Author Topic: Mast Cell Activation Syndrome  (Read 26958 times)

Iwillbeatthis

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Re: Mast Cell Activation Syndrome
« Reply #270 on: July 27, 2020, 11:09:14 AM »
Need some advice guys
I am planning to purchase either Neuro Protek or Histaquel, was just wondering if NeuroProtek contains quercetin phytosome or if it only has quercitin.
Histaquel has double the amount but serving size is two capusles, and its hard to compare the amounts in both products.

Histaquel has no rutin either but does have quercetin phytosome:

https://www.researchednutritionals.com/product/histaquel/?doing_wp_cron=1595866058.4130389690399169921875

https://www.amazon.com/Algonot-NeuroProtek-1-Bottle/dp/B0045JB858

Thanks

Muon

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Re: Mast Cell Activation Syndrome
« Reply #271 on: July 27, 2020, 11:41:47 AM »
Neuroprotek doesn't contain Quercetin phytosome but Quercetin lipsome. Absorption from best to worst: Quercetin Phytosome > Quercetin liposome > Quercetin (it could be liposome or just powder, they never mention this on the supplement facts). I can't compare them because HistaQuel doesn't state the amount per ingredient.

Muon

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« Last Edit: July 28, 2020, 01:19:27 PM by Muon »

Iwillbeatthis

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Re: Mast Cell Activation Syndrome
« Reply #273 on: August 15, 2020, 10:19:07 AM »
Update I have been using histaquel for over two weeks now and haven't seen any difference, for me personally I have doubts now that my issues are mast cell related.

I think Nanna's immune deficiency theory is whats going wrong with me. I have started amitriptyline as of two days ago, I have tried it in the past at a tiny dose (1/4 of 10mg) as advised by my doctor and combined it with piracetam and alpha gpc (I think this is also what caused my severe reactions to showers when i stopped). The trouble was I was still experiencing immune and infectious symptoms back then so I stopped the amitriptyline.

Now I have cleared the infectious symptoms mainly I am trying it again at the full dose of 10mg, as I still have adrenal issues eg: reactions to showers. In a organic acids test it said I had a high HVA/VMA ratio which meant my body was having difficulty converting dopamine into noradrenaline. I have tried co factors for noradrenaline like vitamin c and copper but they aren't strong enough. This also explains why I react badly to bupropion a dopamine antagonist and n acetyl tyrosine.

The test recommends droxidopa - Droxidopa is a synthetic amino acid precursor which acts as a prodrug to the neurotransmitter norepinephrine. Unlike norepinephrine, droxidopa is capable of crossing the protective blood–brain barrier. However I am unable to get this in the Uk as its not licensed here or on any online eu pharmacys.

Vandemolen

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Re: Mast Cell Activation Syndrome
« Reply #274 on: August 22, 2020, 06:07:44 AM »

My excellent doctor found a POIS study using Cromolyn on Pubmed. He said it was only 4 patients and the drug helped only half of them. He prescribed Nalcrom to me to try for a month. I had to have the pharmacy order it because it's not commonly used in Canada. I'll have it in the next day or two to try out and I'll report back. It's very expensive too but luckily my insurance covered it. A 4 week supply was over $400.
My POIS doctor gave me Nalcrom for two months. I hope it will help.
Nalcrom did not help me.
POIS since 2000. Very bad since 2008. I knew that I have POIS since June 2010. Desensitization since March 2011. I stopped with desens in July 2016. I have 50% less POIS. And only 1 day of POIS. Purified CBD works for me, but I am allergic for CBD.

Muon

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Re: Mast Cell Activation Syndrome
« Reply #275 on: August 27, 2020, 04:03:57 PM »
This guy went to Mayoclinic but didn't test for MCAS? What a missed opportunity.

https://www.reddit.com/r/POIS/comments/ihh66g/do_you_think_people_on_nofap_actually_have_pois/

Iwillbeatthis

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Re: Mast Cell Activation Syndrome
« Reply #276 on: August 28, 2020, 05:32:45 AM »
Finished the whole bottle of Histaquel now and it hasn't helped me.

