The role of prevention in reducing the economic impact of ME/CFS in Europe: a report from EUROMENE

Posted on 04/29/2021 by wames

The Role of Prevention in Reducing the Economic Impact of ME/CFS in Europe: A Report from the Socioeconomics Working Group of the European Network on ME/CFS (EUROMENE) by  Derek F H Pheby, Diana Araja, Uldis Berkis, Elenka Brenna, John Cullinan, Jean-Dominique de Korwin, Lara Gitto, Dyfrig A Hughes, Rachael M Hunter, Dominic Trepel and Xia Wang-Steverding in Medicina 2021, 57(4), 388;  [doi.org/10.3390/medicina57040388]

 

Report abstract:

This report addresses the extent to which there may be scope for preventive programmes for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), and, if so, what economic benefits may accrue from the implementation of such programmes. We consider the economic case for prevention programmes, whether there is scope for preventive programmes for ME/CFS, and what are the health and economic benefits to be derived from the implementation of such programmes.

We conclude that there is little scope for primary prevention programmes, given that ME/CFS is attributable to a combination of host and environmental risk factors, with host factors appearing to be most prominent, and that there are few identified modifiable risk factors that could be the focus of such programmes. The exception is in the use of agricultural chemicals, particularly organophosphates, where there is scope for intervention, and where Europe-wide programmes of health education to encourage safe use would be beneficial.

There is a need for more research on risk factors for ME/CFS to establish a basis for the development of primary prevention programmes, particularly in respect of occupational risk factors. Secondary prevention offers the greatest scope for intervention, to minimise diagnostic delays associated with prolonged illness, increased severity, and increased costs.

Read about the EUROMENE Socio-economic working group

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Pathophysiology of skeletal muscle disturbances in ME/CFS

Posted on 04/27/2021 by wames

Pathophysiology of skeletal muscle disturbances in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS), by Klaus J Wirth & Carmen Scheibenbogen in Journal of Translational Medicine vol 19, no. 162 (2021) [doi.org/10.1186/s12967-021-02833-2]

 

Review abstract:

Chronic Fatigue Syndrome or Myalgic Encephaloymelitis (ME/CFS) is a frequent debilitating disease with an enigmatic etiology. The finding of autoantibodies against ß2-adrenergic receptors (ß2AdR) prompted us to hypothesize that ß2AdR dysfunction is of critical importance in the pathophysiology of ME/CFS.

Our hypothesis published previously considers ME/CFS as a disease caused by a dysfunctional autonomic nervous system (ANS) system: sympathetic overactivity in the presence of vascular dysregulation by ß2AdR dysfunction causes predominance of vasoconstrictor influences in brain and skeletal muscles, which in the latter is opposed by the metabolically stimulated release of endogenous vasodilators (functional sympatholysis).

Key symptoms of ME/CFS related to hypoperfusion

An enigmatic bioenergetic disturbance in skeletal muscle strongly contributes to this release. Excessive generation of these vasodilators with algesic properties and spillover into the systemic circulation could explain hypovolemia, suppression of renin (paradoxon) and the enigmatic symptoms.

In this hypothesis paper the mechanisms underlying the energetic disturbance in muscles will be explained and merged with the first hypothesis.

The key information is that ß2AdR also stimulates the Na+/K+-ATPase in skeletal muscles. Appropriate muscular perfusion as well as function of the Na+/K+-ATPase determine muscle fatigability. We presume that dysfunction of the ß2AdR also leads to an insufficient stimulation of the Na+/K+-ATPase causing sodium overload which reverses the transport direction of the sodium-calcium exchanger (NCX) to import calcium instead of exporting it as is also known from the ischemia–reperfusion paradigm. The ensuing calcium overload affects the mitochondria, cytoplasmatic metabolism and the endothelium which further worsens the energetic situation (vicious circle) to explain postexertional malaise, exercise intolerance and chronification.

Reduced Na+/K+-ATPase activity is not the only cause for cellular sodium loading. In poor energetic situations increased proton production raises intracellular sodium via sodium-proton-exchanger subtype-1 (NHE1), the most important proton-extruder in skeletal muscle.

