What is Psoriasis? Causes, Symptoms, and Natural Remedies (2026)

By Ava Huang, Herbal Science Researcher at QICAOGANGMU | Updated: May 2026 | Reading time: 14 minutes

Psoriasis is a chronic, immune-mediated inflammatory skin disease affecting approximately 2-3% of the global population. PMID 32467098. Characterised by rapid skin cell turnover, it typically manifests as thick, red patches covered with silvery scales, often accompanied by intense itching, pain, and discomfort. Beyond the visible symptoms, psoriasis can profoundly impact quality of life and is associated with comorbidities including psoriatic arthritis, cardiovascular disease, and metabolic syndrome. PMID 33812489

This guide covers what psoriasis is, how the immune system drives it, what the different types look like, the limitations of conventional treatments, and what the evidence shows for natural and herbal approaches - including how QICAOGANGMU's five-herb formula addresses psoriasis through non-steroidal mechanisms.

Quick reference: psoriasis facts and QICAOGANGMU mechanisms

Understanding psoriasis: the immune-mediated mechanism

Psoriasis is not merely a skin condition but a systemic inflammatory disease driven by a complex interplay of genetic, immunological, and environmental factors. Its hallmark is the hyperproliferation of keratinocytes - the main cells of the epidermis - leading to the characteristic thick, scaly plaques. PMID 30909615, PMID 29226422

The immune cascade

At the core of psoriasis is a dysregulated immune response involving both innate and adaptive immunity. PMID 24655295

• Trigger phase: Environmental triggers (infections, stress, skin injury, certain medications) activate immune cells in genetically predisposed individuals.
• Immune activation: Antigen-presenting cells (dendritic cells) release pro-inflammatory cytokines, particularly IL-23 and IL-12.
• T-cell differentiation: These cytokines drive naive T cells to differentiate into Th17 and Th1 cells. Th17 cells are the key drivers of psoriasis, producing IL-17, IL-22, and TNF-alpha. PMID 24655295, PMID 30909615
• Keratinocyte hyperproliferation: Released cytokines (IL-17, IL-22, TNF-alpha, IFN-gamma) cause keratinocytes to multiply excessively, accelerating turnover from 28-30 days to 3-5 days and producing thick, scaly plaques.
• Inflammatory amplification: Neutrophils, macrophages, and other immune cells infiltrate the skin, sustaining the inflammatory loop that drives redness, swelling, and itch.

Types of psoriasis

• Plaque psoriasis - the most common type (80-90% of cases). Raised, red patches with silvery scales, typically on elbows, knees, scalp, and lower back. PMID 33812489
• Guttate psoriasis - small, teardrop-shaped spots, often triggered by streptococcal throat infection. More common in children and young adults.
• Inverse psoriasis - smooth, inflamed patches in skin folds (armpits, groin, under breasts) without typical scaling due to moisture.
• Pustular psoriasis - white blisters of non-infectious pus surrounded by red skin. Can be localised or widespread.
• Erythrodermic psoriasis - a severe, rare form causing widespread redness and shedding of skin. Can disrupt body temperature regulation and requires urgent medical care.
• Psoriatic arthritis - affects up to 30% of psoriasis patients, causing joint pain, stiffness, and swelling. PMID 33812489
• Nail psoriasis - pitting, discolouration, thickening, or separation of nails from the nail bed.

Common symptoms

• Red patches of skin covered with thick, silvery scales
• Dry, cracked skin that may bleed
• Itching, burning, or soreness
• Thickened, pitted, or ridged nails
• Swollen and stiff joints (in psoriatic arthritis)

Limitations of conventional psoriasis treatments

Topical therapies

Topical corticosteroids are the most commonly prescribed first-line treatment. They rapidly reduce inflammation, redness, and itch. Limitations with prolonged use include skin thinning (atrophy), rebound flares on stopping, tachyphylaxis (decreased response over time), and increased fungal infection risk. PMID 25862024. Not suitable for long-term continuous use on the face, genitals, or skin folds.

Vitamin D analogues (calcipotriol, calcitriol) slow skin cell growth without skin thinning. Effective for plaque psoriasis long-term but can cause local irritation, particularly on the face. Prescription required.

