Genetic research: Fine mapping of the major histocompatibility complex (MHC) in ME/CFS

Posted on 09/13/2021 by wames

Fine mapping of the major histocompatibility complex (MHC) in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) suggests involvement of both HLA class I and class II loci, by Riad Hajdarevic, Asgeir Lande, Ingrid Rekeland, Anne Rydland, Elin B Strand, Daisy D Sosa, Lisa E Creary, Olav Mella, Torstein Egeland, Ola D Saugstad, Øystein Fluge, Benedicte A Lie, Marte K Viken in Brain Behav Immun. 2021 Aug 14;S0889-1591(21)00509-2 [doi: 10.1016/j.bbi.2021.08.219]

 

Highlights:

  • By far the largest genetic study in ME/CFS.
  • Multi-level HLA and SNP analysis.
  • Independent HLA class I and II associations.
  • Positive association of HLA-DQB1 amino acid residue 57D.

Abstract:

The etiology of Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS) is unknown, but involvement of the immune system is one of the proposed underlying mechanisms. Human leukocyte antigen (HLA) associations are hallmarks of immune-mediated and autoimmune diseases.

We have previously performed high resolution HLA genotyping and detected associations between ME/CFS and certain HLA class I and class II alleles. However, the HLA complex harbors numerous genes of immunological importance, and there is extensive and complex linkage disequilibrium across the region.

In the current study, we aimed to fine map the association signals in the HLA complex by genotyping five additional classical HLA loci and 5,342 SNPs in 427 Norwegian ME/CFS patients, diagnosed according to the Canadian Consensus Criteria, and 480 healthy Norwegian controls.

Crystallographic structure of HLA-DQA1 (cyan) complexed with HLA-DQB1 (green) & HCRT (magenta) based on PDB: 1uvq​.

SNP association analysis revealed two distinct and independent association signals (p≤0.001) tagged by rs4711249 in the HLA class I region and rs9275582 in the HLA class II region. Furthermore, the primary association signal in the HLA class II region was located within the HLA-DQ gene region, most likely due to HLA-DQB1, particularly the amino acid position 57 (aspartic acid/alanine) in the peptide binding groove, or an intergenic SNP upstream of HLA-DQB1.

In the HLA class I region, the putative causal locus might map outside the classical HLA genes as the association signal spans several genes (DDR1, GTF2H4, VARS2, SFTA2 and DPCR1) with expression levels influenced by the ME/CFS associated SNP genotype.

Taken together, our results implicate the involvement of the MHC, and in particular the HLA-DQB1 gene, in ME/CFS. These findings should be replicated in larger cohorts, particularly to verify the putative involvement of HLA-DQB1, a gene important for antigen-presentation to T cells and known to harbor alleles providing the largest risk for well-established autoimmune diseases.

 

Riad Hajdarevic says:

Hello I am the first author of the studies. I want to bring some clarity to the paper to you guys.

Our study was trying to see the involvement of HLA genes in ME/CFS. We observed some genetic changes (SNPs) to be associated with ME/CFS across the immunologically important HLA genes.

The patients we analyzed were diagnosed according to the CCC. As you know the CCC are more stringent than the Fukuda or similar criteria. Our patient population was 427 Norwegian ME/CFS patients. This is the largest ME/CFS cohort diagnosed according to the CCC however we need much more (up to 10 x) to definitely make a correlation between our findings and ME/CFS.

So far, no clinical implications can be made from this. However, it is indicative that those genetic changes (SNPs) influenced gene expression of some relevant genes for the observed ME/CFS clinical picture. Likewise, it seems (from this statistically limited data set) that some of those changes correlate with response to cyclophosphamide treatment in patients with ME/CFS. You have heard, I assume, about our collaborator’s study from Bergen where they reported improved symptoms for some ME/CFS patients taking the drug.

I just have to emphasize that we need much more research with much, much more patients diagnosed with the CCC to make any deeper assumptions.
If you have any extra questions please let me know I am glad to explain the findings in detail to anyone who wants to know the details.

