Ginger for Psoriasis: Skin Inflammation, TNF-α & Keratinocytes

Psoriasis: an autoimmune inflammatory disease

Psoriasis affects 2–3% of the Belgian population (200,000–250,000 people). It is a chronic inflammatory disease mediated by T-lymphocytes (Th1/Th17 axis) with hyperproliferation of keratinocytes. Biologics (anti-TNF, anti-IL-17, anti-IL-23) are effective but expensive and reserved for severe forms. Ginger targets the same inflammatory pathways at a modest and systemic level.

Mechanisms of ginger in psoriasis

1. Inhibition of TNF-α

TNF-α is one of the main cytokines in psoriasis (anti-TNFs like adalimumab are very effective). Gingerols → dermal NF-κB↓ → TNF-α↓ in keratinocytes and dermal fibroblasts. Reduction: −35 to −40% in vitro on human keratinocytes.

2. Reduction of IL-17/IL-23 axis

The Th17 axis (IL-17A, IL-22, IL-23) is central in plaque psoriasis. Gingerols reduce IL-17 production via NF-κB inhibition in antigen-presenting dendritic cells.

3. Inhibition of keratinocyte proliferation

In psoriasis, keratinocytes proliferate 6–10× faster than in normal ginger skin. Intra-epidermal COX-2 contributes to this hyperproliferation. Gingerols → epidermal COX-2↓ → slowing of abnormal keratinocyte turnover.

4. VEGF reduction (anti-angiogenic)

Psoriasis plaques are highly vascularized (red, warm skin). VEGF↓ → reduced neovascularization → reduction of erythema.

INTI protocol for psoriasis

• Internal route: 2–3 INTI shots per day continuously (systemic approach)
• Intensification during flare-ups: 3–4 shots/day during the flare-up
• Evaluation period: Minimum 12 weeks (psoriasis responds slowly to systemic interventions)
• Synergies: Omega-3 EPA, curcumin (IL-17↓, NF-κB↓), vitamin D3 (Th17 regulation), anti-inflammatory diet

Frequently asked questions