The Challenge of Breeding Healthy Dogs
- Jul 16
- 13 min read
When Veterinary Experts Disagree – What Does This Mean for Breeders?
Most dog breeders are women, and many have devoted years—often decades—of their lives to their breeding programmes. Breeding takes time, patience and passion. More often than not, they work alone. Their dogs are not simply breeding animals; they are members of the family.
That is precisely why it is so difficult when a genetic test suddenly delivers an unexpected result. A geneticist tells you:
"Your dog carries a mutation."
From that moment on, the breeder has to make a decision. When it comes to decisions that affect the future of my breeding programme, I need more than opinions. I need reliable scientific evidence. But how can I make an informed decision when scientists themselves interpret the very same data differently?
So I began looking for answers.
Come with me into this scientific jungle.
One warning, though: it requires patience.
How should genetic findings be evaluated under animal welfare law in the future?
Ultimately, this interpretation rests with the competent veterinary authorities responsible for enforcing the legislation. It is precisely at this intersection of science and law that a debate has emerged among veterinary experts—a debate that is likely to have far-reaching consequences for dog breeding.
For me, this issue is personal.
One of my stud dogs tested heterozygous positive for CDDY.
CDDY (Chondrodystrophy) is a genetic variant that affects cartilage and bone development and, in certain breeds, is associated with an increased risk of intervertebral disc disease (IVDD), most notably in the Dachshund. However, its clinical significance depends on the breed and cannot be inferred from a DNA test alone.
My dog shows no clinical signs whatsoever. He is an athletic Dansk–Svensk Gårdshund, measuring approximately 38/39 cm at the withers. Orthopaedic examination is entirely unremarkable. He has no neurological deficits, no clinical evidence of spinal disease, and radiographic examination reveals no signs of intervertebral disc pathology. At least that was my own perspective ....
Suddenly, I found myself asking a question that many conscientious breeders have probably asked themselves:
What does this genetic result actually mean?
Does a positive DNA test automatically mean that a dog should no longer be bred?
Or should science offer more than simply identifying the presence of a genetic variant?
I wasn't looking for opinions.
I wanted to understand.
So I immersed myself in the scientific literature.
I read breeding strategies, peer-reviewed publications, position papers and official guidelines.
To my great surprise and gratitude, Professor Danika Bannasch from the University of California, Davis, even took the time to answer several of my questions personally. she also generously proofread the manuscript and verified the scientific accuracy of its content prior to publication.
The deeper I explored the subject, the more I realised just how complex it really is.
Scientific evidence, legal interpretation, breeding policy and political considerations all intersect—and experts frequently arrive at different conclusions despite evaluating the same scientific data.
CDDY – What the Scientific Literature Actually Says
CDDY (chondrodystrophy) is a genetic variant associated with an increased risk of intervertebral disc disease, particularly in strongly chondrodystrophic breeds such as the Dachshund.
The situation in the Dansk-Svensk Gårdshund, however, appears considerably more nuanced according to the currently available scientific evidence.
The CDDY allele occurs relatively frequently within the breed.
At the same time, the Swedish Kennel Club's official Breed-Specific Breeding Strategy (RAS) explicitly states that insurance data have not demonstrated an increased incidence of intervertebral disc disease in the Dansk-Svensk Gårdshund.
The frequently cited publication by Professor Danika Bannasch's research group illustrates equally well how carefully scientific findings must be interpreted.
The study included six Dansk-Svensk Gårdshunde: five clinically healthy dogs and one dog affected by intervertebral disc disease.
Both the affected dog and one clinically healthy dog each carried a single copy of the CDDY allele.
From these observations alone, no clear cause-and-effect relationship can be established for this breed.
For precisely this reason, the Swedish Kennel Club does not recommend excluding all CDDY carriers from breeding. Instead, it recommends breeding carriers only to genetically clear dogs and testing the offspring.
The objective is to reduce the frequency of the allele over time while preserving valuable genetic diversity.
This Is Where the Real Debate Begins in Germany
As I continued reading, I came across two publications that could hardly be more different.
