How To Naturally Reverse Psoriasis

Get Rid of Psoriasis and Improve Skin Health

There is a lot of bunk info out there about psoriasis and how to treat it, so I want to effectively and scientifically tackle this autoimmune disorder. 

 

 

Contents

  1. Basics
  2. Microbiome
  3. Biomarkers and Tests
  4. Treatment
  5. Stay Away From
  6. Mechanism Of Action
  7. Genetics
  8. More Research

Basics

 

 

Psoriasis is a chronic inflammatory skin disorder that affects 1 to 3 percent worldwide, 3.2% of the US population (8 million Americans). R R

The most common form is plaque psoriasis (psoriasis vulgaris), which accounts for the majority of cases. R

Psoriasis is characterized by well-circumscribed, erythematous plaques with scale that represent a response to an infiltration of inflammatory T-cells producing disease-stimulating cytokines in skin lesions. R

Symptoms

The symptoms of psoriasis are:

  • patches of thick, red skin R
  • skin inflammation R
  • silvery scales R
  • itching R
  • pain R

These symptoms most commonly affect the elbows, knees, scalp, lower back, face, palms, soles of the feet, nails, and soft tissues. R

Depression, anxiety, eating disorders, schizophrenia, sexual disorders, sleep disroders, samatoform disorders, substance abuse/dependence, and bipolar disorder are all commonly linked to psoriasis. R R

Psoriasis is also associated with:

Mircobiome

 

 

Microbiome of the Skin

The microbiome diversity of the skin appears to be less in psoriasis patients. R

There is a high amount of Firmicutes and Actinobacteria on the skin of psoriasis patients, but a lower amount of Proteobacteria and Bacteriodetes. R

Microbiome of the Gut

Psoriasis can be exacerbated by Staphylococcus aureus and fungi like Candida albicans and Malassezia. R

Psoriatic arthritis is similar to the profile commonly observed in the gut of inflammatory bowel disease patients. R

This possibly suggests a decrease of Faecalibacterium prausnitzii and increase of E. coli. R

Gut dysbiosis in psoriatic arthritis has been shown to correlate to an increase of secretory IgA (sIgA) levels and a decrease of receptor activator of nuclear factor kappa-B ligand (RANK-L) levels within the gut luminal content. R

Intestinal Permeability

Toxic-irritative pollutants can cause problems with the gut in patients with skin disorders.R

Serum histamine levels rise when they are exposed to lactose, sucrose, tyramine, serotonine or phenylethylamine. R

This is a very common problem seen in dysbiotic patients. R

Alcohol and other toxins increased intestinal permeability, histamine release and impairment of liver detox functions. R

Psoriasis patients may have a problem in MAO, DAO, and NMT (being inhibited). R

 

 

Biomarkers and Tests

There are the biomarkers commonly found in psoriasis:

  • C4a R
  • alpha-MSH R R R
  • IL-1ß
  • IL-4 R
  • IL-6 R
  • IL-8 R
  • IL-10 R
  • IL-12 R
  • IL-17 R
  • IL-23 R
  • IL-27 R
  • TNF-a R
  • Vitamin A (Retinol) R
  • Vitamin D R R
  • Homocysteine R R R
  • Folate R
  • Uric Acid R
  • Selenium R
  • Prostaglandin E2 R
  • C-Reactive Protein R
  • H. Pylori Infection R
  • CRH R
  • Prolactin R
  • VEGF R

Here are the blood tests you can do to check for these levels.

Treatment

 

 

Actions To Take

Get more sun exposure (UVB inhibits IL-17/TNF-α-induced IL-6, IL-8, and CXCL-1 production and decreases the expression of IL-17 receptors on fibroblasts through TGF-β1/Smad3 signaling pathway) R

Decrease/Deactivate/Inhibit:

  • Alpha-MSH (sun will increase this, so increase it if you have an infection like Candida , Streptococcus, E. coli) R
  • Anxiety R
  • AP-1 R R
  • C4a
  • Homocysteine
  • IFN-gamma R
  • IL-1b
  • IL-6
  • IL-8
  • IL-23
  • Nerve Growth Factor R R
  • NF-kB R
  • Prolactin
  • Prostaglandin E2 
  • mTOR R R R
  • Stress R
  • TNF-a
  • VEGF

Increase/Activate:

Also, fix any underlying Dysbiosis and Histamine Intolerance.

