I don't think the above article is saying any more than
this older March 2017 article covers.
The older article explains that ME/CFS calcium abnormalities are found in natural killer (NK) cells, and that these abnormalities might be due to the lower number of
TRPM3 calcium ion channel receptors found on NK cells in ME/CFS patients.
The recent article is trying to conflate calcium changes with a study they have done showing differences in microRNAs (miRNA) between ME/CFS patients and controls, which they claim might be the basis for a diagnostic test.
In this respect it is similar to the earlier report where the conflation was with TRPM3 receptors, but they are making new claims.
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 which the journalists go on to report.
In the case of the recent claims about miRNA's, 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 -
Due to the small sample size and the heterogeneity of the CFS/ME phenotype we interpreted significance from the unadjusted P-value, without the Benjamini-Hochberg method for False Discovery (FDR) correction. Statistical significance was accepted at P<0.05.
what on earth does this have to do with calcium in cells?
Well nothing but by linking the two the researchers mislead us into thinking that a very small observational study has some causal link. It gives it more gravitas.
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 however - 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.
And there is no reason whatsoever to link this to calcium in cells.
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.
Note there is no reason to think this applies particularly to NK cells. They just chose to study isolated NK cells. The receptors are present on many cell types.
In a similar attempt to give a tiny observational study more gravitas, publicity at the time (in the earlier link above) 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. It leads us to believe the observed differences in calcium have some causal significance however - REALLY DISHONEST in my book.
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.