Research: Limbic perfusion is reduced in patients with ME/CFS

Posted on 11/26/2021 by wames

Limbic perfusion is reduced in patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), by Xia Li, Per Julin and Tie-Qiang Li in Tomography 2021, 7(4), 675-687; [doi.org/10.3390/tomography7040056] 1 Nov 2021

 

Research abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is an illness characterized by a diverse range of debilitating symptoms including autonomic, immunologic, and cognitive dysfunction. Although neurological and cognitive aberrations have been consistently reported, relatively little is known regarding the regional cerebral blood flow (rCBF) in ME/CFS.

In this study, we studied a cohort of 31 ME/CSF patients (average age: 42.8 ± 13.5 years) and 48 healthy controls (average age: 42.9 ± 12.0 years) using the pseudo-continuous arterial spin labeling (PCASL) technique on a whole-body clinical 3T MRI scanner.

Besides routine clinical MRI, the protocol included a session of over 8 min-long rCBF measurement. The differences in the rCBF between the ME/CSF patients and healthy controls were statistically assessed with voxel-wise and AAL ROI-based two-sample t-tests. Linear regression analysis was also performed on the rCBF data by using the symptom severity score as the main regressor.

Hypoperfusion is a term that describes “a reduced amount of blood flow”

In comparison with the healthy controls, the patient group showed significant hypoperfusion (uncorrected voxel wise p ≤ 0.001, FWE p ≤ 0.01) in several brain regions of the limbic system, including the anterior cingulate cortex, putamen, pallidum, and anterior ventral insular area. For the ME/CFS patients, the overall symptom severity score at rest was significantly associated with a reduced rCBF in the anterior cingulate cortex.

In the human brain, the anterior cingulate cortex (ACC) is involved in certain higher-level functions, such as attention allocation, reward anticipation, decision-making, ethics and morality, impulse control (e.g. performance monitoring and error detection), and emotion. [Wikipedia]

The results of this study show that brain blood flow abnormalities in the limbic system may contribute to ME/CFS pathogenesis.

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Research: Analysis of post COVID-19 & its overlap with ME/CFS

Posted on 11/25/2021 by wames

Long COVID overlap with ME/CFS

 

A group of researchers from around the world have joined together to analyse long COVID’s symptom overlap with ME/CFS.

Highlights

  • Serious side effects and post-infection sequelae have been reported in SARS-CoV-2-infected patients after acute disease phase.
  • Long-COVID patient characteristics and symptoms were compared to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
  • The onset, progression, and symptom profile of long-COVID patients have considerable overlap with ME/CFS.
  • Longitudinal monitoring of COVID-19 patients is warranted to understand the virus long-term effects.

 

 

 

 

 

 

 

Analysis of post COVID-19 condition and its overlap with myalgic encephalomyelitis/

chronic fatigue syndrome, by Olga A Sukocheva, Rebekah Maksoud, Narasimha M Beeraka, SabbaRao V Madhunapantula, Mikhail Sinelnikov, Vladimir N Nikolenko, Margarita E Neganova, Sergey G Klochkov, Mohammad Amjad Kamali, Donald R Staines, Sonya Marshall-Gradisnik in  Journal of Advanced Research, Volume 40, September 2022, Pages 179-196 [doi.org/10.1016/j.jare.2021.11.013] Preprint Nov 2021

Research abstract

Background

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) disease (COVID-19) triggers the development of numerous pathologies and infection-linked complications and exacerbates existing pathologies in nearly all body systems. Aside from the primarily targeted respiratory organs, adverse SARS-CoV-2 effects were observed in nervous, cardiovascular, gastrointestinal/metabolic, immune, and other systems in COVID-19 survivors. Long-term effects of this viral infection have been recently observed and represent distressing sequelae recognised by the World Health Organisation (WHO) as a distinct clinical entity defined as post-COVID-19 condition. Considering the pandemic is still ongoing, more time is required to confirm post COVID-19 condition diagnosis in the COVID-19 infected cohorts, although many reported post COVID-19 symptoms overlap with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Aims of Review

In this study, COVID-19 clinical presentation and associated post-infection sequelae (post-COVID-19 condition) were reviewed and compared with ME/CFS symptomatology.

