Transsexualität, die Blut-Hirn-Schranke, Hormonrezeptoren und Aromatase

In einer Twitterdiskussion auch zum Thema Transsexualität führte ich an, dass Transsexualität aus meiner Sicht im wesentlichen eine Abweichung des Gehirngeschlechts und evtl des Bodyplans von dem Geschlecht des übrigen Körpers ist. Gerade aus dieser Abweichung ergibt sich die „Tragik“ der Transsexualität, die viele mit „im falschen Körper stecken“ beschreiben.

Dagegen wurde angeführt, dass es ja keinen Grund gebe, dass man von einem Gehirngeschlecht sprechen müßte, genauso könne man anführen, dass der kleine Finger ein anderes Geschlecht habe. Warum sollte gerade das Gehirn ein anderes Geschlecht haben und nicht andere Körperteile?

Die Frage ist berechtigt, so dass ich es hier – durchaus auch um es für mich selbst einmal darzulegen und mit der Bitte um Input, ob es so richtig ist – auch noch einmal auszuführen versuche.

1. Wie ich es bisher verstanden habe

Der wesentliche Unterschied zwischen dem Gehirn und dem übrigen Körper ist aus meiner Sicht die Blut-Hirn-Schranke.

Dazu aus der Wikipedia:

Als Blut-Hirn-Schranke, auch Blut-Gehirn-Schranke, oder Blut-Hirn-Barriere wird die selektive physiologische Barriere zwischen den Flüssigkeitsräumen des Blutkreislaufs und dem Zentralnervensystem bezeichnet.

Diese besondere Abgrenzung des Bluts (intravasal) vom extravasalen Raum in Gehirn und Rückenmark ist bei allen Landwirbeltieren (Tetrapoda) ausgebildet und ermöglicht es, für das Nervengewebe eigene Milieubedingungen aufrechtzuerhalten (Homöostase). Im Wesentlichen wird diese Barriere von Endothelzellen gebildet, die hier in den kapillaren Blutgefäßen über Tight Junctions eng miteinander verknüpft sind.

Die Blut-Hirn-Schranke schützt das Gehirn vor im Blut zirkulierenden Krankheitserregern, Toxinen und Botenstoffen. Sie stellt einen hochselektiven Filter dar, über den die vom Gehirn benötigten Nährstoffe zugeführt und die entstandenen Stoffwechselprodukte abgeführt werden. Die Ver- und Entsorgung wird durch eine Reihe spezieller Transportprozesse gewährleistet.

Andererseits erschwert diese Schutzfunktion des Gehirns die medikamentöse Behandlung einer Vielzahl neurologischer Erkrankungen, da auch sehr viele Wirkstoffe die Blut-Hirn-Schranke nicht passieren können. Die Überwindung der Blut-Hirn-Schranke ist ein aktuelles Forschungsgebiet, um auch diese Krankheiten behandeln zu können. Nur sehr wenige – ausgesprochen seltene – Erkrankungen stehen in unmittelbarem Zusammenhang mit der Blut-Hirn-Schranke, während sie selbst von einer deutlich höheren Anzahl weitverbreiteter Erkrankungen betroffen sein kann. Eine so hervorgerufene Störung oder Schädigung der Blut-Hirn-Schranke ist eine sehr ernst zu nehmende Komplikation.

Letztendlich ist die Blut Hirn Schranke damit eine Art „Firewall“, die übergriffe auf das Gehirn verhindern soll. Einige Stoffe kommen durch, andere nicht.

Bei den Geschlechtshormonen sieht es so aus, dass Östrogene die Blut-Hirn-Schranke nicht passieren können, Testosteron aber schon. 

Im Gehirn lagert sich das Testosteron an Rezeptoren an, wird dann aromatasiert und damit in Östrogene ungewandelt. Hier liegen spezielle Rezeptoren, die das Östrogen erkennen und dann aufgrund dieses „weiblichen“ Hormons (weiblich aber eben nur in seiner Wirkung _vor_ der Blut-Hirn-Schranke) maskulinisiert.

Da auch Frauen, wenn auch im deutlich geringen Maße Testosteron produzieren (über die Eierstöcke und die Nebennierenrinden) haben sie noch einen besonderen Schutzmechanismus, im Gehirn aus Testosteron aromatisiertes Testosteron wird gebunden und damit unschädlich gemacht. 

Damit liegt eine Situation vor, bei der sich der übrige Körper aufgrund der Wirkung des (sagen wir beim Mann) Testosterons in die männliche Richtung entwickelt, das Gehirn aber zB nicht, weil

• Das Testosteron an den Rezeptoren im Gehirn nicht richtig erkannt wird
• im Gehirn ein Fehler bei der Aromatase eintritt und deswegen das Testosteron nicht oder im geringen Maße in Östrogene umgewandelt
• Das Östrogen nicht richtig erkannt wird 

Daraus würde sich dann Transsexualität (MtF) ergeben. 

Bei einem Transmann könnte:

• der Rezeptor für Östrogene zu empfindlich sein, so dass geringe Mengen Östrogen stärker wirken
• die Bindung des Östrogens nicht richtig funktionieren 

Zur Aromatase:

Die Aromatase (auch CYP19A1) ist das Enzym, das in Wirbeltieren die Umsetzung von Testosteron zu Östradiol bzw. von Androstendion zu Östron katalysiert. Diese Aromatisierung von Androgenen ist der entscheidende letzte Schritt bei der Biosynthese der Östrogene.

Aromatase, auch Östrogen-Synthase genannt, ist eine Monooxygenase (EC 1.14.14.1), die Häm als Kofaktor nutzt und zur Cytochrom P450-Familie 19 zählt. Das daher als CYP19A1 bezeichnete Protein ist in der Membran des Endoplasmatischen Retikulums (ER) von Zellen verschiedener Gewebe lokalisiert. Es findet sich in den Gonaden, der Plazenta, der Brustdrüse, dem Fettgewebe und auch im Gehirn sowie in Haut, Knochen und Blutgefäßen. Mutationen im CYP19A1-Gen können zu erblichem Aromatasemangel oder -überschuss führen.[2]

2. Studien, die ich dazu gefunden habe

a) Fernandez et al, 2014: The Genetics of Transsexualism

Transsexualism is a gender identity disorder with a multifactorial etiology.
Neurodevelopmental processes and genetic factors seem to be implicated.
The aim of this study was to investigate the association between the genotype and female-to-male (FtM) and male-to-female (MtF) transsexualism by performing a karyotype and molecular analysis of three variable regions of the genes ERβ (estrogen receptor β), AR (androgen receptor) and CYP19A1 (aromatase).

Methods: We carried out a cytogenetic and molecular analysis in 273 FtMs, 442 MtFs, 371 control females and 473 control males. The control groups were healthy, ageand geographical origin-matched. The karyotype was investigated by G-banding and by high-density (HD) array in the transsexual group. The molecular analysis involved three tandem variable regions of genes ERβ (CA repeats in intron 5), AR (CAG repeats in exon 1) and CYP19A1 (TTTA repeats in intron 4). The allele and genotype frequencies, after division into short (S) and long (L) alleles, were obtained.

Results: No karyotype aberration has been linked to transsexualism (FtM or MtF), and prevalence of aneuploidy (3%) appears to be slightly higher than in the general population (0.53%). Concerning the molecular study, FtMs differed significantly from control females with respect to the median repeat length polymorphism ERβ (P = 0.002) but not to the length of the other two studied polymorphisms. The repeat numbers in ERβ were significantly higher in FtMs than in the female control group, and the likelihood of developing transsexualism was higher (odds ratio: 2.001 [1.15–3.46]) in the subjects with the genotype homozygous for long alleles.
No significant difference in allelic or genotypic distribution of any gene examined was found between MtFs and control males. Moreover, molecular findings presented no evidence of an association between the sex hormone-related genes (ERβ, AR, and CYP19A1) and MtF transsexualism.

 

Aus der Besprechung der Ergebnisse:

FtMs differed from the female control group with respect to the median length of the ERβ polymorphism but not with respect to the length of the other two studied genes. Considering the data for categorical variables of S and L alleles, and the genotypes SS, SL, and LL, we found significant P values for ERβ gene and genotype frequencies but not for AR and CYP19A1 genes. A greater number of CA repeats corresponds to greater probabilities of FtM transsexualism.
In the case of the AR and CYP19A1 genes, we did not find any relationship between the genes and FtM transsexualism. However, in the case of exon 5 of the ERβ gene, and contrary to that described by Ujike et al. (2009), we found a direct relationship between the length of the variable region and FtM transsexualism, so the greater the number of repeats, the greater
the susceptibility to transsexualism.
Although there are numerous studies showing the inverse relationship between the length of the AR gene and the activity of the hormone-receptor complex (Chamberlain et al., 1994; Kazemi-Esfarjani et al., 1995; Tut et al., 1997), there are no data indicating that this same inverse relationship exists in the case of ERβ. Some works bear on this possibility; Kudwa et al., (2006) found that male mice lacking functional Erβ, when treated with the appropriate hormonal priming, display significantly more female-like sexual receptivity than littermates. Yet, lack of functional ERβ receptors does not impair normal expression of adult masculine
sexual behavior.

They found no evidence showing that masculinization is deficient in ERβKO males (rats genetically modified without the Erβ gene); however, they propose that the defeminization process is incomplete in ERβKO males. Our data, like previous studies (Westberg et al.,  2001; Kudwa et al., 2005), support the finding that a functioning ERβ receptor is directly proportional to the size of the analyzed polymorphism, so a greater number of repeats implies greater transcription activation, therefore, an increase in ERβ receptor function, and finally, an increase in defeminization in females. Thus, one could propose that the greater efficiency of the estrogen-receptor complex by a high number of repeats would lead to a reduction in feminization, favoring a defeminization process (Even et al., 1994). Defeminization of the corticospinal tract has been described in FtMs (Rametti et al., 2011)

Das würde bezüglich der FtM-Transsexuellen durchaus passen: Der ERβ Rezeptor ist der Östrogenrezeptor.

b) Fernandez, 2018: Molecular basis of Gender Dysphoria: androgen and estrogen receptor interaction

Highlights
• Estrogen receptors in humans are implicated in gender development.
• In somatically males, interaction between the ERβ and AR is necessary for a typical development of gender.
• In somatically males, specific genotype interactions of α and β ER and AR decrease the odds ratio of gender dysphoria.
• In somatically males, specific genotype interactions between the ERβ and the AR increase the odds ratio of gender dysphoria.
• In somatically females, specific genotypes of α and β ERs are implicated in an independent manner in gender dysphoria.

Abstract
Background
Polymorphisms in sex steroid receptors have been associated with transsexualism. However, published replication studies have yielded inconsistent findings, possibly because of a limited sample size and/or the heterogeneity of the transsexual population with respect to the onset of dysphoria and sexual orientation. We assessed the role of androgen receptor (AR), estrogen receptors alpha (ERα) and beta (ERβ), and aromatase (CYP19A1) in two large and homogeneous transsexual male-to-female (MtF) and female-to-male (FtM) populations.
Methods
The association of each polymorphism with transsexualism was studied with a twofold subject-control analysis: in a homogeneous population of 549 early onset androphilic MtF transsexuals versus 728 male controls, and 425 gynephilic FtMs versus 599 female controls. Associations and interactions were investigated using binary logistic regression.
Results
Our data show that specific allele and genotype combinations of ERβ, ERα and AR are implicated in the genetic basis of transsexualism, and that MtF gender development requires AR, which must be accompanied by ERβ. An inverse allele interaction between ERβ and AR is characteristic of the MtF population: when either of these polymorphisms is short, the other is long. ERβ and ERα are also associated with transsexualism in the FtM population although there was no interaction between the polymorphisms. Our data show that ERβ plays a key role in the typical brain differentiation of humans.

Und aus der Einführung:

The biological actions of sex steroids are mediated by binding to specific nuclear receptors that are members of an extended family of transcription factors. The ligand–receptor complex translocates to the nucleus and promotes sex-specific gene expression (Matthews and Gustafsson, 2003). The direct induction of gene expression via activation of the estrogen receptors (ERs) α and β and the androgen receptor (AR) is the presumptive route for brain masculinization (Sato et al., 2004; Kudwa et al., 2006).