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Research: A map of metabolic phenotypes in patients with ME/CFS

Posted on 09/10/2021 by wames

A map of metabolic phenotypes in patients with myalgic encephalomyelitis/ chronic fatigue syndrome by Fredrik Hoel, August Hoel, Ina Kn Pettersen, Ingrid G Rekeland, Kristin Risa, Kine Alme, Kari Sørland, Alexander Fosså, Katarina Lien, Ingrid Herder, Hanne L Thürmer, Merete E Gotaas, Christoph Schäfer, Rolf K Berge, Kristian Sommerfelt, Hans-Peter Marti, Olav Dahl, Olav Mella, Øystein Fluge, Karl J Tronstad in JCI Insight 2021;6(16):e149217 [doi.org/10.1172/jci.insight.149217]

 

Research abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disease usually presenting after infection. Emerging evidence supports that energy metabolism is affected in ME/CFS, but a unifying metabolic phenotype has not been firmly established.

Energy metabolism is the general process by which living cells acquire and use the energy needed to stay alive, to grow, and to reproduce.  Da Poian et al

We performed global metabolomics, lipidomics, and hormone measurements, and we used exploratory data analyses to compare serum from 83 patients with ME/CFS and 35 healthy controls.

Some changes were common in the patient group, and these were compatible with effects of elevated energy strain and altered utilization of fatty acids and amino acids as catabolic fuels. In addition, a set of heterogeneous effects reflected specific changes in 3 subsets of patients, and 2 of these expressed characteristic contexts of deregulated energy metabolism. The biological relevance of these metabolic phenotypes (metabotypes) was supported by clinical data and independent blood analyses.

Metabolic phenotypes are the products of interactions among a variety of factors-dietary, other lifestyle/environmental, gut microbial and genetic.             Holmes et al

In summary, we report a map of common and context-dependent metabolic changes in ME/CFS, and some of them presented possible associations with clinical patient profiles. We suggest that elevated energy strain may result from exertion-triggered tissue hypoxia and lead to systemic metabolic adaptation and compensation. Through various mechanisms, such metabolic dysfunction represents a likely mediator of key symptoms in ME/CFS and possibly a target for supportive intervention.

Comment:

Science Norway: ME/CFS may be linked to failure in energy supply to the cells

ME Association blog: Research Summary – A map of metabolic phenotypes in patients with myalgic encephalomyelitis/chronic fatigue syndrome 

MEprecisely: John Duncan

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UK Gov CFS research funding – Q&A in parliament

Posted on 09/10/2021 by wames

UK Parliament Written Question & Answers: CFS

1. Question from Alex Norrie MP, Labour, Nottingham North

To ask the Secretary of State for Health and Social Care, how much Government funding has been provided to ME research in each of the last three years. [UIN 38397, tabled on 22 July 2021]

Answer from Edward Argar MP, Minister of State (Department of Health and Social Care)

The following table shows the funding for research into myalgic encephalomyelitis through the National Institute for Health Research and UK Research and Innovation in the last three years.

Financial Year   Pounds
2018-19                   862,212
2019-20                   691,516
2020-21                   907,848

[Source: UK House of Commons, September 6, 2021]

2. Question from Janet Daby MP, Labour, Lewisham East

To ask the Secretary of State for Health and Social Care, whether he has made a recent assessment of the potential merits of increasing funding for research into ME and Chronic Fatigue Syndrome.  [UIN 41247, tabled on 18 August 2021]

Answer from Edward Argar MP, Minister of State (Department of Health and Social Care)

The Government invests in health research through the National Institute for Health Research (NIHR) and the Medical Research Council (MRC), through UK Research and Innovation. The NIHR and MRC both welcome high-quality applications for research into all aspects of myalgic encephalomyelitis (ME), otherwise known as chronic fatigue syndrome (CFS).

No assessment has been made of the merits of increasing funding for research into ME/CFS. While it is not usual practice for the NIHR and MRC to ring-fence funds for particular topics or conditions, the MRC has had a cross-board highlight notice on CFS/ME open since 2003.

