Listen to what Hugh Easton has to say. We know many DES sons who can confirm that yes, it did happen.
” Among my first discoveries were that I have a type of body structure that’s usually associated with intersex conditions, and that I have symptoms of acute hypogonadism. Basically, my body doesn’t make enough testosterone. Then, I came across a passage in the book “Brain Sex”, about a pattern of very shy, socially withdrawn behaviour that was often seen in teenaged boys who’d been prenatally exposed to an artificial estrogen called DES. It was virtually a perfect match for my own teenage years.
Shortly after that, I joined an online group of DES sons. It was like walking into a disaster zone, with everyone in the group appearing to suffer from health problems of various kinds, including hypogonadism, and various intersex-related abnormalities. One of the first things I noticed was that it was supposed to be a group for DES sons, yet most of the people posting stuff were using women’s names! I later discovered that these people had actually been assigned male at birth… “
Sex can be much more complicated than it at first seems. According to the simple scenario, the presence or absence of a Y chromosome is what counts: with it, you are male, and without it, you are female. But doctors have long known that some people straddle the boundary – their sex chromosomes say one thing, but their gonads (ovaries or testes) or sexual anatomy say another. Parents of children with these kinds of conditions – known as intersex conditions, or differences or disorders of sex development (DSDs) – often face difficult decisions about whether to bring up their child as a boy or a girl. Some researchers now say that as many as 1 person in 100 has some form of DSD.
Claire Ainsworth, Sex redefined, nature, 18 February 2015.
Today the SRY gene is understood as one among the many essential mammalian sex-determining factors that are involved in the genetic pathways of both testicular and ovarian determination. Mammals require cascades of gene product in proper dosages and at precise times to produce functioning male and female gonads, and researchers recognize a variety of healthy sexual phenotypes and sex determination pathways in humans.
In fact, the sex you develop as isn’t directly genetically determined at all, but instead depends on the action of gonadal hormones during the critical period when your prenatal development is taking place. All the X and Y chromosomes do is determine whether you develop testicles or ovaries, it’s the hormones produced by those organs that actually determine whether you develop as male or female.
Unfortunately, most doctors and pharmaceutical industry decision makers also subscribe to the myth that sex is genetically determined, which is why they’ve not appreciated the dangers of giving hormones to pregnant women, and why we’ve ended up in a situation we’re in today (where large numbers of people have been born who’ve undergone partial or complete opposite-sexed brain development, as a result of being exposed to hormone-disrupting drugs such as DES – find out more about DES studies on gender identity).
Sex isn’t chromosomes: the story of a century of misconceptions about X & Y, newstatesman, 23 FEBRUARY 2015. Chromosomes by C. Smith.
The influence of the XX/XY model of chromosomal sex has been profound over the last century, but it’s founded on faulty premises and responsible for encouraging reductive, essentialist thinking. While the scientific world has moved on, its popular appeal remains.
In 1983, researchers “ identified the way DES causes cancer as being through it inducing aneuploidy, or abnormal numbers of chromosomes in cells. It interferes with the process of allocating chromosomes during cell division, so that some cells end up with too many or too few chromosomes. These cells can later become cancerous.
This is something that appears to be related to it’s chemical structure rather than it acting as an estrogen, since tamoxifen, a drug which is an antiestrogen, but whose chemical structure shares some similarities with DES, causes similar changes to cells and is also a carcinogen.
