Neuroimaging studies in people with gender incongruence

Kreukels, Baudewijntje P.C.; Guillamón, Antonio

doi:10.3109/09540261.2015.1113163

Cited by 79 publications

(70 citation statements)

References 71 publications

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“…Also, in that study we replicated the previously observed sex differences in CEOAE response amplitudes with significantly stronger emissions in control girls than in control boys, but there were no sex differences between boys and girls with GD (Burke et al, 2014). These results, in line with several neuroimaging studies, suggest a less pronounced sexual differentiation in transgender individuals (Burke, Manzouri, & Savic, 2017, and for reviews, see Guillamon, Junque, & Gómez-Gil, 2016;Kreukels & Guillamon, 2016).…”

Section: Introductionsupporting

confidence: 89%

Postnatal Effects of Sex Hormones on Click-Evoked Otoacoustic Emissions: A Study of Adolescents with Gender Dysphoria

et al. 2020

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Click-evoked otoacoustic emissions (CEOAEs) are echo-like sounds, generated by the inner ear in response to click-stimuli. A sex difference in emission strength is observed in neonates and adults, with weaker CEOAE amplitudes in males. These differences are assumed to originate from testosterone influences during prenatal male sexual differentiation and to remain stable throughout life. However, recent studies suggested activational, postnatal effects of sex hormones on CEOAEs. Adolescents diagnosed with gender dysphoria (GD) may receive gonadotropin-releasing hormone analogs (GnRHa) in order to suppress endogenous sex hormones and, therefore, pubertal maturation, followed by cross-sex hormone (CSH) treatment. Using a cross-sectional design, we examined whether hormonal interventions in adolescents diagnosed with GD (62 trans boys, assigned female at birth, self-identifying as male; 43 trans girls, assigned male at birth, self-identifying as female), affected their CEOAEs compared to age-and sex-matched controls (44 boys, 37 girls). Sex-typical differences in CEOAE amplitude were observed among cisgender controls and treatment-naïve trans boys but not in other groups with GD. Treatment-naïve trans girls tended to have more female-typical CEOAEs, suggesting hypomasculinized early sexual differentiation, in support of a prominent hypothesis on the etiology of GD. In line with the predicted suppressive effects of androgens, trans boys receiving CSH treatment, i.e., testosterone plus GnRHa, showed significantly weaker right-ear CEOAEs compared with control girls. A similar trend was seen in trans boys treated with GnRHa only. Unexpectedly, trans girls showed CEOAE masculinization with addition of estradiol. Our findings show that CEOAEs may not be used as an unequivocal measure of prenatal androgen exposure as they can be modulated postnatally by sex hormones, in the form of hormonal treatment.

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Section: Introductionsupporting

confidence: 89%

Postnatal Effects of Sex Hormones on Click-Evoked Otoacoustic Emissions: A Study of Adolescents with Gender Dysphoria

et al. 2020

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“…The first line of evidence draws on potential differences in the brain structures between transpeople and controls without a history of GD. Reviews (Guillamon, Junque, & Gómez-Gil, 2016;Kreukels & Guillamon, 2016) concluded that transpeople's brains show some atypical changes away from their natal sex and toward their experienced gender identity. However, independent replications of these findings have not yet been conducted, and therefore some caution is required (e.g., LeBel & Peters, 2011;Open Science Collaboration, 2015).…”

Section: Brain Differences Between People With and Without A History mentioning

confidence: 99%

2D:4D Suggests a Role of Prenatal Testosterone in Gender Dysphoria

et al. 2020

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Gender dysphoria (GD) reflects distress caused by incongruence between one's experienced gender identity and one's natal (assigned) gender. Previous studies suggest that high levels of prenatal testosterone (T) in natal females and low levels in natal males might contribute to GD. Here, we investigated if the 2D:4D digit ratio, a biomarker of prenatal T effects, is related to GD. We first report results from a large Iranian sample, comparing 2D:4D in 104 transwomen and 89 transmen against controls of the same natal sex. We found significantly lower (less masculine) 2D:4D in transwomen compared to control men. We then conducted random-effects meta-analyses of relevant studies including our own (k = 6, N = 925 for transwomen and k = 6, N = 757 for transmen). In line with the hypothesized prenatal T effects, transwomen showed significantly feminized 2D:4D (d ≈ 0.24). Conversely, transmen showed masculinized 2D:4D (d ≈ − 0.28); however, large unaccounted heterogeneity across studies emerged, which makes this effect less meaningful. These findings support the idea that high levels of prenatal T in natal females and low levels in natal males play a part in the etiology of GD. As we discuss, this adds to the evidence demonstrating the convergent validity of 2D:4D as a marker of prenatal T effects.

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“…White matter microstructure studies among transgender individuals who have not yet undergone hormonal interventions revealed white matter connectivity intermediate between controls of the patient's sex assigned at birth and cisgender individuals of their experienced gender (Kreukels & Guillamon, ). These intermediate white matter microstructure phenotypes were found in the superior longitudinal fasciculi, the interior frontooccipital fasciculus, the cingulum, the forceps minor, and the corticospinal tract (Rametti et al., ).…”

Section: Determinants Of Cross‐gender Identificationmentioning

confidence: 99%