Leighvalley Golden Retrievers
General Information

There are several articles listed below that are of interest.
The first article is a review of the eye diseases in Golden Retrievers written by Robin G Stanley Veterinary Eye Specialist March 2001.
The next article is written by Veterinarian Dr Ian Billinghurst regarding Hip & Elbow Dysplasia, Diet
and Exercise.
We thank all parties for their kind permission to use their articles.

Article 1  Eye diseases in Golden Retrievers

Entropion  Entropion (inward rolling of the eyelid onto the eye) usually affects the lower eyelid. It is most common in dogs less than one year of age. Many of the causes that I see have an overly long lower eyelids. Entropion can cause irritation to the eye and in serve cases ulceration of the cornea.
Surgery is required. In young pups temporary stitch can be used to exert the eye lids form the eye.
Most cases require excision of skin to evert the eyelids, and in most cases also require eye lid shortening. I use the operating microscope and fine sutures to minimise the chance of scare tissue forming. A number of genes are involved in the inheritance of entropion. Other factors such as head conformation, eye socket shape and depth, and environment are involved.

Persistent Pupillary Membranes (PPMs)  The mildest form of PPMs affects many Goldens. These are small strands of iris tissue that run across the surface of the iris, and they do not cause clinical signs.
I do not feel that the PPMs are of concern unless they are severe.

Imperforate Tear Punctum  In some Goldens the lower tear duct (punctum) in the eyelid does not form. Affected dogs present with a watery eye as a pup. Using the operating microscope a new tear duct opening is created. The mode of inheritance is unclear, but there is a distinct familiar pattern. This problem seems to be increasing.

Cataracts  Any opacity of the lens is called cataract. There are many causes of cataract, some of which are inherited. If the cataracts are in both eyes and they are mature, the animal may become blind.
Surgery is available in some cases. The posterior polar subcapsular cataract (PPS) is better known as the star cataract. It is usually in both eyes and becomes apparent between 6 to 18 months of age. Some dogs develope this problem as late as 6 to 7 years of age. This cataract may be slowly progressive, but
rarely interferes with vision. It is advised not to breed from affected animals as matings with affected dogs have produced litters of blind pups. Another type of cataract is found in Goldens. This one affects the front of the lens from 3 to 6 monyhs of age. It rarely causes blindness. In the last 12 months we have been seeing a "new" type of cataract in Goldens. This is a juvinile cataract, and affected dogs usually less than 18 months of age. Most of these cataracts cause problems with vision. The centre (nucleus) of the lens is affected, and surgery may be required. In some cases atropine eye drops can be used to dilate the pupil to allow the pup to see around the cataract.

Persistent Hyaloid Artery This is a minor problem, and unlikely to be inherited. It may be associated with a cataract at the back of the lens.

Progressive Retinal Atrophy (PRA) There are two types of PRA in Goldens, one an early onset within the first two years of life, and the other occurring between 5 to 8 years of age. Affected dogs have night blindness, progressing to day blindness and in the later stage cataracts may develop. I have now seen 2 cases of PRA in Goldens. A blood test for PRA is being developed for use in Melbourne.

Glaucoma Golden Retrievers do not seem to be at great risk of glaucoma compared to other breeds such as Bassets or Cocker Spaniels. Affected eyes quickly loose vision and become painful. The eye may be red, blue and have a mid-dilated non-responsive pupil. Urgent specialist treatment is recommended if you are suspicious of glaucoma. This treatment seems to give us the best chance of controlling the glaucoma and saving vision as well.

Distichiasis Disticia (extra eyelashes) grow from glands in the eyelid edge onto the cornea. Depending on a number of factors extra eyelashes may or may not cause irritation to the eyes. I have seen eyes lost because of extra eyelashed. Most of the Golden Retrievers affected in South Australia and Victoria have only 1 to 3 lashes per affected eyelid. Most do not have clinical signs or evidence of corneal irritation. I have seen severely affected dogs. In the United States up to 30% of Goldens, seen at screenings, have extra eyelashes. If there is irriation then surgery is indicated. There are two techniques that Veterinary Eye Specialists will use. My preferred technique is Trans conjunctival Excision (TCE). Using the operating microscope, each individual extra eyelash root is excised. This may cause a light swelling and in some cases a slight ooze of blood for 3 to 5 days. The surgery rarely seems to cause any discomfort for the dogs. In some cases I will use Cryosurgery (freezing). Some of the older techniques can result in scarring. With any extra eyelash surgery, it is possible for new extra eyelashes to grow. At any one time between 10 to 15% of any hair follicles are inactive. Nothing can be done to destroy inactive extra eyelash follicles. In some cases a second extra eyelash surgery may be required, in very rare cases a third extra eyelash surgery may be required. The condition is believed to be inherited in a dominant manner. It may take up to 5 years for the extra eyelashes to grow. Most Goldens are not severely affected, but it is my feeling that we should be breeding away from this condition.

