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In men born between 1906 and 1938 and screened between 1970 and 1973 a strong relation between greater number of siblings and mortality risks was found by Hart and Davey Smith. These risks, however, were also related to adverse behavioural socioeconomic and health measures.1
A great number of children, particularly in lower socioeconomic classes and in the earlier decades of the previous century, implies reproduction at earlier and more advanced maternal age and shorter interpregnancy intervals. These aspects have been neglected in studies on number of siblings in relation to constitutional diseases of complex origin. These casualties seem to be connected with non-optimal maturation of ovarian follicles and in fact, the maturing oocytes they contain. Conceptions at the extremes of maternal reproductive age or during the critical stages of postpartum restoration of the ovulatory pattern (or durante lactatione) are constrained by protraction of the preovulatory phase of the menstrual cycle that entrains preovulatory overripeness of the oocyte (PrOO). This results—in analogy with experiments in animals and observations in humans—in a continuum of pregnancy wastage, perinatal and postnatal mortality, or morbidity.2–4 In addition, mothers with low socioeconomic status are known to suffer disproportiately more from low standards of nutrition, abnormal body mass index, and inherent menstrual disorders. They also use less safe methods of contraception resulting in gradually more unplanned and unwanted pregnancies5 and, in turn, in shorter interpregnancy intervals and intratubal aging of the oocyte (waiting to be fertilised)—that is, postovulatory overripeness of the oocyte (PoOO).2–4
The driving force behind decreasing rates of newborns with neural tube defects or Down’s syndrome was evident long before the introduction of prenatal diagnosis, selective abortion and folate supplementation. The true reason for these decreases has never been revealed and the biased scientific preoccupation with recent changes in lifestyle and risk factors for explaining the enigmatic decrease of cardiovascular diseases has also been blamed. A same scenario, therefore, may exist here and ovopathy might be the common causal pathway for developmental anomalies and “innate” constitutional entities of complex origin. The relentless decrease of conceptopathology, running parallel with increasing socioeconomic levels and improving healthcare provision, would be responsible for their decrease.3,4 Intrauterine mortality, stillbirth, and infant mortality began to decrease at the end of the 19th century, while in fact, cardiovascular diseases only after a lifetime delay since the 1960s. Many other unexplained correlates with cardiovascular diseases (and other chronic diseases) are elucidated by this causal pathway, for example, comorbidity, intergenerational matrilineal transmission and strong social patterning, discordance in monozygotic twins, poor fetal growth and low birth weight, seasonality of conception correlated with geographically latitudinal gradient, and finally, male gender biases.4
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