Environmental, Neuro-immune, and Neuro-oxidative Stress Interactions in Chronic Fatigue Syndrome

Bjørklund, Geir; Dadar, Maryam; Pivina, Lyudmila; Doşa, Monica Daniela; Semenova, Yuliya; Maes, Michaël

doi:10.1007/s12035-020-01939-w

Cited by 31 publications

(27 citation statements)

References 94 publications

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“…Also, circulating lymphocytes often produce increased transcripts of these cytokines ( 129 ). Both COVID-19 and ME/CFS are associated with activation of the protein kinase R and 2- to 5A synthetase antiviral IFN response pathways ( 130 – 132 ).…”

Section: Connecting Redox Imbalance To Inflammation In Covid-19 and Me/cfsmentioning

confidence: 99%

Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome

Paul

Lemle

Komaroff

et al. 2021

Proc. Natl. Acad. Sci. U.S.A.

179

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Although most patients recover from acute COVID-19, some experience postacute sequelae of severe acute respiratory syndrome coronavirus 2 infection (PASC). One subgroup of PASC is a syndrome called “long COVID-19,” reminiscent of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a debilitating condition, often triggered by viral and bacterial infections, leading to years-long debilitating symptoms including profound fatigue, postexertional malaise, unrefreshing sleep, cognitive deficits, and orthostatic intolerance. Some are skeptical that either ME/CFS or long COVID-19 involves underlying biological abnormalities. However, in this review, we summarize the evidence that people with acute COVID-19 and with ME/CFS have biological abnormalities including redox imbalance, systemic inflammation and neuroinflammation, an impaired ability to generate adenosine triphosphate, and a general hypometabolic state. These phenomena have not yet been well studied in people with long COVID-19, and each of them has been reported in other diseases as well, particularly neurological diseases. We also examine the bidirectional relationship between redox imbalance, inflammation, energy metabolic deficits, and a hypometabolic state. We speculate as to what may be causing these abnormalities. Thus, understanding the molecular underpinnings of both PASC and ME/CFS may lead to the development of novel therapeutics.

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Section: Connecting Redox Imbalance To Inflammation In Covid-19 and Me/cfsmentioning

confidence: 99%

Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome

Paul

Lemle

Komaroff

et al. 2021

Proc. Natl. Acad. Sci. U.S.A.

179

View full text Add to dashboard Cite

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“…PTSD has also been frequently related to several further co-morbidities, such as chronic fatigue syndrome (CFS) [261][262][263], fibromyalgia [264][265][266][267][268], irritable bowel syndrome (IBS) [269], and rheumatoid arthritis [270], which all share a very similar underlying neuroendocrinological profile to PTSD (e.g., hypocortisolism, blunted diurnal GC rhythm and HPA axis reactivity) [271][272][273][274][275] and have all been repeatedly associated with increased OXS [276][277][278][279][280][281][282].…”

Section: Other Comorbiditiesmentioning

confidence: 99%

Oxidative Dysregulation in Early Life Stress and Posttraumatic Stress Disorder: A Comprehensive Review

2021

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Traumatic stress may chronically affect master homeostatic systems at the crossroads of peripheral and central susceptibility pathways and lead to the biological embedment of trauma-related allostatic trajectories through neurobiological alterations even decades later. Lately, there has been an exponential knowledge growth concerning the effect of traumatic stress on oxidative components and redox-state homeostasis. This extensive review encompasses a detailed description of the oxidative cascade components along with their physiological and pathophysiological functions and a systematic presentation of both preclinical and clinical, genetic and epigenetic human findings on trauma-related oxidative stress (OXS), followed by a substantial synthesis of the involved oxidative cascades into specific and functional, trauma-related pathways. The bulk of the evidence suggests an imbalance of pro-/anti-oxidative mechanisms under conditions of traumatic stress, respectively leading to a systemic oxidative dysregulation accompanied by toxic oxidation byproducts. Yet, there is substantial heterogeneity in findings probably relative to confounding, trauma-related parameters, as well as to the equivocal directionality of not only the involved oxidative mechanisms but other homeostatic ones. Accordingly, we also discuss the trauma-related OXS findings within the broader spectrum of systemic interactions with other major influencing systems, such as inflammation, the hypothalamic-pituitary-adrenal axis, and the circadian system. We intend to demonstrate the inherent complexity of all the systems involved, but also put forth associated caveats in the implementation and interpretation of OXS findings in trauma-related research and promote their comprehension within a broader context.

