Well-established sex-partner relationships are less common for the DES-exposed
Sexual activity level and sexual functioning in women prenatally exposed to diethylstilbestrol. Helen Taylor.
Study Abstract
Thirty women with a history of prenatal exposure to diethylstilbestrol (DES) underwent a detailed sexual history and were compared to a demographically similar sample of 30 women with a history of an abnormal Pap smear.
The DES women were found to have less well-established sex-partner relationships and less experience with child-bearing, to be lower in sexual desire and enjoyment, sexual excitability, and orgasmic coital functioning, but to be comparable (and low) with regard to such sexual dysfunctions as vaginismus and dyspareunia.
Both potential psychosocial and neuroendocrine explanations are discussed.
DES mothers may manifest increased vulnerability to subsequent stresses in their lives
DES mothers may manifest increased vulnerability to subsequent stresses in their lives. Michael Clesle.
1985 Study Abstract
In utero exposure to diethylstilbestrol (DES) was initially linked to vaginal-cervical cancer and subsequently to reproductive difficulties. These unanticipated and ongoing health risks to female offspring may constitute a chronic source of stress for DES mothers.
We interviewed 60 mothers of exposed daughters and 30 acquaintance controls. Two hypotheses were tested in regard to DES mothers:
DES discovery and its aftermath have a direct, long-term, negative effect on psychological health
and the DES experience intensifies the negative psychological effects of other adverse life circumstances.
To operationalize psychological health, we measured symptoms of “demoralization” and positive health practices–the latter as a behavioral indicator of mastery and personal control. We also measured adversities that may mediate the threat posed by DES, including stressful events, medical problems, and chronic burdens.
We found DES history to be associated with poorer psychological health only when mothers encountered other losses and threats to themselves and their families. We concluded that DES mothers may manifest increased vulnerability to subsequent stresses in their lives.
Sources and more information
Vulnerability to stress among women with in utero diethylstilbestrol (DES) exposed daughters, Journal of human stress, NCBI PMID: 3855173, 1985.
Schweizerische medizinische Wochenschrift, NCBI pubmed 3841230 2;115(44):1555-61, Nov 1985.
Following reports on a few cases in other countries, this 1985 report was the first in a Swiss female, aged 23, with stage III DES-induced adenocarcinoma of the vagina.
1985 Study Abstract
From 1946 to 1971, diethylstilbestrol, a nonsteroid synthetic estrogen, came in for widespread use in the USA, and in other countries only occasional use, for the treatment of high-risk pregnancies.
In 1971 a retrospective epidemiologic study showed a close association of this therapy with occurrence of vaginal and cervical adenocarcinoma in young women (mean age 19 years). Up to 1981 63% of 429 clear cell carcinomas of the vagina and cervix were related to DES exposure in utero in the USA.
Following reports on a few cases in other countries, the present report is the first in a Swiss female, aged 23, with stage III DES-induced adenocarcinoma of the vagina.
The risk of DES-related adenocarcinoma is estimated at about 1%, but benign teratogenic lesions are present in over 50% of patients. Vaginal adenosis is the most frequent finding, but other malformations of vagina (septa), cervix, uterus and fallopian tube may be found. Malformations of the genital tract have also been described in DES-exposed male offspring.
Sources and more information
A case of vaginal adenocarcinoma after uterine exposure to diethylstilbestrol, Schweizerische medizinische Wochenschrift, NCBI pubmed 3841230 2;115(44):1555-61, Nov 1985.
1985 study: the DES women showed increased bisexuality and homosexuality
In this 1985 study, the DES women showed increased bisexuality and homosexuality. Image by torbakhopper.
1985 Study Abstract
Thirty women aged 17 to 30 years with documented prenatal exposure to the nonsteroidal synthetic estrogen diethylstilbestrol (DES) were compared to thirty women of similar demographic characteristics from the same medical clinic who had a history of abnormal Pap smear findings. A subsample of the DES women were also compared to their DES-unexposed sisters. Sexual orientation in its multiple components was assessed by systematic semistructured interviews. In comparison to both control groups, the DES women showed increased bisexuality and homosexuality. However, about 75% of the DES women were exclusively or nearly exclusively heterosexual. Nonhormonal and hormonal interpretations of these findings are discussed.
