a normal pregnancy multiplies the number of Type 1 and 2 lobules. If the pregnancy is aborted, this creates more places for cancers to start, because the third trimester maturation to type 3 and 4 lobules never is allowed to happen.

That is why dozens of published epidemiological studies from around the world, starting as far back as 1957, continue to emerge which show increased breast cancer risk among women who have abortions. This trend even showed up in the World Health Organization (WHO) report back in 1970, wherein the authors noted that their results “suggested increased risk associated with  abortion — contrary to the reduction in risk associated with full-term births.”

Finally, it should be noted that there are two more ways — indirect ways — in which abortion can increase a woman’s future breast cancer risk which often are overlooked.

First, abortion increases the risk of premature birth in subsequent pregnancies. Not only does this have devastating consequences in terms of increasing the incidence of such congenital disabilities as cerebral palsy and autism, but (as noted above) premature deliveries before 32 weeks gestation increase the risk of breast cancer, the same as later-term abortion does.

Second, it is also well established that breast feeding reduces the risk of future breast cancer, and breast feeding is of course not possible after the baby is aborted.

Clearly, nothing reduces the risk of future breast cancer like starting childbearing early. That’s a big reason why teenage and early 20-something mothers in particular should be advised against abortion. Young motherhood will drive their future breast cancer risk way down, while abortion will drive it way up. It really is as simple as that.

But what about abortion of subsequent pregnancies? Again, half a century’s worth of data confirms that the independent effect of abortion – above and beyond the effect of postponing first childbirth — is the same for abortion of any pregnancy. That would be about a 30 percent increased risk on average.

I suspect few women would be willing to take that risk, if only they knew about it.


Joel Brind, Ph.D. is a professor of biology and endocrinology at Baruch College of the City University of New York and co-founder of the Breast Cancer Prevention Institute.  He is a frequent contributor to NRL News and NRL News Today.

This article is reprinted with permission from NRL News Today.

Learn More:
The Abortion-Breast Cancer Link, Part I: Those Stubborn Facts Again
The Abortion Breast Cancer Link, Part II: The Cover Up
The Abortion-Breast Cancer Link, Part III: The Dagger Under the Table
The Abortion-Breast Cancer Link, Part IV: The Biology

For the most complete online library of published studies on the physical and psychological effects of abortion,  visit


The Abortion-Breast Cancer Link: The Biology (Part Four of Four) — 3 Comments

  1. I greatly appreciate Dr. Brinds frank look at all the research that both supports and denies the ABC link. I’ve done a little bit of my own research into the research, but not this extensive. What I still don’t understand, though, is how biologically speaking there is a difference in breast cancer risk between a spontaneous abortion/miscarriage and an induced abortion. The way you explained it biologically, with a surge in type 1 & 2 lobules, this is still happening even if it ends with a miscarriage, no?

    • I’m not an expert either. You may want to contact Dr. Brind or his associates for their best explanation of what they believe is the mechanism. In a broad sense, it is my understanding that in cases of natural miscarriage, the process of miscarriage may essentially take weeks as the body and hormone levels shift toward the miscarriage and through the aftermath of the miscarriage. Since a miscarriage is a “natural” process this process over time allows the body to adjust and “close out” the surge, if any, in growth of type 1 and 2 lobules. (I say, if any, because if the body is signaling a miscarriage weeks before the actual miscarriage, there may not be a surge in type 1 and 2 lobules since the hormone levels to support the pregnancy may not be sufficient.) But abortion is an unnatural process, induced by surgical methods or chemical/medicinal poisoning or shock to the body and so the production of type 1 and 2 lobules is not “naturally” closed but rather disrupted in what may be a “confused” state that may or may not “close” properly as the body tries to adjust to the shock.

      That’s my layperson’s understanding of explanations I have heard, for what it may be worth. It’s also my understanding that all we can say with certainty is that there is a statistically significant association between abortion and breast cancer. The disruption of the natural growth of breast tissue during early pregnancy is a reasonable theory that may explain some or all of the observed effects. Other factors, such as increased risk of depression, smoking, and substance abuse (all of which are also significantly increased after an abortion) may effect the immune system and play a role in increased susceptibility to breast cancer.

      Sorting out the physical (much less the psychological) pathways which may best explain the observed effect is not easy . . . especially in the political environment which makes such research unwelcome. But those who wave their hands and dismiss the statistical association between abortion and breast cancer are putting an ideological commitment to “protecting the liberty of abortion” (the idea that it serves women rather than hurts them) above the right of women to be fully informed about any and all risks that medical research has identified as associated with abortion.

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