Author Topic: Mast Cell Activation Syndrome  (Read 113366 times)

Muon

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Re: Mast Cell Activation Syndrome
« Reply #360 on: December 16, 2021, 04:12:26 PM »

Hopeoneday

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Re: Mast Cell Activation Syndrome
« Reply #361 on: January 01, 2022, 10:38:07 AM »
If histamine( sneezing...), prostagladins(pain...) , leukotrines
(short bresth, astma like symp...)... are involved in pois and
 as far  i can see it is atleast in a half of poisers... Then there must
be a way to test this from blod or urine...
« Last Edit: January 01, 2022, 10:40:49 AM by Hopeoneday »
Dr-pois.


Muon

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Re: Mast Cell Activation Syndrome
« Reply #363 on: February 10, 2022, 08:13:44 PM »
Intensified Hyposensitization Is an Effective Treatment of Postorgasmic Illness Syndrome (POIS)

"The patient had food allergy to wheat, milk, almonds, in an IgE-independent mechanism, with a mild course. Total serum IgE was 66 IU/ml (normal). Celiac disease was excluded (negative Endomysial antibodies and Tissue Transglutaminase antybodies). Patient reported 3 episodes of anaphylactic shock after wasp-sting."

Progecitor

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Re: Mast Cell Activation Syndrome
« Reply #364 on: February 11, 2022, 12:19:09 PM »

The understanding of visceral pain pathways is important in recognizing the serotonin relation and influence of it in pain modulation in IBS. Pain regulation pathways in visceral pain include vagal and spinal afferents that project into the CNS, both facilitating and/or inhibiting the sensory transmission to the spinal cord. Specifically, in visceral pain, there is an antinociceptive action of estrogen on the serotoninergic system due to afferent-driven vagal inhibition of the pain. On the other hand, the pro-nociceptive action occurs because of the enhancement of serotonin secretion in the intestinal mucosal mast cells (IMMCs); cells in which estrogen receptors have been found and that have been associated with its degranulation, increasing the visceral motor response and spinal or supraspinal processing of visceral nociception, mainly in IBS. Furthermore, as described previously, the interference of serotonin in pain modulation depends on the receptors, route of administration, type of pain, and influence of other substances on the release of this neurotransmitter.
https://scholar.google.com/scholar?hl=hu&as_sdt=0%2C5&q=An+Association+of+Serotonin+with+Pain+Disorders+and+Its+Modulation+by+Estrogens&btnG=

The cause is probably the senescence of sexual organs and resultant inducible SASP, which also acts as a kind of non-diabetic metabolic syndrome.

Muon

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Re: Mast Cell Activation Syndrome
« Reply #365 on: March 01, 2022, 11:52:42 AM »
https://www.thenakedscientists.com/forum/index.php?topic=6576.msg330244#msg330244

"For myself I had lots of UTIs and it stopped when I realized that a diet rich in oxalic acid was causing it. I stopped eating soy products and high oxalate foods like rhubarb, parsley, watercress, beet leaves , chard etc. Very occasionally I have the symptoms again and every time I trace it back to a oxalic acid rich food I inadvertently ate. The urethra inflammation really did aggravate the POIS. I am very happy this is basically gone. If you are interested in that topic I can give you more info. I had an urethroscopy back then and my urologist just could not find anything in my urine neither.  He could not help. I am now 99% UTI free.

Pablo
"

https://mastcell360.com/low-histamine-foods-list/

"There are other types of foods that people with MCAS or Histamine Intolerance may react to. These include lectins and oxalates"

UTI
https://youtu.be/lrKqlv6VK_w?t=3309
« Last Edit: March 01, 2022, 12:20:41 PM by Muon »


Muon

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Re: Mast Cell Activation Syndrome
« Reply #367 on: May 14, 2022, 10:08:55 AM »
NAD+-boosting molecules suppress mast cell degranulation and anaphylactic responses in mice
NAD+ precursors nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR)

Muon

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Re: Mast Cell Activation Syndrome
« Reply #368 on: May 24, 2022, 08:46:42 AM »

