Kanchanatawan, Buranee, Thika, Supaksorn, Sirivichayakul, Sunee et al. · Neurotoxicity research · 2018 · DOI
This study examined 80 people with schizophrenia and 40 healthy controls to understand why schizophrenia patients often experience depression, anxiety, and physical symptoms like those seen in chronic fatigue. The researchers found that these symptoms were linked to changes in how the body breaks down tryptophan (an amino acid), problems with memory, and the severity of psychotic symptoms. The findings suggest that toxic byproducts from tryptophan metabolism may contribute to depression, anxiety, and physical symptoms in schizophrenia.
Although this study focuses on schizophrenia rather than ME/CFS, it provides important evidence that depression, anxiety, and physical symptoms can be driven by both cognitive impairment and dysregulated tryptophan metabolism—mechanisms potentially relevant to ME/CFS pathophysiology. The identification of tryptophan catabolites as contributors to systemic symptoms suggests a metabolic pathway that warrants investigation in ME/CFS populations.
This study does not establish causality; the cross-sectional design cannot determine whether tryptophan dysmetabolism causes symptoms or results from them. The findings are specific to schizophrenia and cannot be directly applied to ME/CFS without replication in ME/CFS cohorts. The study does not assess whether these mechanisms are unique to schizophrenia or shared across conditions with similar symptom profiles.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
Spotted an error in this entry? Report it →