Finally, sodium overload is due to diminished sodium outward transport and enhanced cellular sodium loading. As soon as this disturbance would have occurred in a severe manner the threshold for re-induction would be strongly lowered, mainly due to an upregulated NHE1, so that it could repeat at low levels of exercise, even by activities of everyday life, re-inducing mitochondrial, metabolic and vascular dysfunction to perpetuate the disease.

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I already have a job: Energy Limiting Chronic Illness (ELCI), social Inclusion, employment & Social Security

Posted on 04/27/2021 by wames

Centre for Welfare Reform report: I already have a job: Energy Limiting Chronic Illness (ELCI), Social Inclusion, Employment and Social Security.

By Catherine Hale, Stef Benstead, Dr Kate Hardy and Dr Jo Ingold, April 2021

 

This report presents the findings and recommendations from a study into social inclusion, employment and social security for disabled people with energy limiting chronic illness (ELCI).

ELCI is a debilitating mix of physical fatigue, cognitive fatigue and pain alongside other diverse illness symptoms.

The study forms part of the Chronic Illness Inclusion Project (CIIP), a participatory research project by, and with, the chronic illness community in the UK. The first phase of research focused on chronic illness and disability identity, including a survey of over 2,000 disabled people. This report focuses on the second phase of research, involving in-depth discussion of participants’ experiences of employment and social security.

Examples of ELCI include: post viral fatigue syndrome; ME/CFS; fibromyalgia; lupus; MS; chronic pain; IBD; Ehlers Danlos syndrome; MCAS etc.

Main Findings

  • People with energy limiting chronic illness form a discrete sub-group of disabled
    people.
  • Work can be bad for health with ELCI. Energy impairment affects the amount, rather than the type, of activity people can do and aids and adjustments cannot fully mitigate its impact.
  • In the workplace, inflexible, performance-based and rigid human resource policies and practices are a barrier to employment and a lack of autonomy and control risks exacerbating illness.]
  • There is a need for job carving and job brokering agencies, such as Astriid, who can maximise opportunities for people with ELCI by working with employers to specifically create suitable jobs.
  • For social security, disability assessments fail to account for energy impairment,
    especially its key features of payback, reduced capacity and cognitive dysfunction.
  • This report may be timely in addressing the circumstances of those newly
    experiencing ‘Long Covid’, which appears to impact approximately 2% of people who remain ill with Covid after three months

Download the free pdf in your browser here.

RECOMMENDATIONS (excerpt)
Promoting social inclusion for disabled people with ELCI requires a new approach that centres their particular experiences, needs and aspirations. Crucially, measures to improve employment prospects cannot succeed without a robust and enabling social security system. Although we list employment policy recommendations separately from those on social security, joined up policy making is key to improving lives. Employers, government and other stakeholders (including employment support organisations) all have a role to play in:

  1. Recognising ELCI as a type of disability
  2. Promoting employment with ELCI
  3. Social Security Reform
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COVID-19 & post-infectious ME/CFS: a narrative review

Posted on 04/27/2021 by wames

COVID-19 and post-infectious myalgic encephalomyelitis/chronic fatigue syndrome: a narrative review, by Sonia Poenaru, Sara J Abdallah, Vicente Corrales-Medina, Juthaporn Cowan in Therapeutic Advances in Infectious Disease. Jan 2021 [doi:10.1177/20499361211009385]

 

Bottom line

  • Many post-acute COVID-19 symptoms resemble post-infectious ME/CFS
  • Acute disease severity does not clearly correlate with persistent symptoms
  • Long-term monitoring of post-acute COVID-19 symptoms and screening for common comorbid conditions is essential
  • Further research is required to establish COVID-19 as an infectious trigger for ME/CFS as well as to define risk factors, prevalence, natural history, and possible interventional strategies to treat this condition

Review abstract:

Coronavirus disease 2019 (COVID-19) is a viral infection which can cause a variety of respiratory, gastrointestinal, and vascular symptoms. The acute illness phase generally lasts no more than 2–3 weeks. However, there is increasing evidence that a proportion of COVID-19 patients experience a prolonged convalescence and continue to have symptoms lasting several months after the initial infection.

