ArticlePsychoneuroendocrinology2026
Links between hormonal and pubertal development, and adolescent females' risk for affective symptoms.
Article in Psychoneuroendocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Depression and anxiety symptoms surge during adolescence, particularly in females, yet the biological mechanisms underlying this vulnerability remain poorly understood. Although estrogen has traditionally been emphasized, androgens such as dehydroepiandrosterone (DHEA) and testosterone may represent distinct pathways to affective symptom risk. The present study examined whether increases in testosterone predict internalizing symptoms in adolescent females by examining hormonal and physical aspects of pubertal development and testing whether testosterone effects persist beyond estradiol and observable maturation. Using data from 5476 females (ages 9-13) in the Adolescent Brain Cognitive Development Study, we analyzed annual salivary DHEA, testosterone, and estradiol alongside caregiver-reported pubertal development and youth-reported internalizing symptoms. Latent change score models captured developmental dynamics: univariate models characterized growth trajectories, bivariate coupling models tested directional hormonal influences, and the final model evaluated whether testosterone and pubertal development changes predicted internalizing symptoms, controlling for estradiol, age, and assay covariates. Testosterone increased gradually across early adolescence, whereas DHEA showed accelerating, nonlinear growth. Increases in testosterone predicted higher internalizing symptoms between ages 10 and 12 (b = 0.041, 95% CI [0.007, 0.076]; b = 0.075, 95% CI [0.009, 0.142]). Observable pubertal development was negatively associated with internalizing symptoms at one assessment. Estradiol predicted subsequent pubertal development and showed concurrent associations with internalizing symptoms at two assessments but did not explain the testosterone-internalizing link. Increases in testosterone predicted internalizing symptoms after accounting for observable maturation and estradiol, identifying a specific vulnerability window between ages 10-12 with implications for early identification and timing of preventive interventions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.