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Bullmastiff

Bullmastiff
Photo: Fausto Moreno / CC BY-SA 3.0 · Wikimedia

31 Bullmastiffs in the atlas. Every number on this page has a source.

Population-genetic snapshot of Bullmastiffs in the Sniff Atlas, source-graded Mendelian carrier frequencies from Donner 2023, and nutrition guidance tied to the genetic findings above.

The plain version

Bullmastiffs have a moderately diverse genetic background. They are large dogs, typically weighing around 110 pounds, and usually live about 10 years. Their look and size make them close relatives of breeds like the Staffordshire Bull Terrier and French Bulldog. No specific health concerns were found in their gene pool from the tests, but it’s always a good idea to check with your vet for personalized advice.

What the atlas says about Bullmastiff

In the atlas, the Bullmastiff clusters consistently as Bullmastiff (100% of the 31 dogs here). At the trait loci, SMOC2 runs lower than average (26% here vs 75%); FGF5 runs lower than average (16% here vs 64%). Dogs here sit in a relatively sparse region of the atlas, fewer close neighbors than typical.

High breed predictability score (1.36), individual dogs of this breed reliably cluster together genetically.

Genetic dimensions · CanVAS atlas

What the genome says about Bullmastiff

Computed from the 18,477 research dogs in the Atlas.

Dogs in the Atlas
31Founders
20 from Spatola, 11 from Hayward2016
Genetic diversity
0.29Moderate
Mean heterozygosity across the breed. Ranks 32nd most genetically tight of 107 ranked breeds.
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
Splits into two genetic sub-populations
Intra-breed RMS distance: 43.42 · likely working/show-line, regional, or kennel lineage split.
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
Built from
Gave rise to
Distant kin · one shared founding ancestor
In the Working 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
10.2years (life expectancy)
95% CI 9.9–10.5 · VetCompass, McMillan 2024, n=2,188. 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.

Trait genetics
Allele frequencies at named morphology loci

Frequency of the alternate allele in this breed at each locus's representative SNP.

Body size
IGF169%
HMGA224%
SMAD290%
LCORL100%
STC246%
ADAMTS1784%
Leg length
FGF4·CFA1890%
FGF4·CFA12100%
Coat
RSPO278%
FGF516%
KRT7179%
MC1R50%
Ear set
MSRB3100%
Skull shape
BMP3100%
SMOC226%
n = 31 dogs · moderate confidence · CanVAS (Brundage 2026) · Sniff Atlas
Names & origins

Identified as Bullmastiff (VBO:0200261) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs FCI 157 · iDog 59.

What you see when you look at a Bullmastiff

What does the genome say about how a Bullmastiff looks?

Bullmastiffs look the way they do because of a small set of fixed and near-fixed morphology genes that, taken together, define the visible breed. Each translation below pairs the gene with the trait an owner actually sees, the breed's allele frequency at that locus, and a one-clause causal phrase.

Where the breed-defining genes act, mapped on a generic dog-body key — and how fixed each marker is in the Bullmastiff. The figure is the most-settled marker we read in that region; the full per-locus panel is below. (The silhouette is a shared anatomical guide, not this breed's outline.)

Body sizeLCORL · 100%Skull shapeBMP3 · 100%EarsMSRB3 · 100%Leg lengthFGF4 CFA12 · 100%Coat & colorKRT71 · 79%
CanVAS trait-locus panel (Brundage 2026)
15 morphology markers read across 5 regions. Allele frequency = how fixed a marker is in this breed, not whether your dog carries it.

Size and build

IGF1 sits at 69% for the small-body allele. IGF1 is the gene that sets dog body size from Chihuahua to Great Dane. Intermediate frequencies typically keep a breed in the mid-sized range rather than tipping toward the larger working forms.

IGF1what this gene does

IGF1 is a gene that plays a key role in determining a dog's body size. It influences how much a dog grows, affecting overall stature.

For your dog: Knowing about IGF1 gives you insight into your dog's size traits, but it’s just one part of the bigger picture when it comes to their health and care.

Full IGF1 gene page →

HMGA2 is at 24%, leaving most of the size signal to other loci in the panel.

HMGA2what this gene does

HMGA2 is a gene that influences body size in dogs, helping determine how big or small a dog grows.

For your dog: Knowing about HMGA2 helps you appreciate the genetic factors behind your dog's size, but it doesn't signal any health issues.

Full HMGA2 gene page →

SMAD2 is near-fixed at 90%, a chromosome-7 height locus differentiating small from giant breeds.

SMAD2what this gene does

SMAD2 is a gene involved in regulating body size by influencing how cells grow and develop.

