Protective Effect of Hemin Against Experimental Chronic Fatigue Syndrome in Mice: Possible Role of Neurotransmitters, 2020, Kumar et al

Mouse model = mice they have exhausted through over exercising. Therefore this is of dubious use to us.

Paywall, https://link.springer.com/article/10.1007/s12640-020-00231-y
Open access PDF paper, https://sci-hub.tw/10.1007/s12640-020-00231-y

 

Indeed, torturing mice with forced swims might cause fatigue, but it certainly isn't CFS or ME.

Side note: Heme oxygenase is HSP32. Heme is broken down into biliverdin (ultimately bilirubin) and Fe2+
Gilbert's syndrome is not uncommon in CFS patients, suggesting this pathway has increased activity in many patients...

 

Those poor mice

 

This is very interesting ( cc : @wigglethemouse ), Thank you @Andy


Upon searching for hemin i found that hemin is a TSPO ligand :

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520880/



TSPO has been identified by Machine Learning since 2018. To be fair, there was no connection of its function with mitochondrial Calcium metabolism but rather with Cholesterol metabolism. Recall that Prusty also discussed about dysregulated calcium metabolism in one of his slides in his latest presentation.

So, it could be of interest.

 

This isn't ME. It's PTSD. It's horrific. How would the researchers like being 'forced to swim' (i.e., threatened with drowning) for 10 minutes per day?

 

This is about as valid and ethical as experiments where someone takes participants into a room and tell them that their parents were gruesomely murdered and use that state as a proxy for depression.

Which, in mice, would be quite a feat.

But, no, ME, or even CFS, is not the same as a healthy person (or mouse) exercising excessively. The big tell is right there in the name. Chronic. Chro-nic. Words. Mean. Things.

 

@mariovitali Hi Mario, Themos pointed me here after a twitter discussion of TSPO (also with @wigglethemouse)

I find TSPO very interesting for its link to both mitochondrial enzymes and neuroinflammation. The connection to hemin is further intriguing for a number of reasons. I'll be brief here since TSPO perhaps deserves it's own separate thread (if there isn't one already on this site. I don't see one).

I wonder if there are any (tenuous) lines to be drawn between hemin & some of the OMF blood studies, i.e. the RBC deformability study and the "something in healthy serum restores ME-cellular function under stress"-study. It seems too much to hope that hemin is this key factor but it's maybe worth consideration. I'd like to do some digging on how hemin arises endogenously in the body.



Regarding the primary topic of this thread - yeah, what an atrocious mouse study. Mice studies tend to be that way, sadly.

 

Basic biology is very conserved in mammals (and all eukaryotes) so research which tells us how normal biological functions work could lead to benefits finding what is wrong in ME, but animal models of disease are not very useful nowadays.

They worked out what hormones are and how they function in animals and then used that knowledge to treat humans with endocrine diseases saving millions of lives but they did not start by trying to feed sugar into mice to give them diabetes.