In lower mammals ERα is primarily involved in masculinization, while ERβ has a major function in defeminization of sexual behavior (Kudwa et al., 2006). In rodents, estradiol induces two independent developmental processes: masculinization of neural circuits that will support male-typical reproductive behaviors in adults and defeminization, the loss of the ability to display typical adult female behavior, which is also an active developmental process (McCarthy, 2008). However, it is believed that in non-human primates (Wallen, 2005), as well as in humans (Swaab, 2004), estrogenic metabolites from androgens are not critical to masculinization and defeminization (Wallen, 2005).

All these observations have led to the study of the involvement of DNA polymorphisms of ERβ, ERα, AR, and the aromatase (CYP19A1) in transsexuality (Henningsson et al., 2005; Hare et al., 2009; Ujike et al., 2009; Fernández et al., 2014a,b, 2016; Cortés-Cortés et al., 2017). However, the reported results have been inconsistent or negative (Meyer-Bahlburg, 2011). The lack of agreement between different publications might be due to the small samples studied and/or the heterogeneity of the transsexual population in relation to the onset of the gender dysphoria (i.e. before or after puberty) and sexual orientation.

In order to address all these questions, this work studied the implication of the polymorphisms (CA)n-ERβ (rs113770630), XbaI-ERα (rs9340799), (CAG)n-AR (rs193922933) and (TTTA)n-CYP19A1 (rs60271534) in a large and homogenous sample of 549 early onset androphilic MtFs vs 728 male controls and 425 early onset gynephilic FtMs vs 599 female controls. The analyses were conducted independently for a somatically1 female population (FtM vs female controls) and a somatically male population (MtF vs male controls).

Moreover, because it is unknown whether androgen and estrogen genotypes interact with each other in the genesis of gender, we also analyzed the cross interactions between the AR polymorphism and the other above-mentioned polymorphisms (ERβ, ERα and CYP19A1).

Und aus den Ergebnissen:

Our study resulted in three main findings. First, there is an interaction between the ERβ and AR polymorphisms in the development of atypical gender identity in the MtF population involving an inverse relationship between these polymorphisms. Second, the development of gender in the FtM population is associated with ERβ and/or ERα, but no interaction between these polymorphisms was found. Third, both ERs (α and β) are involved in typical male and female gender development.

The androphilic MtF population presents an inverse relationship between ERβ and AR such that the short AR polymorphism is associated with the L/L ERβ genotype, while, on the contrary, the long AR polymorphism is associated with the S/S ERβ genotype.

Neither of these two polymorphisms on its own is associated with MtF. AR is necessary, but insufficient on its own without ERβ for gender development in MtF. The OR for the interaction between ERβ and AR is heightened by a further association with the XbaI-ERα polymorphism. The highest risk for transsexuality is observed in somatically male individuals carrying a short allele (S) for the ERβ polymorphism together with a G allele for XbaI-ERα and a short allele (S) for AR (SGS genotype) compared to the reference category SAS, short allele (S) for the ERβ together with an A allele for XbaI-ERα and a short allele (S) for AR. However, the differences were not significant when Bonferroni corrections were used

Furthermore, there is a lower risk for transsexuality in somatically male individuals when the short allele (S) for AR is associated with the short allele (S) for ERβ and the A allele for ERα (SAS genotype) compared to the reference category SAL, short allele (S) for the ERβ together with an A allele for XbaI-ERα and a long allele (L) for AR.

Previous studies evaluated polymorphism interactions using a binary logistic regression model (Henningsson et al., 2005; Hare et al., 2009; Ujike et al., 2009). However, cross-interaction analysis between polymorphisms is additionally used here. Our results confirmed those obtained by Henningsson et al. (Henningsson et al., 2005), who suggested an interaction between ERβ and AR, but, what is more, we are able to specify the genotypes involved. We found that fewer CAG repeats in the AR polymorphism increases the risk of transsexuality in comparison to the presence of a higher number of CAG repeats, in interaction with the L/L genotype for ERβ (Table 4). Like Hare et al. (2009), we also found an association between the AR polymorphism and MtF. However, we found, the association was restrictive since a low number of CAG repeats in the AR increases the risk of transsexuality in interaction with the L/L genotype for ERβ (Table 4), and, vice versa, more CAG repeats in the AR increases the risk of transsexuality in interaction with the S/S genotype for the ERβ (Table 5). The Ujike et al. study (Ujike et al., 2009) is not really comparable to ours or other studies mentioned above because it used the average instead of the median to establish long and short alleles. Considering the work of Henningsson et al. (2005) and Hare et al. (2009) together with our results, and taking into account the different origins of the analyzed populations, we could say that the implication of the AR in gender dysphoria in MtF is a consistent finding.

ER α and β also play a key role in the gynephilic FtM population. Specific variants of ERβ and ERα polymorphisms are associated with FtM. Interestingly, there is no interaction between these polymorphisms. ERα, particularly the XbaI-ERα polymorphism, has a significant effect: an A/A genotype implied a greater susceptibility to transsexuality, while genotype A/G showed a protective effect. With respect to the ERβ polymorphism, we found a direct association between the number of CA repeats and transsexuality, confirming our previous report (Fernández et al., 2014a).

One important observation that is directly derived from our analysis is that androphilic MtFs and gynephilic FtMs share a common feature: the involvement of the same polymorphisms in the estrogen receptors. Moreover, these polymorphisms have been related to sexually dimorphic behavior like Alzheimer’s disease, depression, obsessive compulsive disorder, schizophrenia, FtM dysphoria and others (Brandi et al., 1999; Ji et al., 2000; Corbo et al., 2006; Boada et al., 2012; Pan et al., 2014).

Estrogen is an important regulator of brain growth and differentiation and the ERs have a key function in sexual differentiation of brain and behavior (McCarthy, 2008). Additionally, ER α and β are found in both the developing (González et al., 2007) and adult human brain (Osterlund et al., 2000). ER expression shows sex differences (Ishunina et al., 2002).

With respect to the typical masculinization of the brain in XY subjects, it was proposed that direct androgen action on the brain is crucial for the development of a male gender identity and heterosexuality and that the aromatization theory, developed from rodent experiments, would be of secondary importance in our species (Swaab, 2004). In contrast, our results show that both ERs and AR receptors are involved in the development of transsexuality in the androphilic MtF population. As well as by androgens acting on AR, ERs can be activated by estradiol resulting from the aromatization of testosterone (Lephart, 1996). The aromatase enzyme is already present in human fetuses (Naftolin et al., 1971). Moreover, dihydrotestosterone, a reduced testosterone metabolite, can be further metabolized to 5α-androstene-3β,17β-diol, a molecule that preferentially binds to ERβ (Kuiper et al., 1997). Our results show the involvement of ERα and β in the typical development of gender in men and women.

Es liegt also ein Zusammenspiel von den Testosteronrezeptoren und den Östrogenrezeptoren vor, 

„First, there is an interaction between the ERβ and AR polymorphisms in the development of atypical gender identity in the MtF population involving an inverse relationship between these polymorphisms“

Wenn man davon ausgeht, dass „Mann zu Frau“ zuerst sehr schwache Testosteronrezpetoren haben (viele Wiederholungen) und dann auch sehr schwache Östrogenrezeptoren (Wenig Wiederholungen) dann würde da durchaus passen. Dann wird erst sehr wenig Testosteron erkannt und umgewandelt und von diesem wenigen umgewandelten noch weniger als Östrogen erkannt. 

Second, the development of gender in the FtM population is associated with ERβ and/or ERα, but no interaction between these polymorphisms was found.

Bei Frau zu Mann Transseuellen scheinen also bestimmte Faktoren bei den Östrogenrezeptoren vorzuliegen. Möglicherweise reicht es aus, wenn einer von beiden besonders scharf eingestellt ist?

Third, both ERs (α and β) are involved in typical male and female gender development.

Der Unterschied zwischen beiden ist mir insoweit noch nicht ganz klar. 

Wenn ich das so richtig verstehe, dann ist mein Model oben allenfalls eine Annährung und die tatsächlichen Abläufe sind noch wesentlich komplizierter

Die Wirkung von Testosteron

Der englische Wikipedia Artikel zu Testosteron gibt einen guten Überblick über die durch Testosteron bewirkten Effekte:

In general, androgens such as testosterone promote protein synthesis and thus growth of tissues with androgen receptors.^[11]Testosterone can be described as having virilising and anabolic effects (though these categorical descriptions are somewhat arbitrary, as there is a great deal of mutual overlap between them).^[12]

• Anabolic effects include growth of muscle mass and strength, increased bone densityand strength, and stimulation of linear growth and bone maturation.
• Androgenic effects include maturation of the sex organs, particularly the penis and the formation of the scrotum in the fetus, and after birth (usually at puberty) a deepening of the voice, growth of facial hair(such as the beard) and axillary (underarm) hair. Many of these fall into the category of male secondary sex characteristics.

Testosterone effects can also be classified by the age of usual occurrence. For postnataleffects in both males and females, these are mostly dependent on the levels and duration of circulating free testosterone.

Before birth

Effects before birth are divided into two categories, classified in relation to the stages of development.

The first period occurs between 4 and 6 weeks of the gestation. Examples include genital virilisation such as midline fusion, phallic urethra, scrotal thinning and rugation, and phallic enlargement; although the role of testosterone is far smaller than that of dihydrotestosterone. There is also development of the prostate gland and seminal vesicles.

During the second trimester, androgen level is associated with sex formation.^[13] This period affects the femininization or masculinization of the fetus and can be a better predictor of feminine or masculine behaviours such as sex typed behaviour than an adult’s own levels. A mother’s testosterone level during pregnancy is correlated with her daughter’s sex-typical behavior as an adult, and the correlation is even stronger than with the daughter’s own adult testosterone level.^[14]

Early infancy

Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4–7 months of age.^[15][16] The function of this rise in humans is unknown. It has been theorized that brain masculinizationis occurring since no significant changes have been identified in other parts of the body.^[17]The male brain is masculinized by the aromatization of testosterone into estrogen, which crosses the blood–brain barrier and enters the male brain, whereas female fetuses have α-fetoprotein, which binds the estrogen so that female brains are not affected.^[18]

Before puberty

Before puberty effects of rising androgen levels occur in both boys and girls. These include adult-type body odor, increased oiliness of skin and hair, acne, pubarche(appearance of pubic hair), axillary hair(armpit hair), growth spurt, accelerated bone maturation, and facial hair.^[19]

Pubertal

Pubertal effects begin to occur when androgen has been higher than normal adult female levels for months or years. In males, these are usual late pubertal effects, and occur in women after prolonged periods of heightened levels of free testosterone in the blood. The effects include:^[19][20]

Growth of spermatogenic tissue in testicles, male fertility, penis or clitoris enlargement, increased libido and frequency of erection or clitoral engorgement. Growth of jaw, brow, chin, nose, and remodeling of facial bone contours, in conjunction with human growth hormone.^[21] Completion of bone maturation and termination of growth. This occurs indirectly via estradiol metabolites and hence more gradually in men than women. Increased muscle strength and mass, shoulders become broader and rib cage expands, deepening of voice, growth of the Adam’s apple. Enlargement of sebaceous glands. This might cause acne, subcutaneous fat in face decreases. Pubic hair extends to thighs and up toward umbilicus, development of facial hair (sideburns, beard, moustache), loss of scalp hair (androgenetic alopecia), increase in chest hair, periareolar hair, perianal hair, leg hair, armpit hair.

