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The Biology

    • It is well known that exposure to estrogen increases breast cancer risk. In fact, most known risk factors for breast cancer can be attributed to some form of excess estrogen exposure.
    • Early (before age 12) menarche, late (after 52) menopause, childlessness, late first full-term pregnancy, use of hormone replacement therapy after menopause, as well as the prolonged use of oral contraceptives by young women, are well known risk factors for developing breast cancer of varying levels of significance. All of these risk factors are the result of an over-exposure to the hormone estrogen. The same biology that accounts for the known hormonal risk factors for breast cancer mentioned above, also accounts for the link between abortion and breast cancer.
    • Before pregnancy, a woman's breast cells consist mainly of immature, non-milk-producing Type 1 and 2 lobules. When pregnancy occurs, estrogen (and to a lesser extent, other growth factors) cause Type 1 and 2 lobules to multiply immensely, in preparation for lactation. Because Type 1 and 2 lobules multiply so readily, this is where most breast cancers arise. When the pregnancy progresses past 32 weeks gestation, progesterone, along with other pregnancy hormones, cause Type 1 and 2 lobules to mature into Type 3 and Type 4 lobules. Mature, milk-producing Type 3 and 4 lobules are resistant to cancer, because they are no longer able to multiply as Type 1 and 2 lobules.
    • Having a full-term pregnancy has been linked to a decrease in breast cancer risk--the earlier the better. A major study of 250,000 women from around the world found that those who have their first child by age 18 have only about one-third the risk of breast cancer faced by women whose first birth occurs at age 35 or later.(1)
    • Breastfeeding has also been associated with a decrease in breast cancer risk. Valerie Beral and colleagues of the Collaborative Group on Hormonal Factors in Breast Cancer have published a large study on the effects of childbirth and lactation on breast cancer risk. They concluded that, "It is estimated that the cumulative incidence of breast cancer in developed countries would be reduced by more than half, from 6.3 to 2.7 per 100 women by age 70, if women had the average number of births and lifetime duration of breastfeeding that had been prevalent in developing countries until recently. Breastfeeding could account for almost two-thirds of this estimated reduction in breast cancer incidence".(2)
    • It is a well established fact that abortion can increase a woman’s risk of developing breast cancer by denying her the protective effect of both a full-term pregnancy as well as breast-feeding. In addition, the abrupt, artificial termination of a healthy pregnancy leaves a woman with an increased number of vulnerable undifferentiated (immature) breast cells which are, in turn, exposed to the massive amounts of estrogen present during early normal pregnancy. Estrogen is a known cancer causing hormone.

      (1) B. MacMahon et al., "Age at First Birth and Breast Cancer Risk," Bulletin of the World Health Organization, 43:209-221, 1970.
      (2) Collaborative Group on Hormonal Factors in Breast Cancer. "Breast Cancer and Breastfeeding: Collaborative Reanalysis of Individual Data From 47 Epidemiological Studies in 30 Countries, Including 50 302 Women With Breast Cancer and 96 973 Women Without the Disease." Lancet 2002; 360: 187-195.

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Biological Changes in Breast Tissue during Pregnancy

When a female child approaches puberty, she has only a few primitive Type 1 lobules in her breast tissue. A rise in estrogen levels at the onset of puberty leads to tissue growth by increasing the number of Type 1 lobules. Type 1 lobules consist of a cluster of approximately 11 small club-shaped end ductules, known as alveolar buds, branched out from a terminal duct. The increase in hormonal activity during puberty causes some Type 1 lobules to develop into Type 2 lobules, in which the alveolar buds branching from each terminal duct become smaller and multiply to an average of 47 buds per terminal duct.(2) The terminal ductal units of the Type 1 and 2 lobules are known to be especially vulnerable to carcinogens, due to their highly proliferative susceptability. (1,3-5) In mid to late pregnancy, after at least 32 weeks gestation(6), the alveolar buds of Type 2 lobules multiply and mature into the grape-like pockets of cells, or alveoli, of Type 3 lobules. Type 3 lobules in turn differentiate into Type 4 lobules, which, after childbirth, secrete milk. Type 3 and 4 lobules, in which the tissues are fully differentiated, are known to be resistant to carcinogens.(1,2,3,4,7,8)

