THE liver is an extraordinary organ which performs many vital functions throughout the entire body. Given these varied roles, the signs of disease it throws at us are also varied and often non-specific.
There are many ways in which we can extend liver patients a helping hand in a clinical setting including (of course) feeding for long-term health.
While liver disease is diagnosed only occasionally in cats, it is a relatively common finding in dogs. It can lead to problems with the metabolism and storage of nutrients and the breakdown of their potentially harmful by-products (or toxins).
One important toxin is ammonia, which is produced by bacteria in the large intestine, created by the breakdown of meat proteins. When absorbed into the bloodstream, these circulating toxins can cause central nervous system signs, collectively known as hepatic encephalopathy (HE).
The owner will commonly see behavioural changes, fits, tremors, excessive salivation (particularly in cats), vacant staring and disorientation.
While it is true to say that the liver has great regenerative capacity, during and after disease it is particularly vulnerable to damage from free radicals, often escalated by the accumulation of copper within the liver cells.
To aid recovery and restore optimal function, the liver requires high levels of energy, high-quality protein, plus the ability to address damaging oxygen free radicals, by way of antioxidant which can be delivered in the diet. We should also consider the positive impact that reducing workload of the liver can make.
This is where Royal Canin Hepatic diets can be beneficial. They are highly palatable and balanced for the dietary support of dogs and cats with liver disease and insufficiency.
The diets are enriched in antioxidants (with a patented synergistic complex of vitamin E, vitamin C, taurine and lutein) to help maintain health and vitality and to help neutralise free radicals in the liver.
In my opinion, a good hepatic diet should have a high caloric density, to provide pets with the energy needed for recovery, without requiring large meal volumes and potential gastric overload, important in a patient which may be showing signs of nausea.
Palatability is also important and is largely responsible for restoring voluntary food intakes, particularly in the face of reduced appetite. Liver formulas also typically contain low copper levels which help minimise copper accumulation and hepatic cell damage and death. Royal Canin’s diet contains a highly-digestible vegetable protein (selected for exceptional digestibility and greater tolerance in the face of HE) to reduce the workload of a compromised liver.
Adapted fibre levels
Another key feature of many hepatic diets is the adapted levels of soluble and insoluble dietary fibre. Dietary fibre helps “trap” ammonia and other toxins in the intestine via incorporation into the dog or cat’s stools. Fermentable fibres also support the healthy growth of intestinal bacteria, further reducing ammonia production.
The food also has a modified zinc content to avoid deficiency but also inhibit uptake of copper at the level of the gut.
Zinc is involved in the detoxification process and as such also helps to remove the ammonia which could affect the nervous system.
In summary, any dietary management of liver disease needs to first correct any malnutrition, before then working to support liver cell regeneration and limit further liver damage. Hepatic diets provide a very precise nutritional solution for liver patients which can reduce the hepatic workload and the toxin levels to which liver cells are exposed.
Nutritional support must be adapted to each individual patient based upon the type of disease (and the extent of dysfunction), levels of tolerance, concurrent conditions and other physiological states for a truly tailored recommendation.
References and further reading
- Biourge, V. (2004) Nutritional support, a key factor in the management of liver disease. WALTHAM Focus 14 (2): 22-27.
- Brewer, G., Dick, R. and Schall, W. (1992) Use of zinc acetate to treat copper toxicosis in dogs. J Am Vet Med Assoc. 201 (4): 564-568.
- Britton, R. and Bacon, B. (1994) Role of free radicals in liver diseases and hepatic brosis. Hepatogastroenterology 41 (4): 343-348.
- Center, S. (1998) Nutritional support for dogs and cats with hepatobiliary disease. Journal of Nutrition 128 (suppl): 2,733S-2,746S.
- Greenhalgh, S., Dunning, M., McKinley, T., Goodfellow, M., Kelman, K., Freitag, T., O’Neill, E., Hall, E., Watson, P. and Jeffery, N. (2010) Comparison of survival after surgical or medical treatment in dogs with a congenital portosystemic shunt. J Am Vet Med Assoc. 236 (11): 1,215-1,220.
- Marks, S. (2012) Nutritional Management of Hepatobiliary Diseases. In: Fascetti J. and Delaney S. (eds), Applied Veterinary Clinical Nutrition. Chichester, John Wiley & Sons, 235-250.
- Michel, K. (1995) Nutritional Management of Liver Disease, Veterinary Clinics of North America: Small Animal Practice 25 (2): 485-501.
- Proot, S., Biourge, V., Teske, E. and Rothuizen, J. (2009) Soy protein isolate versus meat-based low-protein diet for dogs with congenital portosystemic shunts. Journal of Veterinary Internal Medicine 23 (4): 794-800.
- Rutgers, H. and Biourge, V. (2006) Nutritional management of hepatobiliary and pancreatic diseases. In: Pibot, P., Biourge, V., Elliott, D. (eds), Encyclopaedia of Feline Clinical Nutrition.
- Paris, Aniwa, 139-179. Rutgers, H. and Biourge, V. (2006) Nutrition of dogs with liver disease. In: Pibot, P., Biourge, V., Elliott, D. (eds), Encyclopaedia of Canine Clinical Nutrition. Paris, Aniwa, 134-161.