Copper-associated hepatopathy (CAH), also known as copper storage disease, is a well-recognized liver disorder in dogs resulting from excessive copper accumulation within the liver’s cells (hepatocytes). This pathological buildup triggers oxidative stress and inflammation, and progressively may lead to chronic hepatitis, hepatic failure, or even death if left untreated. While certain breeds are genetically predisposed due to defects in copper metabolism, current evidence shows that any breed or mixed-breed dog can be affected.​

Normally, copper—a trace dietary element essential for enzymatic functions—is regulated and excreted by the liver. However, factors such as environmental exposures and dietary changes, especially rising copper content in commercial dog food, have resulted in more cases across a broader range of breeds and ages. Clinically, affected dogs often display vague symptoms (lethargy, poor appetite) until the disease is advanced, highlighting the importance of early awareness and intervention.​

Diagnosis relies on liver biopsy, which confirms copper accumulation and guides treatment recommendations. Management typically involves dietary copper restriction and medications that help remove excess copper from the body—strategies developed from the latest veterinary consensus and research.

Certain breeds have a documented genetic predisposition to copper-associated hepatopathy, including Bedlington Terriers, Labrador Retrievers, Doberman Pinschers, West Highland White Terriers, Dalmatians, and Skye Terriers.​

These predispositions are linked to mutations in genes controlling copper transport (COMMD1, ATP7A, ATP7B), which impair the liver’s ability to excrete excess copper. While these breeds remain at higher risk, current veterinary studies confirm that dietary and environmental factors have caused copper buildup in many dogs outside those genetic groups.

Recent studies by veterinary institutions and the American College of Veterinary Internal Medicine (ACVIM) show a sharp increase in copper-associated hepatopathy across all breeds and mixes. Contributing factors include modern diet formulations with highly bioavailable copper, lack of upper dietary limits, and widespread use of copper chelates in pet foods. Genetics remain important, but the rise in cases—combined with better awareness and diagnostics—means this disease is no longer confined to traditionally at-risk breeds. Veterinary experts now recognize that copper-associated hepatopathy is multifactorial, involving a complex interplay of genetic, nutritional, physiologic, and environmental factors that can cause copper buildup and liver injury in any dog.

Optimal care requires collaboration with veterinarians experienced in hepatic disorders, ideally including a board-certified veterinary internal medicine specialist (DACVIM) and, where possible, a board certified veterinary nutritionist (DACVN).​

These specialists guide diagnostic testing (ultrasound, liver biopsy for copper quantification) and design nutrition and medical protocols for long-term management.

Treatment typically includes chelation therapy, low-copper therapeutic diets, and antioxidant support. Chelation removes stored copper, while dietary management prevents reaccumulation.

Success depends on early diagnosis, ongoing monitoring, and precise specialist guidance.

With early detection and strict compliance to dietary and medical recommendations, many dogs can achieve stabilization or reversal of liver damage, maintaining good quality of life for years.​

However, delayed or incorrect treatment can allow irreversible fibrosis or liver failure to develop

Establish care with qualified veterinary specialists to develop an individualized treatment plan based on your dog’s specific diagnostic findings and clinical presentation. Ideally, your care team should include:

• Board-certified veterinary internal medicine specialist (DACVIM) – for liver disease expertise and diagnostic procedures
• Board-certified veterinary nutritionist (DACVN) – for therapeutic diet formulation and nutritional management
• Veterinary follow-up every 3–6 months to re-evaluate liver enzymes