Key Scientific Concepts of Review

The onset, progression, and symptom profile of post COVID-19 condition patients have considerable overlap with ME/CFS. Considering the large scope and range of pro-inflammatory effects of this virus, it is reasonable to expect development of post COVID-19 clinical complications in a proportion of the affected population. There are reports of a later debilitating syndrome onset three months post COVID-19 infection (often described as long-COVID-19), marked by the presence of fatigue, headache, cognitive dysfunction, post-exertional malaise, orthostatic intolerance, and dyspnoea. Acute inflammation, oxidative stress, and increased levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha), have been reported in SARS-CoV-2 infected patients.

Longitudinal monitoring of post COVID-19 patients is warranted to understand the long-term effects of SARS-CoV-2 infection and the pathomechanism of post COVID-19 condition.

 

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Hypothesis: An attempt to explain the neurological symptoms of ME/CFS

Posted on 11/24/2021 by wames

An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome, by Klaus J Wirth, Carmen Scheibenbogen & Friedemann Paul in Journal of Translational Medicine volume 19, no: 471 (2021)

 

Review abstract

There is accumulating evidence of endothelial dysfunction, muscle and cerebral hypoperfusion in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS).

In this paper we deduce the pathomechanisms resulting in central nervous pathology and the myriad of neurocognitive symptoms. We outline tentative mechanisms of impaired cerebral blood flow, increase in intracranial pressure and central adrenergic hyperactivity and how they can well explain the key symptoms of cognitive impairment, brain fog, headache, hypersensitivity, sleep disturbances and dysautonomia.

Excerpt from Introduction

Key neurological pathomechanisms in ME/CFS

ME/CFS is classified as a neurological disease. This is based on neurological symptoms including mental fatigue, impaired cognition, psychomotor slowing, disturbed sleep, hypersensitivities to noise, light and smells, headache, pain and paresthesias and severe dysautonomia.

Many symptoms are, however, not obviously explained by neurological pathology including the cardiovascular situation with orthostatic intolerance, hypovolemia and a low activity of the renin–angiotensin–aldosterone system (RAAS), or the impaired muscle function (reduced handgrip strength and fatigability) and energetic disturbance. This co-occurrence of seemingly unrelated symptoms and findings prompts to look for a unifying explanation (the most parsimonious explanation).

 The authors discuss:

  • Decreased cerebral blood flow (CBF)
  • Disturbed local blood flow regulation and neurovascular coupling
  • Increase in intracranial pressure
  • Disturbances of reflexes and autonomic function, hypervigilance and hypersensitivity to sensory stimuli such as light, noises and smells and brain fog
  • Hypocapnia, hyperventilation, respiratory alkalosis and possible consequences for skeletal muscle metabolism
  • Sleep disturbances and non-restorative sleep

Conclusion

Neurological symptoms in ME/CFS can be severe and debilitiating, but no clear specific brain pathology or lesions have been detected so far. Whether neuroinflammation or a brain stem pathology exists—where dysautonomia may have its origin as the primary disturbance eliciting ME/CFS—remains to be shown.

Decreased CBF, disturbed local blood flow regulation and neurovascular coupling, central adrenergic hyperactivity, hypocapnia and increase in intracranial presssure seem to play a strong role in the pathophysiology of the neurological symptoms in ME/CFS (Fig. 1). They can well explain cognitive impairment, brain fog, headache, psychomotor slowing, ataxia and loss of coordination of movements, hypersensitivity, sleep disturbances and dysautonomia.

Read full paper

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Research: Understanding the molecular changes of PEM in ME/CFS

Posted on 11/22/2021 by wames

Understanding the molecular changes of Post Exertional Malaise in ME/CFS,  by Jemma Elley (Thesis, Bachelor of Biomedical Sciences with Honours). University of Otago, 2021

 

Research abstract:

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating and often life-long condition affecting over 20,000 New Zealanders. Symptoms include muscle and joint pain, severe fatigue, unrefreshing sleep, hypersensitivity to light and sound, and cognitive dysfunction. However, the condition lacks a reliable diagnostic biomarker, impairing patient diagnosis and treatment development. Previous research has identified several key physiological areas of promise from which markers might come, including mitochondrial dysfunction, HPA-axis impairment, immune alterations, increased oxidative stress and epigenome modifications.

