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The link between abortion and breast cancer What every woman in the world has a right
to know! In 1970 the World Health Organization published the results of its study1 on reproductive experience in relation to the incidence of breast cancer. This study of more than 17,000 women in seven locations on four continents gained knowledge which is still undisputed almost 30 years later: Women who begin bearing children at
a young age are less likely to get breast cancer than those who have children
later, or those who have no children at all. How much protection against breast cancer do they get? Based on their findings, the W.H.O. scientists concluded: "It is estimated that women
having their first child when aged under 18 years
have only about one-third the breast cancer risk of those whose first birth
is delayed until the age of 35 years or more."1 Does this mean that a young woman who gets pregnant lowers her risk of getting breast cancer, even if she has an abortion? In relation to abortion the W.H.O. scientists said their results "suggested increased risk associated with abortion—contrary to the reduction in risk associated with full-term births."1 Research published in respected medical journals has since confirmed these findings2 and the hormonal basis for them: Twenty-five out of 31 epidemiologic studies3-33 worldwide—studies on women of African, Asian and European ancestry—have found that even one abortion increases the risk of getting breast cancer later in life. Importantly, the increased risk from abortion is in addition to the
increased risk from delaying a woman’s first childbirth, so abortion increases breast cancer risk in two
ways! Do you wonder why, in less than half a century, while abortion became legal and common, the incidence of breast cancer in the industrialized world, has more than doubled?34, 35 Do you have questions about the real impact on the women of your
country of importing "reproductive rights" from the industrialized
world? Is your country’s health care system prepared for an epidemic of breast
cancer? The Estrogen Connection: Why induced abortions raise breast cancer risk--and most
miscarriages don't Estrogen is the hormone--the chemical messenger--that turns a girl’s body into a woman’s body at puberty. Acually, there is a whole class of similar steroids, estrogens, which can stimulate the growth of the breasts and other female tissues. The most abundant and important estrogen secreted by a woman’s ovaries is called estradiol. Estradiol is so potent that it’s concentration in a woman’s blood is measured in parts per trillion! There is even some estradiol--about a tenth as much--made in a man’s body, and both men and women need some estradiol for normal growth and maintenance of the bones. After puberty, the levels of estrogen rise and fall twice with each menstrual cycle. Under the influence of the pituitary gland’s follicle stimulating hormone (FSH), new, egg-containing follicles develop in the ovaries during the first half (called the follicular phase) of the menstrual cycle. The follicular, estradiol-secreting cells surrounding the eggs proliferate, and so the ovaries secrete ever larger quantities of estradiol, reaching a peak about one day before ovulation. This preovulatory peak is the highest blood level of estradiol a woman ever normally experiences in the non-pregnant state. It stimulates her pituitary gland to secrete another hormone, luteinizing hormone (LH), which actually triggers ovulation. After ovulation, the follicle which has expelled the egg becomes filled with another kind of cell called a luteal cell. These luteal cells proliferate under the influence of pituitary LH, thus secreting ever larger quantities of both estradiol and the pregnancy hormone progesterone, from which estradiol is made. Since pituitary secretion of LH falls off quite sharply after ovulation, the corpus luteum (as the former follicle is now called) begins to regress about a week after ovulation, unless fertilization of the egg (conception) has taken place. If conception has occurred, the embryo begins--almost immediately--to secrete another chemical messenger, human chorionic godadotropin (HCG)*, which acts like LH to "rescue" the corpus luteum. If conception has not taken place, the corpus luteum essentially dies. Since luteal estrogen and progesterone are needed for (respectively) the growth and maturation of the endometrium (the uterine lining in which the embryo implants), the endometrium is shed as the menstrual flow or menses. If, however, conception has occurred and the corpus luteum has been rescued, it proceeds to generate enormous concentrations of progesterone (necessary to permit implantation of the embryo and maintainance of the pregnancy) and estradiol. Significantly elevated levels (compared to non-pregnant levels at the same time of the menstrual cycle) of estradiol can be detected as early as 5 days after conception36. As shown in Figure 1, by 7 to 8 weeks gestatation (after the last menstrual period, or LMP), a pregnant woman’s blood already contains six times more (i.e., 500% more) estradiol that it did at the time of conception, more than twice the highest level attained in the non-pregnant state (preovulatory peak).37 In marked contrast, pregnancies destined to abort spontaneously (i.e., end in miscarriage) during the first trimester usually do not generate estradiol in quantities exceeding non-pregnant levels37, 38 (Figure 1). One team of Swiss obstetricians, as far back as 1976, was actually able to predict spontaneous abortions with 92% accuracy with just a single measurement of estradiol!38 Theoretically, this makes perfect sense: The very reason for the abortion is an inadequate supply of progesterone from which estradiol is made. It is also widely known that women who start having children at a younger
age lower their risk of getting breast cancer later in life1. The
sooner the breasts become fully mature for the purpose of milk production,
the less likely is the presence of abnormal, potentially cancer-forming
cells, from accumulated carcinogenic insults (and what these are is still
largely unknown). In support of this theory, an experimental study of the
effect of pregnancy and induced abortion on breast cancer incidence in young
rats treated with chemical carcinogens was published in 198039.
