The epigenetic environment: secondary sex ratio depends on differential survival in embryogenesis: Comment 2

P.H. Jongbloet

Department of Epidemiology and Biostatistics,University Medical Centre Nijmegen,P.O.Box 9101, 6500 HB Nijmegen, The Netherlands

Email: p.jongbloet{at}epib.umcn.nl

Sir,

Charles Boklage (2005)Go interferes with the ‘enduring supposition that the ‘primary sex ratio’ at conception ... must be quite high to explain the consistent observation of male excess at birth, in spite of the ‘not-always-but-more-often-than-not’ observed male excess in losses throughout recognized pregnancy’. The author tries to explain the male excess at birth by a supposed excess of female loss before the fetal period, i.e. before recognition of pregnancy, which would be the consequence of abnormal genomic imprinting normally imposed in oogenesis and lethally poor growth of the embryo proper.

This supposed female-biased loss before recognition of pregnancy requires documentation and cannot account for the perennial loss of male fetuses after recognition of pregnancy and of the male bias in mortality from birth on to adulthood, let alone in congenital anomalies and constitutional chronic diseases, such as diabetes, schizophrenia, cardiovascular diseases and cancer. In general these conditions develop at younger age and are more severe in men than in women.

Boklage's move to preferential female loss before recognition of pregnancy might be of interest but it does not seem necessary for explaining his ‘not-always-but-more-often-than-not’ phenomenon, nor the data from Evdokimova et al. (2000)Go which would be consistent with his proposal. It is true that the biases in sex ratio before and after recognized pregnancy cannot originate from a 1:1 bias in the X:Y ratio during spermatogenesis. In the case of fertilization, however, we are left without arguments, whereas there is a possibility that non-optimally matured oocytes associated with non-optimal liquefaction of the cervical mucus—due to inappropriate hormonal balances at the extremes of the fertile window of the menstrual cycle—are more accessible by Y-bearing sperm (Jongbloet, 2004aGo,bGo). Their head, length, perimeter and area are significantly smaller than in X-bearing ones, and their necks and tails shorter. Preferential fertilization of these non-opimally matured oocytes by Y-bearing sperm would in fact explain the perennial loss of male-biased embryos, fetuses and individuals. This ovopathy concept implies a tendency of gradual attrition and disproportionate loss of XY embryos or sex ratio reversal. In particular epigenetic environments, this dose–response fallacy will occur after transition of a critical level of exposition, i.e. extreme constraint of the oocyte.

This occasional female excess explains Boklage's ‘not-always-but-more-often-than-not’ phenomenon throughout recognized pregnancy and the sex ratio reversal during the so-called ‘anovulatory’ seasons (Jongbloet, 2004aGo,bGo) or in pre-eclamptic gestations (Jongbloet, 2004cGo). In relation to the results of Evdokimova et al. (2000)Go, Boklage says: ‘the earlier the failure most likely occurred, the greater fraction female’. It would seem preferable to say: ‘the stronger the attrition of the oocyte most likely occurred, the earlier the male-biased loss and the greater fraction female’.

References

Boklage CE (2005) The epigenetic environment: secondary sex ratio depends on differential survival in embryogenesis. Hum Reprod 20, 583–587.[Abstract/Free Full Text]

Evdokimova VN, Nikitina TV, Lebedev N, Sukhanova NN and Nazarenko SA (2000) Sex ratio in early embryonal mortality in man. Ontogenez 31, 251–257.[Medline]

Jongbloet PH (2004a) Over-ripeness ovopathy. A challenging hypothesis for sex ratio modulation. Hum Reprod 19, 769–774.[Abstract/Free Full Text]

Jongbloet PH (2004b) The ovopathy concept for explaining the secondary sex ratio. Hum Reprod 19, 1036–1038.[Free Full Text]

Jongbloet PH (2004c) Offspring sex ratio at population level versus early and late onset preeclampsia. Early Hum Dev 79, 159–163.[CrossRef][ISI][Medline]

Submitted on April 4, 2005; accepted on May 5, 2005.





This Article
Extract
Full Text (PDF )
Alert me when this article is cited
Alert me if a correction is posted
Services
Email this article to a friend
Similar articles in this journal
Similar articles in ISI Web of Science
Similar articles in PubMed
Alert me to new issues of the journal
Add to My Personal Archive
Download to citation manager
Request Permissions
Google Scholar
Articles by Jongbloet, P.H.
PubMed
PubMed Citation
Articles by Jongbloet, P.H.