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BONE AND JOINT DISEASE IN YOUNG DOGS - ARE WE BARKING UP THE WRONG TREE? |
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Written by Dr Ian Billinghurst
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 Hip Dysplasia, Elbow Dysplasia and Shoulder Dysplasia; these, and a host of related bone and joint diseases continue to mount their attacks on young dogs, particularly pups of the larger breeds, despite mass radiography and ruthless culling. What are we doing wrong? Why do these problems appear and reappear in supposedly disease-free lines? Our failure to eliminate Hip and Elbow Dysplasia, despite elaborate and costly schemes aimed at their eradication, compels us to ask… “Are our efforts entirely misdirected?” Should we be looking elsewhere for a solution?
Are we barking up the wrong tree?
The answer is yes, most definitely. Most dogs that develop Hip and Elbow Dysplasia, (or other juvenile skeletal diseases) are suffering from completely avoidable problems. However, these problems will never be overcome, under the belief system currently maintained by the veterinary profession.
For decades, breeders, veterinarians, academics and anyone with any sort of interest in these problems have held that there is one single cause of these problems; ‘bad genes.'
Bad genes as the cause of hip and elbow dysplasia is a piece of veterinary dogma, which has become accepted “truth.” It is on the basis of this ‘truth' that the veterinary profession, together with a host of breed societies has built its enormous (and largely useless) schemes, designed to eliminate hip and elbow dysplasia from the large breeds of dogs.
On the basis of a belief that these problems are entirely genetic, it is assumed (or maintained) that by eliminating from the breeding population, individuals with radiographic evidence of hip and/or elbow dysplasia, we will be removing those genes, which cause the problem and therefore the problem will disappear. Unfortunately, although numerous beautiful animals have been culled (either euthanased or not allowed to breed) on the basis of this theory or hypothesis, these diseases continues unabated, with all such schemes having little or no success and there is every reason to believe these schemes will continue to fail into the future.
The futility of what we are attempting; is something that we vets as a profession, are not willing to face. We have developed, (in conjunction with breeders), an enormous emotional and professional investment in believing that the bone and joint problems in our young dogs are caused by genes – alone. This leaves us with little choice; we can only attempt to be rid of these problems via a programme of genetic manipulation. Our only basis for decision making in these programmes is radiographic evidence and a belief system that interprets all radiographic abnormalities as being genetic in origin. No consideration is given to any environmental factors, which may or may not have impacted on the radiographic image of the joints in question.
This way of thinking has produced a gargantuan juggernaut of a scheme, which depends on mass radiography, highly questionable interpretations of same, and wholesale culling to eliminate those individuals with radiographic evidence of skeletal disease. People who own giant breed dogs are coerced into participating in these schemes in the vain hope of eliminating from the gene pool, all of the genes, which produce hip and elbow dysplasia. Unfortunately, but predictably, this machine is making very little headway after many decades of rolling roughshod over countless canine corpses which lie strewn in its wake.
However, rather than face the obvious reality of the total uselessness of these eradication schemes, it has clearly been easier, more ‘professional' and definitely more profitable for the veterinary profession to stick its head in the sand and continue with the ‘high tech' approach; involving specialised radiographs and complicated hip scores; schemes run by a tiny elite of veterinary radiographic professionals.
These hip and elbow dysplasia schemes have become major profit centres for a veterinary industry, which like its medical cousin, maintains ill health as its stock in-trade. Could we as a profession make the giant leap of abandoning these schemes and adopting low-cost effective solutions? Perhaps we might ask: “Could we as a profession, both abandon the profit potential these schemes represent and also lose face by admitting our failure?
These universal schemes, apart from generating dollars for the profession and despite their futility, lend enormous credence to the profession and presumably will continue to do so indefinitely. Ironically, they will do so, not because they are effective, but because of their total failure to hit their target. In common with so much ‘established wisdom,' it is the futility of these schemes, which promotes their longevity and maintains their prestige.
