I Was Betrayed by a Pill
The abortion pill was supposed to make termination safe, easy, and discreet. One pro-choice advocate found it anything but.
From the moment it was approved in 2000, I believed in the abortion pill. I thought, Finally! Abortion would at last become what it always should have been: a private medical matter between a woman and her doctor. It held the promise of a swift, at-home termination. There would be no more gauntlets of protesters at clinics, because who would know which physicians were dispensing the pills? Even better, the pill would keep abortion accessible at a time when fewer gynecologists were willing to perform them out of fear of attacks.
Nonetheless, I never expected I'd need to consider using it myself. I had just been at my gyno discussing fertility options. Stewart and I were getting married, and we planned to try for a baby right after the wedding. At 38, I was supremely aware that my window of opportunity was closing. Little did I know, lying there with my feet in the stirrups, pondering whether I ought to freeze my eggs in case we had trouble conceiving later, that I was already pregnant; it was too early to detect with a pelvic exam. But four weeks later, as I stared at the double pink lines (I took three tests to be sure), the facts were undeniable.
I should have been elated. Instead, I was distraught. This was not how things were supposed to go. My concern was about more than tossing middle-class conventionality-wedding first, family second-out the window. At the time, Stewart and I were living in Las Vegas, land of the all-night-and-way-into-the-next-morning party. In order to work all day and party, party, party all night, I'd been relying on a cocktail of caffeine and Peruvian marching powder. When I backtracked through my calendar, I realized I'd gotten pregnant when I was, shall we say . . . marching almost daily.
Stupid! Stupid! Stupid! I cursed myself as I drove home from the Walgreens where I'd bought the third test, hoping against hope that there had been a mistake with the other two. I was so impatient for the results, I ripped open the package in the store bathroom and peed on the wand right there. Oh, I was pregnant all right. How could I have been so irresponsible? You start a pregnancy with a healthy diet and prenatal vitamins, not cocaine-I didn't have to consult a panel of experts to know that. No matter what I did from this point on, there would always be the chance that the baby would have problems-maybe physical ones, maybe psychological issues. I wasn't willing to roll the dice with another life. I could really see only one option. I broke the news to Stewart in one breath: I'm pregnant, and we need to abort.
He didn't need any convincing. The next question was how to abort. There was the surgical option, of course. I'd had one in college (so you'd think I would have learned this lesson already), and I dreaded the needle that would be used to numb my cervix. In the years since college, another option had emerged: A pill called mifepristone (formerly RU-486, now sold under the brand name Mifeprex) could trigger what experts call a "medical abortion." Mifepristone isn't to be confused with Plan B, the morning after, pill that can prevent pregnancy if you take it within 72 hours of unprotected sex.
This one (also called the "early option" or the "abortion pill") is used together with the synthetic hormone misoprostol to abort when you're already pregnant. First, mifepristone blocks the action of progesterone, the hormone that's needed to sustain pregnancy. Then, misoprostol empties the uterus. The Mifeprex literature described some cramping and bleeding, "similar to or greater than a normal, heavy period." This sounded far more appealing than surgical abortion. A few pills, a couple of cramps, and it would all be over. We could move on with our lives.
But as it turned out, things weren't quite that simple.
For starters, the abortion pill is not always easy to get. In Nevada, where the state constitution guarantees the right to abortion, my own gynecologist refused to administer the pill-not because he's antiabortion, but, he explained, somewhat apologetically, just as he didn't do surgical abortions because he feared becoming a target of abortion foes, he didn't do medical abortions, either. Nor would he simply write me a prescription and let me do it myself. "They watch what I prescribe at the pharmacy," he told me. So much for discretion and accessibility.
Fortunately, after searching online, I was able to find a cooperative local clinic. The initial procedure was simple enough. I had an ultrasound to confirm that the pregnancy wasn't lodged in the fallopian tubes (a case where Mifeprex can't be used). I signed a release stating that I understood how the drug worked and all the risks involved. Then I downed the Mifeprex and went home. Two days later, it was time for the misoprostol. This part I could do at home. Clinic staffers had directed me to insert the tablets into my vagina in the morning so I'd have the day to recover. I envisioned recuperating on the couch with some uncomfortable but bearable cramps and soothing myself with bad daytime TV. I kissed Stewart good-bye. He said he'd call later. I went to insert the tablets.
I never made it to the couch.
Nothing-not the drug literature, not the clinic doctor, not even my own gyno-had prepared me for the searing, gripping, squeezing pain that ripped through my belly 30 minutes later. I couldn't even form words when Stewart called to check on me. It was all I could do to gasp, "Come home! Now!" For 90 minutes, I was disoriented, nauseated, and, between crushing waves of contractions that I imagine were close to what labor feels like, racing from the bed to the bathroom with diarrhea. Then, just as quickly, it was over. The next night, I started bleeding. I bled for 14 days. A follow-up ultrasound confirmed I'd aborted. And that's when my problems really began.
