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Androgen Insensitivity Syndrome (AIS), complete (CAIS), partial (PAIS), mild(MAIS)


What is Androgen Insensitivity Syndrome?

CLICK HERE for an in-depth overview of AIS from the AISSG
CLICK HERE for the complete Wikipedia page on AIS

Having AIS means that the body is unable to process (insensitive to) male hormones (called androgens).

AIS is a genetic condition that is caused by a recessive gene which is passed from a mother to a child. AIS or the body's inability to process androgens or male hormones (like testosterone,) affects every person differently that has this recessive gene.
Therefore it operates on a spectrum: some people with AIS are relatively responsive to androgens and have a MILD form; others whom are less responsive to the hormones have a PARTIAL form, while others are COMPLETELY unable to use the androgens.
AIS is not completely uncommon. Estimates put children born with a form of AIS between 1 in every 20,000 babies
with XY chromosomes. There may be even greater numbers since these numbers only reflect medically reported and recognized cases.
These numbers probably do not take into account men that are very minimally affected with a mild form or MAIS, who might not even know that they have it. They may develop as completely 'normal' male or may have only slight issues with virilization.

A mother that is a carrier of the recessive gene for AIS is generally not affected by the gene, but may pass the gene to her children that are genetically XY. She may also have
children with XX chromosomes and some might also be carriers of the recessive gene.
In each of her pregnancies there is a 1 in 4 chance she could have a:
'Normal' XY boy, or
AIS
XY baby, or
'Normal' XX girl, or
Carrier
XX girl
During the fetal stage of development, the body forms basic gonads that either distend and become testicles or remain within the body and become ovaries. A fetus with the recessive gene that causes AIS cannot respond to their own chromosomes properly resulting in the range of this intersexual condition, based on the individual's level of sensitivity to androgens.
Sometimes with partial AIS or PAIS it can lead to ambiguous genitalia or complications with some genital formations. Some of these individuals are diagnosed earlier in life, while others may not be and may also develop pubic and axillary hair or might possibly have an enlarged clitoris. Children with PAIS or with CAIS may also be born with bi-lateral hernias as babies.
When a child is born with complete AIS or CAIS, the baby will probably outwardly appear as a completely 'normal' female. She will typically be raised as a woman and may have internal 'gonads' that produce testosterone, which the brain alters to estrogen for her. Since male hormones are responsible for sexual virilization or facial, pubic and underarm hair, a person with CAIS may have little, if any.
Some of these women do not even find out about having AIS until in their late teens or after puberty when the diagnosis is established because of a lack of menses or a period.

A person with CAIS (although XY) is destined to look female as they cannot take male hormones to change the body's appearance or thus have a 'sexual reassignment' to look male (since the body can't process them). Studies have shown that most women with CAIS (although they technically have XY chromosomes) would not typically choose to be male and are not typically confused about their gender role. Gender identity and genetics are not always one in the same; one's chromosomes do not define "WHO" they are.
Many ("XY") women with forms of AIS have a "blind" ended vagina that can range from very shallow to 3/4 the size of a 'normal' XX woman; and vaginal sexual intercourse is possible for many others with dilation or surgical lengthening, should that be their choice.
Many intersexual XY women with AIS have their internal 'gonads' removed due to an increased cancer risk. Women with CAIS do not have ovaries, fallopian tubes or a uterus and therefore cannot bear children. Many women with AIS take Hormone Replacement Therapy or HRT to replace the estrogen that is lost from removing the gonads.
Having AIS does NOT necessarily imply being inclined to identify one's self specifically with either gender, as this may also occur on a spectrum of feeling more linked to one gender rather than another, or neither, depending on the individual. Having AIS does not imply being homosexual, or having any specific sexual preference. It may not necessarily lead to having gender dysmorphia or the feeling of being "trapped" in the wrong gender. Individuals with intersex conditions might not necessarily consider sexually reassigning themselves (as transsexuals do) or desire to change appearance to become androgynous, or to "gender bend" like transvestites do.
There is debate in both the medical and intersex communities about when is the right time to (if ever) remove the internal gonads or in the cases of PAIS when there is ambiguous genitalia, when to assign a gender.
According the the US-AIS Support Group AISSG- "Based on conservative estimates of frequency, approximately 8000 women in the US and Canada have a DSD (Disorder of Sex Development) identified as Partial or Complete Androgen Insensitivity Syndrome"
Some former terms for AIS have included:
Testicular Feminization Syndrome (Testicular Feminisation Syndrome) or (TFS), Feminizing Testes Syndrome (Feminising Testes Syndrome), and Male Pseudo-hermaphroditism, - all of which are no longer preferred terms since they are inaccurate and stigmatizing.