On one side stands the Task Force Healthy Dog Breeding, an interdisciplinary group of geneticists, veterinarians and scientists from various fields.
Their objective is to translate scientific knowledge into practical guidance for breeders and veterinary professionals.
I find this approach convincing.
Science should not provide simplistic answers.
Its purpose is to support well-informed decision-making—particularly where no simple answers exist.
The central message of the Task Force guideline, "CDDY/CDPA – Responsibly Considering Genetic Variants in Dog Breeding," is therefore not the individual gene.
Its focus is the population. The key principle is straightforward:
Healthy populations are not created by excluding as many genetic carriers as possible from breeding. Healthy populations are created by managing genetic risks responsibly while preserving genetic diversity.
This population-genetic approach has formed the cornerstone of modern conservation breeding for many years. Yet it is precisely here that the controversy begins.
This population-based approach, however, is challenged by an Open Letter addressed to the German Federal Chamber of Veterinary Surgeons (Bundestierärztekammer), initiated by Professor Achim Gruber and supported by numerous board-certified veterinary specialists as well as representatives of the public veterinary authorities.
The authors explicitly caution against adopting the recommendations of the Task Force as a model for other dog breeds.
In their view, a population-genetic approach is not an appropriate foundation for future breeding recommendations and could create substantial difficulties in the practical enforcement of Section 11b of the German Animal Welfare Act.
This illustrates an important point.
The debate is not about whether dogs should be healthy.
Both sides share that objective.
The difference lies in how that objective should be achieved.
The Task Force approaches canine health from the perspective of population genetics.
The Open Letter evaluates the same scientific evidence primarily through the lens of animal welfare legislation and regulatory enforcement.
To me, this is the true heart of the debate.
It is no longer simply about CDDY.
It is about the future role that scientifically sound population genetics will play in responsible pedigree dog breeding.
Why This Development Made Me Rethink My Position
Hardly any dog breed is completely free from inherited genetic variants.
Almost every breed carries recessive mutations or genetic variants associated with certain diseases.
Many of these variants will never result in clinical disease.
Others have only low penetrance.
Still others—such as CDDY—may have a very different clinical significance depending on the breed.
That is precisely why population genetics is so important.
It does not evaluate individual genes in isolation.
It evaluates the population as a whole.
Every breeding decision changes the genetic makeup of a breed.
Population genetics does not mean accepting inherited disease.
It means reducing disease without destroying the genetic diversity that is essential for the long-term health and sustainability of a breed.
So What Should I Do With My Dog's Test Result?
Veterinary experts disagree.
Breeding restrictions are being discussed.
I was confused.
Whose advice should I follow?
The Task Force for Healthy Dog Breeding, including the internationally respected neurologist Professor Holger Volk?
Or the group around Professor Achim Gruber, whose recommendations are increasingly influencing the political and regulatory discussion?
Looking for clarity, I contacted Professor Dr Danika Bannasch once again.
Professor Dr Danika L. Bannasch, veterinary geneticist at the University of California, Davis, is internationally recognised as one of the leading experts in canine genetics.
Her research group played a pivotal role in identifying the FGF4 retrogene on chromosome 12, the genetic variant responsible for CDDY and its association with intervertebral disc disease.
Fortunately for me, she responded.
Her assessment of CDDY in the Dansk-Svensk Gårdshund gave me an entirely new perspective.
Prof Dr Danika Bannasch
Personal communication with the author, July 2026. Translated from English.
"CDDY causes all intervertebral discs to be abnormal. They are hard and no longer provide their normal cushioning function. This was demonstrated by Hansen in the 1950s across many different breeds. We later confirmed these findings in Nova Scotia Duck Tolling Retrievers."
(The "we" refers to Murphy, Dickinson, Bannasch and their co-authors.)
The publication she referred to was:
Murphy BG et al. (2019).
Pathologic Features of the Intervertebral Disc in Young Nova Scotia Duck Tolling Retrievers Confirms Chondrodystrophy Degenerative Phenotype Associated With Genotype. Veterinary Pathology.
This study provides some of the strongest histopathological evidence currently available that the FGF4 retrogene on chromosome 12, associated with CDDY, alters the structure of the intervertebral discs from a very early age.
