https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0083947
Quote from the above study: “We found differences in the regional grey matter (GM) structure of transsexual compared with control subjects, independent from their biological gender, in the cerebellum, the left angular gyrus and in the left inferior parietal lobule. Additionally, our findings showed that in several brain areas, regarding their GM volume, transsexual subjects did not differ significantly from controls sharing their gender identity but were different from those sharing their biological gender (areas in the left and right precentral gyri, the left postcentral gyrus, the left posterior cingulate, precuneus and calcarinus, the right cuneus, the right fusiform, lingual, middle and inferior occipital, and inferior temporal gyri).”
Both MTF and FTM patients were eligible for the study, but only those with homosexual orientation. The rationale for this choice was based on the Blanchard typology [15] which considers two fundamentally different types of transsexualism: homosexual and nonhomosexual. Homosexual transsexual individuals are sexually attracted to the same biological gender, while nonhomosexual transsexual individuals are attracted to either the opposite gender or show no sexual orientation/attraction at all. According to Blanchard, homosexual transsexuals are usually younger at initial presentation of gender identity disorder and show more pronounced and frequent childhood femininity, as well as different anthropometric data [16], [17]. One might argue that mixing individuals from both transsexual groups in one study targeting the neurobiological background of transsexualism might bias the results by introducing heterogeneity in the sample. Thus, in our study, only homosexual transsexual individuals were included preventing our findings from the aforementioned bias. Evaluation of the subjects' sexual orientation was based on self-report.
They don't study how sexual orientation relates to brain structure and how that influences troon brain structure. There's plenty of studies that show that distinction in non-troon populations and it probably accounts for most, if not all, of the differences you might see in the troon populations too.
Yeah, they wilt really fast
Also lots of flies around for some reason.
People say it should take it down but then I'll remind them of the Autobahnhow he burned down that tranny institute and everyone is chill again.
That wet spot tho... but that's probably just the book of the dead...
Is it just me, or are some of the sample sizes from some of these studies rather low?
In this study, the sample size was described here: “Post-mortem brain material was used from 42 subjects: 14 control males, 11 control females, 11 male-to-female transsexual people, 1 female-to-male transsexual subject and 5 non-transsexual subjects who were castrated because of prostate cancer.”
“Seventeen patients with the diagnosis of GID (10 MTF patients and 7 FTM patients), based on the DSM-IV TR [1] diagnostic criteria, before cross-hormonal treatment, and 18 age matched control subjects (11 females and 7 males) were included in the study. “
The study linked above also states this: “These initial results, including the results of our study, need to be further replicated and refined in future studies on larger samples, as well as followed by functional imaging studies that might clarify how these structural differences impact the process of the disturbed evolution of gender identity and/or how disturbed gender identity affect brain structure and functions.”
Anyone have any thoughts on these studies? They observe the differences between the brains of trans and cis people:
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0083947
Quote from the above study: “We found differences in the regional grey matter (GM) structure of transsexual compared with control subjects, independent from their biological gender, in the cerebellum, the left angular gyrus and in the left inferior parietal lobule. Additionally, our findings showed that in several brain areas, regarding their GM volume, transsexual subjects did not differ significantly from controls sharing their gender identity but were different from those sharing their biological gender (areas in the left and right precentral gyri, the left postcentral gyrus, the left posterior cingulate, precuneus and calcarinus, the right cuneus, the right fusiform, lingual, middle and inferior occipital, and inferior temporal gyri).”
I'm not a scientist and only spent a few minutes looking at this first study, but it was a small study (17 trannies of both sexes and 18 non-trannies of both sexes) with post-hoc analysis (which probably means that they were searching for differences and could have easily selected for only those that would reaffirm their desired outcome, AKA p-hacking. These could just be statistical noise that they've chosen to highlight, especially with such small sample sizes). And, a common thing with these studies IME, the trannies are mostly (in this case all) homosexual which obviously poses a major confounding factor.
tl;dr They took a small, unrepresentative group of trannies, and then focused exclusively on the traits that would indicate that they were true and honest men or women instead of actually women or men.
I'm not a scientist and only spent a few minutes looking at this first study, but it was a small study (17 trannies of both sexes and 18 non-trannies of both sexes) with post-hoc analysis (which probably means that they were searching for differences and could have easily selected for only those that would reaffirm their desired outcome, AKA p-hacking. These could just be statistical noise that they've chosen to highlight, especially with such small sample sizes). And, a common thing with these studies IME, the trannies are mostly (in this case all) homosexual which obviously poses a major confounding factor.
tl;dr They took a small, unrepresentative group of trannies, and then focused exclusively on the traits that would indicate that they were true and honest men or women instead of actually women or men.
The problem with all this is that they're asking the wrong questions, they should observe brain differences first, without classification of the subjects, make guesses what they might affect AND THEN look at who the people with them are, instead they're looking for the needle in the haystack after dividing people into true and honest women/men and/or trannies. They subdivide and subdivide until their perspective is so narrow and skewed that they can frame any minute detail any way they want. Everybody knows what a woman is and everyone knows what a tranny is already. The true horror will begin when they agree to some conclusion from this and begin screening newborns for this or that brain area's volume/neuron density/whatever metric and decide their gender like they already do for intersex people. And when that inevitably doesn't work out and they again have reimer cases and blood at their hands, they will backpedal, say there wasn't enough science done, and look for something else - forever and ever and ever.