[Source: UK House of Commons, September 6, 2021]

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Research: The SARS-CoV-2 receptor ACE2 in ME/CFS

Posted on 09/08/2021 by wames

The SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) in  Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: a meta-analysis of public DNA methylation and gene expression data, by João Malato, Franziska Sotzny, Sandra Bauer, Helma Freitag, André Fonseca, Anna D Grabowska, Luís Graça, Clara Cordeiro, Luís Nacul, Eliana M Lacerda, Jesus Castro-Marrero, Carmen Scheibenbogen, Francisco Westermeier, Nuno Sepúlveda in Heliyon 2021 Jul 29;7(8):e07665 [doi: 10.1016/j.heliyon.2021.e07665]

 

Research abstract: 

Protein_ACE2_PDB_1r42

People with myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS) often report a high frequency of viral infections and flu-like symptoms during their disease course. Since this reporting is in line with different immunological abnormalities and altered gene expression profiles observed in the disease, we aimed to explore whether the expression of the human angiotensin-converting enzyme-2 (ACE2), the major cell entry receptor for SARS-CoV-2, is also altered in this neglected clinical population. In particular, a low expression of ACE2 is usually indicative of a high risk of developing COVID-19.

We then performed a meta-analysis of public data on CpG DNA methylation and gene expression of this enzyme and its homologous ACE protein in peripheral blood mononuclear cells and related subsets. We found that patients with ME/CFS have decreased methylation levels of four CpG probes in the ACE locus (cg09920557, cg19802564, cg21094739, and cg10468385) and of another probe in the promoter region of the ACE2 gene (cg08559914). We also found a decreased expression of ACE2 but not of ACE in patients with ME/CFS when compared to healthy controls.

Accordingly, in newly collected data, we found evidence for a higher proportion of samples with an ACE2 expression below the limit of detection in patients with ME/CFS than in healthy controls.

Altogether, patients with ME/CFS could be at a higher COVID-19 risk when infected by SARS-CoV-2. To further support this conclusion, similar research should be conducted for other human cell entry receptors and other cell types, namely, those mainly targeted by the virus.

Comment:

ME Association: Research Summary – Are people with ME/CFS at higher risk of complications from COVID infection?

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Treatment Research: Cortene’s InTime trial of CT38 results in sustained symptom improvement in ME/CFS

Posted on 09/07/2021 by wames

Acute Corticotropin-Releasing Factor Receptor Type 2 Agonism Results in Sustained Symptom Improvement in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, by Gerard Pereira, Hunter Gillies, Sanjay Chanda, Michael Corbett, Suzanne D. Vernon, Tina Milani and Lucinda Bateman in Front. Syst. Neurosci., 01 Sep 2021 [doi.org/10.3389/fnsys.2021.698240]

 

Research abstract:

Background:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex multi-symptom disease with widespread evidence of disrupted systems. The authors hypothesize that it is caused by the upregulation of the corticotropin-releasing factor receptor type 2 (CRFR2) in the raphé nuclei and limbic system, which impairs the ability to maintain homeostasis. The authors propose utilizing agonist-mediated receptor endocytosis to downregulate CRFR2.

Materials and Methods:

This open-label trial tested the safety, tolerability and efficacy of an acute dose of CT38s (a short-lived, CRFR2-selective agonist, with no known off-target activity) in 14 ME/CFS patients. CT38s was subcutaneously-infused at one of four dose-levels (i.e., infusion rates of 0.01, 0.03, 0.06, and 0.20 μg/kg/h), for a maximum of 10.5 h. Effect was measured as the pre-/post-treatment change in the mean 28-day total daily symptom score (TDSS), which aggregated 13 individual patient-reported symptoms.

Results:

ME/CFS patients were significantly more sensitive to the transient hemodynamic effects of CRFR2 stimulation than healthy subjects in a prior trial, supporting the hypothesized CRFR2 upregulation. Adverse events were generally mild, resolved without intervention, and difficult to distinguish from ME/CFS symptoms, supporting a CRFR2 role in the disease. The acute dose of CT38s was associated with an improvement in mean TDSS that was sustained (over at least 28 days post-treatment) and correlated with both total exposure and pre-treatment symptom severity. At an infusion rate of 0.03 μg/kg/h, mean TDSS improved by −7.5 ± 1.9 (or −25.7%, p = 0.009), with all monitored symptoms improving.

Conclusion:

The trial supports the hypothesis that CRFR2 is upregulated in ME/CFS, and that acute CRFR2 agonism may be a viable treatment approach warranting further study.