I had been prepared for the possibility that the pill wouldn't work and I'd still need a sur-gical abortion-that happens in about 5 to 8 percent of cases. I also knew that I might bleed so heavily I'd need surgery to stop it-about 1 percent of women do. What blindsided me, apart from being battered by the misoprostol, were the huge cystic boils that soon covered my neck, shoulders, and back. I was also overcome by fatigue-an utter lack of ability to do anything more strenuous than sleep or lie on the couch. My brain felt so fuzzy, English seemed like a second language, and I couldn't work. On top of all that came depression: I sobbed constantly. I wouldn't leave the house. I stopped showering.
It was only after I described my symptoms to my gynecologist that I discovered my experience wasn't all that unusual. (The Mifeprex literature didn't even mention it.) "I think it's underreported, but probably one in three women have dramatic side effects," he told me. My body was in hormonal chaos-pregnancy hormones clashing with antipregnancy hormones clashing with stress hormones. "I've seen a lot of women go through-I don't want to call it postpartum, but postevent-melancholy that's more dramatic than people want to admit," he said. He prescribed antidepressants. "One day, you'll feel just like your old self." It took nine months.
I'm very reluctant to give antiabortion advocates any more tools for chipping away at our right to safe, legal, accessible abortions. And despite my experience, I'm not suggesting the abortion pill be banned. (Viagra carries a higher risk of death, and no one's calling for a ban on that.) But I am bitterly disappointed that it's not the panacea millions of women like me thought it would be.
It doesn't help that those who dispense mifepristone/misoprostol don't always know as much about the drugs as they should. In fact, at the clinic I visited, the doctor couldn't tell me which hormone the combination used.
Much later, I also learned about several deaths linked to the abortion pill. In one case, it was given to a woman who never should have received it-she had an undiagnosed ectopic pregnancy and died from associated hemorrhaging. But five other women developed mysterious, fatal bacterial infections. Reading about them, my stomach twisted. I'd used the pills exactly as they had. I couldn't help but wonder: Could I have died?
The drug's manufacturer and the FDA have emphasized that a "causal relationship" between the pills and the infection that reportedly killed these women hasn't been established. And given that the rare bacterium, Clostridium sordellii, responsible for the deaths has killed a handful of other people-including a man undergoing surgery-it seems likely that more than just the pills are responsible.
The scary thing is that no one knows what. It's possible that together, the abortion pill and pregnancy suppress immune function enough to make some women more vulnerable to infection. There's also been some suggestion that inserting misoprostol into the vagina might raise the risk of infection. (Although the FDA approved it for oral use, many clinics instruct women to use it vaginally because research shows that the process works just as well but with fewer side effects.) But gynos like Anne Davis, M.D., M.P.H., assistant professor of obstetrics and gynecology at Columbia Presbyterian Medical Center in New York City, pooh-pooh that theory. "Literally hundreds of thousands of women have used it that way. It seems unlikely that a particular woman putting her fingers in her vagina would give herself an infection."
For the moment, we really don't know whether medical abortion carries any greater risk for infection than, say, surgical abortion, miscarriage, or childbirth. Still, to be safe, Planned Parenthood now instructs women to take misoprostol orally. In addition, Mifeprex now carries a black-box warning about the potential risk for excessive bleeding and serious, even fatal, infection. And because C. sordellii infection mimics the process of medical abortion, the FDA also issued a public-health advisory in July 2005 cautioning women and doctors to look out for prolonged nausea, vomiting, diarrhea, weakness, or abdominal pain (even in the absence of fever) in the days after taking misoprostol. (In the U.K., doctors can look for it themselves: Women stay in the hospital after the pills are administered.)
Of course, these are all good steps toward safeguarding women's health. But you know what else would help? If doctors and clinic staff dispelled the misconception many women have that the "early option" is an easy option. In all fairness, my postabortion experience was, according to several gynecologists, more severe than most. It's entirely possible that the aftershocks I suffered were magnified by grief as well as guilt that I'd brought this on myself. But was it the abortion pill that magnified my grief and guilt over ending the pregnancy or the grief and guilt that magnified my reaction to the abortion pill? There's no way to really know.
To date, about 650,000 women in the U.S. have used the abortion pill, and I'm sure many more will, since the medical literature is filled with reports of satisfied customers. And yet, the questions about what role (if any) the abortion pill played in those fatal infections underscores why it's important to keep surgical abortion accessible.
One gynecologist I talked to not long ago confided that she'd absolutely choose surgical abortion over a medical one, because even without the specter of septic shock, the abortion pill can be, as she put it, "a real ordeal." "We could have told you it wasn't going to be easy," a clinic staffer noted when I rattled off my complaints during my follow-up.
Why didn't she speak up sooner?
From the moment it was approved in 2000, I believed in the abortion pill. I thought, Finally! Abortion would at last become what it always should have been: a private medical matter between a woman and her doctor. It held the promise of a swift, at-home termination. There would be no more gauntlets of protesters at clinics, because who would know which physicians were dispensing the pills? Even better, the pill would keep abortion accessible at a time when fewer gynecologists were willing to perform them out of fear of attacks.
Nonetheless, I never expected I'd need to consider using it myself. I had just been at my gyno discussing fertility options. Stewart and I were getting married, and we planned to try for a baby right after the wedding. At 38, I was supremely aware that my window of opportunity was closing. Little did I know, lying there with my feet in the stirrups, pondering whether I ought to freeze my eggs in case we had trouble conceiving later, that I was already pregnant; it was too early to detect with a pelvic exam. But four weeks later, as I stared at the double pink lines (I took three tests to be sure), the facts were undeniable.
