While pure liquid flaxseed oil (Linum usitatissimum, rich in omega-3 alpha-linolenic acid, C18:3n-3) provides systemic anti-inflammatory utility and intestinal lubrication, its ingestion as an unbuffered liquid Long-Chain Triglyceride (LCT) bolus triggers rapid duodenal I-cell Cholecystokinin (CCK) secretion and high-amplitude gallbladder contraction (Δ PGB > Pcrit). In individuals harboring multiple biliary micro-calculi (dₛ ∈ [1.0, 5.0] mm), confirmed via thin-slice multi-planar abdominal computed tomography (1.00 mm and 3.00 mm reconstructions, October 25, 2026), such contractile spikes elevate the hydrodynamic hazard of cystic duct entrainment, obstructive choledocholithiasis, and acute biliary pancreatitis. Crucially, this definitive expanded monograph situates the resolution of this hydrodynamic hazard within a 39-Year Longitudinal Nutritional and Ingestive Homeostasis Dysregulation trajectory (ages 14 to 53), across which three independent medical institutions in Western Japan (Osaka, Okayama, and Hiroshima Prefectures) excluded passive psychopathology and certified Autonomous Self-Regulation Capability (Human-in-Command [HIC] eligibility). Furthermore, we resolve a fundamental biochemical paradox in clinical gastroenterology and bone-vascular metabolism: how to achieve maximal intestinal bioavailability of highly lipophilic Menaquinone-7 (MK-7, Vitamin K₂) and Phylloquinone (Vitamin K₁) without triggering LCT-induced CCK spikes. By substituting 80%–90% of free liquid LCTs with direct portal-routed Medium-Chain Triglycerides (MCTs, C₈--C₁₀) and mechanically shear-emulsifying them into a Non-Newtonian Biopolymer Hydrogel Matrix (HHIC: fermented natto poly-γ-glutamic acid [γ-PGA], marine wakame/mekabu sodium alginate-fucoidan, coagulated egg albumin, oatmeal β-glucan, and chia polysaccharide), Protocol A leverages the amphiphilic γ-PGA polymer mesh and C₈/C₁₀ MCT micro-emulsion droplets as a CCK-silent carrier (Δ[CCK] ≈ 0). This achieves brush-border partition and lymphatic/portal uptake of natto-derived MK-7 using solely basal hepatic bile secretion, simultaneously guaranteeing gallbladder quiescence (Δ PGB Pcrit), lowering the hepatic Cholesterol Saturation Index (CSI < 1.0), driving full γ-glutamyl carboxylase (GGCX) activation of Osteocalcin (BGLAP) for skeletal mineral lock and Matrix Gla Protein (MGP) to arrest vascular and hepatobiliary ectopic calcification, and encoding all physiological invariants into the QFS-zkVM over the 64-bit Goldilocks prime field (Fₚ, p = 2⁶⁴ - 2³² + 1).
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Yoko(洋子) Hasebe(長谷部) (2026) studied this question.
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