HughE Said

You say your Mom was prescribed "progesterone" (which usually means progestins). Does that mean you were exposed to progestins rather than DES? If so, that would support a theory I have that progestins can have similar effects as far as male development is concerned as DES (which if true is quite important, because some progestins are still being given to prenant women).

My Mom was prescribed BOTH DES and progesterone. I was born in 1971. My Mom tried to get pregnant from the year 1962 onwards. In 1967 they declared her infertile. In 1970  August 1970 she began bleeding heavily and was found to have a tubal pregnancy. They started her on both before I was conceived and was kept on it while I was in the womb.  Now I am here today.

A review of my symptoms pre HRT:

* long, slender arms and legs Yes
* feminine looking facial features No
* legs significantly longer than the height of your upper body Yes
* an armspan more than 3cm greater than your height No
* sparse or very fine body hair No
* a female pubic hair pattern (like an upside down triangle and confined to the pubic area) No
* an inability to build upper body muscle Yes
* gynecomastica No
* a female carrying angle Yes, 18°
* a female digit ratio Right hand only

  I had higher than normal T male levels before HRT and during the 6 month time off of Spiro a year ago. Muscle mass gain during HRT could be attributed to a low number of T receptacles in my muscles with possibly higher E ones. Possible due to the lack of T receptacles in certain areas of my body that the effect of the pre-natal DES might have been more selective in my body. The pituitary gland may have allowed that high amount of T in my system to compensate. An increase of prostate problems above the average male over 50 appears to be a symptom of DES sons as well. It is to this late transitioner.

Joelene

I've just set up a photobucket account, so I can share some images here in support of my theory that, through the use of DES as a miscarriage treatment, doctors, the FDA, and the pharmaceutical industry have inadvertently created somewhere in the region of 5 million people, born between 1940 and the early 80s, who have male bodies but brains that developed as female instead of male.


From this diagram you can see that male genital development is already complete by 13 weeks after conception, the only ongoing processes after that point being elongation of the penis and descent of the testicles. It follows that testosterone suppression during the 2nd or 3rd trimester will have minimal effects on the genitals - the penis will just end up shorter than it would otherwise have been, and the baby might be born with undescended testicles or abnormalities associated with testicular descent (such as hydrocele or inguinal hernia).

The standard treatment protocol with DES involved a dose that progressively escalated over the course of the pregnancy, so that by far the heaviest exposure to the drug occurred during the second half of the pregnancy:


(excerpt from "DES: the Complete Story")

This excerpt also gives some idea of the colossal doses that were being used. Gram for gram, DES is roughly the same potency as ethinyl estradiol, so 125mg per day (or even 5mg per day) represents an enormous amount of artificial estrogen. This excerpt also highlights an often overlooked part of the DES story: that DES was often co-prescribed with progestins, most of which at that time were derivatives of testosterone.


This is a slide taken from a webcast about the importance of prenatal testosterone in determining which sex your brain develops as. The earlier diagram about genital development (which shows relatively flat T levels for the duration of the pregnancy), is an oversimplification, and there's actually 2 peaks of T production that are implicated in masculinisation of the brain, one about 17 weeks after conception and the other at about 30 weeks. I think that in my case the first one was more or less completely wiped out by exposure to artificial female hormones, but the second one occurred more or less as normal. The result is that, psychologically, I'm not really a man or a woman but kind of a mixture of the two. There's also been an effect on my body's ability to control hormones, but more on that later.


(excerpt from "Brain Sex" - click on image to enlarge it)

What this shows it that it's been known for a long time (the book was published in 1989, and the research they're discussing was carried out in the 1970s), that prenatal exposure to artificial hormones results in behavioural alterations later in life - feminized behaviour in males exposed to DES, masculinized behaviour in females exposed to artificial androgens (first generation progestins, danazol or anabolic steroids).

One minor quibble is that they've either poorly explained or misunderstood what happened, with their comment about why behaviour was feminized, even though the genitals developed as male. As I was saying earlier, I think that is just a matter of timing. Due to the way DES was being administered, I think testosterone production generally only started to be heavily suppressed after genital development had already completed, and so you've ended up with people with relatively normal looking male genitals, but brains that developed as female instead of male. If DES had been administered in heavy doses from beginning to end, I think the resulting "DES sons" would have had female reproductive organs as well as female brains.

It wouldn't have been apparent at the time "Brain Sex" was written, but I bet if you went back and talked to those hormone-exposed people now, you'd find that a lot of them are trans.