Sources
Sexual orientation after prenatal exposure to exogenous estrogen,Ehrhardt AA, Meyer-Bahlburg HF, Rosen LR, Feldman JF, Veridiano NP, Zimmerman I, McEwen BS., Arch Sex Behav. 1985 Feb;14(1):57-77. NCBI PMID: 3977584.
Medical hypotheses, Lynch HT, Reich JW, March 1985
Abstract
Diethylstilbestrol (DES) is the first example of transplacental carcinogenesis in humans, as evidenced by an excess of clear cell adenocarcinoma of the vagina and cervix in exposed women.
We hypothesize that:
DiEthylStilbestrol usage review buttress the need for adequate and rigorous research into the use of drugs in pregnancy and ensure that they do more good than harm before being introduced.
in utero DES exposure will be responsible for a broader spectrum of cancer with variable age of onset as a function of latency effects in exposed humans of both sexes;
teratogenicity of DES will be more far-reaching than currently recognized and will harbor cancer implications in the face of known associations between teratogenesis and carcinogenesis;
and genetic heterogeneity will be a critical etiologic discriminant in DES associated cancer.
This hypothesis embraces a prodigious body of data at the infrahuman level, as well as extant pharmacogenetic and ecogenetic observations in humans which signify heritable variations in response to environmental carcinogenic exposures. This hypothesis has important implications for drug testing with appropriate preventive strategies. Herein, particular restraints with monitoring through governmental legal channels must be employed. Past experience has clearly indicated negligence in shouldering this responsibility by both the pharmaceutical industry and government regulatory bodies.
Sources
Diethylstilbestrol, genetics, teratogenesis, and tumor spectrum in humans, NCBI, PMID: 3889564, 1985 Mar;16(3):315-32.
DiEthylStilbestrol studies – DES can induce neoplastic cell transformation, mutagenesis, irreversible binding to DNA and protein and unscheduled DNA synthesis
Estrogen receptor mechanism in uterine target cell. E represents estradiol but can also be substituted by DES. Cytosolic form ofreceptor (RC); activated cytosol receptor (Rc), nuclear receptor (Rn), progesterone receptor (PRc), glucose 6 phosphate dehydrogenase (G6PD), Korach, 1981.
1985 Study Abstract
The site and specificity of the tissue response to a toxicant are of central importance; it is in this area of Diethylstilbestrol (DES) toxicity that the estrogen receptor would appear to play its primary role. Compilation of the various sites of DES toxicity in humans and experimental animals indicates that lesions appear predominantly in estrogen responsive target tissues suggesting that the presence of the estrogen receptor in such target tissues may help govern the tissue specificity of the toxic insult. DES and many of its oxidative metabolites interact with high affinity with the estrogen receptor. Such an interaction may be responsible for localizing DES to target tissues. Autoradiographic and biochemical studies have supported the localization of radiolabeled DES in susceptible tissues. The intracellular mechanism of receptor binding of DES and certain metabolites could then result in mobilization of these compounds to the nucleus. Experimental evidence has shown that DES and a number of its metabolites are able to translocate receptor to the nucleus of uterine cells. Such an action by the receptor results in an increased probability of potential chemical interactions with the genome. The actual induction of a chemical lesion in the target cell may, at this point, proceed by non-receptor mediated mechanisms. For example, studies using in vitro cell culture systems which contain no estrogen receptors have shown that DES can induce neoplastic cell transformation, mutagenesis, irreversible binding to DNA and protein and unscheduled DNA synthesis. These results raise the possibility that a part of DES toxicity may follow pharmacologic principles established for chemical carcinogens. Following induction of the molecular lesion, the role of the receptor continues in this process by mediating increased protein synthesis and mitogenesis in responsive target tissues which ultimately permits a more extensive expression of the toxic effects. It has been demonstrated that DES is a potent mitogen in vivo in both uterine and pituitary tissues, subsequently, the lesion will perpetuate itself through this receptor mediated biological response. This is particularly important since a number of DES induced reproductive tract tumors are expressed only after additional estrogen exposure. While other tumors have been shown to be estrogen sensitive and will regress without continued estrogen stimulation. Therefore, it should be considered that the presence of the estrogen receptor and the estrogen receptor mediated biological responsiveness of a particular tissue are most important in explaining the specificity of DES toxicity.
Sources:
The role of the estrogen receptor in diethylstilbestrol toxicity, NCBI, PMID: 3913404, Arch Toxicol Suppl. 1985;8:33-42.