Muon

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Re: Mast Cell Activation Syndrome
« Reply #277 on: September 10, 2020, 02:27:39 PM »
"Combination of triggers is more important than individual ones as they can lower the stimulation threshold of mast cells and ‘prime’ them for additional triggers." Ref

Lower activation threshold due to decreased expression/function of inhibitory molecules/pathways.
Intracellular
PTEN
Chondroitin sulfate
Sergylin
Spermine/spermidine
TGF beta
Extracellular
Deflisinc
IL-10
IL-37
IL-38
TGF beta
« Last Edit: September 10, 2020, 02:29:57 PM by Muon »


Muon

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Re: Mast Cell Activation Syndrome
« Reply #279 on: September 15, 2020, 07:34:13 AM »
While I like flavonoids, but they yet have to eradicate my 3-4 warts (on foot sole).  I think they are due to HPV.  Any method to get permanently get rid of HPV?
I just saw a otolaryngologist (ear, nose and throat doctor) about a growth on the uvula in my throat. He said that the growth was a benign papilloma (wart) and that it was probably caused by viral infection of the uvula. No test were done, but the otolaryngologist seemed confident that the growth was caused by human papillomavirus (HPV). I did not suggest any cause, he came up with this diagnosis on his own after examination of my uvula.

More: https://poiscenter.com/forums/index.php?topic=2301.msg34026#msg34026

Finally I took Diazepam (Valium) the day after O, while in POIS, and it completely removed my brain fog and anxiety.

Mast cells express benzo receptors: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3318920/table/T1/

Some subtypes of adenosine receptors have affinity for benzodiazepines if I'm not mistaken (I could be wrong about that).
« Last Edit: September 15, 2020, 07:49:14 AM by Muon »

hurray

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Re: Mast Cell Activation Syndrome
« Reply #280 on: September 21, 2020, 02:57:57 PM »
I found an interesting paper called "Postural Tachycardia Syndrome (POTS) - Satish R. Raj".

Mast Cell Activation triggered by sexual intercourse?

Quote
Some patients with POTS present with episodic flushing associated with surges in tachycardia and have coexistent mast cell activation
There are many triggers for the flushing, including prolonged standing, exercise, premenstrual cycle, meals, and sexual intercourse.

Mental clouding:

Quote
Many patients are also greatly troubled by mental clouding or troubles concentrating.

Elevated levels of norepinephrine are common in POTS suffers:

Quote
Many patients with POTS have elevated levels of plasma norepinephrine, suggestive of a hyperadrenergic state. This is most commonly secondary to a partial dysautonomia or hypovolemia. In a small subgroup of patients, the primary underlying problem seems to be excessive sympathetic discharge. These patients often have extremely high levels of upright plasma norepinephrine (>1000 pg/mL and occasionally >2000 pg/mL, with an upper limit of normal of 475 pg/mL in our clinical laboratory).

Quote
Norepinephrine Transporter Deficiency and Blockers

A specific genetic abnormality has been identified in a kindred with hyperadrenergic POTS.11 These individuals have a single point mutation causing loss of function in the norepinephrine transporter. The resultant diminished norepinephrine clearance leads to a hyperadrenergic state in response sympathetic nerve activation.

Although functional norepinephrine transporter mutations might be infrequent, many antidepressant and attention deficit medications work at least in part through inhibition of norepinephrine transporter. This includes traditional drugs such as tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors (eg, duloxetine, venlafaxine, or milnacipran), or purer norepinephrine transporter inhibitors (eg, atomoxetine or reboxetine).

https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.112.144501

Muon

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Re: Mast Cell Activation Syndrome
« Reply #281 on: September 21, 2020, 03:51:21 PM »
Evidence of Mast Cell Activation Disorder in Postural Tachycardia Syndrome (P1.277)

"Urinary 11-beta-prostaglandin F2 levels were elevated in 50[percnt], urinary N-methylhistamine levels increase in 16[percnt], while serum tryptase was not elevated in any of the PoTs + MCAD patients."

Urinary 11-beta-prostaglandin F2 alpha is also the one I found being elevated. Norepi has been measured but only in flat position which was normal. There is a paper about a point mutation under atopic dermatitits in the paper thread (receptor not transporter though). Milnacipran could tackle multiple issues at once, catecholamine/dysautonomia related and cytokine/inflammation related symptoms.