Muon

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Re: Mast Cell Activation Syndrome
« Reply #369 on: September 07, 2022, 03:41:53 AM »
We focused on my food allergies for the most part, but I'm going to consult with a urologist to see about attempting Dr. Afrin's (mast cell pseudocelebrity) urethral Cromolyn injection protocol. That's intended to stabilize the mast cells lining the urinary tract, so we'll see if it works for seminal allergies too.

https://www.reddit.com/r/POIS/comments/x7qird/anyone_seen_immunologist_yet/

Muon

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Re: Mast Cell Activation Syndrome
« Reply #370 on: September 11, 2022, 09:24:16 AM »
https://youtu.be/rW2K_WPUQTA?t=1262

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8465360/table/jpm-11-00860-t003/?report=objectonly

Diagnosis Atopic Diseases

Blood
  • IgE, IgG1, IgG4
  • Immune IgE (RAST for alpha-gal, casein, gluten, dust mites, fungi, grass, pollen)
  • Anti-IgE receptor antibody (basophil activation)
  • CCL2, CXCL8 (IL-8)
  • Chromogranin A
  • Eosinophilic cationic protein (ECP)
  • Food Intolerance Panel (IgG4)
  • Heparin
  • IL-4, IL-6, IL-31, IL-33
  • PGD2
  • Tryptase
Urine 24 hours (must be kept and sent cold)
  • Methylhistamine or MIA
  • PGD2
  • 23BPG=2,3-Dinor-11beta-PGF2alpha
So what will the result show if you run down this panel on a group of POIS patients?

Mast cells and cytokines crash course

All inflammation is not the same

Muon

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Re: Mast Cell Activation Syndrome
« Reply #371 on: September 12, 2022, 12:57:00 PM »
I wonder if Chymase plays a role in POIS. It's a major enzyme in mast cells.

Muon

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Re: Mast Cell Activation Syndrome
« Reply #372 on: September 12, 2022, 04:46:05 PM »
https://www.reddit.com/r/POIS/comments/xckj3r/random_pois_triggered/

"Has anyone else had pois symptoms randomly triggered? I haven't ejaculated in months and I haven't had a wet dream in over 2 weeks but I'm feeling a bit how I feel when I'm having pois symptoms can anyone explain!?"

"I ate some home made Chinese food and it used Worcester sauce I believe that's what messed me up"

demografx

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Re: Mast Cell Activation Syndrome
« Reply #373 on: October 03, 2022, 03:00:57 AM »
Posted in NORD’s October newsletter. I’m re-posting this for those of you who see a possible relationship between POIS and mast cell activation.


MAST CELL DISEASE SOCIETY

The Mast Cell Disease Society’s Patient & Provider Symposium on October 15-16 will bring together an international group of patients, well-renowned physicians, and investigators to discuss the opportunities, challenges, and progress made in research and serving patients affected by mast cell disease. Interactive panel discussions and wellness and support sessions for patients and caregivers will also take place.

To learn more:
https://tinyurl.com/2j7xe6rc
« Last Edit: October 04, 2022, 01:03:32 AM by demografx »
10 years of significant POIS-reduction, treatment consisting of daily (365 days/year) testosterone patches.

TRT must be checked out carefully with your doctor due to fertility, cardiac and other risks.

40+ years of severe 4-days-POIS, married, raised a family, started/ran a business

Progecitor

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Re: Mast Cell Activation Syndrome
« Reply #374 on: November 07, 2022, 04:33:21 PM »
https://www.reddit.com/r/POIS/comments/xckj3r/random_pois_triggered/

"Has anyone else had pois symptoms randomly triggered? I haven't ejaculated in months and I haven't had a wet dream in over 2 weeks but I'm feeling a bit how I feel when I'm having pois symptoms can anyone explain!?"

"I ate some home made Chinese food and it used Worcester sauce I believe that's what messed me up"

Worcester sauce has some base ingredients like garlic and tamarind which are considered aphrodisiac. Some optional ingredients could be coriander and clove, which are also aphrodisiac, but there could be more based on the specific recipe.
https://poiscenter.com/forums/index.php?topic=4281.msg45818#msg45818
The cause is probably the senescence of sexual organs and resultant inducible SASP, which also acts as a kind of non-diabetic metabolic syndrome.


