Psychosexual Aspects, Effects of Prenatal Androgen Exposure, and Gender Change in 46,XY Disorders of Sex Development

2019 ◽  
Author(s):  
Loch Batista R ◽  
Inacio M ◽  
Prado Arnhold IJ ◽  
Gomes NL ◽  
Diniz Faria JA ◽  
...  
Keyword(s):  
Disorders Of Sex Development ◽  
Sex Development ◽  
Androgen Exposure ◽  
Prenatal Androgen Exposure ◽  
And Gender ◽  
Prenatal Androgen ◽  
Gender Change

scholarly journals Psychosexual Aspects, Effects of Prenatal Androgen Exposure, and Gender Change in 46,XY Disorders of Sex Development

2018 ◽  
Vol 104 (4) ◽  
pp. 1160-1170 ◽  
Author(s):  
Rafael Loch Batista ◽  
Marlene Inácio ◽  
Ivo Jorge Prado Arnhold ◽  
Nathália Lisboa Gomes ◽  
José Antônio Diniz Faria ◽  
...  
Keyword(s):  
Gender Identity ◽  
Disorders Of Sex Development ◽  
Psychosexual Development ◽  
Estrogen Exposure ◽  
Androgen Exposure ◽  
Tertiary Center ◽  
Prenatal Androgen Exposure ◽  
And Gender ◽  
Prenatal Androgen ◽  
Gender Change

AbstractContextIn 46,XY disorders of sexual development (DSD) patients, several factors may affect psychosexual development, leading to gender identity discrepancy and gender change later in life. Prenatal sexual steroid exposure and external genital virilization are considered to influence human psychosexual development, but their roles not completely understood yet.DesignA total of 144 individuals (18 to 60 years of age) with a clinical/molecular diagnosis of 46,XY DSD from a single tertiary center were enrolled. Psychosexual outcomes (gender role, gender identity, and sexual orientation) were assessed using questionnaires and psychological test. The Sinnecker score was used for genital virilization measurement. Prenatal androgen exposure was estimated according to 46,XY DSD etiology.ResultsWe found a positive association between prenatal androgen exposure and male psychosexual outcomes. Alternatively, prenatal estrogen exposure, age of gonadectomy, and the degree of external genital virilization did not influence any psychosexual outcome. There were 19% (n = 27) with gender change, which was associated with prenatal androgen exposure (P < 0.001) but not with the external genital virilization. The median age of gender change was 15 years, but most of the patients reported the desire for gender change earlier.ConclusionsPrenatal androgen exposure influenced psychosexual development in 46,XY DSD favoring male psychosexuality in all psychosexual outcomes, whereas the degree of external genital virilization did not influence these outcomes. The organizational effect of sexual steroids on psychosexuality at puberty appears to be weak in comparison with the prenatal effects. Prenatal androgen exposure also influenced female-to-male gender change frequency. All 46,XY DSD conditions with prenatal androgen exposure must be followed for gender issues in their management.

Childhood Sex-Typed Behavior and Gender Change in Individuals with 46,XY and 46,XX Disorders of Sex Development: An Iranian Multicenter Study

2018 ◽  
Vol 47 (8) ◽  
pp. 2287-2298 ◽  
Author(s):  
Behzad S. Khorashad ◽  
Ghasem M. Roshan ◽  
Alistair G. Reid ◽  
Zahra Aghili ◽  
Maliheh Dadgar Moghadam ◽  
...  
Keyword(s):  
Multicenter Study ◽  
Disorders Of Sex Development ◽  
Sex Development ◽  
And Gender ◽  
Gender Change

Gender Dysphoria and Gender Change in Disorders of Sex Development/Intersex Conditions: Results From the dsd-LIFE Study

2018 ◽  
Vol 15 (5) ◽  
pp. 777-785 ◽  
Author(s):  
Baudewijntje P.C. Kreukels ◽  
Birgit Köhler ◽  
Anna Nordenström ◽  
Robert Roehle ◽  
Ute Thyen ◽  
...  
Keyword(s):  
Gender Dysphoria ◽  
Disorders Of Sex Development ◽  
Life Study ◽  
Sex Development ◽  
And Gender ◽  
Gender Change

scholarly journals Investigating the reliability and sex differences of digit lengths, ratios, and hand measures in infants