My brother doesn't have POTS but he told me recently that he had a spontaneous POTS-like attack where blood suddenly pooled in the legs and didn't go properly to the brain. He said he underestimated these kind of symptoms. He also tried SNRIs in the past with no benefit I believe, not sure what meds he tried.
« Last Edit: September 21, 2020, 04:01:25 PM by Muon »

hurray

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Re: Mast Cell Activation Syndrome
« Reply #282 on: September 21, 2020, 04:42:08 PM »
Evidence of Mast Cell Activation Disorder in Postural Tachycardia Syndrome (P1.277)

"Urinary 11-beta-prostaglandin F2 levels were elevated in 50[percnt], urinary N-methylhistamine levels increase in 16[percnt], while serum tryptase was not elevated in any of the PoTs + MCAD patients."

Urinary 11-beta-prostaglandin F2 alpha is also the one I found being elevated. Norepi has been measured but only in flat position which was normal. There is a paper about a point mutation under atopic dermatitits in the paper thread (receptor not transporter though). Milnacipran could tackle multiple issues at once, catecholamine/dysautonomia related and cytokine/inflammation related symptoms.

My brother doesn't have POTS but he told me recently that he had a spontaneous POTS-like attack where blood suddenly pooled in the legs and didn't go properly to the brain. He said he underestimated these kind of symptoms. He also tried SNRIs in the past with no benefit I believe, not sure what meds he tried.

Milnacipran could tackle multiple issues at once, catecholamine/dysautonomia related and cytokine/inflammation related symptoms.

Good insight Muon - I think you are right.

re cytokine/inflammation (from the milnacipran thread):

Quote
milnacipran analgesic and anti-inflammatory effects were at least in part exerted through its suppression of MPO activity and inflammatory mediators, such as IL-1?, IL-6 and TNF-?. Carrageenan triggers neutrophil recruitment and MPO activity, and activates the cytokines production, including IL-1?, IL-6 and TNF-?, which are accountable for inflammation and pain

https://sci-hub.tw/10.1007/s10787-020-00726-2

The most common SNRIs are venlafaxine and duloxetine - I tried them both and they were of no benefit to me either.

Prospero

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Re: Mast Cell Activation Syndrome
« Reply #283 on: September 22, 2020, 10:48:30 AM »
Quote
Norepinephrine Transporter Deficiency and Blockers

A specific genetic abnormality has been identified in a kindred with hyperadrenergic POTS.11 These individuals have a single point mutation causing loss of function in the norepinephrine transporter. The resultant diminished norepinephrine clearance leads to a hyperadrenergic state in response sympathetic nerve activation.

Although functional norepinephrine transporter mutations might be infrequent, many antidepressant and attention deficit medications work at least in part through inhibition of norepinephrine transporter. This includes traditional drugs such as tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors (eg, duloxetine, venlafaxine, or milnacipran), or purer norepinephrine transporter inhibitors (eg, atomoxetine or reboxetine).

https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.112.144501

I don't understand this. Dysfunctional norepinephrine transporter -> bad NOR clearance -> too much NOR -> POTS (or POIS), presumably.
If Milnacipran inhibits NOR transporter, it should increase NOR levels, which are believed to be already too high, and thus it should worsen POTS/POIS... What did I get wrong ?

Muon

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Re: Mast Cell Activation Syndrome
« Reply #284 on: September 22, 2020, 05:39:22 PM »
Role of inflammation in the pathogenesis and treatment of fibromyalgia

" Milnacipran, a dual reuptake inhibitor, acts its therapeutic effect partly by targeting glial activation and thereby inhibiting neuroinflammation."



Glial cells

"Furthermore, astrocytes release gliotransmitters such as glutamate"
Milnacipran blocks NMDA receptors. Glutamate receptor activation leads to mechanisms related to intracellular calcium concentration. Also I'm not surprised if (micro)glia crosstalk with mast cells in POIS.

Check education and intelligence polls:
"Recent publications have proposed that the number of glial cells in the brain is correlated with the intelligence of a species."



There might be a link with testosterone somewhere in this story. Mast cells respond to T so that may shutdown communication or it affects glia directly somehow. I haven't looked into literature for the neuroendocrinology of glial cells.
« Last Edit: September 23, 2020, 08:56:09 AM by Muon »