A variety of chronic symptoms have been reported including fatigue, dyspnea, myalgia, exercise intolerance, sleep disturbances, difficulty concentrating, anxiety, fever, headache, malaise, and vertigo. These symptoms are similar to those seen in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a chronic multi-system illness characterized by profound fatigue, sleep disturbances, neurocognitive changes, orthostatic intolerance, and post-exertional malaise. ME/CFS symptoms are exacerbated by exercise or stress and occur in the absence of any significant clinical or laboratory findings.

The pathology of ME/CFS is not known: it is thought to be multifactorial, resulting from the dysregulation of multiple systems in response to a particular trigger. Although not exclusively considered a post-infectious entity, ME/CFS has been associated with several infectious agents including Epstein–Barr Virus, Q fever, influenza, and other coronaviruses.

There are important similarities between post-acute COVID-19 symptoms and ME/CFS. However, there is currently insufficient evidence to establish COVID-19 as an infectious trigger for ME/CFS. Further research is required to determine the natural history of this condition, as well as to define risk factors, prevalence, and possible interventional strategies.

Discussion

The evidence for post-infectious ME/CFS following COVID-19 is not as strong as for other viruses such as EBV. Although persistent fatigue has been described extensively in post-acute COVID-19 symptom studies, no study has used ME/CSF criteria to characterize chronic fatigue in conjunction with other key symptoms and common disease manifestations.5,71,82,83 Another limitation is the degree of variability among different ME/CSF diagnostic criteria. Most post-infectious ME/CFS studies continue to use the 1994 CDC diagnostic criteria, which do not require the presence of other hallmark features of ME/CFS such as post-exertional malaise, cognitive changes, sleep disturbances, or orthostatic intolerance for diagnosis.7,8,16–19 This leads to difficulty interpreting the significance of individual chronic symptoms within the context of a post-infectious ME/CFS diagnosis.

Diagnosis of post-infectious ME/CFS in COVID-19 patients is further limited by its emerging infection status, as a duration of follow-up of at least 6 months is required to make this diagnosis.

Some symptoms seen in post-acute COVID-19 may occur as a consequence of critical illness or as a side effect of treatments such as steroids. For example, dyspnea is seen in up to 36% of people diagnosed with ME/CFS and is considered part of the broader category of orthostatic intolerance, along with postural tachycardia and hypotension.109 However, the dyspnea reported in post-COVID studies is not clearly described as a manifestation of orthostatic intolerance and may in fact represent fibrosis following inflammatory lung injury.76–78 This theory would be supported by the presence of clinically detectable abnormalities on imaging and pulmonary function testing in post-acute COVID-19 patients.73,74 Similar findings can be seen in survivors of acute respiratory distress syndrome, suggesting an organic cause for dyspnea.110–112

Other complications of critical illness and acute respiratory distress syndrome such as loss of muscle mass, deconditioning, steroid-induced myopathy, and multi-organ failure are correlated with poorer long-term health outcomes, chronic fatigue, and decreased functional capacity.111 There is some overlap between these outcomes and symptoms of ME/CFS. However, it is important to note that multiple post-acute COVID-19 studies have found no association between illness severity, presence of chronic symptoms, and objective measures of respiratory function, suggesting an alternate mechanism of pathogenesis.72,73,75,77,82

The importance of the higher rate of psychiatric comorbidities seen following epidemic outbreaks is similarly unclear. This association is likely caused by external stressors rather than due to the infection itself.11,35,42 While specific psychiatric conditions have not been consistently associated with increased risk of post-infectious ME/CFS, other psychosocial factors such as stressful life events, persistent high levels of anxiety, and reduced community support may play a role.7,17,28,29 Evidence from prior viral epidemics suggests that this period of multiple stressful life events may be an independent risk factor for developing ME/CFS; it will be difficult to separate the impact of pandemic-associated stress from the impact of the infection itself in defining COVID-19 as a risk factor for ME/CFS.

Although the symptom patterns seen in post-acute COVID-19 are similar to those seen in ME/CFS, further investigation with longer periods of follow-up and clearly defined diagnostic criteria will be required to establish COVID-19 as an infectious trigger for ME/CFS.

