Stress Hormones Cortisol and Aldosterone, and Selected Markers of Oxidative Stress in Response to Long-Term Supplementation with Omega-3 Fatty Acids in Adolescent Children with Depression

Abstract

Late childhood and adolescence are crucial periods of brain development with high vulnerability to environmental insults. The aim of this study was to test the hypotheses that in adolescents with depression (a) 12 weeks-supplementation with omega-3 fatty acids results in the attenuation of salivary stress hormone concentrations; (b) the mentioned supplementation improves potentially disrupted daily rhythm of stress hormones; (c) stress hormone concentrations correlate with values of selected markers of oxidative stress. The sample consisted of 60 patients suffering from depression aged 11–18 years. Hormone concentrations in saliva were measured in the morning and midday before (baseline) and after (6, 12 weeks) food supplementation with omega-3 or omega-6 (as comparator) fatty acids. Morning cortisol decreased in response to omega-3 but not omega-6 fatty acids at 12 weeks compared to baseline. No changes were observed in aldosterone concentrations. The obtained results show that adolescent children with depression preserved the daily rhythm of both stress hormones. Baseline morning cortisol concentrations correlated positively with depression severity and lipoperoxides, and negatively with docosahexaenoic acid. Aldosterone concentrations correlated positively with 8-isoprostane. Thus, both hormones showed positive correlation with the selected markers of oxidative stress suggesting that enhanced stress hormone secretion may be associated with increased oxidative tissue damage in adolescent children with depression. This study was registered with the ISRCTN registry (DEPOXIN study, ISRCTN81655012).

The kynurenine and serotonin pathway, neopterin and biopterin in depressed children and adolescents: an impact of omega-3 fatty acids, and association with markers related to depressive disorder. A randomized, blinded, prospective study

“…This work is a part of the DEPOXIN project (ISRCTN81655012). A detailed description of the study design, recruitment of patients, inclusion and exclusion criteria, interventions, and previous study results are presented in recent publications ( 7 , 15 , 21 – 23 ). For readers’ convenience, key information about the design of the project is given in Supplements as Supplement - Study design.…”

“…The samples were stored at −20°C until analyzed. Details of saliva collection are described in our paper ( 15 ).…”

“…Oxidative stress is closely associated with inflammation ( 13 ), activating IDO and consequently triggering KYN production. Stress is another initiator of the kynurenine pathway: it activates the HPA axis, which in turn initiates the production of pro-inflammatory mediators such as cortisol ( 14 , 15 ) and thereby activates the IDO enzyme ( Figure 1 ).…”

The role of aldosterone in the pathogenesis of diabetic retinopathy

“…The renin-angiotensin-aldosterone system (RAAS) is a critical part of the vasoactive hormone pathway, in which aldosterone plays a key role. When RAAS is stimulated and activated, angiotensin II stimulates adrenal glomerular cells to release aldosterone, which then causes a series of pathophysiological changes such as tissue inflammation ( 7 ), fibrosis ( 8 ) cell proliferation ( 9 ), oxidative stress ( 10 ) and neovascularization ( 11 – 13 ) ( Figure 1 ). Based on these findings, researchers confirmed that aldosterone is critical in the pathological mechanism of cardiovascular disease and chronic kidney disease ( 14 ).…”

Prenatal stress induces a depressive-like phenotype in adolescent rats: The key role of TGF-β1 pathway

“…Depressed children and adolescents have shown HPA axis dysregulation and higher basal cortisol levels compared to healthy controls (Silberg et al, 1999). This enhanced cortisol secretion is associated with: i) increased oxidative tissue damage in adolescent children with depression (Oravcova et al, 2022); ii) a deficit of serotoninergic system (Hughes et al, 1996) combined with a lower expression/function of the serotonin transporter than in adults and a reduced clinical response to selective serotonin reuptake inhibitors (SSRIs) (Bowman And Daws 2019).…”