Shiba Inu
Shiba Inus have a cited life expectancy of 14.6 years (McMillan 2024 / VetCompass, n=423, 95% CI 14 to 15.1). No carrier testing data for Shiba Inus has been read in yet. Only 16 dogs stand behind the atlas figures here, so little is known yet.
Also known as Japanese Shiba Inu, Japanese Small Size Dog, Shiba, and Shiba Ken.
Other names
The Shiba Inu is also recorded as Japanese Shiba Inu, Japanese Small Size Dog, Shiba, and Shiba Ken.
Identified as Shiba Inu (VBO:0201220) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs FCI 257 · iDog 217.
For researchers Population genetics, disease models and every recorded condition Open the research detail for the Shiba Inu
In the atlas, the Shiba Inu clusters consistently as Shiba Inu (100% of the 16 dogs here).
Only 16 dogs of this breed in the atlas, modestly sampled.
What the atlas genotypes say about Shiba Inu
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.
Not enough dogs in the atlas yet (n=16) for a reliable diversity figure. It fills in as more are added.
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.
Not enough dogs in the atlas yet (n=16) to resolve cluster structure. It fills in as more are added.
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.
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.
Shiba Inus are a natural model for human disease
Because the same genes cause the same conditions across species, the inherited conditions documented in Shiba Inus 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.
- GM1 gangliosidosis type 1, modeled by the breed's Gangliosidosis, GM1 via GLB1, the same underlying biology.
- Duchenne muscular dystrophy, modeled by the breed's Muscular dystrophy, Duchenne type via DMD, the same underlying biology.
- Sandhoff disease, modeled by the breed's Gangliosidosis, GM2, type II (Sandhoff or variant 0) , the same underlying biology.
- OMIM:256450, modeled by the breed's Hyperinsulinemic hypoglycemia , the same underlying biology.
Every condition recorded in the Shiba Inu
Beyond the testable carriers above, OMIA's literature catalogue records 5 genetic conditions in the Shiba Inu, 4 of which have a known human equivalent. This is the documented landscape across all Shiba Inus ever studied, not a prediction for any one dog.
- Gangliosidosis, GM1 Autosomal recessiveHuman equivalent: GM1 gangliosidosis type 1
- Muscular dystrophy, Duchenne type X-linked recessiveHuman equivalent: Duchenne muscular dystrophy
- Gangliosidosis, GM2, type II (Sandhoff or variant 0) Autosomal recessiveHuman equivalent: Sandhoff disease
- Human equivalent: OMIM:256450
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.
Some things about living with a shiba inu never make it into a database. Add what you know as a Keeper, in your words →
Lived experience, kept beside the science.We have 16 shiba inus. We do not have yours.
Every shiba inu added sharpens the breed's genetic neighborhood. Enrollment is free. The data stays open. The star is permanent.
- 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
- Brundage DM (2026). CanVAS: A Harmonized and Imputed Canine Variant Atlas. bioRxiv. doi:10.64898/2026.04.13.718238
- 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).