Curated from a recent article on TheLabradorSite.com
Health screening for Labrador diseases is important. It involves testing dogs to see whether they carry the genes for diseases which could cause them or their future offspring to suffer.
A good deal of research has gone into these Labrador diseases, much of it funded by the Kennel Club, AKC Canine Health Foundation, and the British Veterinary Associaton (BVA).
You can't assume that because you are purchasing a pedigree Labrador that they have undergone health testing.
Love's Labradors screens for Hip and Elbow Dysplasia, EIC, CNM and DM, Annual Eye Exams, Optical Refractory, Optigen DNA-PRA-prcd and RDOSD, and Heart.
A responsible breeder tests his/her dogs for autosommal recessive diseases which are evident in the breed, and only ever mates a 'carrier' (one parent has the gene, the other doesn't) with a dog that is 'clear'.
If you buy a puppy from untested parents and both happen to be carriers, a quarter of all their puppies will be affected puppies. If one parent is a carrier and one is affected, half the puppies will be affected. This is why it's so important to buy from a breeder who does health testing.
With the development of so many available tests, breeding from carriers is not only possible, it is actually a good thing because it helps to keep the gene pool healthy. Breeders can be sure to only breed carriers with clear dogs.
Why don't all Labrador breeders health test? Genetic testing is not cheap. By refusing to purchase a puppy who has untested parents, you can put pressure on breeders to do the testing.
Read more about the various tests by going to Health Screening for Labrador Diseases.
Curated from a recent article on Paw Print Genetics.com
The liver disease, copper toxicosis (CT) has become a hot topic among Labrador retriever breeders and dog owners with the arrival of a new genetic test which identifies two recently described mutations found in Labradors associated with opposite effects on the amount of dietary copper stored in the liver.
Copper toxicosis is an inherited metabolic disease affecting Labrador retrievers and other breeds, which can result in chronic liver failure. Dogs with copper toxicosis have a decreased ability to excrete dietary copper from the body resulting in excessive copper storage in tissues and organs, including the liver, which can result in liver damage, subsequent cirrhosis and the inability of the liver to function properly. In a study published in 2016 by Dr. Hille Fieten and colleagues in the journal, Disease Models and Mechanisms, increased liver storage of copper in Labrador retrievers was associated with a mutation in the canine ATP7B gene.
In contrast, a different mutation in the similarly named, but different gene, the ATP7A gene was found to significantly decrease liver copper storage and provide a protective effect against CT in dogs which had also inherited the ATP7B mutation. Dogs inheriting the ATP7A mutation in the absence of the ATP7B mutation, did not appear to be positively or negatively affected with regard to copper storage and the ability of the body to process copper.
When using the CT test results to make breeding decisions it is important to take into account the level of CT risk. Inheritance of the ATP7B gene mutation increases liver copper storage in an additive fashion. In other words, dogs inheriting two copies of the ATP7B mutation (one from each parent) are at greater risk of excess liver copper accumulation while dogs inheriting a single copy of the mutation (from one parent) have a lesser, but still significantly increased risk for the disease. It is important to note that the copper storage effect caused by the ATP7B mutation is more pronounced in female dogs than males, placing females with the ATP7B mutation at greater risk of developing CT. Both male and female dogs are protected, or have a dampening effect, against liver copper accumulation when they inherit the ATP7A “protective” mutation in combination with the ATP7B disease-causing mutation.
Given that only a fraction of dogs inheriting the ATP7B mutation will develop CT combined with the fact that the mutation appears common, we support a conservative approach to safely eliminating it from the population. In an effort to prevent loss of genetic diversity, we recommend keeping dogs with the ATP7B mutation in the breeding pool with the purpose of breeding them to dogs that are clear of the ATP7B mutation (regardless of their ATP7A mutation status). Using this practice limits the number of copies of the ATP7B mutation in offspring to one copy at most and keeps overall CT risk at a relatively low level while maintaining genetic diversity.
Read more about the Genetic Markers, the Breeding Strategies, and CT treatment in Casey Carl's Article here.