Adult

Testosterone is necessary for normal spermdevelopment. It activates genes in Sertoli cells, which promote differentiation of spermatogonia. It regulates acute HPA (hypothalamic–pituitary–adrenal axis) response under dominance challenge.^[22]Androgen including testosterone enhances muscle growth. Testosterone also regulates the population of thromboxane A₂ receptors on megakaryocytes and platelets and hence platelet aggregation in humans.^[23][24]

Adult testosterone effects are more clearly demonstrable in males than in females, but are likely important to both sexes. Some of these effects may decline as testosterone levels might decrease in the later decades of adult life.^[25]

Health risksEdit

Testosterone does not appear to increase the risk of developing prostate cancer. In people who have undergone testosterone deprivation therapy, testosterone increases beyond the castrate level have been shown to increase the rate of spread of an existing prostate cancer.^[26][27][28]

Conflicting results have been obtained concerning the importance of testosterone in maintaining cardiovascular health.^[29][30]Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many parameters that are thought to reduce cardiovascular disease risk, such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and glycemic control.^[31]

High androgen levels are associated with menstrual cycle irregularities in both clinical populations and healthy women.^[32]

Sexual arousalEdit

See also: Hormones and sexual arousal

When testosterone and endorphins in ejaculated semen meet the cervical wall after sexual intercourse, females receive a spike in testosterone, endorphin, and oxytocin levels, and males after orgasm during copulation experience an increase in endorphins and a marked increase in oxytocin levels. This adds to the hospitable physiological environment in the female internal reproductive tract for conceiving, and later for nurturing the conceptus in the pre-embryonic stages, and stimulates feelings of love, desire, and paternal care in the male (this is the only time male oxytocin levels rival a female’s).^{[citation needed]}

Testosterone levels follow a nyctohemeral rhythm that peaks early each day, regardless of sexual activity.^[33]

There are positive correlations between positive orgasm experience in women and testosterone levels where relaxation was a key perception of the experience. There is no correlation between testosterone and men’s perceptions of their orgasm experience, and also no correlation between higher testosterone levels and greater sexual assertiveness in either sex.^[34]

Sexual arousal and masturbation in women produce small increases in testosterone concentrations.^[35] The plasma levels of various steroids significantly increase after masturbation in men and the testosterone levels correlate to those levels.^[36]

Mammalian studies

Studies conducted in rats have indicated that their degree of sexual arousal is sensitive to reductions in testosterone. When testosterone-deprived rats were given medium levels of testosterone, their sexual behaviors (copulation, partner preference, etc.) resumed, but not when given low amounts of the same hormone. Therefore, these mammals may provide a model for studying clinical populations among humans suffering from sexual arousal deficits such as hypoactive sexual desire disorder.^[37]

In every mammalian species examined demonstrated a marked increase in a male’s testosterone level upon encountering a novelfemale. The reflexive testosterone increases in male mice is related to the male’s initial level of sexual arousal.^[38]

In non-human primates, it may be that testosterone in puberty stimulates sexual arousal, which allows the primate to increasingly seek out sexual experiences with females and thus creates a sexual preference for females.^[39] Some research has also indicated that if testosterone is eliminated in an adult male human or other adult male primate’s system, its sexual motivation decreases, but there is no corresponding decrease in ability to engage in sexual activity (mounting, ejaculating, etc.).^[39]

In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats.^[40]This reaction engages penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters, allowing for more production of successful sperm and a higher chance of reproduction.

Males

In men, higher levels of testosterone are associated with periods of sexual activity.^[41]Testosterone also increased in heterosexual men after having had a brief conversation with a woman. The increase in testosterone levels was associated with the degree that the women thought the men were trying to impress them.^[42]

Men who watch a sexually explicit movie have an average increase of 35% in testosterone, peaking at 60–90 minutes after the end of the film, but no increase is seen in men who watch sexually neutral films.^[43] Men who watch sexually explicit films also report increased motivation, competitiveness, and decreased exhaustion.^[44] A link has also been found between relaxation following sexual arousal and testosterone levels.^[45]

Men’s levels of testosterone, a hormone known to affect men’s mating behaviour, changes depending on whether they are exposed to an ovulating or nonovulating woman’s body odour. Men who are exposed to scents of ovulating women maintained a stable testosterone level that was higher than the testosterone level of men exposed to nonovulation cues. Testosterone levels and sexual arousal in men are heavily aware of hormone cycles in females.^[46] This may be linked to the ovulatory shift hypothesis,^[47]where males are adapted to respond to the ovulation cycles of females by sensing when they are most fertile and whereby females look for preferred male mates when they are the most fertile; both actions may be driven by hormones.

Females

Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal.^[48] Women’s level of testosterone is higher when measured pre-intercourse vs pre-cuddling, as well as post-intercourse vs post-cuddling.^[49] There is a time lag effect when testosterone is administered, on genital arousal in women. In addition, a continuous increase in vaginal sexual arousal may result in higher genital sensations and sexual appetitive behaviors.^[50]

When females have a higher baseline level of testosterone, they have higher increases in sexual arousal levels but smaller increases in testosterone, indicating a ceiling effect on testosterone levels in females. Sexual thoughts also change the level of testosterone but not level of cortisol in the female body, and hormonal contraceptives may affect the variation in testosterone response to sexual thoughts.^[51]

Testosterone may prove to be an effective treatment in female sexual arousal disorders,^[52] and is available as a dermal patch. There is no FDA approved androgen preparation for the treatment of androgen insufficiency; however, it has been used off-label to treat low libido and sexual dysfunction in older women. Testosterone may be a treatment for postmenopausal women as long as they are effectively estrogenized.^[52]

Romantic relationships

Falling in love decreases men’s testosterone levels while increasing women’s testosterone levels. There has been speculation that these changes in testosterone result in the temporary reduction of differences in behavior between the sexes.^[53] However, it is suggested that after the „honeymoon phase“ ends—about four years into a relationship—this change in testosterone levels is no longer apparent.^[53] Men who produce less testosterone are more likely to be in a relationship^[54] or married,^[55] and men who produce more testosterone are more likely to divorce;^[55] however, causality cannot be determined in this correlation. Marriage or commitment could cause a decrease in testosterone levels.^[56] Single men who have not had relationship experience have lower testosterone levels than single men with experience. It is suggested that these single men with prior experience are in a more competitive state than their non-experienced counterparts.^[57] Married men who engage in bond-maintenance activities such as spending the day with their spouse/and or child have no different testosterone levels compared to times when they do not engage in such activities. Collectively, these results suggest that the presence of competitive activities rather than bond-maintenance activities are more relevant to changes in testosterone levels.^[58]

Men who produce more testosterone are more likely to engage in extramarital sex.^[55]Testosterone levels do not rely on physical presence of a partner; testosterone levels of men engaging in same-city and long-distance relationships are similar.^[54] Physical presence may be required for women who are in relationships for the testosterone–partner interaction, where same-city partnered women have lower testosterone levels than long-distance partnered women.^[59]

Fatherhood

Fatherhood also decreases testosterone levels in men, suggesting that the resulting emotional and behavioral changes promote paternal care.^[60] The way testosterone levels change when a child is in distress is indicative of fathering styles. If the levels reduce, then there is more empathy by the father than in fathers whose levels go up.^[61]

Motivation

Testosterone levels play a major role in risk-taking during financial decisions.^[62][63]

Aggression and criminality

See also: Aggression § Testosterone, and Biosocial criminology

Most studies support a link between adult criminality and testosterone, although the relationship is modest if examined separately for each sex. Nearly all studies of juvenile delinquency and testosterone are not significant. Most studies have also found testosterone to be associated with behaviors or personality traits linked with criminality such as antisocial behavior and alcoholism. Many studies have also been done on the relationship between more general aggressive behavior/feelings and testosterone. About half the studies have found a relationship and about half no relationship.^[64]

Testosterone is only one of many factors that influence aggression and the effects of previous experience and environmental stimuli have been found to correlate more strongly. A few studies indicate that the testosterone derivative estradiol (one form of estrogen) might play an important role in male aggression.^{[64][65][66][67]} Studies have also found that testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.^[68]

The sexual hormone can encourage fair behavior. For the study subjects took part in a behavioral experiment where the distribution of a real amount of money was decided. The rules allowed both fair and unfair offers. The negotiating partner could subsequently accept or decline the offer. The fairer the offer, the less probable a refusal by the negotiating partner. If no agreement was reached, neither party earned anything. Test subjects with an artificially enhanced testosterone level generally made better, fairer offers than those who received placebos, thus reducing the risk of a rejection of their offer to a minimum. Two later studies have empirically confirmed these results.^[69][70][71]However men with high testosterone were significantly 27% less generous in an ultimatum game.^[72] The Annual NY Academy of Sciences has also found anabolic steroid use which increase testosterone to be higher in teenagers, and this was associated with increased violence.^[73] Studies have also found administered testosterone to increase verbal aggression and anger in some participants.^[74]

Testosterone is significantly correlated with aggression and competitive behaviour and is directly facilitated by the latter. There are two theories on the role of testosterone in aggression and competition.^[75] The first one is the challenge hypothesis which states that testosterone would increase during puberty thus facilitating reproductive and competitive behaviour which would include aggression.^[75]Thus it is the challenge of competition among males of the species that facilitates aggression and violence.^[75] Studies conducted have found direct correlation between testosterone and dominance especially among the most violent criminals in prison who had the highest testosterone levels.^[75] The same research also found fathers (those outside competitive environments) had the lowest testosterone levels compared to other males.^[75]

The second theory is similar and is known as „evolutionary neuroandrogenic (ENA) theory of male aggression“.^[76][77] Testosterone and other androgens have evolved to masculinize a brain in order to be competitive even to the point of risking harm to the person and others. By doing so, individuals with masculinized brains as a result of pre-natal and adult life testosterone and androgens enhance their resource acquiring abilities in order to survive, attract and copulate with mates as much as possible.^[76] The masculinization of the brain is not just mediated by testosterone levels at the adult stage, but also testosterone exposure in the womb as a fetus. Higher pre-natal testosterone indicated by a low digit ratio as well as adult testosterone levels increased risk of fouls or aggression among male players in a soccer game.^[78] Studies have also found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression in males.^{[79][80][81][82][83]}

The rise in testosterone levels during competition predicted aggression in males but not in females.^[84] Subjects who interacted with hand guns and an experimental game showed rise in testosterone and aggression.^[85] Natural selection might have evolved males to be more sensitive to competitive and status challenge situations and that the interacting roles of testosterone are the essential ingredient for aggressive behaviour in these situations.^[86] Testosterone produces aggression by activating subcortical areas in the brain, which may also be inhibited or suppressed by social norms or familial situations while still manifesting in diverse intensities and ways through thoughts, anger, verbal aggression, competition, dominance and physical violence.^[87] Testosterone mediates attraction to cruel and violent cues in men by promoting extended viewing of violent stimuli.^[88] Testosterone specific structural brain characteristic can predict aggressive behaviour in individuals.^[89]

Estradiol is known to correlate with aggression in male mice.^[90] Moreover, the conversion of testosterone to estradiol regulates male aggression in sparrows during breeding season.^[91] Rats who were given anabolic steroids that increase testosterone were also more physically aggressive to provocation as a result of „threat sensitivity“.^[92]

Brain

The brain is also affected by this sexual differentiation;^[13] the enzyme aromataseconverts testosterone into estradiol that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors.^[93]

There are some differences between a male and female brain (possibly the result of different testosterone levels), one of them being size: the male human brain is, on average, larger.^[94] Men were found to have a total myelinated fiber length of 176,000 km at the age of 20, whereas in women the total length was 149,000 km (approx. 15% less).^[95]

No immediate short term effects on mood or behavior were found from the administration of supraphysiologic doses of testosterone for 10 weeks on 43 healthy men.^[96] A correlation between testosterone and risk tolerance in career choice exists among women.^[62][97]

Attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. Preliminary evidence suggests that low testosterone levels may be a risk factor for cognitive decline and possibly for dementia of the Alzheimer’s type,^{[98][99][100][101]} a key argument in life extension medicine for the use of testosterone in anti-aging therapies. Much of the literature, however, suggests a curvilinear or even quadratic relationship between spatial performance and circulating testosterone,^[102]where both hypo- and hypersecretion (deficient- and excessive-secretion) of circulating androgens have negative effects on cognition.