Corneal Lipidosis/Dystrophy In this condition fat (usually cholesterol) and in some cases minerals (usually calcium) are deposited in to the cornea, and may result in a cloudy appearance to the eye. This condition rarely, if ever, causes problems with vision. The most common  form in Goldens is lipid dystrophy. This is whee the cloudy fat layer is deposited into the cornea without any obvious cause. In these cases it is believed that there may be an inherited problem with fat metabolism in the cornea. Fat degeneration can also occur in the cornea following trauma or injury to the eye. This is most common if the dog has hyperlipidaemia (high fat levels in the bloodstream).

Horners Syndrome Dogs with Horners Syndrome have a sunken in eye, with a prominent third eyelid. The upper eyelid is often droopy, and the pupil is small. This problem is caused by a disruption to the sympathetic nerve supply to the eye. Horners Syndrome can be due to problems in the ear, chest, spine, but often despite testing no specific cause can be found. Most cases of Horners Syndrome improve without specific treatment within 6 weeks. As a breed, Golden Retrievers have been noted to be more at risk to develop Horners Syndrome. No pattern of inheritance has been noted.

Retinal Dysplasis/Focal Retinal Elevations Small folds are seen in the retina. Vision does not seem to be affected. The pattern of inheritance is unknown. In some breeds this condition is inherited, and in severe forms as seen in Labrador Retrievers can cause blindness.

Other problems seen occasionally:

Iris Cysts Black cysts may be seen floating in the eye. They do not cause problems.

Retina/Optic Nerve Variations in the appearance of the retina and optic nerve are common in the Golden Retriever. They are variations of normal. In some cases these normal variations have been confused with disease conditions. Considerable experience and specialised equipment may be required to avoid this mistake.

Iris Tumours Goldens have been noted to be at a greater risk of developing iridal and ciliary body tumors at a young age. No inherited pattern has been demonstrated. but the breed predisposition suggests a genetic tendency.

Robin G Stanley BVSc(Hons), MACVSc(Surgery) FACVSc(Ophthalmology), MRCVS Veterinary Eye Specialist. Prepared March 2nd 2001. 

ARTICLE 2  BONE AND JOINT DISEASE IN YOUNG DOGS
               ARE WE BARKING UP THE WRONG TREE?

Hip Dysplasia, Elbow Dysplasia, Osteochondritis. These diseases continue to mount their attacks on young dogs, particularly the larger breeds, despite mass radiography and culling. What are we doing wrong? Why do these problems appear and reappear in supposedly disease free lines? Our failure to eliminated Hip and Elbow Dysplasia compels us to ask..."Are our efforts entirely misdirected?" Should we be looking elsewhere for a solution?