Since this thread hasn't been updated in a while, I decided to revisit the case(s) of fertility regarding pooners. There have been some studies posted here regarding the effects of testosterone on the vaginal microbiome, but the bulk of it can be found in the SRS thread. There have been a few more studies published since 2021 regarding this issue. None of them are good.
I believe Krakowsky et al has been published here before, but here is a reminder. Predictably, they have a statement regarding gynecological care and trans men:
We will employ the commonly used term “neovagina” to refer to vaginas that are surgically created by vaginoplasty, and “vagina” to refer to vaginas that were present at birth. Furthermore, we will refer to the present-at-birth vaginas of those taking testosterone therapy (tM individuals) as testosterone dominant vaginas (TDV) and vaginas of reproductive-aged individuals who are not taking testosterone therapy (including both cF and TGD individuals not on testosterone therapy) as estrogen dominant vaginas (EDV). The field of transgender medicine is relatively new, and little is known of the effects of testosterone therapy on the TDV nor of estrogen therapy on the neovagina, but it is clear that both genital microenvironments are distinct from the comparatively better studied EDV. As social acceptance increases and access to gender-affirming medical care continues to improve, the number of TGD individuals who will need tailored gynecological care is increasing. The provision of inclusive healthcare is necessary to achieve optimal health and reduce inequities experienced by TGD communities (American College of Obstetricians and Gynecologists’ Committee on Gynecologic Practice and American College of Obstetricians and Gynecologists’ Committee on Health Care for Underserved Women, 2021).
The vaginal mucosa is a stratified squamous epithelium that undergoes continuous renewal through proliferation of basal cells, and thus newly formed epithelial cells are pushed outward towards the lumen by the subsequent cell generations. As basal cells lose contact with the basement membrane, they begin to differentiate, expressing cytokeratins K4/K13 and K1/K10 (which form intermediate filaments, and whose expression is organ-specific), to eventually reach full maturation in the superficial layers (Waseem et al., 1998). Maturation of vaginal epithelial cells is regulated by estrogen, which promotes epithelial cell proliferation and thus increases thickness of the epithelium (Ayehunie et al., 2015). Estrogen also promotes the production of glycogen, a glucose polysaccharide, by vaginal epithelial cells (Cruickshank, 1934; Anderson et al., 2014). Cell-cell junctions are lost during cellular maturation and the loosely connected, glycogen-rich cells of the superficial layer are readily shed into the vaginal lumen. Glycogen from shed epithelial cells is catabolized by both human and bacterial α-amylases in the vaginal lumen to smaller polymers that are a preferred carbon source of beneficial Lactobacillus spp., but also of non-desirable anaerobic bacteria (Mirmonsef et al., 2014; Spear et al., 2014; van der Veer et al., 2019; Nunn et al., 2020). Lactobacilli then metabolize glycogen-derived polymers into lactic acid, which reduces the pH of the vaginal lumen, favoring the proliferation of lactobacilli and inhibiting the growth of pathogenic organisms such as Neisseria gonorrhoeae, Chlamydia trachomatis and those associated with bacterial vaginosis (BV) (Graver and Wade, 2011; O'Hanlon et al., 2011; O'Hanlon et al., 2013; Gong et al., 2014; Mirmonsef et al., 2014; Breshears et al., 2015; Mirmonsef et al., 2016; Nardini et al., 2016; Edwards et al., 2019). In addition to reducing the pH, Lactobacillus spp. also prevent colonization by pathogens through the production of bacteriocins and biosurfactants (Valore et al., 2002). In the absence of Lactobacillus spp., the EDV is colonized by a diverse set of strict and facultative gram-positive and gram-negative anaerobes (e.g., Atopobium, Prevotella, Gardnerella) (Ravel et al., 2013; France et al., 2020; Holm et al., 2020; Turpin et al., 2021). Communities dominated by diverse anaerobes are reminiscent of BV, which is characterized by abnormal discharge, itching, malodour, and an elevated pH (Eschenbach et al., 1988; Schwebke et al., 1996; Redelinghuys et al., 2020). Even in the absence of symptoms, vaginal microbiomes deficient in lactobacilli (“molecular BV”) are associated with impaired epithelial maturation, increased mucosal inflammation, changes in epithelial barrier function, increased susceptibility to sexually transmitted infections (chlamydia, gonorrhea, HIV and HPV, among others), and reproductive risks (Leitich et al., 2003; Wiesenfeld et al., 2003; Brotman et al., 2010; Arnold et al., 2016; Zevin et al., 2016; Joag et al., 2019; Tamarelle et al., 2019; O'Hanlon et al., 2020).