As discussed in this paper:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3146061/

both male genital development and masculinization of the brain are driven by the action of testosterone (and its derivative DHT), not by whether you have a Y chromosome or not. In that paper they induced male development in genetic females by administering testosterone or DHT to the mother. It's only reasonable that administering a testosterone blocking drug (such as DES) to pregnant women should produce the reverse effect, of female development in genetic males. Based on everything I've seen since I first started looking at all this in 2011, that's exactly what's happened with DES, only the numbers affected are so large and the blame for what happened so widely spread that nobody is prepared to admit what happened, and the whole thing's been covered up.

I can't believe that I have never heard of this before. It answers so many questions. I was born in 1957. My mother said that she had a hard time carrying a baby. And her Dr.  told her that if she was ever going to have one it had to be right away. She had me and then had a hystorectomy soon afterward. This helps explain my small stature , low sperm count , cyst on testicles , low sex drive. I am a walking poster child for this and never knew it....WOW !!!! Wouldn't be surprised when I go in for blood tests for HRT that my levels may be closer than I think.

Yep, you're far from alone. Those sort of effects seem to be really widespread among DES "sons".

I recently found a free to view version of a paper, "Follow-up study of Male and Female Offspring of DES-Exposed Mothers",
http://journals.lww.com/greenjournal/Abstract/1977/01000/Follow_up_Study_of_Male_and_Female_Offspring_of.1.aspx

Click on "PDF" and you can download a full copy of the paper.

Although it was fine a couple of days ago, the link wasn't working when I tried it just now, so I've put a copy of the PDF on my Google Drive, just in case anyone has trouble accessing that one:
https://drive.google.com/file/d/0B-U464GiBN9tdjJFQ1FHcG9wUGs/view?usp=sharing

Table 1 shows the (absurdly high) doses that were being used under the standard "Smith and Smith" regimen for prevention of miscarriage (which is what the people in this study were exposed to):

This is of a drug with similar potency to ethinyl estradiol, something which is normally dispensed in micrograms, not milligrams!

If you look at this page about prostate cancer treatment:
http://www.hrpca.org/estrogens.htm

DES at doses of between 1 and 3 mg per day will completely suppress testosterone production in adult men (1mg per day is usually enough; 3mg invariably causes total testosterone suppression).
(as an aside, considering the increased risk of thromboembolism with even those comparatively low doses, there must surely have been a lot of fatalities amongst the women given DES miscarriage treatment!)

Anyway, what this shows is that the exposure was relatively modest during the critical period for genital development (7 - 12 weeks after conception), but very high (50mg+ per day) throughout the second half of the pregnancy, which (according to the monkey research) is when the differences between male and female brains arise. Unless a developing fetus is somehow magically immune to the effects of DES, that makes it more or less inevitable that anyone who was exposed to this treatment had their testosterone heavily suppressed throughout the critical period for sexually dimorphic brain development, which, in theory at least, should result in the brain developing as female instead of male.

Although this particular paper was only looking at the physical effects of DES exposure, there's still some very useful information from it - that there were much higher rates of genital abnormalities and signs of incomplete masculinization among the DES sons than the control group, and even more significantly, massive differences in fertility between the two groups.

"The most striking results are related to the sperm count. The average value of sperm density (count/ml) is approximately 2 times (factor of 1.93) lower in the DES-exposed group...The average quality score is in the pathologic range for the DES-exposed group (6.9) and normal for the control group (1.4.)...Ejaculate volumes of less than 1.5 ml were observed in 10 out of 39 subjects (26%) in the DES-exposed group versus 0 out of 25 in the control group...The results show that only 14 of 39 (36%) of the DES-exposed group can be classified as normal whereas the control group shows 18 of 25 (72%) with normal scores...11 of 39 (28%) of the DES-exposed group received scores greater than 10, classified as "severely pathologic", whereas none of the 25 subjects in the control group received this score."

If sperm counts are on average halved, then production of that other thing the testicles make - testosterone - has probably been halved too. That would explain why I, and seemingly a high percentage of DES sons, have developed a "eunuchoid" body structure and other signs of undervirilization.