This project focuses on post-exertional malaise (PEM), a cardinal symptom of ME/CFS. Post-exertional malaise is defined as an exacerbation of ME/CFS symptoms after physical, mental or emotional exertion. As PEM distinguishes ME/CFS from other fatigue-related conditions, it may aid in identifying the molecular basis of ME/CFS.

To determine the molecular changes leading to this malaise, five ME/CFS-affected individuals and two healthy controls performed an exercise paradigm where they were made to cycle on an ergometer until their peak work rate was reached. 20 mL of blood was taken from each individual before performing the exercise, and after two exercise episodes that were 24 hours apart.

Peripheral blood mononuclear cells (PBMCs) were purified from the blood by centrifuging on Ficol gradients. The mitochondrial function was determined on live cells using the Seahorse XF Cell Mito Stress Test Kit. The genomic DNA was extracted from the PBMCs and 8-hydroxy 2 deoxyguanosine (a marker of oxidative stress) was determined using an 8-hydroxy 2 deoxyguanosine ELISA Kit. Methylome changes were detected in the DNA by digestion of the DNA and preparation of 40-220bp fragment libraries before performing Reduced Representation Bisulfite sequencing.

A decrease in the mitochondrial function after the first exercise was observed in all ME/CFS individuals and one control. Contrary to existing literature, the ME/CFS group had, on average, a lower level of 8-hydroxy 2 deoxyguanosine compared to healthy controls.

An average of 1.25% of DNA fragments were differentially methylated between the baseline 24-hour and baseline and 48-hour samples. Results of a STRING protein network analysis on the differentially methylated fragments present in the promoter show interaction between upregulated mitochondrial, nervous system, immune function, and HPA-axis -associated genes. Additionally, hypermethylation and potentially decreased expression of POU3F4, a transcription factor with high expression levels in the basal ganglia (which regulates motor activity and motivation) provides evidence of how the PEM symptoms of increased fatigue and perceived exertion may arise.

Whilst the molecular changes during PEM are varied and complex, these results contribute to the knowledge of the processes underlying the symptoms, and by proxy, the overall pathophysiology of ME/CFS.

Supervisor: Prof Warren Tate

4.6. Conclusions

In summary, changes were observed in the oxygen consumption rate of ME/CFS subjects, as well as evidence of a difference between ME/CFS patients and healthy controls. The similarity in OCR profiles between ME/CFS-affected individuals and an over-exerted control should be further explored, as it potentially links the “increased perceived exertion” hypothesis with a physiological output.

The statistically significant decrease of ATP production after exercise should also be explored, potentially explaining the fatigue ME/CFS sufferers experience.
8-OHdG levels, as a measure of oxidative stress, did not appear to have drastic changes during the exercise paradigm, nor between ME/CFS individuals and controls. However, the spread of 8-OHdG levels in ME/CFS and healthy individuals should be assessed, as we cannot conclude that this minor difference is not, in fact, significant enough to act as a biomarker for ME/CFS.

Finally, significant differences in the DNA methylation of one individual’s genome was observed throughout the exercise paradigm, especially in genes related to the HPA-axis and immune system, metabolism, and circadian rhythm.

These findings buttress those reported by many other research groups. Whilst many researchers have investigated ME/CFS by comparing it to controls, the investigation of its key symptom, PEM, is underdeveloped. Therefore, this thesis contributes to filling a major gap in the field.

Additionally, this study employs a “precision medicine” approach, using patients as their own controls. Because of the fatigue-induced limitations of those with ME/CFS in partaking in studies, genome-wide investigations employing thousands of participants are not possible. This project provides an alternative, which, with increased sharing of data and machine learning, may provide a better way to approach ME/CFS research and the study of chronic illnesses in general.

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Research review: Immunoglobulin therapy for ME/CFS

Posted on 11/15/2021 by wames

Back to the Future? Immunoglobulin therapy for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, by  Helen Brownlie and Nigel Speight in Healthcare 2021, 9(11), 1546; [doi.org/10.3390/healthcare9111546]   12 Nov 2021 (This article belongs to the Special Issue ME/CFS – the Severely and Very Severely Affected)

 

Review abstract:

The findings of controlled trials on use of intravenous immunoglobulin G (IV IgG) to treat myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are generally viewed as representing mixed results. On detailed review, a clearer picture emerges, which suggests that the potential therapeutic value of this intervention has been underestimated.