As is well-known, and as stated by Valerie Beral in her 2002 study, "pregnancies that result in a birth are known to reduce a woman's long-term risk of developing breast cancer"(9). The protection associated with first full term pregnancy is due to differentiation of the initially primitive ductal end cells into cancer resistant milk producing lobules.(2-4,7,8,10-12)

Differentiation of breast tissue, which occurs after 32 weeks, is a result of the interaction of numerous hormones. After conception occurs, many hormones including estrogens and progesterone prepare breast tissue for lactation. Estrogen levels rise by 2000% in early pregnancy, causing massive proliferation of Type 1 and 2 lobules, in which mutations are more likely to arise.(3)

During normal pregnancy, the proliferative effects of estrogen, prolactin hormone and growth factors are balanced by the actions of other hormones such as human chorionic gonadotropin hormone (hCG), as well as progesterone.(13) hCG has a direct effect on the breast tissue by activating inhibin, which regulates cell growth and induces the activation of genes that control programmed cell death and differentiation. Differentiation also occurs when hCG stimulates release of progesterone.(14) Progesterone induces a new set of chemicals within the breast cell that tell it to stop dividing and mature into a cell that can produce milk, but is no longer capable of replication.(15,16) While estrogen primarily causes proliferation of breast tissue, progesterone primarily causes differentiation.(27,32) Differentiated Type 3 and 4 lobules are not only non-proliferative, they also have a better ability to repair damage induced in the DNA.(4,17)

Differentiation associated with full-term pregnancy increases the overall number of Type 3 and 4 lobules. Type 3 lobules remain as the predominant structure in childbearing women until age 40. Thereafter, and especially after menopause, Type 3 lobules mostly revert back to Type 1 lobules. The breast tissue of a woman who has never become pregnant will consist of mainly Type 1, some Type 2, very few Type 3, and no Type 4 lobules.(18,19) Without the profound rise of progesterone that occurs in late pregnancy(20), few Type 1 and 2 lobules will progress to the stage where progesterone stops cell proliferation, controls programmed cell death, and differentiates the lobules into cells that are better able to repair damage to the DNA. Instead, they are left in the vulnerable state in which carcinogens, including estrogen, (3,21-26) can stimulate the uncontrolled growth of abnormal cells.

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Full-Term Pregnancy versus Terminated Pregnancy

Pregnancy beyond at least 32 weeks causes breast lobules to mature into highly differentiated tissue that is resistant to carcinogens. When pregnancy is terminated by induced abortion before full maturation of her breast tissue, she is left with an increased number of the immature Type 1 and 2 lobules, where cancers are more likely to arise. This results in a greater net risk for breast cancer.

Pregnancy that is terminated by induced abortion results in increased breast cancer risk in two ways. First, estrogen stimulation in early pregnancy causes massive proliferation of Type 1and 2 lobules, where cancers can arise. If abortion terminates the pregnancy before 32 weeks, these lobules are not protected from cancer by progressive maturation to Type 3 and 4 lobules, as they would have been, had the pregnancy continued to term. So the woman is left with a much greater number of cancer-vulnerable cells than she had before she became pregnant. She is also left with a much greater number of cancer-vulnerable cells than she would have had if she had continued the pregnancy to term.

Secondly, this increased number of vulnerable cells are exposed to extremely high levels of estrogen during pregnancy, as well as during subsequent menstruation, which can induce cancer cells to form. Without the balancing effect of the marked progesterone rise of late pregnancy, estrogen promotes the proliferation of both cancer vulnerable breast tissue and existing tumors.(3,20) Estrogen can even initiate cancers in susceptible women.(3,21-26)

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Estrogen Exposure leads to Breast Cancer

Estrogen acts as a carcinogen in several ways. In the first place, estrogen acts as a mitogen, stimulating massive cell division through mitosis. Each time a cell divides into two, it must replicate its DNA. When errors or mutations occur during this process, abnormal cells can result. Cells may lose the ability to stop dividing, or may lose the information that controls programmed cell death. Thus, by stimulating increased cell division, estrogen can cause more abnormal cells to form. Timely exposure to progesterone can stimulate the abnormal cells to either die off, or differentiate, repair themselves, and control their proliferation before they result in full blown cancer. Without progesterone exposure, further estrogen stimulation also causes the abnormal cells to multiply.(3,21-23)