It has a specific term for trans men on T, the 'testosterone dominant vagina':
Testosterone therapy is highly effective in allowing TGD individuals to develop the secondary sex characteristics associated with masculinity, but the suppression of estrogen (Table 2) can induce epithelial thinning reminiscent of the estrogen-deprived post-menopausal cF vagina (Baldassarre et al., 2013).
In the absence of estrogen, vaginal epithelial cell proliferation slows, and the epithelium becomes thinner and more fragile, leading to dryness, irritation, and dyspareunia (pain during intercourse) (Pessina et al., 2006; Perrone et al., 2009; Baldassarre et al., 2013).(...)This microbiota has some overlap with molecular BV in the EDV (e.g., Prevotella, Gardnerella, Dialister), but is clearly distinct, with higher abundance and prevalence of genera such as Streptococcus, Corynebacterium, Finegoldia, Peptoniphilus, Anaerococcus, and Bifidobacterium and lower abundance of BV-associated genera Atopobium, Sneathia, and Megasphaera (Brotman et al., 2014; Mirmonsef et al., 2014; Shen et al., 2016; France et al., 2020). The importance of estrogen in shaping the vaginal microbiome is underscored by the effects of local or systemic estradiol-based hormone replacement therapy post-menopause, which restores lactobacilli dominance, decreases vaginal pH, and alleviates symptoms of vaginal fragility (Brotman et al., 2014; Shen et al., 2016). In TDV, testosterone therapy has been shown to thin the epithelium, with histological evaluation revealing lowered cell proliferation, loss of the intermediate and superficial strata, and reduced glycogen deposition compared to pre-menopausal EDV (Baldassarre et al., 2013). Recently published data indicates that TDV tissue has elevated levels of inflammation, edema, collagen fibrosis, and granulation tissue (Schardein et al., 2021). Transmasculine individuals on testosterone therapy frequently experience symptoms of vaginal atrophy similar to those of the post-menopausal state, including dryness, irritation, bleeding with vaginal penetration (sex or medical examination), and dyspareunia (Peitzmeier et al., 2014; Potter et al., 2015). These symptoms can have a substantial impact on quality of life, and as such some tM individuals opt for topical estriol or estradiol administered directly to the vaginal mucosa via cream, a ring, or tablets (Santen, 2015). While local estrogen-based therapy to treat vaginal atrophy is included in multiple trans care guidelines, the efficacy of this approach has not been documented in tM (Deutsch, 2016; Obedin-Maliver and de Haan, 2017; Bourns, 2020).
They have to take estrogen creams just to save their vaginas. Some refuse to take it because anything related to estrogen triggers them.
And it gets worse:
Despite sharing some similarities with the post-menopausal vagina, the microbiota observed in the TDV was also clearly distinct, with higher abundance of Campylobacter, Fusobacterium, Parvimonas, and Porphyromonas, indicating testosterone augmentation may influence the composition of the vaginal microbiota beyond that of estrogen reduction. It is notable that, of the three individuals who had a Lactobacillus-dominated microbiota, two were prescribed topical estradiol (a total of 4 individuals in the study had been prescribed topical estradiol to treat symptoms of vaginal atrophy). Despite limited statistical power in this relatively small study, the correlation between vaginal estrogen therapy and presence of a Lactobacillus-dominated microbiota was statistically significant (p=0.045). This study provides an important first assessment of the TDV microbiota, suggesting it is distinct from the microbiota observed post-menopause, and that Lactobacillus-dominated microbiota are rare.
They get a post-menopausal vagina, and then some. Testosterone can be prescribed to post menopausal women for their health, but in specific doses. Trans men are trying to take testosterone to reach the T levels of normal men, which is disastrous to their female bodies. Not that they care, though.
Edit: forgot to add this graph.
In this study, testosterone does lead to increased libido, but vaginal pain is experienced by 60% of them.
Overall, 516 (42.3%) had never used testosterone and 602 (49.4%) currently used testosterone. Median duration of use was 37.7 months (range 7 days to >27 years). Most participants (64.6%) reported genital pain/discomfort during sexual activity in the past 30 days, most commonly in the vagina/frontal genital opening (52.2%), followed by the clitoris (29.1%) and labia (24.5%). Current testosterone use was associated with higher interest in sexual activity (β=6.32, 95% CI: 4.91-7.74) and more vaginal pain/discomfort during sexual activity (β=1.80, 95% CI: 0.61-3.00). No associations were observed between current testosterone use and satisfaction with sex life, lubrication, labial pain/discomfort, or orgasm pleasure.
Just give it time, bro. Once that vagina dries up, it won't be fun anymore.
At least 1.6 million transgender adults and adolescents live in the United States,1 among whom an estimated 70% of transgender men have ever used testosterone as gender-affirming hormone therapy (GAHT).2 Vaginectomy is rare (<3%) in this population, and the majority of transgender men and gender diverse people retain their vagina.2 Testosterone GAHT likely impacts sexual function via several complex pathways: Testosterone GAHT is associated with vaginal atrophy, which may be associated with decreased lubrication and/or discomfort during sexual activity.3–5 At the same time, increased gender affirmation through testosterone use may be associated with improved sexual function.
