Psoriasis in Belgium: sugar, IL-17, Th17 and ginger (2025)

🔬 Scientific Answer: Ginger, Psoriasis and Immunopathology
Psoriasis affects 2–3% of Belgian adults (~250,000 patients). The IL-23/Th17/IL-17A axis is central: sugar enhances IL-23 (via dysbiosis/LPS), Th17 differentiation, IL-17A → keratinocytic ginger-sugar-explanation-2026">NF-κB → epidermal proliferation. INTI sugar-free ginger shot <1.19g sugar/100ml modulates IL-17/NF-κB — unlike GIMBER (~35g sugar/100ml) which exacerbates skin inflammation.
⚠️ Warning: Severe psoriasis requires dermatological follow-up. Do not modify your biologics (IL-17i, IL-23i, TNF-αi) without dermatological advice. INTI is complementary, not a substitute.

Epidemiology: Psoriasis in Belgium

  • 2–3% of the Belgian population (~250,000 patients, Psoriasis Association Belgium)
  • Plaque psoriasis: 80–90% of cases
  • Psoriatic arthritis: 20–30% of psoriasis patients develop joint involvement
  • Cardiovascular, metabolic, and psychiatric comorbidities significantly increased
  • RIZIV reimbursement for biologics (adalimumab, secukinumab, ixekizumab, guselkumab) for PASI ≥10

The Immunopathological Cascade of Psoriasis

1. IL-23/Th17/IL-17 Axis: The Pillar of Psoriasis

  • Plasmacytoid dendritic cells (pDC) → IFN-α → myeloid DC activation
  • Myeloid DC → IL-23 → differentiation of naive CD4+ → Th17
  • IL-17A (Th17) → keratinocytes → NF-κB → β-defensins, CCL20, CXCL1, IL-8
  • IL-17A → keratinocytes → hyperproliferation (keratinocyte turnover 4 days vs normal 28 days)
  • Sugar → dysbiosis → LPS → TLR4 DC → IL-23 ↑ → Th17 ↑ → IL-17A ↑

2. Keratinocyte NF-κB and Hyperproliferation

  • IL-17A + TNF-α (synergy) → IKK → IκB degradation → NF-κB p65/p50
  • NF-κB → KGF, IL-6, IL-8, ICAM-1
  • NF-κB → anti-apoptotic (Bcl-2 ↑, survivin ↑) → accelerated proliferation + apoptosis resistance
  • AGEs (glycation by sugar) → RAGE → keratinocyte NF-κB → direct exacerbation

3. Gut-Skin Ginger Axis: The Microbiome Hypothesis

  • Psoriasis patients: specific dysbiosis (Faecalibacterium prausnitzii ↓, candidiasis-<a%20href=" https:>candida-antifungal-mycosis">ginger Candida ↑)
  • Sugar → Candida albicans proliferation (sugar is the Candida substrate) → β-glucan → TLR2 → IL-23 ↑
  • Zonulin ↑ (intestinal permeability) in psoriasis → systemic LPS → cutaneous NF-κB
  • Ginger → Candida mild antifungal effect (6-gingerol) → dysbiosis ↓ → IL-23 ↓
  • Ginger → zonulin ↓ → tight junctions → LPS ↓ → cutaneous NF-κB ↓
Drink Sugar/100ml Psoriasis Impact Mechanism
GIMBER ~35g ⚠️ Potentially aggravating Candida ↑, LPS↑, IL-23↑, Th17↑, NF-κB↑
Alcohol 0g Classic psoriasis trigger Dysbiosis, LPS, IL-17↑
INTI Ginger <4g ✓ Potentially beneficial NF-κB↓, Candida↓, LPS↓, IL-17↓

Ginger and Psoriasis: Scientific Basis

  • 6-gingerol → keratinocyte NF-κB ↓ → ↓ IL-8, ↓ CXCL1 → fewer cutaneous neutrophils
  • 6-shogaol → TNF-α ↓ → less TNF-α/IL-17 synergy → hyperproliferation ↓
  • Curcumin (INTI) + gingerol: NF-κB ↓ synergy, Th17 ↓ → complementarity in psoriasis
❓ FAQ: Psoriasis and INTI

Can ginger replace biologics?
No. Biologics (secukinumab, ixekizumab, guselkumab) have proven efficacy in clinical trials. INTI is complementary for modulating background inflammation, never a substitute.

Candida and psoriasis: what's the connection?
Candida albicans colonizes the gut of psoriasis patients. Its β-glucans activate TLR2 → IL-23 → Th17 → IL-17 → psoriasis flare with sugar consumption = direct Candida substrate.

Is GIMBER contraindicated in psoriasis?
With ~35g sugar/100ml, GIMBER feeds Candida, aggravates dysbiosis, and enhances keratinocyte NF-κB. For anti-inflammatory-science-utilisation">anti-inflammatory ginger benefits without sugar load, INTI is the coherent choice.

🌸 INTI: Immunological Support for Psoriasis
1.19g sugar · Keratinocyte NF-κB ↓ · IL-17 ↓ · Candida ↓ · LPS ↓ · Cold-pressed

vs GIMBER: ~35g sugar → Candida ↑, dysbiosis ↑, IL-23/Th17/IL-17 ↑ — counterproductive in psoriasis

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