The researchers examined four Nova Scotia Duck Tolling Retrievers:
two dogs homozygous for the CDDY-associated retrogene;
two genetically normal (wild-type) control dogs.
The affected dogs were 10 weeks and 31 months old.
The two control dogs were 7 weeks and 10 weeks old.
Despite the young age of one affected puppy, the investigators already observed profound pathological changes.
The nucleus pulposus—the soft, gelatinous centre of the intervertebral disc—had largely been replaced by cartilage.
Normal notochordal cells had almost disappeared.
The tissue already showed unmistakable signs of early chondroid degeneration.
These microscopic findings explain why Danika Bannasch and Brian Murphy repeatedly emphasise that CDDY alters the biology of the intervertebral discs long before a dog develops clinical symptoms.
Importantly, however, the study does not demonstrate that every CDDY-positive dog will inevitably develop a clinically significant disc herniation.
Rather, it shows that the discs are already histologically altered early in life when the CFA12 FGF4 retrogene is present.
Whether a dog later develops clinically apparent intervertebral disc disease (IVDD) or intervertebral disc extrusion (IVDE) depends on additional genetic, anatomical, biomechanical and environmental factors.
Professor Bannasch also clarified an important point that many breeders—including myself—often misunderstand.
Prof Dr Danika Bannasch
Personal communication with the author, July 2026. Translated from English.
"This is IVDD—intervertebral disc disease. What you and many breeders actually want to test for is IVDE, intervertebral disc extrusion. More specifically, you are trying to identify dorsal disc extrusion, where disc material enters the spinal canal and compresses the spinal cord, resulting in acute neurological signs. There is currently no predictive test for that. Disc extrusion is a biomechanical consequence of discs that have become hard and abnormal because of CDDY. In the Bianchi study we demonstrated that Nova Scotia Duck Tolling Retrievers that appeared clinically normal nevertheless had disc extrusions. Their discs were hard, disc material had extruded, and they were very likely experiencing pain at the time this occurred."
Reading this changed my own understanding considerably.
I realised that CDDY is not merely a DNA test result.
It represents a biological change within the intervertebral discs themselves.
I also realised that the likelihood of a clinically significant disc extrusion associated with pain or neurological deficits may be higher than I had previously appreciated.
At the same time, Professor Bannasch made another important point.
At present, there is no diagnostic test that can reliably predict whether, when or where a clinically normal dog will later experience a clinically relevant disc extrusion.
Once an extrusion has occurred, it can be diagnosed using advanced imaging techniques such as CT or MRI.
But conventional radiographs cannot reliably detect or exclude it.
What About the Future of My Breeding Programme?
That left me with one obvious question.
What happens to valuable genetic material if we remove every CDDY-positive dog from breeding?
To begin answering that question, I looked at the publicly available data from Wisdom Panel / MyDogDNA.
The figures for the Dansk-Svensk Gårdshund are particularly interesting.
The database reports:
48 heterozygous dogs
4 homozygous dogs
This tells us that the CDDY-associated variant occurs regularly within the tested Wisdom population of the breed.
Among the genetic variants listed for the Dansk-Svensk Gårdshund, CDDY has one of the highest reported allele frequencies—considerably higher, for example, than Primary Lens Luxation (PLL).
The reported allele frequency is 13.5%.
Based on the published genotype counts, approximately 52 dogs in the dataset carried the variant, representing roughly 25% of the tested dogs.
It is important to understand what this number actually means.
It represents the genotype prevalence within this selected sample.
It is not the prevalence of intervertebral disc disease within the breed.
Nor does it mean that 25% of Dansk-Svensk Gårdshunde will develop IVDD.
The sample itself is relatively small.
Wisdom reports the number of tested dogs only as a category of 100–499 animals.
Using the published genotype counts and allele frequency, the actual sample size can be estimated at approximately 200 dogs.
Nevertheless, this remains only a subset of the global breed population.
The dogs were voluntarily submitted for DNA testing, which means the dataset may be influenced by geographical and breeding-related sampling bias.
