An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (2021, Wirth et al)

Violeta

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Since alpha 1 adrenergic receptors and Beta 2 adrenergic receptors are both stimulated by epi/norepi, if there was a lack of epi/norepi, both would be affected.

I just realized this the other day. Butcher's Broom does help with orthostatic intolerance, and so is helping in some way with a1ar, so I wasn't looking at B2-aR. But now I am thinking it's affecting both.

I suppose insufficient epi/norepi could be the issue, or as nerd said, it could just be compensatory. In which case there would supposedly be autoantibodies (or some other issue) at both sites.

So beta2-adrenergic receptors are found in:
Beta 2 receptors are predominantly present in airway smooth muscles. They also exist on cardiac muscles, uterine muscles, alveolar type II cells, mast cells, mucous glands, epithelial cells, vascular endothelium, eosinophils, lymphocytes, and skeletal muscles.

And yes, I have symptoms related to Beta 2 receptors, too. I am looking for relief from those symptoms by Butcher's Broom, not sure yet. Allergies might also be involved.
 

Violeta

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An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Klaus J. Wirth, Carmen Scheibenbogen and Friedemann Paul

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Abstract
There is accumulating evidence of endothelial dysfunction, muscle and cerebral hypoperfusion in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). In this paper we deduce the pathomechanisms resulting in central nervous pathology and the myriad of neurocognitive symptoms. We outline tentative mechanisms of impaired cerebral blood flow, increase in intracranial pressure and central adrenergic hyperactivity and how they can well explain the key symptoms of cognitive impairment, brain fog, headache, hypersensitivity, sleep disturbances and dysautonomia.
Do you have links to their previous papers that they mentioned in this article? I searched by authors at BMI but couldn't find them.

Oh, silly me, the links are in this paper.
Here's one. Wow.

"We found elevated ß2 adrenergic receptor (ß2AdR) and M3 acetylcholine receptor antibodies in a subset of CFS/ME patients."

https://www.sciencedirect.com/science/article/pii/S1568997220300823?via=ihub
 
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Violeta

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I am thinking molecular mimicry technology would be helpful with determining possible autoantibodies, and maybe there already is info out there relative to a1-aR and b2/aR.

Along that line I found this paper.

Molecular mimicry theory (MMT) suggests that epitope mimicry between pathogens and human proteins can activate autoimmune disease. Group A streptococci (GAS) mimics human cardiac myosin in rheumatic heart disease (RHD) and coxsackie viruses (CX) mimic actin in autoimmune myocarditis (AM). {Beta2-AdR}
https://www.frontiersin.org/articles/10.3389/fped.2014.00085/full
 
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Violeta

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WIth respect to possibility of epi/norepi insufficiency in this issue,

These results clearly demonstrated that pantothenic acid supplementation stimulates the ability of adrenal cells in male rats to secrete corticosterone and progesterone

https://pubmed.ncbi.nlm.nih.gov/18520055/

Adrenal function in rheumatoid arthritis

https://arthritis-research.biomedcentral.com/articles/10.1186/ar3628l

And weak support for this but nevertheless, some support:
"One study found that people with RA may have lower levels of B5 in their blood than healthy people, and the lowest levels were associated with the most severe symptoms."
 

Pyrrhus

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Although it doesn't answer the question of whether there is a lack of chemical (epinephrine/norepi) or if the receptors for some reason aren't responding.
There is a third possibility: there is a problem with the nerve cell that is supposed to release the (nor)epinephrine to the cell that has the adrenergic receptor, and therefore (nor)epinephrine is not getting released in the first place.

In this possibility, there is not a lack of (nor)epinephrine and there is not a problem with the receptors, but there is a problem with the nerve cell that is supposed to release the (nor)epinephrine in the first place.
 
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Violeta

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There is a third possibility: there is a problem with the nerve cell that is supposed to release the (nor)epinephrine to the adjacent nerve cell that has the adrenergic receptor, and therefore (nor)epinephrine is not getting released in the first place.

In this possibility, there is not a lack of (nor)epinephrine and there is not a problem with the receptors, but there is a problem with the nerve cell that is supposed to release the (nor)epinephrine in the first place.
That's interesting, so I had to look up release of neurotransmitter from nerve cell and found this.

"A neuron sending a signal (i.e., a presynaptic neuron) releases a chemical called a neurotransmitter, which binds to a receptor on the surface of the receiving (i.e., postsynaptic) neuron. ... The increase in intracellular Ca2+ concentration triggers the release of neurotransmitter molecules into the synaptic cleft." @Crux

Do you know anything else about this, Pyrrhus?
 
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Pyrrhus

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"A neuron sending a signal (i.e., a presynaptic neuron) releases a chemical called a neurotransmitter, which binds to a receptor on the surface of the receiving (i.e., postsynaptic) neuron. ... The increase in intracellular Ca2+ concentration triggers the release of neurotransmitter molecules into the synaptic cleft."
That's right. So, if there is a problem with the neuron that is supposed to send the signal, the neurotransmitters (nor/epinephrine) will not be released, and will not bind to the (adrenergic) receptors on the receiving cell...
 

nerd

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"A neuron sending a signal (i.e., a presynaptic neuron) releases a chemical called a neurotransmitter, which binds to a receptor on the surface of the receiving (i.e., postsynaptic) neuron. ... The increase in intracellular Ca2+ concentration triggers the release of neurotransmitter molecules into the synaptic cleft."
And we're back at the electrolyte mobilization topic and the question of whether Ca+ influx in ME/CFS enhances or compensates the disease pathogenesis.
 

Violeta

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Stimulating effect of 6R-tetrahydrobiopterin on Ca2+ channels in neurons of rat dorsal motor nucleus of the vagus

We have recently found that 6R-tetrahydrobiopterin (6R-BH4), a natural cofactor for aromatic L-amino acid hydroxylases and nitric oxide synthase, enhances dopamine release.

"we examined the effect of 6R-BH4 on Ca2+ channels in neurons of rat dorsal motor nucleus of the vagus, where dopaminergic neurons are densely located"


https://pubmed.ncbi.nlm.nih.gov/8660332/
 

SlamDancin

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@Violeta Ive been wanting to try Kuvan for a while now, it seems promising. I think you’ve inspired me to ask my doctor how I might be able to get a prescription filled for it.
 

Violeta

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If you try it, keep us posted. I ordered some tyrosine to see if that helps. Trying to figure out the peroxynitrite deal, what to do about it.