Academic journal article Issues in Law & Medicine

Induced Abortion and Breast Cancer

Academic journal article Issues in Law & Medicine

Induced Abortion and Breast Cancer

Article excerpt

Biology of the Abortion Breast Cancer Link

The basic human biology of breast maturation through pregnancy is the basis of the abortion breast cancer link. The protective effect of a full-term pregnancy on breast cancer risk has been known since the Middle Ages when it was noted that nuns had a higher risk of breast cancer than women with children.

Since 1976, there has been a 400% increase risk of in-situ breast cancer in women under 50 by SEER data. There has been a 2% per year increase in metastatic breast cancer in women under 40. Why? An understanding of the biological basis of breast cancer risks makes it possible to understand, predict and minimize those risk factors which will affect a womans future risk of breast cancer.

Medical authorities agree:

* That a full-term pregnancy lowers a womans risk of breast cancer.1

* That each additional pregnancy further lowers her risk by 10%.2

* That for each year after age 20, a woman who delays a full-term pregnancy, increases her risk of premenopausal breast cancer by 5% and postmenopausal breast cancer by 3%.3

* That induced abortion increases the risk of premature birth which in turn increases breast cancer risk if it occurs before 32 weeks.4

These 4 medical facts necessarily cause a pregnant woman who chooses to end her pregnancy by abortion, to increase her risk of Breast cancer.

In practical terms, this is the situation: A woman has an unplanned pregnancy.

If she chooses to continue her pregnancy and has a full-term pregnancy, or one that lasts at least 32 weeks, she will lower her risk of breast cancer.


If she chooses to end her pregnancy with an induced abortion, she will necessarily have an increased risk of breast cancer because:

* She will lose the benefit of a full-term pregnancy.

* She will delay a full-term pregnancy or have no or fewer full-term pregnancies.

* She may have a premature delivery before 32 weeks of another pregnancy.

Biological Basis of Breast Cancer Risk

Inherited genes or genes mutated after birth account for approximately 6-10% of all breast cancers (e.g. inherited BRCA genes 1& 2 or radiation, virus or chemically induced injury). Approximately 90% factors that influence the rate of breast cancer are due to the interplay of two influences: 1) cumulative lifetime exposure to estrogen and 2) amount and timing of breast lobular cell differentiation from Type 1 lobules, the most primitive type to Type 4 lobules, the most differentiated.

It is the biology of the breast lobule maturation that occurs during pregnancy which accounts for the abortion breast cancer link. At full development, the breast is comprised of 15-25 lobes which are in turn comprised of lobules. Lobules in turn are composed of breast cells.

There are 4 types of lobules whose structural differences appear under the microscope.5 Type 1, 2 & 3 lobules are differentiated by the average number of ductules per lobular unit: (Type 1 has 11; Type 2 has 47; Type 3 has 80). Type 4 lobules are fully matured and contain colostrum or milk.

These 4 types of lobules are also metabolically different with different breast cancer potential. Type 1 & 2 lobules have more estrogen and progesterone receptors than Type 3.6 Type 1 and 2 lobules grow through mitosis (cell division) when estrogen and proges- terone levels are elevated. Mitosis requires replication of DNA (genes) and therefore can result in mutations. Mutated cells also undergo mitosis. Multiple mutations can cause cancer cells to form. Cells of Type 1 & 2 lobules also multiply faster than Type 3 resulting in more chances for mutations to occur. This growth (proliferation) under estrogen and progesterone stimulation explains the cancer causing properties of estrogen/progestin combination drugs.

Type 1 lobules mature into Type 2 lobules under the cyclic influence of the female hormones, estrogen and progesterone, during menstrual cycles. …

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