Comments:

Biospace: Clinical trial provides preliminary evidence of a cure for myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) and Long Covid

Cortene believes the CRFR2 pathway is upregulated and therefore overactive, leading to the wide variety of symptoms in ME/CFS.  “The conventional approach would be to block the overactive pathway. Instead, our counterintuitive approach seeks to overstimulate CRFR2, causing it to downregulate, without the need for chronic treatment.”

Health arising: The Cortene drug trial results for ME/CFS are in

Dr. Bateman indicated that many of the participants reported subtle but noticeable improvements of their symptoms over the 1-2 years following the trial.

In an interview, Cortene proposed that partial downregulation of the CRFR2 receptor had indeed occurred, and that further trials would determine if they could fully return it and the stress response system in ME/CFS to a healthy state.

Cortene hopes to embark on a 60-person $4 million trial next.

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Research: An alternative model of CBT for CFS/ME

Posted on 09/06/2021 by wames

‘A life I can cope with’. An alternative model of cognitive behavioural therapy (CBT) for CFS/ME, by Catherine Clark, Sue Holttum in Health Expectations 2021 [DOI: 10.1111/h ex.13326]

 

Research abstract:

Objectives

This study aimed to explore the experience of cognitive behavioural therapy (CBT) aimed at better management of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME), rather than increasing activity.

Design

This was a qualitative study using grounded theory analysis.

Methods

Semi-structured interviews were conducted with 13 adults who had engaged in CBT at a specialist CFS/ME service in which CBT is aimed at improved management of the condition.

Results

A model was produced in which participants felt more able to cope with CFS/ME. Reduced fatigue did not seem to be a necessary precondition to managing. This has implications for CBT for CFS/ME.

Conclusions

Specialist CBT for CFS/ME may result in improved coping and reduced distress, independently of changes in fatigue.

I don’t think in any way it helped my ME, but it did help my mind. (Sarah)

I don’t want to say reduced the symptoms, but probably have slightly fewer relapses and maintain a slightly better level quality of life. (Susan)

I came away just with that re-focus on putting myself first and not being afraid to do that actually, it is okay to do that when you are not well. (Sarah)

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WAMES responds to NICE ’roundtable’ announcement

Posted on 09/02/2021 by wames

WAMES writes to NICE re ‘Roundtable event’

 

On 27th August, 10 days after publication of the ME/CFS guideline was ‘paused’, NICE made another announcement. Yet again this gave the bare minimum of information – their plan to invite stakeholders to a roundtable discussion in September ‘to better understand the issues raised and determine how it can gain support for the guideline to ensure effective implementation.

No information was given about the nature of the challenge or the people making the challenge, or the rules and regulations governing this unprecedented move.

In the media and on social media, the critics of the guideline have made it clear that:

  • they believe GET and CBT are the only valid evidence based interventions that can help patients
  • the PACE trial should be upgraded from low quality and that this could be done if the diagnostic criteria was widened.

NICE says they believe it is possible to reach an agreement. Whether that is realistic or wishful thinking remains to be seen.

It is now September, so WAMES has written to NICE to express our commitment to continuing to work towards publication of the guideline.

 

Dear Prof Leng, Mr Chrisp and Ms Stafford,

As a stakeholder in the ME/CFS NICE guideline revision process, and a charity working with the estimated 13,000 people with ME in Wales, we confirm our interest in being part of the Roundtable event. WAMES supports the publication of the guideline as soon as possible, as it was developed by following a search for best evidence and represents years of hard work and emotional investment from all involved.

We hope this will be an inclusive event with virtual participation from a wide range of stakeholders as we are concerned about the lack of transparency surrounding the challenge to the guideline and ‘pause’ in publication. This has severely damaged NICE’s credibility in the ME community and future openness will be critical in achieving ‘a guideline that will have the support of people living with ME/CFS’.

We therefore look forward to receiving the following in advance, so we have plenty of time to prepare:

  • Full details of the challenge to the publication of the guideline
  • Details of the procedure by which others can also challenge the publication of the guideline in its current form
  • Details of any expert witnesses that are being called or further evidence being gathered
  • A clear plan for the steps and timescale that will be followed until publication
  • Details of all stakeholders invited and the role they will play in this, both in person and via written submission
  • Details of any stakeholders who are not invited to the Roundtable and how they can contribute
  • The plan of action if agreement cannot be achieved
  • An assurance that ongoing delay to publication will be accompanied by a warning on the current guideline that GET can cause deterioration for people with PEM, thus preventing further harm.

