Hypersensitivity Megathread

[Nas]

Some quick examples:
Astilbin suppresses delayed‐type hypersensitivity by inhibiting lymphocyte migration

From this site
"Astilbin can be found in St John's wort, in Dimorphandra mollis, in the leaves of Harungana madagascariensis (Hypericaceae), in the rhizome of Astilbe thunbergii, in the root of Astilbe odontophylla(Saxifragaceae), in the rhizone of Smilax glabra(Chinaroot, Smilacaceae) and in the bark of Hymenaea martiana. It can also be isolated from Kohki tea processed from Engelhardtia chrysolepis (huang-qui). Astilbin is used in traditional Chinese medicine and can be used in supplements."

[Muon]

Perhaps slightly off-topic but I find this interesting:

''When the innervation to substance P nerve terminals is lost, post-synaptic cells compensate for the loss of adequate neurotransmitter by increasing the expression of post-synaptic receptors. This, ultimately, leads to a condition known as denervation supersensitivity as the post-synaptic nerves will become hypersensitive to any release of substance P into the synaptic cleft.''
https://en.wikipedia.org/wiki/Substance_P#Denervation_supersensitivity

''Denervation supersensitivity is the sharp increase of sensitivity of post-synaptic membranes to a chemical transmitter after denervation.[1][2] It is a compensatory change.[3]''
https://en.wikipedia.org/wiki/Denervation_supersensitivity

[Nas]

Perhaps slightly off-topic but I find this interesting:

''When the innervation to substance P nerve terminals is lost, post-synaptic cells compensate for the loss of adequate neurotransmitter by increasing the expression of post-synaptic receptors. This, ultimately, leads to a condition known as denervation supersensitivity as the post-synaptic nerves will become hypersensitive to any release of substance P into the synaptic cleft.''
https://en.wikipedia.org/wiki/Substance_P#Denervation_supersensitivity

''Denervation supersensitivity is the sharp increase of sensitivity of post-synaptic membranes to a chemical transmitter after denervation.[1][2] It is a compensatory change.[3]''
https://en.wikipedia.org/wiki/Denervation_supersensitivity

I think this needs it's own topic, I have no idea how anyone would understand this without getting a bit of background on substance P

[Muon]

I think it fits more into a topic about neurotransmitters. What if there is denervation supersensitivity in the genitourinary tract and POIS is actually a supersensitivity to neuropeptides? These can interact with nerve endings right?

[Nas]

I think it fits more into a topic about neurotransmitters. What if there is denervation supersensitivity in the genitourinary tract and POIS is actually a supersensitivity to neuropeptides? These can interact with nerve endings right?

Again I think you should make a post giving us a background on this subject, cause here other than Nanna I don't think people will understand this topic.

[Hopeoneday]

I think it fits more into a topic about neurotransmitters. What if there is denervation supersensitivity in the genitourinary tract and POIS is actually a supersensitivity to neuropeptides? These can interact with nerve endings right?

Definitely could be , i can fell that something damaging our nerves.

And i have syptomes that prove that to me.

[Muon]

I think it fits more into a topic about neurotransmitters. What if there is denervation supersensitivity in the genitourinary tract and POIS is actually a supersensitivity to neuropeptides? These can interact with nerve endings right?

Definitely could be , i can fell that something damaging our nerves.

And i have syptomes that prove that to me.

Yes I have symptoms that led me to believe there is neurogenic inflammation involved. I suspect something is going on with the nerves whether it's inflammation, neurotransmission, abnormal conduction, I don't know. Like pain in inside of arms, burning sensation, muscle spasms. Neuropeptides play a role in neurogenic inflammation:
https://en.wikipedia.org/wiki/Neurogenic_inflammation
https://en.wikipedia.org/wiki/Neuropeptide#Examples
They can cause inflammation in your brain, spine or even joints. I have no knowledge about these systems though so I will refrain from discussing it further, but this is something that is in the back of my mind.

[Nas]

"A recent (2010) study of the treatment of migraine with CGRP blockers shows promise.[24] In early trials, the first oral nonpeptide CGRP antagonist, MK-0974 (Telcagepant), was shown effective in the treatment of migraine attacks" Neurogenic inflammation wiki

If anyone has access to these drugs, it could be a good way to test the Neurogenic inflammation theory.

''Denervation supersensitivity is the sharp increase of sensitivity of post-synaptic membranes to a chemical transmitter after denervation.[1][2] It is a compensatory change.[3]''
https://en.wikipedia.org/wiki/Denervation_supersensitivity

Denervation reaction in the genitourinary tract could actually be the cause of premature ejaculation due to hypersensitivity in the penis neural endings.

