Nutritional Management of Liver Disease in Birds

Key Points

  • Chronic liver disease may lead to malnutrition, hepatic encephalopathy, and weight loss.
  • Antioxidant supplementation may protect hepatocytes from further damage.
  • Protein restriction is not required except in cases of liver failure and encephalopathy.
  • In liver failure, temporarily restrict protein while feeding a highly digestible diet with moderate amounts of fiber.


In mammals, chronic liver disease is often associated with decreased intake of food, mainly due to anorexia, nausea, and vomiting, as well as taste abnormalities, and the same appears to be true for the avian patient. Chronic liver disease may also lead to maldigestion and malabsorption, as well as metabolic abnormalities such as increased protein and lipid catabolism, glucose intolerance, depletion of hepatic glycogen stores, and decreased glucose oxidation. Therefore chronic liver disease may lead to significant malnutrition and weight loss, particularly in patients with severe hepatic dysfunction.

In general, birds with liver disease may be presented with a wide range of clinical disease signs ranging from mild (e.g. anorexia, depression) to severe (e.g. internal bleeding, death). Clinical signs that are commonly associated with avian liver disease include yellow to green discoloration of the urates or feces, feather discoloration (typically black coloration where the feather should be green or blue) (Fig 1), cachexia, subcutaneous hemorrhaging, prolonged or lack of blood clotting, and poor feather quality.

Black discoloration of plumage that should be green or blue is a possible sign of liver disease in the avian patient

Figure 1. Black discoloration of plumage that should be green or blue is a possible sign of liver disease in the avian patient. Photo credit: Dr. Susan Orosz.

Assessment of the nutritional status of the patient with liver disease is challenging since many indicators are directly altered by liver pathology. One should assume, however, that nutritional deficiencies are associated with liver dysfunction if a poor quality diet is fed, especially if the poor quality diet has been fed for a prolonged period of time.

  • Body weight is an insensitive indicator, especially in end-stage liver disease, when weight may be affected by total body salt and water retention.
  • Measurement of plasma proteins, such as albumin and prealbumin, is also unreliable. Instead, low protein levels reflect a decrease in hepatic synthesis and an increase in catabolism of prealbumin.
  • In birds, enzyme levels commonly analyzed in a plasma chemistry panel [link to]; alanine aminotransferase (ALT), lactate dehydrogenase (LDH), serum alkaline phosphatase (SAP), and aspartate amino transferase (AST) are either not sensitive or specific for liver disease.  In the case of AST and ALT a concurrent elevation in creatine phosphokinase (CK) will elevate both.  If the CK is not elevated there is a great reliability that an elevated AST and ALT is truly the result of liver disease.
  • Measurement of bile acid levels is the best diagnostic test to determine liver function.  Also bile acid testing is recommended for assessing chronic liver disease that results in decreased hepatic function.

Both in human and small animal patients, nutritional therapy of liver disease has been shown to be key in the management of patients, and nutritional therapy is the only effective treatment for hepatic lipidosis. The major goals in the nutritional management of the mammalian patient are to provide enough nutrients to correction malnutrition and support hepatocytes, while preventing complications such as hepatic encephalopathy and ascites. All of the recommendations listed below for the patient with liver disease are directly extrapolated from human and small animal medicine. There is very little bird-specific information available at this time.

In avian species, both liver fat and excess body weight are considered primary contributors to hepatic lipidosis or fatty liver syndrome (FLS). The typical avian patient diagnosed with hepatic lipidosis is overweight, body condition score 5/5, with little to no exercise activity.

Dietary preventative measures that have been recommended for use in avian patients diagnosed with or are susceptible to hepatic lipidosis include:

  • Ground flaxseed (100 g/kg feed) (Harrison and McDonald 2006)
  • Flaxseed oil (40 g/kg feed) (Harrison and McDonald 2006)
  • Palm kernel oil
  • Safflower seed

Amino acid and derivative supplementation

S-adenosylmethionine (SAMe)

A methionine metabolite is an important methyl and sulfur donor for production of a number of amino acids and biochemicals including methylcytosine, glutathione, and taurine. Glutathione is considered a liver protectant and is best synthesized with when adequate levels of SAMe are physiologically present. Vitamin B supplementation is required for optimum SAMe transformation from homocysteine to the liver protectant glutathione. Vitamins B2, B6, B12, and folic acid are recommended supplements to use with SAMe supplementation in avian species diagnosed with liver disease. Unfortunately there is little to no scientific evidence on the usefulness of SAMe as a useful hepatic therapeutic agent in pet bird species. However anecdotal case testimonials indicate there may be clinical effectiveness when treating birds with hepatic disease.


Although the site of L-carnitine production is unknown in birds, in mammals the liver is one of the main sites of L-carnitine synthesis. In patients with severe liver disease or in cases of hepatic lipidosis, carnitine supplementation has been recommended to promote hepatocellular regeneration.


Provided at 6g/kg feed increases the levels of essential amino acids in the body thereby reducing the susceptibility of death to the patient diagnosed with hepatic lipidosis. L-cysteine is recognized for its ability to perform as a powerful antioxidant.

