Data available on possible associations of lipids, steroid levels, and depression are conflicting. This study investigated their possible associations in a sample of youth with depression. Ninety-eight youth with depression and individually matched healthy volunteers on the basis of age and sex were enrolled for the study. The two groups had nearly similar body mass index. After fasting overnight, they underwent blood sampling for triglycerides (TG), total cholesterol, low-density lipoprotein, high-density lipoprotein (HDL)-cholesterol, apolipoprotein A1 (apo A1) and B (apo B), lipoprotein A (LpA), morning cortisol, total testosterone (TT), estradiol (E2), and DHEAS measurements. All participants were evaluated with the semi-structured psychiatric K-SADS-PL interview and filled out the self-rating Children's Depression Inventory (CDI). Salivary cortisol was also determined serially five times a day. Children with depression showed significantly higher levels of plasma TG (p = 0.006), lower apolipoprotein A1 (p = 0.043), higher morning cortisol (p = 0.011) and TT (p = 0.001), as well as lower E2 levels (p = 0.032) compared to those of controls. Positive correlations for the total sample was observed between TG (R = 0.24, p = 0.018), TT (R = 0.35, p <0.001), and morning cortisol (R = 0.29, p = 0.005) with the CDI scores. The depression group showed elevated cortisol levels 30 min after awakening, 15:00, 18:00, 21:00, and increased cortisol awakening Response and Area Under the Curve (AUCg) (p = 0.030, p = 0.007, respectively) compared to those of controls. Higher cortisol and TG levels in children with depression imply an increased metabolic risk, starting early in development; therefore, routine metabolic assessment in this group is of great importance.
CITATION STYLE
Syros, I., Pervanidou, P., Liapi, C., Apostolakou, F., Chrousos, G. P., & Kolaitis, G. (2020). Increased diurnal salivary cortisol and morning serum triglycerides and decreased Apo A1 concentrations in children and adolescents with clinical depression. OBM Neurobiology, 4(2). https://doi.org/10.21926/obm.neurobiol.2002060
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