The pubertal transition is characterized by pronounced sex hormone fluctuation, refinement of affective neural circuitry, and an increased risk of depression in female adolescents. Sex hormones, including testosterone, exert modulatory effects on frontal-limbic brain networks and are associated with emotion dysregulation and depressive symptoms. Weekly changes in hormones predict affective symptoms in peripubertal female adolescents, particularly in the context of stress; however, the biobehavioral mechanisms underlying hormone change and mood relationships during the pubertal transition have yet to be determined and was the objective of the present study. Forty-three peripubertal female adolescents (ages 11–14) collected 8-weekly salivary hormone (estrone, testosterone) samples and mood assessments to evaluate hormone-mood relationships, followed by a biobehavioral testing session with psychosocial stress and EEG. Within-person correlations between weekly hormone changes and corresponding mood were performed to determine individual differences in mood sensitivity to weekly hormone change. Increased frontal theta activity indexing emotion reactivity, reduced cortisol reactivity, and reduced vagal efficiency predicted the strength of the relationship between testosterone and mood. Further, testosterone-sensitivity strength was associated with the enhancement of negative affect following stress testing. Results identify divergent frontal theta and stress responses as potential biobehavioral mechanisms underlying mood sensitivity to peripubertal testosterone fluctuation.

This study investigates relations of maternal N-3 and N-6 polyunsaturated fatty acids (PUFA) intake during pregnancy with offspring body mass index (BMI), height z-score and metabolic risk (fasting glucose, C-peptide, leptin, lipid profile) during peripuberty (8–14 years) among 236 mother–child pairs in Mexico. We used food frequency questionnaire data to quantify trimester-specific intake of N-3 alpha-linolenic acid, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA); N-6 linoleic acid and arachidonic acid (AA); and N-6:N-3 (AA:EPA+DHA), which accounts for the fact that the two PUFA families have opposing effects on physiology. Next, we used multivariable linear regression models that accounted for maternal education and parity, and child’s age, sex and pubertal status, to examine associations of PUFA intake with the offspring outcomes. In models where BMI z-score was the outcome, we also adjusted for height z-score. We found that higher second trimester intake of EPA, DHA and AA were associated with lower offspring BMI and height z-score. For example, each 1-s.d. increment in second trimester EPA intake corresponded with 0.25 (95% CI: 0.03, 0.47) z-scores lower BMI and 0.20 (0.05, 0.36) z-scores lower height. Accounting for height z-score in models where BMI z-score was the outcome attenuated estimates [e.g., EPA: −0.16 (−0.37, 0.05)], suggesting that this relationship was driven by slower linear growth rather than excess adiposity. Maternal PUFA intake was not associated with the offspring metabolic biomarkers. Our findings suggest that higher PUFA intake during mid-pregnancy is associated with lower attained height in offspring during peripuberty. Additional research is needed to elucidate mechanisms and to confirm findings in other populations.