It's time to put
what we have learned about DES together and ask a few questions. On
this page I summarize the things DES can do and then look at some
dosages used in cohort studies. The results are quite startling. I
then ask some pertinent questions.
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DES can affect development
in numerous ways.
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[1] Inhibits
androgen receptor binding16), so the effects of testosterone on the cell are diminished.
"At high dosage, on the other hand, DES produced an
opposite effect, inducing hypospadias and inhibiting prostate growth and
AR binding activity."
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[2] Lower the over all testosterone
levels 27): "DES inhibits luteinizing
hormone secretion by the pituitary, there by inhibiting testosterone secretion."
167)
" In analogy with animal studies showing strong
activational effects of androgens on nuclear AR-ir, the present data
suggest that nuclear AR-ir in the human MBC is dependent on the presence
or absence of circulating levels of androgen."
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[3] DES is a potent synthetic estrogen,
so it can bind to cells estrogen
receptors. It also interferes with Mullerian Duct Regression 125).
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[4] Transgenerational effects are
also being investigated 124).
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[5] Toxic
: Capable of causing injury or death. In fact a recent paper designed
to downplay the psychosexual effects of DES inadvertently indicates
that the death rate to males exposed in utero is 2.5 that of the
control group "Briefly,
1% of the poten-tially eligible women (exposed or unexposed) and 3% of
the men (5% exposed, 2% unexposed) had died before the combined study was implemented ".83) "Diethylstilbestrol can cause fetal toxicity
when given to pregnant women" 27).
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Normally the mother's
estrogen, which passes to the fetus via the placenta, binds with proteins,
making it inert, and thus protecting the fetus from its effects. However,
these proteins do not bind effectively to DES. If they did, then none of
the physiological effects DES is known to cause would occur.
Ample proof exists that prenatal DES exposure affects the physiological
development of the human fetus (CDC , very cautious about what they say). Given this
and given present research on the effects of hormonal exposure on the
physiological and neurological development on the non human fetus, is it
irrational to conclude that DES also has the potential to affect the neurological
development of a human fetus? Was the dosage negligible?
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If we roughly equate the potency of DES to Premarin (see dosing for prostate
cancer: conjugated estrogen's versus diethylstilbestrol). During the course
of a pregnancy, expectant mothers were given up to 11 times the total
amount a transitioning m-to-f transsexual would take during the same period
of time (5mg/day). To start lets look at a table provided by the
NIH on Cohort study dosages 240) .
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From - the web site of the Law Offices
of Aaron M. Levine & Associates 10):
"The drug manufacturers who jumped on the
DES bandwagon either never made the computations or didn't care, but
the recommended dosage of DES given to pregnant women, shown in Slide
B, was the equivalent of the estrogenic effect of 55,666 birth control
pills."
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Slide B of the above
link is a Smith & Smith regimen, enlarging the slide so that it is
easily legible and then adding up the recommended dosage for a pregnant
mother between week 7 to week 35 equals 11.725 grams of DES. (Dosage
varied from week to week but the lowest dosage was 5mg/day) As we will
see below only 3mg/day is required to chemically castrate an adult
male.
Using typical (US) hormone regimens for male to female transsexuals 20)
as a comparison:
In addition to anti-androgens and progesterone one regimen includes
about 5mg of Premarin a day. During the same period of time
(35-6=29 weeks = 203 days) a transitioning adult male would ingest about
1.015 grams of Premarin.
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If we compare the dosage
to that given adult males for the treatment of prostate cancer (see below),
we see that only 3mg a day of DES is required to chemically castrate
an adult male.
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Suggested Dose Options for the use of DES in the
treatment of prostate cancer in adult males: "There
is an abundance of information indicating that 5 mg is too high a dose
given the side effects and that lower doses have similar efficacy against
prostate cancer with a lower toxic profile. The 5mg/day dose results
in castrate levels of testosterone as does the 3mg/day dose. A dose
of 1mg/day is not sufficient to reduce serum testosterone to castrate levels
in all patients. However, the 1mg/day and 3mg/day doses have equivalent effects
on prostate cancer (6)."
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IF
genetic males with cloacal extrophy reassigned
to female at birth and raised as female have male gender identities similar
to people with 5-alpha reductase,
and if
people who are genetically male with CAIS
have feminine gender identities,
and if
the gender identities of people genetically
male with PAIS and partial gonadal dysgenesis range from masculine to
feminine and some switch genders as they mature,
and if
at the cellular level prenatal DES exposure
(higher dosage) equals a combination of chemically induced PAIS (milder
forms) and chemically induced partial gonadal dysgenesis,
then ...........
IF
In the mouse and rat you can do prenatal
or neonatal treatment with estrogens or androgens to feminize or masculinize
behavior,
and if
the behavior of a female rhesus monkey can
be masculinized by prenatal exposure to androgens,
and if
researchers are sure that prenatal hormone
exposure affects the sexual dimorphic development of the mammalian brain,
then ...........
IF
Universities and colleges teach courses
which discuss the possible effects of prenatal hormone exposure on the
development of the brain and thus changes in behavior,
and if
the infamous Dr. John Money, who is the
founder of the “psychosexually neutral theory,” is now admitting that
prenatal hormone exposure may play a part in the formation of gender
identity,
then ...........
What’s wrong with this picture?
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