Download 100 Sexual Development

JBS BioEthics
Sexual Development
2011 - 2012
Remind students about the sensitive nature of the things we will be discussing.
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sex is a biological term which refers to the functional differences between males and females and their
reproductive potential
◦ male and female are biological terms ◦
sex is determined by genes in chromosomes
sexuality is a psychological term which refers to our awareness and reaction to biological sex ◦
masculine and feminine are psychological terms which refer to a person's gender ◦
gender is determined by biological, psychological and sociological factors
gender role: adoption of masculine or feminine behavioral traits that are deemed appropriate or
characteristic of a particular gender
gender identity: a person's private, subjective sense of maleness or femaleness
sexual orientation / preference: erotic desire for people of same or different sex
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In some cases, all of these will be typically associated with one sex.
Other times, a person can have some characteristics associated with two different sexes
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According to a nature view of psychosexual differentiation,
prenatal exposure to androgen influences the
development of gender identity
- the feeling an individual has of being a man or a
woman.
In contrast the nurture position holds that we are psychosexually neutral at birth and
that socialization is responsible for the development of
gender identity.
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Male, identical twin, Canada
Accident with circumcision at 8 months (done because foreskin was not retracting); penis destroyed
Parents took him to Johns Hopkins, psychologist John Money prominent proponent of the theory that
gender identity was relatively "plastic" in infancy and developed primarily as a result of social learning from
early childhood; most liberal academics in the late 1960s felt that all psychological and behavioral
differences between males and females were learned!
!
at the age of 22 months, surgery was performed to remove his testes and construct a vagina; given the
name Brenda; would be used as a test case (WHY? - identical genes, fetal environ., family environ. And no
abnormal prenatal hormones)!
!
Reimer's later account, written with John Colapinto, described how, contrary to Money's reports, Brenda
did not feel like a girl. She was ostracized and bullied by peers, and neither frilly dresses nor female
hormones made her feel female. By the age of 13, Brenda was experiencing suicidal depression, and told
her parents she would commit suicide if they made her see John Money again. In 1980, Brenda's parents
told her the truth about her gender reassignment, following advice from Brenda's endocrinologist and
psychiatrist. Now 15, Brenda decided to assume a male gender identity, calling himself David. After
learning of the new relationship with his ex-sister, Brian began to experience a pattern of mental
disturbance that would develop into schizophrenia. By 1997, David had undergone treatment to reverse
the reassignment, including testosterone injections, a double mastectomy, and two penis reconstruction
operations. He had married a woman, and become a stepfather to her children!
!
Although the book made David Reimer more comfortable financially, many other things went badly in his
life, including a separation from his wife, severe problems for his parents, and the death of his twin brother
Brian in 2002 from an overdose of schizophrenia medication. David Reimer took his own life with a
sawed-off shotgun in 2004.!
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Up to the 9th week of prenatal development, sexes look alike.
Week 5: All embryos develop two unspecialized gonads
Week 5: gonads form near two sets of ducts -- two options
Mullerian ducts -- form the female structures
Wolffian ducts -- form male structures
Week 6: Choice of which ducts develops
Depends on which sex chromosomes present, especially on activation of the SRY gene
on the Y chromosome
SRY activation--> male route
No SRY --> female route
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The Mullerian ducts degenerate (anti Mullerian hormone)
The neutral gonad becomes a teste
All the male structures, internally and externally, develop:
Vas Deferens, prostrate, seminal vesicles, penis,
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No Y, no SRY gene results in female development, no anti mullerian hormone
“Default” program
Gonad develops into an ovary,
Fallopian tubes, uterus, vagina
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Females: homogametic
Males: heterogametic
(Other species: reverse can be true, as in birds)
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X chromosome: 1500 genes
Y chromosome: Maybe 90 protein genes
Y chromosome does not have a complete homolog: How to map it?
Examine men who were missing parts of the chromosome and see how they differed
Now, use genome sequence: Findings: Unusual
Short arm, long arm
Tips: pseudoautosomal (PAR1 and PAR2) 5% - Homologous to the X chromosome
63 pseudoautosmal genes have counterparts on X chromosome
Example of these genes: bone growth, cell division, immunity, signal transduction, syn.
