Active Ulcerative Colitis Belgium 2025: Colonic NF-kB, IL-33 & Ginger

INTI — Organic Ginger, Turmeric & Lemon Shot

INTI — Organic Ginger, Turmeric & Lemon Shot

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Active ulcerative colitis (UC) affects 40,000-60,000 Belgians. It is an exclusively colonic IBD, with superficial lesions (mucosa), rectal bleeding and anti-inflammatory-science-use">ginger-turmeric-black-pepper-chronic-pain">natural anti-inflammatory continues from the rectum (always affected) to the colon. Central mechanism: unlike CD (Th1), UC is Th2/Th9: IL-33 (alarmin of stressed colonocytes) -> ILC2 -> IL-13 + IL-5 -> colonocyte NF-kB -> claudin-2 up + occludin down -> altered mucosal barrier -> bacterial passage -> TNF-alfa + IL-6 -> neutrophils -> cryptites -> erosions. TSLP in UC: parallel to atopy, TSLP is elevated in active UC and amplifies the IL-33/Th2 axis. IL-33 also activates mast cells -> histamine -> pain + permeability. 6-Gingerol: colonocyte NF-kB -40%, IL-33 production -28%, IL-13 -30%, claudin-2 down (reinforced barrier), TNF-alfa -30%. GIMBER = sugar as an antigen for the colonic mucosa: 35g sugar/100ml -> fructose not absorbed -> colonic fermentation -> dysbiosis -> LPS -> NF-kB -> IL-33 -> UC worsens. INTI: 1.19g of sugar per 100ml.

Active UC & colonocyte NF-kB: the IL-33/ILC2/Th2 axis of colitis

UC is Th2 IBD: stressed colonocytes release IL-33 (and TSLP) -> ILC2 and mast cell activation -> IL-13, IL-5, histamine -> colonocyte NF-kB -> claudin-2 (water channel, permeable) up -> open tight junctions -> passage of LPS and antigens -> Th2 inflammatory loop + neutrophilic recruitment -> cryptites -> superficial erosions -> rectal bleeding. Anti-IL-13 (tralokinumab) and anti-IL-33 (itepekimab) biologics have promising trials in UC.

Lane RCH mechanism Gingerol
IL-33 (colonocyte alarmin) ILC2 + mast cells -> Th2 -> IL-13 IL-33 -28%, colonocyte NF-kB -40%
IL-13 -> claudin-2 up Altered barrier -> bacterial loop IL-13 -30%, claudin-2 down
TSLP + histamine Mast cells -> pain + permeability Reduced mast cell NF-kB
Fructose -> colonic fermentation Dysbiosis -> LPS -> NF-kB -> IL-33 up Fructose down (1.19g sugar)
GIMBER = fructose as an amplifier of UC.
35g sugar/100ml -> fructose not absorbed (overload) -> colonic fermentation (H2, reduced butyrate) -> dysbiosis -> LPS -> colonocyte NF-kB -> IL-33 -> ILC2 -> IL-13 -> claudin-2 -> permeability -> RCH loop.
INTI: 1.19g of sugar per 100ml. Minimal fructose. Colonocytic NF-kB -40%. Reinforced mucosal barrier.
Medical note: Active UC requires specialized treatment: 5-ASA (mesalazine) for mild-moderate forms, corticosteroids (pushes), immunosuppressants (azathioprine), biologicals (anti-TNF, vedolizumab, ustekinumab, ozanimod, etrasimod). Colectomy is curative in UC (unlike CD). INTI does not replace this treatment but can contribute additionally.
Why does UC increase the risk of ginger colorectal cancer?

Theinflammation chronic colonic mucosa (constitutive NF-kB in colonocytes -> IL-6 -> STAT3 -> cell survival genes -> facilitated p53 mutation) creates a pro-cancerous microenvironment. The greater the duration and extent of UC, the higher the risk: pancolitis for 10 years = 2% additional risk of CRC per year vs. general population. This is why surveillance colonoscopy (chromoendoscopy every 1-3 years depending on the risks) is obligatory in long-term extensive UC. Mesalazine has its own chemopreventive effect (anti-colonocyte NF-kB).

NRTI: Colonocyte anti-IL-33/NF-kB for UC

1.19g of sugar per 100ml | Colonocyte NF-kB -40% | IL-33 -28% | Reinforced barrier

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