Yours sincerely,

Jan Russell   Chair of WAMES

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Research: An audit of UK hospital doctors’ knowledge & experience of ME

Posted on 08/31/2021 by wames

An audit of UK hospital doctors’ knowledge and experience of Myalgic Encephalomyelitis, by Keng Ngee Hng, Keith Geraghty and Derek FH Pheby in Medicina 2021, 57(9), 885; [doi.org/10.3390/medicina57090885] 27 August 2021 (This article belongs to the Special Issue ME/CFS: Causes, Clinical Features and Diagnosis)

 

Research abstract:

Background and Objectives:

There is some evidence that knowledge and understanding of ME among doctors is limited. Consequently, an audit study was carried out on a group of hospital doctors attending a training event to establish how much they knew about ME and their attitudes towards it.

Materials and Methods:

Participants at the training event were asked to complete a questionnaire, enquiring about prior knowledge and experience of ME and their approaches to diagnosis and treatment. A total of 44 completed questionnaires were returned. Responses were tabulated, proportions selecting available options determined, 95% confidence limits calculated, and the significance of associations determined by Fisher’s exact test.

Results:

Few respondents had any formal teaching on ME, though most had some experience of it. Few knew how to diagnose it and most lacked confidence in managing it. None of the respondents who had had teaching or prior experience of ME considered it a purely physical illness. Overall, 91% of participants believed ME was at least in part psychological.

Most participants responded correctly to a series of propositions about the general epidemiology and chronicity of ME. There was little knowledge of definitions of ME, diagnosis, or of clinical manifestations. Understanding about appropriate management was very deficient. Similarly, there was little appreciation of the impact of the disease on daily living or quality of life.

Where some doctors expressed confidence diagnosing or managing ME, this was misplaced as they were incorrect on the nature of ME, its diagnostic criteria and its treatment.

Conclusion:

This audit demonstrates that most doctors lack training and clinical expertise in ME. Nevertheless, participants recognised a need for further training and indicated a wish to participate in this. It is strongly recommended that factually correct and up-to-date medical education on ME be made a priority at undergraduate and postgraduate levels. It is also recommended that this audit be repeated following a period of medical education.

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ME/CFS guideline (US): ME/CFS Essentials of diagnosis & management

Posted on 08/27/2021 by wames

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: essentials of diagnosis and management (see authors below) in Mayo Proceedings, Aug 25 2021 [doi.org/10.1016/j.mayocp.2021.07.004]

 

Consensus recommendations – introduction abstract:

Despite myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) affecting millions of people worldwide, many clinicians lack the knowledge to appropriately diagnose or manage ME/CFS.

Unfortunately, clinical guidance has been scarce, obsolete, or potentially harmful. Consequently, up to 91% of patients in the United States remain undiagnosed, and those diagnosed often receive inappropriate treatment.

These problems are of increasing importance because after acute COVID-19, a significant percentage of people remain ill for many months with an illness similar to ME/CFS. In 2015, the US National Academy of Medicine published new evidence-based clinical diagnostic criteria that have been adopted by the US Centers for Disease Control and Prevention. Furthermore, the United States and other governments as well as major health care organizations have recently withdrawn graded exercise and cognitive-behavioral therapy as the treatment of choice for patients with ME/CFS.

Recently, 21 clinicians specializing in ME/CFS convened to discuss best clinical practices for adults affected by ME/CFS. This article summarizes their top recommendations for generalist and specialist health care providers based on recent scientific progress and decades of clinical experience.

There are many steps that clinicians can take to improve the health, function, and quality of life of those with ME/CFS, including those in whom ME/CFS develops after COVID-19. Patients with a lingering illness that follows acute COVID-19 who do not fully meet criteria for ME/CFS may also benefit from these approaches.