Estrogen also acts as a genotoxin, or mutagen, which directly attacks the DNA, causing mutations and thus initiating a process that leads to the formation of cancer cells. Along with stimulating cell division, estrogen also activates the production of enzymes, which are required to break down the estrogen and eliminate it from the body. Some forms of estrogens are safely and easily excreted, while others form unstable metabolites and by products that can damage the DNA of cells.(7,20-28) While estrogen can cause cancers to form by damaging DNA, a full-term pregnancy results in more differentiated cells that are better able to resist damage to the DNA as well as better able to repair damaged DNA. Terminating a pregnancy through induced abortion forfeits the protection afforded by cell differentiation, as well as increasing exposure of a greater number (than were present before onset of pregnancy) of vulnerable cells to estrogen.

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Spontaneous Abortion and Breast Cancer Risk

While induced abortion is associated with increased estrogen exposure of vulnerable cells, early spontaneous abortion generally is not. It has been shown that in pregnancies ending in early spontaneous abortion, hormone levels are generally not elevated to the same degree as in 'normal' pregnancies.(29,30) Thus, early spontaneous abortions do not result in increased estrogen exposure with subsequently overall increased breast cancer risk, as has been demonstrated in several studies.(31,1,32,40) Because pregnancies that end in early spontaneous abortion and induced abortion are physiologically unequal in regards to hormone levels and estrogen exposure, studies examining abortion and breast cancer risk should deal with induced and early spontaneous abortion separately.

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Risk Factors Related to Estrogen

It is well known that exposure to estrogen increases breast cancer risk. In fact, most known risk factors for breast cancer can be attributed to some form of excess estrogen exposure, and/or exposure of highly vulnerable Type 1 and 2 lobules to estrogen. Early (before age 12) menarche, late (after 52) menopause, childlessness, late first full-term pregnancy, use of hormone replacement therapy after menopause , as well as the prolonged use of oral contraceptives by young women, are well known risk factors of varying levels of significance.(3,33-36) In fact, the World Health Organization (WHO) reported in its July 29, 2005 press release that a team of scientists has determined that combined oral contraceptives (estrogen plus progestogen) and combined menopausal therapy are "carcinogenic to humans." Menopausal therapy was formerly classified as "possibly carcinogenic to humans." It has been upgraded to a Group 1 classification, "sufficient evidence of carcinogenicity in humans." Oral contraceptives received the same classification.(41) The same biology that accounts for the known hormonal risk factors for breast cancer mentioned above, also accounts for the abortion breast cancer link.

Conversely, events that decrease estrogen exposure decrease breast cancer risk: late menarche, early menopause, early first full-term pregnancy (with its narrower 'window' of exposure of vulnerable cells to cyclic monthly estrogen exposure, due to earlier differentiation of breast tissue into cancer resistant cells), higher total parity, and prolonged lactation.(3,4,36,37) Valerie Beral and colleagues of the Collaborative Group on Hormonal Factors in Breast Cancer have published a large study on the effects of childbirth and lactation on breast cancer risk. They concluded that, "It is estimated that the cumulative incidence of breast cancer in developed countries would be reduced by more than half, from 6.3 to 2.7 per 100 women by age 70, if women had the average number of births and lifetime duration of breastfeeding that had been prevalent in developing countries until recently. Breastfeeding could account for almost two-thirds of this estimated reduction in breast cancer incidence".(38) Induced abortion obviously decreases both number of births, as well as breastfeeding. Induced abortion, by causing loss of the protective effects of both a full-term pregnancy and breastfeeding, as well as increasing exposure of a greater number of more vulnerable cells to estrogen, increases overall breast cancer risk.

