Here's some links, for the curious:
General articles on the subject of the role of hormones on fetal growth:Prenatal testosterone and gender behavior (pdf)Several topics covered, including,
- Behavior, sexual orientation (page 1)
- Normal variability in prenatal testosterone (page 3)
- Gender-differentiated cognitive abilities (page 4)
Sexual Development & Differentiation --Morphological differentiation begins on the 8th week of gestation; see pages 10 through 15.
Fetal testosterone and sex differences --Abstract only; but mentions that "androgens, including testosterone" affect dimorphism
Pregnant mothers producing hormones for their babies to be:No correlation observed between blood serum and amniotic hormonal concentrations --IOW, hormones apparently being produced and regulated exclusively for the benefit of the growing fetus.
Testosterone and other hormones are present inside the placenta, in the amniotic fluid, in different concentrations, depending on whether the growing fetus is male or female; can be measured to predict the baby's sex; and can be changed to prevent (or cause) sexual abnormalities:Amniotic testosterone levels compared (typivally 5.5 times higher amniotic testosterone concentration for male than for female growing fetuses)
Amniotic hormone measurements as fetal sexing indicators --IOW, male babies require a different placental hormanal cocktail from female babies, and sex of the child can be predicted by measurement of hormone concentration levels.
MANAGEMENT OF CONGENITAL ADRENAL HYPERPLASIA DURING PREGNANCY --"Prevention of masculinization of affected female fetuses by corticosteroid suppression has been attempted in both 21-hydroxylase deficiency and 11b-hydroxylase deficiency CAH, with variable degrees of success."
Hormone concentration levels change over time:Hormones in bovine pregnancies --Not about sex hormones, in this study; but there are charts showing how some other hormones in the amniotic fluid change over the time pregnancy.
Confusion caused by discordant gender twins:Discordant sex twins can't seem to get differential treatment --(about amniotic fluid alpha-fetoprotein levels, in this study)
Dena Bodyan's 'Homosexuality' page --"The research team of Vom Saal, Grant, McMullen and Laves ( 10 ) offers another potential cause whose basis is also rooted in prenatal hormones. Fetal female rats were seen to have higher levels of testosterone if they had been situated between two male embryos in utero . The reception of testosterone from adjacent brothers was enough "to alter (a female rat's) behavioral phenotype"( 10 ). According to Edward Miller ( 11 ), the same occurs in humans: women who had male twins (and were therefore exposed to testosterone in utero ) exhibited slightly more masculine characteristics than did women who had not been exposed to testosterone before birth."
Male twins reduce fitness of female co-twins in humans --"In mammals, including humans, female fetuses that are exposed to testosterone from adjacent male fetuses in utero can have mascu-linized anatomy and behavior."
Too much testosterone at the wrong time can cause autism:High amniotic testosterone levels in womb linked to autism --"Children with autism seemed to have an exaggeration of the typical male profile because they have a very strong interest in systems, like numbers, but have difficulties with
empathy, according to Professor Cohen."
Homosexuality determined during early pregnancy, during shaping of the hypothalamus:Homosexuality - natural causes of --"The brain makes its gender committment very early in development and, once committed to either male or female, it can not change. The interference with testosterone in the later stages of pregnancy, or after birth, does little or nothing to inhibit primary gender development of the other organs of the body."
Glen Wilson's 'Science of Sex' page --"In addition, it is necessary to separate brain settings for sex orientation from brain settings for sex-typical behaviour. It is possible, for example, to have an individual who is macho both in body and personality but who prefers male sex partners, or vice versa. This is because the masculinization/feminization effects occur in different parts of the brain and, more importantly,
at different times during pre-natal development."
Homosexual rats born by exposing mothers to even low levels of a chemical normally found leeching out of plastic food containers:Evidence of Altered Brain Sexual Differentiation in Mice Exposed Perinatally to Low, Environmentally Relevant Levels of Bisphenol A --"Here we explore the ability of environmentally relevant exposure to BPA to affect anatomical and functional measures of brain development and sexual differentiation."
This article in Psychology Today says that only sexual organs, the hypothalamus, and fingers differentiate during fetal growth:Sexuality: Your Telltale Fingertips --"Except for genitalia, relative finger length is the only physical trait fixed at birth that is sexually dimorphic—meaning males and females show typical gender differences. Other sexually dimorphic traits, such as height and waist-to-hip ratio, don't appear until puberty. 'Everything you see as far as sex differences in the behavior of toddlers is an aftereffect of prenatal testosterone,' says Dennis McFadden..."
