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The first World Conference on Breast Cancer acknowledged that higher levels of estrogen increased the risk of breast cancer. 27 out of 31 studies have found that even one abortion can increase the risk of developing breast cancer. Having a first child before the age of 18 years reduces the breast cancer risk dramatically. In first trimester miscarriages, the estradiol (estrogen) levels are usually at non-pregnant levels. When a woman has an abortion, she has more cancer-vulnerable cells in her breasts than before pregnancy and exposes herself to increased risk of breast cancer. In a full-term pregnancy, lactating breasts leave fewer cancer-vulnerable cells in her breasts than before pregnancy. Scientists and researchers have collected data since 1957 that indicates early abortion is a risk factor for breast cancer, yet this information is not well known to the public, nor is it acknowledged by many medical associations and journals. Those making the claim say there are two ways in which abortion is linked to breast cancer. Firstly, women who begin bearing children at a young age are less likely to get breast cancer than those who have children later in life, or those who have no children at all. A World Health Organisation (WHO) study reported: "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 Secondly, 27 out of 31 epidemiological studies worldwide have found that having even one induced abortion increases the risk of getting breast cancer later in life. 2-32 The increased risk from abortion is apparently in addition to the risk from delaying a woman's first childbirth. Following the first World Conference on Breast Cancer in July 1997 a Global Action Plan Report was published which acknowledged that higher levels of estrogen increased the risk of breast cancer. It said: "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, are all cited as risk factors for increased estrogens and breast cancer." Read more about the World Conference here. At puberty, the hormone estrogen is what causes the changes in a female that turns her body from a girl to a woman. The most important estrogen is called estradiol and it is so powerful that its concentration in a woman"s blood is measured in parts per trillion. After puberty, the levels of estrogen rise and fall twice with each menstrual cycle. The ovaries secrete ever larger quantities of estradiol, reaching a peak about one day before ovulation. This peak before ovulation is the highest blood level of estradiol a woman will ever normally experience when she is not pregnant. After ovulation larger quantities of estradiol and the pregnancy hormone progesterone, from which estradiol is made, are secreted. About a week after ovulation, unless the egg has been fertilised (i.e. conception has taken place), the hormone levels soon return to normal. If conception has occurred, the embryo begins - almost immediately - to produce a chemical messenger which "rescues" the corpus luteum (the hormone-secreting body). If conception has not taken place, the corpus luteum essentially dies and the endometrium (the uterine lining of the womb) is shed as the menstrual flow or menses. Conception If, however, conception has occurred and the corpus luteum has been rescued, it starts producing enormous concentrations of progesterone 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 conception.33 By 7-8 weeks gestation (after the last normal period) a pregnant woman"s blood already contains six times more (i.e., 500% more) estradiol than it did at the time of conception, more than twice the highest level attained in the non-pregnant state (preovulatory peak).