Our analysis is consistent with the propositions that:

  1. IgG is highly effective for a proportion of patients with severe and well-characterised ME/CFS;
  2. responders can be predicted with a high degree of accuracy based on markers of immune dysfunction.

Rigorous steps were taken in the research trials to record adverse events, with transient symptom exacerbation commonly experienced in both intervention and placebo control groups, suggesting that this reflected the impact of participation on people with an illness characterised by post-exertional symptom exacerbation. Worsening of certain specific symptoms, notably headache, did occur more commonly with IgG and may have been concomitant to effective treatment, being associated with clinical improvement.

The findings emerging from this review are supported by clinical observations relating to treatment of patients with severe and very severe ME/CFS, for whom intramuscular and subcutaneous administration provide alternative options.

We conclude that:

  1. there is a strong case for this area of research to be revived;
  2. pending further research, clinicians would be justified in offering a course of IgG to selected ME/CFS patients at the more severe end of the spectrum.

As the majority of trial participants had experienced an acute viral or viral-like onset, we further suggest that IgG treatment may be pertinent to the care of some patients who remain ill following infection with SARS-CoV-2 virus.

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Research: The characterization of IL-2 stimulation & treatment of TRPM3… in ME/CFS

Posted on 11/15/2021 by wames

Characterization of IL-2 stimulation and TRPM7 pharmacomodulation in NK Cell cytotoxicity and channel Co-Localization with PIP2 in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome patients, by Stanley Du Preez , Natalie Eaton-Fitch, Helene Cabanas, Donald Staines and Sonya Marshall-Gradisnik in Int. J. Environ. Res. Public Health 2021, 18(22), 11879; [doi.org/10.3390/ijerph182211879] 12 Nov 2021  (This article belongs to the Special Issue Chronic Fatigue Syndrome: Medical, Nursing and Public Health Management)

 

Research abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex multisystemic disorder responsible for significant disability. Although a unifying etiology for ME/CFS is uncertain, impaired natural killer (NK) cell cytotoxicity represents a consistent and measurable feature of this disorder.

Research utilizing patient-derived NK cells has implicated dysregulated calcium (Ca2+) signaling, dysfunction of the phosphatidylinositol-4,5-bisphosphate (PIP2)-dependent cation channel, transient receptor potential melastatin (TRPM) 3, as well as altered surface expression patterns of TRPM3 and TRPM2 in the pathophysiology of ME/CFS.

TRPM7 is a related channel that is modulated by PIP2 and participates in Ca2+ signaling. Though TRPM7 is expressed on NK cells, the role of TRPM7 with IL-2 and intracellular signaling mechanisms in the NK cells of ME/CFS patients is unknown.

This study examined the effect of IL-2 stimulation and TRPM7 pharmacomodulation on NK cell cytotoxicity using flow cytometric assays as well as co-localization of TRPM7 with PIP2 and cortical actin using confocal microscopy in 17 ME/CFS patients and 17 age- and sex-matched healthy controls.

The outcomes of this investigation are preliminary and indicate that crosstalk between IL-2 and TRMP7 exists. A larger sample size to confirm these findings and characterization of TRPM7 in ME/CFS using other experimental modalities are warranted.

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mapMECFS: new opportunities for discovery for ME/CFS researchers

Posted on 11/15/2021 by wames

mapMECFS – an interactive data portal

… providing access to research results across many biological disciplines from studies that are focused on advancing our understanding of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS).

 

The mapMECFS website serves as the omics data sharing portal for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) research, created as part of the NIH funded ME/CFS Network.

This website enables researchers to gain a broader view of ME/CFS by:

  • Bringing together the data that researchers have collected across the multiple systems affected by ME/CFS
  • Providing a dynamic navigation portal to search across these domains
  • Facilitating the integration of complementary data types to offer a new, more complete picture of the disorder

Mission
Our mission is to help ME/CFS researchers discover new insights about the disorder, promote data sharing between experts, and present a comprehensive picture of the hallmarks of this disorder. We hope these efforts help millions of people suffering from ME/CFS by enabling a faster path to better diagnostics and treatments.