An Interesting Comparison
Despite these limitations, the Wisdom data correspond surprisingly well with observations published by Bannasch and colleagues.
Compared with highly chondrodystrophic breeds, the Dansk-Svensk Gårdshund appears to have a low to moderate frequency of the CDDY-associated FGF4 retrogene.
An allele frequency of approximately 13–14% is substantially lower than that reported for several strongly chondrodystrophic breeds, where frequencies exceeding 80%, or even approaching fixation, have been described.
This distinction is important.
When a genetic variant is nearly fixed within a population—that is, present in almost every dog—excluding every carrier from breeding would remove a large proportion of the breeding population and could severely reduce genetic diversity.
That is one of the central arguments put forward by the Task Force and many population geneticists.
But does the same argument apply to breeds with a much lower allele frequency, such as the Dansk-Svensk Gårdshund?
I asked Professor Dr Bannasch exactly that question.Her answer was concise.
Prof Dr Danika Bannasch
Personal communication with the author, July 2026. Translated from English.
"The Dansk-Svensk Gårdshund has exceptionally high genetic diversity. It is therefore relatively easy to reduce the frequency of a dominant mutation through targeted breeding."
That statement made me reconsider the TGH recommendations as well the Open letter from a different perspective.
A single breeding strategy cannot automatically be applied to every breed.
In breeds where the retrogene is almost fixed, immediately excluding every positive dog from breeding may dramatically reduce genetic diversity.
In a breed with a comparatively low allele frequency and broad genetic diversity—such as the Dansk-Svensk Gårdshund—a carefully planned breeding strategy may allow a much more decisive reduction of the variant without compromising the genetic health of the population.
In other words, one size does not fit all.
What may be appropriate for a Dachshund is not necessarily the right solution for a Dansk-Svensk Gårdshund.
A View From Clinical Practice
To help explain why this discussion has become so emotional among veterinary specialists, I would like to conclude with one final quotations sbd told me:
"You have to understand what veterinarians see every day. My hospital treats dogs with CDDY-related disease every single day. Nothing has changed in the nine years since the cause of CDDY was discovered. Dogs still arrive screaming in pain following catastrophic disc herniation. Contrary to popular belief, most of our patients are not Dachshunds. The treatment of CDDY-related intervertebral disc disease has become a billion-dollar industry."
Those words had a profound impact on me.
Until then, I had not fully appreciated the biological significance—or the clinical consequences—of these findings.
What I take away from this debate is not that one side is right and the other wrong.
Rather, I have come to realise that the current public disagreement between regulatory veterinary authorities and the Task Force cannot be resolved by applying a single rule to every breed.
What may be appropriate for a breed in which the mutation is almost fixed cannot automatically be applied to a genetically diverse breed with a much lower allele frequency.
The Dansk-Svensk Gårdshund still possesses remarkable genetic diversity.
Responsible, population-based breeding management offers the opportunity to preserve that diversity while gradually reducing the frequency of the CDDY-associated variant.
As a breeder, that is the path I can follow.
Let's do it—for the dogs.
Thank you for taking the time to read what is admittedly a highly technical subject—but one that I believe is of enormous importance.
References
Open Letter of the Veterinary Profession. (2026). How Much Animal Suffering Is Acceptable to Preserve Breed Characteristics? Faculty of Veterinary Medicine, Freie Universität Berlin, 1 July 2026.
This position paper argues that breeding practices should prioritize animal health over breed-specific conformation traits where these are associated with hereditary disease. Referring to the revised German Animal Welfare Act and current scientific literature, the authors advocate a stricter interpretation of breeding regulations and recommend limiting the use of dogs carrying genetic variants associated with inherited disorders, including the FGF4 retrogene (CDDY) where considered relevant. The document represents a professional policy statement rather than original peer-reviewed research.
Healthy Dog Breeding Task Force. (2026). Chondrodysplasia, Chondrodystrophy and Hereditary Increased Risk of Intervertebral Disc Disease. Healthy Dog Breeding (TGH), Guideline, 15 April 2026.
