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The ovulatory homolog model of female orgasm posits that the neuro-endocrine mechanisms underlying female orgasm evolved from and are homologous to the mechanisms mediating copulation-induced ovulation in some mammals. This model predicts that pharmacological agents that affect human orgasm, such as fluoxetine, should also affect ovulation in animals with copulation-induced ovulation, such as rabbits. We tested this prediction by treating rabbits with daily doses of fluoxetine for 2 wk and found that fluoxetine treatment reduces the number of ovulations postcopulation by 30%. In a second experiment we tested whether this result was mediated by an effect on the brain or via peripheral serotonin functions. We treated animals with fluoxetine and induced ovulation with a single injection of human chorionic gonadotropin. In this experiment ovulation rate was nominally reduced by only 8%, which is statistically not significant. We conclude that the effect of fluoxetine on copulation-induced ovulation rate supports the ovulatory homolog model of female orgasm, suggesting that female orgasm has very deep evolutionary roots among the early eutherian mammals. [ABSTRACT FROM AUTHOR]

Recently, we presented the cliff-edge model to explain the evolutionary persistence of relatively high incidences of fetopelvic disproportion (FPD) in human childbirth. According to this model, the regular application of Caesarean sections since the mid-20th century has triggered an evolutionary increase of fetal size relative to the dimensions of the maternal birth canal, which, in turn, has inflated incidences of FPD. While this prediction is difficult to test in epidemiological data on Caesarean sections, the model also implies that women born by Caesarean because of FPD are more likely to develop FPD in their own childbirth compared with women born vaginally. Multigenerational epidemiological studies indeed evidence such an intergenerational predisposition to surgical delivery. When confined to anatomical indications, these studies report risks for Caesarean up to twice as high for women born by Caesarean compared with women born vaginally. These findings provide independent support for our model, which we show here predicts that the risk of FPD for mothers born by Caesarean because of FPD is 2.8 times the risk for mothers born vaginally. The congruence between these data and our prediction lends support to the cliff-edge model of obstetric selection and its underlying assumptions, despite the genetic and anatomical idealizations involved. [ABSTRACT FROM AUTHOR]

The strikingly high incidence of obstructed labor due to the disproportion of fetal size and the mother's pelvic dimensions has puzzled evolutionary scientists for decades. Here we propose that these high rates are a direct consequence of the distinct characteristics of human obstetric selection. Neonatal size relative to the birth-relevant maternal dimensions is highly variable and positively associated with reproductive success until it reaches a critical value, beyond which natural delivery becomes impossible. As a consequence, the symmetric phenotype distribution cannot match the highly asymmetric, cliff-edged fitness distribution well: The optimal phenotype distribution that maximizes population mean fitness entails a fraction of individuals falling beyond the "fitness edge" (i.e., those with fetopelvic disproportion). Using a simple mathematical model, we show that weak directional selection for a large neonate, a narrow pelvic canal, or both is sufficient to account for the considerable incidence of fetopelvic disproportion. Based on this model, we predict that the regular use of Caesarean sections throughout the last decades has led to an evolutionary increase of fetopelvic disproportion rates by 10 to 20%. [ABSTRACT FROM AUTHOR]

A response from the author of the article "Cliff-edge model of obstetric selection in humans" which discuss the reasons for rise in Cesarean sections and the role of natural selection is presented.