The Courier Mail: Australian scientists prove CFS is real and have discovered a test for it

https://www.ncbi.nlm.nih.gov/pubmed/24338648

 

Excellent, now he needs to make wild claims and grandiose proclamations and he will gain the support of more thread members and much more funding
And it would not hurt to publish more of his results since then, might help with the NIH.

 

He has made plenty of those already. I’m suspicious of every group and researcher now personally. Hopefully one day someone will prove me wrong but until then I will be a suspicious bastard about everyone.

The point people were making (I believe) was not to put all our eggs in one omf shaped basket.

 

I keep saying i agree, we need many groups working on this, we don't know who will strike paydirt. But my unpopular view is that we should scrutinize who we support when there is so little money to go around. Fortunately for everyone who disagrees my view is not the one followed.

 

Im honestly not sure where you’re reading that other people don’t want the same. No one is saying we should fling money at everyone left right and centre. Just that the omf isn’t the only game in town.

 

I keep saying i agree, i just don't like this repeated grandiose claim Australian team but i get blowback from that view. If they do discover a treatment i will recant and sing their praises
I would like to put this to bed personally, i don't like how this team does things, its a consequenceless opinion since i control no purse strings, can life go on?

 

I don't think anyone is buying the Australian team's hype ... maybe I missed a post or two where someone was? The difference of opinion seems to be that you think that OMF should be getting preference for funding over other groups, due to apparently having "the best talent" in your opinion, despite a lack of publishing.

OMF and the Australian team also aren't funded from the same sources, being in different countries, so aren't in competition with other. The implication would therefore be that other American teams, namely those recently receiving large grants from the NIH, are somehow less talented and less worthy of receiving that funding when there isn't enough funding for all teams. And on that point, I very much disagree.

 

I'm not saying they are the only ones, i used them as an example of a more reputable team (and i acknowledge their faults), but there are others to choose from, and some that i would not choose like this Australian one. I would like to see more good scientists then we have today come into ME/CFS research, and its insane that people have been told in the past if they research this condition they are putting a stain on their careers Its as if they don't want to acknowledge we exist or admit they are ignoring our suffering
Many teams on many fronts is completely necessary, in almost no condition is only one team working on a problem, from heart disease to Alzheimers there are thousands of teams (if not more) worldwide working on them on many fronts. They also have much more money to go around then we do, not that they can't find uses for more, but in absolute dollars we have peanuts in comparison.

Money can certainly cross international lines (NIH giving money to a UK team for example).

 

Turns out schlepping across the country was knackering so it's taken me a little while to get around to this. Anyhow, here is the patent to which I was referring: https://www.google.co.uk/patents/WO2016023077A1?cl=en

The interesting bit is from paragraph 465 onwards (it's fair to say patent applications aren't the most readable of documents):

Now, if I'm reading this correctly the first study - 'Example 1' - was an underpowered look-at-all-SNPs approach whereas here it appears they've gotten a validation cohort and found the same SNPs when looking for those ones only. That would seem to me that they may have actually hit on something, rather than just always getting a low p-value if you look at enough SNPs in a small sample. The entirely plausible alternative is that I'm not reading their results correctly

 

Measuring miRNAs is not the same as measuring SNPs, but I'd also caution that their miRNA research is subject to the same sort of statistical false positive risk.

 

Doh, you're absolutely right. And I was actually reading miRNA as I was typing SNP - this will teach me to multitask...

On the false positive risk: it's been a looong time since I took Statistics for Engineers so possibly a dumb question - wouldn't the false positive risk be reduced if they've specifically looked to validate a handful of interesting miRNA in the second study as opposed to the 'look at everything' approach in the first? (Assuming that's what they've done)

 

Even if the miRNA study does show a real statistical difference between the test and control patients

(which I doubt since in their original publication they specifically say they didn't correct for multiple comparisons -

)

what on earth does this have to do with calcium in cells?

I am tired of the exaggerated claims coming from this group and the incoherent press reports that bring the claims to us. There may be some problems with reporters incorrectly interpreting scientific information but they wouldn't have made up the statements - the researchers must have made the links between these two completely different and unrelated aspects of their research.

