The science, studies and sociology of the abortion-breast cancer link.

AuthorLanfranchi, Angela

ABSTRACT: This article explains the breast physiology and epidemiologic criteria supporting the abortion breast cancer link and the sociologic factors that cause this risk to remain largely unknown to both medical professionals and the public. Abortion increases breast cancer risk through multiple mechanisms. Pregnancy exposes women to high levels of estrogen acting as a mitogen and genotoxin, and induced abortion then leaves their breasts with more places for cancers to start. They have a higher risk of subsequent premature deliveries that further increase their risks of breast cancer. Rampant breast cancer seen in ever younger women will not allow this issue to be suppressed.

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Abortion is a causal factor in the development of breast cancer in the same way cigarettes cause lung cancer. Both put the users at higher risk, even though the majority will not be affected. Like cigarettes, which cause lung cancer to form in 15% of those who smoke, abortion causes breast cancer in about 5% of women who have an abortion. This results in approximately 10,000 cases of breast cancer attributable to abortion a year, approximately the same number as is caused by the inheritable BRCA gene. The vast majority of smokers never get lung cancer yet we tell the public not to smoke. Women considering abortion need to know about the abortion breast cancer link (ABC link) so they can give an informed decision. Women who have had an abortion need to know they are at higher risk of showing symptoms of the disease earlier than other women so that they can be screened for breast cancer at an appropriate age.

This article will explain the breast physiology and the epidemiologic criteria supporting the ABC link and the sociologic factors which cause this risk to remain largely unknown to both medical professionals and the public.

Breast Cancer in U.S. Women

Only 15% of women with breast cancer have a family history of the disease. At most, 10% of women with breast cancer have inherited a faulty gene such as the BRCA gene. Yet over the last 30 years, the number of new cases of breast cancer has increased by 40%. Most of this increase has occurred in the Roe v. Wade generation, i.e. those women of reproductive age when the ruling was made in 1973. These women were young during the time of the "Women's Lib" movement and the "sexual revolution." Many delayed childbearing well into their thirties to pursue higher education and a career, widely using "the pill" so that sexual activity need not be postponed until marriage. When the pill failed, abortion became the frequently chosen option. Abortion is a consequence of equality in pursuing the sexual license that men have traditionally enjoyed by being free of the worry of becoming pregnant. The tobacco industry's ad told us, "You've come along way baby," and we have. Lung cancer rates were much higher in men than in women in the '70s; now we are nearly equal. The benzopyrenes in cigarette smoke not only increased lung cancer but also the incidence of cervical and breast cancer in women. The childless rate for women increased from 10% to 18% by the year 2000. Delayed child bearing, never having children, taking "the pill" and abortion as well as cigarettes are all well established risk factors for breast cancer, and can account for this increased incidence.

Relative Risk

Risk can be expressed in many ways. Relative risk (RR) is a useful way to compare different factors and is derived from epidemiologic studies. A RR of 1.0 means that factor is neutral or has no effect on risk. A RR of less than 1.0 means that a factor causes a decrease in risk. For example, a factor with a RR of .5 means that factor reduces risk by 50%. A RR over 1 means that factor increases risk. For example, 1.5 means 50% increase in risk and RR 2.0 means 100% increase in risk. Most women who hear that a risk factor has caused them to be at 100% increased risk think that this means they are 100% certain to get the disease. However, in regards to breast cancer, if a woman has no risk factors she has only a 3.3% risk of developing breast cancer. A factor which then increases her risk 100% causes her to have a 6.6% chance of developing cancer.

Cumulative Lifetime Risk

Many women have been alarmed by the widespread use of the statistic, cumulative lifetime risk of breast cancer. This is a statistically derived number that assumes all women will live to the age of 82 and not die of other causes before then. In 1975 the risk was one in 12 women would develop breast cancer. In 2004 that risk increased to one in seven, reflecting the increase in incidence of breast cancer over the last 30 years. However, it does not mean that if seven women are in a room one will now get breast cancer.

Three Major Influences on Breast Cancer Risk

The risk for development of breast cancer can be understood by considering three major influences: genetic factors and damage to the DNA, lifetime exposure to estrogen and breast lobule maturation.

Genetic Factors and Damage to the DNA

While it is true the root cause of all cancers is damaged genes, when considering breast cancer risk it is useful to realize that only 8% to 10% of all breast cancers occur because women inherited a faulty gene such as the BRCA genes from one of their parents.

Direct damage to the DNA (long strands of genes in the nucleus of the cell) can also be caused by large doses of radiation to the breast, such as when women are treated for Hodgkin's disease in the chest with radiation or have frequent X-rays over many years during treatment for a curved spine. These account for only a few percent of cancer cases. Benzopyrenes in cigarette smoke can damage breast DNA.

There is also the interaction of these two factors in regard to the timing of the exposures that impact risk. For example, exposure to radiation damages breast tissue most when the cells are actively developing and dividing, as when the breast is growing during puberty. For example, the atomic bomb radiation in Hiroshima caused breast cancers to form in teenagers who were exposed but did not affect post menopausal women. Benzopyrenes in cigarette smoke increase breast cancer risk in teenagers who have not had children by as much as 600%. Postmenopausal women who have had children do not have this increase in risk. Overall, these factors account for only approximately 10% of breast cancers in the population. Therefore, lifetime exposure to estrogen and breast lobule maturation accounts for approximately 90% of the other cases of breast cancer.

Lifetime Exposure to Estrogen

Estrogen is the major female hormone which makes women womanly. Without estrogen women would not have breasts or be able to bear children. It is difficult to grasp why such a beneficent hormone could also cause breast cancer. Yet one has only to remember that some of the most effective and used breast cancer treatments available are drugs which block the effect of estrogen or keep it from forming in the patient in order to understand the large impact estrogen exposure has on the risk of developing breast cancer. The class of anti-cancer drugs known as SERMs alter the effect of estrogen on breast cells. For example. Tamoxifen, a drug used both to treat breast cancer and prevent it, blocks estrogen receptors. Another class of drugs such as Arimidex blocks an enzyme aromatase from converting another hormone into estrogen. Before such drugs were available, breast cancer was treated by removing the patient's ovaries to decrease the estrogen in her body.

DES, diethyl stilbesterol, a potent estrogen used to prevent miscarriages, also increased the risk of breast cancer in the mother and the female child exposed in utero. In order to understand why lifetime exposure to estrogen increases breast cancer risk, it is necessary to understand its role as a mitogen and genotoxin.

Estrogen as a Mitogen. Estrogen in the presence of progesterone causes breast cells to undergo mitosis, i.e., multiply through division. Once a breast cell duplicates its DNA (long strands of genes in the nucleus of the cell) it...

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