I should have been elated. Instead, I was distraught. This was not how things were supposed to go. My concern was about more than tossing middle-class conventionality-wedding first, family second-out the window. At the time, Stewart and I were living in Las Vegas, land of the all-night-and-way-into-the-next-morning party. In order to work all day and party, party, party all night, I'd been relying on a cocktail of caffeine and Peruvian marching powder. When I backtracked through my calendar, I realized I'd gotten pregnant when I was, shall we say . . . marching almost daily.
Stupid! Stupid! Stupid! I cursed myself as I drove home from the Walgreens where I'd bought the third test, hoping against hope that there had been a mistake with the other two. I was so impatient for the results, I ripped open the package in the store bathroom and peed on the wand right there. Oh, I was pregnant all right. How could I have been so irresponsible? You start a pregnancy with a healthy diet and prenatal vitamins, not cocaine-I didn't have to consult a panel of experts to know that. No matter what I did from this point on, there would always be the chance that the baby would have problems-maybe physical ones, maybe psychological issues. I wasn't willing to roll the dice with another life. I could really see only one option. I broke the news to Stewart in one breath: I'm pregnant, and we need to abort.
He didn't need any convincing. The next question was how to abort. There was the surgical option, of course. I'd had one in college (so you'd think I would have learned this lesson already), and I dreaded the needle that would be used to numb my cervix. In the years since college, another option had emerged: A pill called mifepristone (formerly RU-486, now sold under the brand name Mifeprex) could trigger what experts call a "medical abortion." Mifepristone isn't to be confused with Plan B, the morning after, pill that can prevent pregnancy if you take it within 72 hours of unprotected sex.
This one (also called the "early option" or the "abortion pill") is used together with the synthetic hormone misoprostol to abort when you're already pregnant. First, mifepristone blocks the action of progesterone, the hormone that's needed to sustain pregnancy. Then, misoprostol empties the uterus. The Mifeprex literature described some cramping and bleeding, "similar to or greater than a normal, heavy period." This sounded far more appealing than surgical abortion. A few pills, a couple of cramps, and it would all be over. We could move on with our lives.
But as it turned out, things weren't quite that simple.
For starters, the abortion pill is not always easy to get. In Nevada, where the state constitution guarantees the right to abortion, my own gynecologist refused to administer the pill-not because he's antiabortion, but, he explained, somewhat apologetically, just as he didn't do surgical abortions because he feared becoming a target of abortion foes, he didn't do medical abortions, either. Nor would he simply write me a prescription and let me do it myself. "They watch what I prescribe at the pharmacy," he told me. So much for discretion and accessibility.
Fortunately, after searching online, I was able to find a cooperative local clinic. The initial procedure was simple enough. I had an ultrasound to confirm that the pregnancy wasn't lodged in the fallopian tubes (a case where Mifeprex can't be used). I signed a release stating that I understood how the drug worked and all the risks involved. Then I downed the Mifeprex and went home. Two days later, it was time for the misoprostol. This part I could do at home. Clinic staffers had directed me to insert the tablets into my vagina in the morning so I'd have the day to recover. I envisioned recuperating on the couch with some uncomfortable but bearable cramps and soothing myself with bad daytime TV. I kissed Stewart good-bye. He said he'd call later. I went to insert the tablets.
I never made it to the couch.
Nothing-not the drug literature, not the clinic doctor, not even my own gyno-had prepared me for the searing, gripping, squeezing pain that ripped through my belly 30 minutes later. I couldn't even form words when Stewart called to check on me. It was all I could do to gasp, "Come home! Now!" For 90 minutes, I was disoriented, nauseated, and, between crushing waves of contractions that I imagine were close to what labor feels like, racing from the bed to the bathroom with diarrhea. Then, just as quickly, it was over. The next night, I started bleeding. I bled for 14 days. A follow-up ultrasound confirmed I'd aborted. And that's when my problems really began.
I had been prepared for the possibility that the pill wouldn't work and I'd still need a sur-gical abortion-that happens in about 5 to 8 percent of cases. I also knew that I might bleed so heavily I'd need surgery to stop it-about 1 percent of women do. What blindsided me, apart from being battered by the misoprostol, were the huge cystic boils that soon covered my neck, shoulders, and back. I was also overcome by fatigue-an utter lack of ability to do anything more strenuous than sleep or lie on the couch. My brain felt so fuzzy, English seemed like a second language, and I couldn't work. On top of all that came depression: I sobbed constantly. I wouldn't leave the house. I stopped showering.
It was only after I described my symptoms to my gynecologist that I discovered my experience wasn't all that unusual. (The Mifeprex literature didn't even mention it.) "I think it's underreported, but probably one in three women have dramatic side effects," he told me. My body was in hormonal chaos-pregnancy hormones clashing with antipregnancy hormones clashing with stress hormones. "I've seen a lot of women go through-I don't want to call it postpartum, but postevent-melancholy that's more dramatic than people want to admit," he said. He prescribed antidepressants. "One day, you'll feel just like your old self." It took nine months.
