Early MASH Reversal: Mediterranean Diet and Naturopathic Co-Management

Anna Kolomitseva, ND

A 51-year-old woman with severe steatosis and minimal fibrosis achieved early liver and metabolic improvements through a Mediterranean-style diet, low-impact activity, sleep support, and adjunctive nutraceuticals co-managed with conventional diabetes care.

Abstract

Nonalcoholic steatohepatitis (NASH) with type 2 diabetes and obesity remains difficult to manage with monotherapy. We report hepatic and metabolic signals in a 51‑year‑old woman with severe steatosis by vibration‑controlled transient elastography and minimal fibrosis who pursued a gastrointestinal‑first, multimodal program co‑managed with conventional care. 

The program emphasized Mediterranean‑pattern meals with explicit protein/fiber targets, low‑impact activity, and sleep consolidation. In addition, magnesium bisglycinate, methylcobalamin with folate lozenge, and deglycyrrhizinated licorice were added as needed during proton‑pump‑inhibitor reduction, and a silymarin‑based liver support that was initiated at full dose, down‑titrated to maintenance, and later re‑escalated. 

Aminotransferases fell 33% to a nadir, then rose after down‑titration. The dose was re‑escalated, and confirmatory laboratories are pending (October 2025). Secondary signals included 12% lower continuous‑glucose‑monitoring mean, 5% smaller waist circumference, improved home blood pressure, and fewer reflux flares on once‑daily proton‑pump inhibitor. 

This data‑tracked N‑of‑1 case illustrates a co‑management template in early disease with lifestyle‑led care and pre‑specified titration linked to objective measures, while underscoring the need for prospective validation.

Introduction

MASLD/MASH terminology reframes fatty‑liver disease within cardiometabolic risk, with consensus guidance emphasizing noninvasive staging and lifestyle‑first care.^1-3 Stepwise case‑finding (eg, FIB‑4 followed by elastography) helps risk‑stratify patients; on VCTE, values <8 kPa generally rule out advanced fibrosis, values ≥12 kPa rule it in, and values between 8 and 12 kPa are indeterminate and warrant further evaluation.^2-4 Lifestyle interventions such as weight loss, exercise, and diet quality are repeatedly associated with histologic and biochemical improvement. This includes NASH resolution with ≥7–10% weight loss and exercise‑mediated reductions in intrahepatic fat independent of weight loss.^3,5-7 Mediterranean‑pattern diets and higher‑polyphenol variants improve liver fat and metabolic indices.^8,9 Pharmacotherapy is evolving: resmetirom gained approval in 2024 for non‑cirrhotic MASH with moderate‑to‑advanced fibrosis as an adjunct to diet and exercise¹⁰, and incretin‑based agents (GLP‑1 and dual GIP/GLP‑1) show liver‑fat and metabolic benefits.^11,12 Within this context, we present a patient with severe steatosis and minimal fibrosis who pursued an integrative, GI‑first program co‑managed with conventional therapy. 

Case Presentation

Patient Profile
A 51‑year‑old woman with type 2 diabetes, obesity, dyslipidemia, eosinophilic esophagitis, irritable bowel syndrome, and osteoarthritis presented in January 2025 for adjunctive management of probable NASH. Physician‑managed therapies during the case included metformin (extended‑release), a sulfonylurea (later discontinued), incretin‑based therapy (initial GLP‑1 receptor agonist, later dual GIP/GLP‑1), ezetimibe, a PPI (tapered to once daily), and an anti-IL-4–IL‑4/IL‑13 monoclonal antibody for EoE/asthma.

Symptoms and Examination
She reported reflux with intermittent dysphagia since youth, IBS with stress‑sensitive cramping/diarrhea, chronic knee/ankle pain limiting activity, mid‑day fatigue, and variable sleep. Home metrics (waist, blood pressure, continuous‑glucose‑monitoring summaries) were tracked longitudinally.

Diagnostic Testing

Baseline VCTE (Jan 6, 2025) showed severe steatosis (grade 3) with F0–F1 fibrosis; biopsy was not performed. Laboratory anchors immediately preceding adjunctive care included ALT 39 U/L and AST 24 U/L, fasting glucose 173 mg/dL, and total cholesterol 230 mg/dL. An autoimmune screen was negative for ANA/RF (June 2025). Longitudinal monitoring employed CGM summaries, home blood‑pressure logs, and weekly waist measurements at the midpoint between the costal margin and the iliac crest.

Timeline

At intake, we initiated Mediterranean‑pattern meals rich in protein and fiber, fermented foods as tolerated, graded low‑impact activity (pool kicking; quadriceps lean‑backs), sleep consolidation, and a silymarin‑based liver support at full dose (three capsules nightly). Within 2–4 weeks, sleep and GI comfort improved, stools became more formed, and CGM variability tightened. By 8 weeks, the PPI was reduced to once daily; labs were repeated. Over the subsequent two months, life stressors coincided with partial adherence drift; Mid‑summer labs guided refinements; by late summer 2025, the patient re‑engaged consistently with nutrition, activity, and sleep prescriptions under ongoing physician‑managed therapy.

Differential Diagnosis

1. MASH/NASH with metabolic risk (type 2 diabetes, obesity, dyslipidemia): working diagnosis; elastography-supported steatosis with minimal fibrosis.
   
