Error Of the Millenium In Veterinary Medicine

The background: Diseases of the musculoskeletal system in dogs have been a considerable veterinary problem for decades. Statistics compiled by the canine science associations indicate that 70-75% of the entire canine population are affected. More than half of the dogs of all breeds exhibit pathological changes, especially of the acetabulum and femur, known as hip dysplasia (HD) or canine hip dysplasia (CHD). The etiological or causal background to canine hip dysplasia has hitherto generally been assumed to be multifactorial heredity. This term originates from farm and slaughter animal breeding and postulates that not only heredity but also environ-mental factors - especially nutrition - play a role in determining characteristics. The relative importance of these factors is expressed as the degree of heritability. For CHD, percentage values of up to 60 % have been assumed or, with reference to 1, of 0.2 to 0.6.

The dog breeding associations in the United States, United Kingdom, France and Germany developed X-ray systems designed to detect and combat hip dysplasia. But only in Germany and several other European countries was it attempted to eliminate CHD through selection, by excluding the dogs exhibiting this condition from breeding in the populations of the different breeds. These genetic measures, however, proved fruitless over a period of three decades. The Verband für das Deutsche Hundewesen (VDH) (German Kennel Club) failed in its attempts to gain approval for this initiative from the American Kennel Club (AKC), The Kennel Club (KC) or the Société Centrale Canine (SCC) in France. The incidence of hip dysplasia still persists at around 60-65 % in all the canine populations of the Western countries. When other pathological changes are included, the total skeletal morbidity rate is as high as 70-75 %. In most cases HD is accompanied by other skeletal diseases.

Veterinarians in the Western countries have traditionally advocated a "balanced diet" - without specifying further details - and have left it to the animal foodstuffs industry to provide dogs with "optimized complete diets". At present, around 80-85% of the total canine population is being fed completely or partially with industrially manufactured preformulated food, which has consequently become accepted as "healthy dog food". These new feeding methods, however, have been unable to significantly improve morbidity in terms of canine hip dysplasia. Indeed, there is also a very high total morbidity level of numerous nutritional diseases affecting various organ systems.

Marc Torel and Klaus Dieter Kammerer - a veterinarian and a scientific journalist with medical training - believe that breeding programs and industrially produced dog food in its present form cannot hope to bring about any fundamental improvements in the incidence of canine hip dysplasia because CHD is not heritable and because existing dog food does not prevent, but is in fact the original cause of CHD. In these authors' view, canine hip dysplasia is induced solely by malnutrition.

In 1996, the respected German journal "Tierärztliche Umschau" (TU) (Veterinary Review) published the continuation article "Topical notes on canine hip dysplasia" by Marc Torel and Klaus Dieter Kammerer, in which these authors traced the entire history of the development of canine hip dysplasia. They claimed that the hereditary nature of CHD had never been conclusively proven and is not supported by any objective evidence, and that breeding programs over three decades were thus inevitably doomed to failure (Tierärztliche Umschau, Volume 51, pp. 455 ff., 1996).

In the opinion of Torel/Kammerer, everything points to the probability that CHD has an alimentary/hormonal etiology and pathogenesis associated with malnutrition and increased production of somatotropin, triiodothyronine (T3), thyroxine (T4), parathormone and insulin-like growth factor IGF-I in the canine organism. The authors went on to draw conclusions regarding the nutrition and keeping of dogs and gave recommendations for the prevention of their skeletal diseases. The essence of their argument is that CHD is of nutritional and hormonal origin. Malnutrition causes increased production of growth hormone, the thyroid hormones tri-iodothyronine and thyroxine, parathormone and insulin-like growth factor in dogs. The authors give a detailed analysis of the malnutrition and its adverse skeletal effects.

The book aroused great interest among veterinarians and met with a worldwide response. The authors and the editors of TU have received consistently positive feed-back from the USA, the whole of Europe, South Africa and Australia.