The question remains. Why have these schemes been so uniformly unsuccessful? Why will they continue to fail?
Could it be that such schemes are based on an unsound hypothesis? Clearly, if these schemes are not working, the theory on which they are based must have holes in it and of course it does! The problem is simple. There is one very obvious flaw in these schemes and it relates to a basic law of genetics: an animal's phenotype (what an animal looks like, what it IS like) is never exactly the same as might be predicted from its genotype, its genetic inheritance. In other words, what an animal actually turns out to be, including any faults it may or may not develop during its lifetime, will never be exactly as one might predict simply by knowing what genes it has inherited. This is because phenotype is very much dependent upon the interaction between an individual's genes and the environment the individual experiences during its lifetime. This interaction between an animal's genotype and the environment is the single vital factor that is not being taken into account by the veterinary profession in its attempt to eradicate hip and elbow dysplasia.
The veterinary profession has never asked the question “Is it possible that the genes responsible for these bone and joint diseases in young dogs will only cause such problems under particular environmental conditions?
And this is despite the fact that the veterinary profession knows only too well that there are two vital and controllable components of a puppy's environment, which play a vital role in bone development and are totally amenable to manipulation. Those two environmental factors, which vary widely between different breeders and different puppy owners, are DIET and EXERCISE.
Both diet and exercise play a vital role in bone development. The role of diet and exercise in bone production is crucial. Diet and exercise interact with genes, producing either sound or unsound bones and joints. Numerous scientific papers have demonstrated the potentially destructive role that poor application of these two environmental factors play in the development of skeletal disease in pups.
However, despite this body of knowledge, when it comes to schemes designed to eliminate skeletal problems in pups, all questioning, all reference to the vital role of these two specific and totally malleable factors, in causing or preventing skeletal disease is totally ignored. Hip and Elbow Dysplasia schemes take no account of them.
The originators and the perpetuators of these schemes, act as if environment plays no role in producing these crippling diseases. When radiographs are read and the fate of puppies (most particularly their role as future breeding stock) is decided, it is assumed that all radiographic abnormalities are caused only, by faulty genes. Diet and exercise are ignored as if they play no role in skeletal health. Nobody asks what and how much did each pup eat and how was each pup exercised while its bones were developing? And yet the answers to these questions are the key to solving these major health problems in young large and giant breed dogs.
The truth is that most of the blame for these problems should be laid at the door of incorrect nutrition and poor exercise regimes, rather than ‘bad' genes.
For any dog with skeletal disease, we must ask “what was the relative contribution of genes, poor diet and inappropriate exercise?” If diet and exercise were the major contributors, logic would dictate that these must be the first areas we should look to when seeking a solution. We must also ask the question “What do we gain by eliminating these individuals from the breeding program?
We might also ask at this point… “Does the failure of these schemes rule out genes as the basic cause of these bone and joint problems?” The answer is that genes are most definitely involved, but their role, for the most part is limited and that the genes involved are, for the most part, not available for removal or elimination. In other words, most of the genes that are involved in producing these problems are genes that we may actually want to keep!
Let me now ask with you, the following question. “Has anybody ever bothered to ask: exactly which genes are we trying to eliminate?” To the best of my knowledge, proponents of these schemes have never actually identified the ‘bad' genes. Unfortunately, if we don't know which genes we are looking for, what chance do we have of getting rid of them? And even if we could get rid of them, would this be a good idea? Genes code for proteins and proteins play diverse roles in mammalian bodies. The elimination of a particular gene may well eliminate traits we actually want to keep!
That is, would we be throwing the baby out with the bathwater, even if we could successfully eliminate these so-called ‘bad' genes? The elimination of good genes is not what we are aiming for with these schemes, but it is what we are getting in so many instances.
Clearly, under the current set of schemes designed to eliminate skeletal disease, where the only criteria considered is the reading of a set of radiographs, there is little chance of success. For example, breeders know only too well that two sound parents will produce unsound offspring if the pups are raised badly. They also know that unsound parents will produce sound pups if the puppies are raised with care. In practice, this works out as follows.