I'm very reluctant to give antiabortion advocates any more tools for chipping away at our right to safe, legal, accessible abortions. And despite my experience, I'm not suggesting the abortion pill be banned. (Viagra carries a higher risk of death, and no one's calling for a ban on that.) But I am bitterly disappointed that it's not the panacea millions of women like me thought it would be.
It doesn't help that those who dispense mifepristone/misoprostol don't always know as much about the drugs as they should. In fact, at the clinic I visited, the doctor couldn't tell me which hormone the combination used.
Much later, I also learned about several deaths linked to the abortion pill. In one case, it was given to a woman who never should have received it-she had an undiagnosed ectopic pregnancy and died from associated hemorrhaging. But five other women developed mysterious, fatal bacterial infections. Reading about them, my stomach twisted. I'd used the pills exactly as they had. I couldn't help but wonder: Could I have died?
The drug's manufacturer and the FDA have emphasized that a "causal relationship" between the pills and the infection that reportedly killed these women hasn't been established. And given that the rare bacterium, Clostridium sordellii, responsible for the deaths has killed a handful of other people-including a man undergoing surgery-it seems likely that more than just the pills are responsible.
The scary thing is that no one knows what. It's possible that together, the abortion pill and pregnancy suppress immune function enough to make some women more vulnerable to infection. There's also been some suggestion that inserting misoprostol into the vagina might raise the risk of infection. (Although the FDA approved it for oral use, many clinics instruct women to use it vaginally because research shows that the process works just as well but with fewer side effects.) But gynos like Anne Davis, M.D., M.P.H., assistant professor of obstetrics and gynecology at Columbia Presbyterian Medical Center in New York City, pooh-pooh that theory. "Literally hundreds of thousands of women have used it that way. It seems unlikely that a particular woman putting her fingers in her vagina would give herself an infection."
For the moment, we really don't know whether medical abortion carries any greater risk for infection than, say, surgical abortion, miscarriage, or childbirth. Still, to be safe, Planned Parenthood now instructs women to take misoprostol orally. In addition, Mifeprex now carries a black-box warning about the potential risk for excessive bleeding and serious, even fatal, infection. And because C. sordellii infection mimics the process of medical abortion, the FDA also issued a public-health advisory in July 2005 cautioning women and doctors to look out for prolonged nausea, vomiting, diarrhea, weakness, or abdominal pain (even in the absence of fever) in the days after taking misoprostol. (In the U.K., doctors can look for it themselves: Women stay in the hospital after the pills are administered.)
Of course, these are all good steps toward safeguarding women's health. But you know what else would help? If doctors and clinic staff dispelled the misconception many women have that the "early option" is an easy option. In all fairness, my postabortion experience was, according to several gynecologists, more severe than most. It's entirely possible that the aftershocks I suffered were magnified by grief as well as guilt that I'd brought this on myself. But was it the abortion pill that magnified my grief and guilt over ending the pregnancy or the grief and guilt that magnified my reaction to the abortion pill? There's no way to really know.
To date, about 650,000 women in the U.S. have used the abortion pill, and I'm sure many more will, since the medical literature is filled with reports of satisfied customers. And yet, the questions about what role (if any) the abortion pill played in those fatal infections underscores why it's important to keep surgical abortion accessible.
One gynecologist I talked to not long ago confided that she'd absolutely choose surgical abortion over a medical one, because even without the specter of septic shock, the abortion pill can be, as she put it, "a real ordeal." "We could have told you it wasn't going to be easy," a clinic staffer noted when I rattled off my complaints during my follow-up.
Why didn't she speak up sooner?
Abortion and The Pill
Most people assume that the common oral contraceptive pill acts only as a contraceptive and that it does not cause abortion. A recent medical article in the Archives of Family Medicine shows that this assumption is incorrect. The authors studied much of the medical literature since 1970 that discussed most of the types of oral contraceptives (from here on in, OCs), low dose phasic combined OCs (which contain estrogen and progestin), and progestin only pills (POPs).
How the Pill Acts
The mechanisms involved are:
* As a contraceptive,
* As an abortifacient,
* As a cause of ectopic pregnancy.
The organs affected are
* The ovary, by inhibition of ovulation ... which action is contraception.
* The cervical mucus, by impeding penetration by sperm which is contraceptive.
* The fallopian tubes; there is indirect evidence that the OCs slow the transport of the embryo through the tube. This may result in implantation of the embryo in the tube (ectopic pregnancy).
* The uterus, by alteration of the endometrium (the lining of the uterine cavity), which either prevents implantation or renders the embryo, after implantation, unable to maintain itself (abortion).
Does the Pill always prevent ovulation?
There is strong evidence that the OC does not always prevent ovulation and that, as a result, so-called 'break-through' or 'escape' ovulation occurs. [1] Conception sometimes does occur despite the use of OCs. The pregnancy rates following 'break-through' ovulation are often underestimated. [2] How often does 'break through' ovulation occur in women on OCs ? For COGs, the rate ranged from 1.7% to 28.6% per cycle. [3] For POPs it ranged from 33% to 65%. In one study the ovulation varied from 14% to 84% [5].
Pregnancy Rates in OC Users
A study accounting for underreporting of elective abortions gave these figures:
4% in the first year ... for 'compliant' users,
8% in the first year ... for 'poor compliance',
29% for some users.
