We have known that the American Cocker Spaniel is susceptible to the heritable accumulation of abnormal amounts of copper in the liver with resultant chronic liver failure. This disease has previously been called chronic active hepatitis. It appears that the problem has been present sporadically in some of the best bloodlines of all three American Cocker Spaniel varieties for at least 30 years. Whether it was present before that, when the cocker spaniel breed was divided into the American and English Cocker Spaniels in the 1940s is unclear.
The American Cocker Spaniel is one of the best known breeds genetically susceptible to copper toxicosis, other susceptible breeds such as Bedlington Terrier, Doberman Pinscher, Dalmatian, Labrador Retriever, West Highland White Terrier, and Skye Terrier have also been identified.
Identified Genetic Variants
DNA tests for copper accumulation are available for Labrador Retrievers, Doberman Pinschers, Black Russian Terriers and Bedlington Terriers at University of California Davis. Embark offers the test for Doberman Pinschers and Labrador Retrievers.
- ATP7B (Accumulating variant). The mode of inheritance for ATP7B is incomplete dominance, meaning that one or two copies of this gene can cause the disorder.
- ATP7A (Attenuating variant). The mode of inheritance for ATP7A is complex (X-chromosome linked). This variant has been shown to decrease copper accumulation in dogs with one or two copies of the ATP7B The ATP7A gene is most beneficial in males with one copy. Females with one copy likely have less benefit than females with two copies.
- RETN (Attenuating variant). The mode of inheritance for RETN is complex. One or two copies of this variant may reduce the accumulation of copper in the liver of Labrador Retrievers with one or two copies of the APT7B variant and may help reduce disease severity.
Breeds with known genetic variants include Labrador Retrievers (ATP7B, ATP7A, and RETN) and Doberman Pinschers (ATP7B and ATP7A).
Dietary Copper Restriction
Thus, because of the risk of accumulating excessive copper, especially in families known to be affected or closely related to animals with the problem, published data and common sense indicates that reducing dietary sources of copper both in food and in water supplies should be helpful in minimizing the amount of copper. For this reason, commercial or homemade diets should be selected that have lower amounts of copper.
Dietary copper restriction should still provide a dietary level equivalent to the NRC minimum of 0.8 mg/1000 kcal ME. This translates to a minimum of 7.3 ppm (7.3 mg/kg) copper for adult maintenance, whereas a truly low copper diet would have < 0.5 ppm copper; but no commercially available diet is this low in copper. Copper-restricted diets are available, and they usually contain about 7-9 ppm (7-9 mg/kg). Some diets that contain higher amounts of copper (18-30 ppm; 18-30 mg/kg) also add higher amounts of zinc, which they claim offsets the higher copper level. [Copper is still an essential nutrient, because of its importance in several key body functions.]
Nutritional therapy in the above situation aids in the management of animals already diagnosed as having copper toxicosis, and for those relatives or families of dogs that are also at increased risk. In addition to feeding diets with lower amounts of copper, zinc is known to bind intestinal copper and prevent its absorption, thereby reducing the amount of copper absorbed. Thus, zinc is often used as a supplement when given at physiological doses to help bind excess copper. Typical doses of zinc for a dog of American Cocker Spaniel size would be 15 mg of zinc sulfate daily. Zinc acetate or gluconate can also be used at the relatively high levels of 5-10 mg/kg twice daily. Zinc supplement should be given 1 hour before feeding, as food interferes with its absorption. In affected patients, the reduced copper absorption due to zinc supplementation lowers elevated liver copper levels too, presumably by increasing release of liver copper stores to compensate for the lowered intestinal copper absorption.
The protein source in foods for animals with compromised or potentially compromised liver function should be of high quality and easily digestible, so that the diet should have lower amounts of poor quality protein. Homemade diets designed to provide high quality overall protein or diets for senior pets are suitable examples.
Copper Levels in Common Foods
Low Copper Content
- Beef
- Cheese
- Cottage Cheese
- Eggs
- Oils
- Fats
- Rice
Medium Copper Content
- Turkey
- Chicken
- Potatoes
- Breads
- Peas
- Peanut Butter
High Copper Content
- Lamb
- Pork
- Duck
- Goose
- Salmon
- Liver
- Heart
- Kidney
- Soybean Meal
- Tofu
- Brewers’ Yeast
- Mushrooms
- Broccoli
- Avocado
- Wheat Germ
- Bran Breads
- Bran Cereals
- Granola
- Quail
- Pheasant
- Shellfish
- Meat Gelatin
- Nuts and Seeds
- Mineral Water
Precautions with Commercial Raw Diets
As more raw pet food manufacturers add organs to their foods, because of their rich source of vitamins and minerals, they may also include a vitamin pack without considering the potential health risks such as copper accumulation. A good example of copper toxicity is a dog diet that includes beef liver and is also enriched with copper. And, yes; I prefer organ meats as sources of vitamins and minerals. However, if a balance is not achieved, a companion animal’s health is at risk.
References
Dodds W J, Donoghue S. Interactions of clinical nutrition with genetics, Chapter 8. The Waltham Book of Clinical Nutrition of the Dog and Cat. Pergamon Press Ltd., Oxford, 1994, p.105-117.
Dodds W J. Pet food preservatives and other additives, Chapter 5. Complementary and Alternative Veterinary Medicine. Mosby, St. Louis, 1997; pp 73-79.
Volhard W, Brown K L. The Holistic Guide for a Healthy Dog. Howell Book House, New York, 1995, 294 pp.
Burkholder W J, Swecker W S Jr. Nutritional influences on immunity. Sem Vet Med Surg (Sm An), 5(3): 154-156, 1990.
Fieten H, Gill Y, Martin AJ, et al. The Menkes and Wilson disease genes counteract in copper toxicosis in Labrador retrievers: a new canine model for copper-metabolism disorders. Dis Model Mech. 2016 Jan;9(1):25-38. doi: 10.1242/dmm.020263. PMID: 26747866; PMCID: PMC4728329.
Wu X, Mandigers PJJ, Watson AL, et al. Association of the canine ATP7A and ATP7B with hepatic copper accumulation in Dobermann dogs. J Vet Int Med 2019, 33(4), 1646-1652. https://pmc.ncbi.nlm.nih.gov/articles/PMC6639496
Wu X, den Boer ER, vos- Loohuis M et al. Investigation of genetic modifiers of copper toxicosis in Labrador retrievers. Life 2020, 10(11), 266; https://doi.org/10.3390/life10110266
Rodrigues A, Leal RO, Girod M, et al. Canine copper-associated hepatitis: A retrospective study of 17 clinical cases. Open Vet J. 2020 Aug;10(2):128-134. doi: 10.4314/ovj.v10i2.2. Epub 2020 Apr 13. PMID: 32821657; PMCID. PMC7419071. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7419071/
Peterson L. Embark adds copper toxicosis DNA test. EMBARK, updated May 6, 2024.
Originally Published: February 15, 2015; Updated: August 15, 2024