 

Geschlechterrollenwechsel in der Pubertät aufgrund 5a-reductase-2 Ausfall (5a-RD-2)

Ein interessanter Bericht schildert den Verlauf einer biologischen Besonderheit,  der 5a-reductase-2 deficiency (5a-RD-2):

Ich hatte dazu schon einmal einen Artikel:

Gender development and 5a-reductase-2 deficiency (5a-RD-2) and 17bhydroxysteroid dehydrogenase-3 deficiency (17b-HSD-3) Children with 5α-RD-2 have an enzyme defect that prenatally blocks the conversion of testosterone into dihydrotestosterone. Consequently they are born with external genitals that are female in appearance. They are usually raised as girls and seem to have a female gender identity, but, if the condition is not discovered in childhood, these children develop male sex characteristics in puberty: growth of their “clitoris” and scrotum, lowering of the voice, beard growth, masculine muscle development, and masculine body fat distribution. After puberty, many of these youngsters start living as males and develop a sexual attraction toward females. These transitions have been primarily documented in non-Western cultures. When raised as boys, these children have a male identity and behave like boys.

Dazu dann aus dem Artikel:

A study of this form of pseudo-hermaphroditism in the Dominican Republic found 18 cases, all of whom had been unambiguously assigned a female sex and socialized as girls by parents who had no idea that their daughters might be sons. This occurred in a traditional, rural, unsophisticated, Latin American society with clear and distinct differences in male and female sex role behaviour. At the time of their sex change, several of the subjects were already engaged to be married to men. All had girls’ names, dressed as girls, and regarded themselves as girls until the sex change.

Following puberty, all the subjects developed male genitals along with the other secondary sexual characteristics of adolescent males. One of the first signs of the sex change in the erstwhile girls was a sudden interest in playing football! The ages at which subjects first experienced morning erections, nocturnal emissions, masturbation and sexual intercourse were not appreciably different between those raised as girls who changed to a male-gender identity and a control group raised as boys from the beginning.

Vermutlich würde man hier im feministischen sagen, dass eben die Zuordnung des Männlichen zu den Genitalien so eindeutig ist, dass sie trotz aller Erziehung ihre Rollen vergessen und männlich werden.

Dazu aus meinem Butlerartikel:

Butler überträgt diesen Gedanken, wie Foucault bereits vor ihr auf das Geschlechterverhältnis, wo nach ihrer Auffassung ebenfalls bestimmte Geschlechternormen errichtet worden sind, die die Errichtung der Geschlechter und deren Verhalten bewirken. Diese knüpfen an die unterschiedlichen Körper von Mann und Frau an, die aber insoweit lediglich das Unterscheidungsmerkmal bilden, dass dann über verschiedene kulturell geschaffene Regeln zur Errichtung der Geschlechterrollen führt. Körper materialisieren sich nie unabhängig von ihrer kulturellen Form, sind also immer an ihre kulturspezifische Wahrnehmung gebunden.
Diese kulturspezifischen Merkmale der Geschlechterrollen werden dann durch beständige Wiederholung gleichsam eingeübt.
Nach dieser Vorstellung gibt es ersteinmal keine Frau als Subjekt, sondern das was als Frau definiert wird ist beständig einer kulturellen Betrachtung und Veränderung unterworfen. Eine „Frau“ mit einem männlicheren Körper ist in dieser Hinsicht teilweise schon wieder den männlichen Regeln unterworfen, ist also nicht per se Frau, sondern irgendwo dazwischen. Ein Transsexueller wäre nach erfolgter Operation über seinen Körper neuen Geschlechternormen unterworfen, die aber wiederum im Fluss sind und wer welchen Normen unterworfen ist, ist ebenso im Fluss, was die Abgrenzung der Geschlechter schwierig macht. Allein der Diskurs kann nach diesen Vorstellungen festlegen, was eigentlich eine Frau und was ein Mann ist. Denn der Diskurs hätte nach diesen Theorien etwa die Macht, einem Mann mit einem zB geringen Bartwuchs die Männereigenschaft abzusprechen und ihn den Frauen zuzuordnen (wenn ich es richtig verstehe). Darauf, dass die Abgrenzung dennoch in den meisten Kulturen abgesehen von den geringen Zahlen der Intersexuellen und Transsexuellen unproblematisch ist, geht sie meines Wissens nach nicht ein.

Für Butler schafft der Diskurs damit auch gleichzeitig den Körper -durch die Sprache materialisert sich das Geschlecht, Diskurs und Materie sind insofern miteinander verbunden. Die Sprache und der Diskurs stehend damit auf einer Stufe mit der Materie. Das Sprache und Diskurs die Materie nicht verändern und die Materie unterschiedlich bleibt ist nicht relevant, weil das übergeordnete Subjekt aus den drei Elementen, Diskurs, Sprache und Materie, eben durch diese alle drei geschaffen wird. Eine Frau kann nicht Frau sein, wenn die Eigenschaft Frau nicht durch den Diskurs in seiner gerade gültigen Form geschaffen, dies durch Sprache vermittelt wird und die Unterscheidung zu anderen Geschlechtern anhand körperlicher Faktoren, an denen diese Normen ansetzen können, erfolgen kann. (vgl auch „Butler zur Konstruktion der Geschlechter„)

Weil also deren Körper männlicher werden übernehmen sie dann nach dieser Vorstellung auch männliche Normen. Allerdings scheint mir die Erklärung nach der Biologie wesentlich realistischer und natürlich müsste man sich dann auch entscheiden, ob Erziehung leicht änderbar ist, ebenso wie Geschlechterrollen oder nicht.

The study found that all but two (89 per cent) made a full sex-role change and were living with women at the time of the study despite parental consternation, their own initial shock, and social pressure not to do so.

Gerade wenn man diesen Druck dazu nimmt und auch berücksichtigt, dass sie nicht plötzlich körperlich Männer geworden sind, sondern nur männlicher, passen auch die oben genannten Theorien nach meiner Auffassung nicht. Eine so hohe Quote passt aber sehr gut zu den biologischen Theorien.

Auch die anderen beiden Personen haben aber erhebliche Veränderungen mit dem Einsetzen der Hormone erlebt.

One of the remaining two continued to dress as a woman, had sexual relations with women but not men, and had masculine ways. The other persisted in the female role and lived with a man for a year until he left her. She was described by the study as having masculine build and mannerisms but wore false breasts and at the time of the study desired a sex change operation to make her a more normal woman.

Auch sicherlich keine einfachen Schicksale plötzlich eine solche Umkrempelung des eigenen Lebens zu erfahren und alles auf den Kopf gestellt zu bekommen, was bisher galt.

Of the 18, she was the only one who persisted in all respects with the female sex role that she had been assigned at birth. The researchers conclude: “These subjects demonstrate that in the absence of sociocultural factors that could interrupt the natural sequence of events, the effect of testosterone predominates, over-riding the effect of rearing as girls.”

Es würde in der Tat ganz neue Modelle erfordern um diese Phänomene darzustellen, wenn man nur auf die Erziehung abstellt. Denn dieses Abstreifen der Erziehung scheint mir mit den bisherigen Theorien nicht wirklich zu erklären.

Ein anderes Beispiel:

The Simbari Anga of Papua New Guinea have a radically different culture from that of the Dominican Republic: after male initiation rites (prior to puberty) the two sexes are kept rigorously separate, and ritualized oral sex occurs between men from puberty until premarital age. Yet in spite of this barrier between the sexes,

most of the affected individuals changed their gender identities from female to male at puberty, albeit with much turmoil … The fact that these individuals adopted male gender identity at puberty suggests that prenatal exposure of the brain to testosterone, combined with normal activational events of male puberty, overrides any effect of rearing in the determination of adult gender identity.

Bei vollkommener Trennung konnten sie dennoch eine andere Geschlechteridentität entwickeln. Aber eben auch nur die davon betroffenen, die eine hormonelle Umstellung erlebten.

The researchers conclude:

It has been proposed that gender identity becomes fixed by 18 months to 4 years of age, at the approximate time of language development (…). During this time a child becomes aware of his or her gender. Awareness of one’s gender and being unalterably fixed in that gender appear to be two separate issues. Subjects with 5α-reductase deficiency who have undergone a gender change suggest that gender identity in man is not fixed in childhood but is continually evolving, becoming fixed with or following pubertal events.

In humans, androgens, and not just environmental or sociocultural factors, make a strong and definite contribution to the formation of a male gender identity (…).

Es ist ein interessanter Sonderfall, der sicherlich weiterer Forschung wert ist. Natürlich funktioniert ansonsten bei anderen Jungs und Mädchen auch die Umwandlung von Testosteron auch, so dass da bestimmte Abläufe früher beginnen und abgeschlossen werden könnten.

In terms of the diametric model(link is external), sexuality is a complex issue, as I argued in a previous post, with a real, mechanistic, genetically-determined part—sex—and an imaginary, mentalistic part—gender. Furthermore, as I also pointed out in another post, even the purely genetic/hormonal aspect of sex is much more complicated in reality than it might seem. But however you look at it, the score seems to be: Nature 9, Nurture 1! At the very least, it certainly isn’t the draw we’re usually told it is.

Es zeigt aus meiner Sicht auch die starke Wirkung der Biologie, die selbst einen so komplexen Wandel bewirken kann.

Geschlechterunterschiede im Gehirn sind bereits im Alter von einem Monat vorhanden

Ein interessante Studie zu Geschlechterunterschieden im Gehirn bei Säuglingen:

The developing brain undergoes systematic changes that occur at successive stages of maturation. Deviations from the typical neurodevelopmental trajectory are hypothesized to underlie many early childhood disorders; thus, characterizing the earliest patterns of normative brain development is essential. Recent neuroimaging research provides insight into brain structure during late childhood and adolescence; however, few studies have examined the infant brain, particularly in infants under 3 months of age. Using high-resolution structural MRI, we measured subcortical gray and white matter brain volumes in a cohort (N = 143) of 1-month infants and examined characteristics of these volumetric measures throughout this early period of neurodevelopment. We show that brain volumes undergo age-related changes during the first month of life, with the corresponding patterns of regional asymmetry and sexual dimorphism. Specifically, males have larger total brain volume and volumes differ by sex in regionally specific brain regions, after correcting for total brain volume. Consistent with findings from studies of later childhood and adolescence, subcortical regions appear more rightward asymmetric. Neither sex differences nor regional asymmetries changed with gestation-corrected age. Our results complement a growing body of work investigating the earliest neurobiological changes associated with development and suggest that asymmetry and sexual dimorphism are present at birth.

Quelle: Investigation of brain structure in the 1-month infant (Scihub Volltext Link)

Aus der Studie:

Unterschiede Gehirn Mann Frau 1 Monat

Da geht es um die

1. Größe des Gehirns von männlichen und weiblichen Babies nach Geburt.
2. Das Volumen der weißen Substanz im Gehirn
3. Das Volumen der grauen Substanz im Gehirn

Wie man sieht ist das Gehirn der männlichen Babies im Durchschnitt zB größer, und zwar über die hier erfassten Alter hinweg, auch wenn es einzelne männliche Babies mit relativ kleinen und einige Mädchen mit relativ großen Gehirnvolumen gibt. Der Trend ist aber recht deutlich.

Auch die Daten zu den verschiedenen Bereichen zeigen deutliche Unterschiede:

Unterschiede Gehirn Mann Frau 1 Monat

Es wird schwer das mit einer unterschiedlichen Sozialisiation zu erklären. Sie müsste dann wohl bereits im Mutterleib ansetzen. Was allerdings pränatale Hormone in der Tat machen, wie man beispielsweise an dem Testosteronspiegel sieht:

Testosteron Maenner Frauen

Aus einer Besprechung der Studie:

Dean’s team found that the boys’ brains were 8.3 per cent bigger, in line with the sex difference in brain volume found in adults and the few other available infant studies. Also as seen in adults, male brains had relatively more white matter (connecting tissue) and female brains more grey matter, relative to total brain size.

A number of specific neural areas were larger in males, such as parts of the limbic system involved in emotions, including the amygdala, insula, thalamus and putamen. The researchers also found evidence for relatively larger hippocampi, an area involved in memory, which has more commonly been found to be larger in females, although not universally so. Meanwhile female brains were relatively larger in other limbic areas such as parts of the cingulate gyrus, caudate and parahippocampal gyrus, and they had a few white-matter structures that were relatively larger.