There is limited research on the sexual function of transgender men and gender diverse people assigned female at birth (AFAB). What does exist suggests that, although testosterone GAHT is associated with increased desire and arousal,6 a high proportion of transgender men also reported dyspareunia (painful sex), a common symptom of vaginal atrophy. The prevalence of dyspareunia may be as high as 60-62% among transgender men,7,8 markedly higher than the prevalence reported among cisgender women (3-48%).9 Several studies also suggest that transgender men using testosterone may experience chronic genital pain and discomfort, with one study reporting that 10-16% of transgender men had been diagnosed with vulvodynia (defined as chronic burning, stinging, or irritating vulvovaginal pain for three consecutive months or longer).7,8 Only one prior small study directly assessed the impact of testosterone GAHT on genital pain during sexual activity. Although 30% of transgender men reported that testosterone had caused genital dryness and 14% experienced genital tearing since initiating testosterone, they did not observe an association between testosterone use and vulvodynia or dyspareunia symptoms.10
Our analysis included 1,219 participants ages 18-72 years old (median age 27.1; Table 1). Most participants (61.1%) endorsed more than one gender identity: most commonly non-binary (54.2%), transgender man (46.0%), genderqueer (33.6%), and man (21.5%). Participants were diverse in sexual orientation, although most identified as queer (65.1%). The majority (80.6%) of participants only reported White race and/or ethnicity and 12.0% of participants selected more than one racial and/or ethnicity.
Table 2 reports participants’ pelvic health histories. Current testosterone users were more likely to have a hysterectomy (17.9% v. 5.4%, p<0.001) and oophorectomy (14.5% v. 3.3%, p<0.001), and less likely to currently use hormonal contraceptives (5.8% v. 17.8%, p<0.001) compared to participants who never used testosterone. Current testosterone users were also more likely to have a past year bacterial STI diagnosis (3.0% v. 1.6%, p=0.001). Testosterone use was not associated with pelvic inflammatory disease, polycystic ovary syndrome, uterine fibroids, inflammatory bowel disease, irritable bowel syndrome, pregnancy history, or intrauterine device use.
Participants reported very high levels of lifetime experiences of sexual abuse, sexual assault, and ever having received a depression and PTSD diagnoses (Table 2). Testosterone use was associated with lower scores (i.e., better mental health) for current depressive and PTSD symptoms. Testosterone use was also associated was substance use, including current smoking (7.5% v. 4.3%, p=0.033) and higher AUDIT scores.
Their 'front holes' are bothering them, and they don't know why:
Among the 1,091 sexually active participants, most (n=693, 64.6%) reported genital pain/discomfort during sexual activity in the past 30 days, most commonly in the vagina/FGO (52.2%), followed by the clitoris (29.1%) and labia (24.5%; Table 3). There were 103 (9.6%) participants who reported pain at all three genital sites. T-scores for pain/discomfort were higher than the population mean (p-values<0.001) while T-scores for orgasm pleasure (mean T-score 45.0, p-value<0.001) and satisfaction with sex life (mean T-score 45.6, p-value<0.001) were lower than the population mean. Figure 1 shows the correlation between each sexual function T-score among participants. Interest in sexual activity, satisfaction, lubrication, orgasm ability and pleasure were positively correlated. Measures of pain/discomfort were negatively correlated with all other domains.
Compared to participants who never used testosterone, current testosterone users were less likely to report difficulty with lubrication (58.5% v. 66.7%, p=0.01), more like to report any vaginal pain/discomfort (56.0% v. 49.2%, p=0.04), and more likely to achieve orgasm (p=0.003; Table 3). In the minimally adjusted regression models (Table 4), current testosterone use was associated with higher interest in sexual activity (β=6.32, 95% CI: 4.91-7.74), higher ability to orgasm (β=1.50, 95%CI: 0.19-2.81), pain/discomfort during sexual activity in the vaginal/FGO (β=1.80, 95% CI: 0.61-3.00) and in the clitoris (β=1.20, 95%CI: 0.10-2.30). The association between testosterone use, ability to orgasm, and clitoral pain/discomfort were not statistically significant in the robustly adjusted model. No associations were observed between current testosterone use and satisfaction with sex life, lubrication, labial pain/discomfort, or orgasm pleasure.
Our findings are consistent with prior studies which found that testosterone use is associated with increased desire and interest in sex.6 GAHT is associated with significant improvements in overall mental health, quality of life, and body image,31–33 which in turn likely have positive impacts on other areas of wellbeing, including sexual function. For example, other studies have found that access to gender-affirming chest reconstruction surgery is associated with higher sexual function scores, while experiencing barriers to accessing gender-affirming care is associated with lower sexual function scores.25Although prior studies have not observed an association between testosterone use and orgasm,6 testosterone use was associated with a higher ability to orgasm in our study.
Nice. Now let's see that five years on. Replicate that when their vagina starts cracking.