The rates are higher for POP users.
How the Pill acts after conception - the evidence
It is a reasonable assumption that, after conception, the pill can cause the death of the embryo (fertilized ovum) prior to or during implantation (the nesting of the embryo in the wall of the uterine cavity). No method has, as yet, been used to measure directly the rate of this embryo death prior to, or up to, the time of implantation. This could theoretically be achieved by the assay of certain pregnancy-related hormones, but such studies have never been done on women using OCs. There are, however, three lines of indirect evidence that strongly suggest that abortion of the embryo caused by the OC occurs in at least some women taking OCs.
1)The significance of the ratio of ectopic (tubal) pregnancies to intrauterine pregnancies in women using OCs: If it were true that the only actions of the pill were impairment of ovulation and alteration of the cervical mucus, then OCs should reduce the rate of tubal pregnancies to the same extent as they reduce the rate of intra-uterine pregnancies. But all of the published data used by Larimore and Stanford, in their article published in the Archives of Family Medicine, and by other authors, indicate that significantly more ectopic pregnancies, relative to intrauterine pregnancies, occur in women who use OCs [7-11. This constitutes good evidence that OC use seems to be associated with risk of ectopic pregnancy or unrecognized loss of embryos from the uterine cavity.
In one publication [12] the authors assumed that in a woman who is taking OCs, and who has break-through ovulation, it is "highly probable" that the endometrium is primed and ready for implantation, simply because ovulation has not been suppressed. Yet no one has studied the tissue characteristics (histology) of the endometrium at the time of implantation in women using OCs. The authors provide no direct or indirect evidence to support their assumption. If this assumption were true, some women should experience a normal cycle (in terms of menstrual flow) as they would if they were not taking the pill. This has never been described in the medical literature.
2) The effect of OCs on the endometrium: The endometrium is thinned -- up to 58% thinner than normal. Its glands are fewer and are atrophied. Its cell structure is altered. Its biochemical composition is altered. [13] Thinness of the endometrium is related to its functional receptivity, and when it becomes too thin, implantation does not occur. [14] The average thickness of the endometrium in women taking OCs is 1.1mm. The minimal endometrial thickness required to maintain a pregnancy in patients undergoing in vitro fertilization ranges from 5 to 13mm. This is strong evidence that changes in the endometrium reduce the likelihood of implantation. [15] The Food and Drug Administration (USA) has accepted the assumption that OCs render the endometrium inhospitable to the implantation of the embryo.
3) Integrins: These are a group of 'cell-adhesion' peptide molecules which are accepted as the markers of the receptivity of the endometrium for implantation and normal fertility. They are conspicuously absent in patients with unexplained infertility. [16] Three of these integrins have been shown to appear locally in the uterus for a brief interval at the precise time in the menstrual cycle that corresponds to the window of maximal uterine receptivity to successful implantation. They are also conspicuously changed in OC users, and this fact is believed to contribute to the failure of implantation. [17]
To sum up, it can be reasonably stated that OCs can not only prevent ovulation and therefore conception, but also can, at least some of the time, cause an embryo, which was conceived despite the fact that the mother had been taking OCs, to be aborted, due to a failure of implantation. Further, OCs can cause an embryo to implant in the fallopian tube, which almost invariably results in the death of the embryo, and sometimes the death of the mother. These facts are recorded in the Physicians 'Desk Reference, in Drug Facts and Comparisons and in most standard gynecological, family practice, nursing, and public health text books. Nonetheless, few physicians and patients are aware of them.
It is important also to realize that the abortifacient potential of OCs is magnified by the concomitant use of certain antibiotics and anti-convulsants which decrease the effectiveness of the OCs in suppressing ovulation. These drugs include barbiturates, anti-depressants, and virtually all classes of antibiotics. Antibiotic use among OC users is not uncommon, such women being more susceptible to bacterial, yeast, and fungus infections, secondary to OC use.
Failure on the part of the physician to provide the patient with information about the potential of OCs to produce abortion and ectopic pregnancy is a failure to provide complete informed consent. Nonetheless, many physicians have consistently tried to conceal these facts by arguing that
* Fertilization results in a 'pre-embryo', not an embryo.
* Fertilization results in a 'fertilized egg' and not an embryo.
* Pregnancy occurs only after implantation, not at the moment of fertilization.
* That the 'pre-embryo' becomes an embryo only after fourteen days when its nervous system begins to develop.
These falsehoods are stated in order to rationalize the view that contraceptive pills are never abortifacient, and that known abortifacients such as the intrauterine device and the morning-after pill are merely contraceptive. These arguments are also used to justify the discarding of embryos in in vitro fertilization and the performance of research on embryos, such as stem cell research, in the first fourteen days of the life of the embryo. Recently some physicians have been promoting the idea that such research is justifiable after fourteen days. Note the similarity to the rationalization of partial-birth abortion and infanticide.
