Liver Cirrhosis

Authored by Chris McDermott, APRN, practicing with autonomous authority in Florida

Introduction

Liver cirrhosis is a serious and progressive condition that results from long-standing liver damage. It involves the replacement of healthy liver tissue with scar tissue (fibrosis), which impairs the liver’s structure and function. Once cirrhosis develops, the liver’s ability to detoxify the body, metabolize nutrients, regulate hormones, and produce proteins is significantly compromised.

While cirrhosis is often viewed as an irreversible end stage of liver disease, a functional medicine practitioner approach seeks to identify root causes, slow disease progression, manage complications, and improve overall quality of life through nutrition, supplementation, toxin reduction, and biomarker-guided care.

What Is Liver Cirrhosis?

Cirrhosis is the result of chronic liver injury that leads to inflammation, necrosis, and fibrosis. Over time, fibrotic tissue disrupts the normal architecture of the liver, limiting blood flow and hepatocyte function. The liver becomes nodular and firm, and its vital roles—including bile production, protein synthesis, and toxin clearance—are significantly impaired.
Cirrhosis can remain asymptomatic for years, but it eventually leads to complications such as portal hypertension, variceal bleeding, ascites, hepatic encephalopathy, and liver cancer.

Early and Advanced Symptoms

In early stages, cirrhosis may go unnoticed, especially if liver enzymes remain within reference range. As liver function deteriorates, however, more recognizable symptoms develop.
Common Symptoms of Liver Cirrhosis Include:

• Fatigue and weakness
  
• Loss of appetite and weight loss
  
• Easy bruising or bleeding (due to reduced clotting factor production)
  
• Jaundice: Yellowing of the skin and sclera from bilirubin accumulation
  
• Pruritus: Persistent itching, especially on the hands and feet
  
• Ascites: Fluid accumulation in the abdominal cavity
  
• Peripheral edema: Swelling in the legs and ankles
  
• Spider angiomas: Dilated blood vessels near the skin surface
  
• Hepatic encephalopathy: Confusion, slurred speech, and sleepiness from toxin buildup

   

In advanced stages, patients may experience muscle wasting, increased infections, gastrointestinal bleeding, or coma.

Functional Medicine Evaluation of Liver Cirrhosis

At Intercoastal Health, we use a combination of physical exam findings, biomarker panels, imaging, and clinical history to identify cirrhosis and monitor its progression. Our approach places strong emphasis on early detection, inflammatory markers, and organ system interconnection.

1. Physical Examination
   
   • Jaundice, ascites, hepatomegaly, splenomegaly, and asterixis
     
2. Laboratory Testing

   Biomarker	Standard Range	Functional Insight
   ALT (Alanine Aminotransferase)	7–56 U/L	May normalize in late-stage cirrhosis despite severe disease
   AST (Aspartate Aminotransferase)	10–40 U/L	Often elevated in early injury; ratio helps identify etiology
   GGT (Gamma-glutamyl Transferase)	0–65 U/L	Elevated with biliary stress and alcohol use
   ALP (Alkaline Phosphatase)	45–115 U/L	Elevated in bile duct disorders or bone disease
   Bilirubin – Total	0.1–1.2 mg/dL	Elevated in cholestasis or advanced disease
   Albumin	3.5–5.5 g/dL	Declines with reduced synthetic function
   INR (Prothrombin Time)	0.8–1.2	Prolonged in impaired clotting factor production
   Platelet Count	150–450 ×10³/µL	Often reduced due to splenic sequestration
   Ammonia	15–45 µg/dL	Elevated in hepatic encephalopathy

3. Imaging Studies
   
   • Ultrasound with Doppler: Assesses liver texture, vascular changes, and ascites
     
   • Elastography (FibroScan): Measures liver stiffness to estimate fibrosis
     
   • CT/MRI: Evaluates nodularity, cancer risk, or thrombosis
     
4. Liver Biopsy (if needed)
   
   • Confirms diagnosis, stages fibrosis, and rules out other etiologies

Underlying Causes of Cirrhosis

Functional medicine prioritizes the identification and treatment of root causes, many of which are modifiable:

1. Chronic Alcohol Use
   
   • Acetaldehyde toxicity drives inflammation and fibrosis
     
2. Chronic Viral Hepatitis
   
   • Hepatitis B and C cause persistent hepatocyte injury
     
3. NAFLD / NASH
   
   • Insulin resistance, obesity, and high-fructose diets lead to fat accumulation and inflammation
     
4. Autoimmune Hepatitis
   
   • Immune-mediated hepatocyte attack
     
5. Inherited Metabolic Conditions
   
   • Hemochromatosis (iron overload)
     
   • Wilson’s disease (copper accumulation)
     
   • Alpha-1 antitrypsin deficiency
     
6. Biliary Cirrhosis
   
   • Chronic inflammation and obstruction of bile ducts

      

Interfering Factors in Test Interpretation

Several factors may influence biomarker accuracy:

• Hemolysis or muscle injury may falsely elevate AST
  
• Malnutrition or fluid overload can lower albumin
  
• Recent alcohol intake can acutely raise enzymes
  
• Medications and supplements may skew results
  
• “Burned-out” cirrhosis can present with normal LFTs

   

Functional Medicine Strategy at Intercoastal Health

Our protocol focuses on slowing progression, managing symptoms, and preventing complications through root-cause management:

1. Nutritional Interventions
   
   • Low-sodium, anti-inflammatory, whole-foods diet
     
   • Emphasize cruciferous vegetables, garlic, turmeric, beets, and berries
     
   • Adequate protein within encephalopathy guidelines
     
   • Eliminate alcohol and ultra-processed foods
     
2. Targeted Supplementation
   
   • N-acetylcysteine (NAC) for glutathione support
     
   • Milk thistle (silymarin) for hepatoprotection
     
   • Vitamin D, zinc, selenium for deficiency correction
     
   • CoQ10 and omega-3s for mitochondrial and anti-inflammatory support
     
3. Toxin and Medication Review
   
   • Minimize hepatotoxic drugs (e.g., NSAIDs, excess acetaminophen)
     
   • Use filtered water, non-toxic cookware, and chemical-free personal care
     
4. Addressing Underlying Conditions
   
   • Treat viral hepatitis
     
   • Correct insulin resistance through diet and movement
     
   • Manage iron/copper overload as indicated
     
5. Managing Complications
   
   • Ascites: Sodium restriction, diuretics, paracentesis
     
   • Variceal bleeding: Endoscopic surveillance, beta-blockers
     
   • Hepatic encephalopathy: Lactulose, dietary adjustments
     
   • Portal hypertension: Monitoring and medical management
     
   • HCC surveillance: Imaging and AFP every 6 months

      

Monitoring and Follow-Up

• Recheck LFTs every 3–6 months
  
• INR, CBC, albumin to assess synthetic function
  
• Ultrasound or FibroScan every 6–12 months
  
• Ongoing symptom monitoring (encephalopathy, bleeding, infection)