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Introducing WAMES volunteers: Simon Horsman

Posted on 04/26/2021 by wames

Introducing WAMES volunteers: the treasurer

 

Early a nomad, by adoption, I’m a Brummie. My school song included the worthy thought “Die of service, not of rust.”   Wales is not the land of my fathers but it is the land of a grandfather, a grandmother and a mother – which, let’s face it, is just hard to get into a song.  Family connections meant that Mid and North Wales was where I went for many holidays and some Scout trips.  I can bring to mind the wonderful Mawddach Estuary any time I want to – which is quite often.  And I’ve always supported Wales playing England at any sport.

Though employed 50% as a university lecturer in accounting and business subjects, when in 2019 my wife’s job moved us to Swansea, I cast around to offer my services.  The Swansea Council for Voluntary Service linked me with WAMES in late 2020 and though I know nothing about ME, CFS or anything similar I was very happy to help.

WAMES treasurer role is to:

    • maintain an overview of WAMES’ financial affairs and advise the committee on budgets
    • ensure that proper financial records and procedures are maintained

Things are at their best when, with money in the bank, treasurers have little to do – which has been my lot so far with WAMES.   As everyone else feels they have to be optimistic, it’s normally left to accountants and treasurers to play the sceptical negative cards. Of course the converse can be the case: I have been in a position where I’m the one to say “Things are fine – spend a bit of money!”

I see the role of Treasurer as primarily ensuring that everybody else has the maximum of information.   Secondarily, the Treasurer is there in a “sweeper” role making sure in an anticipatory fashion, that everything is going to turn out well.  Formally, and in this case, I’m a Trustee of WAMES which means I share the responsibility for ensuring the charity is run effectively and legally.

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Ross River virus immune evasion strategies & the relevance to Post-Viral Fatigue & ME onset

Posted on 04/26/2021 by wames

Ross River virus immune evasion strategies and the relevance to Post-Viral Fatigue, and Myalgic Encephalomyelitis onset, by Brett A Lidbury in Front. Med.  Vol 8, 2021 pp 298 [doi: 10.3389/fmed.2021.662513]

 

Article abstract:

Ross River virus (RRV) is an endemic Australian arbovirus, and member of the Alphavirus family that also includes Chikungunya virus (CHIK). RRV is responsible for the highest prevalence human disease cases associated with mosquito-borne transmission in Australia, and has long been a leading suspect in cases of post-viral fatigue syndromes, with extrapolation of this link to Myalgic Encephalomyelitis (ME).

Research into RRV pathogenesis has revealed a number of immune evasion strategies, impressive for a virus with a genome size of 11 – 12kb (plus strand RNA), which resonate with insights into viral pathogenesis broadly. Drawing from observations on RRV immune evasion, mechanisms of relevance to long term idiopathic fatigue are featured as a perspective on infection and eventual ME symptoms, which include considerations of; (1) selective pro-inflammatory gene suppression post antibody- dependent enhancement (ADE) of RRV infection, (2) Evidence from other virus families of immune disruption and evasion post-ADE, and (3) how virally-driven immune evasion may impact on mitochondrial function via target of rapamycin (TOR) complexes.

In light of these RRV measures to counter the host immune – inflammatory responses, links to recent discoveries explaining cellular, immune and metabolomic markers of ME will be explored and discussed, with the implications for long-COVID post SARS.CoV.2 also examined.

Compelling issues on the connections between virally-induced alterations in cytokine expression, for example, will be of particular interest in light of energy pathways, and how these perturbations manifest clinically.

Conclusions

The history of ME features regular “outbreaks,” which have been associated with virus infections. At the time of writing, the COVID (SARS-CoV-2) pandemic has revealed a sub-population of recovered patients who have developed long-term symptoms that resemble classic ME. Therefore, a perspective is presented herein that aims to link the viral manipulation of host antiviral and inflammatory-immune responses to mitochondrial function, with TOR proteins as the critical interface between deranged cytokine expression and energy regulation.