Consider a smart breeder whose breeding stock has (according to radiographic evidence) a supposedly marginal genetic background in relation to skeletal health. This breeder grows the pups well, that is, with appropriate diet and exercise. These pups, the progeny of relatively unsound parents (radiographically) will have their radiographs assigned a tick of approval. Such individuals will be allowed to pass on their (supposedly marginal) genes to future generations. In stark contrast, consider a novice breeder. This breeder pays big dollars for breeding stock, stock with a supposedly first-class genetic background in relation to skeletal health, according to radiographic evidence. Such a breeder will usually make many mistakes in growing the pups, with inappropriate diet and exercise. Such pups will have their supposedly excellent genes eliminated from the gene pool as they demonstrate radiographic evidence of skeletal disease.
It gets even more confusing. Veterinarians are well aware of the phenomenon where dogs, which are clinically sound, produce radiographic readings regarded as woeful, while other dogs, with brilliant radiographs, can hardly walk. Under the current paradigm, the crippled dogs with healthy radiographs are classified as sound, while the agile dogs are condemned as unsound! The question must surely be asked, under the current scheme, what logic do we use as we attempt to decide how these dogs are viewed and which ones are kept for breeding?
This raises the question of exactly which genes we are attempting to eliminate in our hip and elbow dysplasia ‘schemes' and exactly what is the relationship between genes, the environment and clinical soundness or otherwise? This is a question the veterinary profession needs to answer; it needs to develop a true understanding of the role of both genes and the environment, and how they relate to each other in producing these diseases. It needs to understand which are the most important environmental factors to consider, could they be diet and exercise?
As you may be realising, what we veterinarians DO NOT KNOW about Hip and Elbow Dysplasia, far outweighs what we do know! Fortunately, there ARE answers to the problem. Those answers are to be found in the history relating to when these diseases were first seen to be a problem in the dog population. The answers, embodied in that history have stared us in the face for decades, but we veterinarians, as a profession, have, for whatever reason, chosen to ignore them.
Let me ask a very simple but fundamentally important question. “How long have these skeletal problems plagued our dogs: tens, hundreds or thousands of years? Are these diseases a new phenomenon or have they been around for only a short period of time?” The surprising answer is that these bone and joint abnormalities are a product of the twentieth century. Their story begins with the sudden appearance of Hip Dysplasia in the mid 1930's. At that time, Hip Dysplasia was considered a rare disease; it was practically unknown before the 1930's. Elbow Dysplasia did not appear until a decade or so later. Was there a reason for this? Most definitely; the great depression of the late 1920's and early 1930's had a profound (and lasting) effect on the dietary habits of modern dogs.
It was in the 1930's that the traditional meat, bones, offal and table scrap diet fed to dogs for centuries was abandoned as people were at that time forced to eat these foods themselves. It was the food that the dogs of the day were switched to, which became life-changing and health threatening; and not only for dogs, but ultimately also for cats. This was the beginning of the enormous pet-food industry as we know it today. This industry arose because in the 1930's, the dog owners of the day began to feed dogs with stock feed; grain-based feed, to which was added extra protein and calcium in the form of what was basically fertiliser – meat meal, blood and bone. To make a long story short, grain producers, realising the profits to be made from the wastes of their industry, began what has become the ubiquitous and damaging (to companion animal health) modern pet food industry.
So it was from the late 1920's onwards that dog owners abandoned the gold standard diet for canines (the evolutionary or genetically (genomically) determined diet) in favour of the artificial diets produced by the pet food companies.
