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Collie

Lifespan
13.3 years
95% CI 13.3 to 13.6 · McMillan 2024, n=2,171
Most carried variant
Collie Eye Anomaly
72% of 1,207 tested · Donner 2023
Behind this page
20 dogs
in the atlas · an early sketch · 1,207 tested for variants

Collies have a cited life expectancy of 13.3 years (McMillan 2024 / VetCompass, n=2,171, 95% CI 13.3 to 13.6). The most carried tested variant is Collie Eye Anomaly, in 72% of 1,207 Collies tested (Donner 2023), then MDR1 (56%) and Degenerative Myelopathy (13%). 20 dogs stand behind the atlas figures here, so treat this page as an early sketch.

Collie
Photo: Yasu w · CC BY-SA 4.0 · Wikimedia
Mendelian-disease genetics

What genetic diseases do Collies carry?

From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), Collies carry 5 of them at observable frequency. Carrier frequency is not clinical risk. Most recessive variants require two copies for disease expression; many dominant variants show incomplete penetrance. Read this as a population fingerprint of what's in the gene pool, not a per-dog prediction.

Collie Eye Anomaly (CEA)
Autosomal recessive
high 72.2%
n = 1,207 dogs · 1 variant tested · OMIA:000218-9615 · omia.org →
NHEJ1what this gene does

NHEJ1 is a gene involved in repairing breaks in DNA, helping maintain the integrity of genetic information in cells.

For your dog: If your dog belongs to one of the breeds known to carry this gene variant, it's worth discussing testing with your vet to understand any potential eye health risks.

n = 1,207 dogs · 1 variant tested · OMIA:001402-9615 · omia.org →
ABCB1what this gene does

ABCB1 is a gene that helps control how certain drugs are processed and cleared from a dog's body.

For your dog: If your dog is from a breed that carries this gene variant, ask your vet about medication sensitivities before giving any new drugs.

Degenerative Myelopathy (DM)
Autosomal recessive (Incomplete penetrance)
moderate 12.6%
n = 1,207 dogs · 1 variant tested · OMIA:000263-9615 · omia.org →
SOD1what this gene does

SOD1 is a gene that helps protect cells from damage caused by harmful molecules called free radicals.

For your dog: If your dog is a carrier of SOD1 variants, it's worth discussing with your vet, but remember carrier status doesn't mean your dog will get the disease.

n = 1,207 dogs · 1 variant tested · OMIA:002484-9615 · omia.org →
Exercise-Induced Collapse (EIC)
Autosomal recessive (Incomplete penetrance)
low <0.1%
n = 1,207 dogs · 1 variant tested · OMIA:001466-9615 · omia.org →
DNM1what this gene does

DNM1 is a gene that helps nerve cells communicate properly by managing how they send signals during muscle activity.

For your dog: If your dog belongs to one of the breeds known to carry this gene variant, it's worth discussing EIC with your vet, especially if your dog is very active or shows signs of weakness during exercise.

Source: Donner J et al. 2023. Genetic prevalence and clinical relevance of canine Mendelian disease variants in over one million dogs. PLOS Genetics 19(2):e1010651 · Evidence: Limited (DTC ascertainment, tag-SNP proxy) · Confounding MEDIUM · License CC-BY-4.0 · Phene IDs from OMIA (Sydney School of Veterinary Science, The University of Sydney; DOI 10.25910/2AMR-PV70).
Sample size in this breed: 1,207 dogs from the Donner 2023 cohort.
In plain terms

What these results mean for a Collie

56.4% of Collies in the Donner 2023 cohort carried it (n=1,207).