These sex differences were smaller than has been observed in adults, which suggests that maturation continues this differentiation, likely through the high volume of sex steroid receptors in these brain areas. The alternative suggestion is that the subsequent differentiation is due to socialisation, but for the forces of socialisation to work along the same lines as pre-existing biological forces would suggest that socialisation is at most a feedback loop between biology and society.

There were a lot of brain areas that differed structurally between the sexes, but it would be irresponsible to draw any firm conclusions about what they might mean for function and behaviour. For instance,  what could differences in overall insula size possibly mean psychologically when the area is associated with “compassion and empathy, perception, motor control, self-awareness, cognitive functioning”, “interpersonal experience” and “psychopathology”?

Insofern liegt noch viel Arbeit vor den Forschern, bis sie die Unterschiede wirklich verstehen. Aber dennoch entzieht diese Studie vielen, die auf einen Blank Slate abstellen und annehmen, dass Geschlechterunterschiede nur auf Sozialisiation zurück gehen können einiges an Boden bzw. erfordert, dass diese ihre Thesen kritisch hinterfragen.

Vgl auch:

• Geschlechterunterschiede im Gehir
• Die Rolle von Testosteron und dem Y-Chromosom bei der Maskulinisierung des Gehirns
• Metastudie zu Geschlechterunterschieden in der Gehirnstruktur
• Geschlechterunterschiede in den strukturellen Verbindungen des menschlichen Gehirns
• „Das menschliche Gehirnmosaik“: Unterschiede im Gehirn von Mann und Frau
• Unterschiede im Gehirn von Männern und Frauen: Struktur
• Weiße und graue Gehirnzellen und Transsexualität
• Gehirn von Männern und Frauen: Unterschiede und Theorien
• Geschlechtliche Differenzierung des menschlichen Gehirns in Bezug auf geschlechtliche Identität und sexuelle Orientierung
• Wie Geschlechtsunterschiede im Gehirn durch pränatale Hormone entstehen
• Sprache und Unterschiede im Gehirn von Mann und Frau
• Unterschiede im Gehirn von Männern und Frauen: Warum sie in Bedeutung haben
• Männliche Geschlechtsidentität und männliches Verhalten: Die Rolle von Sexhormonen in der Gehirnentwicklung
• Sexuelle Differenzierung des menschlichen Gehirns und männliches bzw. weibliches Verhalten
• Die Organisation des Gehirns durch Testosteron
• Unterschiede im Gehirn von Mann und Frau
• Genatlas: 6500 Unterschiede zwischen Männern und Frauen

Homosexualität am Gesicht erkennen

Die Studie war bereits Thema in den Kommentaren:

We show that faces contain much more information about sexual orientation than can be perceived and interpreted by the human brain. We used deep neural networks to extract features from 35,326 facial images. These features were entered into a logistic regression aimed at classifying sexual orientation. Given a single facial image, a classifier could correctly distinguish between gay and heterosexual men in 81% of cases, and in 74% of cases for women. Human judges achieved much lower accuracy: 61% for men and 54% for women. The accuracy of the algorithm increased to 91% and 83%, respectively, given five facial images per person. Facial features employed by the classifier included both fixed (e.g., nose shape) and transient facial features (e.g., grooming style). Consistent with the prenatal hormone theory of sexual orientation, gay men and women tended to have gender-atypical facial morphology, expression, and grooming styles. Prediction models aimed at gender alone allowed for detecting gay males with 57% accuracy and gay females with 58% accuracy. Those findings advance our understanding of the origins of sexual orientation and the limits of human perception. Additionally, given that companies and governments are increasingly using computer vision algorithms to detect people’s intimate traits, our findings expose a threat to the privacy and safety of gay men and women.

Quote: Deep neural networks are more accurate than humans at detecting sexual orientation from facial images.

Aus dem Spiegelartikel dazu:

Sie zeigten, wie ein Computer mithilfe von Gesichterkennungssoftware die sexuelle Orientierung von Menschen erkennt.

Und das mit extrem hoher Trefferquote: Ausgehend von nur einem Foto erkannte das Programm 81 Prozent aller schwulen Männer und 74 Prozent aller homosexuellen Frauen. Menschliche Probanden, denen die gleichen Bilder vorgelegt wurden, kamen hier nur auf 61 und 54 Prozent Trefferquote. Noch gruseliger wurden die Ergebnisse, wenn man dem Rechner fünf Bilder einer Person vorlegte. Dann erkannte die Software 91 Prozent der homosexuellen Männer und 83 Prozent der Frauen.

Auch interessant: Das dort verlinkte Bild:

homosexuell Gesicht

Das linke Gesicht wurde aus heterosexuellen Personen zusammengesetzt, das rechte aus homsoexuellen Personen.

Interessanterweise kommen mir in beiden Fällen die heterosexuellen Gesichter unattraktiver vor. Vielleicht auch nur, weil  sie jeweils dicker aussehen.

Aus meiner Sicht ein durchaus zu erwartendes Ergebnis:

Die vorherrschende Theorie führt an, dass Homosexualität in einer engen Verbindung mit insbesondere pränatalen Hormonen steht:

• Hormone und sexuelle Orientierung
• Pränataler Stress und Medikamente als Ursache für Homosexualität und abweichendes Geschlechterverhalten

Und auch Gesichter sind männlicher oder weiblicher unter der Einwirkung der Hormone:

vgl zB diese Studie:

Prenatal testosterone may have a powerful masculinizing effect on postnatal physical characteristics. However, no study has directly tested this hypothesis. Here, we report a 20-year follow-up study that measured testosterone concentrations from the umbilical cord blood of 97 male and 86 female newborns, and procured three-dimensional facial images on these participants in adulthood (range: 21–24 years). Twenty-three Euclidean and geodesic distances were measured from the facial images and an algorithm identified a set of six distances that most effectively distinguished adult males from females. From these distances, a ‘gender score’ was calculated for each face, indicating the degree of masculinity or femininity. Higher cord testosterone levels were associated with masculinized facial features when males and females were analysed together (n = 183; r = −0.59), as well as when males (n = 86; r = −0.55) and females (n = 97; r = −0.48) were examined separately (p-values < 0.001). The relationships remained significant and substantial after adjusting for potentially confounding variables. Adult circulating testosterone concentrations were available for males but showed no statistically significant relationship with gendered facial morphology (n = 85, r = 0.01, p = 0.93). This study provides the first direct evidence of a link between prenatal testosterone exposure and human facial structure.

Ich hatte einmal zu den Gründen für Homosexualität ausgeführt:

1. Männliche Homosexualität:

• Die Hoden des Fötus produzieren nicht genug Testosteron
• Die Hoden des Fötus entwickeln sich zu spät und produzieren erst nach der entscheidenen Phase Testosteron
• Das Testosteron wird mangels entsprechender Rezeptoren an der Blut-Hirn-Schranke/im ganzen Körper nicht erkannt.
• Das Testosteron wird mangels entsprechender Rezeptoren an der Blut-Hirn-Schranke nur teilweise/abgeschächt erkannt
• Das Östrogen wird im Gehirn mangels entsprechender Rezeptoren nicht erkannt.
• Die Mutter stellt in der entscheidenden Phase nicht genug Testosteron bereit.
• Der Schwellenwert ist überhoch eingestellt, so dass das weibliche Programm trotz ausreichend Testosteron nicht durchgeführt wird.
• Antiandrogene blockieren die Rezeptoren in der entscheidenden Phase.
• Medikamente/andere Stoffe senken den Testosteronspiegel in der entscheidenden Phase
• Umweltbedingungen senken des Testosteronspiegel in der entscheidenden Phase
• Ein Zusammenspiel dieser Faktoren

2. Weibliche Homosexualität:

• Der Fötus hat einen erhöhten Testosteronspiegel (über eine Überproduktion der Nebennierenrinde und der Eierstöcke)
• Die Mutter stellt ein Übermass an Testosteron bereit.
• Der Schwellenwert für das 2.  Bauschema Mann ist in diesem Bereich extrem niedrig angesetzt.
• Medikamente sorgen für eine Erhöhung des Testosteronspiegels in der empfindlichen Phase
• überempfindliche Rezeptoren suggerieren einen erhöhten Testosteronspiegel.
• Ein Zusammenspiel dieser Faktoren

Wie man sieht muss damit nicht zwangsläufig die Homosexualität sich auch im Gesicht zeigen. Etwa weil der „Schwellenwert“ niedrig angesetzt ist oder der Wert nur in einer bestimmten Phase sehr hoch ist. Gerade wenn der Hormonspiegel aber dauerhaft erhöht ist spricht vieles für eine Übereinstimmung.

Insofern aus meiner Sicht ein sehr nachvollziehbares Ergebnis

 

Studiensammlung 5: (Prenatale) Hormone und Geschlechterunterschiede im Gehirn und Verhalten

Und weil wir heute eh schon eine Studie hier zu Gehirnunterschieden haben hier ein paar weitere Studien:

1.

Fetal Testosterone Influences Sexually Dimorphic Gray Matter in the Human Brain

In nonhuman species, testosterone is known to have permanent organizing effects early in life that predict later expression of sex differences in brain and behavior. However, in humans, it is still unknown whether such mechanisms have organizing effects on neural sexual dimorphism. In human males, we show that variation in fetal testosterone (FT) predicts later local gray matter volume of specific brain regions in a direction that is congruent with sexual dimorphism observed in a large independent sample of age-matched males and females from the NIH Pediatric MRI Data Repository. Right temporoparietal junction/posterior superior temporal sulcus (RTPJ/pSTS), planum temporale/parietal operculum (PT/PO), and posterior lateral orbitofrontal cortex (plOFC) had local gray matter volume that was both sexually dimorphic and predicted in a congruent direction by FT. That is, gray matter volume in RTPJ/pSTS was greater for males compared to females and was positively predicted by FT. Conversely, gray matter volume in PT/PO and plOFC was greater in females compared to males and was negatively predicted by FT. Subregions of both amygdala and hypothalamus were also sexually dimorphic in the direction of Male > Female, but were not predicted by FT. However, FT positively predicted gray matter volume of a non-sexually dimorphic subregion of the amygdala. These results bridge a long-standing gap between human and nonhuman species by showing that FT acts as an organizing mechanism for the development of regional sexual dimorphism in the human brain.

Ergänzung:

(FT was measured from amniotic fluid samples collected between 13 and 20 weeks of gestation (mean FT, 0.79 nmol/L; SD, 0.34 nmol/L; range, 0.25–1.70 nmol/L).

2.

The Impact of Sex, Puberty, and Hormones on White Matter Microstructure in Adolescents

Background: During adolescence, numerous factors influence the organization of the brain. It is unclear what influence sex and puberty have on white matter microstructure, as well as the role that rapidly increasing sex steroids play. Methods: White matter microstructure was examined in 77 adolescents (ages 10–16) using diffusion tensor imaging. Multiple regression analyses were performed to examine the relationships between fractional anisotropy (FA) and mean diffusivity (MD) and sex, puberty, and their interaction, controlling for age. Follow-up analyses determined if sex steroids predicted microstructural characteristics in sexually dimorphic and pubertal-related white matter regions, as well as in whole brain. Results: Boys had higher FA in white matter carrying corticospinal, long-range association, and cortico-subcortical fibers, and lower MD in frontal and temporal white matter compared with girls. Pubertal development was related to higher FA in the insula, while a significant sex-by-puberty interaction was seen in superior frontal white matter. In boys, testosterone predicted white matter integrity in sexually dimorphic regions as well as whole brain FA, whereas estradiol showed a negative relationship with FA in girls. Conclusions: Sex differences and puberty uniquely relate to white matter microstructure in adolescents, which can partially be explained by sex steroids.

Ergänzung:

Hormonal Assessment
Four milliliters of blood was collected via venipuncture between the hours of 7:00 to 10:00 AM at the Oregon Clinical and Translational Research Institute in the same week as the imaging session.

3.

