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    Hormonal Contraceptives: Are They Abortifacients?
    A Physicians’ Report

    Hormonal Contraceptive Report
    January 1998

    Currently the claim that hormonal contraceptives [birth control pills, implants (Norplant), injectables (depoprovera)] include an abortifacient mechanism of action is being widely disseminated in the prolife community. This theory is emerging with the assumed status of “scientific fact,” and is causing significant confusion among both lay and medical prolife people. With this confusion in the ranks comes a significant weakening of both our credibility with the general public and our effectiveness against the tide of elective abortion.

    This paper is meant to provide some clarifying information on the issue based on current knowledge and experience regarding the mechanism of action of hormonal contraceptives. It has been compiled in consultation with, and by cooperative effort of, several practicing obstetrician-gynecologists, perinatologists, and reproductive endocrinologists (all among the undersigned), each being a physician committed to the sanctity of human life from conception.

    We begin with the recognition that within the Christian community there is a point of view which holds that artificial birth control per se is wrong. We would consider this a personal matter of conscience and belief, and this paper is not intended to argue for or against this issue.

    In this discussion we accept the time honored definition that conception occurs when a sperm penetrates an egg. Disruption of the fertilized egg after this point represents abortion. We consider fertilization, not implantation, to be the beginning of human life.

    Most literature dealing with hormonal contraception ascribes a three-fold action to these agents. 1) inhibition of ovulation, 2) inhibition of sperm transport, and 3) production of a “hostile endometrium,” which presumably prevents or disrupts implantation of the developing baby if the first two mechanisms fail. The first two mechanisms are true contraception. The third proposed mechanism, IF it in fact occurs, would be abortifacient. (Note: the developing baby at the time of implantation is called a “blastocyst,” and will be referred to as such in this paper. “Endometrium” is the lining of the uterus into which the blastocyst implants.)

    The entire “abortifacient” presumption, therefore, depends on “hostile endometrium” actually being hostile to the blastocyst, resulting in the loss of blastocysts that would otherwise prosper and grow. Since there are no scientific studies demonstrating the validity of this presumption, abortifacient proponents appeal to the writings of scientists and clinicians involved in the production or study of these contraceptive products. Nearly all of these sources freely use the term “hostile endometrium” to describe the changes which occur in the uterine lining when these medications are used. And most make the presumption that these changes contribute to birth control effectiveness. On the surface, this would seem to be nearly incontrovertible evidence that the “pill” is, at least occasionally, an abortifacient. However, we again emphasize that there are no scientific studies that we are aware of which substantiate this presumption.

    Let us examine this “abortifacient presumption” by asking several questions:

    What is meant by the term “hostile endometrium?” Where did it come from? Is it actually “hostile?”

    The term “hostile endometrium” originated as a descriptive term for the less vascular, less glandular, thinner lining of the uterus produced by these hormones. The early pill literature from the late 1950’s established the descriptive term. Over time, the descriptive term “hostile endometrium” progressed to be an unchallenged assumption, then to be a proof text. And all with no demonstrated scientific validation.

    All pill manufacturers list this “hostile endometrium” presumption in their drug literature, implying it is a safeguard against pill failure. (Each company’s literature says essentially the same thing as they comply with FDA labeling requirements.) Understandably, their literature has a marketing agenda. However, to our knowledge, not one company will offer data to validate the “hostile endometrium” presumption. It should be noted that intertwining histologic fact (changes in endometrium) with presumptive action (makes the endometrium hostile) leads to a conclusion compatible with the pill marketing strategies, but not necessarily compatible with the truth.

    The fact that scientific authors in general all use the term “hostile endometrium” to refer to pill induced changes to the lining of the uterus adds nothing to establish the validity of the presumption that these changes cause loss of blastocysts. They are simply using long established descriptive terminology standard in the literature.

    Does the blastocyst require a “friendly endometrium” to thrive, or even to survive?

    The nature of the blastocyst is important to this discussion. There is much we do not understand about the role of the blastocyst in implantation. But we do know it has an invasive nature, with the demonstrated ability to invade, find a blood supply, and successfully implant on various kinds of tissue, whether “hostile,” or even entirely “foreign” to its usual environment-decidualized (thinned) endometrium, tubal epithelium (lining), ovarian epithelium (covering) cervical epithelium (lining) even peritoneum (abdominal lining cells).

