Evidence map›Paper›PMID 37333619›Full record

ArticleFrontiers in molecular neuroscience2023

Tryptophan catabolites, inflammation, and insulin resistance as determinants of chronic fatigue syndrome and affective symptoms in long COVID.

Hussein Kadhem Al-Hakeim, Anwar Khairi Abed, Shatha Rouf Moustafa, Abbas F Almulla, Michael Maes

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
10.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  4. Network-based integration of metabolomics data from large-scale repositories.Metabolomics : Official journal of the Metabolomic Society · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 5 countries.

Hussein Kadhem Al-HakeimDepartment of Chemistry, College of Science, University of Kufa, Kufa, Iraq.
Anwar Khairi AbedDepartment of Chemistry, College of Science, University of Kufa, Kufa, Iraq.
Shatha Rouf MoustafaClinical Analysis Department, College of Pharmacy, Hawler Medical University, Erbil, Iraq.
Abbas F AlmullaDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Michael MaesDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
University of Kufa · IQBarwon Health · AUChulalongkorn University · THHawler Medical University · IQ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Critical COVID-19 disease is accompanied by depletion of plasma tryptophan (TRY) and increases in indoleamine-dioxygenase (IDO)-stimulated production of neuroactive tryptophan catabolites (TRYCATs), including kynurenine (KYN). The TRYCAT pathway has not been studied extensively in association with the physiosomatic and affective symptoms of Long COVID. In the present study, we measured serum TRY, TRYCATs, insulin resistance (using the Homeostatic Model Assessment Index 2-insulin resistance, HOMA2-IR), C-reactive protein (CRP), physiosomatic, depression, and anxiety symptoms in 90 Long COVID patients, 3-10 months after remission of acute infection. We were able to construct an endophenotypic class of severe Long COVID (22% of the patients) with very low TRY and oxygen saturation (SpO2, during acute infection), increased kynurenine, KYN/TRY ratio, CRP, and very high ratings on all symptom domains. One factor could be extracted from physiosomatic symptoms (including chronic fatigue-fibromyalgia), depression, and anxiety symptoms, indicating that all domains are manifestations of the common physio-affective phenome. Three Long COVID biomarkers (CRP, KYN/TRY, and IR) explained around 40% of the variance in the physio-affective phenome. The latter and the KYN/TRY ratio were significantly predicted by peak body temperature (PBT) and lowered SpO2 during acute infection. One validated latent vector could be extracted from the three symptom domains and a composite based on CRP, KYN/TRY, and IR (Long COVID), and PBT and SpO2 (acute COVID-19). In conclusion, the physio-affective phenome of Long COVID is a manifestation of inflammatory responses during acute and Long COVID, and lowered plasma tryptophan and increased kynurenine may contribute to these effects.

Indexed as

affective symptomschronic fatigue syndromeindoleamine-2,3-dioxygenaseinflammationneuro-immuneneurotoxicity

Identifiers

PMID37333619
PMCPMC10272345
OpenAlexW4379958514

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.