The Catholic Church teaches that the practice of contraception is seriously sinful. The fact that it is probable that OCs are, at least sometimes, abortifacient, adds another seriously sinful aspect to their use. What are the implications of these facts for the regulation of births? The Catechism of the Catholic Church teaches that one aspect of parents' duty to fulfill their responsibility to transmit human life and to educate their children concerns the regulation of births. Parents may wish to space the births of their children in a spirit of generosity appropriate to responsible parenthood, but not for selfish or ungenerous reasons. To achieve this goal, methods of birth regulation based on self-observation and the use of fertile periods may be used, because they are in conformity with the objective criteria of morality. These methods respect the bodies of the spouses, encourage tenderness between them, and favour the education of an authentic freedom. [18]
Dr. Thomas Hilgers founded the Pope Paul VI Institute for the study of human reproduction in Omaha, Nebraska (affiliated with Creighton University). He was appointed by Pope John Paul II to the Pontifical Council for the Family. He is also a member of the Pontifical Academy of Science. He and his colleagues have developed a new scientific approach to human fertility, called Natural Procreative Technology. It provides for procreative health care as well as responsible parenthood, and instructs couples on how to achieve, as well as avoid, pregnancy. It also has the potential for preventing uterine, ovarian, and breast cancer. Dr. Hilgers has suggested that the term 'natural family planning', which has negative connotations, be replaced by the term 'fertility care', a totally new approach to fertility. A textbook on this new reproductive science is in preparation at the Pope Paul VI Institute. More information about 'fertility care' can be obtained from the Marguerite Bourgeoys Family Center, Fertility Care Pro gramme, in Toronto. Telephone (416) 465-2868
REFERENCES:
(1.) Walter L. Larimore, M.D., and Joseph B. Stanford, M.D., MSPH. Postfertilization Effects of Oral Contraceptives and their Relationship to Informed Consent. Arch. Fam. Med./Vol. 9. Feb. 2000
(2.) Potter, L.S. How effective are contraceptives? The determination and measurement of pregnancy rates. Obstet. Gynecol. 1996:88 (suppl. 3): 13S-23S.
(3.) Grimes, D.A. et al., Ovarian and follicular development associated with three low dose contraceptives: A randomized controlled trial. Obstet. Gynecol. 1994 83:29-34.
(4.) Chowdry, V. et al. 'Escape' ovulation in women due to the missing of low dose combination oral contraceptive pills. Contraception. 1980:22:241-247.
(5.) Landgren, B.M. et al., Hormonal effects of the 300 micrograms norethendrom (NET). minipill. 1-Daily Administration. Contraception. 1980: 21: 87 - 113. 5
(6.) Potter, as above.
(7.) The WHO task force on intrauterine devices for fertility regullation. Clin. Rep rod. Fertil 1985:3: 131 -143.
(8.) Mol, B.W.J. et al. Contraception and the risk of ectopic pregnancy: meta analysis. Contraception 1995; 52; 337 - 341.
(9.) Job, Spira et al. Risk of Chlamydia PID and oral contraceptives. J. Am. Med. Assoc. 1990: 264: 2072-4
(10.) Thorburn, J. et al. Background factors for ectopic pregnancy. Eur J. Obstet. Gynecol. Reprod. Bid. 1986: 23: 321 -331.
(11.) Coste, J. et al. Risk factors for ectopic pregnancy. The Am. J. Epidemiol. 1991: 133: 839-49.
(12.) Susan, A. Crocket et al. Hormone Contraceptives Controversies and Clarifications. April 1999.
(13.) Brown, H.K. et al. Uterine junctional zone: correlation between histologic findings and M.R. Imaging. Radiology: 1991: 439-413.
(14.) Oliveria, J.B. et al. Endometrial ultrasonography as a predictor of pregnancy in an in vitro fertilization programme after ovulation stimulation and gonadotrophin - releasing hormone and gonadotrophins. Hum. Repro. 1997: 12: 2515 -2518.
(15.) McCarthy, S. et al. Female pelvic anatomy. M.R. assessment of variations during the menstrual cycle and with the use of oral contraceptives. Radiology 1986: 160: 119-123.
(16.) Somkuti,S.G. et al. Epidermal growth factor and sex steroids dynamically regulate a marker of endometrial receptivity in Ishikawa cells.J. Clinical Endocrin. Metab. 1997: 82: 2192-2197.
(17.) Sulz, L. et al. The expression of alpha (V) and beta 3 Integrin subunits in the fallopian tube epethelium suggest the occurrence of a tubal implantation window. Hum. Repro. 1996: 13:2916-2920.
(18.) Catechism of the Catholic Church 2368 - 2370: 482 -483. CCCB.
Author: Shea, J. B.
Date: Oct 1, 2000
Words: 1980
Publication: Catholic Insight
ISSN: 1192-5671
How the Pill Acts
The mechanisms involved are:
* As a contraceptive,
* As an abortifacient,
* As a cause of ectopic pregnancy.
The organs affected are
* The ovary, by inhibition of ovulation ... which action is contraception.
* The cervical mucus, by impeding penetration by sperm which is contraceptive.
* The fallopian tubes; there is indirect evidence that the OCs slow the transport of the embryo through the tube. This may result in implantation of the embryo in the tube (ectopic pregnancy).
* The uterus, by alteration of the endometrium (the lining of the uterine cavity), which either prevents implantation or renders the embryo, after implantation, unable to maintain itself (abortion).
