A possible role for mitochondrial-derived peptides humanin and MOTS-c in patients with Q fever fatigue syndrome and CFS, 2019, Raijmakers et al

I posted about Raijmakers' talk at the recent Emerge conference here (post#39), mostly about the part of the talk that was about CBT.

It's interesting that QFS warrants its own name, whereas syndromes arising after various other illnesses seem to get lumped into CFS. At the conference, Raijmakers seemed quite confident that QFS and CFS are different illnesses but I don't think there's much evidence for that. If this team's mitochondrial peptides are relevant, it doesn't look as though QFS and CFS are different. I wonder whether it might just be that these researchers have a stereotype of the CFS sufferer, and she doesn't look much like most of the farmers and meat processors that get Q fever and go on to develop QFS.

I thought the comment at the conference about the bacteria that causes Q fever being found in bone marrow was interesting, especially given a number of researchers at the conference mentioned bone marrow in passing. It seems that it is quite accepted that the bacteria can lie latent in a person, with the infection resurfacing some years later.

 

I should be asleep, but ffs. There was a small benefit on a subjective outcome at the end of the trial which completely disappeared at followup.

more swearing from me...

 

From the abstract:

No figure for humanin in the healthy controls is given in the abstract, and I mistakenly interpreted those figures as decreases in humanin production relative to the healthy controls. Actually they are absolute values. Here's the control result from the Results section:

So, actually the data can be lined up with increasing humanin levels:
asymptomatic Q fever seropositive controls = 354 (292-393)
CFS patients = 364 (316-387)
QFS patients = 371 (325-384)
healthy controls = 395 (372-409)

Hmm. Here's the chart.


With only 10 people in each cohort, that's not a convincing result. And, for the other peptide MOTS-c, there was no difference between the 4 cohorts.


So maybe the major finding from this study is a negative one:

Of the two genes they found that were a bit different, the peptides they code for were either present in the same amount (MOT-c) or not convincingly different from the two control cohorts (humanin).

I didn't really follow all the washing of the cells and other preparatory processes including stimulation with LPS. Maybe part of the problem is that they washed away a substance that might have made the cells perform differently? Maybe they need to be using tissue cells rather than blood cells?

Anyway, I don't think there is much to get excited about here, at least yet. Good on them for poking about in the biology, but the reflexive reaching for a 'psychological incentive' explanation when they don't know what is going on doesn't inspire confidence.