Hormones, energy met.
MYS = Male-specific region (formerly called nonrecombining region) - 27 genes
Does NOT recombine with the X chromomosome
male fertility: SRY gene!!
also has the AZF gene - codes for a protein needed to
make sperm (Azoospermia factor)
Azoospermia factor (AZF) refers to one of several proteins or their genes, which are coded from the AZF
region on the human male Y chromosome.[1] Deletions in this region are associated with inability to
produce sperm.
Recall how the SRY gene was discovered (1990) XX males (had part of Y)
and XY females (missing part of the Y)
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early in week 4 primordial germ cells from the yolk sac migrate to the gonadal ridges. During
week 6 the germ cells become incorporated into the gonad.
SRY gene - codes for Transcription factors control expression of other genes (found on X chromosomes)
Sustenacular (Seritoli) cells produce Anti-Mullerian Hormone (AMH)
Sustenacular cells are cells in the semeniferous tubules
The production of AMH is controlled by at least two autosomal gene loci. One codes for the
hormone and one for its receptor.
Appropriately, the gene is expressed only in Sertoli cells of the primordial gonad shortly
before testis differentiation.
The SRY gene is believed to initiate the development of the testes by repressing an X-linked
gene, the "Z" gene, which would otherwise direct the fetus toward female development.
[IGNORE: A complex series of steps must occur in gonadal differentiation. A number of genes are critical
to appropriate male genital development. SRY (sex determining region of the Y chromosome), a gene on
the short arm of the Y chromosome, is a testis determining factor. The SOX9 gene is also important in
male sexual differentiation. DAX1, an orphan member of a nuclear hormone receptor family located on the
X chromosome, interacts with steroidogenic factor 1 (SF-1). Other genes involved in male gonadal
differentiation include the tumor-suppressor gene WT1 (Wilms' tumor 1), and the M lerian inhibiting
substance gene (MIS) and its receptor, MIS-R.]
http://www.carolguze.com/text/442-6-sexual_differentiation.shtml
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Internal structures
Recall, hormones work by connecting with receptors on target cells
Wolffian Ducts are male structures
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Androgens govern the development of human external genitalia. Exposure to androgens beginning
around the eighth week of pregnancy causes undifferentiated tissue to develop in the male form. In the
absence of androgens development is in the female form. This effect is independent of the genetic sex of
the fetus.
http://salmon.psy.plym.ac.uk/year1/psychosexualanimation/psychosexualDifferentiationAnimations.htm
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The colors shown below illustrate homologous sexual structures, those that share the same
embryological origins.
http://images.google.com/imgres?imgurl=http://faculty.southwest.tn.edu/rburkett/A%26P
%2520Hu6.jpg&imgrefurl=http://faculty.southwest.tn.edu/rburkett/A%26P%2520Human
%2520Development%2520%26%2520Body%2520Sections.htm&h=406&w=542&sz=59&tbnid=FM3EiQNlEIJ:&tbnh=97&tbnw=130&hl=en&start=13&prev=/images%3Fq%3Dsexual%2Bdevelopment
%26svnum%3D10%26hl%3Den%26lr%3D%26sa%3DG
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1. Anus
2. Labioscrotal folds
3. Legs
4. Genital tuber
7. Urethral groove
8. Urogenital folds
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Think about the various points in the development pathway.
Things can go differently, in a variety of places
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46,XX testicular disorder of sex development is a condition in which individuals with two X chromosomes
in each cell, the pattern normally found in females, have a male appearance. People with this disorder
have male external genitalia. They generally have small testes and may also have abnormalities such as
undescended testes (cryptorchidism) or the urethra opening on the underside of the penis (hypospadias).
A small number of affected people have external genitalia that do not look clearly male or clearly female
(ambiguous genitalia). Affected children are typically raised as males and have a male gender identity.
At puberty, most affected individuals require treatment with the male sex hormone testosterone to induce
development of male secondary sex characteristics such as facial hair and deepening of the voice
(masculinization). Hormone treatment can also help prevent breast enlargement (gynecomastia). Adults
with this disorder are usually shorter than average for males and are unable to have children (infertile).
