The Dalmatian Low Uric Acid Project had nearly reached extinction circa 2005 with only two remaining LUA Descendants available for breeding, and frozen semen on storage for only two LUA Descendant sires.  To address this, Denise Powell first employed a "gene conservation" breeding strategy, which simply stated was to rapidly and significantly increase the number of individuals carrying the dominant [U] gene.  The next step, "gene expansion" is intended to yield LUA Descendants carrying the dominant [U] gene in many different breeding lines or strains.

All of the LUA/HUA Descendant progeny from 2005 forward have undergone extensive health testing, including spot urine testing as puppies, DNA analysis (dewclaws), BAER hearing testing, and routine temperament and conformational analysis, as part of litter evaluations.  Since most of the Descendants are placed in pet homes, and are not AKC registered, they have not had further core health testing leading to CHIC registration.  Some individuals used in the breeding program have had OFA hip or CERF evaluations (data available upon request).

Typical records of coat color, eye color, patches, etc. are recorded and available through this website (see statistics page).  Ten LUA Descendant adults have undergone spot urine testing to determine their urinary uric acid to creatinine ratio and were found to maintain a six fold difference versus their recessive [uu] high uric acid AKC registered Dalmatian counterparts.  Four LUA Descendants have undergone bladder ultrasound and were found to be clear of "sludge".

It is important to note that the LUA/HUA Descendants produced from the "gene conservation" and "gene expansion" efforts are still young dogs - just over two years or less - at this time.  Their overall health and longevity are still being observed.  As of the date of this writing, none of the Descendants have exhibited symptoms or signs of urate stone disease.


During the roughly three decades of the "Backcross Project" preceding 2005, Dr. Robert Schaible persevered as a single breeder without national club support, and without AKC registration.  His breeding program was neither a scientific research program, nor funded by any resource other than by himself.  He was a hobby (but serious) Dalmatian breeder working within parameters typical of a hobby kennel.  To his credit, he rigorously tested the progeny of each litter by spot urine testing to determine LUA or HUA status, and additionally, he maintained both a database and a blood & serum sample library in anticipation of future testing.

The blood samples and pedigree information were provided to Dr. Danika Bannasch at the University of California at Davis for DNA analysis that led to the identification of the single gene responsible for the Dalmatian breed specific uric acid defect.  Dr. Bannasch's retrospective analysis of Dr. Schaible's pedigree and parentage data, and her correlation to his spot urine testing records, revealed that zero mistakes had been made.  The DNA test results confirmed a 100% accuracy of the pedigree and urine testing records.

Other health records and longevity data followed typical patterns of a hobby breeder.  Many health testing methods available today, such as OFA, CERF, BAER, etc, were either not available, or not widely implemented in the early days of the Backcross Project.  Further, working essentially alone, it was not possible for Dr. Schaible to keep every individual puppy within his own kennel.  Instead, typical of most hobby breeders, he kept the individual(s) from a given generation that he intended to breed into future generations, and placed as pets the littermates.  Again, as is the common experience of most hobby breeders, those pet placement families love and cherish their dog, but they do not feel an inordinate responsibility over the decade or so of its life to keep in close touch with their breeder.

Some records and recollections are available.  For example, Dime - the Pointer sire that was used in the initial Dalmatian Pointer Cross - was reported to be free of any dominant health defects, to have remained healthy during his lifespan, and to have lived until old age when he expired.  Lady Godiva similarly lived a healthy life, produced six litters the last of which was whelped when she was ten years old, and died of old age.  An excerpt from Dr. Schaible's personal report is illustrative:

"I raised three litters from Lady Godiva: one by a homozygous merle Collie for pigmentation studies, one by Chuck-A-Luck for show and purebred breeding and one by Rapid Transit to introgress the normal uric acid allele into the Dalmatian breed.  After that I gave her to my feed dealer who raised and showed Appaloosa horses.  She had at least three more purebred litters,  the last when ten years old.  The feed dealer said that she went down in the rear but could still move fast enough to catch and kill chickens!   Lady had an excellent pedigree, being from the last litter bred by Dr. Robert Knowles, Dapplewhite Kennels and Stables, but was not show quality (too heavily spotted, low tail set, but well angulated front and rear)."   --Robert Schaible, PhD to Irvin B. Krukenkamp, MD December 18, 2007.


One and only one AKC registered Champion Pointer was used to form the Dalmatian Pointer cross to introduce the canine dominant normal uric acid gene [U].  As far as can be determined, Dime - the Pointer - was healthy, and specifically did not exhibit any known or outwardly recognizable health defects.

Those individuals concerned whether this one Pointer may introduce untoward health problems in the Descendants of the Dalmatian Pointer cross may consider the following reasoning why that should not be a significant concern.