(See Fig.1) In marked contrast, pregnancies destined to abort spontaneously (i.e., end in micarriage) during the first trimester usually do not generate estradiol in quantities exceeding non-pregnant levels.34,35 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. The very reason for the miscarriage is an inadequate supply of progesterone from which estradiol is made.35 Estradiol relation to breast cancer risk It is estradiol, or estrogens in general, that makes the breasts grow to mature size at puberty and again during pregnancy (at least the first two trimesters). The cells in the breast which are responsive to estradiol are those which are primitive and have not undergone change. Once fully changed into milk-producing cells, breast cells can no longer be stimulated to reproduce. The drawings, in Fig. 2,of a breast in (a) a never-pregnant woman and (b) at the end of a full-term pregnancy, show how the never-pregnant breast tissue consists of primitive, terminal end buds and ducts, which are vulnerable to carcinogens (substances that increase the risk of cancer), while the lactating (milk producing) breast consists mostly of mature lobules - clusters of milk-secreting alveoli - which are resistent to carcinogens. When a woman has an abortion, she has substantially more cancer-vulnerable cells in her breasts than before pregnancy. In addition, any abnormal, potentially cancer-forming cells already in her breasts will also have been stimulated to multiply. All this translates into a statistically greater probability that a cancerous tumor may occur in later years. 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 is how a full-term pregnancy lowers the risk for breast cancer. Estrogen overexposure. Most known risk factors for breast cancer involve some form of estrogen. For example, women who attain puberty at an early age, or who enter the menopause at a late age, or who have few or no children, are exposed to more surges of estradiol that come with more menstrual cycles and are therefore more at risk of breast cancer. Women who breast feed their children also experience fewer menstrual cycles, thereby helping to lower their risk. Spontaneous abortion (miscarriage) Most miscarriages occur in the first trimester, and over 90% of these are characterised by abnormally low maternal estradiol levels. 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 paralleled by estradiol) are likely to raise breast cancer risk, just as induced abortions do. 36 In January 2005, the All Women"s Health Services of Portland, Oregon settled a lawsuit filed by a woman who accused them of failing to inform her that abortion could increase her risk of breast cancer. The case is the first such suit to be settled in the United States although settlements have been made in other countries. You can go here for greater technical details. Related stories here and here. References 1. MacMahon B, et al. Bull Wld Health Org 1970;43-209-21 2. Pike MC et al. Br J Cancer 1981;43:72-6 3. Brinton L et al. Br J Cancer 1983;47:757-62 4. Rosenberg et al. Am J Epidemiol 1988;127:981-9 5. Howe HL et al. Int J Epidemiol 1989;18:300-4 6. Laing AE et al. J Natl Med Assoc 1993;85:931-9 7. Laing AE et al. Genet Epidemiol 1994;11:A300 8. Daling JR et al. J Natl Cancer Inst 1994;86:1584-92 9. Daling JR et al. Am J Epidemiol 1996;144:373-80 10. Newcomb et al. JAMA 1996;275:283-7 11. Wu AH et al. Br J Cancer 1996;73:680-6 12. Palmer JR et al. Cancer Causes Control1997;8:841-9 13. Moseson M et al Int J Epidemiol 1993;22:1000-9 14. Segi M et al GANN 1957;48(Suppl):1-63 15. Watanabe H, Hirayama T Nippon Rinsho 1968;26:1853-9 (in Japanese) 16. Dvoirin VV, Medvedev AB Meth Progr Breast Cancer Epidemiol Res, Tallin, 1978. Moscow: Oncol Sci Ctr USSR Acad Sci 1978;58-63 17. Burany B Jugosl Ginekol Opstet 1979:19:237-47 (in Serbo-Croatian) 18. Nishiyama F Shikoku Ichi 1982;38:333-43 19. Le M-G In: Wolff J-P, Scott JS, eds. Hormones and Sexual Factors in Human Cancer Aetiology. Amsterdam:Elsevier 1884:139-47 20. Hirohata et al NCI Monogr 1985;69:187-90 21. Ewertz M, Duffy SW Br J Cancer 1988;58:99-104 22. Adami HO et al Br J Cancer 1990;62:122-6 23. La Vecchia C et al Int J Epidemiol 1993;53:215-9 24. Andrieu N et al Cancer Detect Prev 1994;18:51-5 25. Lipworth L et al Int J Cancer 1995;61:181-4 26. Rookus M, van Leeuwen FE JNCI 1996;88:1759-64 27. Bu L et al Am J Epidemiol 1995;141:S85 28. Talamini R et al Eur J Cancer 1996;32A:303-10 29. Melbye M et al N Engl J Med 1997;336:81-5 30. Luporsi E in Andrieu N et al Br J Cancer 1995;72:744-51 31. Rohan TE, and 32. Zaridze DG, in #30 above 33. Stewart, et al J ClinEndoMetab 1993;76:1470-6 34. Witt, et al Fertil Steril 1990;53:1029-36 35. Kunz J, Keller PJ, Br J Ob Gyn 1976;83:640-4 36. Pike: 140% increased risk; Brinton: 90% increase; Hadjimichael: 250% increase; Ewertz: 163% increase; and Rookus: 40% increase.



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