Coal tar is one of the oldest established psoriasis treatments, reducing skin cell turnover and inflammation. Available OTC in many countries. Downsides: strong smell, staining, and photosensitivity. Not suitable for the face, groin, or underarms.

Phototherapy

Controlled UV exposure slows skin cell growth and reduces inflammation. Limitations: requires multiple clinic visits, can cause sunburn-like reactions, and carries increased skin cancer risk with long-term exposure.

Systemic medications

For moderate to severe psoriasis, systemic drugs including methotrexate, ciclosporin, and acitretin may be prescribed. Biologic therapies targeting specific immune pathways (TNF-alpha, IL-17, IL-23 inhibitors) are highly effective for severe psoriasis but require injections, carry immunosuppression risks, and are expensive. PMID 32189327

These limitations highlight why many people with psoriasis seek natural alternatives for long-term daily management - where steroids are not sustainable and biologics are not accessible or needed.

Natural approaches for psoriasis relief: the evidence

Natural and herbal approaches for psoriasis have attracted growing research interest. A systematic review confirmed efficacy and safety of topical Chinese herbal medicine for atopic eczema, with many of the same herbs directly relevant to psoriasis. PMID 24821063

Sophora flavescens (Ku Shen) - the strongest herbal evidence for psoriasis

Flavonoids and alkaloids from Sophora flavescens - including sophoraflavanone G - have been shown to suppress inflammatory cytokines (IL-6, IL-8, CXCL1) and reduce psoriasiform inflammation in vitro, with effects comparable to topical steroids. PMID 38358770. Oxymatrine specifically inhibits keratinocyte proliferation and has improved PASI scores in clinical studies. PMID 28450041. This targets the core pathology of psoriasis - excess keratinocyte proliferation driven by NF-kB activation - without the side effects of corticosteroids.

Cnidium monnieri (She Chuang Zi) - TRPV3 antipruritic and antifungal

Osthole from Cnidium monnieri inhibits TRPV3 itch receptors, directly addressing psoriasis itch through a non-histaminergic pathway that antihistamines cannot reach. PMID 30108138. Its documented antifungal activity against Trichophyton rubrum provides broad dermatophyte coverage. PMC8417377. For scalp psoriasis, where secondary Malassezia colonisation worsens scaling, this antifungal coverage addresses a common complicating factor that steroids do not. Synergistic antipruritic effect with Ku Shen confirmed. PMC6151778

Borneolum Syntheticum (Bing Pian) - penetration through the psoriasis scale barrier

Plaque psoriasis presents a unique challenge for topical treatment: the thick keratinocyte scale creates a physical barrier most preparations cannot cross effectively. Borneolum disrupts stratum corneum lipid structure, significantly increasing transdermal absorption of all co-applied actives. PMC5452010. It also relieves both acute and chronic itch by modulating TRPA1 and TRPM8 ion channels. PMID 37290679. This penetration-enhancing role is the critical advantage QICAOGANGMU has over single-herb preparations for psoriasis specifically.

Stemonae Radix (Bai Bu) - Staph aureus protection and COX-2 suppression

Secondary Staphylococcus aureus colonisation worsens psoriasis inflammation and promotes barrier disruption. Stemonae Radix alkaloids provide antibacterial activity against Staph aureus and COX-2/NO anti-inflammatory action. PMID 35295975. This addresses the microbial amplification of psoriasis inflammation that steroids cannot and may worsen.

Menthol - immediate TRPM8 cooling relief

Menthol activates TRPM8 cold receptors within minutes of application, providing immediate itch and heat relief - overriding the itch-scratch cycle that damages psoriatic plaques. PMID 30067875. This is the fastest-acting component in the formula and the one patients feel most immediately.