1. Since only one Pointer was used, that individual contributed only one gene copy (of his two copies) to his Descendants.  The other gene copy for any trait, healthy or unhealthy, originated from the Dalmatian dam (Lady Godiva).  As they say, "it takes two to tango".  If the gene from the Pointer coded for a dominant health problem then all of the progeny would exhibit that.  Neither the Pointer nor the progeny are reported to have exhibited any dominant health problems.  If the Pointer carried and contributed a recessive gene to his progeny, then again, "it takes two to tango" and the other copy must have come from the Dalmatian lineage, especially since in subsequent generations only Dalmatians were used.  The resultant "disease" if evident (none have been evident to date after 12 generations of breeding) would have originated just as equally, if not more likely, from the Dalmatian than the Pointer parental lineage.

2. Of the ~350 known canine diseases, the large majority exhibit a polygenic inheritance pattern.  A few diseases, like the Dalmatian specific uric acid defect, follow a single gene inheritance pattern.  After 12 generations of breeding, it is known that about 0.02% of the DNA of the Dalmatian Pointer Cross Descendants is not the same as AKC registered Dalmatians.  We know that this small percentage includes three genes on chromosome #3 that are closely linked, and one of those is responsible for normal uric acid metabolism.  The others are thought to be so-called housekeeping genes that deal with intracellular processes only.  The selection pressure placed by the breeder's choices over the 12 generations selected for these three closely linked genes, and not others.  Whether the residual DNA even codes for other genes, and whether those genes may or may not code for health problems per se, is unknown.  However, the likelihood that this small amount of residual Pointer DNA codes only for a unique Pointer breed related disease is quite low.  If that were the case, the disease would either have to be dominant (which is extremely unlikely as discussed in #1), or the disease would have to be recessive, in which case the Dalmatian lineage would have had to contribute the other genetic component.

3. Current Descendants of the Dalmatian Pointer Cross are at the 12th generation.  In the 12th generation, the Pointer is one of 4,096 dogs, thereby contributing 0.0244% of the genetic material in that generation to the next generation - the 11th generation.  From the perspective of the entire 12-generation pedigree, the Pointer is one of 8,190 dogs and contributes 0.0122% of the genetic material to the progeny.  These percentages appear miniscule when framed in comparison to the sire and the dam of a litter that each contributes 50% of their genetic material to their get.

4. If the Pointer were carrying a recessive health defect, and if the  LUA/HUA Descendants carried that defect forward, then the only way that it could be expressed is by breeding a Descendant to another carrier.  If breedings in successive generations only to AKC registered Dalmatians produced a recessive defect or disease, then it is at least equally attributable that the recessive trait originated from the Dalmatian parental lineage, if not more so given the overwhelming percentage of AKC Dalmatians in the pedigree versus the single Pointer.

5. Breeding an LUA Descendant to an LUA Descendant is one theoretical way to uncover a recessive gene carrier.  Again, only one Pointer was used, so you would have to theorize that the Pointer contributed the exact same recessive gene copy to every one of his get.  That may or may not be true.  If one used identical twins (which have never been produced) it is theoretically possible to have the exact same copy culprit recessive gene passed to the get.  The mathematical probabilities become even more unlikely when one considers that most canine diseases result from multiple genes - polygenic inheritance.  The same Pointer - the only Pointer ever used - would have had to contribute the exact same copy (recessive, diseased) of each of the genes responsible for a specific health defect, to each of his get, and those get would have to be mated in order to make the homozygous condition to produce the disease.  The odds are extremely unfavorable for that to happen.  Such a mating has never been done.

6. Matings of 12th generation LUA Descendants to produce the 13th generation LUA progeny, even if done as LUA x LUA, puts the Pointer as 1 of 16,382 dogs and results in 0.006% of the genome originating from the Pointer.  The likelihood of passing any relevant genetic material that may cause disease from the Pointer is approaching zero in this scenario. If one gene (out of the estimated 20,000 canine genes) spontaneously mutated and caused disease, the chance could be estimated as 1 in 20,000 or 0.005%.  Thus if an unanticipated disease presents in the 13th generation (or higher) Descendants, the attribution could be equally argued to be the Pointer, spontaneous mutation, or chance alone.

7. Lastly, it is important to point out that LUA/HUA Descendants at the 12th generation may have significant common ancestor effects.  Depending on the pedigree, there can be as many as 50 crosses to popular sires such as CH. Coachman's Chuck-A-Luck and CH. Count Miquel of Tuckaway.  From the perspective of estimating probabilities on pedigree analysis of specific traits (healthy or unhealthy), these popular ancestors may have up to a 50 fold chance of impacting that trait than a single ancestor, or in particular the single Pointer that is 12 or more generations back in the pedigree.

The national Pointer breed club has recently completed a national health survey and when those results are available they will be posted on this website as well.


Three decades of breeding have produced numerous boxes of records maintained by Dr. Schaible.  He has indicated his willingness to share these data with the LUA Study Group.  As these data are reviewed, tabulated, and cross-checked, they will be made public through this website.  The review, correlation and interpretation of 30 years of breeding records is not a small task however, so the LUA Study Group kindly requests indulgence and **patience** while this work is being done.