Abstract
BackgroundThe aim of this cross-sectional study was to identify important biopsychosocial correlates of major depression. Biological mechanisms, including the inflammatory and the tryptophan-serotonin deficiency hypotheses of major depression, were investigated alongside health-related quality of life, life satisfaction, and social support.MethodsThe concentrations of plasma tryptophan, plasma kynurenine, plasma kynurenic acid, serum quinolinic acid, and the tryptophan breakdown to kynurenine were determined alongside health-related quality of life (Medical Outcome Study Form, SF-36), life satisfaction (Life Satisfaction Questionnaire, FLZ), and social support (Social Support Survey, SSS) in 71 depressive patients at the time of their in-patient admittance and 48 healthy controls.ResultsCorresponding with the inflammatory hypothesis of major depression, our study results suggest a tryptophan breakdown to kynurenine in patients with major depression, and depressive patients had a lower concentration of neuroprotective kynurenic acid in comparison to the healthy controls (Mann–Whitney-U: 1315.0; p = 0.046). Contradicting the inflammatory theory, the concentrations of kynurenine (t: −0.945; df = 116; p = 0.347) and quinolinic acid (Mann-Whitney-U: 1376.5; p = 0.076) in depressive patients were not significantly different between depressed and healthy controls. Our findings tend to support the tryptophan-serotonin deficiency hypothesis of major depression, as the deficiency of the serotonin precursor tryptophan in depressive patients (t: −3.931; df = 116; p < 0.001) suggests dysfunction of serotonin neurotransmission. A two-step hierarchical linear regression model showed that low tryptophan concentrations, low social support (SSS), occupational requirements (FLZ), personality traits (FLZ), impaired physical role (SF-36), and impaired vitality (SF-36) predict higher Beck Depression Inventory (BDI-II) scores.DiscussionOur study results argue for the validity of a biopsychosocial model of major depression with multiple pathophysiological mechanisms involved.
Highlights
Traditional biomedical models of clinical medicine focus on pathophysiology and biological approaches to illness
The basic sociodemographic, clinical (BDI-II) and treatment characteristics of the 71 depressive patients and the 48 healthy controls have already been reported in detail in previously published studies about nitric oxide-related biological pathways and about the impact of branched-chain amino acids (BCAAs) as new biomarkers of major depression (Baranyi et al, 2016)
There were no significant sociodemographic differences between the study participants suffering from major depression and the healthy controls regarding their sex, age, marital status, employment status and living arrangements
Summary
Traditional biomedical models of clinical medicine focus on pathophysiology and biological approaches to illness. Biological mechanisms apply in several hypotheses, including the Tryptophan-Serotonin (TRP-5-HT) deficiency hypothesis as well as the inflammatory and neurodegeneration hypothesis of major depression (Bijanki et al, 2014; Patten, 2015). The aim of this cross-sectional study was to identify important biopsychosocial correlates of major depression. Biological mechanisms, including the inflammatory and the tryptophan-serotonin deficiency hypotheses of major depression, were investigated alongside health-related quality of life, life satisfaction, and social support. Corresponding with the inflammatory hypothesis of major depression, our study results suggest a tryptophan breakdown to kynurenine in patients with major depression, and depressive patients had a lower concentration of neuroprotective kynurenic acid in comparison to the healthy controls (Mann–Whitney-U: 1315.0; p = 0.046). Our study results argue for the validity of a biopsychosocial model of major depression with multiple pathophysiological mechanisms involved
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