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Copper accumulation in the liver occurs gradually. In the first phase,- clinical signs are  usually absent.  In progression of the disease, when a large part of the liver Is affected, dogs start to show symptoms of illness  such as vomiting, decreased appetite, lethargy, jaundice, blood clotting problems, and increased abdominal size due to fluid in the abdomen.

An elevation of the liver enzyme ALT in the blood may indicate liver damage. This elevation may be caused by copper accumulation, but other causes that cause liver damage can also lead to elevated ALT. In addition, not all dogs with copper accumulation have elevated ALT. It is possible that the abnormal amount of copper has not yet caused an inflammatory reaction in the liver. A normal ALT value is therefore no guarantee that the dog is free of copper accumulation. 

The definitive diagnosis can only be made by taking a liver biopsy: removing a small piece of liver tissue and examining it for copper and inflammation. 

There may be two reasons to test your Labrador retriever's DNA for copper accumulation. First, for the purpose of breeding. The spread of the ATP7B mutation in the population should be prevented as much as possible. Breeding with dogs with two copies of the mutation is not recommended. Breeding with a dog with one copy of the mutation in combination with a dog free of the mutation should be considered critically. Such a combination could bring forth pups with one copy of the mutation and therefore an increased risk of copper accumulation. The mutation in ATP7A has no proven adverse effects on the dog. There is no scientific justification for selecting parent dogs without the ATP7A mutation.  

Another important reason to perform a DNA test for copper accumulation for your dog is to determine the risk of copper accumulation in your dog and, if there is an increased risk, to take appropriate measures to prevent your dog from becoming ill from copper accumulation. 

Several factors play a role in the likelihood of disease: 

• Whether a protective mutation is also present in ATP7A 
• The age of the dog
• The dog's diet (copper content, zinc content) 
• Whether the liver has suffered damage, eventually from other causes.  

We recommend foods with a low copper content (preferably foods without additional added copper, but at least <5 mg/kg dry weight). Unfortunately, usually only added copper is listed, and not the total copper content. Veterinary diets Hill's L/D, Purina Hepatic and Royal Canin Hepatic have copper levels below 5mg/kg. Nowadays, zinc does not play an important role anymore in dietary foods. If you want specific nutritional advice, please contact our

If a liver biopsy reveals copper accumulation, treatment with D-penicillamine is advised. The duration of treatment depends on the amount of copper present. 

Zinc prevents the absorption of copper from the gut.

The function of the RETN gene in the pathology of copper accumulation has not been sufficiently elucidated to recommend this DNA test. In the Dobermann, the mutation in ATP7B has also been shown to be associated with copper accumulation. Dogs of other breeds are currently under investigation. 

There is no proven connection between the symptoms and the presence of a mutation in the ATP7A gen with Labrador Retrievers. You can breed with Labrador retrievers with this mutation. There is, however, a recommendation to adjust the copper and sink levels in the nutrition based on DNA-tests for ATP7A and ATP7B (page in Dutch) so that, for example, with a carriage of females with two copies of the ATP7A mutation that do not have ATP7B mutations, copper deficiency can be prevented.

The ATP7A gen does not play a role in the copper absorption in the colon. Mutations in this gen could allow a reduced absorption of copper from the colon. In Labrador Retrievers we notice that dogs with a mutation in the ATP7A gen overall have lower levels of copper. We have not noticed that these dogs will immediately have or develop a copper deficiency Those dogs do not show symptoms of Menkes disease which exists in humans with mutations in the ATP7A gen. Dogs with the ATP7A mutation would, in theory, develop a copper deficiency if they’re fed a diet that is limited in copper. Thus the advice would be to test Labradors for both the ATP7A mutation and the ATP7B mutation and adjust the nutrition accordingly. These tests can be requested at the Expertise Centre for Veterinary Genetics where research to copper accumulation is already being conducted. [Page in Dutch]

The ATP7A gen is attached to the X-chromosome. Males have just one X-chromosome and thus don’t have this mutation. Females have two X-chromosomes, and could be homozygous mutant (two copies of the mutation), heterozygous (one copy of the mutation) or absent of mutations.

The ATP7B gen is attached to chromosome 22 and inherits autosomal in an additive way. Each extra copy of the mutation increases the chance for an elevated copper level. This means that dogs with two copies of the mutation would be prone to a higher risk of copper accumulation than dogs with just one copy. Dogs without copies of the ATP7B mutation would have the lowest copper levels in the liver. However, this is also dependent on the presence of the mutation in the ATP7A gen and the copper and sink levels in their nutrition.