Related article: Skin conditions
Related article: Skin conditions
Psoriasis is an autoimmune disease that affects the skin that varies in severity from minor localized patches to complete body coverage. The richness of the skin microbiome and the emerging discrepancies between the microbial composition between health and disease point to a microbial etiology for psoriasis.
The Marshall Protocol treats psoriasis by reactivating the innate immune response. In the course of treatment, patients' disease symptoms may become worse due to a process called immunopathology.
A decade ago, Chiller et al. concluded, “The skin is a poor media for bacteria given the large number of inherent defense mechanisms.”1) This assessment was undermined seven years later by Fierer et al.’s work, which found that the average human palm harbors at least 150 bacterial species – an order of magnitude greater than previous estimates.2) A 2009 Science study expanded on this understanding of microbial diversity in skin, showing that forearms and underarms, though located just a short distance apart, are as “ecologically dissimilar as rainforests are to deserts.”3) Trillions of bacteria, fungi, viruses, archaea, and small arthropods colonize the skin surface, collectively comprising the skin microbiome.4) One prominent researcher called human skin a “virtual zoo of bacteria.”5)
Novel insights are being revealed about the extent to which skin microbiota affects health. For example, odors produced by skin microbiota are attractive to mosquitoes as shown by in vitro studies, and variation in bacterial species on the human skin may explain the variation in mosquito attraction between humans.6)
For many physicians, immunosuppressive medications are a first-line treatment for psoriasis. These drugs suppress the innate immune response, which provides some patients with temporary symptom palliation, because they reduce immunopathology, the bacterial die-off reaction.
Antimicrobial peptides (AMPs) are strongly expressed in lesional skin in psoriasis and play an important role as proinflammatory “alarmins” in this chronic skin disease. Vitamin D analogs like calcipotriol have antipsoriatic effects and might mediate this effect by changing AMP expression. In this study, keratinocytes in lesional psoriatic plaques showed decreased expression of the AMPs beta-defensin (HBD) 2 and HBD3 after topical treatment with calcipotriol. At the same time, calcipotriol normalized the proinflammatory cytokine milieu and decreased interleukin (IL)-17A, IL-17F and IL-8 transcript abundance in lesional psoriatic skin. In contrast, cathelicidin antimicrobial peptide expression was increased by calcipotriol while psoriasin expression remained unchanged. In cultured human epidermal keratinocytes the effect of different vitamin D analogs on the expression of AMPs was further analyzed. All vitamin D analogs tested blocked IL-17A induced HBD2 expression by increasing IkappaB-alpha protein and inhibition of NF-kappaB signaling. At the same time vitamin D analogs induced cathelicidin through activation of the vitamin D receptor and MEK/ERK signaling. These studies suggest that vitamin D analogs differentially alter AMP expression in lesional psoriatic skin and cultured keratinocytes. Balancing AMP “alarmin” expression might be a novel goal in treatment of chronic inflammatory skin diseases. 17)
I've had lots of experience with psoriasis (which looks like sarc lesions, BTW). I've found a cream that helps it feel better. It's a combo of mango and shea butter that I buy at Walmart, made by Tree Hut. It's very soothing.
Reenie, MarshallProtocol.com