It's also completely at odds with what the CDC says on its DES sons page:
http://www.cdc.gov/des/consumers/about/effects_sons.html

DES Sons are not at an increased risk for infertility

Obviously both statements can't be correct, either Bibbo et al (and quite a few people that I've chatted to on facebook and on this forum it seems) were somehow mistaken, or the CDC are telling a pack of lies. I think it's the CDC, and the FDA before them. They, the pharma industry along with whatever doctors were in the know, have all closed ranks to cover up the fact that, through promoting and prescribing this phoney quack remedy DES, they've inadvertently created several million people who are genetically male and were assigned male at birth, but have various intersex-related abnormalities and female brains.

Born between 1940 and 1971 (US) or 1980 (elsewhere) - Yes - 1962

Undescended testicles - No

Micropenis - a fully formed but considerably shorter than normal penis - Meh.... it was unremarkable

Hypospadias - No

Epidiymal cysts of the testicles (these are apparently Mullerian remnants - fragments of female tissue that would have been absorbed in normal male development) - Not sure

Vestigial female organs or organ remnants - Not that i'm aware of

Intersexed genitals similar to grade 3 PAIS - No

Other genital abnormalities - Yes - Found out i'm infertile when the ex and I tried to start a family. Got a brief exam down there and the doc noted what he thought was a varicocele. Don't know if there is anything else going on.

Feminine-looking facial features, developing a body structure that's more like the female members of your family than the male ones - Yes! Look at my avatar picture - female. I have always had a feminine face

Other symptoms of low testosterone such as a lack of body hair, gynecomastica and an inability to build upper body muscle - Yes - very little body hair, small wrists and ankles, feminine legs and butt, my feminine face

Very shy, socially passive behaviour as a teenager - Yes!

Difficulty forming friendships with boys; having a special affinity with girls - Yes

Being bullied a lot; having an inability to fight back - Oh Lord yes!

Having no interest in sport - I royally sucked at playing pretty much all of them, and being a physically small kid the deck was stacked against me.

People tending to assume you're gay; lots of men being attracted to you - Not sure about this one; maybe. No one ever hit on me in an obvious gay pick up attempt, but guys would take a look at me and would immediately not respect me.

Identifying as a woman, or part of you identifying as a woman while part identifies as a man - Yes, I even thought I was nonbinary for a time.  I don't ID as male at all anymore.  It was just part of an act that kept me from getting bullied.

Depression- Yes, but I'm not since transitioning.

ADHD - Ye..... what were we talking about again?

Other seemingly non gender related psychological problems - Yep - Alcohol abuse and some other stuff.

The weird thing about me is that my mom swears she didn't take DES when she was carrying me. Yet, the infertility, the abnormalities on my testicles, my very feminine appearance, and the fact that I am a transsexual all seems to fit perfectly with in utero DES exposure. This was the early 60's and there were all kinds of shenanigans going on with the chemical and pharmaceutical companies back then so who knows what I might have been exposed to it if wasn't DES.

I also was a physically small guy (110 lbs, 5'7", size 26 waist jeans) until I was about 25-26 and then I had a growth spurt and I filled out. I still don't know what that was all about.

I have assumed for years that DES was to blame for my GID.  Born in 1966 with my mom on a number of doctor prescribed things including vitamins which back then carried DES. 
I have two kids though, grew lots of body hair, had a feminine body, curvy hips (wah.. it went away when I filled out around 24), feminine bones, etc, etc, etc... I'm not just mentally a girl but have physical traits too. 
My hormone levels don't seem too crazy though. 

I very well could have been.  Our local hospital was/is used as a teaching facility.  I was born in late '68 and have always had slender arms that were highly resistant to building muscles.  When I come out to my mothere I'll have to ask her.  I'd always wondered if there might be some kind of link between gynecomastia and my gender disphoria.  Funny, when they started to grow I wanted them to grow more. 

-Alana

Quote from: HughE on January 15, 2015, 09:04:50 AM
"The most striking results are related to the sperm count. The average value of sperm density (count/ml) is approximately 2 times (factor of 1.93) lower in the DES-exposed group...The average quality score is in the pathologic range for the DES-exposed group (6.9) and normal for the control group (1.4.)...Ejaculate volumes of less than 1.5 ml were observed in 10 out of 39 subjects (26%) in the DES-exposed group versus 0 out of 25 in the control group...The results show that only 14 of 39 (36%) of the DES-exposed group can be classified as normal whereas the control group shows 18 of 25 (72%) with normal scores...11 of 39 (28%) of the DES-exposed group received scores greater than 10, classified as "severely pathologic", whereas none of the 25 subjects in the control group received this score."