These sensational "Topical notes" formed the basis for the Compendium "The Thirty Years' War 1966-1996" published in 1997. The book, described with a certain selfirony by the authors Torel/ Kammerer as a controversial pamphlet, provided further data, facts and back-ground on the subject of canine hip dysplasia, especially in the expanded and revised 2nd edition published in March 1999 (ISBN 3-9807236-1-5). The title is a deliberate reference to the religious war of 1618-1648 in Central Europe, since the attempts to combat hip dysplasia in the associations and societies, as described by the authors with more than a touch of irony, were not only characterized by the ferocity of a military campaign but, in the face of prevailing dogmatism, were also ultimately futile.

With its "furor teutonicus" - its teutonic fury - the Compendium created an uproar. The authors Torel/Kammerer were not only skilled in verbal cut-and-thrust when deploying their arguments, but also brought up heavy artillery to support their attack. The hostilities, with their attacks and counter-attacks between the authors and their opponents in industry and veterinary medicine, are a cause of ongoing concern to various official agencies. The Bundestierärztekammer (BTK) (Federal German Veterinary Authority), the VDH (German Kennel Club) and the Waltham/Effem company boycotted the book on the basis of cartel agreements and suppressed reviews and reports in the veterinary literature, the societies and the media.

When these measures failed to prevent the distribution of the Compendium by word of mouth, Waltham/ Effem persuaded the BTK and the VDH to apply to Dortmund District Court to have the book banned. When even a temporary injunction obtained from the biased and prejudicially influenced 7th Civil Division on 23 Sept.1999 failed to halt the sale of the book, the VDH intrigued with the Association of Publishers and Booksellers of the Federal Republic of Germany in Frankfurt and on 10 Feb. 2000 the book title was deleted from the list of available books (VLB list) This meant that "The Thirty Years' War" was effectively placed on the index of prohibited books, since it was no longer available through the book trade, or only with great difficulty. The first legal actions taken against the Association at Frankfurt District Court have so far been unsuccessful due to behind the scenes manipulation among the judges in Dortmund and Frankfurt resulting in agreements preferential to the VDH and its backers. Meanwhile, however, a promise has been extracted that the book will be reinstated and available once more through the book trade.

On the basis of predetermined decisions irreconcilable with the existing legal order and without any statutory basis, and in gross violation of the law of civil procedure, the 7th Civil Division of Dortmund District Court on 16 Mar. 2000 granted the applications of the VDH to have the book banned, thereby effectively curtailing the basic constitutional right of freedom of the press. The proceedings are not yet finalized and the judgement does not yet have the force of law, but is subject to judicial review by the Cartel Division of Duesseldorf Higher Regional Court following an appeal.

On the other hand, Christa Bremer, 3rd President of the VDH, its Secretary Bernhard Meyer and permanent legal adviser Claudia Marienfeldt are now under investigation by Dortmund Public Prosecutors Office on suspicion of making a false statutory declaration and giving false evidence in the course of proceedings. Investigative proceedings are also pending at the same Office into the incorrect and biased presiding judge Becker of the 7th Civil Division and his associate judges Altemeier and Meyer-Tegenthoff due to the suspicion of perverting the course of justice. The presiding judge of Hamm Higher Regional Court is also conducting a disciplinary review into manipulation and suspicion of corruption in Dortmund.

Proceedings are ongoing at the Public Prosecutors Office, Division for Commercial and Medical Crime in Mannheim, against the "trio infernale" of BTK, VDH and Waltham/ Effem due to suspicion of fraud, unfair competition and corruption with active and passive bribery. The computerized breeding value estimation system of Dr. Beuing at the Institute of Animal Breeding and Domestic Animal Genetics of Gießen University, as a piece of profitable charlatanism, will be among the objects of the Public Prosecutor's inquiries.

The "trio infernale" have no alternative but to defame and attempt to completely discredit the authors Torel/Kammerer, whose charges, if proved correct, would disgrace and compromise in an unprecedented manner the leading figures of canine science, the veterinary profession and animal foodstuffs industry for their blundering and charlatanism continuing over decades. The Compendium "The Thirty Years' War" has become a full-blown political issue.

Bone and Joint Disease In Young Dogs - By Dr. Ian Billinghurst
	The following was taken from an article written by Dr. Ian Billinghurst.

