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Liver Disorders

January 2, 2021
8 min read
Liver Disorders

Liver is the main organ that carries out various functions such as detoxification, nutrition metabolism, protein synthesis, glycogen storage. These functions get disturbed due to various chronic liver diseases. Liver disease accounts for approximately 2 million deaths per year worldwide1. Chronic liver diseases could arise due to various risk factors including infections, autoimmune conditions, inheritance, harmful use of alcohol, obesity, insulin resistance and metabolic syndrome. Among the different types of liver diseases, both alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) could be adequately prevented and managed through lifestyle changes as part of medical nutrition therapy.

Irrespective of the type of liver disease, the liver damage progresses in the same four stages:

  • Stage 1: In this stage , inflammation starts in the liver and the liver becomes tender and enlarged.
  • Stage 2: If the inflammation is left untreated then tissues start scarring and these replace healthy liver tissues. This process is known as fibrosis. If the liver is treated at this stage then there are high chances of healing of the liver by itself.
  • Stage 3: Cirrhosis - this is the stage where maximum complications start arising. Healthy liver tissues are replaced by hard scarred tissue thus interrupting the function of the liver. As this condition progresses it ultimately leads to liver failure leading to a host of complications such as:
    • Bruising and bleeding rapidly
    • Water retention in the hands and feet
    • Yellow discoloration of skin and eyes
    • Profuse itching of the skin
    • Rupture of the blood vessels leading to the liver due to blockage
    • Increased sensitivity to medications and frequent side effects
    • Insulin resistance and type 2 diabetes
    • Accumulation of toxins in the brain affects concentration, memory, sleep and other mental functions.
    • At this stage, prompt treatment is required to save the healthy liver tissues from damage.
  • Stage 4: End-Stage Liver Disease (ESLD) is a stage where maximum damage has occurred and is irreversible with medical management. The only option for such individuals is liver transplantation2.

In a recent study by Varol and coworkers, it was found that intensive lifestyle interventions and medical nutrition therapy are effective in attaining 5% body weight loss and NAFLD remission in both lean as well as obese patients3.

Interventions promoting weight loss are necessary for patients with non-alcoholic fatty liver disease as such persons with obesity consume high amounts of calories and other nutrients when compared to healthy individuals4.

Obese and severely obese had a 1.6 and 1.9 times higher risk of transplantation or death from acute liver failure (ALF). Obese patients had 3.4 times higher risk of dying after transplantation5.

A study was conducted to evaluate dietary modifications as a form of treatment in NAFLD. It was assessed that 31 subjects who adhered to diet protocols of reduced-calorie and fat intake for a period of 6 months had a greater reduction in baseline weight of 5%, BMI, waist circumference, ALT and GGT values, hepatic, visceral fat, and HOMA IR index6.

In another randomized trial conducted by Zivkovic et al with 12 non-diabetic persons with biopsy-confirmed NAFLD, the effect of the Mediterranean diet on insulin resistance and hepatic steatosis was evaluated. After 18 weeks of follow up though there was no change in weight loss while there was a decrease in hepatic steatosis and improved insulin sensitivity7.

In a clinical trial conducted by Capanni et al, it was found that prolonged supplementation of omega 3 fatty acids for a period of 12 months in non-alcoholic fatty liver disease patients improved liver function to some extent during a biochemical evaluation8.

In a double-blind controlled study conducted by Marchesini et al, it was found that long-term supplementation with oral branched-chain amino acids is useful to prevent individuals from progressing into liver failure9.

Synbiotics which are a combination of prebiotics and probiotics are very helpful in reducing the liver enzymes and other biomarkers. In a randomized, double-blind, placebo-controlled clinical trial of 52 patients with non-alcoholic fatty liver disease were advised to take synbiotics and a placebo capsule twice daily along with lifestyle modification for a period of 28 weeks. During the evaluation, it was found that there was a great reduction in the levels of liver enzymes (ALT, AST, GGT), C-Reactive Protein, and inflammatory cytokines compared to that of the placebo group10.

The following are the tests done to determine the severity of liver disease. A liver panel is a group of tests that are performed together to detect, evaluate, and monitor liver disease or damage.

Liver enzymes:

  • Alanine aminotransferase (ALT) – an enzyme mainly found in the liver; the best test for detecting hepatitis
  • Alkaline phosphatase (ALP) – an enzyme related to the bile ducts but also produced by the bones, intestines, and during pregnancy by the placenta (afterbirth); often increased when bile ducts are blocked or damaged
  • Aspartate aminotransferase (AST) – an enzyme found in the liver and a few other organs, particularly the heart and other muscles in the body Proteins:
  • Albumin – measures the main protein made by the liver; the level can be affected by liver and kidney function and by decreased production or increased loss.
  • Total protein (TP) – measures albumin and all other proteins in the blood, including antibodies made to help fight off infections
  • Bilirubin – two different tests of bilirubin often used together (especially if a person has jaundice): total bilirubin measures all the bilirubin in the blood; direct bilirubin measures a form that is conjugated (combined with another compound) in the liver.

