Effect of an emergency contraceptive pill intervention on pregnancy risk behavior a logical argument

We thank Dr. Raine for her interest in our research and particularly for her kind words acknowledging the quality of our randomized trial. We regret that the reasoning presented in our recent paper from that trial was apparently not entirely clear. We appreciate this opportunity to review our key points. In our paper we concluded that our emergency contraception (EC) access intervention likely caused an increase in coital acts with the potential to lead to pregnancy. Our primary argument for this conclusion was based on two premises: that EC is efficacious in preventing pregnancy and that the intervention group as a whole had more EC failures (pregnancies that occurred despite use of EC) than the control group. We inferred from these premises that the intervention group probably also had more EC successes (coital acts that would have led to pregnancy but for the use of EC). Given that the two groups had the same number of observed pregnancies if the intervention group indeed had more EC successes then it must have had more coital acts at risk for pregnancy. Because our trial was randomized all post-randomization differences between groups - whether directly observed or not - are attributable either to the randomized assignment or to chance. Therefore we have at least as much confidence in the assertion that our intervention caused the inferred increase in high-risk coital acts as we would in an assertion that it caused a similar difference detected post hoc for any conventionally ascertained trial outcome. In fact our conclusion is in retrospect quite plausible: when we make a new method available to people we should expect that some will substitute it for their old methods. Dr. Raine is mistaken in her claim that to reach our conclusion we needed to examine data from women who did not become pregnant. As long as our two premises are valid our pregnancy ascertainment was complete and the trial was properly randomized our conclusion is logically indisputable. In addition to this logical argument our paper also included a separate analysis comparing contraceptive use in pregnancy cycles between the two groups. Although the implications of this second analysis are consistent with those of the first the two analyses were utterly independent. Neither is necessary to support the other. We dispute Dr. Raines allegation that the conclusions in our recent paper are inconsistent with the findings presented in our initial trial report in which we failed to find evidence of a difference between groups in self-reported contraceptive use and coital activity at 6 and 12 months after enrollment. Absence of evidence is not evidence of absence and accepting a null hypothesis based on a nonsignificant result is generally inappropriate. In addition the pertinent analyses in the two papers were based on distinct data sources that most likely differ in their reliability. We do agree with Dr. Raine however that our new conclusions should be interpreted with equanimity. The intervention tested in our trial wasextremely aggressive and its effects may differ from those of "real world" EC provision approaches in other populations. (full text)