Abstract
The tryptophan catabolite (TRYCAT) pathway is induced by indoleamine 2,3-dioxygenase (IDO), which upon activation depletes plasma tryptophan (TRP) and increases the synthesis of TRYCATs. Both phenomena are associated with somatization and depression. The aims of this study are to examine whether disorders in the TRYCAT pathway are specific to depression or somatization and whether the diagnoses somatization, depression, and comorbid depression+somatization reflect qualitatively distinct clinical and biological categories. Plasma TRP, the kynurenine (KY)/TRP and KY/kynurenic acid (KA) ratios were measured in 36 patients with somatization, 35 depressed and 38 depressed+somatization patients and 22 controls. Using pattern recognition methods, the diagnosis comorbid depression+somatization could not be validated, while there was an important overlap between depression and somatization, which form one continuum. Cluster analysis detected a) a control cluster; b) a cluster with lower tryptophan, and higher KY/TRP and KY/KA ratios and somatization scores; and c) a cluster with increased depression but lower KY/TRP values. The differences between both patient clusters were quantitative and not qualitative. Within the patient group, cluster analysis has generated a “pathway phenotype”, i.e. aberrations in the TRYCAT pathway, which are associated with somatization rather than with depression.
Published Version
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