The same research team has also published an excellent study of the
differentiation in human breast tissue as a function of pregnancy and age.40 In addition, since there are always some undifferentiated cells (and even some abnormal cells) in a woman’s breasts, overexposure to the growth-promoting effects of estradiol or other estrogens, whenever the exposure takes place, contributes to breast cancer risk. Not surprisingly, then, most known risk factors for breast cancer involve some form of estrogen overexposure. For example, women who attain puberty at an early age, or who enter the menopause at a late age, or who have fewer or no children, are exposed to more surges of estradiol that come with more menstrual cycles. Women who breast feed their children also experience fewer menstrual cycles, thereby helping to lower their risk. Even risk factors which are unrelated to reproduction seem to operate via an estrogen-mediated mechanism. For example, post-menopausal obesity increases risk, presumably because adipose (fat) cells actually synthesize estrogens, thus raising an obese woman’s blood estrogen levels. Even chronic alcohol consumption seems to raise breast cancer risk by increasing estrogen levels in a woman’s blood. Likewise for a diet high in animal fat, compared to a vegetarian diet. Conversely, certain vegetables known to help protect against cancer, such as members of the broccoli and cabbage family, help a woman’s body to eliminate estrogens more rapidly. Since the effect of estrogens on breast cancer risk has been well recognized for many years, doctors have been wary of prescribing such medications as post-menopausal estrogen replacement therapy for older women, especially those with any family history of breast cancer. As it turns out, such medications do seem to raise the risk of breast cancer risk slightly, when they are used for several years. One would think, therefore, that doctors would long ago have been concerned about possible increases in breast cancer risk attributable to induced abortion, given the extremely high estradiol levels experienced by women even in the first several weeks of a normal pregnancy. Finally, there is one additional and crucial aspect of spontaneous abortion vis-a-vis breast cancer risk that must be noted, namely the effect of post-first trimester miscarriages. Most miscarriages occur in the first trimester, and over 90% of these are characterized by abnormally low maternal estradiol levels38. However, there is reason to believe that pregnancies which survive the first trimester (and they couldn’t survive without adequately high progesterone levels, which are parallelled by estradiol) are likely to raise breast cancer risk, if they go on to miscarry. *Although HCG is commonly referred to as a hormone, in fact, it is not. Since it is a chemical message between two individuals of a species (in this case, mother and child), it is more properly described as a pheromone. Since it is not normally secreted by a woman’s body at all, specific detection of the presence of HCG is the basis of every pregnancy test. How estradiol, or estrogens in general, relate to breast cancer risk, has to do with their role in the growth of breast tissue. It is estradiol which makes the breasts grow to mature size at puberty, and which makes them grow again during pregnancy (at least the first two trimesters). The cells in the breast which are responsive to estradiol are those which are primitive, or undifferentiated. Once terminally differentiated into milk-producing cells, something which happens under the influence of other (still largely unknown) factors, breast cells can no longer be stimulated to reproduce. It is the undifferentiated cells,
which are also vulnerable to the effects of carcinogens (radiation, certain
chemicals, etc.), which can give rise to cancerous tumors later in life. If a
woman therefore has gone through some weeks of a normal pregnancy, and then
aborts that pregnancy, she is left with more of these cancer-vulnerable cells
than she had in her breasts before she was pregnant. In addition, any
abnormal, potentially cancer-forming cells already in her breasts (and such
cells are present to some extent in all people) have also been stimulated to
multiply. All this translates into a statistically greater probability that a
cancerous tumor may eventually arise. In contrast, a full term pregnancy
results in full differentiation of the breast tissue for the purpose of milk