Watch the video

mapMECFS: a portal to enhance data discovery across biological disciplines and collaborative sites

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World ME Alliance writes to WHO re long COVID definition

Posted on 11/12/2021 by wames

Will the World Health Organization’s long COVID definition help or hinder?

 

WAMES has joined other members of the World ME Alliance in writing to the World Health Organization (WHO) concerning their recently published definition of “post COVID-19 condition”, commonly known as long COVID.

 

While we commend the work undertaken to ensure people with long COVID are receiving a diagnostic label and subsequent support we remain concerned that a vague definition alone could hinder research and care efforts.

Further work, including stratification of sub-types is vital, and we call on the WHO to engage disease experts from areas such as ME in this.

 

Read our letter below:

Dear Dr Tedros Adhanom Ghebreyesus, Dr Ren Minghui and Dr Janet Diaz,

On 6th October, the World Health Organization published its definition of post COVID-19 condition (PCC).

Post COVID-19 condition occurs in individuals with a history of probable or confirmed SARS-CoV-2 infection, usually 3 months from the onset of COVID-19 with symptoms that last for at least 2 months and cannot be explained by an alternative diagnosis. Common symptoms include fatigue, shortness of breath, cognitive dysfunction but also others* and generally have an impact on everyday functioning. Symptoms may be new onset following initial recovery from an acute COVID-19 episode or persist from the initial illness. Symptoms may also fluctuate or relapse over time.

The undersigned organisations work for the benefit of people with myalgic encephalomyelitis (ME), a noncommunicable disease (NCD) with great experience of vague diagnostic definitions. There are now so many definitions of ME that research often isn’t comparable. Many of these definitions select such a broad population that research outcomes are considered of low or very low quality in systematic reviews. In fact, there is remarkable similarity between some of the definitions of ME and the recent definition of PCC published by the WHO.

We are concerned that this definition will lead to some of the same outcomes for people experiencing PCC as has happened for people with ME. Defined clinical pathways are clearly needed, and we commend the WHO on working towards this. However, now is the time to prioritise the categorisation of subtypes in order to expedite the delivery of appropriate treatment or management approaches for people presenting with different symptoms.

As research into this novel phenomenon develops, various phenotypes are being differentiated, and the WHO definition could emphasise this. (1) In particular, it is of vital importance that post-exertional malaise (PEM) is screened for, and where present people are supported to pace their energy levels within known limits (as per new guidance from the UK’s National Institute for Health and Care Excellence). (2) The findings of the Patient Led Research Collaborative, that “89.1% of participants reported experiencing either physical or mental PEM”, (3) affirm this.

There are many overlaps between the symptomology presenting in PCC and in ME. However, certain subgroups do not experience the symptoms of ME. We must now ensure that people diagnosed with PCC are appropriately sub-categorised, to ensure that we do delay the advancement of scientific understanding through:

  • misleading data and insignificant findings in research
  • inappropriate one-size-fits-all care

It is critical to identify and track the disease progressions of different subtypes, including those with ME, to identify risk and resiliency factors when compared to those who recover from COVID and healthy controls. As written, this definition alone will be harmful to critical research in the field.

We strongly encourage the WHO to work with NCD disease experts in related fields to develop guidance for clinical care and researchers that enables screening and tracking of ME and other conditions related to PCC, and fully defines the subgroups and their differentiating/differential symptoms.

The WHO has an opportunity here to make a difference for people with PCC, those with ME, and other NCDs who for many years have been out of the spotlight and largely ignored.

We therefore urge you to work with ME organisations and disease experts to make a statement on the similarities between PCC and ME, and the necessary differences in management approach for those experiencing post-exertional malaise.

Secondly, we urge you to ensure ME organisations and disease experts are central to future efforts to develop clinical care and research into PCC.

And finally, we urge the WHO to initiate education and research into PEM, as it remains such a misunderstood and highly disabling characteristic.