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Luisa Ernsten ◽  
Lisa M. Körner ◽  
Martin Heil ◽  
Gareth Richards ◽  
Nora K. Schaal
Keyword(s):  
Sex Differences ◽  
Measurement Techniques ◽  
Directional Asymmetry ◽  
Computer Assisted ◽  
Sexually Dimorphic ◽  
Digit Ratios ◽  
Androgen Exposure ◽  
Prenatal Androgen Exposure ◽  
Test Retest Reliability ◽  
Prenatal Androgen

AbstractHands and digits tend to be sexually dimorphic and may reflect prenatal androgen exposure. In the past years, the literature introduced several hand and digit measures, but there is a lack of studies in prepubertal cohorts. The available literature reports more heterogeneous findings in prepubertal compared to postpubertal cohorts. The comparability of the available studies is further limited by the study design and different measurement techniques. The present study compared the reliability and sex differences of available hand and digit measures, namely digit lengths of 2D, 3D, 4D, 5D, digit ratios 2D:4D, 2D:5D, 3D:4D, 3D:5D, 4D:5D, relative digit lengths rel2, rel3, rel4, rel5, directional asymmetry of right and left 2D:4D (Dr-l), hand width, length, and index of 399 male and 364 female 6-month-old German infants within one study using only indirect and computer-assisted measurements. The inter-examiner reliability was excellent while the test-retest reliability of hand scans was only moderate to high. Boys exhibited longer digits as well as wider and longer hands than girls, but smaller digit ratios, with ratios comprising the fifth digit revealing the largest effect sizes. Other hand and digit ratios revealed sex differences to some extent. The findings promote the assumption of sexual dimorphic hand and digit measures. However, by comparing the results of the available literature, there remains an uncertainty regarding the underlying hypothesis. Specifically in prepubertal cohorts, i.e. before the influence of fluctuating hormones, significant effects should be expected. It seems like other factors than the influence of prenatal androgens contribute to the sexual dimorphism in hand and digit lengths.

P–632 Examination of temporal changes in phenotype and gut microbiome during the process of growth in polycystic ovary syndrome (PCOS) model induced by prenatal androgen exposure

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
A Kusamoto ◽  
M Harada ◽  
J M Azhary ◽  
C Kunitomi ◽  
E Nose ◽  
...  
Keyword(s):  
Body Weight ◽  
Gut Microbiota ◽  
Estrous Cycle ◽  
Gut Microbiome ◽  
Sesame Oil ◽  
Rrna Genes ◽  
Obese Adolescent ◽  
Androgen Exposure ◽  
Prenatal Androgen Exposure ◽  
Prenatal Androgen