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References

(1) Daling JR, Malone KE, Voigt LF, White E, Weiss NS. "Risk of Breast Cancer Among Young Women: Relationship to Induced Abortion." Journal of the National Cancer Institute 1994; 86: 1584-1592.
(2) Dickson RB, Russo J. Biochemical Control of Breast Development. In: Harris JR, Lippman ME, Morrow M, Osborne CK, eds. Diseases of the Breast, 2nd ed. Philadelphia: Lippincott, Williams and Wilkins 2000: 15-31.
(3) ____. The Breast Cancer Prevention Institute. Fact sheet: The Biological Cause of the Abortion Breast Cancer Link: The Physiology of the Breast. May, 2003. http://www.bcpinstitute.org/physiology.htm (12/6/04).
(4) Russo J. in Lee JR, Zava D, Hopkins V. What Your Doctor May Not Tell You About Breast Cancer. New York: Warner Books 2002: 55-57.
(5) LaVelle FW. "Embryology and Abnormal Development of the Breast". In: Isaacs JH, ed. Textbook of Breast Disease. St. Louis, Missouri: Mosby-Year Book Inc, 1992: 15-20.
(6) (as cited in 1) Salazar H, Tobon H. "Morphologic Changes of the Mammary Gland During Development, Pregnancy and Lactation." In: Josimovich J, ed. Lactogenic Hormones, Fetal Nutrition and Lactation. New York: Wiley, 1974: 221-227.
(7) Lee JR, Zava D, Hopkins V. What your Doctor May Not Tell You About Breast Cancer. New York: Warner Books, 2002.
(8) Drife JO. "Breast Development in Puberty". In: Angeli A Breadlow HL, and Dogliottti, eds. Annals of the New York Academy of Sciences, vol 464. Endocrinology of the Breast: Basic and Clinicla Aspects. New York: New York Academy of Sciences 1986: 58-65.
(9) Collaborative Group on Hormonal Factors in Breast Cancer. "Breast Cancer and Abortion: Collaborative Re-analysis of Data from 53 Epidemiological Studies, Including 83 000 Women from 16 Countries." Lancet 2004; 363: 1007-1016.
(10) Russo J, Lynch H, Russo IH. "Mammary Gland Architecture as a Determining Factor in the Susceptibility of the Human Breast to Cancer." Breast Journal 2001; 7(5): 278-291.
(11) Russo J, Russo IH. "Development of the human breast." Maturitas 2004; 49(1): 2-15.
(12) Russo J, Mailo D, Yun-Fu Hu, et al. "Breast differentiation and its implication in cancer prevention." Clinical Cancer Research. January 2005; 11: 931s-936s.
(13) Faber KA, Hammond CB. "Endocrine Aspects of Breast Disease and Breast Function." In: Isaacs, ed . Textbook of Breast Disease. St. Louis, Missouri: Mosby-Year Book, Inc, 1992: 143-154.
(14) Lee, et al. p. 33.
(15) Lee, et al. p. 129.
(16) Malet C, Gompel A, et al. "Effect of Estradiol and the Synthetic Progestin Promegestone (R5020) on the Proliferation of Human Mammary Cells in culture." In: Angeli A, Bradlow HL, and Dogliotti L, eds. Annals of the New York Academy of Sciences, Vol 464. Endocrinology of the breast: Basic and Clinical Aspects. New York: New York Academy of Sciences 1986: 489-492.
(17) Willet WC, Rockhill B, et al. "Epidemiology and Non Genetic Causes of Cancer." In: Harris J, Lippman ME, Morrow M, Osborne CK, eds. Diseases of the Breast, 2nd ed. Philadelphia: Lippincott Williams and Silkins 2000: 175-220.
(18) Russo J, Russo IH. "Experimentally Induced Mammary Tumors in Rats." Breast Cancer Research and Treatment 1996; 39(1): 15-18.
(19) Russo J, Riveira R, Russo IH. "Influence of age and parity on the development of the human breast." Breast Cancer Research and Treatment 1992; 23(3): 211-218.
(20) Lee, et al. p. 154.
(21) Miller K. "Estrogen and DNA Damage: The Silent Source of Beast Cancer?" Journal of the National Cancer Institute 2003; 95: 100-102.
(22) Yager JD. "Endogenous Estrogens as Carcinogens through Metabolic Activation." Journal of the National Cancer Institute Monographs 2000; 27: 67-73.