Some synonymous terms for AIS have included:
Androgen Resistance Syndrome, Morris's Syndrome (CAIS), Goldberg-Maxwell Syndrome, Reifenstein Syndrome (PAIS), Gilbert-Dreyfus Syndrome (PAIS), Rosewater Syndrome (PAIS), Lubs Syndrome (PAIS)
Karyotype=46,XY
Women with a 46,XX karyotype that have the gene for AIS in their family may not have any symptoms/notable physical effects but can possibly be a carrier for the recessive gene.

Other biological conditions that can lead to intersexuality -
XY conditions other than AIS:
5 alpha-reductase deficiency, 17-beta-hydroxysteroid dehydrogenase deficiency, XY or pure gonadal dysgenesis (Swyer Syndrome), Leydig cell hypoplasia, ovo-testes, Mixed gonadal dysgenesis, embryonic testicular regression syndrome, persistent müllerian duct syndrome, Denys-Drash Syndrome, Smith-Lemli-Opitz Syndrome,
XX conditions other than AIS:
Mayer Rokitansky Kuster Hauser (MRKH) Syndrome, Mullerian dysgenesis, vaginal atresia.
More conditions that CAN lead to intersex conditions include but are not limited to:
Congenital adrenal hyperplasia (there are different forms), Klinefelter's Syndrome-XXY, XYY Syndrome, XXYY Syndrome, Turner Syndrome-X, Triple X Syndrome, XXXX Syndrome, XXXXX Syndrome, and sometimes Mosaicism and Chimerism

Hermaphrodite VS. Intersex- the preferred and MORE ACCURATE terminology


AND NOW...ON TO THE BLOG POSTS:

Saturday, May 10, 2008

Great Article on Genetics: The X-factor

The New York Times: 'The Wild Side' Column/Opinion- by-Olivia Judson
Posted: May 6, 2008, 8:19 pm
"When Genes Go Retro"
For the full article please follow this link
The article begins with "Pssst! I’m going on a tour of the genome — want to come?" and takes you on a wild ride into our genetic makeup.
This week, a very astute member of the intersex community, whom shall be referred to as "K" made a wonderful summary of this article in a way that was easy to understand which follows here:

"This is definitely a really cool article, and she does a great job of
explaining where new genes come from. This is how scientists have
come to understand how new species arise, specifically through the
development of brand-spanking new traits in older, familiar species.
For example, a species of cat might evolve that's better able to see
in the dark because of a specific protein that's expressed in its
eyes. None of the other cats in the world have this protein--it' s
just this one, special cat who does, and if she passes that new gene
along to her kittens, then we might have a new, more nocturnal
species of cat.

This doesn't really apply to our conditions, though. The genes that
make us insensitive to androgens, or deficient in 17-b hydroxysteroid
dehydrogenase or 5-a reductase, are already coded in the DNA of the
human species. They've been there for millions of years, and they're
the basis of how people become male or female. What happens to most
of us (as I understand it) is that we happen to get copies of the
genes that have "typos" in them. Nothing new is made, it's just a
change in the original copy. Before it gets passed on, DNA has to be
duplicated, like making a Xerox, and it's really easy for there to be
a single change in the new copy. Sometimes the changes are silent
(like you might not notice if someone wrote "your" instead of
"you're"), but other times they're more important and have a bigger
impact (like "I have dogs" and "I hate dogs"). Like Dr. Quigley
says, in the grand scheme of things, this is like 1 letter in 1 book
of an entire volume of encyclopedias, but if the "typo" is in the
gene that makes the body sensitive to androgens, for example, it will
change the way the gene is "read" and have an impact on how the body
develops.

I know this probably sounds like silly stuff, but I think it's
amazing that this is how it works--it's what motivates me to learn
about biology! Especially since these "typos" are SUPPOSED to happen--
it's how species evolve and people look different from each other.
It's all part of an amazing, gorgeous, and unending ballet! The only
problem is that we, as a society, can't really appreciate the
beautiful differences, so we decide that they're "wrong." That's
what the problem is--not the gene or the body it helps create, but
the inability of other people to understand how perfect it all is."

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