If we move forward three decades from that time, we find that by 1965, hip and elbow dysplasia had been identified in 55 breeds of dogs worldwide and both of these diseases were regarded as common problems. In just thirty years, the dog world had experienced the sudden appearance and rapid spread of these two problems, but not just these two problems. Hip and elbow dysplasia had, over this short period of time, been joined by a multitude of related skeletal problems, including shoulder, hock and stifle dysplasia; all having gone from rare or non-existent diseases prior to the mid 1930's, to syndromes that were and continue to be today, exceedingly common.
I should point out that as early as the late 1940's it had become standard “truth” that the causes of Hip and Elbow Dysplasia were ‘purely' genetic. From that time forward, that particular clinical “truth” has never been questioned, despite masses of peer reviewed research (reported in all the major veterinary journals) demonstrating the pivotal role of exercise and diet in the production of these diseases. The net result is that to date, each and every Hip and Elbow Dysplasia elimination scheme, relies on the hypothesis that these problems are purely genetic. And that is why they have failed utterly; that is why both these problems remain, as serious and as prevalent and as seemingly impossible to eliminate as ever.
Let us return to the simple fact that clinically, these diseases did not exist before the time of the great depression of the 1930's; this raises the question: “If we are to believe the current hypothesis that the origin of these diseases is purely genetic (with no contribution from the environment), we need to ask the question, if that is the case, where did these diseases come from? What caused them to appear and spread rapidly? Why are they now so common?”
Basic biology dictates that a mass of bone wrecking genes can not suddenly appear in the dog population and spread like wild-fire – in two or three decades – through most breeds of dogs, specifically targeting the larger breeds. The basic biological fact is that those genes must always have been present, but not causing any problems prior to the 1930's. The sudden appearance at that time of hip dysplasia, the forerunner of all the other canine developmental skeletal diseases, indicates strongly that there must have been some major change in the environment at that time; a change, which allowed the expression of a whole series of bone and joint damaging genes.
Clearly, we need to ask the question… “What major environmental change occurred in the life of the dog in the 1930's, which allowed genes, with the potential to cause these skeletal problems, to express themselves. As I have already indicated, we do not have to look very far to discover the answer.
During the 1930's, the diet our dogs evolved to eat was drastically changed. Until that time, most people fed their dogs an evolutionary-type diet of raw foods, whole foods and not a lot of grain. In the 1930's this was replaced with masses of cooked grain plus meat and bone meal, together with calcium supplements. The new diet was no longer raw, it was no longer animal based, it no longer included bones, organ meat, fish or birds, it no longer contained the gut contents, the vegetable materials that dogs have eaten for millions of years.
During the depression of the 1930's, dog owners sought cheap alternatives to the fresh food they normally fed their dogs because they were were now feeding such material to themselves; what they discovered, was grain-based stock food. Grain producers of the day realised the potential profit available to them; all they needed to do was take their formerly useless grain waste and add a cheap protein and calcium source; then label the product as pet food.
For the first time in millions of years of canine evolution, our dogs were deprived of fresh whole raw foods and forced to eat a diet based on masses of cooked grain, meat meal and bone meal together with artificial calcium. For the first time in their long evolutionary history, dogs were deprived of the diet they had evolved to require. That massive dietary change was followed in succeeding decades by breeders selecting larger breeding stock with rapid growth rates; they teamed this with an increasing emphasis on excessive exercise.
These changes, but most especially the dietary change, proved to be the ideal set of conditions to allow certain genes to express themselves in the form of skeletal disease.
The two greatest dietary dislocations suffered by our dogs from the 1930's onwards have been the removal from their diet of whole raw foods, particularly the raw meaty bone and the addition to the diet of masses of starch. The removal of raw meaty bones from the canine menu has removed from our dogs' diet, their usual source of calcium and other healthy bone forming nutrients. The use of starch, a seemingly harmless substance as the major source of energy in the canine diet is also far from innocent. In fact, this problem alone is responsible, not only for much of the skeletal disease in young pups, but also for most degenerative disease suffered by older dogs raised on grain-based pet foods.
