Exposure to several factors in utero and in early life may lead to reduced semen parameters in adulthood and potentially to a decline in male fertility
On the question of environmental “endocrine disruptors” as an explanation for a decline in semen quality, Professor Hart added: “The extent of the risk posed by environmental endocrine disrupters is still unclear, but some researchers do attribute the perceived decline in sperm counts to these chemicals within the environment. We do not have any evidence to suggest such a link in our study, but we do intend to measure the fetal exposure to endocrine disrupting chemicals from maternal blood that was stored in 1990, prior to the study recruits’ birth, and to relate these chemical exposures to the men’s semen counts in 2012-3.”
The incidence of testicular cancer has increased among American males over 15 years of age for more than 20 years and while overall incidence is still highest among Caucasian males, the greatest increase was observed in the Hispanic community, according to a new study at the 108th Annual Scientific Meeting of the American Urological Association.
DES Action USAcommented: ” Experts speculate prenatal estrogen exposures may be to blame. All men – and especially DES Sons – should practice testicular self-exam regularly! ”
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!
Les “petits-garçons DES” issus de “grands-mères distilbène” sont 40 à 50 fois plus exposés au risque de malformations du pénis
Une étude montre que les petits-enfants des femmes traitées avec l’hormone de synthèse Distilbène® DES, médicament prescrit aux femmes enceintes jusqu’à la fin des années 70 et sensé prevenir les fausses couches, sont 40 à 50 fois plus exposés au risque de malformations du pénis.
” 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. ”
” … Should the drug DES be recognized as a major cause of transgender and should the public be educated with regard to this, then perhaps over time there may be a change towards those who are transgendered. I am sure that we, as transgendered, would still be open to a lot of prejudice but perhaps not to the extent that we are because we are thought of ‘as just men who want to wear women’s clothes’. Perhaps the slant will over time change to ‘those women who were born into the wrong body’… ”
The orphan nuclear receptor small heterodimer partner mediates male infertility induced by diethylstilbestrol in mice
2009 Study Abstract
Studies in rodents have shown that male sexual function can be disrupted by fetal or neonatal administration of compounds that alter endocrine homeostasis, such as the synthetic nonsteroidal estrogen diethylstilbestrol (DES). Although the molecular basis for this effect remains unknown, estrogen receptors likely play a critical role in mediating DES-induced infertility. Recently, we showed that the orphan nuclear receptor small heterodimer partner (Nr0b2), which is both a target gene and a transcriptional repressor of estrogen receptors, controls testicular function by regulating germ cell entry into meiosis and testosterone synthesis. We therefore hypothesized that some of the harmful effects of DES on testes could be mediated through Nr0b2. Here, we present data demonstrating that Nr0b2 deficiency protected mice against the negative effects of DES on testis development and function. During postnatal development, Nr0b2-null mice were resistant to DES-mediated inhibition of germ cell differentiation, which may be the result of interference by Nr0b2 with retinoid signals that control meiosis. Adult Nr0b2-null male mice were also protected against the effects of DES; however, we suggest that this phenomenon was due to the removal of the repressive effects of Nr0b2 on steroidogenesis. Together, these data demonstrate that Nr0b2 plays a critical role in the pathophysiological changes induced by DES in the mouse testis.