How to use QICAOGANGMU for psoriasis

1. Wash with plain warm water only - no soap or cleanser on the psoriatic plaques. Pat gently dry, leaving skin slightly damp. Avoid vigorous rubbing which can irritate plaques.
2. Patch test first - apply a small amount to the inner forearm for 24 hours before first widespread use. Discontinue immediately if any irritation develops.
3. Apply a thin, even layer - a pea-sized amount covers a palm-sized area. Gently pat until absorbed. Do not rub vigorously over plaques. Borneolum drives all actives through the scale layer - thin application is sufficient.
4. Apply 2-3 times daily during active flares. Reduce to once daily for maintenance once plaques begin clearing.
5. Continue after symptoms improve - QICAOGANGMU is steroid-free and designed for continuous long-term use. Consistent daily application builds cumulative anti-inflammatory protection.
6. Layering: if using other topical treatments (vitamin D analogues, etc.), apply QICAOGANGMU first, allow to absorb (5 minutes), then apply other products. Inform your dermatologist of all topical products.

Safety considerations

• For external use only. Avoid contact with eyes and mucous membranes.
• Patch test is mandatory before first widespread use, especially on sensitive skin.
• For infants under 12 months: consult a paediatrician before use. For children over 12 months: patch test required. See our infant safety guide.
• Do not apply to actively infected skin (pus, fever, rapidly spreading redness) without medical advice - secondary infections require medical treatment.
• Botanical allergies: although natural, some individuals may have sensitivities to specific ingredients. The patch test identifies these before widespread use.

Holistic psoriasis management

Effective long-term management of psoriasis extends beyond topical treatment. The following are consistently supported in the clinical literature:

• Consistent moisturising: apply emollient immediately after bathing to maintain skin hydration and barrier function. Reduced barrier function is both a consequence and a driver of psoriasis flares.
• Identify and avoid triggers: stress, streptococcal infections, skin injury (Koebner phenomenon), certain medications (beta-blockers, lithium), smoking, and alcohol are the most consistently documented triggers. PMID 26025581
• Stress management: stress is a major documented psoriasis trigger. Mindfulness, yoga, regular exercise, and adequate sleep reduce HPA axis activation that worsens inflammatory conditions.
• Diet: reduce alcohol (strong evidence for worsening), refined sugar, and processed foods. Increase omega-3 fatty acids (oily fish, flaxseed). Gluten elimination benefits confirmed gluten-sensitive individuals. In TCM terms: avoid Blood Heat-generating foods (spicy food, alcohol, red meat in excess).
• Weight: obesity is an independent comorbidity that worsens psoriasis severity and reduces treatment response.

Frequently asked questions

What is psoriasis caused by?

Psoriasis is caused by a dysregulated immune response - specifically T-cell (Th17/Th1) activation that drives the release of inflammatory cytokines including IL-17, IL-22, and TNF-alpha. These cytokines signal keratinocytes to multiply rapidly, accelerating skin cell turnover from 28-30 days to 3-5 days and producing the characteristic thick silvery plaques. Genetic predisposition is required but not sufficient - environmental triggers (stress, infection, skin injury, certain medications) are needed to initiate the inflammatory cascade in susceptible individuals. PMID 30909615

Is psoriasis the same as eczema?

No - they are distinct conditions, though both cause red, itchy skin. Psoriasis is Th17/Th1-driven (IL-17, TNF-alpha dominant) and produces thick, well-defined silvery plaques on extensor surfaces (elbows, knees). Eczema (atopic dermatitis) is Th2-driven (IL-4, IL-13 dominant) and produces weeping, poorly defined patches in skin creases. QICAOGANGMU is effective for both conditions - its five herbs address inflammatory and itch pathways common to both, and Borneolum's penetration enhancement is specifically valuable for psoriasis's thick scale barrier.

Can psoriasis be cured naturally?

No treatment currently cures psoriasis - natural or pharmaceutical - because psoriasis reflects a permanent alteration in immune programming that cannot be reversed. The realistic goal with natural treatment is reducing flare frequency and severity, extending remission, and reducing dependence on corticosteroids. Many people achieve extended periods of clear skin through consistent QICAOGANGMU use combined with dietary and trigger management. See our full guide: psoriasis herbal treatment guide.

Is QICAOGANGMU suitable for all types of psoriasis?

QICAOGANGMU is suitable for plaque psoriasis, inverse psoriasis, scalp psoriasis (applied directly to plaques), and nail psoriasis on surrounding skin. For erythrodermic or severe pustular psoriasis, seek emergency medical care first - these are serious conditions requiring systemic treatment. QICAOGANGMU can be used alongside conventional treatment for all types once acute phase is managed.