BUT, the article ignores that although morphological differentiation of the other parts of the body may be subtle and not readily apparent at birth, it is well known that the differentiations ARE there, already (in humans as in turtles, etc.):Sexually dimorphic mandibular morphology in the first few years of life --"Sex differences in the youngest skeletons are very subtle, and any method that can separate males and females significantly better than chance will be of value. Compounding the problem is a paucity of immature skeletons of documented age and sex. In 1992, S.R.L. examined 62 juvenile mandibles of white and black South Africans of known age and sex (from birth to 19 years) from the Dart Collection to determine if the sexes could be differentiated by morphologic traits. By age 6 years, adult chin shapes were already recognizable. Prior to that age, differences were observed in the shape of the inferior border of the symphysis and outline of the body. The male chin base extends steeply downward relative to the adjacent body, coming to a point or squaring off at the symphysis. In females, the symphysis descends gradually to a more rounded base, and even when pointed, the transition is not abrupt. On the outer border of the corpus, the sides diverge sharply to form a \_/ shape from a roughly horizontal anterior region in males, while the female contour is rounded, reflecting the smoothly curved transition from front to sides. These traits were manifest from the eruption of the central incisors until about 4 years of age. The features were tested on all 19 Dart Collection mandibles in that age range. Average accuracy for three different testers was 81%, and males were consistently identified more accurately than females. This new method was then tested on a known sex sample of 11 individuals from 0 to 7 years of age. These included CT scans of 9 French children and the remains of 2 South African black forensic cases. Sexing accuracy was 82% (9/11). The only two missexed cases were both female and over age 6 years. In conclusion, the results of this study indicate that it is possible to determine the sex of very young mandibles. The new sexually dimorphic morphologic configurations introduced here have demonstrated repeatable discrimination with the highest level of accuracy (81%) reported and tested for this age group. Preliminary research indicates that both the male and female shapes are clearly recognizable in archaeologic and premodern hominids as well as chimpanzees. Am J Phys Anthropol 115:179-186, 2001. © 2001 Wiley-Liss, Inc."
--IOW, although anatomical dimorphism may become more evident with age, it is already present and detectable at earier ages (and probably present already at birth, IMO).Geometric Morphometric Sex Estimation for Hatchling Turtles: A Powerful Alternative for Detecting Subtle Sexual Shape Dimorphism --"Identifying sex of hatchling turtles is difficult because juveniles are not obviously externally dimorphic, and current techniques to identify sex are often logistically unfeasible for field studies. We demonstrate a widely applicable and inexpensive alternative to detect subtle but significant sexual dimorphism in hatchlings, using landmark-based geometric morphometric methods." (IOW, sexual dimorphism is not readily appearent in new-born turtles, but it IS there already.)
And, more importantly, although hormonal levels of males and females are different during puberty, the differences are not enough to fully account for dimorphic development. Apparently, male and female tissue's sensitivities to androgens plays a major role:Autoradiographic Localization of Dihydrotestosterone Binding in the Major Salivary Glands and Other Androgen-responsive Organs of the Mouse --in plain English, features grow dimorphically after birth due to distinct concentrations of androgen receptors in the tissues of males and females.
Prenatal testosterone exposure permanently masculinizes anogenital distance, nipple development and reproductive tract morphology in female Sprague-Dawley rats. Evidence that the androgen receptor mediates sexual differentiation of mouse renal cytochrome P450 expression.Androgen receptor mRNA expression in Xenopus laevis CNS: Sexual dimorphism and regulation in laryngeal motor nucleusAndrogen receptors are required for full masculinization of the ventromedial hypothalamus (VMH) in rats --I call your special attention to the fact that the hypothalamus, incidentally, is the primary area of the brain showing sexual dimorphism; --which dimorphism develops during fetal growth.
Induction of Androgen Receptor Formation by Epithelium-Mesenchyme Interaction in Embryonic Mouse Mammary Gland --the formation of androgen receptors in tissues and organs which are responsible for sexually dimorphic development at later stages, appears to be determined during fetal growth: "The role of tissue interaction in the development of hormone responsiveness was studied in the embryonic mammary gland of the mouse, which becomes sensitive to testosterone on day 14."
A Novel Androgen Receptor Mutation Resulting in Complete Androgen Insensitivity Syndrome and Bilateral Leydig Cell Hyperplasia --"Androgens drive male secondary sexual differentiation and maturation. Mutations in the androgen receptor (AR) gene cause a broad spectrum of abnormal phenotypes in humans, ranging from mild through partial to complete androgen insensitivity."
Last but not least:Wikipedia's
Defeminization and masculinization page.
