Lowered Quality of Life in Long COVID Is Predicted by Affective Symptoms, Chronic Fatigue Syndrome, Inflammation and Neuroimmunotoxic Pathways
Michael Maes (),
Haneen Tahseen Al-Rubaye,
Abbas F. Almulla,
Dhurgham Shihab Al-Hadrawi,
Kristina Stoyanova,
Marta Kubera and
Hussein Kadhem Al-Hakeim
Additional contact information
Michael Maes: Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Haneen Tahseen Al-Rubaye: College of Medical laboratory Techniques, Imam Ja’afar Al-Sadiq University, Najaf 54001, Iraq
Abbas F. Almulla: Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Dhurgham Shihab Al-Hadrawi: Al-Najaf Center for Cardiac Surgery and Transcatheter Therapy, Najaf 54001, Iraq
Kristina Stoyanova: Department of Psychiatry, Medical University of Plovdiv, 4002 Plovdiv, Bulgaria
Marta Kubera: Laboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna St., 31-343 Krakow, Poland
Hussein Kadhem Al-Hakeim: Department of Chemistry, College of Science, University of Kufa, Kufa 54002, Iraq
IJERPH, 2022, vol. 19, issue 16, 1-21
Abstract:
The physio-affective phenome of Long COVID-19 is predicted by (a) immune-inflammatory biomarkers of the acute infectious phase, including peak body temperature (PBT) and oxygen saturation (SpO2), and (b) the subsequent activation of immune and oxidative stress pathways during Long COVID. The purpose of this study was to delineate the effects of PBT and SpO2 during acute infection, as well as the increased neurotoxicity on the physical, psychological, social and environmental domains of health-related quality of life (HR-QoL) in people with Long COVID. We recruited 86 participants with Long COVID and 39 normal controls, assessed the WHO-QoL-BREF (World Health Organization Quality of Life Instrument-Abridged Version, Geneva, Switzerland) and the physio-affective phenome of Long COVID (comprising depression, anxiety and fibromyalgia-fatigue rating scales) and measured PBT and SpO2 during acute infection, and neurotoxicity (NT, comprising serum interleukin (IL)-1β, IL-18 and caspase-1, advanced oxidation protein products and myeloperoxidase, calcium and insulin resistance) in Long COVID. We found that 70.3% of the variance in HR-QoL was explained by the regression on the physio-affective phenome, lowered calcium and increased NT, whilst 61.5% of the variance in the physio-affective phenome was explained by calcium, NT, increased PBT, lowered SpO2, female sex and vaccination with AstraZeneca and Pfizer. The effects of PBT and SpO2 on lowered HR-QoL were mediated by increased NT and lowered calcium yielding increased severity of the physio-affective phenome which largely affects HR-QoL. In conclusion, lowered HR-Qol in Long COVID is largely predicted by the severity of neuro-immune and neuro-oxidative pathways during acute and Long COVID.
Keywords: Long COVID; depression; myalgic encephalomyelitis/chronic fatigue syndrome; depression; neuro-immune; inflammation; psychiatry (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2022
References: View complete reference list from CitEc
Citations: View citations in EconPapers (1)
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