2. Alcohol‑associated disease: history did not suggest sustained excess intake.
   
3. Drug‑induced liver injury: pattern improved with lifestyle and silymarin escalation; no clear new hepatotoxin temporally linked. 

4. Viral hepatitis (HBV/HCV): standard part of transaminase work‑up; no risk factors recorded here and no supportive laboratory features noted.
   
5. Autoimmune hepatitis: female sex is a risk factor; antinuclear antibodies were negative, and no autoimmune phenotype was documented; consider disease‑specific serology if elevation persists.

Interventions

Treatment Overview
A multimodal, GI‑first program combined the dietary pattern above, graded low‑impact activity, and sleep consolidation. Adjuncts included magnesium bisglycinate at bedtime; methylcobalamin with folate (lozenge); deglycyrrhizinated licorice as needed during PPI reduction; homeopathic combination analgesic (sublingual) and a topical arnica‑containing botanical for musculoskeletal pain; and a silymarin‑based liver support at bedtime. In late summer, marine omega‑3 fatty acids (EPA+DHA, triglyceride form) with meals and coenzyme Q10 with food were added for lipid‑inflammation balance and energy support. Home monitoring comprised CGM summaries, morning blood‑pressure checks several times weekly, and weekly waist measurements. See Table 1 for a concise nutraceuticals‑and‑rationale summary.

Rationale
First‑line lifestyle interventions (diet quality, movement, sleep) are associated with lower intrahepatic fat, aminotransferase improvement, and better glycemic control in MASLD, while being feasible in real‑world care.^1-3,7-9 Incretin‑based therapies, prescribed by the patient’s physicians, were maintained to complement lifestyle effects.^11,12 Adjuncts were positioned as supportive: silymarin‑based hepatoprotective support used within a lifestyle‑first framework with serial enzymes to track; omega‑3 (EPA+DHA, TG form) and coenzyme Q10 were selected for dyslipidemia and energy support within guideline‑consistent cardiometabolic care.³ Magnesium and methylcobalamin‑with‑folate addressed sleep and medication‑related nutrient considerations in the setting of long‑term PPI/metformin exposure; deglycyrrhizinated licorice aided comfort during PPI taper. 

Adjustments

• Liver support titration: full nightly dose → maintenance once daily after nadir → re‑escalation when enzymes rose on mid‑summer labs.
  
• GI comfort with PPI taper: deglycyrrhizinated licorice as needed; PPI reduced to once daily.
  
• Lipids/energy: added omega‑3 (EPA+DHA, TG form) and coenzyme Q10 in late summer.
  
• Micronutrients: continued methylcobalamin with folate and bedtime magnesium; timing separated from prescription agents when feasible.

Outcomes and Follow-Up

Within two months, ALT/AST fell 33% to a nadir, then rose to ALT 32 U/L/AST 38 U/L mid‑summer; re‑escalation of liver support followed (Figure 1). Secondary signals (Table 2): CGM mean 200→175 mg/dL (12% decrease), waist 47″→44.5″, and home blood pressure lows of 114/65 mmHg. Reflux episodes decreased, and patients were comfortable on once‑daily PPI; IBS shifted toward formed stools. Functionally, sleep initiation and daytime energy improved, with better tolerance of low‑impact activity. No adverse events attributable to adjunctive nutraceuticals were observed. No follow‑up elastography was available within the reporting window. 

Discussion

This case supports a GI‑first, lifestyle‑anchored approach to early steatotic liver disease co‑managed with physician‑directed pharmacotherapy. Severe steatosis with minimal fibrosis, enzyme improvement with lifestyle plus adjunctive support, and partial rebound after down‑titration illustrate both the responsiveness of early disease to behavior‑centered care and the fragility of gains when dose or adherence wanes.^1-3

A Mediterranean‑pattern diet rich in protein and fiber, low‑impact movement, and sleep consolidation likely drove early improvement. These measures are consistently linked with lower intrahepatic fat, better enzymes, and improved glycemia.^1-3,5-9 Under medical care, incretin‑based therapy was optimized and likely amplified these effects.^11,12 Adjunctive silymarin‑based support was supportive and not the primary driver. Its N‑of‑1 pattern (33% decline at full dose, rise at maintenance) informed titration while more definitive outcomes (e.g., repeat elastography) are pending. Omega‑3 and coenzyme Q10 addressed dyslipidemia and energy, while magnesium, methylcobalamin with folate, and DGL supported sleep, medication‑related nutrient considerations, and upper‑GI comfort. Tracking percent change in enzymes with waist, BP, and CGM summaries helped interpret variability and guide timely adjustments while keeping visuals parsimonious.

Conclusion

In a patient with severe steatosis and minimal fibrosis, a GI‑first, lifestyle‑anchored program implemented alongside physician‑managed diabetes and lipid therapies produced clinically meaningful hepatic and cardiometabolic signals: aminotransferases improved early (33% decline to nadir), glycemic variability tightened (12% lower CGM mean), waist circumference decreased (5%), and blood‑pressure readings trended down. Gains were dose‑ and adherence‑sensitive, supporting pre‑specified, data‑driven titration and simple home metrics to guide care. Adjunctive nutraceuticals functioned as supportive, not substitutive, to foundational diet, sleep, and movement, and to incretin‑based pharmacotherapy. The pattern is hypothesis‑generating and merits prospective validation of titration algorithms that integrate enzyme percent change, waist, glycemia, and function.^1-3,11,12

References

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