Does the Pill always prevent ovulation?
There is strong evidence that the OC does not always prevent ovulation and that, as a result, so-called 'break-through' or 'escape' ovulation occurs. [1] Conception sometimes does occur despite the use of OCs. The pregnancy rates following 'break-through' ovulation are often underestimated. [2] How often does 'break through' ovulation occur in women on OCs ? For COGs, the rate ranged from 1.7% to 28.6% per cycle. [3] For POPs it ranged from 33% to 65%. In one study the ovulation varied from 14% to 84% [5].
Pregnancy Rates in OC Users
A study accounting for underreporting of elective abortions gave these figures:
4% in the first year ... for 'compliant' users,
8% in the first year ... for 'poor compliance',
29% for some users.
The rates are higher for POP users.
How the Pill acts after conception - the evidence
It is a reasonable assumption that, after conception, the pill can cause the death of the embryo (fertilized ovum) prior to or during implantation (the nesting of the embryo in the wall of the uterine cavity). No method has, as yet, been used to measure directly the rate of this embryo death prior to, or up to, the time of implantation. This could theoretically be achieved by the assay of certain pregnancy-related hormones, but such studies have never been done on women using OCs. There are, however, three lines of indirect evidence that strongly suggest that abortion of the embryo caused by the OC occurs in at least some women taking OCs.
1)The significance of the ratio of ectopic (tubal) pregnancies to intrauterine pregnancies in women using OCs: If it were true that the only actions of the pill were impairment of ovulation and alteration of the cervical mucus, then OCs should reduce the rate of tubal pregnancies to the same extent as they reduce the rate of intra-uterine pregnancies. But all of the published data used by Larimore and Stanford, in their article published in the Archives of Family Medicine, and by other authors, indicate that significantly more ectopic pregnancies, relative to intrauterine pregnancies, occur in women who use OCs [7-11. This constitutes good evidence that OC use seems to be associated with risk of ectopic pregnancy or unrecognized loss of embryos from the uterine cavity.
In one publication [12] the authors assumed that in a woman who is taking OCs, and who has break-through ovulation, it is "highly probable" that the endometrium is primed and ready for implantation, simply because ovulation has not been suppressed. Yet no one has studied the tissue characteristics (histology) of the endometrium at the time of implantation in women using OCs. The authors provide no direct or indirect evidence to support their assumption. If this assumption were true, some women should experience a normal cycle (in terms of menstrual flow) as they would if they were not taking the pill. This has never been described in the medical literature.
2) The effect of OCs on the endometrium: The endometrium is thinned -- up to 58% thinner than normal. Its glands are fewer and are atrophied. Its cell structure is altered. Its biochemical composition is altered. [13] Thinness of the endometrium is related to its functional receptivity, and when it becomes too thin, implantation does not occur. [14] The average thickness of the endometrium in women taking OCs is 1.1mm. The minimal endometrial thickness required to maintain a pregnancy in patients undergoing in vitro fertilization ranges from 5 to 13mm. This is strong evidence that changes in the endometrium reduce the likelihood of implantation. [15] The Food and Drug Administration (USA) has accepted the assumption that OCs render the endometrium inhospitable to the implantation of the embryo.
3) Integrins: These are a group of 'cell-adhesion' peptide molecules which are accepted as the markers of the receptivity of the endometrium for implantation and normal fertility. They are conspicuously absent in patients with unexplained infertility. [16] Three of these integrins have been shown to appear locally in the uterus for a brief interval at the precise time in the menstrual cycle that corresponds to the window of maximal uterine receptivity to successful implantation. They are also conspicuously changed in OC users, and this fact is believed to contribute to the failure of implantation. [17]
To sum up, it can be reasonably stated that OCs can not only prevent ovulation and therefore conception, but also can, at least some of the time, cause an embryo, which was conceived despite the fact that the mother had been taking OCs, to be aborted, due to a failure of implantation. Further, OCs can cause an embryo to implant in the fallopian tube, which almost invariably results in the death of the embryo, and sometimes the death of the mother. These facts are recorded in the Physicians 'Desk Reference, in Drug Facts and Comparisons and in most standard gynecological, family practice, nursing, and public health text books. Nonetheless, few physicians and patients are aware of them.
It is important also to realize that the abortifacient potential of OCs is magnified by the concomitant use of certain antibiotics and anti-convulsants which decrease the effectiveness of the OCs in suppressing ovulation. These drugs include barbiturates, anti-depressants, and virtually all classes of antibiotics. Antibiotic use among OC users is not uncommon, such women being more susceptible to bacterial, yeast, and fungus infections, secondary to OC use.
Failure on the part of the physician to provide the patient with information about the potential of OCs to produce abortion and ectopic pregnancy is a failure to provide complete informed consent. Nonetheless, many physicians have consistently tried to conceal these facts by arguing that
* Fertilization results in a 'pre-embryo', not an embryo.
* Fertilization results in a 'fertilized egg' and not an embryo.
* Pregnancy occurs only after implantation, not at the moment of fertilization.
* That the 'pre-embryo' becomes an embryo only after fourteen days when its nervous system begins to develop.
