Addison’s disease in dogs does have a hereditary component. The condition is classified as multifactorial, meaning genetics play a significant role but aren’t the only factor. Multiple genes, likely interacting with environmental triggers, determine whether a dog develops the disease. Certain breeds carry a much higher risk than others, and research has identified specific genetic regions linked to the condition.
How Genetics Influence Addison’s Disease
Addison’s disease, also called hypoadrenocorticism, occurs when a dog’s immune system attacks and destroys the outer layer of the adrenal glands. These small glands near the kidneys produce hormones that regulate electrolytes, blood pressure, and stress responses. In affected dogs, immune cells infiltrate all three layers of the adrenal cortex, progressively destroying the tissue until the glands can no longer produce enough hormones to keep the body functioning normally.
The genetic basis is well established but complex. Rather than a single “Addison’s gene,” the disease appears to involve multiple genetic factors. Research has identified associations with genes that regulate the immune system, particularly a set of genes called the dog leukocyte antigen (DLA) system. These genes help the immune system distinguish the body’s own tissues from foreign invaders. Certain versions of these immune-regulating genes appear to make dogs more likely to mount an autoimmune attack against their own adrenal glands. Variations in another immune gene, CTLA4, have also been linked to the disease.
A 2020 genome study in Bearded Collies pinpointed a significant region on chromosome 18 associated with the disease, with additional regions of interest on chromosomes 11, 16, and 29. This kind of multi-chromosome involvement is typical of complex inherited conditions.
Breeds With the Highest Risk
Addison’s disease can occur in any breed, including mixed breeds. However, several breeds are consistently overrepresented in diagnosis data. Cornell University’s College of Veterinary Medicine lists the following as predisposed breeds:
- Standard Poodle
- West Highland White Terrier
- Bearded Collie
- Great Dane
- Portuguese Water Dog
- Nova Scotia Duck Tolling Retriever
- Labrador Retriever
- Rottweiler
- Wheaten Terrier
The clustering of cases within these breeds is itself strong evidence of heritability. Standard Poodles have been studied extensively, and the disease is described as “highly heritable” in that breed. A study by Famula et al. found suggestive evidence that a single recessive gene may be responsible in Standard Poodles, though a polygenic model (multiple genes contributing) hasn’t been ruled out. In Portuguese Water Dogs, heritability was estimated at 0.49, meaning roughly half the variation in disease risk comes from genetics. That study also found suggestive evidence for inheritance through a single autosomal recessive gene, with no difference in risk between males and females.
Inbreeding amplifies the problem. A 2015 study on Standard Poodles found that genetic bottlenecks and inbreeding within the breed increased the incidence of Addison’s disease, alongside another autoimmune condition called sebaceous adenitis.
Is Genetic Testing Available?
For most breeds, no commercial genetic test exists for Addison’s disease. The genes responsible haven’t been fully identified in Standard Poodles, Bearded Collies, or most other predisposed breeds, so there’s nothing to screen for yet.
The one exception is the Nova Scotia Duck Tolling Retriever. The UC Davis Veterinary Genetics Laboratory offers a test for juvenile Addison’s disease (JADD) in this breed, priced at $55 per dog. The test identifies a variant in a gene called RESF1 that follows an autosomal recessive pattern with incomplete penetrance. That means a puppy needs two copies of the variant (one from each parent) to be at risk, and even then, about 75% of those puppies will develop Addison’s disease by one year of age. The remaining 25% with two copies may never develop it. Dogs carrying a single copy are unaffected but will pass the variant to half their offspring. Breeders of Nova Scotia Duck Tolling Retrievers can use this test to avoid pairing two carriers.
For other breeds, breeders rely on pedigree analysis. If you’re considering a puppy from a predisposed breed, asking the breeder whether Addison’s disease has appeared in their lines is a reasonable step. Dogs closely related to affected individuals carry a higher risk of harboring disease-causing gene variants.
Recognizing the Signs
Addison’s disease is typically diagnosed in young to middle-aged dogs, with a median age of about 4 years. The juvenile form seen in Nova Scotia Duck Tolling Retrievers can appear before age 1. Symptoms often develop gradually and can be vague, which is why the condition is sometimes called “the great pretender.”
The most common signs include lethargy, poor appetite, vomiting, diarrhea, weight loss, and muscle weakness. These symptoms may come and go, sometimes improving with basic veterinary care like fluids, only to return weeks or months later. Some dogs present in what’s known as an Addisonian crisis, a sudden collapse with severe dehydration, low blood pressure, and dangerously abnormal electrolyte levels. This is a veterinary emergency.
In the “typical” form, both types of adrenal hormones are deficient: mineralocorticoids (which control sodium and potassium balance) and glucocorticoids (which help manage stress and inflammation). The electrolyte imbalance, specifically high potassium and low sodium, is often the first clue on routine bloodwork. In “atypical” cases, only glucocorticoid production is affected, and electrolytes remain normal, making the condition harder to catch. Diagnosis is confirmed with a hormone stimulation test that measures how the adrenal glands respond to a synthetic signaling hormone.
What Treatment Looks Like
Addison’s disease requires lifelong treatment, but the good news is that well-managed dogs typically live normal, active lives with a normal lifespan.
Treatment replaces the two types of hormones the adrenal glands can no longer make. For the mineralocorticoid component, the standard approach is an injection given roughly every 25 to 30 days. Your vet will check your dog’s electrolyte levels at specific intervals after injection to fine-tune both the dose and how often it’s needed. An oral alternative exists for dogs that don’t tolerate injections or when the injectable form isn’t available.
For the glucocorticoid component, dogs take a small daily oral steroid dose. Most dogs need very little. Before stressful events like boarding, travel, or surgery, the daily dose is typically doubled or tripled to mimic what healthy adrenal glands would do naturally during stress.
The adjustment period during the first few months requires regular vet visits and blood draws, but once the right dose is established, monitoring becomes less frequent. Most owners settle into a routine that feels manageable. The main ongoing costs are the hormone injections, daily medication, and periodic bloodwork.
What This Means for Breeding Decisions
Because Addison’s disease is heritable and the genetic picture is still incomplete for most breeds, responsible breeding practices are the primary line of defense. Affected dogs should not be bred. In breeds where the condition is common, avoiding breeding close relatives of affected dogs reduces risk, though it doesn’t eliminate it entirely since unaffected carriers likely exist. For Nova Scotia Duck Tolling Retrievers, the available DNA test makes it possible to identify carriers before breeding and plan pairings that won’t produce affected puppies.
If you own a predisposed breed, awareness is your best tool. Knowing that your dog’s breed carries a higher genetic risk means you and your vet can keep Addison’s disease on the radar if vague, recurring symptoms appear. Early diagnosis leads to earlier treatment and better outcomes.