They go on T to escape the pain of being assaulted:
Notably, we observed that a majority of transgender and gender diverse people AFAB using testosterone (67%) experienced vulvovaginal pain during sexual activity. This prevalence is consistent with prior studies, which have reported that 60-62% of transgender men experience dyspareunia.7,8 Although testosterone was associated with vaginal/FGO pain in all regression analyses, the prevalence of any genital pain among individuals who were testosterone naïve was also quite high (63%). The causes of genital pain during sex (including dyspareunia, vulvodynia, and vaginismus) are multifactorial.24 Although physiological factors (such as vaginal atrophy, endometriosis, and pelvic floor injury) are associated with genital pain during sex,5 there are complex associations with psychological and social factors, including co-occurrence with other pain disorders, mental health, substance use, and sexual trauma.22,23Our sample reported an alarmingly high level of sexual abuse (78%), sexual assault (50%), depression (81%) and PTSD diagnoses (40%)—factors that are correlated with chronic pelvic pain among presumably cisgender women.17–21 This may partially account for the high prevalence of pain in our study.
Transmasculine people on testosterone may experience atrophic vaginitis. It is thought to be due to the suppressive effects of testosterone on estrogen, leading to an estrogen-deprived state that appears to be similar to the experience of many post-menopausal cis women. Atrophic vaginitis is a reflection of poor skin barrier function and low tissue resilience, and is associated with bacterial vaginosis (BV). In a study of 28 trans men on testosterone, the vaginal microbiome was found to have fewer lactobacillus and a significantly higher diversity of bacteria compared to 8 cisgender women, likely explaining the predisposition of trans men to BV. Atrophic vaginitis can be quite distressing for patients, as it can also cause dyspareunia and dysuria. The current treatment for vaginal atrophy in transmasculine people is adapted from the recommendation for postmenopausal women: topical estrogen and lubrication.
Furthermore, the use of topical estrogen in trans men may lead to systemic absorption and the development of feminizing features, thereby exacerbating gender dysphoria. At this time, there is no research that has been conducted to quantify the prevalence of vaginal atrophy amongst the trans population, to assess for efficacy of estrogen in resolving atrophic vaginitis, or to evaluate for feminizing effects and gender dysphoria. Atrophic vaginitis in trans men is but one example of an LGBTQ+ health issue that is not discussed in medical education, is poorly understood and is unexplored.
They won't use the topical creams because it might just remind them they're women. Enjoy those cracked and bleeding vaginas, dood.
Now, I don't remember posting this one, but this one discusses ovarian health and trans men.
Androgens are essential in normal ovarian function and follicle health, but hyperandrogenism, as seen in polycystic ovary syndrome, is associated with disordered follicle development. There are few data on the effect of long-term exposure to high levels of testosterone as found in transgender men receiving gender-affirming endocrine therapy. In this study, we investigate the effect of testosterone on the development, morphological health and DNA damage and repair capacity of human ovarian follicles in vivo and their survival in vitro. Whole ovaries were obtained from transgender men (mean age: 27.6 ± 1.7 years; range: 20–34 years, n = at oophorectomy taking pre-operative testosterone therapy. This was compared to cortical biopsies from age-matched healthy women obtained at caesarean section (mean age: 31.8 ± 1.5 years; range: 25–35 years, n = . Cortical tissues were dissected into fragments and either immediately fixed for histological analysis or cultured for 6 days and subsequently fixed. Follicle classification and morphological health were evaluated from histological sections stained with hematoxylin and eosin and expression of γH2AX as a marker of DNA damage by immunohistochemistry (IHC). In uncultured tissue, testosterone exposure was associated with reduced follicle growth activation, poor follicle health and increased DNA damage. After 6 days of culture, there was enhanced follicle activation compared to the control with further deterioration in morphological health and increased DNA damage. These data indicate that high circulating concentrations of testosterone have effects on the primordial and small-growing follicles of the ovary. These results may have implications for transgender men receiving gender-affirming therapy prior to considering pregnancy or fertility preservation measures.
However, despite 54% of transgender men expressing a desire to have their own biological children (Wierckx et al. 2012), the uptake of fertility preservation interventions is as low as 3% (Birenbaum-Carmeli et al. 2021). Ovarian tissue cryopreservation is also potentially of value to the transgender population, with the aim of utilising immature oocytes from the preserved ovarian cortex (De Roo et al. 2016). Tissue culture systems have been developed over decades with the goal of producing developmentally competent oocytes (Bertoldo et al. 2018, Telfer & Andersen 2021). Complete in vitro growth of primordial follicles with subsequent in vitro maturation (IVM), IVF and production of live offspring has been achieved in the mouse (Eppig et al. 1996, O'Brien et al. 2003) and systems that support the development of human immature follicles to antral stages (Telfer et al. 2008) and to the development of mature oocytes that can reach Metaphase II have been developed (McLaughlin et al. 2018). There are, however, limited data on the effects of long-term gender-affirming testosterone treatment on the ovary.
To identify whether testosterone exposure was associated with DNA damage, five sections per patient from both transgender and control groups were used to identify expression of γH2AX as a marker of DNA damage in oocytes and the granulosa cells of ovarian follicles (Fig. 2A 1–5). Both D0 and D6 tissue was analysed and included 840 follicles (transgender 573 follicles, control 267 follicles).
