MSH in CFS?

Have you tested MSH?

  • Yes, and it was high.

    Votes: 0 0.0%
  • Yes, and it was low.

    Votes: 1 16.7%
  • Yes, and it was normal.

    Votes: 0 0.0%
  • No.

    Votes: 5 83.3%

  • Total voters
    6

Remy

Administrator
I ran across this article that suggests that high levels of MSH are common in MECFS, at least in the first five years of illness.

CFS patients with a disease duration of ≤ 5 years had significantly higher levels of α-MSH in their peripheral blood. α-MSH could be a potent biological marker for the diagnosis of CFS, at least during the first 5 years after onset of the disease.
I think this runs contrary to Shoemaker's observations and CIRS in general...and my experience too. My MSH has always been low to very low, even within the first five year period.

Wonder what your experience has been? Have you tested MSH?
 
Last edited:

Remy

Administrator
Richie Shoemaker with Chris Kresser:

But what if there is a complication from a cytokine event early on in the course of the illness? This cytokine activity can actually bind in the brain to a receptor for the most important calming neuroregulatory peptide called melanocyte-stimulating hormone, MSH. MSH will correct innate immune excess beautifully if it’s present in normal levels and normal amounts. But cytokines bind to the receptor that is needed to make MSH, and if those cytokines log on and stay attached to the receptor in the hypothalamus, you now will go to the second phase where you have your IL-10. Your anti-inflammatory cytokines now don’t have anything to regulate them. They will initiate additional cascades, C3a, C4a coming out within 4 to 24 hours, TGF-beta1 coming out within 16 to 24 hours. So in terms of symptoms, it doesn’t take too long before a headache and muscle ache and feeling bad and red eyes turns into exhaustion to the point that you can’t get your head off the pillow, and someone looks at you and says, “Well, you look fine to me.”
Low MSH can apparently also drive leptin...

And cause gluten sensitivity:

If you think that you have the non-celiac gluten intolerance syndrome — and Alessio Fasano, who is kind of the father, in my mind, of the immune thought about celiac disease, is really looking at this more carefully. MSH is hugely invested throughout the GI tract, and in MSH-deficient states, Tregs are allowed to reside just underneath the tight junctions primarily of cells in the jejunum and ileum, and they loosen those tight junctions to the point that gliadin — remember that’s about an 18-amino-acid piece, a fairly large molecule, as far as the body goes — can actually get beyond the tight junctions. They’re loosened from zonulin and all this, but they get into the Tregs. The Tregs say, “Here’s a foreign invader,” and they set off this autoimmune response to gliadin. It all comes from eating gluten, but when you break down the mechanism, the mechanism is MSH deficiency, which comes from early on in the stages of reduction of MSH due to cytokine excess.
 

Seanko

Well-Known Member
PS brief explanations of medical terminology are always welcome. There are different medical encyclopaedias online. One example below from the the US Library of Medicine.

Medical Dictionary
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
This is fascinating stuff. He's able to bring hypothalamic dysfunction, low IL-10, complement activation and TGF-beta 1 all together. All have been found in ME/CFS....

I can see why Richie Shoemaker excites people.

But cytokines bind to the receptor that is needed to make MSH, and if those cytokines log on and stay attached to the receptor in the hypothalamus, you now will go to the second phase where you have your IL-10. Your anti-inflammatory cytokines now don’t have anything to regulate them. They will initiate additional cascades, C3a, C4a coming out within 4 to 24 hours, TGF-beta1 coming out within 16 to 24 hours. So in terms of symptoms, it doesn’t take too long before a headache and muscle ache and feeling bad and red eyes turns into exhaustion to the point that you can’t get your head off the pillow, and someone looks at you and says, “Well, you look fine to me.”
 

Remy

Administrator
If you read the link I posted above from Selfhacked, you will notice this section which I found particularly interesting...

Dr Ritchie Shoemaker has coined this CIRS.

People with CIRS often have lower MSH.

Shoemaker says that the normal range is 35-81 pg/mL (R).

However, I’m not sure where he gets this information because he doesn’t cite a study backing this range. Actually, I’ve only found studies that contradict this range in healthy people.
In 30 healthy controls, the average was a-MSH level was 14.5 pg/mL (R).

Not a single healthy person had an MSH over 35, so it’s a bit odd that his reference range is 35-81 pg/mL (R).
I'd be very curious to know who is right regarding the optimal range...Because my level of 38 is just barely into Shoemaker's range...but it is high according to Selfhacked. And that goes along with the paper that found high levels in MECFS. Hmmm.
 

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