If sperm counts are on average halved, then production of that other thing the testicles make - testosterone - has probably been halved too. That would explain why I, and seemingly a high percentage of DES sons, have developed a "eunuchoid" body structure and other signs of undervirilization.

I've made a couple of posts on another thread expanding on what I've said there, so I thought I'd transfer the gist of them to this one, in case anyone's interested and to keep everything in the one place.

In Bibbo 1977 (where the above quote came from) and a couple of other papers I've seen looking at the same cohort of DES sons, they're briefly mentioned the results of blood tests of the DES sons vs controls. The total T is a bit lower on average, but the results don't look very different from the control group. However, the blood work they've published is incomplete. All they've shown are the total testosterone, LH and FSH. They haven't shown two key measurements: sex hormone binding globulin (SHBG), and free testosterone.

Free T, not total T, is the important thing as far as the biological effects of T are concerned. SHBG is important because, if it's high, then it binds up almost all of the T in your body and you can end up with what looks like a quite respectable T level based on total T, even though free T is well below normal. From reading what people have said in some hypogonadism forums I belong to, a common problem they encounter through badly administed T replacement is that their estradiol (E2) goes high, and this in turn causes their SHBG to go high. They end up with what looks like quite a respectable total T level, but their free T remains low, and they continue experiencing the symptoms of hypogonadism.

The ideal SHBG level for males is apparently around 20 ng/dl. In the blood work I've had done, and in the blood work of 2 DES sons I've chatted to about this, our SHBG levels have all been around 40 ng/dl. None of us know our E2 levels (doctors hardly ever request E2 in blood work for males), however I've got gynecomastica and so has at least one of the DES sons I've been chatting to. As most of you probably know, breast development is a good indication of higher than normal male E2!

What I think is going on is that, in biologically male people who've been feminised by prenatal exposure to drugs such as DES, our bodies try to generate a hormonal state in between male and female. They do this by increasing E2 production to above normal male (perhaps by ramping up expression of the aromatase enzyme), and reducing T production to about half normal male. As a side effect, the lowered T production means the testicles don't grow to full size and only produce about half as much sperm as normal. Meanwhile, the elevated E2 causes SHBG to rise well above what it would otherwise have been, and all this excess SHBG results in a large reservoir of inactive T, which means the total T doesn't look too bad even though both the production and consumption of T are only about half of normal.

All this is speculation of course, since none of us had our hormone levels tested in our 20s, and the published research hasn't included measurements of SHBG or free T. However it would tie in with my developing a eunuchoid body structure and other signs of low T, something which (judging by the comments on this thread and what I've seen people saying on facebook), happens a lot amongst DES exposed individuals!

The two DES sons I've been chatting to (both of whom have gender dysphoria, but for personal reasons aren't currently in a position to transition), both have symptoms of hypogonadism and were refused treatment by their doctors because their T levels were "normal". One had a total T of about 500 ng/dl and the other 350ng/dl (which is actually well below normal), however the free T in both cases was very low - 60pg/ml and 71pg/ml, due to their SHBG being quite high. I don't have their blood work written down, but from memory the one with total T 500 had SHBG 45 and free T of 60 pg/ml, the one with total T 350 had SHBG about 35 and free T of 71 pg/ml. These are extremely low values for free T.

From a study aimed at determining what T levels should be in normal, healthy men:
http://press.endocrine.org/doi/full/10.1210/jc.2010-3012

"In a reference sample of 456 men, mean (sd), median (quartile), and 2.5th percentile values were 723.8 (221.1), 698.7 (296.5), and 348.3 ng/dl for TT and 141. 8 (45.0), 134.0 (60.0), and 70.0 pg/ml for FT, respectively. In all three samples, men with low TT and FT were more likely to have slow walking speed, difficulty climbing stairs, or frailty and diabetes than those with normal levels. In EMAS, men with low TT and FT were more likely to report sexual symptoms than men with normal levels. Men with low TT and FT were more likely to have at least one of the following: sexual symptoms (EMAS only), physical dysfunction, or diabetes."

I read this as saying that "normal" (within 1 standard deviation of the mean) total T in men ranges from 500 to 950 ng/dl, and free T 100 to 195 pg/ml. If your total T is below 348 or free T below 70 pg/ml you're in the bottom 2.5 percent of the range, the people with "slow walking speed, difficulty climbing stairs, frailty and diabetes". Both of the people I've been chatting to have free T levels at or below 70 pg/ml, and problems with low enegy, depression, brain fog, ED etc, typical symptoms of hypogonadism. One has already developed type 2 diabetes which has become insulin dependent. Yet they've both been refused treatment by their doctors. I don't know what doctors are basing these decisions on, but it certainly isn't based on science or improving the health of their patients!