[Muon]

''Denervation supersensitivity is the sharp increase of sensitivity of post-synaptic membranes to a chemical transmitter after denervation.[1][2] It is a compensatory change.[3]''
https://en.wikipedia.org/wiki/Denervation_supersensitivity

Denervation reaction in the genitourinary tract could actually be the cause of premature ejaculation due to hypersensitivity in the penis neural endings.

Maybe. Waldinger has a background on this matter, he should know something about this.
These antagonists are experimental, which means they are not available to the public. Another one might be a NK1 blocker, those are used in cancer and very expensive, statins is an option. Are there free nerve endings in the mucosal layer of the lower urinary tract? It could be denervation of these nerves interacting with molecules in sperm or there is something wrong with signal transduction. When using the terms denervation and premature ejaculation I stumbled upon this paper, which is again off-topic (LOL):
The hormonal control of ejaculation
''Evidence shows that oxytocin is actively involved in regulating orgasm and ejaculation via peripheral, central and spinal mechanisms''

[Muon]

The link you gave me about neurogenic inflammation mentions Botox. They used this for my Bell's Palsy. There was a problem with recovery. When I contract 1 facial muscle one other facial muscle contracted as well and vice versa. The neurologist told me the same signal probably were shared between two nerves which were intertwined in the repair phase and he proposed to use Botox to destroy the end plates which then had a chance to regrow properly, this helped somewhat but not much. So could my Bell's palsy be caused by neurogenic inflammation?

Edit: Or there is demyelination where two nerves were making contact. Could this make the signal jump over like in an electrical circuit?

[Nas]

These antagonists are experimental, which means they are not available to the public. Another one might be a NK1 blocker, those are used in cancer and very expensive, statins is an option.

erenumab
fremanezumab
galcanezumab
Are all FDA approved. They are probably rare and expensive, yet if anyone has access to them, trying them would be a good experiment when it comes to this theory.

When using the terms denervation and premature ejaculation I stumbled upon this paper, which is again off-topic (LOL):
The hormonal control of ejaculation
''Evidence shows that oxytocin is actively involved in regulating orgasm and ejaculation via peripheral, central and spinal mechanisms''

What are the coexisting peptides of oxytocin? If we consider that ejaculation is the trigger for POIS then knowing the neurotransmitter that gets expressed right in that moment would let us pinpoint coexisting neuropeptides that are potentially auto-immunogenic.

So could my Bell's palsy be caused by neurogenic inflammation?

Given your situation, you definitely seem to have some sort of nerve issue. And neuro-inflammation us highly likely.

We should totally open up a lab Muon, we have such great theories but no means of testing for their validity lol

[demografx]

Tell me when the ‘Muon and Nas on the road show' comes to my city.

I assume you offer Senior discounts!

[Nas]

Cytokine Targets in the Brain: Impact on Neurotransmitters and Neurocircuits


"In human studies, increases in kynurenine and decreases in tryptophan have been associated with major depression and depressive symptom severity in patients administered IFN-alpha for cancer or infectious disease.[58,59] Of note, kynurenine can be converted to kynurenic acid (KYNA) in astrocytes and quinolinic acid (QUIN) in microglia, and patients treated with IFN-alpha has been found to exhibit increased KYNA and QUIN in the CSF, indicating that kynurenine can access the brain and be converted to its neuroactive metabolites"

Really recommend this article, it talks alot about the potential ways certain cytokines effect the nervous system. From what it written their, it seems that IFN-alpha is a recurring cytokine in many of these metabolic disruptions. 

[Muon]

IFN alpha doesn't play a role in hypersensitivity as far as I know.

[Nas]

IFN alpha doesn't play a role in hypersensitivity as far as I know.

Hmmmm, so completely irrelevant?

[Muon]

IFN alpha doesn't play a role in hypersensitivity as far as I know.

Hmmmm, so completely irrelevant?

Irrelevant if the hypersensitivity theory is true, which is a big IF.

[Nas]

Irrelevant if the hypersensitivity theory is true, which is a big IF.

Is IFN-alpha related to auto-immunity though? Cause auto-immunity is technically a type v hypersensitivity.

[Muon]

I went through a lot of papers considering hypersensitvity but have never seen involvement of IFN-alpha. You can share papers if you find any.

[demografx]

Tell me when the ‘Muon and Nas on the road show' comes to my city.

I assume you offer Senior discounts!

Yes and we will reserve a special chair for you as our VIP:

As a bonus we will serve premium quality caviar!

Thank you, Muon!!
Demo

[Muon]

Hahah good one demo.