This new artificial dog (puppy) food produced both subtle and overt nutritional excesses and deficiencies, including a total loss of protective nutrients found only in fresh whole raw foods. We now recognise the enormous nutritional contribution that cartilage makes to normal bone growth; artificial foods totally lack this vital nutrient. What these artificial foods do contain, is artificial calcium. Artificial calcium is added to these foods in excessive amounts. We now recognise this as a major cause of skeletal disease, interfering as it does with normal bone growth. Being based on starchy foods, this new artificial dog food is a diet designed to support rapid growth and fat deposition; as it does with livestock. Puppies forced to eat this food experience accelerated growth rates and obesity. Part of the reason for this is that diets high in starch cause damaging hormonal changes, most particularly hyperinsulinaemia. Excessive insulin is a potent growth promoting factor. Insulin promotes fat storage and it also promotes inflammation. The net result has been and continues to be, enormous physiological insults to the skeletons of growing pups; producing pathological bone growth, which may be summarised as young inflamed bones, way too soft and too sick to support the massive weight and trauma, to which they are subsequently exposed.
This catastrophic change in food (and exercise) began to wreak havoc on our dogs' bones and joints from the 1930's onward and continues to do so with our dogs today. These health damaging attributes of modern pet foods remain unchanged from the original formulations of the 1930's; these damaging effects are noted particularly with the larger and giant breeds, whose genetic makeup renders them particularly susceptible.
In summary, excessive exercise, will traumatise, inflame and re-shape soft, rapidly growing, poor quality bones. Genetically susceptible pups of the giant breeds develop skeletal disease as their rapidly increasing weight outstrips the ability of their inflamed, soft and badly formed bones to support them.
As you can see, the causes behind Hip and Elbow Dysplasia are much more than genetic, but a question remains, where do the genes fit in to this story? If genes are the basis of the problem, why has the attempted removal of these genes failed to fix the problem? The answer is, simple. We have not fixed the problem because the genes have not been removed.
Despite years of not breeding from dogs, which demonstrated faulty skeletal structure (according to radiographic evidence) and only breeding from dogs with (relatively) sound bones and joints, (according to radiographic evidence), the genes which cause those problems still remain. Why is this so? Because nobody has asked– “which genes are we trying to eliminate?”
The genes we must eliminate are very well known. They appear in most articles dealing with Hip and Elbow Dysplasia but nobody has recognised them as such.
Could it be that simple? Yes it could; that simple and that difficult. The major difficulty is that these genes also happen to code for the very distinctive characteristics of the particular breeds that are susceptible to these skeletal diseases as young pups.
The genes which pre-dispose for skeletal problems in our young dogs are the genes which code for the following characteristics: 1) large size, 2) fast growth rate, 3) small muscles, 4) great obesity, and finally… 5) genes that code for poor engineering, or to put that another way, genes that code (very often) for the very essence of the breed.
The genes we want to eliminate to solve these bone and joint problems are the exact same genes we want to keep! To retain our breeds in their recognisable form, most of the genes which pre-dispose to skeletal disease are the genes we must not remove; they are ones we select for as being the genes, which build the unique characteristics, the distinctive look and character of our giant and large breed dogs.
And so it has been that from the 1930's onwards, we have been producing the perfect conditions for skeletal disease in young dogs, with these problems being particularly noted in the larger, faster growing, more poorly muscled, more obese, and poorly engineered breeds.
This makes any attempt to remove skeletal disease from young dogs using a genetic solution, an exercise in futility. To solve the problem of bone and joint disease in our young dogs, we have to re-visit the basic underlying factors, which caused these problems to appear in the 1930's; the factors, which continue to this very day. These are the factors we must eliminate.
The key to eliminating skeletal disease in our dogs is found in diet and exercise which (happily) are the two factors over which each breeder and dog owner can have maximum control.
We must return our dogs to their evolutionary diet and their evolutionary exercise regime. Of greatest importance is to find modern foods that are equivalent in nutritional terms to the evolutionary diet. This is simple.