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“…People with COVID-19 also frequently suffer from mental fatigue, physical fatigue, mild loss of concentration, neurocognitive deficits, headache and myalgia ( Borges do Nascimento et al, 2020 ; Liu et al, 2020b ; Zhang et al, 2020c ; Zhu et al, 2020 ), symptoms which are reminiscent of Myalgic Encephalomyelitis / chronic fatigue syndrome (ME/CFS) ( Maes and Twisk, 2010 ). As with mood disorders, patients with ME/CFS show activated neuro-immune pathways with increased levels of pro- and anti-inflammatory cytokines, an acute phase response and multiple signs of nitro-oxidative damage ( Bjørklund et al, 2020b ; Morris and Maes, 2013 ). Nevertheless, no research has delineated the immune pathways of affective and ME/CFS-like symptoms in people with COVID-19.…”

Section: Introductionmentioning

confidence: 99%

Intersections between pneumonia, lowered oxygen saturation percentage and immune activation mediate depression, anxiety, and chronic fatigue syndrome-like symptoms due to COVID-19: A nomothetic network approach

Al-Jassas

Al‐Hakeim

Maes

2022

Journal of Affective Disorders

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Background : COVID-19 is associated with neuropsychiatric symptoms including increased depressive, anxiety and chronic fatigue-syndrome (CFS)-like and physiosomatic symptoms. Aims : To delineate the associations between affective and CFS-like symptoms in COVID-19 and chest computed tomography scan anomalies (CCTAs), oxygen saturation (SpO 2 ), interleukin (IL)-6, IL-10, C-Reactive Protein (CRP), albumin, calcium, magnesium, soluble angiotensin converting enzyme (ACE2) and soluble advanced glycation products (sRAGEs). Method : The above biomarkers were assessed in 60 COVID-19 patients and 30 heathy controls who had measurements of the Hamilton Depression (HDRS) and Anxiety (HAM-A) and the Fibromyalgia and Chronic Fatigue (FF) Rating Scales. Results : Partial Least Squares-SEM analysis showed that reliable latent vectors could be extracted from a) key depressive and anxiety and physiosomatic symptoms (the physio-affective or PA-core), b) IL-6, IL-10, CRP, albumin, calcium, and sRAGEs (the immune response core); and c) different CCTAs (including ground glass opacities, consolidation, and crazy paving) and lowered SpO2% (lung lesions). PLS showed that 70.0% of the variance in the PA-core was explained by the regression on the immune response and lung lesions latent vectors. One common “infection-immune-inflammatory (III) core” underpins pneumonia-associated CCTAs, lowered SpO2 and immune activation, and this III core explains 70% of the variance in the PA core, and a relevant part of the variance in melancholia, insomnia, and neurocognitive symptoms. Discussion : Acute SARS-CoV-2 infection is accompanied by lung lesions and lowered SpO2 which may cause activated immune-inflammatory pathways, which mediate the effects of the former on the PA-core and other neuropsychiatric symptoms due to SARS-CoV-2 infection.

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Environmental, Neuro-immune, and Neuro-oxidative Stress Interactions in Chronic Fatigue Syndrome

Cited by 31 publications

References 94 publications

Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome

Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome

Oxidative Dysregulation in Early Life Stress and Posttraumatic Stress Disorder: A Comprehensive Review

Intersections between pneumonia, lowered oxygen saturation percentage and immune activation mediate depression, anxiety, and chronic fatigue syndrome-like symptoms due to COVID-19: A nomothetic network approach

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