This book appears to confirm that DES induces cancer through inducing aneuploidy, not by acting as a hormone. ”
1983 Study Abstract
Diethylstilbestrol (DES) has been demonstrated previously to induce morphological and neoplastic transformation of Syrian hamster embryo cells in the absence of any measurable induction of gene mutation. To determine if DES induces cell transformation by a genetic mechanism at the chromosomal level, the effect of DES on structural aberrations and numerical chromosome changes was examined in asynchronous and synchronized cells. Over the concentration range which is optimal for cell transformation, DES failed to induce any increase in chromosome aberrations in the cells. In contrast, significant numerical chromosome changes were observed in DES-treated cultures. The percentage of metaphases with a near diploid chromosome number increased to 19% at 48 hr after treatment. By comparison, cells from control cultures contained only 1 to 2% aneuploid metaphases with a near diploid chromosome number. No significant increase in the number of metaphases with a near tetraploid number (>70) of chromosomes was observed in the DES-treated cultures. DES induced both chromosome loss and gain, and no significant difference was detected between the number of hyperdiploid and hypodiploid cells. Chromosome loss or gain was observed for chromosomes in each karyotype group. These findings suggest that DES induces chromosome nondisjunction. Synchronized cell cultures were obtained by first growing the cells in 1% serum and then in 10% serum with hydroxyurea which blocked the cells at the G1-S border. Upon release of the hydroxyurea block, the cells entered into S phase in a very synchronous manner. The cells were treated for 3 hr during one of four time periods after hydroxyurea release. During the first period, the cells were primarily in early S phase, while the second period included cells in late S phase. During the third period most of the cells were undergoing mitosis, while in the fourth period most of the cells were in G1 phase, although some mitotic cells were observed. Treatment of the synchronized cells with DES during early or late S phase resulted in little morphological transformation. However, treatment during the third period, when the majority of the cells were in mitosis, resulted in a peak of transformation which was 15 times the level observed in cultures treated in early or late S phase. Treatment during the fourth time period resulted in a reduced level of cell transformation. Treatment of synchronized cultures with DES resulted also in a cell cycle-dependent induction of aneuploid cells which paralleled the induction of cell transformation, with the greatest level observed following treatment during mitosis. No increase in the percentage of polyploid metaphases or chromosome aberrations was observed in the DES-treated synchronized cells. Parallel dose-response curves for cell transformation and aneuploidy induction by DES were observed when the synchronized cultures were treated during the mitotic phase of the cell cycle. Possible mechanisms for DES-induced aneuploidy and the evidence supporting a role for nonrandom numerical chromosome changes in neoplastic development, as well as significance of aneuploidy in cancer, are discussed.
Sources and more information
Aneuploidy Induction and Cell Transformation by Diethylstilbestrol: A Possible Chromosomal Mechanism in Carcinogenesis, Cancer Research August 1983 43; 3814.
This petition is to ask the FDA to acknowledge that, when a pregnant woman is given medical treatment with synthetic hormones, these substances can cross the placenta and cause abnormalities of sexual development in her unborn child, including both physical intersex conditions and transgender.
There are a variety of situations in which medical treatments involving high doses of synthetic hormones are given to pregnant women. Many of these treatments would, if given in the same dose to an adult man, suppress his testosterone production and have other feminising effects on him. Based on my own experiences and what I’ve seen of the effects of an artificial estrogen called DES, they can do the same thing to a male foetus, the main difference being that the effects are permanent. Due to the way foetal development takes place and the fact that most medical use of these drugs tends to be during the second half of the pregnancy, brain development is more likely to be affected than physical development.
Few day later, Brynn Tannehill, Director of Advocacy, SPART*A, published a paper with no less than 15 studies showing a biological origin of gender dysphoria… One of them is a mention about DES: “In this study, more than 150 individuals with confirmed or suspected prenatal diethylstilbestrol (DES) exposure reported moderate to severe feelings of gender dysphoria across the lifespan.”
My own opinion is that DES caused intersexed development in the DES sons by blocking testicular testosterone production. DES is a potent chemical castration agent that for many years the treatment of choice for hormone-sensitive prostate cancer. Just 3mg of DES per day is enough to fully chemically castrate an adult man; the starting dose as a miscarriage treatment was 5mg per day (and often went much higher during the later stages of the pregnancy). It’s a not widely appreciated fact, but male development isn’t driven directly by genes, but instead by hormones (primarily testosterone) produced in the testicles of a male fetus. Given the ability DES has to block testosterone production, it’s no surprise that many DES sons are physically and/or psychologically intersexed. The surprising thing is that there’s so little public awareness of it!
If the problem is just one of testosterone production being suppressed during the critical time sexual development was taking place, then I don’t see any reason for there to be any long term genetic effect or 3rd generation effects. However, one thought that’s occured to me is that DES daughters often have a great deal of difficulty getting pregnant and carrying the pregnancy to term, which puts them at vastly increased risk of medical intervention – and potentially being given hormonal medication during the pregnancy. If one of these hormonal treatments for miscarriage (DES) can cause problems with intersexed development, then the likelihood is that others can too. There’s one drug in particular called hydroxyprogesterone caproate, which is in widespread current use to prevent miscarriages and premature births, and is being given in doses which I’m sure would have some serious gender-bending effects if you were to give the same dose to an adult man.
In short, although DES was phased out 40 years ago, there’s plenty of other sex hormone derivatives still finding their way inside pregnant women and potentially causing many of the same problems. That’s why I’ve been trying so hard to get people to take me seriously, and see whether there’s a link between exposure to these drugs before birth and endocrine and intersex-related problems later in life!
” I’m convinced there’s a major unrecognized problem when exposure before birth to medicines containing artificial female hormones is causing intersexed or opposite-sexed development in males, particularly where brain development is concerned … … The fact that the whole thing with the DES sons has remained a secret for so long has added to my suspicions that there could be similar problems being caused by some of the other pregnancy hormone treatments that are still in current use. ”