Progecitor

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Re: Mast Cell Activation Syndrome
« Reply #376 on: March 07, 2023, 09:24:40 AM »
Phosphatidylserine (PS) externalized by activated cells or apoptotic cells or extracellular vesicles is a potential source of substrate for the production of unsaturated lysoPS species by PLA1A. Maturation and functions of many immune cells, such as T cells, dendritic cells, macrophages, and mast cells, can be regulated by PLA1A and lysoPS.
The externalization of PS has been reported in viable monocytes, activated mast cells, CD8+ T cells, regulatory B cells, cancer cells and cancer cell-derived extracellular vesicles (EVs).
Compared with secreted phospholipase A2 group IIa (sPLA2-IIa), PLA1A produces lysoPS more efficiently and is more potent in inducing histamine release from rat peritoneal mast cells and stimulating alkaline phosphatase-tagged TGFalpha release. 2-acyl-lysoPS is a lipid mediator for mast cells, T cells, and neural cells.
Kawamoto et al. found that nerve growth factor (NGF) could stimulate the release of histamine from rat peritoneal mast cells incubated with activated rat platelets. NGF antibodies or inhibition of NGF receptor tyrosine kinase activity can completely block histamine release by rat peritoneal mast cells. Furthermore, histamine release by rat peritoneal mast cells incubated with PS+ erythrocytes and NGF required the presence of PLA1A, thereby suggesting a role for PLA1A-derived lysoPS in mast cell activation. GPR34 is a highly expressed functional lysoPS receptor in rat mast cells. PLA1A-mediated production of 2-acyl-lysoPS may also contribute to histamine release by rat peritoneal mast cells in response to cross-linking of the high-affinity IgE receptor, known as Fc(epsilon)RI. Histamine release was blocked by heparin, suggesting that PLA1A activity required binding to cellular heparan sulfate proteoglycans.

https://sci-hub.st/https://www.sciencedirect.com/science/article/abs/pii/S016378272100028X

Fisetin (3,30,40,7-tetrahydroxyflavone), another flavonoid, is most highly concentrated in strawberries and is also found in apples, persimmons, and onions. Like luteolin and resveratrol, fisetin has purported anti-inflammatory, antioxidant, and neuroprotective properties. Fisetin exerts anti-inflammatory effects on mast cells and suppresses activation of microglia when stimulated by LPS, blocking LPS-induced production of nitric oxide, TNF-alpha and prostaglandin E2.
https://www.mdpi.com/1660-4601/18/5/2483/htm
« Last Edit: March 07, 2023, 09:27:20 AM by Progecitor »
The cause is probably the senescence of sexual organs and resultant inducible SASP, which also acts as a kind of non-diabetic metabolic syndrome.

Muon

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Re: Mast Cell Activation Syndrome
« Reply #377 on: April 11, 2023, 08:58:47 AM »
See Figures:
Cluster Analytic Identification of Clinically Meaningful Subtypes in MCAS: The Relevance of Heat and Cold (Open access)

Mast cell activation: beyond histamine and tryptase (Locked)

Clusters of non specific multisystem symptoms are involved in MCAS.
Clusters of non specific multisystem symptoms are involved in POIS.

The question becomes: do mast cells play a role in POIS?
« Last Edit: April 29, 2023, 03:14:41 PM by Muon »

Muon

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Re: Mast Cell Activation Syndrome
« Reply #378 on: April 20, 2023, 08:10:24 AM »
https://twitter.com/chydorina/status/1648795519492448256

Time will tell about mast cells: Circadian control of mast cell activation



Fig 2. The circadian clock system in mammals. The mammalian circadian clock con- sists of the central oscillator, located in the suprachiasmatic nucleus (SCN) of the hy- pothalamus called “central clock”, and peripheral oscillators present in virtually all cell types, including mast cells, called “peripheral clock”. The SCN receives innervation from the retina, allowing it to be entrained by solar light/dark cycles. In turn, the SCN transmits time-of-day information to peripheral clocks via the hormonal and/or the autonomic nervous pathways. Recently, diet timing, in particular breakfast, is also shown to have ability to reset peripheral clock. This system keeps the central and peripheral clocks (e.g. a huge number of mast cells) in phase with each other and synchronizes temporal programs of physiology across many tissues.



