The Emerge Australia Media and Research Digest (029) 9th August 2019

Friday 9th August 2019

 

Welcome to the Twenty-Ninth Emerge Australia Media and Research Digest!

The fortnightly summary of research and media about Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS)


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1- Rethinking ME/CFS diagnostic reference intervals via machine learning, and the utility of activin B for defining symptom severity
Authors: Lidbury, B., Kita, B., Richardson, A., Lewis, D., Privitera, E., Hayward, S., … Hedger, M.
Link: https://www.mdpi.com/2075-4418/9/3/79

Australian researchers explored a potentially effective method of identifying ME/CFS by using a combination of cytokines. By grouping activin B with 24-hour urinary creatinine clearance and serum urea together for analysis, the results show good potential for use in diagnosing ME/CFS. Activin B is a complex protein found to have biological effects in numerous bodily functions.

A previous pilot study showed a significant increase of activin B in ME/CFS patients as compared to healthy controls. The researchers found that including activin B in the panel of pathology markers improved prediction rates for mild and moderate cases of ME/CFS. Additionally, activin B was also found to help with the prediction of symptom severity as represented by weighted standing time tests.

**This paper is from the Emerge Australia sponsored issue of Diagnostics

2  – Pathological mechanisms underlying Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Authors: Missailidis, D., Annesley, S. J. & Fisher, P. R.
Link: https://www.mdpi.com/2075-4418/9/3/80/htm

A new paper from researchers based at La Trobe University has summarised current research evidence on the pathological mechanisms underlying ME/CFS. Research shows that ME/CFS patients are likely to experience their symptoms due to changes in muscle and mitochondrial function, metabolism, immune system, neurological system, adrenal system and their gut.

Overall, it is difficult to determine which of the pathological mechanisms is the original cause of ME/CFS. Grouping patients into disease characterising subtypes (as known as patient subtyping), may allow for better diagnosis. This, in turn, helps researchers find the cause of each of these subtype’s symptoms.

**This paper is from the Emerge Australia sponsored issue of Diagnostics

3 –  Medically documenting disability in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) cases
Authors: Comerford, B. & Podell, R.
Link: https://www.frontiersin.org/articles/10.3389/fped.2019.00231/full

A new perspective article from researchers in the US discusses how physicians can best support ME/CFS patients in documenting disability in order to access disability welfare programs.

To provide a more accurate picture of a patient’s health, the article recommends that ME/CFS patients demonstrate to their physician-specific examples of ME/CFS symptoms or incidents that they have experienced. Patients should also include any activities that they have abandoned as a result of ME/CFS. Child claimants should ensure that they provide documentation that shows marked and severe functional limitations as a result of ME/CFS.

Finally, ME/CFS claimants should not participate in the standard functional capacity evaluations that private insurers often schedule, as these evaluations have been shown to be unable to predict the ability of a person with ME/CFS to work.

4 – The IDO trap hypothesis for the etiology of ME/CFS
Authors: Kashi, A. A., Davis, R. W., & Phair, R. D.
Link: https://www.mdpi.com/2075-4418/9/3/82/htm

Researchers from the Open Medicine Foundation have published a new paper outlining the idea of a ‘metabolic trap’, representing a new way of thinking about ME/CFS. The theory proposes that if the levels of tryptophan in a cell become too high, the IOD1 genes will stop producing kynurenine, and this high level of tryptophan will be maintained. ‘IOD1 and IOD2’ genes code for enzymes that transform tryptophan (an essential amino acid) into kynurenine (an important regulator of the immune system) in our cells.

When there are high levels of tryptophan in a cell the IOD2 enzyme increases its yield of kynurenine, while the IOD1 enzyme decreases its yield of kynurenine. If a person has particular mutations in the IDO2 gene – which has been found to be common in the human population – then it is solely up to the IDO1 to convert kynurenine from tryptophan.

It is thought that a significant combination of factors, including pathogens, stressors, and the environment, play a role in triggering the levels of tryptophan in a cell to become high enough to trigger the ‘trap’.

**This paper is from the Emerge Australia sponsored issue of Diagnostics

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