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The receptors on target cells are non-functional or only partly functional ==>
make testosterone but you are not aware of it
Do have testes -- they are just on the inside; they do have the SRY gene
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Defect in the androgen receptor (testosterone and DHT)
Androgens are steroids
Receptors are located inside cell and carries hormones to the DNA where they act to turn on other genes
(hormones cross cell membrane)
Must have receptor to function!
Many different mutations exist, many different alleles ==> many different phenotypes
Totally non-functional receptor ==> full Androgen Insensitivity Syndrome (AIS)
AIS individuals present as normal appearing females who are tall (due to the Y chromosome
genes) and thin with primary amenorrhea (no menstruation).
When karyotyped they are found to be 46,XY and upon physical examination will have a
blind vagina and internal testes.
The gonads must be removed in an XY female because they have a high probability of
developing gonadal blastomas (cancer).
At the opposite end of the spectrum, those with milder mutations are normal appearing
males with reduced fertility.
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Diagram may be incorrect
SRY Gene present ==>
Testes are produced
AMH (Anti-Mullerian Hormone) is produced so internal female structures
disappear
Ressive gene, autosomal Don’t make 5-Alpha Reducase which converst Testosterone into DHT
(dihydrotestosterone)
==> appears female on the outside
The described clinical abnormalities range from infertility with normal male genital anatomy to
underdeveloped male with hypospadias to predominantly female external genitalia, most often with mild
clitoromegaly. The uterus and fallopian tubes are absent because of the normal secretion of the m lerianinhibiting factor. Testes are intact, as are wolffian structures (epididymis, vas deferens, seminal vesicles).
Male internal ducts are present but terminate either in a blind pseudovaginal pouch or on the perineum. A
hypoplastic prostate may be present, regardless of degree of undervirilization of the external genitalia.
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Autosomal Recessive disorder
5-alpha-reductase deficiency (5-ARD) is a condition caused by a mutation of the 5-alpha reductase
gene. !
This gene encodes an enzyme that converts testosterone to dihydrotestosterone (DHT). !
DHT is necessary for the development of male genitalia in utero, and the resulting DHT deficency results
in ambiguous external genitalia at birth. !
The condition affects only chromosomal males (i.e., those with XY chromosomes). Individuals with 5-ARD
lack a uterus and Fallopian tubes (due to the normal action of Mullerian inhibiting factor), and possess
testicles and Wolffian structures. !
Their external genitalia, however, can vary from normal male external genitalia, to ambiguous genitalia, to
normal female genitalia (although with a tendency towards an enlarged clitoris). !
!
In the later cases the Wolffian ducts terminate in the perineum or in a pseudovagina.!
5-ARD constitutes a variety of intersexualism.Individuals with 5-ARD have XY chromosomes and
testicles, and tend to have a vagina and labia, but with a small penis capable of ejaculation instead of a
clitoris (this penis, however, appears to be a clitoris at birth). !
These individuals are normally raised as girls. However, come puberty, adenal glands produce testerone,
their testes will descend, their voice will deepen, muscles build to masculine physique and they often will
develop a male sexual identity. !
No breasts or menstruation. Clitoris can enlarge so large that it appears penis like. !
However, they develop only limited facial hair, and will not experience male-pattern baldness.!
!
Presentation of males at puberty
Clear signs of virilization predominate at this age
. The escutcheon is male in distribution. The phallus exhibits definite enlargement
. The shoulders are relatively broad and the hips are narrow
. Muscularity and body hair may increase.
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During the early 1970s, Dr. Julianne Imperato, a Cornell endocrinologist, conducted an expedition to the
Dominican Republic to investigate reports of an isolated village where children appearing to be girls turned
into men at puberty.
In the village, these children were known as 'guevedoces' (literally, eggs/balls at 12 years).