Established for many virus families (Table 1), ADE post-infection is the particular perspective focus. ADE currently has renewed interest in relation to potential COVID vaccine safety, but in a more general context also raises questions on ME pathogenesis due to the dramatic consequences for immediate antiviral defenses, later innate immune responses, and thereafter guidance from ADE-impacted cells (e.g., antigen-presenting cells) for the formation of an appropriate adaptive immune response to support long term homeostasis.

The unraveling of the interactions between the viral manipulation of cells, bioenergetics and mitochondrial function will reveal the differences, at a cellular level, to explain why some individuals go on to develop chronic long-term health challenges like ME or long-COVID, while others do not.

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Hand grip strength & fatigability: correlation with clinical parameters & diagnostic suitability in ME/CFS

Posted on 04/22/2021 by wames

Hand grip strength and fatigability: correlation with clinical parameters and diagnostic suitability in ME/CFS, by Bianka Jäkel, Claudia Kedor, Patricia Grabowski, Kirsten Wittke, Silvia Thiel, Nadja Scherbakov, Wolfram Doehner, Carmen Scheibenbogen & Helma Freitag in Journal of Translational Medicine vol 19, article no: 159 (2021)

 

Research abstract:

Background

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex and debilitating disease accompanied by muscular fatigue and pain. A functional measure to assess muscle fatigability of ME/CFS patients is, however, not established in clinical routine. The aim of this study is to evaluate by assessing repeat maximum handgrip hand grip dynamometerstrength (HGS), muscle fatigability as a diagnostic tool and its correlation with clinical parameters.

Methods

We assessed the HGS of 105 patients with ME/CFS, 18 patients with Cancer related fatigue (CRF) and 66 healthy controls (HC) using an electric dynamometer assessing maximal (Fmax) and mean force (Fmean) of ten repetitive measurements. Results were correlated with clinical parameters,  (LDH).

Further, maximum isometric quadriceps strength measurement was conducted in eight ME/CFS patients and eight HC.

Results

ME/CFS patients have a significantly lower Fmax and Fmean HGS compared to HC (p < 0.0001). Further, Fatigue Ratio assessing decline in strength during repeat maximal HGS measurement (Fmax/Fmean) was higher (p ≤ 0.0012). The Recovery Ratio after an identical second testing 60 min later was significantly lower in ME/CFS compared to HC (Fmean2/Fmean1; p ≤ 0.0020). Lower HGS parameters correlated with severity of disease, post-exertional malaise and muscle pain and with higher CK and LDH levels after exertion.

Conclusion

Repeat HGS assessment is a sensitive diagnostic test to assess muscular fatigue and fatigability and an objective measure to assess disease severity in ME/CFS.

Excerpt from paper:

Conclusion
HGS measurement is a simple diagnostic tool to assess the severity of muscle fatigue in ME/CFS. Repeat HGS assessment further allows to objectively assess fatigability and impaired recovery. Advantages of HGS measurement are easy handling, low cost and the low risk of causing PEM. Thus, it can be implemented easily in both primary care and research as an objective outcome parameter in clinical studies and drug development.

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Re-analysis of genetic risks for CFS from 23andMe data finds few remain

Posted on 04/21/2021 by wames

Re-analysis of genetic risks for Chronic Fatigue Syndrome from 23andMe data finds few remain, by Felice L Bedford, Bastian Greshake Tzovaras in medRxiv 2020.10.27.20220939  [doi.org/10.1101/2020.10.27.20220939]

Data from 23andMe had been compared with a control database that was found to contain errors. A re-analysis found only 3 of 50 previously reportedly significant SNPs survived initial study criterion of at least twice as prevalent in patients. The authors conclude that 23andMe data can be useful but only ‘if caution is taken with chips and SNPs. [s4ME]

 

Research abstract:

SNP model by David Eccles, Wiki commons

It is tempting to mine the abundance of DNA data that is now available from direct-to-consumer genetic tests, but this approach has its pitfalls A recent study put forth a list of 50 single nucleotide polymorphisms (SNPs) that predispose to Chronic Fatigue Syndrome (CFS), a potentially major advance in understanding this still mysterious disease. However, only the patient cohort data came from a commercial company (23andMe) while the control was a genetic database.