Abstract Study question From when do abnormality in gut microbiome and phenotypes of PCOS appear during the process of growth? Summary answer Reproductive phenotypes of PCOS appear from 6 weeks and metabolic phenotypes from 12 weeks onward. Alteration in gut microbiome appears as early as 4 weeks. What is known already The etiology of PCOS remains largely unknown, however PCOS is considered as a complex multigenic disorder with strong epigenetic and environmental influence. Previous studies have suggested that fetal over-exposure to androgens could be the main factor of the development of PCOS after birth. On the other hands, recent studies on both human and PCOS rodent models have demonstrated the association between PCOS and alteration of gut microbiome in adulthood. Furthermore, it was recently reported that gut microbiome in obese adolescent with PCOS is different from obese adolescent without PCOS. Study design, size, duration A rodent PCOS model induced by prenatal dehydroepiandrosterone (DHT) exposure was applied to this study. Phenotypes and gut microbiome were compared between PCOS model mice (n = 12/group) and control mice (n = 10/group) at each stage of growth; 4 weeks (prepuberty), 6 weeks (puberty), 8 weeks (adolescent), 12 weeks (young adult), and 16 weeks (adult). The determinants for PCOS phenotypes are onset of puberty, estrous cycle, morphology of ovaries, serum testosterone level, body weight, and insulin resistance. Participants/materials, setting, methods Pregnant dams were subcutaneously injected on days of 16, 17, and 18 of gestation with either sesame oil for control groups or sesame oil containing 250µg of DHT for prenatal DHT groups. The evaluation of PCOS phenotypes and gut microbiome in female offspring were performed at each stage of growth. For examination of gut microbiota, next generation sequencing and bioinformatics analysis of 16S rRNA genes were performed on DNA extracted from mouse fecal samples. Main results and the role of chance Prenatal DHT mice exhibited delayed puberty onset, disrupted estrous cycle, and significantly increased testosterone levels from 6 weeks onward. Significantly increased atretic antral follicles were observed in prenatal DHT mice at 6, 12, and 16 weeks. Prenatal DHT mice showed significantly decreased body weight at 4, 6, 8 weeks and increased body weight from 12 weeks onward. As for gut microbiome, alpha-diversity was significantly different between control and prenatal DHT mice from 8 weeks onward and beta-diversity was significantly different at 6 and 8 weeks. Altered composition of gut microbiota was observed as early as 4 weeks. At phylum level, Firmicutes are significantly increased in prenatal DHT mice at 4 and 8 weeks and decreased at 16 weeks. Actinobacteria phylum showed significant decrease at 6 and 8 weeks in prenatal DHT mice. At genus level, relative abundance of several bacterial taxa significantly differed between control and prenatal DHT mice; some taxa, such as Allobaculum, Adlercreutzia, Bilophila, Clostridium, Gemella, Gemmiger, Roseburia, Ruminococcus, Staphylococcus, and Sutterella, exhibited constant increase or decrease in prenatal DHT mice during the process of growth. Interestingly, Roseburia was never detected in prenatal DHT mice, while approximately half of control mice harbored Roseburia at 12 and 16 weeks. Limitations, reasons for caution It is not clearly determined whether alteration in gut microbiome is cause or result of PCOS development, although the changes in gut microbiome seemed to precede the appearance of typical PCOS phenotypes in the present study. Mouse model does not completely recapitulate human PCOS. Wider implications of the findings: Our findings suggest that prenatal androgen exposure causes alteration of gut microbiome from pre-puberty onward, even before PCOS phenotypes become apparent. Intervention for girls at risk of PCOS with pre/pro-biotics may prevent them from developing PCOS in future. Trial registration number Not applicable

scholarly journals Prenatal androgen exposure causes hypertension and gut microbiota dysbiosis

Gut Microbes ◽  
2018 ◽  
pp. 1-22 ◽  
Author(s):  
Shermel B. Sherman ◽  
Nadeen Sarsour ◽  
Marziyeh Salehi ◽  
Allen Schroering ◽  
Blair Mell ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Androgen Exposure ◽  
Prenatal Androgen Exposure ◽  
Prenatal Androgen ◽  
Gut Microbiota Dysbiosis

scholarly journals Origins and Impact of Psychological Traits in Polycystic Ovary Syndrome

2019 ◽  
Vol 7 (8) ◽  
pp. 86 ◽  
Author(s):  
Elisabet Stener-Victorin ◽  
Maria Manti ◽  
Romina Fornes ◽  
Sanjiv Risal ◽  
Haojiang Lu ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Anxiety Disorders ◽  
Maternal Obesity ◽  
Steroid Receptors ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Psychological Traits ◽  
Androgen Exposure ◽  
Prenatal Androgen Exposure ◽  
Prenatal Androgen

Women with polycystic ovary syndrome (PCOS) exhibit compromised psychiatric health. Independent of obesity, women with PCOS are more susceptible to have anxiety and depression diagnoses and other neuropsychiatric disorders. During pregnancy women with PCOS display high circulating androgen levels that may cause prenatal androgen exposure affecting the growing fetus and increasing the risk of mood disorders in offspring. Increasing evidence supports a non-genetic, maternal contribution to the development of PCOS and anxiety disorders in the next generation. Prenatal androgenized rodent models reflecting the anxiety-like phenotype of PCOS in the offspring, found evidence for the altered placenta and androgen receptor function in the amygdala, together with changes in the expression of genes associated with emotional regulation and steroid receptors in the amygdala and hippocampus. These findings defined a previously unknown mechanism that may be critical in understanding how maternal androgen excess can increase the risk of developing anxiety disorders in daughters and partly in sons of PCOS mothers. Maternal obesity is another common feature of PCOS causing an unfavorable intrauterine environment which may contribute to psychiatric problems in the offspring. Whether environmental factors such as prenatal androgen exposure and obesity increase the offspring’s susceptibility to develop psychiatric ill-health will be discussed.

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