Over the last 50 years it has become apparent that numerous breeds of dogs carry genes capable of causing problems such as hip and elbow dysplasia in growing pups. It is also clear that numerous individuals within each of these breeds carry these genes. Because genes are involved in producing these problems, veterinary scientists have attempted to eliminate hip and elbow dysplasia from the dog world by not beeding from animals carrying damaging genes.

To identify young dogs carrying the genes capable of causing skeletal diseases, specialists perform hip and/or elbow radiography. The data is assessed by a panel of experts and given a grading to indicate the degree of hip or elbow dysplasia present - that is, the degree of departure from normal those particular joints exhibit.

Because dogs exhibit varying degrees of hip and elbow dysplasia, it is clear that skeletal disease in young dogs is not an all-or-nothing situation. Geneticists explain this in terms of these problems having a polygenic nature: hip and elbow dysplasia are dependent upon the interplay of numerous genes. In other words, to eliminate these problems entirely involves eliminating numerous genes from the dog population. Vets and breeders are also aware that the diet and exercise to which young pups are subjected can influence the degree of health or ill health existing in any given joint.

After five decades of attempting to remove the genes involved in skeletal disease, almost zero success has been achieved. Despite enormous efforts using radiography and culling, Hip Dysplasia, Elbow Dysplasia and related conditions regularly appear in individuals from supposedly sound lines. The battle against bone and joint disease in young dogs is a war that is not being won.

This forces us to ask "What are we doing wrong?" Are we looking for answers in the wrong place? Part of the dilemma is that the genes causing these skeletal diseases have never been identified. In fact, nobody is even looking for them. Another problem is thta in all the current hip and elbow dysplasia schemes, nobody is asking two simple questions of the participating animals: firstly, what and how much did each dog eat while its bones were developing, and secondly, how was each dog exercised during that same period? These two vital factors in bone development are not even considered an issue by authorities attempting to deal with hip and elbow dysplasia.

Modern veterinary science assumes any deviation from normal observed on the radiographs is one hundred percent due to faulty genes. And yet basic high school biology and first year university genetics would tell us this cannot be so. To use standard geneticist' jargon: "Phenotype does not necessarily equal genotype." In other words, what you see - either in the dog or as demonstrated radio graphically, does not necessarily reflect a genetic cause.

Modern veterinary science accepts that diet and exercise play a vital role in bone production. That being the case, the veterinary profession should also be asking for each and every dog involved in its hip and elbow dysplasia schemes - "How much influence did diet and exercise have, and how much influence did the genes have in producing this dog's skeletal system?" Unfortunately, nobody is asking these questions. By 1950 it had become standard "truth" that because the underlying cause of problems such as Hip Dysplasia was genetic, seeking solutions to these problems elsewhere would be a futile exercise. That basic "truth" has never been questioned despite the fact that all methods to eliminate skeletal disease which have relied on that "truth," have failed utterly! These problems are as bad as they have ever been, if not worse, particularly in breeds such as the Newfoundland, Labrador Retriever, and Rottweiler, where they remain as serious, prevalent, and seemingly impossible to eliminate, as ever.

If we take ourselves back to when these bone diseases first appeared, or were first recognized, we find they have only been with us a short time. They are a product of the Twentieth Century. Hip Dysplasia appeared suddenly in the 1930's. It was virtually unknown before that time. However, by 1965, Hip Dysplasia was regarded as exceedingly common and had been identified in 55 breeds of dogs worldwide. During that very short period of time we also saw the appearance and rapid spread of a multitude of other skeletal problems. These included shoulder, elbow, hock and stifle dysplasia, all of which in just a few decades went from rare or previously non-existent, to exceedingly common.

If these problems did not exist before the 1930's, where did they come from? High school biology says it is unlikely a mass of bone and joint wrecking genes should suddenly appear in the dog population some 60 to 70 years ago and then spread like wildfire through almost all breeds of dogs. Clearly, the genes responsible for these bone and joint problems in our young dogs must always have been present. Present, but not expressing themselves as disease until the 1930's.

