Deep phenotyping of myalgic encephalomyelitis/chronic fatigue syndrome in Japanese population: Kitami, Fukuda et al 2020

https://www.nature.com/articles/s41598-020-77105-y

 

Are these profiles causing the sleep disruption or are they being caused by the sleep disruption?

 

I don't have anything to offer about how the research was performed but would wish that anyone doing proper (as in biomed) research might consider orthostatic intolerance issues as they seem to be wide spread among us.

 

Correlation does not mean causation; it is an association to be explored (maybe).

 

I would have liked to see objective assessment of sleep disturbance e.g. using sleep monitors.

Haven't tried to research it but the technique they used (1h-nmr spectroscopy) is generally considered to be a reference technique i.e. gives accurate results.

Not sure about urea results "decreased uric acid, urea nitrogen, and total bilirubin" - Reference might give insight:
14.
Yamano, E. et al. Index markers of chronic fatigue syndrome with dysfunction of TCA and urea cycles. Sci. Rep. 6, 34990 (2016).
EDIT: yes, the 2016 study found low urea levels [https://www.nature.com/articles/srep34990]

Chris Armstrong found increase in use of protein (certain amino acids) for energy.

@Jonathan Edwards has made an interesting suggestion re MR spectroscopy:
"I still think for any of this to have any plausibility it should be possible to find real-time changes in metabolites in ME patients during exercise using MR spectroscopy."
https://www.s4me.info/threads/subst...-with-cfs-tomas-et-al-2020.17464/#post-297239

Chris Armstrong (from memory) is looking at the whole protein metabolism thing. Also, check out Cara Tomas's paper - comments here https://www.s4me.info/threads/subst...-in-patients-with-cfs-tomas-et-al-2020.17464/

 

Slightly unusual responding to your own post.

I received a few questions re my post
--- Chris Armstong found specific amino acids used-
Chris's study was way back in 2015; subsequently Fluge and Mella added to that (2016) -- might be others
Supplementation with amino acids - search this forum and you'll find stuff - it's come up recently - suggestions?

Re whether - imaging study was sound ---
MRI (really same as magnetic resonance spectroscopy - which was used in this study) is generally considered to be sound i.e. it's a fundamental property which is being measured. I've heard PET referred to as something artificial i.e. created and thus not as reliable as MRI/MRS.
The scan studies I've seen are mostly PET i.e. since MRI scans are only sensitive enough to pick up glutathione and a few other things [Dikoma C. Shungu - http://vivo.med.cornell.edu/display/cwid-dcs7001 - check out his MRI studies]

 

One thing I've noticed in myself is that paradoxically I often have a subjectively better day following a more disturbed night's sleep (cat, dreams, noise). I'm presumed Long Covid, just under 18 months in, and around 9 months from becoming life-changed. I've been quite curious as to why this is. Noting that sleep quality affects hormones (and vice versa), I've recently started doing 24 hour interstitial glucose monitoring. (I'm not diabetic and had not shown any indicators of glucose intolerance, including normal HbA1C). I was particularly interested in what's happening with glucose overnight.

Generally, I seem to be more hypoglycaemic than expected. With two days of 24 hour data I'm <3.9 54% of the time. The highest spike I've seen is a brief 6.1 following a carby meal.

Mornings and overnight, I'm 3-4 mmol/L. Day 1 my pre-breakfast 0750 reading was LO rising to 2.9 at 0902, and then to 5.3 at 0930 following a protein smoothie. Day 2 I seem to have had a more normal early morning response, with an 0713 rise to 5.2 and then 4.5 at 0736 (both prior to food).

Day 1 I was using the cheap handheld reader, so I only had results-on-scan. Now I'm using the iPhone app which graphs the continuous readings the sensor is recording. I'll see what patterns I'm showing over a month. I'm guessing this may reflect compensation in my metabolism +/- pacing.

I haven't looked into the papers on this yet, so might find this is all well established, but thought I'd mention in this thread. Among others, I need to read Fluge and Mella more thoroughly. I do note some comments on the forum relating to higher glucose levels, so I'd appreciate any other thoughts on this (perhaps in a new thread).

In LC there seems to be a suggestion of a bi-modal population of those more commonly being diagnosed: both obese/unfit/diabetic and but also very fit/athletes. Glucose would also seem to be implicated in immune and thrombosis dysregulation.