How It Forms
- Inflammation upregulates Notch signaling
- Excessive Notch blocks goblet cell maturation
- Mucus layer thins dramatically
- Bacteria contact epithelium directly
Self-Reinforcement
- Less mucus → more bacterial contact
- Bacterial antigens → more inflammation
- Inflammation → more Notch activation
- Goblet cells remain suppressed
Breaking This Cycle
BREAK Protocol Interventions
- EGCG - Inhibits γ-secretase and Notch1
- DIM - Activates AhR→IL-22 pathway
- Tributyrin - Supports goblet cell function