At D0, the proportion of oocytes from non-growing and primary follicles expressing γH2AX was significantly higher in transgender compared to control tissue (non-growing: transgender 49.1 ± 8.5% vs control 28.6 ± 8%, primary 40 ± 12.7% vs 3.3 ± 3.3%, both P < 0.05) (Fig. 2B). Insufficient numbers of secondary follicles were identified for analysis.
The proportion of non-growing follicles expressing γH2AX in the granulosa cells at D0 did not significantly differ between groups (Fig. 2C), with comparable proportions of granulosa cells per follicle affected (Fig. 2C). In primary follicles, a higher proportion of follicles expressed γH2AX in the granulosa cells in the transgender tissue compared to control (19 ± 9.2% vs 6.6 ±6.7%, P < 0.05) but with comparable proportions of granulosa cells per follicle affected (20.8 ± 14.7% vs 26.3 ± 2.1%, P = 0.67).
An increased proportion of primordial follicles in transgender ovarian tissue compared to control suggests that testosterone therapy has a suppressive effect on follicle activation in vivo. Similar proportions of primordial follicles were found in other studies (De Roo et al. 2017, Borrás et al. 2021), but our study found a smaller proportion of primary follicles. These studies concluded that testosterone-exposed ovaries had a similar cortical follicle distribution to cisgender females. However, those studies did not use contemporaneous controls and used historic data from the literature (Gougeon & Chainy 1987a) where the age range was 19–49 or based on data from cisgender females who were known to be infertile (Lass et al. 1997). This study used closely aged women who donated ovarian cortical tissue at the time of caesarean section with samples analysed at the same time by the same observer. In pregnancy, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels are persistently low for the duration of pregnancy as a result of the inhibitory effects of high levels of circulating oestradiol and progesterone on the hypothalamus and pituitary, suppressing ovulation (Choi & Smitz 2014, Stilley & Segaloff 2018). However, the process of follicle recruitment and early growth is gonadotrophin-independent; therefore, pregnancy is likely to have no effect on this process (Hsueh et al. 2015, Zhang et al. 2023). In transgender men taking gender-affirming endocrine therapy, FSH and LH levels are also low or similar to the follicular phase of the menstrual cycle in cisgender women (De Roo et al. 2017, Greene et al. 2021) with low levels of oestradiol (Chan et al. 2018). In this study, testosterone levels were within the male range, without marked gonadotrophin suppression.
There is limited information regarding the long-term impact of testosterone on ovarian follicles. Reassuringly, after cessation of testosterone therapy, many transgender men successfully conceive naturally (Light et al. 2014) or through artificial reproductive techniques (Adeleye et al. 2019, Leung et al. 2019). Testosterone has been reported to have marked effects on ovarian morphology with abnormalities including stromal hyperplasia, thickened ovarian cortex and polycystic ovary morphology (Futterweit & Deligdisch 1986, Spinder et al. 1989, Grynberg et al. 2010, Ikeda et al. 2013). Testosterone therapy does not appear to deplete the primordial follicle pool from the ovarian cortex of transgender men (Van Den Broecke et al. 2001) or affect the in vitro maturation potential of cumulus–oocyte complexes (COCs) harvested from the ovarian medulla (De Roo et al. 2017, Lierman et al. 2017). It has however been reported to enhance follicle activation in the mouse ovary through the nuclear exclusion of Forkhead box O3X (FOXO3A) (Yang et al. 2010) although others have found that androgen receptors are not expressed by primordial follicles (Gervásio et al. 2014, Walters et al. 2018), The dense, fibrous nature of normal human ovarian cortical tissue contributes to suppression of primordial follicle growth, thus preventing mass and premature activation, which would result in early depletion (Silber et al. 2018). The ovarian cortex in transgender tissue has been found to be stiffer in comparison to tissue from cancer patients (De Roo et al. 2019). This increased resting tissue rigidity may enhance the suppression of residing primordial follicles and be an explanation for the finding here of reduced follicle activation in vivo.
Following 6 days of culture, the proportion of non-growing follicles in transgender tissue was significantly lower than in controls, despite being higher before culture. This suggests that the rate of activation of non-growing follicles in vitro is higher than in controls. The process of tissue dissection mechanically loosens the ovarian cortex and reduces intrinsic tissue pressure, increasing follicle activation (Smitz & Cortvrindt 2002, Telfer et al. 2008, McLaughlin et al. 2018, Grosbois & Demeestere 2018). This may have had a greater effect on the testosterone-exposed tissue as accelerated activation can have a detrimental impact on follicle quality (Smitz & Cortvrindt 2002, McLaughlin et al. 2014). In studies where primordial follicle activation was enhanced by suppressing phosphatase and tensin homolog deleted on chromosome 10 (PTEN) using Dipotassium bisperoxo oxovanadate (V) (bpV(HOpic)), an increase in the proportion of growing follicles was accompanied by a significant reduction in morphological health in both human (McLaughlin et al. 2014, Maidarti et al. 2019) and bovine ovarian follicles (Maidarti et al. 2019). In this study, with increased follicle activation in cultured transgender ovarian tissue, there was a significant decline in the morphological health of growing follicles compared to the control. This highlights that further optimisation of this stage of the culture process is needed to control follicle activation to ultimately produce a population of high-quality oocytes (Telfer & Zelinski 2013).