Diet/Lifestyle Actions

Supplements To Take

Drugs

  • Adalimumab (for nails) R
  • Apremilast R
  • Itolizumab R
  • Liarozole (inhibits cP450) R
  • Low Dose Naltrexone (LDN) R R
  • Metformin R
  • RA
    MBAs
    R
  • Scedosporium Dehoogii R
  • Thiazolidinediones (by regulating PPAR-gamma and retinoic acid receptor activity) R

Treatments, Lotions, and Devices

  • 453nm of Blue Light R
  • Adapalene R
  • Ammonium Lactate Lotion R
  • Carbon 60 Olive Oil R
  • Ixekizumab (inhibits il-17) R
  • Low-Level Laser Therapy (LLLT) R
  • Methotrexate (better results combining it with calcium) R
  • Possibly Ammonia-Oxidizing Bacteria 
  • Tazarotene R R
  • Tretinoin R
  • Topical Corticosteroids (can have unwanted cutaneous side effects) R
  • Topical Vitamin D3 R
  • UV-B therapy (decreases MMP2) R

Other

  • BAY 11-7082 (by inhibiting NF-kB and NLRP3 ) R
  • Calcipotriol and betamethasone dipropionate R
  • Cardarine R
  • CD1a blockade R
  • Fullerene Nanomaterials (by inhibiting the allergic response) R
  • Givinostat R
  • Methylene Blue R
  • PLA2 inhibition R

Stay Away From

These have all shown to bring about psoriasis:

  • Beta-blockers R
  • Lithium R
  • Synthetic Antimmalrials R
  • NSAIDs R
  • Tetracyclines R

Avoid excessive:

  • Methionine R R R
  • Leucine (via inhibiting mTOR) R
  • Taurine (still debated) R

Mechanism Of Action

 

 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229247/figure/F1/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229247/figure/F1/

 

Like many other autoimmune conditions, psoriasis is mediated by T cells and dendritic cells. R

Inflammatory myeloid dendritic cells release IL-23 and IL-12 to activate IL-17-producing T cells, Th1 cells, and Th22 cells to produce abundant psoriatic cytokines IL-6, IL-17, IFN-γ, TNF, and IL-22. R R

These cytokines mediate effects on keratinocytes and mast cells to amplify psoriatic inflammation. R R

Activation of IL-17-producing T cells, leading to IL-17 release, activates CCL20, CXCL1, CXCL2, and CXCL8/IL-8 synthesis, leading to recruitment of more IL-17-producing T cells and neutrophils into the skin. R

TNF-a also stimulates VEGF and activation of NF-kB. R

Elevated levels of Nerve Growth Factor have been found in psoriasis. R

In psoriasis, skin cells have lots of Tregs but reduced Foxp3. Butyrate would help this. R R

Psoriasis patients who have itches usually have increased histamine. R

CD49a

Psoriasis is characteriszed by the accumulation of a subgroup of T cells called CD49a- and it in the afflicted skin and produces the inflammation-causing protein IL-17. R

Also, in vitiligo another kind of T cell is accumulated, called CD49a+, which recognise and are ready to kill pigment cells. R

In healthy skin, CD49a+ and CD49a cells are dormant, but quickly respond with inflammatory and cytotoxic effects when stimulated by IL-15, a protein secreted from skin cells as a rapid-response defence against microbial attack. R

Genetics

MTHFR

C677T – CC is involved with psoriasis (38.46%). R

SOD

SOD activities were significantly decreased in mild (P < 0.01), moderate (P < 0.01), severe (P < 0.01) psoriasis patients, as compared with healthy controls. R

Decreased SOD activity might be related to epidermal hyper proliferation, because the ROS are thought to induce cell proliferation in various cell systems. R

CARD

CARD14 mRNA was found to be elevated 2.7-fold in the psoriasis transcriptome (activating Bcl10 and NF-κB). R

CDKAL1

rs6908425 – CC homozygotes were significantly more common responders to anti-TNF biological drugs among Psoriasis (Psor) patients. R

NLRP3

rs3806265- increased susceptibility to psoriatic juvenile idiopathic arthritis. R

PSORS

rs3823418 – mutation in this can predict psoriasis in 68% of patients. R
rs3130457 – mutation associated with psoriasis in Chinese. R

TNFα

rs361525 – associated with psoriasis in several populations worldwide R

VDR

An increased association of the A allele for the VDR was found in patients with psoriasis. R

VEGFR

 

 http://www.discoverymedicine.com/Wei-Li/2014/09/targeting-vegf-vegfr-in-the-treatment-of-psoriasis/
http://www.discoverymedicine.com/Wei-Li/2014/09/targeting-vegf-vegfr-in-the-treatment-of-psoriasis/

 

Vascular endothelial growth factor is a powerful mediator of inflammatory diseases. R

VEGF is significantly up-regulated in psoriatic skin lesions. R

More Research

  • Psoriasis and stress: NPF grantee Theoharis Theoharides discusses his psoriasis research V
  • Treating Asthma and Eczema With Plant-­Based Diets V
  • Glycine Regulates Protein Turnover by Activating Protein Kinase B/Mammalian Target of Rapamycin and by Inhibiting MuRF1 and Atrogin-1 Gene Expression in C2C12 Myoblasts. R