Dysplasia, (or other juvenile skeletal diseases) are suffering from completely avoidable problems. Most of the blame, are we barking up the wrong tree? The answer is yes, most definitely. Most dogs that develop Hip and Elbow problems should be laid at the dor of incorrect nutrition and poor exercise regimes, rather than 'bad genes'. Let me explain. Unfortunately, what we vets DO NOT KNOW about Hip and Elbow Dysplasis, far outweigh what we do know! Fortunately there are answers, they are found in the history of these diseases. Understanding that history allows the basic causes of Hip and Elbow Dysplasia to leap out at us, making solutions crystal clear. Ironically, those causes and those solutions have stared us in the face for decades. It is accepted "truth" that bad genes cause Hip and Elbow Dysplasia. We assume that schemes to remove these genes have proved impossible. Yet nobody has asked "exactly which gene are we trying to eliminate?" Those genes have never been identified because nobody is looking for them. And 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 their elimination remove traits we actually want to keep? DIET and EXERCISE play a vital role in bone development. In all the Hip and Elbow Dysplasia schemes, nobody is asking what and how much did each dog eat and how was each dog exercised while its bones were developing? Diet and exercise are ignored as we assume they play no role in bone health, As we assume that all radiographic abnormalities are caused only by faulty genes, we ignore basic biology and genetics which tell us this cannot be. 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. 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. There is a more fundamental question. How long have these problems plagued our dogs? Tens, hundreds or thousands of years? Are these diseases a new phenomenon? The surprising answer is that these bone and joint abnormalities are a product of the twentieth century. The story begins with a sudden appearance of Hip Dysplasia in the 1930's when it was considered a rare disease, unknown before that time. By 1965, Hip and Elbow Dysplasia had been identified in 55 breeds of dogs worldwide. They were known common problems. In just thirty years, the dog world had experienced the sudden appearance and rapid spread of these and a multitude of other skeletal problems, including shoulders, elbows, hock and stifle dysplasia, all having gone from rare or non-existent, to exceedingly common. By 1950 it was standard "truth" that the causes of Hip and Elbow Dysplasia were genetic. The "truth" has never been questioned despite all Hip and Elbow Dysplasia elimination schemes (which rely on that "truth"), having failed utterly! Both these problems remain as serious, as prevalent and as seemingly impossible to eliminate as ever. If these diseased did not exist before the 1930's, where did they 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 wildfire in two or three decades through most breeds of dogs, specifically targeting the larger breeds. These genes must always have been present, but not causing any problems until the 1930's when some environmental change occurred which allowed these genes to express themselves. We vets are not willing to face this possibility because 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 and can therefore ONLY be eliminated by breeding. We have produced a gargantuan juggernaut of an elimination scheme which depends on mass radiography, highly questionable interpretation of same, and wholesome culling to eliminate the genes which produce Hip and Elbow Dysplasia. Unfortunately, this machine is making very little headway after many decades of rolling roughshod over countless canine corpses which lie strewn in its wake. This begs the question. Does the failure of these schemes rule out genes as the basic cause of these bone and joint problems? Not at all. Our fifty years of futility clearly points to a major environmental change which occurred in the 1930's. This change allowed genes which cause these problems, to express themselves. But what was that environmental change? Fortunately, 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 1030's this was replaced with masses of cooked grain plus meat and bone meal and calcium supplements. The new diet lacked the raw whole animals- including bones and organ meat, fish, birds, plants, faeces and soil, dogs had eaten for millions of years. This change occurred during the depression of the 1930's. Dog owners were looking for cheap alternatives to the fresh food they normally fed their dogs. Astute businessmen of the day, realising the enormous money-making potential in the pet food market, obliged by changing the labels of commercially produced pig, calf and poultry feeds and throwing in some extra calcium. For the first time in millions of years of canine evolution, our dogs were deprived of fresh whole foods and forced to eat a diet based on masses of cooked grain, meat meal and bone meal together with artificial calcium rather than raw bones. That massive dietary change occurred in conjunction with a more aggressive approach to exercise. These changes, and 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. Modern commercial dog foods have changed very little. However, there is now an enormous body of evidence that this catastrophic change in food (and exercise) wreaked havoc on our dogs' bones and joints, particularly the larger and giant breeds, whose genetic makeup renders them particularly susceptible to these changes. The new starchy diet, designed to support the rapid growth and fattening of livestock, produced accelerated growth rates and obesity in our pups. Their rapidly increasing weight out-stripped the ability of their soft young bones to support them. High starch resulted in damaging hormonal changes which wreaked further havoc on bone growth. Nutritional excesses and deficiencies, together with a total loss of protective nutrients found only in fresh whole raw foods, added further insult to bone growth. Excessive artificial calcium added further problems. Throw in excessive exercise to traumatise and re-shape these soft badly growing bones, and we have the perfect conditions for skeletal disease in young dogs. These problems were particularly noted in the larger, faster growing, more poorly muscled, more obese, the poorly engineered breeds. As you can see, the causes behind Hip and Elbow Dysplasia are much more than genetic! But what about the genes? 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? 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. The genes which predispose for skeletal problems in our young dogs are the genes which code for large size, fast growth rate, small muscles, great obesity, and finally genes that code for poor engineering. Could it be that simple? Yes it could, that simple and that difficult. The major difficulty is that those genes also happen to code for the very distinctive characteristics of each and every breed. The genes we want to eliminate to solve the 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! This makes any attempt 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. These are the factors we must eliminate. The key to eliminating skeletal disease in our dogs is found in diet and exercise which thankfully are the two factors over which each breeder and dog owner can have maximum control. We must return our dogs to 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 50-60% raw meaty bones, 20-30% raw and crushed vegetables and fruit, 10% offal, no artificial calcium, together with simple additives such as kelp, flax meal, cod liver oil and yoghurt. This diet is not to be fed in enormous amounts. Pups are grown slowly, as nature intended. Enough is fed to ensure that the pups grow at about 60-70% 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 grow sound and healthy with little or no trace of Hip and Elbow Dysplasia. However a few pups will still develop skeletal problems, these pups have directly acting genes, genes that express themselves no matter what the diet or the exercise, Now is the time to cull the animal from the breeding program that carries them. Should we still radiograph our dogs? Yes! By combining a radiographic program with sound management, we will maximise the chance of raising sound pups and eliminate any genes directly responsible for causing skeletal problems, while keeping most of our predisposing genes so as to maintain our breed characteristics. In a nutshell, pups must be grown slowly, kept slim without artificial calcium supplements on an evolutionary type diet-high in raw meaty bones. 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 simple but powerful tools, they have kept dogs' skeletons sound for millions of years. Employing them will eliminate most Juvenile Bone Disease, no matter what "nasty" genes are present. Are you 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.

By Dr Ian Billinghurst