The Abortion and Breast Cancer Link:

Advances in Human Biology and Continued Epidemiologic Studies Increasingly Point to a Link

I. INTRODUCTION::

In the past 30 years, landmark advances in the developmental and the molecular biology of the breast coupled with the repeated epidemiologic studies from around the world have more and more tightly linked induced abortion as an independent factor in breast cancer. The “independent link” refers to the fact that induced abortion before 32 weeks gestation will change the breast in a way that makes it more likely to develop breast cancer in later years.

Indisputable ways induced abortion increases breast cancer risk

Given the present state of knowledge of breast physiology and reproductive risks described in standard medical texts, it is indisputable that induced abortions cause an increase in breast cancer incidence.

It is well known that different pregnancy outcomes lead to changes in the rates of breast cancer among women:

· Once pregnant, if a woman chooses to maintain her pregnancy and achieves a full term pregnancy, she will lower her risk of breast cancer. This is well known and undisputed in medical circles.

· If she chooses to have an induced abortion she may remain childless, a condition which increases her risk of breast cancer.

· Or if she chooses abortion and then has another pregnancy, the abortion will have delayed this pregnancy which delay also increases her risk of breast cancer.

· If she already had a full term pregnancy and chooses to abort a subsequent pregnancy she loses the risk reduction that an additional full term pregnancy would have afforded her.

· The use of instruments such as dilators during an abortion increases the risk of having a premature delivery in future births. If that premature delivery is before 32 weeks, she will have an increased risk of breast cancer.

The well established research conclusions that underpin this indisputable increase in the risk of breast cancer from induced abortions are:

1) A full term pregnancy decreases the risk of breast cancer.

2) Delay of a full term pregnancy increases breast cancer risk.

3) Every full term pregnancy after the first pregnancy further decreases the risk of breast cancer risk.

4) Induced abortion increases the risk of premature delivery, thus increasing the risk of breast cancer if the delivery is before 32 weeks

Long Established Insight on Childlessness and Breast Cancer:

It has been known for centuries that remaining childless increases a woman’s risk for breast cancer and conversely, is was also known that pregnancy was protective. In 1743, Ramazzini of Padua observed that there was an increased number of breast cancer among nuns. In 1842, a hundred years later, Rigioni-Stern noted a 3 fold increase risk of breast cancer among nuns. Nuns were largely childless whereas the rest of the population had pregnancies early on in their reproductive lives.

Delayed first pregnancy: The longer a woman waits to have her first full term pregnancy (FFTP, used hereafter), the higher her risk of breast cancer as her immature, cancer-vulnerable breast tissue is exposed to carcinogens for a longer duration. A woman who has her FFTP at 20 years of age has a 90% lower risk of breast cancer than a woman who remains childless or waits until she is 30 for her FFTP.[1]

Each year a woman delays pregnancy she has a 5% increase in risk for pre-menopausal breast cancer and a 3% increase in risk for postmenopausal breast cancer.[2] For example, having an induced abortion at age 20 followed by a full term pregnancy at age 30 would increase her risk of premenopausal breast cancer by 50%. Other studies have shown that breast cancer risk increases 0.7% for each year subsequent births were delayed after her first birth.[3] Yet another study has shown that if a woman has a pregnancy and lactates within five years after an abortion, she will decrease her risk by 20% compared to if she waits 10 or more years to lactate for the first time.[4]

Increased number of pregnancies: For each pregnancy she has subsequent to her first, her risk of breast cancer will decrease another 10% [5].

