Australian scientists make breakthrough in Chronic Fatigue Syndrome testing

sarah darwins

I told you I was ill
Cornwall, UK


Senior Member
Usually it just means someone found a couple raised or lowered values of something in ME/CFS patients, but still with a lot of overlap with healthy controls.

These can be interesting findings, but nowhere close to being diagnostic biomarkers. For that to happen, a high rate of accuracy needs to be shown ... it's not a useful biomarker if it diagnoses a lot of healthy people with ME/CFS, or says that a lot of people with ME/CFS don't have it. There should also be a lot of replication, to show that these results are not a false positive from a single group of patients.

These types of claims are almost invariably nothing more than hype.
Sonya Marshall-Gradisnik is a signatory to The OMI-MERIT initiative. Is the research being done at Griffith really that bad? Why the dismissive comments about her work? Am I missing something here?

Lucinda Bateman, MD (Fatigue Consultation Clinic & Univ of Utah, UT, US)
Alison Bested, MD (Complex Chronic Disease Clinic, Canada)
Yenan Bryceson, PhD (Karolinska Institute, Sweden)
Ron Davis, PhD (Stanford Genome Technology Center, CA, US)
David Dreyfus, MD, PhD (Yale/Private practice, US/Israel)
Oystein Fluge, MD (Haukeland University Hospital, Norway)
Mady Hornig, MD, PhD (Columbia Univ, NY, US)
Nancy Klimas, MD (NOVA Univ, FL, US)
Andy Kogelnik, MD, PhD – Chair (Open Medicine Institute, CA, US)
Charles Lapp, MD (Hunter Hopkins Center, NC, US)
Jay Levy, MD (UCSF, CA, US)
Alan Light, PhD (University of Utah, UT, US)
Kathleen Light, PhD (University of Utah, UT, USA)
Sonya Marshall-Gradisnik, PhD (Griffith University, Australia)
Mauro Malnati, MD, PhD (San Raffaele Scientific Institute, Italy)
Olav Mella, MD (Haukeland University Hospital, Norway)
Jose Montoya, MD (Stanford University, CA, US)
David Patrick, MD, PhD (Complex Chronic Disease Clinic, Canada)
Dan Peterson, MD (OMI and Sierra Internal Medicine, NV, US)
Simone Pensieroso, PhD (San Raffaele Scientific Institute, Italy)
Charles Shepherd, MD (Private practice, UK)
Ila Singh, MD, PhD (Mount Sinai School of Medicine, NY, US)
Carmen Scheibenbogen, MD (Charité Berlin, Germany)
Chris Snell, PhD (University of the Pacific, US)
Eleanor Stein, MD (Private practice, Canada)
Staci Stevens (Pacific Fatigue Lab, US) and
Rosamund Vallings, MD (Private practice, New Zealand).


Senior Member
A single test for CFS will 'never' happen because it is not one disease. Also it takes years before this test can be used for a subgroup of patiënts. Don't talk about a breakthrough at this point, i have seen it many, many times and it never was. But these scientists are not quackers so maybe maybe maybe they have found something usefull. I hope so! But i am very sceptical.


Science breeds knowledge, opinion breeds ignorance
Intriguing. Did they say that the biomarker lies in the white blood cells? This is already extensively phenotyped, but as JE has pointed out before: The tests might have to be improved..


Senior Member


Senior Member
Logan, Queensland, Australia
Its an early news release. So it is hard to evaluate.

There is a huge way to go from a possible diagnostic test to having one marketed that is proven to be reliable.

The devil is in the details. We do not know the details and so cannot evaluate it.

Its possible this is a big leap forward, or another dud.

I would like to remind people that this research is based on some very strict identification of subjects in at least some of their studies, such as the CCC. They also use Fukuda though. They are aware of diagnostic issues at least.

Its also possible they only have a test for a subset of patients. Or that other diseases share the marker, its just that nobody looked.

I am hoping its right. So far I do not see the science behind why it is right .... if it is.

Its also worth remembering that a diagnostic biomarker does not have to be about the cause, just a unique identifying marker. Is even possible they have a marker for a secondary effect with multiple causes.

Its early days. We can be hopeful but shouldn't pin all our hopes on them. Yet.


Senior Member
Logan, Queensland, Australia
We're looking at changes in very specific parts of gene that then translate to certain receptors or proteins in the body that have key roles in metabolism, neuronal function, cardiovascular function and so on, so it's probably not surprising that it's taken this long to work it out.
It sounds like a change in actual gene expression. Not so much about activation of the gene/s, but post modification. Such modification can cut and paste parts of the gene, truncate it, add methyl groups, or maybe other things such as different conformational folding. Its very hard to say what for sure, or even what genes they are looking at.

The wording of the quote is grammatically funny. Are they talking about one or more than one gene?


Senior Member
Somewhere near Glasgow, Scotland
Is even possible they have a marker for a secondary effect with multiple causes.
IMHO, the similarity of symptoms in a bunch of illnesses:
M.E.; M.S.; organophosphate related ones; possibly Lupus and some others,
suggests to me that there is a single common "pathway" in the immune system being screwed up
and the variations in the initial cause and effects it *uniquely* has on the body over all, and then genetics, plus possible damage in various ways from environmental causes (long term heavy metal exposure for example)
possibly a retrovirus or the like being the prime thing that makes a specific weakness in the immune system "pathway"
results in a myriad of very similar health problems

We've been to used to the simple "mechanistic" dogma of the Cult of Health and Big Business, (indeed, of our societies):
one simple disease, one drug to cure it
Reality is NOT like that. There are always so many subtleties, synergies and knock on effects etc that have been overlooked.
A sort of simple and deadly example is the horrible cocktail of syphilis, HIV and Tuberculosis in the poor in the USA. Resulting in immune compromised and deeply troubled and screwed up people which then gives rise to extremely dangerous resistant and communicable TB.
Simple mechanistic experimentation in a laboratory will usually not show such things.

So, with the mindset of "simple obvious cause, then provide specific approved medicine to treat"
the medical Profession has had entirely the wrong view point about a lot of health problems.
Thus when a patient presents with something they cannot explain easily, the cultural stand by is: "well the tests cannot be wrong therefor the patient must be making it up!"
Which in real Science is bullshit: if you cannot understand something but are presented with clear obvious mass of evidence, then your Theories and/or detection/measurement equipment must lack, and then you work on it but do not dismiss it!
Took astrophysicists decades to work out what a quasar probably is, and the smart ones will know they do NOT "know" what it truly is even now, just best evidence suggests what it probably is, until we can reach one and see it's formation with our own eyes there's no "proof", just evidence and hypothesis.

We don't know what diabetes truly is, as we don't know what causes the autoimmune attack, but we're getting closer. There is no cure as yet, but some therapies look like they may offer such in the foreseeable future. Not merely treatment, but actual cure.
that's after vast sums of money and research and decades of work on this very common deadly disease many Humans suffer from
The colossal arrogance and stupidity of dismissing "stealth"/unusual illnesses to the realms of "they are making it up", is outrageous