  • MDR1 is a drug sensitivity, not a disease. A dog with the variant lacks a pump that keeps certain drugs out of the brain.
    OMIA 001402-9615

    “Multidrug resistance 1 is caused by a lack of P-glycoprotein drug transporter in the blood-brain barrier, which is characterized by neurotoxicity after administration of certain drugs.” OMIA 001402-9615

  • Heartworm prevention is safe. At the dose on the label, every FDA-approved heartworm preventive sold in the United States is safe even for a dog with two copies of the variant.
    Mealey 2008

    “at the manufacturer's recommended dose, all FDA-approved heartworm preventive products marketed in the United States are safe, even for dogs with the ABCB1 mutant/mutant genotype” Mealey 2008

  • The risk is dose. The same drug family (ivermectin, milbemycin and their relatives) causes toxicity in these dogs at doses other dogs tolerate, and some chemotherapy drugs are handled by the same pump.
    Mealey 2008

    “renders affected animals extremely susceptible to toxicosis induced by substrate drugs, such as the macrocyclic lactones at doses well below those tolerated by dogs with the wild-type ABCB1 gene” Mealey 2008

    “Many drugs used in veterinary medicine are substrates for P-gp, including many chemotherapeutic agents and macrocyclic lactones” Mealey 2008

What to do
Keep heartworm prevention going at the label dose. Tell your veterinarian the dog's MDR1 status before any off-label parasite treatment or chemotherapy.

No test, or a mix
No test yet, or a mix that may have herding ancestry: label-dose heartworm prevention is safe either way. For any higher-dose decision, tell your veterinarian the dog is untested so it can be treated as a possible carrier.

12.6% of Collies in the Donner 2023 cohort carried it (n=1,207).

  • DM is a loss of function in the spinal cord that begins in adulthood and progresses to paralysis of the back legs. There is no treatment that stops it.
    OMIA 000263-9615

    “This is an adult onset degeneration of the spinal cord that progresses to paraplegia and tetraparesis. There is no successful treatment. A genetic test is available.” OMIA 000263-9615

  • Two copies of the SOD1 variant mean at risk, not affected. Some dogs with two copies never show signs.
    OMIA 000263-9615

    “some homozygous mutant dogs had no signs of degenerative myelopathy, which suggests incomplete penetrance or other causative loci” OMIA 000263-9615

  • One copy makes a dog a carrier. In the study that found the variant, every affected dog tested had two copies.
    OMIA 000263-9615

    “All affected dogs tested were homozygous mutant.” OMIA 000263-9615

What to do
A DNA result is not a diagnosis. Take the result, and any change in how the dog walks, to a veterinarian.

No test, or a mix
Without a test nobody can say how many copies a dog has. A breed's carrier frequency describes the breed, not this dog.

Which Mendelian variants matter most for Collies?

The Mendelian-disease table above lists variants screened in 1,207 Collies (Donner 2023). Two dominate by carrier frequency and clinical impact.

Collie Eye Anomaly (CEA)

Collie Eye Anomaly in Collies is an autosomal-recessive developmental eye condition caused by a variant in the NHEJ1 gene. Affected dogs have retinal hypoplasia, choroidal hypoplasia, or in severe cases retinal detachment and blindness. The condition is present at birth and does not progress after early development.

72.2% of Collies in the Donner cohort carry at least one copy of the variant (n=1,207). That is nearly three in four. Testing is widely available through breed-club recommended laboratories. The Collie Club of America health committee recommends testing breeding stock and has maintained CEA screening protocols for decades.

Bardet-Biedl Syndrome 2 or Progressive Retinal Atrophy (BBS2-PRA) and Exercise-Induced Collapse (EIC)

Bardet-Biedl syndrome 2 (BBS2-PRA) in Collies is an autosomal-recessive retinal degeneration causing progressive vision loss. Exercise-Induced Collapse in Collies is an autosomal-recessive condition with incomplete penetrance that causes collapse during or after intense exercise.

Both variants appear at less than 0.1% carrier frequency in the Donner cohort (n=1,207). Neither is a present breeding concern in the current population.

How should I test my Collie?

A breed-specific panel from a CLIA-accredited laboratory is the high-yield path. The essential set for Collies is CEA, MDR1, and DM. The Collie Club of America maintains a list of recommended testing laboratories on their health pages.

