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To: ckca
I disagree that anyone on the Pill is killing babies. I don't think there is evidence to prove that the low dose combination hormonal contraceptive pills - which result in hormonal changes that are less than those caused by the hormones produced by the corpus luteum after ovulation - cause abortions. One example is the amount of normal pregnancies on these pills.

It appears to me that the body treats an embryo the same, whether or not a woman is taking combination pills as usually prescribed.

On the other hand, the progestin-only pills slow the movement of the oocyte or embryo down the fallopian tube, resulting in 4 to 10 times the rate of ectopic pregnancies in women who are on these pills, compared to women who are on no exogenous hormones at all.

Another option is the injectible progestin, Depo-provera, that blocks ovulation for 3 or more months. The greater risk with this contraception is that a woman may not ovulate for 6 months to a year after stopping the medicine.
162 posted on 12/18/2003 9:10:06 PM PST by hocndoc (Choice is the # 1 killer in the US)
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To: hocndoc
I disagree that anyone on the Pill is killing babies. I don't think there is evidence to prove that the low dose combination hormonal contraceptive pills - which result in hormonal changes that are less than those caused by the hormones produced by the corpus luteum after ovulation - cause abortions. One example is the amount of normal pregnancies on these pills.

Do you see the obvious contradiction in this statement? Think about it. (Hint, compare your last sentence to the first. If there are live births as well as contracepted births, is it not possible that a percentage of the prevented full term births were due to failed implantation of released and fertilized ova? If they can be released and fertilized and born, as the failure rate proves, why is it not possible they can be released and fertilized and not born?)

See Postfertilization Effects of Oral Contraceptives and Their Relationship to Informed Consent in "Archives of Family Medicine", February 2000, Volume 9 Number 2, Pages 126 - 133:

Our analysis of the evidence involved a review of the abstracts of all studies of OCs published since 1970 available on MEDLINE that discussed the commonly used OCs, including low-dose (<50 µg of estrogen) phasic combined oral contraceptives (COCs), low-dose monophasic COCs, and progestin-only OCs (progestin-only pills [POPs]).

...If the action(s) of OCs on the fallopian tube and endometrium were such as to have no postfertilization effects, then the reduction in the rate of intrauterine pregnancies in women taking OCs should be proportional to the reduction in the rate of extrauterine pregnancies in women taking OCs. If the effect of OCs is to increase the extrauterine-to-intrauterine pregnancy ratio, this would indicate that one or more postfertilization effects are operating. All published data that we could review indicated that the ratio of extrauterine-to-intrauterine pregnancies is increased for women taking OCs and exceeds that expected among control groups of pregnant women not currently using OCs. These case-controlled series come from 33 centers in 17 countries and include more than 2800 cases and controls.72-77 The odds ratios in these studies ranged from 1.7 (95% confidence interval [CI], 1.1-2.5)72 to 1.8 (95% CI, 0.9-3.4)73 to 4.3 (95% CI, 1.5-12.6)74 to 4.5 (95% CI, 2.1-9.6)75 to 13.9 (95% CI, 1.8-108.3).76 The letter by Job-Spira et al74 seems to represent the same data set of 279 cases and controls as the study by Coste et al.76 The meta-analysis by Mol et al73 includes 2 of the publications,72, 75 but one of these may include women taking POPs.72 Therefore, of the 5 publications, only 2 allow review of the association of COCs with ectopic pregnancy.75, 76 These 2 studies from 7 maternity hospitals in Paris, France, and 3 in Sweden involved 484 women with ectopic pregnancies and 289 pregnant controls and suggest that at least some protection against intrauterine pregnancy is provided via postfertilization preimplantation effects. We recognize that studies that have used nonpregnant controls have not shown a risk of increased ectopic pregnancy for users of COCs. In our review, we restricted our analysis to studies using pregnant controls, because we concur with researchers73, 76 in this field that " . . . when considering the situation where a woman became pregnant during contraceptive use, one should focus on pregnant controls."73 Therefore, COC use seems to be associated with an increased risk of ectopic implantation or unrecognized loss of preembryos. We considered this level II.2 (good to very good) evidence (Table 1). Ectopic pregnancy is a particular form of postfertilization loss that involves substantial risks to the woman, and thus the absolute risk of ectopic pregnancy for women taking OCs will be of interest to clinicians and patients. Converting a relative risk of ectopic pregnancy to an absolute risk has many inherent difficulties that have been reviewed elsewhere.78 Nevertheless, adapting the method suggested by Franks et al78 would allow one to predict that the ectopic pregnancy rate for women taking OCs would be the product of 3 factors: (1) the overall pregnancy rate per 1000 woman-years among those taking OCs, (2) the proportion of extrauterine pregnancies compared with all pregnancies for a comparable control population not taking OCs, and (3) the relative risk for ectopic pregnancy in women taking OCs compared with the control population, which may be estimated by the odds ratio from case-control studies. For factor 1, Potter29 suggests 40 for good compliers and 80 for poor compliers. For factor 2, the proportion of ectopic pregnancies in the 1990s is estimated to range from 1 in every 5679 to 6480, 81 pregnancies (0.0156 to 0.0179). A reasonable range for factor 3 would be 1.1 to 13.9, based on the studies discussed above. This model would predict an absolute risk ranging from 0.7 (40 X 0.0156 X 1.1) to 19.9 (80 X 0.0179 X 13.9) ectopic pregnancies per 1000 woman-years. We could only find one study, from Zimbabwe, which reported an absolute risk of ectopic pregnancy in women taking OCs of 0.582 per 1000 woman-years. The risk of ectopic pregnancy is higher with POPs, and ectopic pregnancy has been discussed at length by a number of investigators as a clinically significant potential complication of POPs.82-84 The odds ratio of an extrauterine pregnancy for a woman taking a POP (compared with pregnant controls) was reported in only one study and was 79.1 (95% CI, 8.5-735.1).74 Assuming an overall clinical pregnancy rate of 30 to 70 per 1000 woman-years, this equates to a predicted absolute risk of 4 to 99 ectopic pregnancies per 1000 woman-years ([30 or 70] X [0.0156 or 0.0179] X [8.5 or 79.1]) in women taking POPs. This is reasonably concordant with absolute rates of ectopic pregnancy in women taking POPs, which have been reported to range from about 382, 83, 85 to about 2084, 86 per 1000 woman-years. Data from case-controlled series demonstrate that women with clinically recognized pregnancy are no more or less likely to miscarry based on whether they were taking an OC after their pregnancy was clinically recognized.87-90 However, the epidemiology, biology, and recognized risk factors of clinically recognized embryo or fetal loss (spontaneous abortion after clinically recognized pregnancy) do not seem to apply to early (unrecognized) preembryo or embryo loss, as the available evidence suggests that the mechanisms of early establishment and maintenance of pregnancy and later maintenance of pregnancy are qualitatively and substantially different.90

200 posted on 12/19/2003 11:49:50 AM PST by ckca
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