Long-term effects of delayed parenthood

The present study aims to define, characterize and compare the long-term effects on offspring of delayed parenthood. Data published so far on this topic show that maternal and paternal ageing may affect offspring by different mechanisms. Delayed motherhood is characterized by increased probability of obstetric complications and/or fetal and perinatal problems which, in turn, may increase the risks of mortality and morbidity in newborns and later life. Furthermore, maternal ageing is distinguished by a decreased ratio of male to female infants and higher odds of conceiving a trisomic child and/or an individual suffering from mitochondrial DNA disorders. In contrast, delayed fatherhood is associated with higher risks of conceiving an individual suffering from new inheritable-mutation disorders. The different pattern of disease in offspring associated with maternal and paternal ageing may be explained, among other factors, by the fact that (i) oocytes of middle-aged women may suffer oxidative stress because their mitochondria produce higher amounts of reactive oxygen species; (ii) diplotene oocytes and to a lesser extent metaphase I and II oocytes have an efficient DNA repair system which is essentially independent of maternal age; and (iii) mitochondria are transmitted to the next generation along the matrilineal line. Moreover, (i) the activities of antioxidant enzymes within the seminal plasma and spermatozoa from older men may be reduced and so spermatozoa may be more vulnerable to mutational changes than spermatozoa from younger men; and (ii) late spermatids, and immature and mature spermatozoa do not have a DNA repair system.