Additional tests:

  • Gamma-glutamyl transferase (GGT) – another enzyme found mainly in liver cells; it is a very sensitive marker for liver diseases, but it is not specific as it cannot differentiate between various causes of liver diseases. GGT is not recommended for routine use. It is used in conjunction with ALP to determine the source of increased ALP, either from bone or liver. High levels of GGT can be found with alcohol consumption.
  • Lactate dehydrogenase (LD) – an enzyme released with cell damage; found in cells throughout the body
  • Prothrombin time (PT) – the liver produces proteins involved in the clotting (coagulation) of blood; the PT measures clotting function and, if abnormal, may indicate liver damage.
  • Alpha-fetoprotein (AFP) – associated with the regeneration or proliferation of liver cells and can be produced by certain types of tumors.
  • Autoimmune antibodies (e.g., ANA, SMA, anti-LKM-1) – associated with autoimmune liver diseases (autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC)

Reference Range For Liver Panel11,12,13

ParameterReference Range
ALT7 to 55 units per liter (U/L)
AST8 to 48 U/L
ALP40 to 129 U/L
Albumin3.5 to 5.0 grams per deciliter (g/dL)
Total protein6.3 to 7.9 g/dL
Bilirubin0.1 to 1.2 milligrams per deciliter (mg/dL)
GGT8 to 61 U/L
LD122 to 222 U/L
PT9.4 to 12.5 seconds


  1. Asrani SK, Devarbhavi H, Eaton J, Kamath PS.. J Hepatol. 2019 Jan;70(1):151-171. Burden of liver diseases in the world

  2. The Progression of Liver Disease

  3. Hamurcu Varol P, Kaya E, Alphan E, Yilmaz Y. Role of intensive dietary and lifestyle interventions in... : European Journal of Gastroenterology & Hepatology. Eur J Gastroenterol Hepatol. 2020 Oct;32(10):1352-1357.

  4. A. R. Moschen and H. Tilg, “Nutrition in pathophysiology and treatment of nonalcoholic fatty liver disease,” Current Opinion in Clinical Nutrition and Metabolic Care, vol. 11, no. 5, pp. 620–625, 2008.

  5. Canbay A, Chen SY, Gieseler RK, Malago M, Karliova M, Gerken G, et al.Overweight patients are more susceptible for acute liver failure Hepatogastroenterology 2005; 52(65):151.

  6. M. C. Elias, E. R. Parise, L. D. Carvalho, D. Szejnfeld, and J. P. Netto, Nutrition and Physical Activity in Nonalcoholic Fatty Liver Disease” Nutrition, vol. 26, no. 11-12, pp. 1094–1099, 2010.

  7. A. M. Zivkovic, J. B. German, and A. J. Sanyal, Comparative review of diets for the metabolic syndrome: implications for nonalcoholic fatty liver disease” The American Journal of Clinical Nutrition, vol. 86, no. 2, pp. 285–300, 2007.

  8. M. Capanni, F. Calella, M. R. Biagini et al., “Prolonged n-3 polyunsaturated fatty acid supplementation ameliorates hepatic steatosis in patients with non-alcoholic fatty liver disease: a pilot study,” Alimentary Pharmacology and Therapeutics, vol. 23, no.8, pp. 1143–1151, 2006.

  9. G. Marchesini, G. Bianchi, M. Merli et al., .Nutritional supplementation with branched-chain amino acids in advanced cirrhosis: a double-blind, randomized trialGastroenterology, vol. 124, no. 7, pp. 1792–1801, 2003

  10. Tannaz Eslamparast, Hossein Poustchi, Farhad Zamani, Maryam Sharafkhah, Reza Malekzadeh, Azita Hekmatdoost, Synbiotic supplementation in nonalcoholic fatty liver disease: a randomized, double-blind, placebo-controlled pilot study, The American Journal of Clinical Nutrition, Volume 99, Issue 3, March 2014, Pages 535–542

  11. Smith et al, Lab tests online; American Association for Clinical Chemistry (AACC)2001-2020.

  12. Wintrobe's Clinical Hematology. 14th ed. Greer J, editor. Philadelphia, PA: Wolters Kluwer: 2019.

  13. Henry's Clinical Diagnosis and Management by Laboratory Methods. 22nd ed. McPherson R, Pincus M, eds. Philadelphia, PA: Elsevier Saunders; 2011.

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