Hemorrhoids in Belgium: sugar, microcirculation, and ginger (2025)

Pathophysiology of Hemorrhoids: Far Beyond Varicose Veins

Hemorrhoids are not simply anal ginger varicose veins. They are normal vascular cushions (arterio-venous) that become pathological under certain conditions:

1. Vascular Dysfunction and NF-κB

• Increased venous pressure (constipation, prolonged sitting, ginger and ginger and pregnancy) → distension of the hemorrhoidal plexus
• Local ischemia-reperfusion during exertion → ROS production → NF-κB in endothelial cells
• Endothelial NF-κB → ICAM-1, VCAM-1 → neutrophil recruitment → local inflammation
• NF-κB → COX-2 → PGE2 → vasodilation → congestive aggravation
• Local TNF-α → MMP-9 → degradation of supporting connective tissue → hemorrhoidal prolapse

2. Sugar and intestinal dysbiosis → constipation

Sugar directly contributes to hemorrhoidal pathogenesis via dysbiosis:

• Refined sugar → growth of pro-fermentative Firmicutes → dysbiosis → slow transit
• Slow transit → increased straining during defecation → increased anorectal venous pressure → hemorrhoids
• GIMBER (~35g sugar/100ml) × 3 times/day = +105g sugar → aggravated dysbiosis → cyclical constipation
• Fructose → excessive colonic fermentation → abdominal distension → increased straining during defecation

3. VEGF and pathological angiogenesis

VEGF (Vascular Endothelial Growth Factor) is overexpressed in symptomatic hemorrhoids:

• NF-κB → VEGF-A → angiogenesis → hemorrhoidal vascular hyperplasia
• Sugar → HIF-1α (relative wall hypoxia) → increased VEGF → pathological vascular expansion
• Sclerosing injection (conservative treatment): targets this same VEGF/angiogenesis axis

4. Anorectal microbiome and inflammation

• Intestinal dysbiosis → LPS → local TLR4 activation → anorectal NF-κB
• Reduced Akkermansia muciniphila (protective bacteria) → increased mucosal permeability
• Butyrate-producers ↓ (with refined sugar) → anorectal epithelial cells without fuel → inflammation

Ginger and Hemorrhoidal Pathology

6-Gingerol: NF-κB and microcirculation

• 6-gingerol → inhibition of endothelial NF-κB → reduction of local ICAM-1/COX-2/PGE2
• Ginger → eNOS activation → increased NO → physiological vasodilation (improves flow, reduces stasis)
• Mild anti-platelet aggregation properties → prevention of hemorrhoidal microthrombi

Prokinetic 5-HT₄ effect and transit

• Ginger → partial 5-HT₄ agonism (enteric receptor) → accelerated colonic transit
• Normalized transit → reduced straining during defecation → reduced anorectal venous pressure → less stress on hemorrhoids
• This prokinetic effect is well-documented for managing nausea (5-HT₃/5-HT₄)

Curcumin: local anti-inflammatory ginger synergy

• Curcumin → NF-κB ↓, COX-2 ↓ → complementarity with 6-gingerol
• Curcumin → MMP-9 ↓ → protection of submucosal connective tissue → less prolapse