Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Baranyi, A; Amouzadeh-Ghadikolai, O; von Lewinski, D; Breitenecker, RJ; Rothenhäusler, HB; Robier, C; Baranyi, M; Theokas, S; Meinitzer, A.
Revisiting the tryptophan-serotonin deficiency and the inflammatory hypotheses of major depression in a biopsychosocial approach.
PeerJ. 2017; 5(46):e3968-e3968
Doi: 10.7717/peerj.3968
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- Führende Autor*innen der Med Uni Graz
- Baranyi Andreas
- von Lewinski Dirk
- Co-Autor*innen der Med Uni Graz
- Meinitzer Andreas
- Robier Christoph
- Rothenhäusler Hans-Bernd
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- Abstract:
- 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. The 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. 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). 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. Our study results argue for the validity of a biopsychosocial model of major depression with multiple pathophysiological mechanisms involved.
- Find related publications in this database (Keywords)
- Major depression
- Tryptophan-serotonin deficiency hypothesis
- Inflammatory hypothesis
- Life satisfaction
- Social support
- Health-related quality of life