Abortion and Subsequent Premature Births: Two large meta-analyses show that induced abortion increased a woman’s risk of premature delivery.[6] Also, the more induced abortions a woman has the higher her risk of subsequent premature births.[7] In 2006 the Institutes of Medicine listed induced abortion as an immutable cause of premature birth in its publication on prematurity.[8]

No matter the length of her pregnancy, in the first 32 weeks she will have changes in her breast tissue which will increase her risk of breast cancer. When a woman gives birth naturally, it takes many hours to dilate the cervix for birth. During an abortion the cervix is forcibly dilated and subjected to injury. Due to use of instruments such as dilators during an abortion she may have a premature delivery. If the premature delivery is before 32 weeks, she will have an increased risk of breast cancer. Approximately 3% of all premature deliveries are before 32 weeks.[9]. Approximately 12.5% of all births are before 37 weeks and are considered premature [10]

Breast Tissue Changes in First Pregnancy: When a woman becomes pregnant for the first time, her immature and cancer-vulnerable breast tissue matures into cancer-resistant tissue. Eighty-five percent of her breast will become fully mature type 4 lobules which contain the first milk, colostrum. After weaning, theses lobules regress to type 3 lobules which are also cancer resistant. This biological change accounts for the known fact that never having a full term pregnancy (nulliparity) increases a woman’s risk of breast cancer (as in the case of nuns). After a full term pregnancy, only 15% of her breast tissue remains susceptible to forming cancer.[11] It is the genetic changes that occur in the breast lobules during a full term pregnancy which gives lifelong protection. [12] Molecular biologists have also determined that progenitor or stem cells in the breast do not become terminally differentiated (reached their full potential growth or matured) until they have undergone the environment of pregnancy and have lactated. [13]

Premature Births and Increased Risk of Breast Cancer: Several studies have shown that prematurity before 32 weeks more than doubles breast cancer risk.[14] In fact, the biologic mechanism for premature delivery, induced abortion and second trimester miscarriage as causes for increase risk of breast cancer is the same mechanism for all three: Abortion, premature delivery or 2nd trimester miscarriage all leave the breast with more places for cancers to start when the pregnancy ends. The woman’s breasts have been exposed to the same pregnancy hormones (estrogen, progesterone, human chorionic gonadotropin (hCG) and human placental lactogen hPL) all of which lead to the same breast changes. Elevated levels of estrogen and progesterone, stimulated by hCG, cause more cancer vulnerable breast tissue to form. It is only after 32 weeks of gestation that the elevated levels of hPL, concert with other pregnancy hormones, allow the full maturation to cancer-resistant breast tissue to occur. Therefore, whether the pregnancy ends with a premature birth before 32 weeks, a 2nd trimester miscarriage (which generally have normal hormonal levels) or an induced abortion, breast cancer risk is increased.

II. Developmental Biology Supports The Independent Link Between Breast Cancer And Induced Abortion

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.

Lobules are units of breast tissue comprised of a milk duct with surrounding mammary (milk) glands, which are in turn composed of individual breast cells. Each breast cell contains a nucleus—a center space that contains DNA, the coded complete blueprint of genetic information that every cell in the body contains.

After puberty a woman has only Type 1 and 2 lobules in her breasts. During the first half of pregnancy of Type 1 and 2 lobules increase in number as the breast doubles in volume. . 85% of breast cancers arise in Type I lobules which form ductal cancers.. 10-15% of all breast cancers arise in Type 2 lobules which form lobular cancers.. Type 1 lobules have a greater number of estrogen and progesterone receptors in their cells’ nuclei than Type 2 lobules. Type 2 lobules have more of thes receptors than Type 3 lobules, which have significantly fewer.

The source of any cancer that develops in a body results from a mutation or damage done to the blueprint of the cell’s DNA. Unless the mutation is a critical one, such as in a gene that fixes errors in DNA when it is copied during cell division, most cancers form after several mutations have built up in a cell over a number of years, When cancer cells arise in the milk ducts but do not penetrate the basement membrane (outer layer of the duct) it is said to be in-situ cancers. These cancers are curable because they haven’t penetrated or invaded the basement membrane where the lymphatic channels on blood vessels are located, so they can’t spread to other parts of the body. Invasive cancers have penetrated the basement membrane and can spread throughout the body becoming metastatic and life-threatening.

Most invasive cancers start as in-situ cancers.