Also known locally as machihembras ('first women, then man'), these pseudohermaphrodites were
documented serially in the following photographs published originally in the American Journal of Medicne
(Am. J. Med. 62: 170-191, 1977):
In an isolated village of the southwestern Dominican Republic, 2% of the live births were, in the 1970's,
guevedoces (actually male pseudohermaphrodites). These children appeared to be girls at birth, but at
puberty these 'girls' sprout muscles, testes, and a penis. For the rest of their lives they are men in nearly
all respects (see photograph 6 below). Their underlying pathology was found to be a deficiency of the
enzyme, 5-alpha Reductase.
There is VIDEO Segment on “The Third Sex”
http://www.usrf.org/news/010308-guevedoces.html
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1.  At 18 months, the appearance is female though un-descended testes are present.
2.  Lacking dihydrotestosterone (DHT) in utero, this boy's external genitalia develop as female.
However, internally the gonadal tissue is that of normal male and his karyotype is 46 XY
(normal male). There are no internal female structures because the AMH was present and they
degenerated.
3.  In utero, DHT is essential for the normal male development of the external genitalia. After
complete maturation, DHT seems to have no important biological function.
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Just before puberty, prior to the testosterone outpouring, the phenotype is still female
With the testosterone surge at puberty, the phenotype changes to male: the voice deepens, the
testes descend, the phallus grows, erection and ejaculation begin, and a male psychosexual
orientation develops.
Presentation of males at puberty
Clear signs of virilization predominate at this age
. The pubic hair is male in distribution. The phallus exhibits definite enlargement
. The shoulders are relatively broad and the hips are narrow
. Muscularity and body hair may increase.
No breast development is generally present
. A prominent Adam's apple may start to develop.
Facial hair develops.
The child's voice may begin to deepen
. The mucosa of the vaginal introitus remains atrophic in appearance (remaining red) rather than the
thickened pink of estrogen-stimulated mucosa.
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And for the rest of their lives, the guevedoces resemble the other Dominican men in all respects
except:* Beard growth is scanty. * There is no hairline recession. * None has acne. * The prostate
remains small.
Today: Specific inhibition of 5-alpha Reductase is the mechanism of action of the prostate drug,
finasteride (Proscar), which in adults, shrinks the prostate without affecting the male phenotype.
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Adrenal glands secretes too little cortisol (stress hormone); doesn’t do negative feedback on pituitiray
(ACTH); much ACTH produced which stimulates not only cortisol production but androgens (testosterone)
from adrenal gland
Remember:
a child will develop female external genitalia unless it is exposed to dihydrotestosterone (DHT)
a child will develop male external genitalia if it is exposed to dihydrotestosterone
If XX fetus exposed to high androgens levels, then ambiguous/male external genitalia develop.. CAH is
one form of pseudohermaphroditism.
Also called androgenital syndrome (AGS)
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congenital adrenal hyperplasia
Most common cause of ambiguous genitalia
b XX "male" - Congenital Androgenital Syndrome (CAS) not in XY individuals
chromosomal sex is female (XX); gonads are ovaries with oviducts, uterus, and vagina (inside)
external genitalia appear male-like with penis and scrotum but vaginal opening may be present
adrenal glands larger than normal and produce increased amounts of testosterone
inherited as autosomal recessive
Such ambiguous genitalia can now be corrected surgically at birth or soon afterward.
Injections of cortisol can reduce the amount of testosterone produced
Other problems: salt balance and dehydration
Autosomal recessive with 100s of possible alleles; variations exist in phenotypes
(Rtphoto: http://salmon.psy.plym.ac.uk/year1/inttopic/gender.html#)
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Male Mounts
Female
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Feminization of male rat by castration in infancy
Early brain organization determines the adult's reaction to gonadal hormones.
(A)  An male rat castrated at birth reacts to an injection of estrogen (red) by exhibiting lordosis, a female
sexual response.
(B)  A normal male injected with estrogen shows no lordosis response because the presence of
testosterone (blue) in his brain shortly after birth established male circuits and inhibited the
development of female circuits. The blue dot within the rat represents the testes.
(C)  The activational effects of the hormones testosterone, estrogen and progesterone were discussed in
the last lecture. Activational effects refer to effects in the adult organism. Organisational effects
occur during the early development of an animal Castration of male rats in infancy causes them to
become◦ demasculinised and◦ feminised Treatment of female rats with testosterone in infancy causes
them to become◦ masculinised and◦ defeminised
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Summary showing effects of male castration and female testosterone treatment
Adult sexual behavior in the rat depends on whether the brain was organised by gonadal
hormones during the first few days after birth.
