Analysis by Dr. John B. Shea, MD. FRCP(C)
TORONTO, May 28, 2007 (LifeSiteNews.com) – In a recent article in Fertility and Sterility R.T. Mikolajczyk and J.B. Stanford proposed a model experiment that estimated the effectiveness of the disruption of ovulation by Levonorgestrel used as an “emergency contraceptive,” based on the prevention of fertilization.
They also demonstrated what was termed the “effectiveness” of levonorgestrel with or without “mechanisms acting after fertilization.” If disruption of ovulation were the only significant mechanism of action of levonorgestrel, its “effectiveness” could not be much more than 50% if given immediately after intercourse. With delays in its administration, it would be substantially less.
This finding contrasts sharply with “effectiveness” rates reported in clinical trials, where rates as high as 95% are reported if administered within 24 hours after intercourse.
The authors suggest that mechanisms other than disruption of ovulation contribute to this “reduction of clinical pregnancy.” Those mechanisms were said to include inhibition of sperm migration and reduction of sperm capacity for fertilization (both contraceptive mechanisms) and “mechanisms that act after fertilization,” that is, prevent implantation of the embryo in the uterus.
That mechanism causes an abortion and does not “reduce clinical pregnancy.” Only numbers can be reduced. The pregnancies are aborted, not reduced.
The word “effectiveness” is used by the authors in an ambiguous way. One meaning refers to disruption of ovulation, contraception, and the other refers to reduction in fecundity, but does not indicate whether this was the result of contraception, abortion, or both. This study does, however, provide strong evidence that levonorgestrel administered as an “emergency contraceptive” may act as an abortifacient.
The abstract can be found at: