In 2021, an opinion piece was published in the Journal of the American Veterinary Medical Association raising concerns regarding the copper content of commercial pet food. Written by a panel of internal medicine specialists lead by Dr Sharon Center from Cornell University, Colorado State, Tufts and Cambridge, the piece requests the American Association of Feed Control Officials (AAFCO), to implement a maximum copper level within both canine and feline formulations [1].
AAFCO is an independent regulatory body that sets standards for pet foods and animal feeds in the United States [2].
Recent trends in the pet food industry include the increased inclusion of organ meat which can potentially account for the greater copper content. Grain-free and vegetarian or vegan diets may also be using more novel vegetable sources such as sweet potato and peas, again known to be rich in copper [1, 3]. Currently there is no maximum limit on copper content, only a minimum guideline in the United States, regulated by AAFCO [4].
Copper can be added to a formulation as a ‘pre-mix’ if the ingredients in the formulation are low in copper. This supplementation can be in the form of copper sulphate or copper oxide- it is important to note the bioavailability between the two sources vary, with copper oxide being unavailable to the animal to metabolise and absorb [1].
Copper is a trace element essential for several biochemical processes including collagen synthesis, mitochondrial energy generation and is utilised in redox reactions [1]. As free copper is damaging to cells, the metabolism and absorption of copper is very tightly regulated [5]
Copper is absorbed in the proximal small intestine and is transported to the liver in both free and protein bound forms [5]. Copper is eliminated in the bile and faecally excreted ultimately.
Copper toxicity impairs mitochondrial function and protein synthesis and increases in oxidative activity result in localized inflammation and cellular damage.
There are three causes of hepatic copper toxicity in companion animals.
- A primary inherited defect with copper metabolism resulting in copper accumulation in the hepatocytes. This condition is also recognized in humans as Wilson’s disease. Bedlington terriers, Labrador retrievers and Dobermanns are known to be at risk of primary copper-associated hepatic disease [6].
- Chronic hepatobiliary disease such as fibrosis or cholestasis may alter copper homeostasis and impair excretion resulting in secondary disease. [6]
- Prolonged dietary excess [1], the concern raised by the panel of experts in 2021.
Owners of Labrador retrievers and Dobermann can opt for genetic testing to look for the ATP7A and ATP7B variants- in both breeds, a female predisposition to the disease is observed [5, 7].
For Bedlington terriers, there is a known deletion in the COMMD1 gene. It is a recessive trait; for breeding purposes, carriers should be neutered to prevent further risk. DNA screening has been a very effective tool in managing this mutation and the incidence of disease in this breed has greatly reduced [5].
One challenge with this condition is identification of early subclinical disease, when clinicians have the best chance at limiting or even reversing further damage. Subclinical detection in patients of breeds not known to have a suspected genetic predisposition is difficult. Where prolonged dietary excess is the concern, biochemistry will likely only reveal increased ALT and ALKP when hepatocellular damage is extensive and so is not a useful screening tool to detect early copper accumulation [5].
Symptoms of copper-associated hepatopathy are non-specific;
- anorexia,
- jaundice,
- weight loss,
- GI symptoms including vomiting
- PUPD [5]
Definitive diagnosis regardless of cause requires histopathology post hepatic biopsy- via surgery or percutaneous sampling with ultrasound guidance [5]. Specialist staining with rubeanic acid or rhodamine is required to detect the copper accumulation [5].
An effective and non-invasive screening tool would be invaluable, as invasive procedures may not possible- coagulopathy associated with hepatic disease, concurrent conditions or financial constraints can rule this out as an option in some cases.
Treatment of copper-associated hepatopathy regardless of the cause includes the use of copper chelators such as D- penicillamine and/or dietary management- selecting an adjusted diet with restricted copper and zinc levels [5]. Individual variation in tolerance of dietary copper levels are suspected particularly in cases of hereditary primary disease; repeated biopsy to assess treatment response should be considered [5]. It is also important to note that many of the “Low Copper” diets on the market are also protein-restricted, aimed at the management of chronic or end stage hepatobiliary disease. For patients with subclinical copper associated-hepatopathy, these diets are less than ideal [5].
An AAFCP 13-member panel issued a report in response to the JAVMA article on August 1st, 2022, rejecting a call for a maximum level to be set [4].
Royal Canin products supplied here in the UAE, Qatar, Oman and Bahrain are manufactured in Europe and, as such, comply with FEDIAF standards (the trade body representing the European pet food industry).
FEDIAF have stated minimum and maximum values for copper for dogs and cats (see below table), at both growth and maintenance life stages [8]. The use of copper oxide as a source is also discouraged by FEDIAF due to the low bioavailability [8].
| Lifestage | FEDIAF min-max range in mg /100g dry matter basis |
| Adult maintenance (dog) | 0.72-2.8 |
| Adult maintenance (cat) | 0.5-2.8 |
| Growth and Reproduction (dog) | 1.1-2.8 |
| Growth and Reproduction (cat) | 1.0-2.8 |
For reference, all dry Royal Canin diets contain 1.50mg/100g on an as fed basis, which places diets well within the FEDIAF reference range. In a dry food with a moisture content of 5.5%, with 1.50mg this would equate to 1.59mg/100g and just exceeds the level the expert panel assembled by AAFCO used to allow a food to claim it is “Low Copper” [4].
Royal Canin VHN Hepatic diets are a “Low Copper” option and have copper included at 0.3mg/100g as fed for dogs and 0.36mg/100g as fed for cats, so contain approximately 20% of the copper content of a maintenance diet and are aimed at those patients who have a diagnosis of hepatic disease. This diet will only be recommended and supplied under veterinary supervision due to the concurrent protein restriction.
- Center, S.A., et al., Is it time to reconsider current guidelines for copper content in commercial dog foods? Journal of the American Veterinary Medical Association, 2021. 258(4): p. 357-364.
- Association of American Feed Control Officials. 2023 [cited 2023 18th October 2023]; Available from: https://www.aafco.org/.
- Zafalon, R.V.A., et al., Nutritional inadequacies in commercial vegan foods for dogs and cats. PLoS ONE, 2020. 15(1): p. 1-17.
- Association of American Feed Control Officials. March 2023 [cited 2023 18th October 2023]; Available from: https://www.aafco.org/wp-content/uploads/2023/01/Copper_in_Dog_Foods_Expert_Panel_Report_to_the_PFCkv2136684-2136685.pdf.
- Dirksen, K. and H. Fieten, Canine Copper-Associated Hepatitis. Veterinary Clinics of North America: Small Animal Practice, 2017. 47(3): p. 631-644.
- Smedley, R., T. Mullaney, and W. Rumbeiha, Copper-Associated Hepatitis in Labrador Retrievers. Veterinary pathology, 2009. 46(3): p. 484-490.
- Wu, X., et al., Association of the canine ATP7A and ATP7B with hepatic copper accumulation in Dobermann dogs. Journal of Veterinary Internal Medicine, 2019. 33(4): p. 1646-1652.
- FEDIAF Nutrional Guidelines. FEDIAF Nutritional Guidelines for Complete and Complementary Pet Food for Cats and Dogs 2021 [cited 2022 08/06/2022].
Written on October 27, 2023