On 2015 Aug 14, David Mage commented:

The authors have done an excellent job in reviewing the effect of fetal sex on prenatal development. However, they seem to reach an incongruous conclusion above that "male fetuses exposed to prenatal adversities are more highly impaired than those of female fetuses." Given that the numbers of X and Y sperm in the race to conception must be identical if Dad is XY, the human primary gender distribution at the instant of conception must be 0.5 XY and 0.5 XX. However, given the nominal 5% excess male live birth rate, there must be an excess of female fetal loss during pregnancy, between the moment of conception and moment of exit from the birth canal. Conceptus and fetal loss in the first trimester can occur even before Mom knows she is pregnant, and later without fetal recovery for gender identification. Even if there is a male excess of observed fetal loss in the third trimester, from spontaneous abortion or stillbirth, it cannot be greater than the prior female fetal loss. The authors also do not appear to consider as valid Naeye et al. (1971)'s page 905 concluding explanation for the male infant disadvantage: "The biologic difference must originate in the genetic difference between the sexes and those genetic differences are the consequences of the disparity in the number of the X chromosomes." Indeed, Mage and Donner, Scandinavian Journal of Forensic Science, 2015;21(1) doi:10:1515/sjfs-2015-0001 show that an X-linked gene in Hardy-Weinberg Equilibrium with a dominant allele protective against respiratory failure with frequency p = 1/3 and non-protective recessive allele with frequency q = 1 - p = 2/3, can explain the 50% male excess rate of infant death from respiratory failures,such as SIDS, and the 25% male excess rate of ALL infant mortality up to their 5th birthday.

David Mage, PhD (WHO retired)

On 2015 Aug 14, David Mage commented:

The authors have done an excellent job in reviewing the effect of fetal sex on prenatal development. However, they seem to reach an incongruous conclusion above that "male fetuses exposed to prenatal adversities are more highly impaired than those of female fetuses." Given that the numbers of X and Y sperm in the race to conception must be identical if Dad is XY, the human primary gender distribution at the instant of conception must be 0.5 XY and 0.5 XX. However, given the nominal 5% excess male live birth rate, there must be an excess of female fetal loss during pregnancy, between the moment of conception and moment of exit from the birth canal. Conceptus and fetal loss in the first trimester can occur even before Mom knows she is pregnant, and later without fetal recovery for gender identification. Even if there is a male excess of observed fetal loss in the third trimester, from spontaneous abortion or stillbirth, it cannot be greater than the prior female fetal loss. The authors also do not appear to consider as valid Naeye et al. (1971)'s page 905 concluding explanation for the male infant disadvantage: "The biologic difference must originate in the genetic difference between the sexes and those genetic differences are the consequences of the disparity in the number of the X chromosomes." Indeed, Mage and Donner, Scandinavian Journal of Forensic Science, 2015;21(1) doi:10:1515/sjfs-2015-0001 show that an X-linked gene in Hardy-Weinberg Equilibrium with a dominant allele protective against respiratory failure with frequency p = 1/3 and non-protective recessive allele with frequency q = 1 - p = 2/3, can explain the 50% male excess rate of infant death from respiratory failures,such as SIDS, and the 25% male excess rate of ALL infant mortality up to their 5th birthday.

David Mage, PhD (WHO retired)