They know they are unrelated but persist in conflating things to mislead us into thinking that there is more to their results than a series of tiny observations.

They have engaged in this dishonest behaviour in the past and all it does is diminish confidence in everything they do.

Just for the record - the miRNA study which I linked above could conceivably form the basis for a way of discriminating between patients and controls, provided very large numbers of people are tested and the differences observed to date are shown to hold up with statistically robust analysis.

There is no known biological link between this difference and the disease - ie we have no idea what such a difference means, assuming that the difference is real. We do know a little bit about the particular miRNA's but nothing whatsoever about how they might be acting in ME/CFS.

I suspect the researchers threw in the stuff about calcium so they could lead us to think that the test is related to mechanism and so give it more gravitas.

There is no link - the two things have nothing to do with each other.

And as for changes in calcium being behind the disease, well they would need to do an enormous amount more work than they have so far published before I would give that claim any credence.

Their claim to fame on the calcium front is a small in vitro study on isolated NK cells.

All they showed was that in cells isolated from CFS/ME patients, there are fewer TRPM3 receptors (one type of calcium channel) on the surface of the minor sub-group of NK cells (about 10% of the total NK cell population), but the major group had normal numbers.

When these two populations of NK cells were stimulated in a test tube with a natural ligand for the receptor, there were differences in intracellular calcium response, both between the two groups of NK cells from patients and between cells from patients and controls.

That is as far as the study went. We don't even know if this effect happens in the body or if it is an in vitro artefact. Assuming it is real, we don't know where it fits in to the wider scheme of things. It could be causal or it could be a downstream consequence of some other problem.

In a similar attempt to give a tiny observational study more gravitas, publicity at the time tried to link this observation with their SNP studies on TRPM3, ie tried to imply the changes were the result of a defect in an ion channel. The waters were made even murkier at the time with the first round of claims about a new test to detect CFS hinting that it might be based on these SNP differences.

Yet they themselves went on to do a study on SNPs where they finally did what everyone criticised them for not doing in the first place, namely correct for multiple comparisons, and actually showed the SNP differences in TRPM3 didn't exist. To try to salvage something they tried to fudge a difference in one other SNP but really this doesn't exist either.

This didn't stop them from continuing to claim in publicity that they have discovered a defect in a cell surface receptor involved in calcium signalling, even though they know this is not true, because it leads us to believe the observed differences in calcium have some causal significance - REALLY DISHONEST.

They flit from tiny observational study to tiny observational study. Some of these are interesting but we will only know if they mean something when this group does in depth follow-up studies that convince other scientists that here is something here that is worth trying to replicate and examine further.

So far there doesn't seem to be any evidence of substantial studies of underlying mechanisms coming from the group, surely a hallmark of serious research. Instead there is periodic and vigorous beating of the publicity drum to make us think these studies mean something, but it's no substitute for the real thing.

 

Agreed. Anecdotally, I've been taking a calcium channel blocker (Verapamil) at high dosages (240 to 480mg/day) for about 30 years as treatment for cluster headaches. While they work for that purpose, if they are alleviating any CFS/ME symptoms, I'm not aware of it.

 

As soon as I saw that this article was published in the Courier-Mail, I decided not to waste my precious energy reading it. This awful Murdoch rag regularly competes for the least trustworthy position in the bottom of the barrel rankings in Australia, so you can expect the headline grab would have little meaningful relationship to the content, such as it would be, given the audience it is directed at. I would also place a bit more trust in the article if the writer, the National Health and Medical Reporter for News Corp, had (apparently) more than a secondary education. As for the research- maybe it is important, maybe it isn't. I'm going to wait until it appears somewhere that has at least a smidgen of credibility. It might be a long wait. Besides which, this is not a new 'discovery' - http://www.amjmed.com/article/S0002-9343(88)80052-4/abstract - from 1988! (oops, I see that it has been mentioned earlier that this is nothing new.)