    The presumption that implantation of a blastocyst is thwarted by “hostile endometrium” is contradicted by the “pill pregnancies” we as physicians see. Pill company literature estimates 3 to 5 pregnancies per 100 women per year for pill users. Many of these women take the “pill” an additional month or two before finding out they are pregnant. These pregnancies generally progress with no more difficulty than non-pill pregnancies. To our knowledge, there are no studies showing that the spontaneous abortion rate in these cases is any greater than in pregnancies with a “friendly endometrium.”

    The blastocyst regularly and successfully implants on tubal ciliated epithelium (commonly referred to as tubal, or ectopic, pregnancies). Approximately 1 percent of pregnancies in the USA are tubal pregnancies. The tubal epithelium is a tissue with an entirely different function and structure than the endometrium. Unlike endometrium, it has no glands with secretions, no rich vascular stroma. Yet these pregnancies implant and generally thrive until interrupted by treatment or rupture of a fallopian tube due to size constraints.

    Is there actual clinical evidence of early miscarriage in pill users?

    The typical clinical picture of spontaneous abortion (heavy bleeding, severe cramping, passage of tissue is rarely, if ever, seen by most practicing physicians dealing with pill pregnancies, and is not substantiated in any literature we are acquainted with. The “hostile endometrium is abortifacient” proponents theorize that the losses are pre-implantation, and thus would have no tell-tale clinical or laboratory findings. However, since the actual rate of demonstrable ovulation for women on the pill roughly approximates the pregnancy rate for women on the pill, this type loss would seem extremely unlikely.

    What is the conception rate for women on hormone contraception?

    It is impossible to say. Ovulation suppression rates vary from about 95 percent with the combined 35 mcg estrogen pill to about 50 percent with the minipill or Norplant in place 3-4 years. Cervical mucus factors enter in. Most pill literature estimates 3 to 5 percent of pregnancies per year for combined OCs, less for depoprovera, more for Norplant and minipills.

    One may get an idea of the frequency of conception on hormonal contraceptives by considering the ectopic (tubal) pregnancy rates. The ectopic rate in the USA is about 1 percent of all pregnancies. Since an ectopic pregnancy involves a preimplantation blastocyst, both the “on-pill conception” and normal “non-pill conception” ectopic rate should be the same-about 1 percent (unaffected by whether the endometrium is “hostile” or “friendly.”) Ectopic pregnancies in women on hormonal contraception (except for the minipill) are practically unreported. This would suggest conception on these agents is quite rare. If there are millions of “on-pill conceptions” yearly, producing millions of abortions, (as some “BC pill is abortifacient” groups allege), we would expect to see a huge increase in ectopics in women on hormonal birth control. We don’t. Rather, as noted, this is a rare occurrence.

    Is it possible that hormonal contraceptives may be responsible for the loss of blastocysts in some instances? In medicine, anything is possible. Does the known medical information suggest that “on-pill” conceptions have a higher rate of blastocyst loss than normal “non-pill conceptions?” We believe the answer is “No.”

    There are 1,200,000 medical and surgical abortions of unborn babies that take place every year in the United States. The “hormonal contraception is abortifacient” theory is not established scientific fact. It is speculation, and the discussion presented here suggests it is in error. How happy the abortionists must be to find us training our guns on a presumption, causing division/confusion among prolife forces, and taking some of the heat off the abortion industry. Ought we not rather be spending our energies to eliminate the convenience destruction of the innocent unborn?

    In Summary

    1. We know of no existing scientific studies that validate the “hormonal contraception is partly abortifacient” theory. “On-Pill” pregnancy rates roughly parallel “on-pill” ovulation rates (about 3-5 percent on 35 mcg pill). Increased spontaneous abortion of on-pill pregnancies is not noted.

    2. There is regular successful implantation of the invasive blastocyst on surfaces a great deal more “hostile” than “hostile endometrium” (e.g. fallopian tube lining). “Hostile endometrium” is not a demonstrated clinical reality.