What should I feed a Collie?

Feeding a Collie well means feeding around the breed’s known genetic vulnerabilities. The most consequential is MDR1 medication sensitivity, which shapes medication choices for every Collie. Two other genetics matter: DM’s mid-life onset window and the breed’s moderate hip dysplasia signal.

Heartworm prevention is safe for Collies at the label dose, whatever their MDR1 status. Every FDA-approved heartworm preventive sold in the United States is safe at the manufacturer’s dose, even for a dog with two copies of the variant (Mealey 2008). The danger is above that dose: the same drug family (ivermectin, milbemycin and their relatives) causes toxicity in carriers at doses other dogs tolerate. Which product and at what dose remains a decision for the veterinarian. The diet itself does not change.

Joint care matters for the breed’s hip dysplasia frequency. The Orthopedic Foundation for Animals reports 4.4% hip dysplasia prevalence across 10,547 Collie evaluations (OFA breed statistics, ofa.org/diseases/hip-dysplasia/, accessed 2024). This is lower than many large breeds but not negligible. A large-breed puppy formulation with controlled calcium (0.8-1.2% dry matter) and a calcium-to-phosphorus ratio between 1.1:1 and 2:1 supports healthy skeletal development. Adult-life weight management and moderate exercise (avoiding sprinting and jumping in growing puppies until 12 months of age) are equally important.

Degenerative Myelopathy becomes relevant in the second half of life. DM typically emerges between ages 5 and 14 in affected dogs, based on reported SOD1-associated DM case series (Awano et al. 2009, PNAS 106:2794-2799). There is no proven dietary prevention, but maintaining a lean body condition and joint mobility through appropriate exercise may slow progression. Antioxidant support (vitamin E and selenium at NRC 2006 levels or modestly above) is often recommended by neurologists, though the evidence base is limited. Standard adult maintenance diets with adequate antioxidants are sufficient unless a veterinarian flags a specific need.

Grain inclusion or exclusion is not a genetic vulnerability for Collies. The breed has no documented association with diet-related dilated cardiomyopathy as Goldens do. A grain-inclusive diet is no more protective for Collies than a grain-free one from a genetic standpoint. The choice is nutritional and economic, not a breed-specific mandate.

What we don’t know

The penetrance of MDR1 sensitivity is incompletely characterized. Donner S4 phenotype-confirmed 1 of 2 at-risk dogs, which is too few to state a penetrance figure. Whether an individual dog with two copies reacts, and how severely, is not predictable from the genotype alone, and nothing in the data yet says which dogs will.

Degenerative Myelopathy’s incomplete penetrance is also unsettled. Not every Collie homozygous at the SOD1 locus becomes symptomatic. Environmental and genetic modifiers may govern whether a carrier develops clinical signs. The published analyses have not yet identified those modifiers.

CEA’s severity is heritable but incompletely predictable from genotype alone. Two affected littermates from the same cross may show different degrees of retinal involvement. The breed-club health surveys have documented this variation but the genetic basis remains unresolved.

Frequently asked questions about Collies

Are Collies good with children? Collies were bred for herding and have strong herding instinct toward moving objects, including small children. With socialization and training, they are typically gentle and patient. Supervision with young children is important, as is teaching children not to trigger herding behavior through running.

What is the most common genetic disease in Collies? Collie Eye Anomaly, caused by a variant in the NHEJ1 gene. 72.2% of Collies carry at least one copy (Donner 2023, n=1,207). Severity ranges from subclinical to blindness, with most carriers showing mild hypoplasia that does not affect vision.

Should I do a DNA test on my Collie? For breeding stock, yes. The Collie Club of America recommends testing for CEA, MDR1, and DM. Pet owners should know their Collie’s MDR1 status before any off-label parasite treatment or chemotherapy; label-dose heartworm prevention does not depend on it.

