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
function.
Mast cells and inflammationPsoriasis 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 cellsZinc and Th1Table 2 Clinical studies on neuropeptides and cutaneous innervation in psoriasis:
The role of neuropeptides in psoriasis