Antioxidant supplementation

Elevation of liver enzymes alone does not generally warrant a dietary change, however if liver enzymes are consistently elevated, supplemental antioxidants may partially protect hepatocytes from further damage. Healthy hepatocytes maintain an elaborate antioxidant system. Interruption of the free radical scavenger defense system by inflammation, infection, hypotension, and/or accumulation of copper is thought to play a major role in the pathogenesis and the progression of hepatic lesions. Dosing, efficacy, and the exact mechanism of action of these supplements is not fully understood, however antioxidants are known to be more effective when given in combination because of their synergistic action.

  • Silymarin (milk thistle): 100-150 mg/kg divided q8-12h
  • Vitamin C: 20-50 mg/kg IM q1-7d
  • Vitamin E: 0.06 mg/kg IM q7d or 15 mg/kg PO once

Energy and protein requirements

An adequate supply of energy and protein is essential to prevent weight loss and muscle wasting. Initially, calories should be provided as carbohydrates, an important energy source in chronic liver disease. Lipids may then be cautiously added to provide more calories. Restrict fat only in cases of significant steatorrhea (pale, bulky, foul-smelling stools).

Provide an adequate supply of high quality protein (i.e. highly digestible with an optimal amino acid profile). Protein restriction does not appear to be necessary in most patients with liver disease. In fact, unnecessary protein restriction can reduce the production of important proteins like albumin putting the patient at risk for abnormal fluid accumulation. Protein restriction is only crucial in treating patients with hepatic encephalopathy or ascites. Additionally, a moderate restriction of dietary sodium is indicated for ascites.

To avoid overwhelming the metabolic capacity of the liver, divide daily nutritional intake into smaller, more frequent meals. Whenever possible, feeding should be enteral. The first-pass effect of nutrients provides beneficial trophic effects on the liver and gastrointestinal tract.

Vitamin/mineral supplementation

In mammals with liver failure, the most commonly reported deficiencies are for potassium, zinc, vitamin K, and vitamin B-complex.

  • Hypokalemia may easily be corrected by fluid therapy [link to]. Dietary supplements may also be used cautiously.
  • Zinc deficiency is essentially the result of anorexia and should correct when feeding resumes.
  • B-vitamins are found in very high levels in the liver where they are stored as coenzymes. Therefore the need for vitamin B should be considered when refeeding. Supplement vitamin B-complex to satisfy at least twice the minimum requirements (Vitamin B1 or thiamine at 1-2 mg/kg IM q24h or 50 mg/kg PO q24h.
  • In cases of abnormal bleeding, vitamin K injections (2.5 mg/kg IM q12-24h) are indicated.
  • Depending upon the bird species, ascorbic acid synthesis may occur predominantly in the liver, kidneys, or both; therefore vitamin C supplementation may also be indicated (20-50 mg/kg IM q1-7d).

Liver failure

Patients with liver failure generally benefit from the same nutritional approach treatment described above for liver disease. Moderate amounts of dietary fiber are also recommended as they promote the uptake of ammonia by intestinal flora. These proteins are then excreted in the feces. By decreasing colonic pH, fermentable fibers also reduce the production and absorption of ammonia and potentially other toxins as well. Temporary protein restriction is also recommended for patients with liver failure with hepatic encephalopathy to minimize ammonia production.

A common feature of liver disease recognized in mammals is a decrease in plasma levels of branched chain amino acids (BCAA) (leucine, valine, isoleucine) and a rise in aromatic amino acids (phenylalanine, tyrosine). Because these latter amino acids are precursors of different neurotransmitters, changes in their concentrations could explain the clinical signs of encephalopathy. Diets enriched in BCAA have been used to theoretically normalize plasma amino acid levels in the hope of improving nitrogen balance and hepatic encephalopathy. However these formulas are not yet recommended in veterinary medicine due to their expense and controversial efficacy.

Iron storage disease

Hemochromatosis or iron accumulation within the hepatocytes is a common disease condition of many birds that eat primarily a fruit (e.g. toucan) or insect diet (mynah birds). The dietary recommendation for birds that are predisposed to iron storage disease (ISD) is to provide food with minimal iron concentrations; toucan species < 100 mg/kg and mynah species < 25 mg/kg. Even if fed diets specifically formulated to reduce the incidence of ISD, birds genetically predisposed may develop the disease.

The most important concepts for a diet fed to the patient with liver disease is that it be high quality and easily digestible. Although there is no empirical research to support its use, there is one formulated diet currently marketed for liver disease: Roudybush AL Liver Care. The two main ingredients of this product are barley and corn, and it contains a minimum crude protein of 7.5%, a minimum crude fat of 3.0%, and maximum crude fiber of 4.0%.


In most cases of hepatic disease, nutritional modifications will be necessary for the life of the patient. The exception to this rule of thumb is hepatic lipidosis. Following treatment, the liver may return to normal function allowing the patient to return to its normal maintenance diet.



DrugDose (mg/kg)RouteFrequencyComments
PO: per os IM: intramuscular q: every h:hours
Silymarin (milk thistle)100-150PODivided q8-12hSelect a low-alcohol or alcohol-free formulation
Vitamin B11-2IMq24h
Vitamin C20-50IMq1-7d
Vitamin E0.06IMq7d
Vitamin K12.5IMq12-24h