Normal adult males display mounting behavior because their brains were subjected to a dose of
testosterone from the gonads just after birth. The same effect can be produced in females by injecting the
hormone testosterone. Depriving the male pups of testosterone by castrating them at birth results in a
female brain organization. As adults these feminized males, like normal females, display very few attempts
to mount but a high frequency of lordosis when mounted.
http://salmon.psy.plym.ac.uk/year1/SEXDIFF.HTM
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CAH = Congenital Adrenal Hyperplasia
Ehrhardt (1975) studied 17 female CAH patients: age 4.3 to 19.9 years, most of the girls were in middle
childhood and early adolescence.
The comparison sample (n=11) consisted of the girls' sisters who did not have CAH.
All the patients were under long-term corrective treatment with replacement cortisol and had undergone
surgical correction of the external genitalia, usually in infancy or early childhood.
Interviews with children and their mothers, fathers and siblings were tape-recorded. Interview transcripts
were rated according to coded scales to elicit information about the child's behaviour.
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Girls with CAH were more often described as having high levels of energy expenditure compared to their
unaffected siblings.
They also tended to prefer to play with boys rather than other girls.
Although they tended to start fights more frequently than their sisters, this difference was not statistically
significant.
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This diagram shows that girls with CAH were not very interested in playing with dolls, instead they tended
to play with cars, trucks and blocks; toys that are generally preferred by boys.
They showed little interest in future roles as brides or mothers, but were much more concerned with their
careers.
Their relatives described them as being indifferent to - or avoiding - contact with babies.
For example, they did not participate in caring for infants at home or go out baby-sitting.
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Relatives and girls with CAH describe themselves as 'tomboys' during all of their childhood.
35% of the sample were unsure or said that they might have chosen to be a boy if they could start their
lives over again.
However, Ehrhardt points out that none of the girls were unsure about their gender identity.
They did not feel that they were boys and being a girl did not make them unhappy.
In other words - as a group - they did not exhibit gender dysphoria.
Conclusion: CAH appears to have a significant effect on gender role behaviours.
Patients exhibit significantly more male-typical behaviors than unaffected siblings.
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They were big muscular plain women, complete with Adam's apples.
Both had some facial hair. Tamara had thick muscular thighs like a weightlifter, and a powerful torso with just the barest suggestion of
breasts showing through her singlet.
As spectators watched the two women go into action, waves of buzz ran through the stands.
Instantly the Press sisters were pegged as the latest "monstrosities." Tamara, the older and bigger of the two, provoked the most
curiosity and outrage. .
Right away the grumbling and rumors went to orange-alert level.
Not only were the Press sisters trained by millions of Soviet rubles, but no "normal" women could perform like they did.
They must be using some kind of unfair advantage.
There was buzz about drug use. Though the IOC had not yet outlawed doping, some athletes on both sides were already pumping
their performance with amphetamines, anabolic steroids, etc.
Indeed, many in sports were OK with men bulking up on steroids Allegations had it that communist women, notably the Press sisters,
were being forced by their governments to use a lot of steroids.
It was NOT OK for women to look and act like Superman. But most of the buzz about the Press sisters focused obsessively on
their gender. They couldn t possibly be real women.
"Real women" were what the most popular American athletes looked like. For instance the "graceful" Wilma Rudolph, whose three
gold medals in track gave Americans one of their few happy moments in Rome.
The Presses had to be men in women's clothes. The IOC should demand to look inside the sisters shorts to see if the right sex
organs were there
http://www.outsports.com/history/gendertesting.htm
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The test made its first appearance in 1966, at the European Track and Field Championships in budapest.
In its first and most primitive form, it was a physical exam.
The women had to stand naked before a panel of gynecologists and submit to having their bodies and genitals
fingered. There had to be a real vagina, and no penis.
Some women felt horribly degraded by the ritual grope, and said so. Their countries complained to the IOC.