Fig. 3. Clock-controlled genes (CCGs) in mast cells. CLOCK temporally regulates the expression of Fc?RI?, ST2, and OCT-3 through its binding to the E-box sequence in the promoter of these genes. As a result, expressions of these receptors exhibit time-of-day-dependent variation in mast cells. Specifically, Fc?RI, ST2, and OCT-3 show increased expressions in the resting phase compared with in the active phase. Consequently, in the cases of Fc?RI and ST2, high-intensity Fc?RI or ST2 signaling occurs in the resting phase whereas low-intensity Fc?RI or ST2 signaling occurs in the active phase, upon IgE or IL-33 stimulation.



Fig. 4. De-synchronization of the mast cell clockworks can affect net response of mast cell activation. De-synchronization of the mast cell clockworks by genetic and/or environmental factors such as corticosterone insufficiency in mice can dampen the rhythmicity of the circadian clockworks in mast cells at the population levels. As a net result, the intensity and temporal profiles of mast cell activation could be altered. A. When mast cell clockworks are synchronized at the population levels, expression of CCGs and mast cell activation show clear circadian rhythms as a net. B. When mast cell clockworks are de-synchronized, expression of CCGs and mast cell activation lose circadian rhythms as a net.
« Last Edit: April 20, 2023, 08:45:53 AM by Muon »

Progecitor

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Re: Mast Cell Activation Syndrome
« Reply #379 on: April 23, 2023, 02:26:46 AM »
Some bitter substances may inhibit mast cell activation. Besides yellow gentian tea other bitter teas could be tested for this purpose.

Here, we investigated the impact of amarogentin on substance P-induced release of histamine and TNF-a from the human mast cell line LAD-2. Amarogentin inhibited in LAD-2 cells substance P-induced production of newly synthesized TNF-a, but the degranulation and release of stored histamine were not affected. In HaCaT keratinocytes histamine and TNF-a induced IL-8 and MMP-1 expression was reduced by amarogentin to a similar extent as with azelastine.
However, it is unclear whether amarogentin the bitterest substance in nature that is also present in high amount in the alpine flora Gentiana lutea can also modulate immune reactions in inflamed skin. As amarogentin is an agonist for several bitter taste receptors (TAS2R1, TAS2R4, TAS2R39, TAS2R43, TAS2R46, TAS2R47, and TAS2R50) and the expression of at least the bitter taste receptors TAS2R1 and TAS2R38 can be found on keratinocytes, amarogentin could influence cutaneous inflammation.

https://www.hindawi.com/journals/mi/2015/630128/

In man, 8 of the 25 bitter taste receptors (hTAS2Rs) are closely related members of such an expanded subfamily of receptor genes. This study identified two natural bitter terpenoids, andrographolide and amarogentin, that are agonists for the orphan receptor hTAS2R50, the most distant member of the subfamily.
https://pubs.acs.org/doi/abs/10.1021/jf9014334

Some other teas with bitter compounds:
White horehound, yellow gentian, wormwood, common centaury, blessed thistle and buckbean belong to the herbs rich in bitter compounds, for which the degree of dilution ranges from 6,000 to 16,000. Elecampane, hops and sweet flag belong to the herbs of medium bitterness, for which the degree of dilution ranges from 1,000 to 5,000. Extracts of chicory (leaf and root), sage, common dandelion and ribwort, with a degree of dilution ranging from 200 to 1000 exhibited little bitterness.
https://agris.fao.org/agris-search/search.do?recordID=SK1999000538
The cause is probably the senescence of sexual organs and resultant inducible SASP, which also acts as a kind of non-diabetic metabolic syndrome.