It is interesting to know, the authors well know about of the biology of the human fetus? Physiology of human pregnancy is that between the fetus and the mother's body, there is a organ that up to 24 perform of the function of the endocrine system of the fetus, that is the placenta. This is the first thing. Secondly to maintain a normal pregnancy need huge concentration of estrogen and progesterone, but androgens are not, the content of which is negligible (if at all they circulate in the blood of the fetus) during pregnancy. That is why the male fetus in contrast to in the female fetuses for at least of the period of fetal development and several years after spermatogenesis is not occurs, as it requires at least a minimum amount of androgens. That's why when any threats abortion obstetricians artificially increases the concentration of estrogens and progestins in pregnant women to prevent miscarriage. Third, start the production of hormones in fetus begins only at 20-24 weeks of development, after maturation of the pituitary gland, which is coincident with the first of brain potentials. And at the end, placenta - a powerful factor in hormone metabolism and almost all steroids and androgens generally transformed by aromatase necessary to maintain pregnancy in estrogens. Therefore, the big question is level of which hormones increases by congenital adrenal hyperplasia of fetus? What kind of estrogen-androgen balance is all about? But hypotheses is the hypotheses, whatever it was.
Article Digit Ratio (2D:4D): A Biomarker for Prenatal Sex Steroids a...
From FETAL AND NEONATAL PHYSIOLOGY Volume 2 PN 9996076415 FOURTH EDITION 2011, p. 319: (hopefully this helps)
Gonadal sex steroids exert an important influence on the pubertal growth spurt, but absence of these factors is not noticeable in prepubertal growth.197 But even in early life, gonadal and adrenal sex steroids in excess can cause a sharp increase in growth rate as well as the premature appearance and progression of secondary sexual features. Sex steroids exert a direct effect on long bone growth, mainly through conversion to estrogen, and can increase GH secretion, once GH receptors are present in adequate supply. Untreated virilizing congenital adrenal hyperplasia is compatible with survival, sometimes for years, as long as severe hypoglycemia or shock does not develop; in those children who have achieved such a state of stability, growth acceleration may occur early in infancy; if the adrenopathy also is of the salt-losing type, the failure to thrive will mask any tendency toward increased growth rate, and the child will grow poorly until treatment is supplied or the child dies from hyponatremia, hyperkalemia, and hypoglycemic shock. Familial Leydig and germinal cell maturation may also cause increased growth early in the first year. If unabated, increased sex steroids will cause advancement of skeletal age, premature epiphyseal fusion, and short adult stature. Thus, just as growth deceleration requires evaluation, growth acceleration can be just as abnormal and may be a sign of precocious puberty or virilizing congenital adrenal hyperplasia
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