PD354 - DETERMINISTIC BIOPHYSICS IN ADVANCED NASH: AN IN-SILICO NUTRITIONAL APPROACH

PD354

DETERMINISTIC BIOPHYSICS IN ADVANCED NASH: AN IN-SILICO NUTRITIONAL APPROACH

P. I. Herrera Gutiérrez^1,*

¹ Department of Clinical Nutrition, Precision Health Herrera, Badajoz, Spain

Rationale: Phenotypic nutritional models fail to address the specific thermodynamic friction driving non-alcoholic steatohepatitis (NASH) progression. This case evaluates a deterministic biophysical algorithm to audit allostatic load and formulate in-silico nutritional interventions for advanced fibrosis.

Methods: A 52-year-old female with advanced NASH (liver stiffness measurement 12.5 kPa, F3) and severe insulin resistance (HOMA-IR 6.6) was evaluated computationally. Clinical inputs, including elastography and a 75-polymorphism nutrigenetic panel, were mapped into a strict thermodynamic framework. The system computed structural capital against friction vectors (glucocentric lipotoxicity, systemic metaflammation) driven by high-risk PNPLA3 (rs738409 G/G), IL6 (-174 G/G), and MTHFR (C677T) variants to engineer a targeted negentropic blueprint.

Results: The computational audit identified critical systemic failures in metabolic and inflammatory vectors, exacerbated by constitutive genetic bottlenecks. An exact in-silico blueprint was generated, overriding probabilistic dietary guidelines. The prescription delivered 1.4 g/kg/day of high-biological-value protein to stabilize skeletal muscle mass, and strictly modulated lipids (80-90 g/day) to mathematically suppress metaflammation. Concurrently, targeted epigenetic modulators were deployed: N-Acetylcysteine (600 mg twice daily) to reinforce hepatic clearance, Berberine (500 mg three times daily) to suppress insulin resistance, and 5-MTHF (800 mcg/day) to bypass the constitutive MTHFR logistical bottleneck.

Conclusion: Standard caloric guidelines are mathematically inadequate for complex metabolic insolvencies like NASH F3. Thermodynamic modeling enables precise, genome-aligned nutritional engineering, targeting specific pathophysiological friction to halt entropic progression toward cirrhosis.

Disclosure of Interest: None declared