These falsehoods are stated in order to rationalize the view that contraceptive pills are never abortifacient, and that known abortifacients such as the intrauterine device and the morning-after pill are merely contraceptive. These arguments are also used to justify the discarding of embryos in in vitro fertilization and the performance of research on embryos, such as stem cell research, in the first fourteen days of the life of the embryo. Recently some physicians have been promoting the idea that such research is justifiable after fourteen days. Note the similarity to the rationalization of partial-birth abortion and infanticide.
The Catholic Church teaches that the practice of contraception is seriously sinful. The fact that it is probable that OCs are, at least sometimes, abortifacient, adds another seriously sinful aspect to their use. What are the implications of these facts for the regulation of births? The Catechism of the Catholic Church teaches that one aspect of parents' duty to fulfill their responsibility to transmit human life and to educate their children concerns the regulation of births. Parents may wish to space the births of their children in a spirit of generosity appropriate to responsible parenthood, but not for selfish or ungenerous reasons. To achieve this goal, methods of birth regulation based on self-observation and the use of fertile periods may be used, because they are in conformity with the objective criteria of morality. These methods respect the bodies of the spouses, encourage tenderness between them, and favour the education of an authentic freedom. [18]
Dr. Thomas Hilgers founded the Pope Paul VI Institute for the study of human reproduction in Omaha, Nebraska (affiliated with Creighton University). He was appointed by Pope John Paul II to the Pontifical Council for the Family. He is also a member of the Pontifical Academy of Science. He and his colleagues have developed a new scientific approach to human fertility, called Natural Procreative Technology. It provides for procreative health care as well as responsible parenthood, and instructs couples on how to achieve, as well as avoid, pregnancy. It also has the potential for preventing uterine, ovarian, and breast cancer. Dr. Hilgers has suggested that the term 'natural family planning', which has negative connotations, be replaced by the term 'fertility care', a totally new approach to fertility. A textbook on this new reproductive science is in preparation at the Pope Paul VI Institute. More information about 'fertility care' can be obtained from the Marguerite Bourgeoys Family Center, Fertility Care Pro gramme, in Toronto. Telephone (416) 465-2868
REFERENCES:
(1.) Walter L. Larimore, M.D., and Joseph B. Stanford, M.D., MSPH. Postfertilization Effects of Oral Contraceptives and their Relationship to Informed Consent. Arch. Fam. Med./Vol. 9. Feb. 2000
(2.) Potter, L.S. How effective are contraceptives? The determination and measurement of pregnancy rates. Obstet. Gynecol. 1996:88 (suppl. 3): 13S-23S.
(3.) Grimes, D.A. et al., Ovarian and follicular development associated with three low dose contraceptives: A randomized controlled trial. Obstet. Gynecol. 1994 83:29-34.
(4.) Chowdry, V. et al. 'Escape' ovulation in women due to the missing of low dose combination oral contraceptive pills. Contraception. 1980:22:241-247.
(5.) Landgren, B.M. et al., Hormonal effects of the 300 micrograms norethendrom (NET). minipill. 1-Daily Administration. Contraception. 1980: 21: 87 - 113. 5
(6.) Potter, as above.
(7.) The WHO task force on intrauterine devices for fertility regullation. Clin. Rep rod. Fertil 1985:3: 131 -143.
(8.) Mol, B.W.J. et al. Contraception and the risk of ectopic pregnancy: meta analysis. Contraception 1995; 52; 337 - 341.
(9.) Job, Spira et al. Risk of Chlamydia PID and oral contraceptives. J. Am. Med. Assoc. 1990: 264: 2072-4
(10.) Thorburn, J. et al. Background factors for ectopic pregnancy. Eur J. Obstet. Gynecol. Reprod. Bid. 1986: 23: 321 -331.
(11.) Coste, J. et al. Risk factors for ectopic pregnancy. The Am. J. Epidemiol. 1991: 133: 839-49.
(12.) Susan, A. Crocket et al. Hormone Contraceptives Controversies and Clarifications. April 1999.
(13.) Brown, H.K. et al. Uterine junctional zone: correlation between histologic findings and M.R. Imaging. Radiology: 1991: 439-413.
(14.) Oliveria, J.B. et al. Endometrial ultrasonography as a predictor of pregnancy in an in vitro fertilization programme after ovulation stimulation and gonadotrophin - releasing hormone and gonadotrophins. Hum. Repro. 1997: 12: 2515 -2518.
(15.) McCarthy, S. et al. Female pelvic anatomy. M.R. assessment of variations during the menstrual cycle and with the use of oral contraceptives. Radiology 1986: 160: 119-123.
(16.) Somkuti,S.G. et al. Epidermal growth factor and sex steroids dynamically regulate a marker of endometrial receptivity in Ishikawa cells.J. Clinical Endocrin. Metab. 1997: 82: 2192-2197.
(17.) Sulz, L. et al. The expression of alpha (V) and beta 3 Integrin subunits in the fallopian tube epethelium suggest the occurrence of a tubal implantation window. Hum. Repro. 1996: 13:2916-2920.
(18.) Catechism of the Catholic Church 2368 - 2370: 482 -483. CCCB.
Author: Shea, J. B.
Date: Oct 1, 2000
Words: 1980
Publication: Catholic Insight
ISSN: 1192-5671
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