Going on my experiences, your body seems to be able to handle having abnormally low hormone levels OK while you're young, but as you get older the hormone imbalance gets worse and worse, and you start developing all sorts of health problems as a result in middle age. Incidentally, going on female HRT protects you from all this, because the estradiol you take as part of your HRT replaces the missing T.

Those two haven't yet started on any kind of HRT. Unfortunately I don't have any blood work from prior to taking hormones, but here's two sets of blood work I had done last year, by which time I'd been on fertility meds for about 3 years.

In this first one,



I'd been taking my usual combination of fertility meds (clomid and HCG) and progesterone cream. Everything in that test looked OK, not just that part of the panel but everything else too (apart from my cholesterol being slightly elevated, but not enough to warrant taking action).

Using a separate online calculator, my calculated value for free T is 128 pg/ml, which is just a little bit below the average for free T (141.8 pg/ml) in that study of healthy men I linked to earlier. I felt pretty good the day of that test, alive, full of energy and with no aches or pains.

In this second test,


(15.2 nmol/L = 438 ng/dl)

I'd stopped taking fertility meds for 5 days. You can see how the total T has fallen by about a third, and the LH and FSH readings have basically collapsed. The FSH is flagged as being below the lower limit of the lab range (and probably the LH reading would have been too, except there would still have been some HCG in my system, which shows up as LH unless they do a special test to exclude it). That second test is basically what secondary hypogonadism looks like - LH and FSH are low, and so is total T.

Using the online calculator, my free T would have been 86 pg/ml, so it had fallen below the "normal" (100 - 195pg/ml) range for healthy men, but was still higher than what the 2 people I've been chatting to are having to put up with. I'd felt rough the day before the test and quite unwell on the morning the blood was drawn (I was actually supposed to wait a further 2 days before having it done, but by that stage had decided enough was enough, why make myself sick for a further 2 days).

Unfortunately, the doctor I saw following that second blood test (who is the senior doctor at that practice) turned out to be a total bastard. He refused to refer me on to an endocrinologist, or for a DEXA scan to assess my bone density, or for an MRI scan to see whether I have a brain injury that might explain my being hypogonadal. This is despite the fact that, apart from the blood work, I look kind of intersexed, and a physical examination would show that I have eunuchoid proportions and other symptoms of hypogonadism. I got a very strong impression that, if it had been up to him, I wouldn't have even had the tests I've had done, and I was quite lucky that I saw a junior doctor there on my first couple of visits who ordered them for me. So I'm not sure what was going on there, perhaps the practice has to bear some of the costs for those tests, or maybe he was just one of those doctors who turn eugenicist when dealing with trans and intersex folk. Either way, he's basically trying to condemn me to a slow and horrible death, and it hasn't done a lot to restore my faith in medicine. It makes me wonder how many other people like me are out there with endocrine systems damaged by drugs such as DES, whose health is now failing as a result, and are being lied to and denied treatment by their doctors.

Interesting:
http://www.jaacap.com/article/S0890-8567(09)64914-5/abstract
"This report concerns the role of prenatal hormones in normal and abnormal psychosexual differentiation. Several studies indicate that perinatal treatment of infrahuman female mammals with diethylstilbestrol (DES) masculinizes certain features of their brain and behavior."

Quote from: anjaq on January 24, 2015, 09:54:42 AM
Interesting:
http://www.jaacap.com/article/S0890-8567(09)64914-5/abstract
"This report concerns the role of prenatal hormones in normal and abnormal psychosexual differentiation. Several studies indicate that perinatal treatment of infrahuman female mammals with diethylstilbestrol (DES) masculinizes certain features of their brain and behavior."

They haven't said what animal species they were studying in the abstract, however I gather that DES causes brain masculinisation in the two most commonly used lab animals, rats and mice. This is because, in rodents, brain masculinisation is mainly driven through estrogen receptors rather than androgen receptors. In rodent fetal brain cells, testosterone is converted into estradiol via the aromatase reaction, and this estradiol then activates estrogen receptors and switches on their genes for brain masculinisation. However, that's something that appears to be specific to rodents. It doesn't apply to human beings or Rhesus monkeys anyway. There's two lines of evidence showing this, firstly this paper:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3146061/

in which two androgenic hormones, testosterone (aromatatizable) or DHT (non-aromatizable), both proved equally effective in masculinizing female monkeys' brains. This shows that estradiol isn't necessary for brain masculinization in Rhesus monkeys, and is a strong indication that the whole thing's being driven through androgen receptors, not estrogen receptors.