The extent to which 23andMe data agree with genetic reference databases is unknown. We reanalyzed the 50 purported CFS SNPs by comparing to control data from 23andMe which are available through public platform OpenSNP. In addition, large high-quality database ALFA was used as an additional control. The analysis lead to dramatic change with the top of the leaderboard for CFS risk reduced and reversed from an astronomical 129,000 times to 0.8.

Errors were found both within 23andMe data and the original study-reported Kaviar database control. Only 3 of 50 SNPs survived initial study criterion of at least twice as prevalent in patients, EFCAB4B involving calcium ion channel, LINC01171, and MORN2 genes. We conclude the reported top-50 deleterious polymorphisms for Chronic Fatigue Syndrome were more likely the top-50 errors in the 23andMe and Kaviar databases.

In general, however, correlation of 23andMe control with ALFA was a respectable 0.93, suggesting an overall usefulness of 23andMe results for research purposes but only if caution is taken with chips and SNPs.

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How peptic ulcer disease could potentially lead to the lifelong, debilitating effects of CFS

Posted on 04/21/2021 by wames

How peptic ulcer disease could potentially lead to the lifelong, debilitating effects of chronic fatigue syndrome: an insight, by Chien-Feng Kuo, Leiyu Shi, Cheng-Li Lin, Wei-Cheng Yao, Hsiang-Ting Chen, Chon-Fu Lio, Yu-Ting Tina Wang, Ching-Huang Su, Nai-Wei Hsu & Shin-Yi Tsai in Scientific Reports vol 11, no.: 7520 (April 2021)

 

Research abstract: 

Chronic Fatigue Syndrome (CFS) has been defined as unexplained relapsing or persistent fatigue for at least 6 consecutive months. Immuno-inflammatory pathway, bacterial infection, and other causes play essential roles in CFS.

Helicobacter pylori infection is one of the most common causes of foregut inflammation, leading to peptic ulcer disease (PUD). This study aimed to analyze the risk of CFS development between patients with and without PUD. Other related factors were also analyzed.

We performed a retrospective, nationwide cohort study identifying patients with or without PUD respectively by analyzing the Longitudinal Health Insurance Database 2000 (LHID2000), Taiwan.

The overall incidence of CFS was higher in the PUD cohort than in the non- PUD cohort (HR = 2.01, 95% CI = 1.75–2.30), with the same adjusted HR (aHR) when adjusting for age, sex, and comorbidities. The sex-specific PUD cohort to the non-PUD cohort relative risk of CFS was significant in both genders. The age-specific incidence of CFS showed incidence density increasing with age in both cohorts. There is an increased risk of developing CFS following PUD, especially in females and the aging population. Hopefully, these findings can prevent common infections from progressing to debilitating, chronic conditions such as CFS.

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Introducing WAMES volunteers: Sharon Williams

Posted on 04/19/2021 by wames

The second in a series introducing WAMES volunteers: the Volunteer Coordinator 

 

Hi! My name is Sharon Williams.

Sharon 2021

I have been involved with WAMES for many years, initially helping to raise awareness and fundraising, but now as Volunteer Coordinator and Volunteer Support Officer, meaning that I recruit, induct and support volunteers. I can’t wait to welcome more people to the team!

My role is key because we need more volunteers with varied skills as we seek to expand and help more people with ME throughout Wales.

This mission is important to me on a personal level. Until the age of 17, I was a healthy and active young person. I was an A grade student and represented Wales at gymnastics.

Then, out of the blue, I got Glandular Fever. After the fever went, I was left with profound fatigue and I was eventually diagnosed with Post Viral Fatigue Syndrome and ME. I was very ill for 20 years but in recent years my symptoms have lessened.

WAMES has helped me in the past so it is nice to give back as a volunteer and turn a negative into a positive.

I am a self-employed French and German teacher and translator. I am married and live in Pembrokeshire, enjoy walking in beautiful landscapes, swimming, knitting and spending time with my friends and family and updating my cat’s Twitter account!

Jan: the chair

Michelle

Mia

Tony

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