For your dog: Knowing about SMAD2 helps understand your dog's size traits but isn't linked to health issues; no immediate action needed.

Full SMAD2 gene page →

LCORL is near-fixed at 100%, the NCAPG/LCORL height locus that is one of the strongest single contributors to canine body size.

LCORLwhat this gene does

LCORL is a gene that influences body size in dogs. It helps determine how big or small a dog might grow.

For your dog: Knowing about LCORL helps you appreciate the genetic factors behind your dog's size, but it’s just one piece of the bigger picture when it comes to health and care.

Full LCORL gene page →

STC2 sits at 46%.

ADAMTS17 sits at 84%. ADAMTS17 is a body-size locus also linked to lens disorders.

ADAMTS17what this gene does

ADAMTS17 is a gene that influences body size and also plays a role in certain eye conditions. It affects the structure of tissues in the eye and elsewhere in the body.

For your dog: If your dog belongs to a breed known to carry ADAMTS17 variants, it’s worth discussing genetic testing and eye exams with your vet to stay ahead of potential issues.

Full ADAMTS17 gene page →

Leg length

The FGF4 retrogene on chromosome 18 is near-fixed in this breed at 90%. This is the leg-length variant. The breed is fully committed to the long-legged form rather than the short-legged Corgi-and-Dachshund body plan.

The FGF4 retrogene on chromosome 12 is near-fixed at 100%, the chondrodystrophic variant associated with intervertebral disc disease risk in breeds that carry it.

Coat type, length, and color

RSPO2 sits at 78% for the furnishings variant. Furnishings (the eyebrow-and-mustache pattern seen in Schnauzers and Wheaten Terriers) vary across the population at this intermediate frequency, and visible expression depends on the specific allele combination each dog carries.

RSPO2what this gene does

RSPO2 influences the texture and appearance of a dog's coat, particularly the presence of 'furnishings' like mustaches and eyebrows. It helps determine whether a dog has that distinctive wiry or textured look.

For your dog: If your dog has those wiry eyebrows or a mustache, RSPO2 is part of the reason—no health worries, just a coat feature worth knowing about.

Full RSPO2 gene page →

FGF5 is at 16% for the long-coat variant, which keeps the breed in the short-coated form.

FGF5what this gene does

FGF5 is a gene that influences the length of a dog's coat. It acts like a natural switch, telling hair follicles when to stop growing longer fur.

For your dog: If your dog has a notably long or short coat, FGF5 is likely part of the reason—no action needed, but it’s a neat genetic detail to know.

Full FGF5 gene page →

KRT71 sits at 79% for the wavy/curly variant. Coat curl varies across individuals at this intermediate frequency, and visible expression is also influenced by modifier loci.

KRT71what this gene does

KRT71 is a gene that influences the curliness of a dog's coat. It helps determine whether a dog's fur is straight or has a distinctive curl.

For your dog: If your dog has a curly coat, KRT71 is likely part of the reason; it’s a natural variation, not a health concern.

Full KRT71 gene page →

MC1R sits at 50% at the representative SNP. MC1R controls the switch between red-to-gold pigment and black-to-brown pigment, with the e/e homozygous genotype producing the gold-to-red spectrum. Substrate frequencies at this SNP depend on the array's polarity, so visible coat color in the breed is a more reliable indicator than this single number.

MC1Rwhat this gene does

MC1R is a gene that influences coat color in dogs, affecting how pigments are produced in the fur.

For your dog: Knowing about MC1R gives insight into your dog's coat color but doesn't relate to health issues.

Full MC1R gene page →

Ears

MSRB3 is at 100% for the drop-ear allele, the genetic basis of the breed's signature dropped ear set.

MSRB3what this gene does

MSRB3 is a gene involved in the development of ear shape and structure in dogs.

For your dog: Understanding MSRB3 helps explain why your dog's ears look the way they do, but it isn't linked to any health issues.

Full MSRB3 gene page →

Skull shape

BMP3 is at 100%, contributing to the breed's brachycephalic skull shape.

BMP3what this gene does

BMP3 is a gene that influences the shape of a dog's skull, particularly contributing to a shorter, broader head shape known as brachycephaly.

For your dog: If your dog has a broad, short skull, it's worth discussing with your vet how this might impact their health, even though BMP3 isn't directly tied to illness.

Full BMP3 gene page →

SMOC2 is at 26%, leaving the breed in the long-headed dolichocephalic form.

SMOC2what this gene does

SMOC2 influences the shape of a dog's skull, particularly affecting how flat or short the face appears.

For your dog: If your dog has a short nose, it's worth discussing with your vet how this trait might impact their health over time.

Full SMOC2 gene page →
Mendelian-disease genetics

What genetic diseases do Bullmastiffs carry?

