The Stubborn Biological Facts regarding the Abortion-Breast Cancer link (ABC link) Part Four of Four
Joel Brind, Ph.D.
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% 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% 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 cancer 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 chosen abortion. 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 increases 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% increased risk on average.
I suspect few women would be willing to take that risk, if only they knew about it.
Source: NRLC News
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