Secondly, there's the fact that CAIS women seem to universally identify as women, and have female rather than male behaviour. The sole difference between CAIS women and the genetically male people who turn into men is that they have a mutation which renders their androgen receptors inoperative, so all their development takes place as if there were no androgenic hormones present. Their aromatase enzyme, estradiol production and estrogen receptors are all completely unaffected by the mutation. If brain masculinisation were driven through estrogen receptors in human beings, there'd be large numbers of FTM CAIS women queing up for SRS etc. That's not what happens though, which basically proves that brain masculinization in humans is essentially entirely driven through androgen receptors, and estrogen plays no role.

That one odd quirk of rodent physiology appears to have led to a lot of confusion about the effects of DES on human beings, and to most researchers in the field barking up completely the wrong tree (as the paper you've linked to shows). DES is a powerful testosterone-suppressing drug, and the standard dosing scheme for miscarriage prevention resulted in doses more than 10x higher that what will totally suppress testosterone in an adult man, being administered throughout the second half of the pregnancy (which appears to be the crucial time as far as the brain development responsible for gender identity later in life is concerned).

   Hi Hugh, your testosterone description was interesting.My tt just before hrt was almost 1400 but the FT was only 80 and my e was over 40. The other one was tested also and was high but I am to lazy to look for it right now.They also checked a couple of more and I believe they were very borderline also.All that is ancient history now as my levels look like what I am  a woman.

   Hey Hugh I have another question. Has there been any research on those of us with cysts being more prone to hernias. My father his brother and myself all had to have the lower unit screened due to hernias. As far as I know my brothers did not have the cyst and never had to have a hernia repair.

Hi Hugh,

My being intersex my T before hrt was 38 while my E was 74 pg/ml. As a female hermaphrodite(Yes, I hate the "H" word and prefer IS. but for purpose of others understanding what I am it will suffice). Being born in 1964 I'm quite confident I may fall in this group despite being genetically female and the fact I was born on a reservation. I was also an 8 month preemie too but being a preemie I doubt has anything to do with it.

I truly thank you for all your work and study, also your time it took to research the information you've posted here. Finally i may possibly have some answers to the many questions i have, but am unable to ask my biological mom given she's deceased.

Again, thank you.
Ally

Quote from: justpat on January 25, 2015, 06:19:04 PM
   Hey Hugh I have another question. Has there been any research on those of us with cysts being more prone to hernias. My father his brother and myself all had to have the lower unit screened due to hernias. As far as I know my brothers did not have the cyst and never had to have a hernia repair.

Yes. I was born with a hydrocele, which worsened during my childhood until a loop of my intestine forced its way through the gap, producing an inguinal hernia.

I've recently found a paper which confirms that defects involving incomplete closure of the Processus Vaginalis (inguinal hernia, hydrocele, and cryptorchidism), and epididymal abnormalities, are all linked defects.
http://www.ncbi.nlm.nih.gov/pubmed/8911389

Association of epididymal anomalies with patent processus vaginalis in hernia, hydrocele and cryptorchidism.
RESULTS: A closed, partially closed and open processus vaginalis was associated with an abnormal epididymis in 14, 36 and 69% of cases, respectively. Epididymal anomalies were more frequent in association with undescended (72%) than descended (34%) testes.
CONCLUSIONS: These data confirm the observation of a higher incidence of epididymal anomalies associated with patency of the processus vaginalis irrespective of testicular position, and they support the theory that androgenic stimulation may be required for closure of the processus vaginalis as well as epididymal development.