Regional sex differences in grey matter volume are associated with sex hormones in the young adult human brain

Previous studies suggest organizing effects of sex hormones on brain structure during early life and puberty, yet little is known about the adult period. The aim of the present study was to elucidate the role of 17β-estradiol, progesterone, and testosterone on cortical sex differences in grey matter volume (GM) of the adult human brain. To assess sexual dimorphism, voxel-based morphometry (VBM) was applied on structural magnetic resonance images of 34 healthy, young adult humans (17 women, 17 men, 26.6 ± 5 years) using analyses of covariance. Subsequently, circulating levels of sex hormones were associated with regional GM using linear regression analyses. After adjustment for sex and total GM, significant associations of regional GM and 17β-estradiol were observed in the left inferior frontal gyrus (β = 0.39, p = 0.02). Regional GM was inversely associated with testosterone in the left inferior frontal gyrus (β = −0.16, p = 0.04), and with progesterone in the right temporal pole (β = −0.39, p = 0.008). Our findings indicate that even in young adulthood, sex hormones exert organizing effects on regional GM. This might help to shed further light on the underlying mechanisms of both functional diversities and congruence between female and male brains.

4.

Pubertal hormones organize the adolescent brain and behavior

Maturation of the reproductive system during puberty results in elevated levels of gonadal steroid hormones. These hormones sculpt neural circuits during adolescence, a time of dramatic rewiring of the nervous system. Here, we review the evidence that steroid-dependent organization of the adolescent brain programs a variety of adult behaviors in animals and humans. Converging lines of evidence indicate that adolescence may be a sensitive period for steroid-dependent brain organization and that variation in the timing of interactions between the hormones of puberty and the adolescent brain leads to individual differences in adult behavior and risk of sex-biased psychopathologies.

5.

Prenatal hormones and childhood sex-segregation: Playmate and play style preferences in girls with congenital adrenal hyperplasia

We investigated playmate and play style preference in children with congenital adrenal hyperplasia (CAH) (26 females, 31 males) and their unaffected siblings (26 females, 17 males) using the Playmate and Play Style Preferences Structured Interview (PPPSI). Both unaffected boys and girls preferred same-sex playmates and sex-typical play styles. In the conflict condition where children chose between a same-sex playmate engaged in an other-sex activity or an other-sex playmate engaged in a same-sex activity, boys (both CAH and unaffected brothers) almost exclusively chose playmates based on the preferred play style of the playmate as opposed to the preferred gender label of the playmate. By contrast, unaffected girls used play style and gender label about equally when choosing playmates. Girls with CAH showed a pattern similar to that of boys: their playmate selections were more masculine than unaffected girls, they preferred a boy-typical play style and, in the conflict condition, chose playmates engaged in a masculine activity. These findings suggest that prenatal androgen exposure contributes to sex differences in playmate selection observed in typically-developing children, and that, among boys and girls exposed to high levels of androgens prenatally, play style preferences drive sex segregation in play.

6.

Prenatal Hormones and Postnatal Socialization by Parents as Determinants of Male-Typical Toy Play in Girls With Congenital Adrenal Hyperplasia

Toy choices of 3- to 10-year-old children with congenital adrenal hyperplasia (CAH) and of their unaffected siblings were assessed. Also assessed was parental encouragement of sex-typed toy play. Girls with CAH displayed more male-typical toy choices than did their unaffected sisters, whereas boys with and without CAH did not differ. Mothers and fathers encouraged sex-typical toy play in children with and without CAH. However, girls with CAH received more positive feedback for play with girls’ toys than did unaffected girls. Data show that increased male-typical toy play by girls with CAH cannot be explained by parental encouragement of male-typical toy play. Although parents encourage sex-appropriate behavior, their encouragement appears to be insufficient to override the interest of girls with CAH in cross-sexed toy

7.

Increased aggression and activity level in 3- to 11-year-old girls with congenital adrenal hyperplasia

Experimental research in a wide range of mammals has documented powerful influences of androgen during early development on brain systems and behaviors that show sex differences. Clinical research in humans suggests similar influences of early androgen concentrations on some behaviors, including childhood play behavior and adult sexual orientation. However, findings have been inconsistent for some other behaviors that show sex differences, including aggression and activity level in children. This inconsistency may reflect small sample sizes and assessment limitations. In the present study, we assessed aggression and activity level in 3- to 11-year-old children with CAH (38 girls, 29 boys) and in their unaffected siblings (25 girls, 21 boys) using a questionnaire that mothers completed to indicate current aggressive behavior and activity level in their children.

Data supported the hypotheses that:

• 1. unaffected boys are more aggressive and active than unaffected girls;
• 2. girls with CAH are more aggressive and active than their unaffected sisters; and
• 3. boys with and without CAH are similar to one another in aggression and activity level.

These data suggest that early androgens have a masculinizing effect on both aggressive behavior and activity level in girls.

8.

Prenatal androgen exposure alters girls’ responses to information indicating gender-appropriate behaviour

Individual variability in human gender-related behaviour is influenced by many factors, including androgen exposure prenatally, as well as selfsocialization and socialization by others postnatally. Many studies have looked at these types of influences in isolation, but little is known about how they work together. Here, we report that girls exposed to high concentrations of androgens prenatally, because they have the genetic condition congenital adrenal hyperplasia, show changes in processes related to selfsocialization of gender-related behaviour. Specifically, they are less responsive than other girls to information that particular objects are for girls and they show reduced imitation of female models choosing particular objects. These findings suggest that prenatal androgen exposure may influence subsequent gender-related behaviours, including object (toy) choices, in part by changing processes involved in the self-socialization of gendered behaviour, rather than only by inducing permanent changes in the brain during early development. In addition, the findings suggest that some of the behavioural effects of prenatal androgen exposure might be subject to alteration by postnatal socialization processes. The findings also suggest a previously unknown influence of early androgen exposure on later processes involved in self socialization of gender-related behaviour, and thus expand understanding of the developmental systems regulating human gender development.

9.

How early hormones shape gender development

Highlights
• Prenatal androgens influence sex-related characteristics to varying degrees.
• Androgens facilitate male-typed activities through interest in things versus people.
• Androgens are associated with some aspects of brain structure and activation.
• Current work is focused on interplay of hormones and social environment.
• Relevant to questions regarding sex-related psychopathology, prenatal programming.
 
Many important psychological characteristics show sex differences, and are influenced by sex hormones at different developmental periods. We focus on the role of sex hormones in early development, particularly the differential effects of prenatal androgens on aspects of gender development. Increasing evidence confirms that prenatal androgens have facilitative effects on male-typed activity interests and engagement (including child toy preferences and adult careers), and spatial abilities, but relatively minimal effects on gender identity. Recent emphasis has been directed to the psychological mechanisms underlying these effects (including sex differences in propulsive movement, and androgen effects on interest in people vs things), and neural substrates of androgen effects (including regional brain volumes, and neural responses to mental rotation, sexually arousing stimuli, emotion, and reward). Ongoing and planned work is focused on understanding the ways in which hormones act jointly with the social environment across time to produce varying trajectories of gender development, and clarifying mechanisms by which androgens affect behaviors. Such work will be facilitated by applying lessons from other species, and by expanding methodology. Understanding hormonal influences on gender development enhances knowledge of psychological development generally, and has important implications for basic and applied questions, including sex differences in psychopathology, women’s underrepresentation in science and math, and clinical care of individuals with variations in gender expression.

10.

The organizing actions of adolescent gonadal steroid hormones on brain and behavioral development

Highlights

• Adolescence is a sensitive period for the effects of hormones on brain and behavior.
• Testicular hormones masculinize and defeminize social and reproductive behaviors.
• Ovarian hormones have both feminizing and defeminizing effects on female behavior.
• Gonadal steroid hormones drive many brain structural changes during adolescence.
• Adolescence may be part of a protracted postnatal steroid-sensitive period.

Abstract
Adolescence is a developmental period characterized by dramatic changes in cognition, risk-taking and social behavior. Although gonadal steroid hormones are well-known mediators of these behaviors in adulthood, the role gonadal steroid hormones play in shaping the adolescent brain and behavioral development has only come to light in recent years. Here we discuss the sex-specific impact of gonadal steroid hormones on the developing adolescent brain. Indeed, the effects of gonadal steroid hormones during adolescence on brain structure and behavioral outcomes differs markedly between the sexes. Research findings suggest that adolescence, like the perinatal period, is a sensitive period for the sex-specific effects of gonadal steroid hormones on brain and behavioral development. Furthermore, evidence from studies on male sexual behavior suggests that adolescence is part of a protracted postnatal sensitive period that begins perinatally and ends following adolescence. As such, the perinatal and peripubertal periods of brain and behavioral organization likely do not represent two discrete sensitive periods, but instead are the consequence of normative developmental timing of gonadal hormone secretions in males and females.

11.

Effects of chromosomal sex and hormonal influences on shaping sex differences in brain and behavior: Lessons from cases of disorders of sex development

Sex differences in brain development and postnatal behavior are determined largely by genetic sex and in utero gonadal hormone secretions. In humans however, determining the weight that each of these factors contributes remains a challenge because social influences should also be considered. Cases of disorders of sex development (DSD) provide unique insight into how mutations in genes responsible for gonadal formation can perturb the subsequent developmental hormonal milieu and elicit changes in normal human brain maturation. Specific forms of DSDs such as complete androgen insensitivity syndrome (CAIS), congenital adrenal hyperplasia (CAH), and 5α-reductase deficiency syndrome have variable effects between males and females, and the developmental outcomes of such conditions are largely dependent on sex chromosome composition. Medical and psychological works focused on CAH, CAIS, and 5α-reductase deficiency have helped form the foundation for understanding the roles of genetic and hormonal factors necessary for guiding human brain development. Here we highlight how the three aforementioned DSDs contribute to brain and behavioral phenotypes that can uniquely affect 46,XY and 46,XX individuals in dramatically different fashions

Aus der Studie:

CAH, CAIS und 5-alpha reductace Deficiency: ein Schaubild

Weiteres aus der Studie:

Research focused on cases of DSD have helped the scientific community better understand the interplay between gonadal hormones and sex chromosome complement with regard to generating some of the sex differences observed in humans. These works have shed light on the likelihood that testosterone exposure, as opposed to sex chromosomes, is a larger contributing factor for guiding one’s sexual orientation and to a lesser extent gender identity. We see that 46,XX CAH individuals that have been exposed to in utero testosterone experience a greater degree of dissatisfaction in gender assignment in addition to above-average levels of homosexual and bisexual fantasies, a proxy for sexual preference. As previously mentioned, other variables are present in CAH cases such as life-long medical interventions and psychosocial confounds. These variables may constitute an environmental factor that, when coupled with biological predispositions, generates variations in sexual orientation and gender identity. That sexual orientation is determined solely by in utero hormonal milieu is unlikely. We see that the vast majority of CAH women, despite having been exposed to above-average levels of testosterone, identify as heterosexual as measured by both partners and sexual fantasies. The science of sexual orientation is still weakly understood at the mechanistic level; however, considerable amounts of research have proposed many possibilities for the causes of same-sex attraction (LeVay, 2012; Bailey et al., 2016).

The strongest evidence that adds support for the influence of testosterone in structuring gender identity comes from the work focused on 46,XY CAIS, in which nearly all individuals researched indicate feelings typical of female gender. In addition to self-reports and clinical evaluations, recent fMRI studies have also demonstrated that CAIS women not only feel female but also neurologically respond more similarly to 46,XX women than to 46,XY men when observing sexual images. However, new studies are continually emerging suggesting that gender identity and sexual orientation in individuals with CAIS are not as clear as once thought, and the rates of nonheterosexual and gender dysphoria may be much higher than currently stated. In addition to CAH and CAIS, 5α-reductase deficiencies have also demonstrated the strong role of testosterone’s ability to organize the human brain hormonally and influence adult gender identity and behavior. If early in utero exposure had no influence in guiding brain gender, we would expect considerable difficulty with the female-to-male transition observed in pubertal years in those with 5α-reductase deficiency. What we observe, however, is that an overwhelming majority of individuals with this condition comfortably transitioned into the new gender role at puberty, a worldwide observation occurring throughout many different types of social environments. Despite the convincing findings for the role of testosterone in generating these observations, the influence of social and other environmental variables are also factors that require consideration.