What should I avoid giving my Collie? High doses of ivermectin and related parasite drugs, if your Collie carries the MDR1 variant or has not been tested. Doses other dogs tolerate can cause severe neurological toxicity. Heartworm preventives at the label dose are the exception and are safe either way (Mealey 2008). Ask your veterinarian before any other use of those drugs.

How long do Collies live? Breed-club surveys and OFA data align on a median lifespan near 13.3 years (McMillan 2024 / VetCompass) for Collies (Collie Club of America health pages, collieclub.net). Breed-club estimates align with this range. Collies are generally considered a long-lived breed within the large-breed category.

What is the best diet for a Collie? A balanced, age-appropriate diet from a manufacturer that runs feeding trials. For puppies, prioritize controlled calcium and a calcium-to-phosphorus ratio of 1.1:1 to 2:1. Keep heartworm prevention at the label dose, which is safe whatever the MDR1 status (Mealey 2008). In middle age and beyond, maintain lean body condition to support joint health and potentially slow DM progression if your dog is at genetic risk.

Can Collies compete in agility or dock diving? Yes, with caveats. Collies are athletic and capable of competitive sports. However, if your Collie carries the Exercise-Induced Collapse variant (currently rare in the breed), intense sprinting or sustained high-intensity activity may trigger collapse. Genetic testing is available; most Collies are not carriers and can safely train intensively.

Do Collies need special grooming? Collies have a double coat that sheds heavily. Brushing several times per week is standard maintenance. Shedding intensifies during spring and fall coat blows. This is cosmetic, not health-related, but it is worth planning for if you are a new owner.

Names & origins

Identified as Collie (VBO:0200375) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs iDog 79 · VeNom 13879.

For researchers Population genetics, disease models and every recorded condition Open the research detail for the Collie
What the atlas says about Collie

In the atlas, the Collie clusters consistently as Collie (100% of the 20 dogs here). Dogs here sit in a relatively sparse region of the atlas, fewer close neighbors than typical.

Ranks 12 of 107 on the bottleneck severity scale, well into the upper quartile of population contraction. High breed predictability score (2.85), individual dogs of this breed reliably cluster together genetically. Only 20 dogs of this breed in the atlas, modestly sampled.

Genetic dimensions · CanVAS atlas

What the atlas genotypes say about Collie

Computed from the 14,478 CanVAS dogs in the Atlas, on an imputed genotype backbone: 77,215 directly typed sites per dog, imputed to 9.67 million variants.

The confidence below counts dogs, not reads: it is the size of the sample, and it is separate from how the genotypes were measured.

Dogs in the Atlas
20Founders
10 from Spatola, 10 from Hayward2016
Genetic diversity
0.24Tight
Mean heterozygosity across the breed. 12th tightest of 107 ranked populations.
What does genetic diversity mean?

How varied a breed's gene pool is — the share of gene spots where a typical dog of the breed carries two different versions rather than two identical ones.

How to read it: Higher = more diverse. Among well-sampled breeds it ranges roughly 0.22 (least diverse) to 0.33 (most diverse).

Diversity is a strength, not a verdict on any individual dog. Lower diversity means it's worth paying attention to recessive-risk testing — not that a dog is doomed.

Cluster structure
Single tight cluster
Intra-breed RMS distance: 24.54
What does within-breed variation mean?

How much individual dogs within the breed differ from each other genetically.

How to read it: Higher = more internal variety among individuals of the breed.

Sensitive to how many dogs of the breed we've sampled.

Related breeds
Gave rise to
In the Herding group
Explore the full lineage map →
VBO foundation stock (breeding records) · AKC breed group
Relatedness is documented lineage + kennel family. Genetic-ancestry distance measures diversity, not kinship, so it isn't used here.
How long they live
13.3years (life expectancy)
95% CI 13.3–13.6 · VetCompass, McMillan 2024, n=2,171. source
What does typical lifespan mean?

The median age dogs of the breed tend to reach.

