Author Topic: Mast Cell Activation Syndrome  (Read 30693 times)


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Re: Mast Cell Activation Syndrome
« Reply #345 on: January 11, 2021, 05:34:28 PM »
Yes, i don't want to take them because of addiction, only when needed.
Nothing else really work for me but coffee in pois , for pain and cfs,
but coffee has side effects if not dosing smart.

Catechin synergistically potentiates mast cell-stabilizing property of caffeine

I haven't checked the sources:

The average caffeine content of an 8-oz, brewed cup of coffee is 95 mg. A single espresso or espresso-based drink contains 63 mg, and decaf coffee contains about 3 mg of caffeine (on average).

1 mol of caffeine= 194,1906 gram
1 gram = 0.0051495798457804 mol
95 mg = 0.000489210085 mol = 0.48921 millimol

95 mg ~ 8 oz (=236.588237 ml?)

0.4015 mg/mL = 2,07 mM

Paper at top:

"Caffeine anhydrous, purchased from Wako Pure Chem Ind. (Osaka, Japan), was dissolved in the external solution at the final concentrations of 1 mM (194 ug/ml), 5 mM (971 ug/ml), 10 mM (1.94 mg/ml), 25 mM (4.86 mg/ml), 50 mM (9.71 mg/ml) and 100 mM (19.4 mg/ml)"

At least 10mM for some suppression. Your average cup is ~ 2mM

"However, this amount varies between different coffee drinks, and can range from almost zero to over 500 mg."

For 500 mg caffeine per cup ---> concentration = 2.113 mg/mL = 10.89 mM, so this one is sufficient.

But there is catechin in coffee (how much?) so the concentrations of caffeine needed could be lower.

Another reason why caffeine could work:
However, in the presence of 10 mM caffeine, a potent scavenger of ROS

« Last Edit: January 13, 2021, 01:08:41 PM by Muon »


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Re: Mast Cell Activation Syndrome
« Reply #346 on: January 13, 2021, 12:08:56 PM »
Ah now I understand why the coffee enema in a POISer might have worked out. If you want to cover as much surface area (mucosal MCs) of your GI tract as possible you will need more than 1 cup of coffee + argument in previous post.
« Last Edit: January 13, 2021, 12:14:10 PM by Muon »


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Re: Mast Cell Activation Syndrome
« Reply #347 on: January 13, 2021, 01:54:55 PM »
I tried coffee enemas twice, the first time I felt really weak and shaky afterwards, using the recommended amount, the second I used much less but still felt bad and weird, found it hard to speak. And normally I can drink strong coffees and feel normal. I also tried an enema also with just water and electrolytes and this made me feel really good.


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Re: Mast Cell Activation Syndrome
« Reply #348 on: January 15, 2021, 03:15:26 PM »
Hello, I have started taking Zinc Picolinate 40mg and I have noticed a slight improvement in my POIS symptoms (a bit more alert and my psoriasis is not so bad).

Could this mean that my POIS is hormone-related given Zinc is linked to testosterone, etc? Is there anything else I should try alongside Zinc given I have seen some improvements with Zinc?

Simultaneous measurement of multiple Th1 and Th2 serum cytokines in psoriasis and correlation with disease severity

"We observed that IFN-g and IL-8 cytokines were elevated in psoriatics and correlated with parameters of disease severity while IL-10 and IL-12 were decreased."

Susceptibility-associated genetic variation at IL12B enhances Th1 polarization in psoriasis

Tuning the brain:
"If NGF levels are too high, a phenomenon called apoptosis occurs. Apoptosis is associated with cell death. Using zinc in fairly
physiologic concentrations attenuates the apoptosis induced by NGF.

Zinc can block NMDA receptors acutely and can also induce a Src family-mediated (tyrosine kinase) up-regulation of NMDA-receptor

Mast cells and inflammation

Psoriasis is also triggered or exacerbated by acute stress [105,200-202]. We showed that psoriasis is associated with increased serum CRH and decreased lesional skin CRHR-1 gene expression possibly due to downregulation [203]. Psoriasis is characterized by keratinocyte proliferation and inflammation, as well as mast cell accumulation and activation [106,204]. Mast cells are increased in lesional psoriatic skin [105,106]. Neuropeptides [205], especially SP [206], are involved in the pathogenesis of psoriasis. In particular, SP reactive fibers are localized close to mast cells [105,207]. SP can stimulate mast cells [208,209] and contributes to inflammation [210,211].

SP-positive nerve fibers are more dense in psoriatic lesions and have an increased number of mast cell contacts compared to normal skin [207,212,213]. SP-positive nerve fibers and mast cell contacts are also increased by acute stress in mice [214], leading to dermal mast cell degranulation [201,208,215]. Keratinocytes also express neurokinin (NK) 2 receptors and can be stimulated by SP [216], to release IL-1 [217]. Keratinocyte proliferation is accelerated by PAF, which can be secreted from mast cells [218], and stimulates human mast cells [219].

Psoriasis is associated with chronic inflammation and it often co-exists with inflammatory arthritis [220], in which IL-33 was recently implicated [221]. IL-33 is one of the newest members of the IL-1 family of inflammatory cytokines [222], and can mediate IgE-induced anaphylaxis in mice [223]. IL-33 also induces release of IL-6 from mouse bone marrow-derived cultured mast cells [224], and IL-8 from hCBMCs [225]. We showed that IL-33 augments SP-stimulated VEGF release from human mast cells and IL-33 gene expression is increased in lesional skin from patients with psoriasis [226]. Mast cells may, therefore, be involved in the pathogenesis of psoriasis and other inflammatory skin diseases.

Zinc and mast cells

Zinc and Th1

Table 2 Clinical studies on neuropeptides and cutaneous innervation in psoriasis:
The role of neuropeptides in psoriasis
« Last Edit: January 15, 2021, 03:40:29 PM by Muon »