production, which leaves fewer cancer-vulnerable cells in the breasts than
were there before the pregnancy began. This translates into the well known
breast cancer risk lowering effect of a full term pregnancy. The World Conference on Breast Cancer acknowledges the
link between abortion and breast cancer The first World Conference on Breast Cancer took place in July of 1997 in At the conference, Dr. Joel Brind, Ph.D.,
Professor of Endocrinology at A year later, in the fall of 1998,the World Conference published its Global Action Plan Report41, in which the organization outlined its agenda for the ultimate eradication of breast cancer. Under the subject of risk factors related to hormones, the Report reads in pertinent part: "Today, women in general are exposed to higher levels of estrogen during their lifetime than was the case in previous generations. It is believed that women now face excess levels of both natural and synthetic estrogens, increasing their risk of breast cancer. Prolonged use of the birth control pills, late or lack of pregnancies and breast-feeding, INDUCED TERMINATION OF PREGNANCIES, a diet high in fat, meat or dairy products, and hormone replacement therapy following menopause, all are cited as risk factors for increased estrogens and breast cancer." (Emphasis added.) Remember: Reproductive
rights are meaningless without the right of women to know all the
consequences of the choices they may make. References cited 1. MacMahon B, et al. Bull Wld Health Org 1970;43-209-21 2. Brind J, et al. J Epidemiol Community Hlth 1996;50:481-96 3. Pike MC et al. Br J Cancer 1981;43:72-6 4. Brinton L et al. Br J Cancer 1983;47:757-62 5. Rosenberg et al. Am J Epidemiol 1988;127:981-9 6. Howe HL et al. Int J Epidemiol 1989;18:300-4 7. Laing AE et al. J Natl Med Assoc 1993;85:931-9 8. Laing AE et al. Genet Epidemiol 1994;11:A300 9. Daling JR et al. J Natl Cancer Inst 1994;86:1584-92 10. Daling JR et al. Am J Epidemiol 1996;144:373-80 11. Newcomb et al. JAMA 1996;275:283-7 12. Wu AH et al. Br J Cancer 1996;73:680-6 13. Palmer JR et al. Cancer Causes Control1997;8:841-9 14. Moseson M et al Int J Epidemiol 1993;22:1000-9 15. Segi M et al GANN 1957;48(Suppl):1-63 16. Watanabe H, Hirayama T Nippon Rinsho 1968;26:1853-9 (in Japanese) 17. Dvoirin VV, 18. Burany B Jugosl Ginekol Opstet 1979:19:237-47 (in Serbo-Croatian) 19. Nishiyama F Shikoku Ichi 1982;38:333-43 20. Le M-G In: Wolff J-P, Scott JS, eds. Hormones and Sexual Factors in
Human Cancer Aetiology. 21 Hirohata et al NCI Monogr 1985;69:187-90 22. Ewertz M, Duffy SW Br J Cancer 1988;58:99-104 23. Adami HO et al Br J Cancer 1990;62:122-6 24. La Vecchia C et al Int J Epidemiol 1993;53:215-9 25. Andrieu N et al Cancer Detect Prev 1994;18:51-5 26. Lipworth L et al Int J Cancer 1995;61:181-4 27. Rookus M, van Leeuwen FE JNCI 1996;88:1759-64 28. Bu L et al Am J Epidemiol 1995;141:S85 29. Talamini R et al Eur J Cancer 1996;32A:303-10 30. Melbye M et al N Engl J Med 1997;336:81-5 31. Luporsi E in Andrieu N et al Br J Cancer 1995;72:744-51 32. Rohan TE, and 33. Zaridze DG, in #31 above 34. Harris JR et al N Engl J Med 1992;327:319-28 35. Remennick LI Int J Epidemiol 1989;18:498-510 36. Stewart et al J Clin Endo Metab 1993;76:1470-6 37. Witt et al Fertil Steril 1990;53:1029-36 38. Kunz J, Keller PJ Br J Ob Gyn 1976;83:640-4 39. Russo J, Russo IH Am J Path 1980;100:497-512 40. Russo J et al Brst Cancer Res Trt 1992;23:211-8 41. 1997 World Conference on Breast Cancer Global Action Plan Report. 1997, p. 15 This pamphlet has been produced as a joint effort of Endeavour Forum, Inc., 12 Denham Place, Toorak, Victoria 3142, Australia Phone: +613-9822-5218; Fax: +613-9822-3069, Babette Francis, National and Overseas Coordinator, and the Abortion-Breast Cancer Quarterly Update, P.O. Box 3127, Poughkeepsie, NY, 12603 USA; phone & Fax: 914-463-3728 e-mail: jbrind@abortioncancer.com., Joel Brind, Ph.D., Editor and Publisher. Reproduction and distribution of this pamphlet is encouraged.
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Figure 1 Blood Estradiol |
Figure 2 Schematic representation of a breast a) in a never pregnant woman, and b) at the end of a full-term pregnancy. Never pregnant breast tissue conists of primitive, terminal end buds and ducts, which are vulnerable to carcinogens, while lactating breast consists mostly of mature lobules--clusters of milk- secreting alveoli --which are resistant to carcinogens. (Adapted from references #39 and 40) |