With regards,

Sonya Chowdhury,
Chair of the World ME Alliance

On behalf of the World ME Alliance members:

Action for M.E.
ACAF – Associació Catalana d’Afectades i Afectats de Fibromiàlgia i d’altres Síndromes de Sensibilització Central
AMMES – The American ME and CFS Society
ANZMES – The Associated New Zealand Myalgic Encephalomyelitis Society
AQEM – Association québécoise de l’encéphalomyélite myalgique
Forward M.E.
#MEAction
Plataforma Familiars FM-SFC-SQM Síndromes de Sensibilització Central
Solve M.E.
The ME CFS Foundation South Africa
WAMES – Welsh Association of ME & CFS Support

 

(1) Estiri, Hossein, Zachary H. Strasser, Gabriel A. Brat, Yevgeniy R. Semenov, Chirag J. Patel, and Shawn N. Murphy. “Evolving Phenotypes of non-hospitalized Patients that Indicate Long Covid.” medRxiv (2021).

(2) NICE. “Myalgic encephalomyelitis (or encephalopathy)/chronic fatigue syndrome: diagnosis and management” Available at https://www.nice.org.uk/guidance/ng206 (2021)

(3) Davis, Hannah E., Gina S. Assaf, Lisa McCorkell, Hannah Wei, Ryan J. Low, Yochai Re’em, Signe Redfield, Jared P. Austin, and Athena Akrami. “Characterizing long COVID in an international cohort: 7 months of symptoms and their impact.” Available at SSRN 3820561 (2021).

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Research review: Pain-related post-exertional malaise in ME/CFS & FM

Posted on 11/12/2021 by wames

Pain-related post-exertional malaise in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia: a systematic review and three-level meta-analysis, by Ellen E Barhorst, Alex E Boruch, Dane B Cook in Pain Medicine, October 2021 [DOI:10.1093/pm/pnab308]

 

Review abstract:

Objective:

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia (FM) are two debilitating, moderately comorbid illnesses in which chronic musculoskeletal pain symptoms are prevalent. These individuals can experience post-exertional malaise (PEM), a phenomenon where symptom severity is worsened 24hr or longer following physical stress, but the pain-related component of PEM is not well characterized.

Design:

Systematic review and meta-analysis.

Methods:

Case-control studies involving adults with ME/CFS or FM and measuring pain symptoms before and after exposure to a standardized aerobic exercise test were included. Hedges’ d effect sizes were aggregated using random effects models and potential moderators were explored with meta-regression analysis. Results were adjusted for nesting effects using three-level modeling.

Results:

Forty-five effects were extracted from 15 studies involving 306 patients and 292 healthy controls. After adjusting for nesting effects, we observed a small-to-moderate effect indicating higher post-exercise pain in patients than controls (Hedges’ d=0.42; 95% CI: 0.16, 0.67). The mean effect was significantly moderated by pain measurement timepoint (b = -0.19, z = -2.57, P = 0.01) such that studies measuring pain 8-72hr post-exercise showed larger effects (d = 0.71, 95% CI = 0.28-1.14) than those measuring pain 0-2hr post-exercise (d = 0.32, 95% CI = 0.10-0.53).

Conclusions:

People with ME/CFS and FM experience small-to-moderate increases in pain severity following exercise which confirms pain as a component of PEM and emphasizes its debilitating impact in ME/CFS and FM. Future directions include determining mechanisms of pain-related PEM and developing exercise prescriptions that minimize symptom exacerbation in these illnesses.

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Diagnostic test research: Saliva fatigue biomarker for severe ME/CFS

Posted on 11/10/2021 by wames

Saliva fatigue biomarker index as a marker for severe myalgic encephalomyelitis/ chronic fatigue syndrome in a community based sample, by Leonard A Jason, John Kalns, Alicia Richarte, Ben Z Katz, Chelsea Torres in Fatigue: Biomedicine, Health & Behavior, October 27, 2021 [doi/full/10.1080/21641846.2021.1994222]

 

Research abstract:

Objective

The prevalence of pediatric Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS) has been estimated from an ethnically and sociodemographically diverse community-based random sample of 10,119 youth aged 5-17. We assessed whether a salivary biomarker of fatigue could identify youth with ME/CFS.

Study design

We examined the ratio of the concentrations of 2 peptide fragments in saliva, referred to as the Fatigue Biomarker Index (FBI), in participants from our study diagnosed with ME/CFS (n=59) and matched controls (n=39).

Results

Significant overall differences were found in the FBI between those participants with severe ME/CFS and those with ME/CFS and the controls.

Conclusions

If confirmed in other populations, the FBI could serve as an objective test to aid in the diagnosis of severe ME/CFS.

Full article behind a paywall

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