In 1968, reacting to this criticism, the IOC hastened to substitute a new, less invasive technique at the Mexico City
summer games.
The buccal smear made it possible to examine a woman's sex chromosomes under a microscope, in cells swabbed
from the inside of her mouth.
If female gender was "verified" in the form of two X chromosomes, the woman got a certificate that let her compete.
If anything different was seen, the ax fell. The IOC allowed her to pretend sudden injury or illness, and go home
quietly.
But her future in international competition was over -- the International Amateur Athletic Federation (IAAF), the Asian
Games, the Commonwealth Games and others were adopting the test.
Buccal Smear stayed as the test even tho the medical community found it unreliable
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1964
In 1967, Polish sprinter Eva Klobukowska was eliminated from the European Cup, banned from
competition and publicly humiliated worldwide, all because she had an XXY result, one chromosome too
many to be declared a woman. She probably had AIS (Androgen Insensitivity Syndrome)A few years later,
she became pregnant and gave birth to a healthy baby.
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At virtually every Olympic event, however, abundant rumors circulated;
in one instance, this author was informed that women athletes who were detected as "positive" were
instructed to feign injuries or in some cases were actually fitted with casts.
In 1 celebrated case, a Spanish hurdler, Maria Patino, was publicly disclosed after failing her femininity
test during an event in Tokyo, at the cost of public disgrace and loss of her athletic scholarship.
It took 2 years and the active intercession of a number of medical authorities for Ms. Patino, who has
androgen resistance( AIS), to be reinstated
It was this test that Maria Patino took in 1985 to prove she had no unfair advantage over the
other women hurdlers. When her results came back, however, there were no Barr bodies in
her cells - genetically she was a male, the test said. Meet officials told her she would not be
allowed to compete, and advised her to fake an injury and leave. But convinced that she was
just as female as the other competitors, she continued training and entered a meet in Spain
several months later. Ignoring a warning not to compete from the president of the Spanish
athletic federation, she won her event, but the following week she was kicked off the Spanish
national team, stripped of her titles and barred from competition. Two and a half years later
she was reinstated by the International Amateur Althetics Federation
Buccal test looked for the presence of barr bodies. She had no Barr body so she couldn’t be
female.
AIS
http://christielee.net/med9.htm
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Circumstances such as these and the efforts of a number of dedicated professionals resulted in some
changes by the early 1990s.
The International Amateur Athletic Federation (IAAF) for a Workshop on Methods of Femininity
Verification held in late 1990 in Monte Carlo concluded that laboratory-based sex determination should be
discontinued,[9] a recommendation that was accepted shortly thereafter by the IAAF and subsequently by
all but 4 of the international athletic federations.
The IOC, however, instead replaced sex chromatin with DNA-based methods to detect Y chromosomal
material, principally the SRY sex-determining locus on the Y chromosome, implementing this procedure at
the 1992 winter games in Albertville.[10]
At the insistence of the organizers, the 1996 Summer Olympic Games in Atlanta included a
comprehensive process for screening, confirmation of testing, and counseling of individuals detected.
Eight of 3387 female athletes (1:423) had positive test results. Of these, 7 had androgen insensitivity, 4
incomplete, and 3 complete; the other athlete had previously undergone gonadectomy and is presumed
to have 5-alpha-steroid reductase deficiency.
All individuals were given appropriate gender verification certificates and were permitted to compete.[11]
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After the Atlanta Olympics, efforts continued to persuade the IOC to abandon gender verification.