Since epididymal cysts are a very common marker of DES exposure, in my mind, the likely explanation for these defects all being linked is that they're all common side effects of DES exposure, and a lot of the people who have them are DES babies (particularly in light of them also talking about a lack of androgenic stimulation as the cause!).

http://en.wikipedia.org/wiki/Processus_vaginalis

something  to  keep  in  mind. 
  back  when,  was  not  the  age  of  information.    so  mom  walks  into  the  docs  office,  the  rabbit  dies,  and  shes  handed  a  handfull  of  pills. 
  back  then,  there  were  no  real  questions,  or  answers.  mom  just  swallows  the  pills,  as  doctor  knows  best.
  I  read  stuff  on  this  issue  a  decade  ago.    most  women  simply  dont  know  if  they  took  it,  or  if  they  did,  in  what  frequency, duration   or  dose. 
  paper  records,  long  lost.  deceased  mothers,  long  list  that  makes  the  info  hard  to  find. 
  there  was enough  info  and  research  to  say  it  could,  and  probably  did  have  some  effect,  but  past  that,  its  history,  plain  and  simple. 
my  mom  passes  last  feb,  in  1014.  she  was  born  in  1917.    she  was  43  when  i  was  born.  I  am  57.   there  are  studies  that  suggest  a  womans  age affects  transgender  identifacaton,  especialy  if  conception  was  during  the spikes  or  lulls of  hormone  producton  of  menapause. 
  at  a  point,  we  are  what  we  are.  we  cant  change  it,  most  wouldnt  if  they  could. 
  point  being,  unless  there  are  underlying  medical  issues,  dont  lose  the  sleep  over  it. 

Quote from: lilredneckgirl on January 30, 2015, 01:05:24 AM
she  was  born  in  1917.    she  was  43  when  i  was  born.  I  am  57. 

I know this is silly but I just have to ask.   Something doesn't add up, 1917 + 43 = 1960, then you should be 55 or 54.  You're younger than you think ;-)

Paige

I recently acquired a book about medical diasters, "Worse than the Disease", that includes a fairly substantial section on DES. This is what the authors had to say about the role of the regulatory authorities in the disaster.


They're talking about the FDA and USDA, however, as I was saying earlier, it looks like much the same applies to the CDC too. I've just found a transcript of a teleconference in which a bunch of senior doctors at the CDC are blatantly lying about the incidence of genital abnormalities and fertility disorders in DES sons.
http://www.cdc.gov/des/consumers/tele/DESSonsTeleconference.pdf

Referring back to what it says in the paper I've linked to earlier (with similar findings in two other studies of that group of DES sons, the Dieckmann cohort).
"The most striking results are related to the sperm count. The average value of sperm density (count/ml) is approximately 2 times (factor of 1.93) lower in the DES-exposed group...The average quality score is in the pathologic range for the DES-exposed group (6.9) and normal for the control group (1.4.)...Ejaculate volumes of less than 1.5 ml were observed in 10 out of 39 subjects (26%) in the DES-exposed group versus 0 out of 25 in the control group...The results show that only 14 of 39 (36%) of the DES-exposed group can be classified as normal whereas the control group shows 18 of 25 (72%) with normal scores...11 of 39 (28%) of the DES-exposed group received scores greater than 10, classified as "severely pathologic", whereas none of the 25 subjects in the control group received this score."

Compare that to what the senior CDC official in the teleconference, Dr. Titus-Ernstoff, says:

"As most of you know, DES exposure has strong effects on fertility and reproductive outcomes in women. Consequently, the influence of DES on these outcomes in men is of key interest. Results from a few studies, including those based on the Dieckmann and Mayo men, provide little evidence of sperm abnormalities, although one study suggested that sperm motility might be lower in the DES exposed men. DES exposure does not appear to be associated, however, with low sperm counts or with Eliasson scores, which seem to be unaffected by DES exposure. "

There's no two ways about it, she's telling a total pack of lies!

Reading through it, that whole teleconference was nothing short of a whitewash. Along with outright lies about the incidence of genital abnormalities and fertility disorders, they've dodged the gender identity issue and talked about sexual orientation instead. I don't see how it can be a mistake or misunderstanding. The whole thing reeks of a cover up to me.

Looking at the Q&A section, some very valid points were raised which the CDC officials completely evaded:

Q:
"Dr. Titus-Ernstoff, I am with the DES International Network, and I'm pleased to connect with you and Dr. Messing as well. We've not had a chance to actually talk before, but I think it might be worthwhile in the future.
I have a question briefly. Our network is about five years old, and I'm quite familiar with your research study on psychosexual effects and have been through actually the entire range of studies going back to the 1970s that have looked at psychosexual effects and gender issues in DES exposed people. I wonder if you would briefly just address the question of why it could be possible that although your study seems to be finding "no or very little impact on adult sexual behavior," we have, in fact, in our network found over 100 individuals with known or likely exposure who also have a history of gender variance experiences or transsexualism."