Pregnancy causes Type 1 lobules to increase the number of ductules (which become mammary glands) from an average of eleven ductules per lobule to forty-seven, becoming Type 2 lobules. Type 2 lobules mature still more fully into Type 3 lobules at which stage there is an average of eighty ductules in each lobule. Type 3 lobules have very few estrogen and progesterone receptors and do not quickly copy their DNA, thereby decreasing the possibility of mutations and carcinogenesis.[15] By 32 weeks these Type 3 lobules start to produce colostrum, the first milk, thereby becoming Type 4 cancer-resistant lobules.

We know exactly which genes have been turned off and on (down-regulated and up-regulated) throughout a full-term of pregnancy.[16]

During this time of maternal breast maturation, in the womb at 32 weeks gestation, a parallel development is occurring in the fetus: the solid cords of epithelial cells on the fetal chest wall become canaliculized (become hollow), thereby developing the milk ducts and glands of the newly forming fetal breasts.[17]

A mother’s breasts enlarge very soon after conception, making sore and tender breasts one of the first signs of pregnancy. Even before the embryo (or blastocyst) implants in its mother’s womb, a chemical signal, hCG (human chorionic gonadotropin) produced by the embryo, causes its mother’s ovaries to increase production of estrogen and progesterone in order to sustain the pregnancy. The maturation process that protects a woman from breast cancer happens only because the child in her womb produces the hormones hCG and hPL which prepare the mother to breast feed. In the first half of pregnancy, hCG stimulates estrogen and progesterone levels which cause the breast to enlarge with increased numbers of Type 1 and Type 2 lobules. In the later half of the pregnancy, hPL rises three times higher than the mother’s prolactin levels by the end of pregnancy, and enables full differentiation to Type 4 lobules which produce colostrum (the first milk). Thus the baby causes the mother’s breasts to get ready to feed him.

To summarize: Infants are born with Type 1 lobules in their breast tissue. During puberty in girls some Type 1 become Type 2 lobules, at which point she has a mixture of approximately 75%Type 1 and 25%Type 2 lobules. Pregnancy after 32 weeks causes Type 4 to develop with the milk the baby will need. After weaning these Type 4 lobules regress to Type 3 lobules but with the genetic changes of Type 4 remaining in the new Type 3 lobules (regressed Type4 lobules). After menopause, the Type 3 morph yet again into what appear to be Type 1 lobules, however the genetic changes which have afforded cancer resistance remain. Therefore the woman who has a full term pregnancy with Type 4 lobules gets lifelong benefits from these genetic changes, even without breastfeeding.

After about eleven weeks gestation it is the fetus and placenta --- not the mother --- which produces most of the needed estrogen and progesterone to sustain the pregnancy. Fetal developmental abnormalities that prevent adequate production of those hormones cause miscarriage (spontaneous abortion) in the first trimester. The levels of the pregnancy hormones (estrogen, progesterone, and hCG) during an abnormal pregnancy that result in a spontaneous abortion (miscarriage) in the first trimester were insufficient to stimulate breast development and thus leave the mother’s breasts unchanged. Therefore, following a first-trimester spontaneous abortion, the mother typically has no change in breast-cancer risk as her breasts were never stimulated to grow. Often a mother who spontaneously aborts (miscarries) in the first trimester will often remark that she never “felt” pregnant before she miscarried; she had no morning sickness nor sore and tender breasts that she may have experienced in prior pregnancies. Thirty-one percent of all conceptions will end in a spontaneous abortion.[18] Thus such miscarriages are not cancer-risk-raising events, because there is something wrong with the embryo so that hCG is not stimulating the mother’s ovaries to produce more estrogen and progesterone, or something is wrong with the mother’s ovaries which can’t produce enough estrogen/progesterone, resulting in the spontaneous termination of the pregnancy (miscarriage). After 11 weeks the fetus produces enough estrogen/progesterone to maintain the pregnancy. Most miscarriages are in the 1st trimester.