(23) Leihr JG. "Is Estradiol a Genotoxic Mutagenic Carcinogen?" Endocrine Reviews 2000; 21(1): 40-54.
(24) Cavalieri EL, Frenkel J, Liehr JG, et al. "Estrogens as Endogenous Genotoxic Agents - DNA Adducts and Mutations." Journal of the National Cancer Institute Monographs 2000; 27: 75-94.
(25) Cavalieri EL, Stack DE, Devanesan PD, et al. "Molecular Origin of Cancer" Catechol Estrogen-3,4-quinones as Endogenous Tumor Initiators. Proceedings of the National Academy of Sciences of the USA,
1997; 94: 10937-10942.
(26) Russo J, Hasan Lareef M, Balogh G, Guo S, Russo IH. "Estrogen and its metabolites are carcinogenic agents in human breast epithelial cells." Journal Steroid Biochemical Molecular Biology. Oct, 2003; 87(1): 1-25.
(27) Rinzler CA. Estrogen and Breast Cancer. New York: MacMillan Publishing Company 1993: 174.
(28) Lee, et al. p.116-135.
(29) Stewart DR, Overstreet JW, Nakajima ST, Lasley BL. "Enhanced Ovarian Steroid Secretion Before Implantation in Early Human Pregnancy." Journal of Clinical Endocrinology and Metabolism 1993; 76(6): 1470-1476.
(30) Norman RJ, McLoughlin JW, Borthwick GM, Yohkaichiya T, Matthews CD, MacLennan AH, de Kretser DM. "Inhibin and Relaxin Concentrations in Early Singleton, Multiple and Failing Pregnancy: Relationship to Gonadotropin and Steroid Profiles." Fertility Sterilty 1993; 59(1): 130-137.
(31) Brind, Joel, Chinchilli VM, Severs WB, Summy-Long J. "Induced Abortion as an Independent Risk Factor for Breast Cancer: A Comprehensive Review and Meta-analysis." Journal of Epidemiology and Community Health 1996; 50: 481-496.
(32) Lipworth L, Katsouyanni K, Ekbom A, et al. "Abortion and the Risk of Breast Cancer: a Case Control Study in Greece." International Journal of Cancer 1995; 63(5): 761.
(33) Lee, et al. p. 26-43.
(34) Rinzler, p. 125, 168-9, 174.
(35) Marshall JR. "Epidemiology of Breast Cancer." In: Isaacs JH, ed. Textbook of Breast Disease. St. Louis, Missouri: Mosby-Year Book, Inc, 1992: 143-154.
(36) ____. National Cancer Institute. Cancer Facts: Oral Contraceptives and Cancer Risk. 2003. Http://cis.nci.nih.gov/fact/3_13.htm#ref (1/26/05).
(37) ____. Coalition on Abortion and Breast Cancer. Fact Sheet: Exposure to Estrogen and Breast Cancer Risk. http://www.abortionbreastcancer.com/exposuretoestrogen.htm (12/9/04).
(38) Collaborative Group on Hormonal Factors in Breast Cancer. "Breast Cancer and Breastfeeding: Collaborative Reanalysis of Individual Data From 47 Epidemiological Studies in 30 Countries, Including 50 302 Women With Breast Cancer and 96 973 Women Without the Disease." Lancet 2002; 360: 187-195.
(39) Rinzler, C. "The Female Principle" in Estrogen and Breast Cancer. New York: MacMillan Publishing Company 1993: 9,10. "The body makes three principal forms of estrogen: estrone, estradiol, and estriol. Estradiol, (in scientific terms, the word estrogen usually refers specifically to a form of estradiol called 17-b estradiol) the most potent, most plentiful estrogen, is secreted by the ovaries, the testes, the placenta, and the cortex (outer covering) of the adrenal glands…Estradiol is metabolized in the liver, where it is converted to estrone, a much less active estrogen, which is eventually excreted in the urine." In this paper, "estrogen" generally refers to estradiol.
(40) Kunz J , Keller PJ, "hCG, Oestradiol, Progesterone and AFP in Serum in Patients with threatened abortion", British journal of Obstetrics and Gynaecology 83.8 (Aug 1976):640-644
(41) Press Release No. 167, "IARC Monographs Programme Finds Combined Estrogen-Progestogen Contraceptives (the "pill") and Menopausal Therapy Are Carcinogenic to Humans," World Health Organization International Agency for Research on Cancer, July 29, 2005. See <http://www.iarc.fr/ENG/Press_Releases/pr167a.html>.