A:
"Sure. I'd be happy to address that. First of all, I think what I'd like to do is talk about why you are seeing something that's very different from what we've seen. I think that we can start with the possibility that some of the people that are in the network do not have confirmed DES exposure. A very important strength of the NCI study is that every single person in that study has DES exposure confirmed by medical records. While medical records may not be infallible, that's about as close to perfection as we can get."

What she fails to mention is that, firstly, in their research, they were only looked at sexual orientation, not gender identity. Since they never looked for it, it's hardly surprising they found no effects on gender identity. Secondly, the study group of DES sons they used, the Mayo cohort, aren't typical DES sons at all - their average exposure was much lower than under the standard "Smith and Smith" regimen for prevention of miscarriage (720mg over the course of of a pregnancy vs 12 grams under "Smith and Smith", according to one of the CDC's own papers, or a 15x lower dose than most typical DES babies were exposed to).

...
Q:
"Yes. I have a question, please. My son, I was a DES mother, and it wasn't found until he was 40 that his testicles did not develop. What I was wondering, they did the testosterone test on him, but I worked in the medical field ,and what I was wondering, is it important to monitor the testosterone and the estrogen level? Because from what I understand if the estrogen level creeps up sometimes that can destroy the testosterone. I may be wrong. I don't know."

A:
(a completely nonsensical answer from one of the other Drs at the teleconference to what was a very valid question)

...

Q:
"Hi. Given Dr. Titus-Ernstoff's psychosexual study did not include gender identity and given the large amount of studies which indicate that proper testosterone levels are very important to the masculinization in men ... and that many university lecturers discuss the relationship between prenatal hormone levels and gender identity, i.e., Harvard Medical School, University of South Florida, etc., and even the Merck Manual states biological factors such as gender complement and the prenatal hormone largely determine gender identity, does the CDC have any plans to acknowledge any of these studies and university lecturers and their continuing research on DES exposure to genetic males?"

A:
"...In our study, we had a hard time evaluating homosexual orientation, even though it's not that rare. To look at something more subtle, like gender identity, or more rare, like transsexuality, would be almost impossible in our study..."

Really? Being trans is harder to spot than being gay? What planet do these people live on? From memory it was something like 150 out of 500 DES "sons" who identified as women in the Kerlin/Beyer study, which is hardly rare either.

The whole thing just reinforces my opinion that there are plenty of people in the pharma industry and the upper echelons of organisations such as the CDC and FDA, who know all too well about the link between DES exposure and trans/intersex, and they've all closed ranks to keep the public and the unfortunate victims in the dark about it.

Quote from: HughE on January 30, 2015, 09:10:20 PM
The whole thing just reinforces my opinion that there are plenty of people in the pharma industry and the upper echelons of organisations such as the CDC and FDA, who know all too well about the link between DES exposure and trans/intersex, and they've all closed ranks to keep the public and the unfortunate victims in the dark about it.

Thanks HughE,

Interesting reading.   It's interesting that the U.S. avoided the Thalidomide horror story, but didn't manage to avoid the DES mess.  On the other hand, if you look at all the things being done by chemical and pharmaceutical companies during this time, I'm guessing they just got very lucky with Thalidomide.

Paige

HughE, thanks so much for this series of posts regarding DES.  I recently had a bout of testicular pain, and at age 61 and a DES son, this was particularly alarming.  In the ultrasound, sure enough, multiple epididymal abnormalities were noted.  By the time I got to see a urologist, though, the pain had gone away, so he dismissed the abnormalities when he found out that I was a DES son.

Another thing that's odd is my body's reaction to T and to E.  I've been on light doses of both at different times in my life.  (I'm currently considering transition, so I'm pre- a normal transitioning dose of HRT.)  T made me angry, sullen, depressed, in short a real a** to live with.  E on the other hand calmed me, made my anti-depressant work better and improved my overall focus and mental abilities.  That shouldn't have happened if I were a "normal" male.

I'm also quite hypo-thyroid, the first instance of such in either side of my family.

Some else here mentioned a growth spurt at age 25 or so.  I had that same experience.  I was this skinny underdeveloped something until around that time, then bam, finally grew shoulders and chest and began to look a lot more "male-ish", at around 24 or 25. 

In any case, it's apparent that DES upended the normal operation of my endocrine system as well as causing all of the developmental issues.

Thanks again.  This has made fascinating reading.