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This study concluded that the digit-length ratio (2D:4D) does not predict androgenic alopecia development, suggesting prenatal androgen exposure does not predispose men to this condition.

This study found that prenatal exposure to finasteride in rats led to permanent changes in developmental endpoints like anogenital distance and nipple retention, which were predictive of further reproductive tract malformations.

This study observed that low-dose intrauterine exposure to finasteride alters postnatal prostate development in male and female Mongolian gerbils, showing sex-specific differences in receptor expression and tissue changes.

In this study, D-004 did not affect androgen-dependent development in rats exposed in utero, while finasteride caused significant changes in male offspring's androgen-dependent tissues.

In this study, researchers found that pregnant mice exposed to excessive androgen led to thinner ventricular walls and cardiac hypertrophy in offspring, suggesting that prenatal androgen exposure adversely affects cardiac health through reduced cardiomyocyte proliferation.

This review discusses the 2011 publications on the side effects of sex hormones and related compounds, without reporting new clinical results.

This study found that women with PCOS were more likely to have longer anogenital distances, indicating possible intrauterine origins linked to prenatal androgen exposure.

This study observed that both prenatal androgen exposure and postnatal early-life environment influence the development of PCOS-like phenotypes and changes in the gut microbiota in prenatally androgenized offspring.

In this study, male rats exposed in utero to low-dose chemical mixtures had permanent reproductive tract alterations, suggesting additive effects even at doses below individual adverse levels.

This study observed that male fetuses exposed to finasteride in utero may develop external genital anomalies, with the outcome dependent on the timing of exposure.

This study observed that a longer anterior clitoral anogenital distance (AGDAC) is associated with polycystic ovary syndrome in adult Mediterranean women.

The study found that males with androgenetic alopecia had a significantly lower left-hand 2D:4D digit ratio compared to healthy controls, suggesting this ratio may help estimate future AGA risk.

This article reviews the characteristics, diagnosis, and management of premature adrenarche and suggests it may predict future ovarian hyperandrogenism in some adolescents; no new clinical results are reported.

This study found that prenatal exposure to androgens caused long-lasting heart remodeling and left ventricular hypertrophy in female mice offspring, suggesting potential cardiac risks for daughters of mothers with PCOS.

This review discusses the multifactorial etiology of hypospadias, including genetic predispositions and possible environmental factors, and highlights the need for further studies on genetic and environmental contributions to its increasing prevalence, without presenting new findings.

This review examines the diverse roles of SRD5α enzymes across species, focusing on their involvement in steroid synthesis, sexual development, and various physiological processes, but reports no new clinical results.

This review discusses the hypothesis that polycystic ovary syndrome may originate in fetal life due to prenatal androgen exposure, but reports no new clinical results.

This article reviews the updated ESHRE/ASRM criteria for diagnosing polycystic ovary syndrome, emphasizing the need for continued research and collaboration, but reports no new clinical results.

In this study, prenatal androgen exposure was linked to altered sexual behaviors in both male and female mice, with specific effects on mounting and lordosis behaviors.

This study found that oral administration of finasteride to pregnant rats caused dosage-related developmental toxicities, including hypospadias and decreased anogenital distance in male offspring.

This study found that males with androgenetic alopecia had a significantly lower 2D:4D digit length ratio in the right hand compared to healthy controls, which may indicate prenatal androgen exposure.

This review discusses the etiology of polycystic ovary syndrome, emphasizing the role of genetic and environmental factors, and reports no new experimental findings.

This study found that prenatal exposure to certain pesticides may lead to earlier breast development in girls, potentially associated with higher androgen levels.

This review suggests that "polycystic ovarian syndrome" is a misleading name, as the disorder involves complex metabolic and reproductive issues beyond ovarian dysfunction and may stem from factors affecting the fetus in utero.

Finger length ratios are not linked to the number of specific gene repeats affecting testosterone sensitivity.

This study found that prenatal exposure to finasteride in pregnant rats significantly disrupted male reproductive development, confirming its use as a positive control for androgen-related reproductive effects.

This review discusses the hypotheses surrounding the developmental origins of polycystic ovary syndrome, particularly the role of prenatal androgen exposure, and reports no new experimental results.

This review explores the hypothesis that polycystic ovary syndrome may originate in fetal life due to genetic predispositions and environmental influences, but it reports no new clinical findings.

This article reviews polycystic ovary syndrome in adolescents, highlighting its endocrine and metabolic features, and reports no new clinical findings; the etiology may involve early-life abnormalities in androgen production.

Finasteride negatively affects fish reproduction and gonadal development.