    3. The extremely rare reporting of ectopic pregnancies associated with hormonal contraception would indicate the rarity of actual conception by patients using these modalities. (Minipill and Norplant apparently are less effective in preventing pregnancies, and ectopics per pregnancy are more frequent with these medications.)

    4. Many factors play a part in how a family plans and spaces their children. It is not the purpose of this paper to promote nor to oppose hormonal contraception. However, if a family, weighing all the factors affecting their own circumstances, decides to use this modality, we are confident that they are not using an abortifacient.

    5. This paper is not meant to be the “final word” on this issue. If scientific study should validate that a hormonal contraceptive agent is partly abortifacient in its action, we would oppose that agent just as we oppose elective medical and surgical abortions.

    We must constantly examine valid data as it becomes available in our effort to discern what is abortifacient v. what is appropriate birth control to be used or prescribed by those who hold to the sanctity of human life from the time of conception.

    Watson A. Bowes, Jr., MD, Professor, Maternal-Fetal Medicine, University of North Carolina, Chapel Hill, NC

    Matthew J. Bulfin, MD, DFACOG, general OB-GYN, Founder of American Association of Prolife Obstetricians-Gynecologists, Ft. Lauderdale, FL

    Byron Calhoun, MD, FACOG, Assoc. Professor of Clinical OB-GYN, Uniformed Services, University of Health Sciences, F. Edward Hebert School of Medicine, Madigan Army Medical Center, Tacoma, Wash.

    Steve Calvin, MD, FACOG, Asst. Professor, Dept. OB-GYN, University of Minnesota Medical School, Minneapolis, Minn.

    Denis Cavanagh, MD, FACOG, Professor of Obstetrics and Gynecology, University of South Florida College of Medicine, Tampa, FL

    Curtis Cook, MD FACOG, Asst. Clinical Professor, Maternal Fetal Medicine, Michigan State University College of Human Medicine, Grand Rapids, Mich.

    Susan A. Crockett, MD, FACOG, Assistant Clinical Professor, University of Texas Medical Branch and Director of Maternal Services for Santa Rosa Family Practice Residency Program, San Antonio, TX

    Steven Cruikshank, MD, FACOG, Professor of OB-GYN, Wright State University School of Medicine, Dayton, Ohio

    Joseph L. DeCook, MD, FACOG, Assistant Secretary, American Association of Prolife Obstetricians-Gynecologists, Holland, Mich.

    William G. Dodds, MD, FACOG, Director Reproductive Medicine, Butterworth Hospital, Assoc. Professor, Michigan State University, Grand Rapids, Mich.

    R. Don Gambrell, Jr., MD, FACOG, Clinical Professor of Endocrinology and Obstetrics and Gynecology, Medical College of Georgia, Augusta, GA

    David Hager, MD, FACOG, Professor, Dept. of OB-GYN, Women’s Care Center, Lexington, KY

    Donna Harrison, MD, FACOG, Southwestern Medical Center, Berrien Springs, Mich.

    Camilla Hersh, MD, FACOG, Asst. Clinical Professor, Obstetrics and Gynecology, Georgetown University, Washington, DC

    Nathan Hoeldtke, MD, FACOG, Maternal Fetal Medicine, Tripler Army Medical Center, Honolulu, Hawaii

    Antony Paul Levitino, MD, FACOG, Associate Professor, OB-GYN, Albany Medical Center, Albany, NY

    Robert W. Lobel, MD, FACOG, Asst. Clinical Professor of Uro-Gynecology, Albany Medical Center, Albany, NY

    Joe McIlhaney, MD, OB-GYN, FACOG, Infertility, Austin, TX

    Gwendolyn Patterson-Hobbs, MD, OB-GYN Clinical Associate, Virginia Women’s Health Association, Vienna, VA

    William Stalter, MD, FACOG, Associate Clinical Professor, Wright State University School of Medicine, Dept. of OB-GYN, Dayton, Ohio

    Roy Springfellow, MD, FACOG, Advanced Gynecology, Colorado Springs, CO

    Robert L. Weeldreyer, MD, FACOG, President Physician’s Resource Council of Michigan Family Forum, Holland, Mich.

    All signators are speaking as individuals, not spokespersons for the organizations that employ them.




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