Reduced serum cortisol, IGF-1, GLP-1, and T3 levels in medication-free children and adolescents with...

Obsessive-compulsive disorder (OCD) frequently emerges during childhood and adolescence and has been associated with alterations in multiple neurobiological systems. Neuroendocrine pathways involved in stress regulation, neurodevelopment, metabolic signaling, and thyroid function interact closely to influence brain circuits implicated in OCD. However, studies simultaneously examining several neuroendocrine parameters in pediatric OCD remain limited.

This case-control study included 52 medication-free children and adolescents with OCD and 42 healthy controls aged 8-17 years. Psychiatric diagnoses were established using the Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version (K-SADS-PL) according to DSM-5 criteria. Obsessive-compulsive symptom severity was assessed using the Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS). Anxiety and depressive symptoms were evaluated using the Screen for Child Anxiety Related Emotional Disorders (SCARED) and the Children's Depression Inventory (CDI), respectively. Serum levels of adrenocorticotropic hormone (ACTH), cortisol, growth hormone (GH), Insulin-like growth factor-1 (IGF-1), Glucagon-like peptide-1 (GLP-1), relaxin-3 (RLN-3), triiodothyronine (T3), and thyroid-stimulating hormone (TSH) were measured using ELISA. Group differences were examined using covariance-based models controlling for age, sex, BMI percentile, anxiety (SCARED), and depressive symptoms (CDI).

Initial analyses showed that children and adolescents with OCD had significantly lower serum levels of cortisol, IGF-1, GLP-1, and T3 compared with healthy controls. These differences remained significant after controlling for age, sex, BMI percentile, and the SCARED and CDI total score, with adjusted analyses showing lower levels of cortisol (p = 0.003), IGF-1 (p = 0.013), GLP-1 (p = 0.017), and T3 (p = 0.015) in the OCD group. Correlation analyses did not reveal significant associations between biochemical parameters and OCD symptom severity after correction for multiple comparisons.

These findings suggest that pediatric OCD may be associated with alterations in several neuroendocrine pathways rather than isolated changes within a single hormonal system. Further longitudinal studies are needed to better clarify the biological basis and clinical significance of these findings.