This evidence-based guideline reviews the current scientific knowledge on the FGF4 retrogenes responsible for chondrodysplasia (CDPA, CFA18) and chondrodystrophy (CDDY, CFA12). It concludes that CDPA is not associated with an increased risk of intervertebral disc disease (IVDD), whereas CDDY represents a genetic risk factor for IVDD in some, but not all, dog breeds. The guideline emphasizes that IVDD is a multifactorial disease influenced by additional genetic and environmental factors, and recommends breed-specific breeding strategies, radiographic screening where appropriate, preservation of genetic diversity, and avoidance of excluding dogs from breeding solely on the basis of their CDDY genotype. It further calls for prospective breed-specific studies to better quantify the clinical significance of the CDDY allele.
Brown, E.A., Dickinson, P.J., Mansour, T., Sturges, B.K., Aguilar, M., Young, A.E., Korff, C., Lind, J., Ettinger, C.L., Varon, S., Pollard, R.E., Penderis, J., Garosi, L., Shelton, G.D., Rusbridge, C., Vernau, K.M., Drögemüller, M., Drögemüller, C., Leeb, T., Bannasch, D.L. (2017). FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs. Proceedings of the National Academy of Sciences of the United States of America (PNAS), 114(43), 11476–11481. https://doi.org/10.1073/pnas.1709082114
This landmark study identified the FGF4 retrogene insertion on canine chromosome 12 (CFA12) as the genetic variant responsible for chondrodystrophy (CDDY) and strongly associated with intervertebral disc disease (IVDD), reporting an odds ratio of 51.23 for IVDD.
Batcher, K., Dickinson, P.J., Giuffrida, M.A., Sturges, B.K., Vernau, K.M., Knipe, M.F., Rasouliha, S.H., Drögemüller, C., Leeb, T., Maciejczyk, K., Jenkins, C.A., Mellersh, C.S., Bannasch, D.L. (2019). Phenotypic Effects of FGF4 Retrogenes on Intervertebral Disc Disease in Dogs. Genes, 10(6), 435. https://doi.org/10.3390/genes10060435
This study investigated the phenotypic effects and breed distribution of the CFA12 FGF4 retrogene, reporting CDDY allele frequencies ranging from 0.02 to 1.00 among different dog breeds.
Murphy, B.G., Dickinson, P.J., Marcellin-Little, D.J., Batcher, K., Raverty, S., Bannasch, D.L. (2019). Pathologic Features of the Intervertebral Disc in Young Nova Scotia Duck Tolling Retrievers Confirm a Chondrodystrophic Degenerative Phenotype Associated with FGF4 Retrogene Genotype. Veterinary Pathology, 56(6), 886–894. https://doi.org/10.1177/0300985819852128
This pathological study confirmed premature intervertebral disc degeneration associated with the CFA12 FGF4 retrogene genotype in young Nova Scotia Duck Tolling Retrievers.
Bannasch, D.L., Batcher, K., Leuthard, F., Bannasch, M., Hug, P., Marcellin-Little, D.J., Dickinson, P.J., Drögemüller, M., Drögemüller, C., Leeb, T. (2022). The Effects of FGF4 Retrogenes on Canine Morphology. Genes, 13(2), 325. https://doi.org/10.3390/genes13020325
This study distinguished the effects of the CFA12 (CDDY) and CFA18 (CDPA) FGF4 retrogenes. One copy of the CFA12 retrogene reduced limb length by approximately 6%, while two copies resulted in an average reduction of about 10%. Unlike the CFA18 retrogene, the CFA12 variant is additionally associated with susceptibility to intervertebral disc disease.
Olby, N.J., Batcher, K., Dickinson, P.J., Bannasch, D.L., et al. (2020). Current Understanding of the Genetics of Intervertebral Disc Degeneration. Frontiers in Veterinary Science, 7, 431. https://doi.org/10.3389/fvets.2020.00431
This review summarizes the current understanding of the genetics of canine intervertebral disc degeneration. It emphasizes that prospective longitudinal studies are still needed to accurately quantify the clinical IVDD risk associated with the CFA12 FGF4 retrogene, particularly in breeds with very high allele frequencies such as Dachshunds, Beagles, and French Bulldogs.
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