γH2AX is a DNA repair protein that binds to the location of DNA damage and controls recruitment of DNA repair proteins (Winship et al. 2018). In this study, the proportion of oocytes expressing γH2AX in uncultured D0 non-growing follicles was significantly higher in the transgender group compared to the control, consistent with the histological findings of reduced follicle health. After 6 days of culture, levels of γH2AX in the non-growing and primary follicles from transgender tissue remained stable. The cause of increased DNA damage in testosterone-exposed follicles is not clear, but studies that have used an experimental hyperandrogenic model in culture (Bertoldo et al. 2019) found increased levels of reactive oxidative species (ROS) resulting in DNA damage. Oxidative stress is a state whereby ROS outbalances anti-oxidant levels, resulting ultimately in DNA damage and/or cell apoptosis (Lee et al. 2022). There is also an increasing body of literature on the role of ROS in the pathogenesis of PCOS (Karadeniz et al. 2008, Zhang et al. 2008). Increased levels of biochemical markers of oxidative stress have been reported in women with PCOS compared to controls (Sabuncu et al. 2001, Palacio et al. 2006, Murri et al. 2013) whilst others have found variable findings when looking for markers for anti-oxidative stress levels (Sabuncu et al. 2001, Zhang et al. 2008, Seleem et al. 2014). Given that similar histological findings have been identified in both transgender male ovaries and females with PCOS, for example stromal hyperplasia, tunica albuginea thickening (Baba et al. 2007), it is possible that ROS could be responsible for the increased DNA damage seen in testosterone exposed ovarian follicles.
PCOS still doesn't have the same levels of T as trans men, as this study showed that these trans men were on male levels of T. So they're frying their ovaries, slowly but surely.
As for the 'no differences' bit:
Similar levels of expression of DNA repair proteins in oocytes were found between the transgender and control groups despite differing levels of expression of γH2AX and morphological health. Small numbers of subjects and follicles being included in the analysis may explain the lack of statistical significance in these experiments. However, a lack of increased expression of DNA repair proteins with increased levels of DNA damage in transgender tissue could indicate suboptimal DNA repair protein recruitment. Ineffective DNA repair is pathognomonic in reproductive aging, resulting in accumulating DNA DSBs (Karanjawala & Lieber 2004, Gorbunova et al. 2007, Winship et al. 2018). DSBs have been found to accumulate in ovarian follicles of aging mice, with the downregulation of key DNA repair proteins (Oktay et al. 2010, Titus et al. 2013). It is possible that testosterone may impair the DNA repair capacity of ovarian follicles, resulting in compromised genetic integrity and reduced oocyte quality. However, this study only looks at the first step of follicle growth; therefore, the results of these experiments cannot take into consideration the potential for DNA repair at later stages. This would however align with findings that when COCs harvested from the ovarian medulla of transgender men on testosterone therapy were fertilised, there were significantly impaired fertilisation rates and embryo development (Lierman et al. 2021).
Observational study: A study in which the subject is observed to see if there is a relationship between two or more things (eg: the consumption of diet drinks and obesity). Observational studies cannot prove that one thing causes another, only that they are linked.
People: This is a study based on research using people.
Observational study: A study in which the subject is observed to see if there is a relationship between two or more things (eg: the consumption of diet drinks and obesity). Observational studies cannot prove that one thing causes another, only that they are linked.
People: This is a study based on research using people.
According to the link, the authors' postulate cause anyway, and of course, it's due to discrimination, not, you know, that surgically/hormonally altering oneself is rarely a good answer to mental health issues.
Observational study: A study in which the subject is observed to see if there is a relationship between two or more things (eg: the consumption of diet drinks and obesity). Observational studies cannot prove that one thing causes another, only that they are linked.
People: This is a study based on research using people.
The study itself doesn't seem wholly incompetent. Their methodology seems sound but their conclusions are so whack. I have a sinking feeling that people in the field are getting not-so-subtly pressured to overlook the obvious cause of their findings, instead of everyone being brainwashed into actually believing the muh generational trauma marginalized groups bullshit. Sad to see JAMA of all places is pushing shit like this. 10 years ago this would have gotten torn apart for ignoring such a jarringly confounding variable. Even fucking NIH studies aren't safe, case in point:
The increased prevalence and severity of psychological distress and suicidality among TGD individuals may best be understood within the gender minority stress model. Building on the contributions of Brooks33 and Meyer34, Hendricks and Testa proposed that distal stressors (e.g., discrimination), which are external to the individual, and proximal stressors (e.g., internalized transphobia), which are internal and are often the byproduct of repeated exposure to distal stressors, act on biobehavioral pathways to contribute to the health disparities impacting TGD individuals.35 For example, bullying, which disproportionately affects TGD youth,36,37 is a distal stressor that may contribute to low self-esteem, and feelings of worthlessness and burdensomeness,38,39 which are risk factors for suicide.35,40 Consistent bullying may also lead to the development of proximal stressors; for instance, TGD individuals may conceal their identity and experience anxiety about anticipated discrimination, and thus be less buffered by protective factors, including lower community connectedness and social support.35,41,42 Similar pathways to increased suicide risk have been examined among sexual minority youth.41,42
Courtesy of Kirakosian et al. (2023), a study with a much larger sample size, albeit from 2015-18. Not one mention of their butchery as a contributory factor. The blatant bias would be comical if it wasn't so sad. I see this 'gender minority stress model' come up time and again in these papers, might be worth looking into for the blackpill lulz.
