Consequences of the Sex Difference in Rates of Fetal Growth

Abstract

Accessible online at: www.karger.com/journals/hre De Zegher et al. [1] note that male fetuses grow faster than females. This being so, a higher proportion of them may reach developmental windows too early and consequently may be programmed for postnatal susceptibility to disease. I wish to make two points in connection with this hypothesis: (1) The authors write as if a difficulty were posed by the facts that in the male fetus, serum testosterone reaches a peak before mid-gestation, while maximum weight gain occurs in late gestation. These facts would pose no difficulty if – as seems likely – weight gain (expressed e.g. in grams per day) were dependent not only on testosterone level, but on current weight. (2) However, complexity is introduced by the good evidence that within a fruitful cycle, the regression of p (the probability that a conceptus is male) is U-shaped across the fertile interval, that period of time during the cycle when a woman can conceive. In other words, if a woman conceives early or late in this interval, she is more likely to have a boy: and if she conceives in the centre of that interval, she is more likely to have a girl [2]. I have suggested that the reason for this is that the sexes of offspring are dependent (inter alia) on maternal hormone levels at the time of conception [3]. However, it is irrelevant to the present argument whether that hypothesis is true. The crucial point is that if the Ushaped regression exists, it suggests another possibility. If the subsequent developmental window is temporally related to ovulation, rather than conception, male fetuses are bound to be more likely to be suboptimally timed in relation to that window. For this reason it is important to assess the evidence for (a) that hypothesized U-shaped regression and (b) the time origin of the window. References