Why do topical steroids stop working for psoriasis?

Two reasons: tachyphylaxis (the skin's glucocorticoid receptors downregulate with continuous exposure, requiring stronger steroids to achieve the same effect) and the fact that steroids suppress the inflammatory response without modifying the underlying immune dysregulation. When stopped, the immune activation resumes - often more intensely (rebound). QICAOGANGMU's NF-kB modulation targets the inflammatory pathway more specifically without creating receptor dependency, and does not produce rebound on stopping.

Related articles

• Psoriasis Causes, Symptoms and Natural Treatment: Complete Chinese Herbal Guide
• Herbal Remedies for Psoriasis: How QICAOGANGMU Aligns with TCM
• QICAOGANGMU vs Steroid Creams: Full Mechanism and Safety Comparison

Clinical references

1. Lowes MA, Suárez-Fariñas M, Krueger JG. Immunology of psoriasis. Annual Review of Immunology. 2014;32:227-255. PMID 24655295
2. Griffiths CEM et al. Psoriasis. Lancet. 2021;397(10281):1301-1315. PMID 33812489
3. Rendon A, Schäkel K. Psoriasis pathogenesis and treatment. International Journal of Molecular Sciences. 2019;20(6):1475. PMID 30909615
4. Ogawa E et al. Pathogenesis of psoriasis and development of treatment. Journal of Dermatology. 2018;45(3):264-272. PMID 29226422
5. Parisi R et al. Global epidemiology of psoriasis: a systematic analysis. BMJ. 2020;371:m1590. PMID 32467098
6. Boehncke WH, Schön MP. Psoriasis. Lancet. 2015;386(9997):983-994. PMID 26025581
7. Smith CH et al. British Association of Dermatologists guidelines for biologic therapy for psoriasis 2020. British Journal of Dermatology. 2020;183(6):628-637. PMID 32189327
8. Barnes L, Kaya G, Rollason V. Topical corticosteroid-induced skin atrophy: a comprehensive review. Drug Safety. 2015;38(5):493-509. PMID 25862024
9. Pan YJ et al. Anti-inflammatory activity of flavonoids and alkaloids from Sophora flavescens alleviates psoriasiform lesions. Phytotherapy Research. 2024;38(4):1951-1970. PMID 38358770
10. Zhou H et al. Oxymatrine improves PASI scores in psoriasis and inhibits keratinocyte proliferation. Journal of Dermatological Treatment. 2017;28(5):463-472. PMID 28450041
11. Sun X-Y et al. Antipruritic effect of natural coumarin osthole through selective inhibition of TRPV3 channels. International Journal of Molecular Sciences. 2018;19(10):3007. PMID 30108138
12. Cao Y et al. Antifungal Mechanism of Cnidium monnieri Against Trichophyton rubrum. Frontiers in Microbiology. 2021. PMC8417377
13. Chao X et al. Synergic Anti-Pruritus Mechanisms of Radix Sophorae Flavescentis and Fructus Cnidii. Evidence Based Complementary and Alternative Medicine. 2018. PMC6151778
14. Dai H et al. Clinical and mechanistic study of topical borneol-induced analgesia and enhanced transdermal delivery. Experimental and Therapeutic Medicine. 2017;13(6):3267-3272. PMC5452010
15. Tian W et al. Topical borneol relieves nonhistaminergic pruritus via TRPA1 inhibition and TRPM8 activation. Journal of Investigative Dermatology. 2023;143(10):2389-2398. PMID 37290679
16. Xu Y et al. Alkaloids from Stemona tuberosa and their anti-inflammatory activity. Frontiers in Chemistry. 2022;10:847595. PMID 35295975
17. Misery L et al. Anti-itching effects of a TRPM8 agonist cream in atopic dermatitis. Journal of the European Academy of Dermatology and Venereology. 2019;33(2):e67-e69. PMID 30067875
18. Gu S et al. Topical Chinese herbal medicine for atopic eczema: systematic review with meta-analysis. Dermatology. 2014. PMID 24821063