Isn't it great when no one ever has to take responsibility for their own identity? "Oh poor me, I have the wrong body. Please, drop any insecurity and issue you have and deal with ME!"
I'll say it a thousand times to anyone who will listen: transgenderism encourages the kind of unhealthy mental mindset and habits that would otherwise require correction in virtually anyone else.
It's why any medical professional or adjacent profession should immediately look at anyone who claims to be trans and say: we'll deal with you being trans, but let's get you mentally stable and able to cope without being a pain in the ass to other people first.
According to the link, the authors' postulate cause anyway, and of course, it's due to discrimination, not, you know, that surgically/hormonally altering oneself is rarely a good answer to mental health issues.
And the fun thing is: the authors didn't even attempt to assess the degree of perceived discrimination; the conclusion about "minority stress theory" is an ass-pull. And they don't even assess the usual suicide indicators like education level and relationship status.
Whole paper attached. I'm not sure it warrants a passing grade as an undergrad project.
I found that study on r/psychology and a few toons have left comments outright saying that they were mentally ill before they thought about transitioning. Which is the entire problem with studies on troons: you can't find any without a history of mental illness, so there's no control group!
There are tons of differences between male and female brains. Brain size, sizes of different structures in the brain, cortical thickness, all sorts of stuff. However troon activists never point to any of these differences, you never see them saying that mtf troons have the same surface area or cortical thickness as women when they try to argue they have female brains. Instead they always point to this vague shit that can only be seen in some brain scans and that nobody can explain what it means or why it's important. I think that says it all, actually.
Instead they always point to this vague shit that can only be seen in some brain scans and that nobody can explain what it means or why it's important. I think that says it all, actually.
There are tons of differences between male and female brains. Brain size, sizes of different structures in the brain, cortical thickness, all sorts of stuff. However troon activists never point to any of these differences, you never see them saying that mtf troons have the same surface area or cortical thickness as women when they try to argue they have female brains. Instead they always point to this vague shit that can only be seen in some brain scans and that nobody can explain what it means or why it's important. I think that says it all, actually.
Add that they actively protested when researchers actually did want to do a bigger study that would improve the method and weed out the causes to the differences. The truth is that they probably did measure some sort of similarity - perhaps natural effeminacy or same-sex attraction aka HSTS. I imagine if they did the brain scan on your average hon it wouldn't show up.
I found that study on r/psychology and a few toons have left comments outright saying that they were mentally ill before they thought about transitioning. Which is the entire problem with studies on troons: you can't find any without a history of mental illness, so there's no control group!
I get that the world isn't a perfect place where people act logically and all problems are solved immediately. But I do have a thing about "minimum standards".
And the minimum standard in almost every other case of depression and suicidal ideation is to get a person over those feelings and into a place of self-validation rather than lean into whatever happens to be claimed to be causing those feelings, including the idea that everyone ELSE is the problem.
It would be nice if we could ask for some fucking ethical behavior from the medical field, and I know that after COVID, that's a dream and useless to wish for, but god fucking damn it, it doesn't mean I shouldn't say it out loud.
Isn't it great when no one ever has to take responsibility for their own identity? "Oh poor me, I have the wrong body. Please, drop any insecurity and issue you have and deal with ME!"
I'll say it a thousand times to anyone who will listen: transgenderism encourages the kind of unhealthy mental mindset and habits that would otherwise require correction in virtually anyone else.
It's why any medical professional or adjacent profession should immediately look at anyone who claims to be trans and say: we'll deal with you being trans, but let's get you mentally stable and able to cope without being a pain in the ass to other people first.
Ok, lets say for arguments sake that "discrimination" was the reason troons have poor mental health. What does the author of that study expect people to do? Force straight men to have sex with trans women because saying no to these people will cause them to kill themselves? These people talk about wanting people to respect them and yet whenever anyone tells these people no they threaten suicide. "Oh your daughters are uncomfortable being in the shower room with a boy who thinks he's a girl? Too bad because the boy will kill himself if he can't shower with the girls." Transgenderism is the only kind of mental health issue that encourages bullying and everyone having to play along. Its no wonder the community is seen as extremely toxic.
at oophorectomy taking pre-operative testosterone therapy. This was compared to cortical biopsies from age-matched healthy women obtained at caesarean section (mean age: 31.8 ± 1.5 years; range: 25–35 years, n =