Why did these genes "choose" to begin expressing themselves in the 1930's? This is a question we are not asking. Instead of seeking and eliminating the factor or factors that have allowed these genes to express themselves as skeletal disease since that time, we have concentrated on getting rid of the genes.

It is high time we asked the question, "what calamitous environmental change occurred during the 1930's that allowed previously dormant genes to suddenly wreak joint and skeletal havoc in practically all breeds of dogs?" Fortunately, we do not have to look very far to discover the answer to this canine conundrum.

It was during the 1930's that the diet our dogs evolved to eat was drastically changed. Until that time, the food people fed their dogs was fundamentally the same as the dog's evolutionary diet. The evolutionary diet of dogs consists of whole animals, fish, birds, bones, meat, organ meat, ingesta, other plant material including berries and nuts, together with such "delicacies" as vomit, feces and soil. The new diet that took its place was cooked and grain-based. It contained added calcium in a form totally foreign to the canine digestive system. It totally lacked the raw meaty bones, the organ meat, the ingesta rich in vegetable material, and all the other raw whole elements dogs had eaten for millions of years. Clearly, this new diet, suddenly thrust upon them, was a radical departure from what our canine friends were designed to eat.

This diet change was a consequence of the great depression of the 1930's, as dog owners sought cheaper alternatives to the fresh food they normally fed their dogs. Their search led many dog owners to grain-based pig, calf, and poultry feeds. Astute businessmen of the day began adding calcium and meat meal to stock foods, changed the label, and called them dog foods. Grain waste, worthless rubbish from the production of human food, became the major component of pet food and to this day there has been little change in that basic composition of commercial pet foods.

For the first time in millions of years, dogs were deprived of fresh whole raw foods and began eating masses of cooked grain together with heat damaged fat and protein, plus artificial calcium. A cooked and grain-based diet, high in carbohydrates and low in protein, is completely foreign to a species designed to thrive on fresh whole raw foods with plenty of meat and bones.

Dogs were being fed a high carbohydrate diet designed to support rapid growth and fattening of livestock. This diet allowed the larger breeds of dogs to grow more rapidly and at the same time produced subtle changes in their bone growth. The bones were softer and more easily damaged. Fast growth, combined with excessive excercise to traumatize and re-shape soft poor quality bones, has the potential to produce skeletal disease, particularly in the larger, faster growing, more poorly muscled, more obese, and poorly engineered breeds. Because this drastic change of diet has wrought such havoc on the bones and joints of our dogs, it would seem sensible to get rid of the new diet rather than the genes - particularly as our attempts to remove those genes has been an utter failure. Unfortunately, the veterinary profession has not recognized any of this.

Nor has the veterinary profession specified the genes whic need to be eliminated - and yet most of those genes are well known. They are the genes coding for large size, fast growth rate, small muscles, great obesity and poor engineering. Unfortunately, these genes, which predipose an animal to skeletal disease, also code for the distinctive characteristics of each and every breed prone to skeletal diseases. They are the genes we continually select for as we maintain the characteristics of each breed.

It makes little sense to both select for and eliminate the same genes within one breeding program. To eliminate skeletal problems such as hip and elbow dysplasia, it would make much more sense to remove the modern skeleton-damaging program of diet and excercise and replace it with the dogs' evolutionary program of diet and excercise.

In a nutshell, to avoid most forms of skeletal disease in our young pups, puppies must be kept slim and grown slowly, without artificial calcium supplements, on an evolutionary type diet, high in raw meaty bones, offal and vegetables. Their excercise must consist only of play - not rough play, but play where the puppy stops as soon as it becomes tired. These are the simple but powerful tools which have kept dogs' skeletons sound for millions of years. These tools are available today to any dog owner or breeder who cares to use them. They have the power to make most Juvenile Bone Disease in young dogs - of any breed - a thing of the past.

A final point: it is important to keep radio-graphing our dogs for soundness! By combining a radiographic program with sound management, we will not only maximize the chance of raising sound pups, we will also eliminate any genes which directly cause skeletal problems, as opposed to those that merely predispose to skeletal problems.