How to read it: Higher = longer-lived. Compare to longevity-for-size to see whether it's just a size effect.

Drawn from population lifespan records; individual dogs vary widely with care, genetics, and luck.

n = 20 dogs · moderate sample · CanVAS (Brundage 2026) · Sniff Atlas
A gift to human medicine

Collies are a natural model for human disease

Because the same genes cause the same conditions across species, the inherited conditions documented in Collies help researchers understand, and work toward treating, the human diseases they model. This is the dog advancing human medicine. The breed models the human disease; it does not have it, and this is not a prediction for your dog.

Human equivalents via OMIA → Mondo / OMIM. Model-of, not identity. The named gene is the canine locus, not a claim that a pet has the human disease.
Documented in OMIA

Every condition recorded in the Collie

Beyond the testable carriers above, OMIA's literature catalogue records 10 genetic conditions in the Collie, 9 of which have a known human equivalent. This is the documented landscape across all Collies ever studied, not a prediction for any one dog.

Online Mendelian Inheritance in Animals (OMIA); Nicholas, Tammen & Sydney Informatics Hub, DOI 10.25910/2AMR-PV70
Documented in the breed's literature is not carrier status and not a forecast for an individual dog. Human equivalents are mapped via Mondo/OMIM. Carrier frequencies (above) are the separately-measured testable subset (Donner 2023).
The data behind this page

Where every number on this page came from.

This page draws on three primary data sources. Carrier frequencies for the Mendelian section come from Donner et al. 2023 (CC-BY-4.0). We grade these data at evidence Limited because the cohort is a direct-to-consumer ascertainment, which biases toward owners who chose to test their dogs. The panel also uses tag-SNP proxies for some variants rather than direct causal-variant assays. Limited is a study-design grade, not a quality grade: the Donner cohort is the largest open canine-genotype dataset in existence and we are grateful for it. We rate the confounding MEDIUM.

Population-genetic dimensions (heterozygosity, intra-breed PCA distance, nearest neighbors, trait-locus frequencies) come from CanVAS (Brundage 2026), harmonized through the Sniff Atlas. The exact release date and verification commit are pinned at the bottom of the page so a researcher can trace a number back to a specific snapshot. The disease-gene-variant graph comes from OMIA (Online Mendelian Inheritance in Animals; Nicholas, Tammen, and the Sydney Informatics Hub at the Sydney School of Veterinary Science, The University of Sydney; retrieved April 2026, DOI 10.25910/2AMR-PV70).

What this page does not yet have. Inheritance modes and per-disease penetrance evidence from Donner 2023 are in the structured data for every variant the panel covers. Mondo, OMIM, Ensembl, and HGNC cross-references live on the gene and disease pages this page links to, rather than being repeated here. What is still absent from this breed page is anything not in the cited panel, and each such gap carries its cause where it appears.

How to cite this page. The computed dimensions on this page are derived from the open Sniff Atlas v1.0.1 (Gehring 2026, doi:10.5281/zenodo.20566358, CC-BY 4.0). Full citation formats including BibTeX, RIS, and CITATION.cff at sniff.world/cite.

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References
  1. Donner J, Freyer J, Davison S, Anderson H, Blades M, Honkanen L, et al. (2023). Genetic prevalence and clinical relevance of canine Mendelian disease variants in over one million dogs. PLOS Genetics 19(2):e1010651. doi:10.1371/journal.pgen.1010651
  2. Brundage DM (2026). CanVAS: A Harmonized and Imputed Canine Variant Atlas. bioRxiv. doi:10.64898/2026.04.13.718238
  3. Nicholas, F.W., Tammen, I., & Sydney Informatics Hub. (2026). Online Mendelian Inheritance in Animals (OMIA) [dataset]. The University of Sydney. https://omia.org. doi:10.25910/2AMR-PV70 (retrieved April 2026).
Last updated
Sources: CanVAS (Brundage 2026) · Donner 2023 · OMIA