Cognitive Conclusions
Studying cases of DSDs has also provided insight into some of the biological parameters that generate sex differences in cognitive abilities such as visuospatial awareness and targeting ability. From studies with 46,XX CAH individuals it has been well established that in utero androgen exposure seems to enhance the ability to mentally rotate objects as well as improving hand–eye coordination during targeting tasks. This trait appears to be dependent on sex chromosome complement in addition to hormone exposure, insofar as 46,XY males with CAH actually perform worse than their matched controls, which is unexpected given the fact that CAH males would have equal or elevated levels of circulating testosterone. This raises the notion, as mentioned above, that proper timing and dosage are also likely to be important for enhancing such abilities and that simply having above-average levels of testosterone during development would not generate a “super-male.” CAIS provides another insight into this matter, demonstrating that the ability to respond to testosterone on an XY background is critical to establishing baseline spatial performance abilities. fMRI studies demonstrate that 46,XY CAIS had less inferior parietal lobe neuroactivation when performing spatial rotation tasks, a feature that resembles 46,XX females more than control genetic males. These fMRI studies on CAIS individuals once again minimize social influences and allow for a more unbiased assessment of the requirement for testosterone over genetic composition for shaping these cognitive performance sex differences.
Structural Conclusions
From the MRI studies that have been conducted in patients with CAH, it is clear that DSDs affect more than gonadal development. As highlighted, the central nervous system is highly sensitive to various hormones, and imbalances of these can greatly affect downstream behavior as well as overall brain structure. Variations in amygdala volume seem to be present in some individuals with CAH; however the effect is different depending on sex chromosome composition. Specifically, 46,XY males with CAH show unilateral reductions in the left amygdala, whereas 46,XX females with CAH show bilateral reductions in overall volume. Alterations in amygdala volume seem to be consistent with long-term glucocorticoid replacement therapies because findings for non-CAH patients on such hormone regiments also show amygdala abnormalities. The documentations of white matter irregularities seem to be unaffected by chromosomal sex and to cause similar variations in both males and females with CAH. The explanations for these results are not agreed upon, and more research will be needed before causations can be associated with the unusual white matter findings. Although limited, these discoveries have opened a new area for potential investigation focusing on the role of glucocorticoid influences in the developing brain in addition to the more frequently studied gonadal hormonal contributions. Unfortunately, no extensive structural studies have been conducted in patients with CAIS or 5α-reductase deficiencies. These findings would be invaluable in determining the direct effect of testosterone on the structures that in MRI studies have shown alterations in CAH. Future work focusing on outcomes in individuals with DSD will continue to aid in deciphering the contributions of chromosomal sex and hormones to shaping the sexually dimorphic human brain.

12.

Feminists wrestle with testosterone: Hormones, socialization and cultural interactionism as predictors of women’s gendered selves 

Sociology of gender has developed beyond a personality-centered idea of ‘‘sex-roles’’ to an approach that stresses interaction and social structure. At the same time, there has been a concurrent development in the psychological sex-differences and medical literatures toward including the biological bases of sex-typed behavior and gender identities. In this paper, while we conceptualize gender as a social structure, we focus only on the individual level of analysis: testing the relative strength of (maternal circulating) prenatal hormones, childhood socialization, and the power of expectations attached to adult social roles (cultural interactionist) as explanations for women’s self-reported feminine and masculine selves. Our findings are complex, and support some importance of each theory. Prenatal hormones, childhood socialization, and cultural interactionism were all influential factors for gendered selves. While cultural expectations predicted only feminine selves, prenatal hormones were more robust predictors of masculine sense of self. While personality may be a relatively stable characteristic influenced by the body and childhood socialization, our results reinforce the importance of studying how the social world responds to and reinforces gendered personality.

12.

Genetic association suggests that SMOC1 mediates between prenatal sex hormones and digit ratio

Abstract

Men and women differ statistically in the relative lengths of their index and ring fingers; and the ratio of these lengths has been used as a biomarker for prenatal
testosterone. The ratio has been correlated with a wide range of traits and conditions including prostate cancer, obesity, autism, ADHD, and sexual orientation. In a genome-wide association study of 979 healthy adults, we find that digit ratio is strongly associated with variation upstream of SMOC1 (rs4902759: P = 1.41 9 10-8) and a meta-analysis of this and an independent study shows a probability of P = 1.5 9 10-11. The protein encoded by SMOC1 has recently been shown to play a critical role in limb development; its expression in prostate tissue is dependent on sex hormones, and it has been implicated in the sexually dimorphic development of the gonads. We put forward the hypothesis that SMOC1 provides a link between prenatal hormone exposure and digit ratio.

Anmerkung: Finde ich interessant: Wenn das Protein, welches Einfluss auf die Entwicklung der Gliedmaßen hat, wiederum abhängig von Testosteron ist, dann würde das durchaus erklären, warum die Digit Ratio ein Indikator  für pränatales Testosteron ist, es könnte je nach Zusammenspiel auch zeigen, warum es ein teilweise unzuverlässiger Anzeiger ist, eben weil die Mechanismen unterschiedlich sind.

13.

Exposure to prenatal life events stress is associated with masculinized play behavior in girls

Previous research has shown that prenatal exposure to endocrine-disrupting chemicals can alter children’s neurodevelopment, including sex-typed behavior, and that it can do so in different ways in males and females. Non-chemical exposures, including psychosocial stress, may disrupt the prenatal hormonal milieu as well. To date, only one published study has prospectively examined the relationship between exposure to prenatal stress and gender-specific play behavior during childhood, finding masculinized play behavior in girls who experienced high prenatal life events stress, but no associations in boys. Here we examine this question in a second prospective cohort from the Study for Future Families. Pregnant women completed questionnaires on stressful life events during pregnancy, and those who reported one or more events were considered “stressed”. Families were recontacted several years later (mean age of index child: 4.9 years), and mothers completed a questionnaire including the validated Preschool Activities Inventory (PSAI), which measures sexually dimorphic play behavior. In sex-stratified analyses, after adjusting for child’s age, parental attitudes towards gender-atypical play, age and sex of siblings, and other relevant covariates, girls (n=72) exposed to prenatal life events stress had higher scores on the PSAI masculine sub-scale (β=3.48, p=0.006) and showed a trend towards higher (more masculine) composite scores (β=2.63, p=0.08). By contrast, in males (n=74), there was a trend towards an association between prenatal stress and higher PSAI feminine sub-scale scores (β=2.23, p=0.10), but no association with masculine or composite scores. These data confirm previous findings in humans and animal models suggesting that prenatal stress is a non-chemical endocrine disruptor that may have androgenic effects on female fetuses and anti-androgenic effects on male fetuses.

Anmerkung: Die Werte sind allerdings anscheinend sehr gering

14.

Relations between prenatal testosterone levels and cognitive abilities at 4 years.

Relations between prenatal testosterone (T) levels and cognitive abilities at age 4 were examined for 28 girls and 30 boys. Prenatal T levels were measured in 2nd trimester amniotic fluid samples obtained by amniocentesis and were examined in relation to scores on tests of cognitive abilities. For girls, prenatal T levels showed a curvilinear (inverted U-shaped) relation to language comprehension and classification abilities. Linear relations also were observed in that prenatal T levels were inversely related to girls‘ scores on tasks assessing counting and number facts. Similarly, girls with high average block building scores had lower prenatal T and cognitive abilities were not observed. The observation of relations in girls and not boys is discussed, and the findings are examined in relation to theories of hormone-behavior relations.

15.

Relations between prenatal testosterone and cerebral lateralization in children.

Several theorists have proposed that the sex steroid testosterone acts on the fetal brain during a critical period of development to influence cerebral lateralization (N. Geschwind & A. M. Galaburda, 1987; M. Hines & C. Shipley, see PA, Vol 71:8996; S. F. Witelson, see PA, Vol 79:26441. In the present study. relations were examined between prenatal testosterone levels in 2nd trimester amniotic fluid and lateralization of speech, affect, and handedness at age 10. Girls with higher prenatal testosterone levels were more strongly right-handed and had stronger left-hemisphere speech representation. Boys with higher prenatal testosterone levels had stronger right-hemisphere specialization for the recognition of emotion. This pattern of results is most consistent with Witelson’s (1991) claim that prenatal testosterone leads to greater lateralization of function.

Testo-kain oder Koka-steron? Zur Wirkung von Testosteron

Dies ist ein Gastartikel von Nina Radtke

Vor nicht all zu langer Zeit habe ich Testosteron mit Kokain verglichen. Zu diesem Schluss bin ich gekommen, da ich, im Gegensatz zu den meisten Menschen, in meinem Leben bereits verschiedenste Mengen an Testosteron im Blut hatte.

Dazu muss ich nun erst einmal kurz meine Vorgeschichte erklären: Bis ich 21 wurde, war ich der männlichen Adoleszenz unterworfen. Je mehr die Männlichkeit mein Ich bestimmte, umso schlechter fühlte ich mich. Das lag allerdings an meinem inneren Konflikt, dem Umstand, das ich trotz bereits lange vorher bestehendem andersartigem Bedürfnis, ein Mann werden sollte statt eine Frau.

Nun, ich habe dann, zuerst in Eigenregie und später mit ärztlicher Unterstützung eine Hormontherapie begonnen (und viele Operationen mitgemacht), dabei war mein Androgenspiegel oft signifikanten Änderungen unterworfen und ich habe inzwischen Alles erlebt von Testosteron quasi auf 0 bis hin zu den furchtbar hohen Testosteronspiegeln die ich angesichts meiner damals sehr ausgeprägten Muskulatur und Maskulinität gehabt haben muss.

Natürlich ist Testosteron nur ein Faktor, auch die Östrogenspiegel sowie mein weiterer Lebensweg hatten und haben sicher einen Einfluss auf mein Verhalten.

Dennoch ist es meine persönliche Empfindung, das Testosteron / Dihydrotestosteron (Wird mit Hilfe einer Aromatase zB in Prostata und Haarfolikeln aus Testosteron hergestellt und wirkt deutlich stärker) folgendermaßen wirkt:

• Testosteron gibt Selbstvertrauen
  Wenn mein Testosteronspiegel sehr sehr niedrig ist, dann geht mir zunehmend das Selbstvertrauen flöten. Als mein Testosteronspiegel deutlich höher war, hatte ich im Umgang mit Menschen keine Selbstzweifel. Und auch keine Selbstzweifel (nur Verbitterung) beim Blick in den Spiegel. Bei sehr niedrigem Testosteron fühle ich mich einfach nicht sicher, aber es ist mehr. Mit viel Testosteron hat mein Selbstvertrauen oft dazu geführt, das Leute ohne Wiederworte Dinge mitgemacht haben, um die ich sie jetzt wirklich bitten müsste. Ich stand auch sehr viel mehr im Mittelpunkt.
• Testosteron macht aktiv
  Kaum Testo – Lange Schlafen | „Normales Testo“ (Wert den ich die meiste Zeit hatte, etwas über weibl. Norm) – Halbwegs Aktiv | Hohes Testo – Aufgedreht (zB hin und her laufen beim Warten) ——- Hab aber glaub ich auch ADHS was sich überwiegend in sprunghaften Gedanken aber auch in physischer Unruhe äußert
• Testosteron macht Unangreifbar
  Keine Angriff hätte mein Ego treffen können. Sowieso ist Ego glaube ich ein Produkt des zirkulierenden Testosterons, jedenfalls hat der Wettbewerbsgeist und der Geltungswahn mit der Hormontherapie schrittweise abgenommen und hat nun (T < weibliche Norm) Nichts mehr zu sagen. Ich bin jetzt auf mein Potential fokussiert und nicht auf den Vergleich mit Anderen. Ich ordne mich ohne Hierachiebewusstsein in eine Gruppe ein, früher undenkbar, aber vielleicht war mein Fokus auf Hierachie auch teilweise durch die Tipps in den Flirtratgebern statt nur durchs Testosteron bestimmt.
• Testosteron macht Triebhaft
  Drogen, Party, Alkohol, Fressen – früher konnte ich mir den Driss jeden Tag geben und habs auch getan weil ich immer Bock drauf hatte. Eine neurobiologische Erklärung könnte sein, das Testosteron die Dopaminausschüttung stimuliert: Der gleiche Belohnungsreiz wirkt mit viel Testosteron deutlich stärker als mit wenig Testosteron. Vermutlich ein Grund, warum exzessives Verhalten bei Männern verbreiteter ist: Mehr Dopamin = Mehr Risikobereitschaft.
• Testosteron macht gefühllos
  Schlimmer als unter Antidepressiva hat das Testosteron damals wie eine unsichtbare Mauer meine Gefühle eingesperrt. Ich konnte Gefühle ansatzweise fühlen, aber es gab immer einen Punkt, wo die Gefühle geblockt waren. Nur besonders starke „Einschläge“ konnten mich emotional aus der Ruhe bringen. Emotionen sind unter Östrogen ohne Testosteron weit fließender und natürlicher.