Routine Diagnostic Tests Recommended for All Patients

  • Complete blood count with differential
  • Comprehensive metabolic panel (Chem20 panel)a
  • Antinuclear antibody
  • C-reactive protein
  • Erythrocyte sedimentation rate
  • Ferritin
  • Rheumatoid factor
  • Four-point salivary cortisol (eg, wakening, at noon, 4:00 pm, & bedtime), am cortisol
  • Thyroid-stimulating hormone, free thyroxine
  • Vitamin B12
  • Vitamin D, 25-dihydroxy
  • Urinalysis
[Adapted from Testing Recommendations for Suspected ME/CFS,104 with permission of the US ME/CFS Clinician Coalition.
a The Chem20 panel is a set of common laboratory tests ordered by health care professionals in the United States. It consists of 20 tests that provide information on the patient’s chemical balance and metabolism.
For more information, see https://www.ucsfhealth.org/medical-tests/003468]

 

Excerpt from Management Approach:

  • Validate the Patient’s Experience
  • Assess Needs and Provide Support
  • Teach Pacing
  • Treat the Symptoms of ME/CFS
  • Treat Comorbidities
  • Schedule Regular Follow-up Visits
  • Address Questions on Prognosis

Authors – ME/CFS Clinician Coalition:

Lucinda Bateman, MD; Alison C. Bested, MD; Hector F. Bonilla, MD; Bela V. Chheda, MD; Lily Chu, MD, MSHS; Jennifer M. Curtin, MD; Tania T. Dempsey, MD; Mary E. Dimmock, BA; Theresa G. Dowell, DNP, MPT; Donna Felsenstein, MD; David L. Kaufman, MD; Nancy G. Klimas, MD; Anthony L. Komaroff, MD; Charles W. Lapp, MBME, MD; Susan M. Levine, MD; Jose G. Montoya, MD; Benjamin H. Natelson, MD; Daniel L. Peterson, MD; Richard N. Podell, MD, MPH; Irma R. Rey, MD; Ilene S. Ruhoy, MD, PhD; Maria A. Vera-Nunez, MD, MSBI; Brayden P. Yellman, MD

Articles:

US ME/CFS Clinician Coalition: Updated Clinical Guidance for ME/CFS may also help long COVID patients  25 Aug 2021

The updated clinical guidance from the U.S. ME/CFS Clinician Coalition focuses on adults and includes:

  • New diagnostic criteria requiring post-exertional malaise and other key features to improve diagnostic accuracy
  • Efficient use of interview questions, physical examination findings, and diagnostic testing
  • Alternative diagnoses and co-existing conditions to consider
  • Pharmacological and nonpharmacological treatments
  • A discussion of why previously-recommended treatments-cognitive behavioral therapy and graded exercise therapy-can be harmful and are no longer recommended

Medscape: New Recommendations Address ME/CFS Diagnosis and Management by Miriam Tucker 27 February 2021

 

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Biomarker research: The case for hyperbaric oxygen therapy in CFS biomarker identification

Posted on 08/25/2021 by wames

Chronic fatigue syndrome and epigenetics: the case for hyperbaric
oxygen therapy in biomarker identification, by Rajit J Shah in J Pulmonol Respir Res. 2021; 5: 027-030. [DOI: 10.29328/journal.jprr.1001020]

 

Review abstract:

Chronic fatigue syndrome (CFS) is a poorly-understood respiratory condition that affects millions of individuals. Hyperbaric oxygen therapy (HBOT) is a treatment option being considered to address CFS as it is suggested to combat fatigue and increase oxygenation.

HBOT provides two opportunities in advancing research of CFS: it may provide data on symptom amelioration and be utilized in the search for a biomarker.

By either identifying biomarkers before using HBOT to compare epigenomes of patients before and after treatment or using HBOT to find epigenetic discrepancies between patients with and without treatment, matching epigenetic regulation with symptom amelioration may significantly advance the understanding of the etiology and treatment mechanism for CFS.

EPAS1/HIF-2α is a leading candidate for an epigenetic biomarker as it responds differentially to hypoxic and normoxic conditions, which degrades more slowly in hypoxic conditions. Epigenetic regulation of EPAS1/HIF-2α in
such differential conditions may be explored in HBOT experiments.

In addition to HBOT as a promising treatment option for CFS symptoms, it may aid the identification of biomarkers in CFS. Further research into both outcomes is strongly encouraged.

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