From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), Bullmastiffs carry 4 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.

n = 209 dogs · 1 variant tested · OMIA:001444-9615 · omia.org →
BEST1what this gene does

BEST1 is a gene that helps maintain the health of the retina, the light-sensitive layer at the back of the eye. It plays a role in keeping the cells in the retina functioning properly.

For your dog: If your dog is from a breed known to carry BEST1 variants, it’s worth discussing retinal health with your vet, especially if you notice any vision changes.

Degenerative Myelopathy (DM)
Autosomal recessive (Incomplete penetrance)
low 2.2%
n = 209 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.

low 1.9%
n = 209 dogs · 3 variants tested · OMIA:000256-9615 · omia.org →
SLC3A1what this gene does

SLC3A1 is a gene that helps transport certain amino acids in the kidneys. It plays a key role in preventing the buildup of cystine, which can form stones.

For your dog: If your dog is from a breed known to carry SLC3A1 variants, it’s worth discussing cystinuria risks with your vet, especially if urinary issues arise.

n = 209 dogs · 1 variant tested · OMIA:002015-9615 · omia.org →
FAM20Cwhat this gene does

FAM20C is a gene that plays a key role in the mineralization of teeth, helping them develop properly and stay strong.

For your dog: If your dog is from one of these breeds, it's worth mentioning FAM20C to your vet when discussing dental care, but being a carrier doesn't mean your dog will have problems.

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: 209 dogs from the Donner 2023 cohort.

Which Mendelian variants matter most for Bullmastiffs?

The Mendelian-disease table above lists variants screened in 209 Bullmastiffs (Donner 2023). Four rise above the background noise of rare recessive carriers, though all are low-frequency in this breed.

Canine Multifocal Retinopathy 1 (CMR1)

Canine Multifocal Retinopathy 1 in Bullmastiffs is an autosomal-recessive retinal condition caused by variants in a gene discovered in Mastiff-related breeds. The condition has not produced a single phenotype-confirmed case in the Donner 2023 cohort of 209 Bullmastiffs. Retinal lesions are the canonical sign in affected breeds, but expression in Bullmastiffs remains unconfirmed. 9.1% of Bullmastiffs in the Donner cohort carry one copy of the variant (n=209).

No dogs in the phenotype-confirmed cohort expressed the disease, which suggests either incomplete penetrance or that homozygous affected individuals are rare enough that none appeared in the study sample. Testing is available through commercial DNA panels.

Degenerative Myelopathy (DM)

Degenerative Myelopathy in Bullmastiffs is an autosomal-recessive condition with incomplete penetrance that causes progressive spinal-cord degeneration, typically beginning with hind-limb weakness. Not every dog with two copies of the variant becomes clinically affected. 2.2% of Bullmastiffs in the Donner cohort carry one copy (n=209).

The low carrier frequency and incomplete penetrance mean DM is not a breed-wide concern. Testing is available and recommended for breeding stock if there is a family history.

Cystinuria Type I-A and Dental Hypomineralisation

Cystinuria Type I-A in Bullmastiffs is an autosomal-recessive condition that causes excess urinary cystine excretion and predisposes to bladder stones. 1.9% of Bullmastiffs carry one copy (n=209). Affected dogs are managed with diet and monitoring.

Dental Hypomineralisation in Bullmastiffs is an autosomal-recessive condition affecting tooth enamel formation. 0.24% carry one copy (n=209). Both conditions are sufficiently rare in the breed that they do not materially change breeding or screening decisions for most breeders.

How should I test my Bullmastiff?

A breed-specific panel from a CLIA-accredited lab covering CMR1, degenerative myelopathy, and cystinuria Type I-A provides the highest-yield screening for breeding stock. The carrier frequencies are low enough that testing is more useful as a genetic-transparency step than as a population-level risk mitigation.

What should I feed a Bullmastiff?

Bullmastiffs go from 1 pound at birth to 110 to 130 pounds at adulthood. The growth rate is so fast that the calcium-to-phosphorus ratio in the puppy formula is the single most important food decision an owner makes. Deviation from the optimal range during the first year of life increases the lifetime risk of orthopedic disease, and that damage is irreversible.

Large-breed puppy formulations are non-negotiable. The National Research Council’s 2006 nutrient standard for large-breed puppies specifies a calcium-to-phosphorus ratio between 1.1:1 and 2:1 (NRC 2006). Most adult and all-life-stage kibbles exceed this range. A Bullmastiff puppy fed adult kibble receives excessive calcium, which disrupts bone remodeling and predisposes to hip dysplasia, elbow dysplasia, and developmental orthopedic disease. Use a large-breed puppy formula from a manufacturer that runs AAFCO growth trials for large breeds.

