A Biopsychosocial Model of Adolescent Gender Dysphoria

Abstract

Gender dysphoria is a mental health condition characterized by clinically significant distress or impairment associated with marked gender incongruence, a feeling of discordance between one’s gender identity and biological sex. Gender incongruence and dysphoria prevalence have risen substantially in recent years, particularly in adolescent females. My dissertation aims to understand the etiology of these phenomena through a historical overview of clinical gender dysphoria, case studies of gender reassignment in populations with disorders of sex development, theories of the neurobiology of sexual development, and four empirical studies examining gender incongruence across early adolescent development. My empirical chapters make use of the Adolescent Brain Cognitive Development (ABCD) Study sample, a demographically diverse longitudinal sample of 11,864 youths in the United States followed from ages 9-10 years in 2016-2018 to ages 14-15 years in 2021-2023. Chapter 1 reports developmental trajectories of self- and parent-reported gender incongruence, gender expression, and gender identity across five timepoints. While gender expression was stable with age, gender incongruence and transgender or nonbinary (TNB) self-identification increased with age, particularly in females. At baseline, 0.5% of males and 1.1% of females identified as TNB. By Wave 5, 1.2% of males and 9.6% of females identified as TNB. Females were also more likely to report gender incongruence and elevated gender nonconformity (i.e., sex-atypical gender expression). TNB youth reported elevated gender nonconformity across all ages, but showed increased gender incongruence only at later timepoints. Parents reported lower gender incongruence across all measures. Chapter 2 makes use of ABCD’s large sample of 1,970 same-sex twins to estimate the heritability of gender incongruence. Gender incongruence was more common in females, and concordance was higher in female twin pairs than male twin pairs. Binary probandwise concordance for TNB gender identity was 46% among monozygotic pairs compared to 13% among dizygotic pairs. ACE models revealed that genetic factors explained 47% of the variance of gender incongruence, with the remaining variance explained by non-shared environmental factors. Estimates had large standard errors, and thus high uncertainty, but suggest a large genetic contribution to gender incongruence in adolescents. Chapter 3 examined concurrent and longitudinal cross-lagged associations between self-reported gender incongruence and a range of biopsychosocial variables known or hypothesized to be associated with gender dysphoria: internalizing symptoms, autism spectrum traits, sexual orientation, pubertal timing, body mass index, family conflict, peer victimization, cyberbullying, screen time, and number of TNB friends. All predictors of interest were significantly associated with gender incongruence except family conflict and number of TNB friends. Cross-lagged models tested competing hypotheses between the theory of rapid-onset gender dysphoria (ROGD) and minority stress theory on the directionality of these associations. Higher internalizing symptoms and screen time predicted later gender incongruence, but not vice versa, in females across all timepoints, while other associations were mixed. Longitudinal results largely favored predictions made by ROGD over minority stress theory. Chapter 4 aimed to document predictors of longitudinal persistence and desistance of TNB gender identity within the subsample of 670 TNB adolescents, and to test whether a three-cluster solution of latent gender incongruence classes resembled a hypothesized typology distinguishing between classical gender dysphoria, autogynephilia, and ROGD. Finite mixture regression identified three latent profiles of gender incongruence, but these appeared to describe mild, moderate, and pronounced subtypes of ROGD rather than the triune typology. Participants in the “mild” cluster were exclusively nonbinary (as opposed to transgender-identified), had a 100% longitudinal desistance rate, sex-typical gender expression, and low levels of internalizing symptoms and social stress. Conversely, participants in the “pronounced” cluster had the highest rates of transgender identification, nonheterosexual orientation, internalizing symptoms, and social stress, and the highest longitudinal persistence rates at 45%. Biopsychosocial correlates of gender incongruence largely did not predict longitudinal TNB persistence or desistance; the strongest predictors were gender identity and sexual orientation. I conclude by proposing a new biopsychosocial model of adolescent gender dysphoria, synthesizing these findings on adolescent gender incongruence with existing clinical and neurobiological theories of gender dysphoria. This model accounts for recent rises in nonbinary identification among adolescents without gender dysphoria symptoms by introducing a subtype of gender incongruence not captured in existing typologies, characterized by identity exploration, low persistence rates, and sex-typical gender expression and psychosocial adjustment. Sociocultural and neuroendocrine pathways to gender incongruence are discussed.