Mehr kann ich dazu nicht sagen, es ist noch heftig wie stark anabol Testosteron wirkt, ich merke es innerhalb weniger Wochen wenn mein Testosteron mal wieder sinkt oder steigt, das die Einkaufstasche mal schwerer und mal leichter ist. Aber das weiß glaub ich Jeder über das Hormon Testosteron^^

Zur Ergänzung des Gastartikels noch einige Links:

• Wirkung von Östrogen (Nina Radtke)
• Die Wirkung von Testosteronpräparaten
• Testosteron und seine Wirkung auf den Sexualtrieb
• Schilderung des Journalisten Andrew Sullivan
• Transsexualität, Hormonbehandlung und die Libido
• Fähigkeiten in Verbindung mit den Hormonen (Östrogen / Testosteron)

„Gender ist kein soziales Konstrukt“

Liebe als Sucht bzw. Sucht als Liebe und das Liebesleben von Wühlmäusen

Ich habe das sehr interessante Buch „The Chemistry between us“ gelesen, welches ich empfehlen kann. Es werden einige sehr interessante Punkte dargestellt, sowohl zur Forschung von Geschlechterunterschieden als auch insbesondere dazu, wie wir Lieben und wie sich Bindung entwickelt.

Es sind interessante Punkte in dem Buch enthalten, zu denen man dutzende Artikel schreiben könnte. Ich fange mal mit einem an, der auch in dieser Kurzzusammenfassung hier dargestellt wird:

Young has devoted his career to studying the behaviors and neural circuitry of love in the prairie vole, a rodent whose monogamous tendencies resemble our own. Once a prairie vole has found “the one,” the pair will most likely remain companions for life. Young’s research has implicated a range of chemical activities—mainly during sex—that build this lifelong bond. In particular, he uncovered how two hormones in the brain, vasopressin in male voles and oxytocin in female voles, regulate social behavior and memory—promoting the recognition of a loved one and the urge to cuddle or defend. In addition, the circulation of dopamine and opioids allows the vole to associate his or her partner with pleasure, thus strengthening their bond. Many of these molecules are identical to those activated in human bonding.

Interessant ist daran, dass es zwei Arten von Voles (Wühlmäuse) gibt, die eine ist monogam, die andere nicht. Der Wesentliche Unterschied ist wohl eben der, dass bei dem einen über Vasopressin und Oxytocin eine Bindung erfolgt und bei dem anderen nicht. Der Unterschied zwischen den beiden Arten ist relativ gering, die Unterschiede im Verhalten aber enorm.

Young führt dann verschiedene Tests auf, die nahelegen, dass die gleichen Mechanismen eben auch beim Menschen wirken.

That loving feeling comes at a price. A hormone called corticotropin-releasing factor, or CRF, builds up in the brains of paramours and parents alike. The CRF system activates a stress response, and this system elicits the painful sensations you feel when your baby cries or your boyfriend dumps you. The system may seem like a nasty trick, but it has its uses. Even when passion fades or a diaper needs changing, the sharp pangs of the CRF system keep families and loved ones together. The CRF system also contributes to the agony an addict feels after the elation wears off. Thus, the authors argue, the highs of intimacy and withdrawals of separation parallel the highs and lows that drug addicts experience.

Wenn ich mich recht erinnere, dann stellt der Autor es so dar, dass die erste Liebe (oder der erste Kick bei einer Droge) oft noch tatsächliches Glück ist, weil man in Oxytocin gebadet ist und andere glücklichmachende Hormone ausgeschüttet werden. Das bewirkt eine Bindung. Wie bei vielen positiven Reizen wird diese Ausschüttung von reinen Glückshormonen aber mit der „Gewöhnung“ an den Partner immer geringer. Es greift dann ein anderes System: Wenn man das, was einen bisher glücklich gemacht hat, nicht mehr hat, dann baut sich das oben genannte Stresshormon auf und dieser lässt dann nach, wenn man den „Reiz“ wieder ausgesetzt ist. Das bewirkt dann den Trennungsschmerz und kann in bestimmten Fällen zu einem „ich kann nicht mit ihr und ich kann nicht ohne sie“ führen: Wenn sie da ist hat man dann eben „Belohnungseffekt“ mehr, weil dieser zu abgestumpft ist, ist sie aber weg, dann stellt sich der Trennungsschmerz ein.

Ähnlich ist es wohl auch bei Drogennutzern, die eine Droge eben wie eine Liebe empfinden: Am Anfang ist es pures Glück, dann brauchen sie eine immer höhere Dosis und schließlich ist es schlicht der „Trennungsschmerz“ der bekämpft wird und man hält es nicht mehr aus und will diesen beseitigen. Hat man ihn beseitigt, dann meint man vielleicht jederzeit aufhören zu können, aber dann treten wieder die Entzugserscheinungen auf.

Hier eine andere Besprechung des Buches in der man auch sieht, wie sich dieser „Liebesentzug“ auswirkt:

To investigate the rodent version of getting hugs, and what happens in the absence of hugs from a bonded partner, Bosch took virgin males and set them up in vole apartments with roommates—either a brother they hadn’t seen in a long time or an unfamiliar virgin female. As males and females are wont to do, the boy-girl roommates mated and formed a bond. After five days, he split up half the brother pairs, and half the male-female pairs, creating what amounted to involuntary vole divorce. Then he put the voles through a series of behavioral tests.

The first is called the forced-swim test. Bosch likens it to an old Bavarian proverb about two mice who fall into a bucket of milk. One mouse does nothing and drowns. The other tries to swim so furiously the milk turns into butter and the mouse escapes. Paddling is typically what rodents will do if they find themselves in water; they’ll swim like crazy because they think they’ll drown if they don’t. (Actually, they’ll float but apparently no rodent floaters have ever returned to fill in the rest of the tribe.)

The voles that were separated from their brothers paddled manically. So did the voles who stayed with their brothers and the voles who stayed with their female mates. Only the males who’d gone through vole divorce floated listlessly as if they didn’t care whether they drowned.

„It was amazing,“ Bosch recalls. „For minutes, they would just float. You can watch the video and without knowing which group they were in, you can easily tell if it’s an animal separated from their partner, or still with their partner.“ Watching the videos of them bob limply, it’s easy to imagine them moaning out „Ain’t No Sunshine When She’s Gone“ with their tiny vole voices.

Die armen Wühlmäuse.

Man stelle es sich mit ihm an der Gitarre vor:

Prairie vole (Prärie Wühlmaus) (ein Bild mit Gitarre war nicht zu finden, aber er schaut immerhin traurig)

Das Leben von Laborwühlmäsuen ist allerdings auch so hart:

Next Bosch subjected the voles to a tail-suspension test. This test uses the highly sophisticated technique of duct taping the end of an animal’s tail to a stick and suspending it. As in the swim test, a rodent thus suspended will usually flail and spin his legs like a cartoon character who’s run off the edge of a cliff. Once again, though, while the other males did just that, the divorced males hung like wet laundry.

In a final behavior test, Bosch placed the voles on an elevated maze, like the ones we’ve already described that tested anxiety. On such a maze, the animal’s desire to investigate fights with its fear of exposed areas. Compared to the other voles, the divorced males were significantly less likely to explore the open arms of the maze.

All these tests, commonly used to test lab animals for depression, showed that if you separate a pair-bonded male vole from his mate, you’ll get a very mopey vole who uses what’s called passive-stress coping to deal with the overwhelming anxiety of partner loss. „When the separation takes place, this is what causes the animals to feel so bad,“ Bosch explains. „We found this increased depressive behavior and that tells us the animal is not feeling well.“ He doesn’t mean „under the weather,“ he means the divorced voles are emotionally miserable. „It is like when my wife went to the States for a post-doc for one year, so I knew I wouldn’t see her for at least six months. Well, I was sitting at home, laying on the couch, not motivated to do anything, not to go out and meet friends like I usually would.“

Es ist interessant, dass wir hier den Tieren ganz ähnlich sind und das in beiden Fällen bestimmte Chemikalien am Werk sind, ohne die wir uns nicht auf diese Weise verhalten würden (wie die andere Art von Voles zeigt, die nicht monogam ist).

Dann wurde versucht, die Wirkung mit Drogen nachzustellen:

Koob and others have used drugs to create the very same behavior in other lab animals. When the drugs are taken away from rats and mice, they display the same passive responses to elevated mazes. They withdraw socially. They mope. Human addicts do the same, Koob points out, mentioning characters in movies like Leaving Las Vegas and Trainspotting as examples.

To explain the physiology behind this passive depression state in the separated voles, Bosch checked their chemistry. The males separated from their mates had much higher levels of corticosterone, a stress chemical, in their blood than did any of the other groups, including voles separated from their brothers. Their HPA axis was working so hard, their adrenal glands weighed more. Bosch nailed CRF’s role in driving both the HPA axis overdrive and the mopey behavior by blocking CRF receptors in the voles‘ brains. When he did, the divorced voles no longer hung limply from the sticks. They didn’t float for as long in the water. They still remembered their mates, and were still bonded to them; they just didn’t worry about it when they left them.

Das finde ich recht eindrucksvoll: Wenn bestimmte Rezeptoren blockiert sind, dann gab es keinen Liebeskummer mehr. Was die „Macht“ biologischer Systeme aus meiner Sicht gut darlegt. Theoretisch könnte man dies sicherlich auch bei Menschen machen, aber entsprechende Tests wären unethisch. Ich würde aber vermuten, dass es Menschen mit einer geringeren Ausschüttung an Stresshormonen oder schwächeren Rezeptoren gibt, die dann eben eher auf „Short Time Mating“ setzen und nicht sehr anfällig für Liebeskummer sind. Ich vermute, dass sie dann eben auch ein anderes Verhalten zeigen.

But here’s the strange thing: both the voles who stayed with their female mates and the voles who were forced to split from the females had much more CRF in the BNST than did males who lived with, or were separated from, their brothers. In other words, loads of this stress-related hormone were being pumped in both the voles who got depressed after separation and voles who were still happily bonded and didn’t show signs of passive-stress coping.

„Bonding itself produces high CRF,“ Bosch says. „But this does not mean the system is also firing.“ There is something fundamental about living with a mate that results in more CRF stress hormone in the brain, but that also prevents the engagement of the HPA stress axis as long as the mates stay together. Using an interesting metaphor for bonding, Bosch says „I compare it to a rifle. As soon as they form a pair-bond, the rifle is loaded with a bullet. But the trigger isn’t pulled unless there is separation.“ He thinks that vasopressin serves as the chemical trigger to fire off the HPA axis during separation, though the exact roles of both oxytocin and vasopressin are still unclear.

Addicted drug users load the rifle, too. The gun won’t fire unless they stop taking the drug. For the bonded voles, „it won’t fire unless the partner leaves the nest,“ Bosch says.

Das ist ein interessanter Mechanismus. Er bewirkt zum einen Bindung, aber er lässt uns wahrscheinlich auch gleichzeitig eher die Möglichkeit, den Partner zu wechseln. Bei einem neuen Partner wird eben dann wieder Vasopressin, Oxytocin etc ausgeschüttet und damit das System wieder in Schach gehalten. Weswegen derjenige mit neuem Partner die Trennung auch besser verkraftet während der Verlassene das weit weniger kompensieren kann. Es verhindert also ein Verlassen sofern man nicht etwas besseres findet (statt wie beim ersten Verliebt sein den Partner unter der Ausschüttung der Hormone zu verklären). Wobei der Trennungsschmerz den Wechsel auch nicht zu einfach machen wird.

Hormone