An evolutionary diet is based on 50 to 60 percent raw meaty bones, 20 to 30 percent raw crushed vegetables and fruit, ten to twenty percent offal, no artificial calcium, together with simple additives such as kelp, cod liver oil, fish oil, flax meal, eggs and yoghurt. This diet is not to be fed in enormous amounts. Pups are to be grown slowly, as nature intended. Enough is fed to ensure that the pups grow at about 60 to 70 percent of their maximum growth rate.
Exercise along evolutionary lines is vital; bones require normal stresses for normal growth; neither too much nor too little.
The only “bone healthy” exercise for juvenile dogs is PLAY. Plenty of play, not rough play, but play where the puppy stops as soon as it becomes tired. Until the bones are mature, that is the only exercise that should be allowed - as Nature/God/Evolution intended.
Raised this way, no matter what genes they have inherited, the vast majority of pups will develop a sound and healthy skeletal structure, with little or no trace of Hip or Elbow Dysplasia. However, it must be understood, that even if we adhere to these principles, a small percentage of pups will be found that develop skeletal problems. These pups have directly acting genes. Genes that express themselves no matter what the diet or the exercise regime. Now is the only time we would consider the possibility of removing this individual from the breeding programme, this individual has genes we definitely do not want.
Should we still radiograph our dogs? Yes! By combining a radiographic programme with sound management, we will maximise the chance of raising sound pups, and be able to eliminate any genes, which are directly responsible for causing skeletal problems. Meanwhile, we have no choice; we must keep most of our predisposing genes, so as to maintain our breed characteristics.
In a nutshell, healthy management requires that pups are grown slowly, kept slim, without artificial calcium supplements, on an evolutionary type diet, high in raw meaty bones, offal and vegetable material, together with other whole raw foods. This is the only logical way to ensure normal healthy bone growth. Until the pup's bones are mature, the only exercise that should be allowed is play with age and size matched peers. This will produce normal stresses allowing normal growth.
These are the simple but powerful tools, which have kept dogs' skeletal structures, sound for millions of years. Employing them will eliminate most Juvenile Bone Disease, no matter what “nasty” genes are present.
Are you, as a breeder or a veterinarian or a dog owner barking up the wrong tree when it comes to producing sound skeletons in young dogs? Think carefully before dismissing the ideas in this article. To not use those simple but profoundly effective tools, can make breeding and rearing dogs a difficult and painful exercise, and very costly from a monetary, an emotional and a genetic loss point of view. On the other hand, by adopting sound dietary and exercise regimes for growing pups, makes rearing healthy dogs with a sound skeletal framework a simple and pleasurable exercise.
Also realise, when these basically sound ideas are opposed by veterinary professionals, those professionals, mostly have no idea, no understanding of the material being presented in this article. They have no idea of the damage wreaked on the health of companion animals by modern diets; they have no idea of the value of evolutionary nutrition in producing sound bones and joints and maintaining healthy longevity.
Additionally, as a profession, veterinarians have a huge stake in maintaining the status quo. It appears more ‘professional' and has definitely been far more profitable, to stick with the ‘high tech' approach to eliminating hip and elbow dysplasia. The use of specialised radiographs and complicated hip scores that can only be assigned by highly trained veterinary radiologists fosters elitism and generates dollars. There is no kudos and no on-going profit to be made from pursuing low-cost effective solutions. It does not matter that the high tech solutions are useless. Indeed, the fact that they are useless ensures their ongoing value to the veterinary industry. Such procedures, because of their futility, have the ability to generate dollars indefinitely. Hip and elbow dysplasia have become yet another major profit centre for a veterinary industry, which sadly, like its medical cousin, maintains ill health, based on poor diet, as its stock in-trade.
For more detailed information about feeding and exercising young dogs according to evolutionary principles, may I suggest you read my book “Grow Your Pups With Bones”
Click here to purchase Grow Your Pups With Bones
Copyright Ian Billinghurst.
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