Indeed, by the time of the 1996 Summer Olympic Games in Atlanta, essentially all of the relevant
professional societies had endorsed resolutions that called for elimination of gender verification, including
the American Medical Association, the American Academy of Pediatrics, the American College of
Physicians, the American College of Obstetrics and Gynecology, the Endocrine Society, the Lawson
Wilkins Pediatric Endocrine Society, and the American Society of Human Genetics.[12]
It was argued that the current clothing used in athletic competition, as well as the requirement that
urine for doping control be voided under direct supervision, made it virtually certain that male
impostors could not escape detection[7];
Furthermore, gender verification procedures are complex, expensive, and counterproductive.[11]
Still, it was not until the IOC's Athletes' Commission called for discontinuation of the IOC
system of gender verification that the IOC's executive board, at its June 1999 meeting in
Seoul, decided to discontinue the practice on a trial basis at the forthcoming summer
Olympic games in Sydney. The proposal by the Athletes' Commission, similar to the IAAF
plan that has been in place for track and field since the early 1990s, permits intervention and
evaluation of individual athletes by appropriate medical personnel if there is any question
regarding gender identity.[13] Since the IAAF policies were instituted in 1992, this has never
been invoked
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http://www.time.com/time/world/article/0,8599,1919562,00.html
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From the NYT:
The testing done on Semenya takes weeks to complete. It requires a physical medical evaluation, and
includes reports from a gynecologist, an endocrinologist, a psychologist, an internal medicine specialist
and an expert on gender. The effort, coordinated by Dr. Harold Adams, a South African on the I.A.A.F.
medical panel, was conducted at hospitals in Berlin and South Africa.It is unclear what the exact threshold
is, in the eyes of the I.A.A.F., for a female athlete being ineligible to compete as a woman.
2012: For the 2012 Games, officials have implemented a test of testosterone levels. However, unlike past
tests which were given to all competitors in women's events, this test will be administered only when the
chief medical officer of a national Olympic committee or a member of the IOC's medical commission
requests it. The new rules disqualify athletes from women's events if they have testosterone levels in the
normal male range, which is 7 to 30 nanomoles per liter in the blood. The top range for women is just
below 3 nanomoles per liter. Athletes with complete androgen insensitivity will be allowed to compete.
Under current IOC rules, transsexuals (those who have had a sex change from male to female) can
compete in women's events at the Olympics as long they wait two years after the operation and are
undergoing hormone therapy.
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Still, it was not until the IOC's Athletes' Commission called for discontinuation of the IOC system of gender
verification that the IOC's executive board, at its June 1999 meeting in Seoul, decided to discontinue the
practice on a trial basis at the forthcoming summer Olympic games in Sydney.
The proposal by the Athletes' Commission, similar to the IAAF plan that has been in place for track and
field since the early 1990s, permits intervention and evaluation of individual athletes by appropriate
medical personnel if there is any question regarding gender identity.[13]
Since the IAAF policies were instituted in 1992, this has never been invoked, nor is it likely to be in Sydney
under the circumstances described above, especially because of the requirement for freshly voided urine
for doping testing.
NOTE: Meanwhile, on the U.S. political front, gender realities continue to be ignored by many
conservatives -- as in Texas, where the 4th Court of Appeals ruled in 1999 that only couples with standard
XY and XX chromosomes could be married
http://www.outsports.com/history/gendertesting.htm
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http://salmon.psy.plym.ac.uk/year1/psychosexualanimation/psychosexualDifferentiationAnimations.htm
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Female (left)
Red: genital tubercle develops into glans clitoris
Blue: abioscrotal fold develops into labia majora
Green: urogenital fold develops into labia minora
Dark Green: cloacal membrane develops into urogenital membrane
Male
Red: genital tubercle develops into glans penis
Blue: labioscrotal fold develops into scrotum
Green: urogenital fold develops into scrotal raphe
Dark Green: cloacal membrane develops into urogenital membrane
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Black: anus
Female:
Dark Green: Vaginal Orifice
Male:
Green: scrotal raphe developed from fused urogenital folds corresponds to labia minora
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Female
Dark Green: urethral groove develops from urogenital membrane
Male
Dark Green: urethral groove develops from urogenital membrane
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Female:
Blue: labia majora developed from labioscrotal fold corresponds to scrotum
Red: Glans Clitoris
Light Green: labia minora developed from urogenital fold corresponds to scrotal raphe
Light Green circle: urethral orifice forms end of developed urethral groove
Dark Green: vaginal orifice
Black: anus
Male
Blue: scrotum developed from labioscrotal folds corresponds to labia majora
Red: glans penis developed from glans tissue corresponds to glans clitoris
Lt Green: scrotal raphe developed from fused urogenital folds corresponds to labia minora
Dark Green Circle: urethral orifice forms end of developed urethral groove
Black: anus
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