Transition to adult food at 12 to 14 months, not 18 months. Bullmastiffs generally reach skeletal maturity by 12 to 14 months, earlier than the very largest breeds. Staying on puppy formula beyond 12 months risks overfeeding calories and calcium once growth has substantially slowed.

Weight management matters more in this breed than in most. The OFA reports hip dysplasia in Mastiff-related breeds at notable rates (ofa.org breed statistics). No published Bullmastiff-specific prevalence figure exists, but the breed’s size and structure place it in a higher-risk category. Adult-life leanness reduces the mechanical load on dysplastic joints and extends functional lifespan. Body condition scoring at every vet visit is the baseline.

The breed’s median lifespan from the atlas is 10.2 years, which is typical for a 120-pound breed. Senior-life feeding should shift toward joint support (glucosamine, adequate omega-3) and calorie restriction to prevent obesity-driven decline in the final years.

What we don’t know

The Bullmastiff atlas contains 31 dogs, one of the smallest cohorts in the dataset. That sample size is insufficient to detect rare Mendelian variants or to settle questions about disease prevalence beyond the four variants in the substrate. The breed’s true genetic architecture remains unmapped.

We do not yet know which Bullmastiffs in the 9.1% CMR1 carrier pool are at genuine risk for vision loss and which are silent carriers. The zero phenotype-confirmed cases in the study sample could mean either that the penetrance is genuinely low, or that the phenotype is subtle enough to have gone undetected in the dogs that were studied.

Cancer and dilated cardiomyopathy are reported in Bullmastiffs by individual breeders and veterinarians, but published prevalence data do not exist. The honest summary is that no breed-specific epidemiology has been published for either condition, so predicting risk or feeding to prevent it remains speculative for this breed.

Frequently asked questions about Bullmastiffs

How long do Bullmastiffs live? The atlas median lifespan is 10.2 years. Large-breed dogs age faster than small breeds, and Bullmastiffs are no exception. Lifespan varies, and the upper range for the breed is not well documented in published studies.

What is the most common genetic disease in Bullmastiffs? Canine Multifocal Retinopathy 1 is the most common genetic variant by carrier frequency, at 9.1% (Donner 2023, n=209). No phenotype-confirmed cases appeared in the study cohort, which means the condition is either very rare in expression or has low penetrance.

Should I do a DNA test on my Bullmastiff? For breeding stock, testing for CMR1, degenerative myelopathy, and cystinuria Type I-A is reasonable as a transparency measure. The carrier frequencies are low, but knowing your dog’s status prevents surprise carrier-by-carrier pairings.

Are Bullmastiffs good with kids? Bullmastiffs were originally bred to guard estates and have a protective temperament. Many are gentle with family children, but they are large, powerful dogs that require early socialization and supervision with small children. Breed-club resources emphasize that supervision is essential.

What is the best diet for a Bullmastiff puppy? A large-breed puppy formula with a calcium-to-phosphorus ratio between 1.1:1 and 2:1 is essential (NRC 2006). Adult or all-life-stage kibbles contain too much calcium for growing giant-breed puppies and increase the lifetime risk of hip and elbow dysplasia.

Do Bullmastiffs have breathing problems? Bullmastiffs are not brachycephalic like Bulldogs or French Bulldogs. They have normal muzzle proportions and do not typically have upper-airway obstruction. They are prone to overheating in warm weather and should not be exercised in heat.

What health conditions should I screen for before breeding? OFA hip and elbow screening before breeding is a standard recommendation for large breeds; check the Mastiff Club of America website (mastiff.org) for the current breed health protocol. The four Mendelian variants in the substrate (CMR1, degenerative myelopathy, cystinuria, and dental hypomineralisation) are each low-frequency, but a breed-specific DNA panel provides a baseline genetic transparency.

Are Bullmastiffs prone to bloat? Bloat (gastric torsion) is a risk in deep-chested, large-breed dogs and has been reported in Bullmastiffs. Feeding multiple small meals rather than one large meal, avoiding exercise immediately after eating, and knowing the signs of bloat (distended abdomen, unproductive retching, restlessness) are recommended precautions.

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 now in the structured data for every variant the panel covers. Mondo, OMIM, Ensembl, and HGNC cross-references on gene pages remain pending, they arrive in December 2026 alongside the imputed 9.67M-variant CanVAS dataset via the OMIA SQL dump absorption. Until then, gene IDs carry NCBI Gene and OMIA phene URLs only; the wider human-homolog and disease-ontology cross-reference set fills in with that release.

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 J, et al. (2026). CanVAS: a harmonized 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