REFERENCES (back to Dog Food page)
Phasic Diets
Puppy Diets
Hips / Elbows - Wyburn
Development
Permission
was granted to pass this e-mail along
-----Original Message-----
From: Michelle + Rick Stopps
[mailto:michelle@silmaril.on.ca]
Sent: Monday, 11 August 2003 5:32 a.m.
To: ukgoldens@yahoogroups.com
Subject: Golden Retrievers Re: Food for thought - "Bird" Dogs
--- In ukgoldens@yahoogroups.com, "Garlis" <garlis@s...> wrote:
Hi Rick. Jim and I are very interested in your article about puppy feeding.
The idea of phasic diets originated in . . . poultry !!! (Ah, Michelle the
Animal Science nutritionist that she is - says Rick !!!)
In order to grow bigger 'broiler' chickens faster, breeding programs sought to
have faster maturing birds with a higher proportion of breast meat . . . and
using a strict breeding protocol it was possible to have a marketable bird in a
mere 6 weeks from hatching. The problem was that the muscle and weight gain
outstripped the ability of the legs and pelvis to support them, and they got
severe "spraddle" and inability to stand, eat and drink. Chickens being
cannibals picked on the spraddled birds ! Heart disease and heart failure was
rampant in the juvenile birds since their rapidly growing muscle and body mass
demanded a higher cardiac output!
The first correction was to only breed these hybrid birds as F1 crosses ! Neither parent breed had the rapid weight, spraddle (leg) problems or heart failure ! And the F1 "chicks" went to slaughter before they got big enough to have the leg or heart problems as adults ! So every generation of such high growth rate hybrid chicks is a new F1 generation !!!
Secondly, it was reasoned that a "phasic diet" with initial high protein (starter ration), then reduced protein (maintenance) to slow muscle mass and growth (allowing the legs and hips to 'catch up in strength and maturity !) followed finally by a high protein food (finishing ration) fuelling the rapid muscle and high quality meat growth. The genes determined the ultimate weight and height, but the nutrition controlled the rate of 'getting there' !!!
It worked ! Reduced risk of spraddle and other leg problems in juveniles. More 'finished' birds for every chick started ! And even the heart was allowed to grow to maturity before the muscle growth demands. Fewer heart failure losses condemned by Food Inspection at slaughter for ascites.
So while Goldens are "bird" dogs . . . this attempted manipulation of osteochondral growth in Golden retriever puppies (by dietary means) to reduce hip dysplasia . . . really DID originate with "the birds" !!
Michelle
Seaborn & Rick Stopps
For Silmaril Kennels (Canada)
____________________
Golden Retrievers in Cyberspace
contributed by
Kathy P.
Atelier Goldens
In an earlier post re: calcium supplementation of young dogs, I had said, "Many people don't even feed puppy foods as they *encourage rapid bone growth and weight gain which are other proven risk factors* for orthopedic problems." I received a private post asking for proof of this, the poster saying "I have yet to see any manuscripts in refereed scientific journals. There are plenty of antecdotal reports, but nothing solid."
Well, there's plenty to be found in the journals; here are three citations. I decided to post it to the whole list, as I think it will probably be of interest to many (all are from peer reviewed veterinary journals):
See "Special Symposium, Osteochondrosis: How to identify and treat its manifestations in dogs" by Steven M. Fox, MS, DVM and Alexander M. Walker, BVSc, MACVSc, in Veterinary Medicine (a peer-reviewed journal), Feb. 1993, pp 116-153. On page 121 it says, "the etiology of OCD is multifactorial. The most consistent finding in experimental and clinical studies incriminates rapid growth and weight gain. Most dogs affected with [OCD] are of medium to large size. And male dogs, which generally grow faster than female dogs, are affected twice as often as females. The relationship between nutrition, hormonal disturbances, and genetic factors for rapid growth and disturbances of endochondral osteogenesis suggests a metabolic origin...Dietary factors incriminated in OCD are high-energy, high-protein diets, excessive intake of calcium and phosphorus, and imbalances of calcium, phosphorus, and vitamin D. Excessive intake of nutrients accelerates growth and induces hormonal disturbances. In an experimental study in Great Dane puppies, free-choice feeding resulted in increased growth and multiple skeletal abnormalities. The high-protein, high-carbohydrate diet accelerated both growth and weight gain, and excessive calcium intake caused a persistently high level of calcitonin...Regardless of the specific nutrients involved, there is general agreement that the incidence and severity of OCD can be substantially reduced by normalizing the diet and slowing the rate of growth and weight gain." (Several studies were cited)
Also, from "Effects of dietary electrolyte balance on subluxation of the femoral head in growing dogs", by RD Kealey, et al. (8 authors on this one), Am J Vet Res, Vol. 54, No. 4, April 1993 (pp 555-562): "Although hip dysplasia has a genetic basis, several studies have indicated that its development can be influenced by excess food consumption, weight gain, or both. Increased weight gain from excess consumption accelerated development of hip dysplasia, whereas slower weight gain during the first several months of life delayed the appearance or reduced the severity of hip dysplasia." (Several studies were cited)
And from "Effects of limited food consumption on the incidence of hip dysplasia in growing dogs", by RD Kealy et al., in JAVMA, Vol. 201, No. 6, Sept. 15, 1992 (pp 857-863), "The first report of a correlation of early rapid growth and weight gain to severity of CHD was published in 1964...In a study of Gread Danes, it was shown that excessive intake of food accelerated growth thereby contributing to the development of hip dysplasia. In a study of 31 dogs...with a high parental frequency of hip dysplasia, it was found that CHD was more frequent, developed earlier, and became more severe in dogs with rapid weight gain caused by increased caloric intake, compared with dogs with low weight gain because of restricted feeding." And in the discussion of this study, "On the basis of our findings in the long-term study reported here, limited food intake has a beneficial effect on development of the hip joints in growing and adolescent dogs. Labrador Retrievers fed 25% less food than those fed ad libitum had less hip joint laxity when they were 30 weeks old than their ad-libitum-fed counterparts. Furthermore, by maintaining the dogs on the same feeding regimen until they were 2 years old, this beneficial effect was still present at that age, as demonstrated by the significantly lower frequency of hip dysplasia in the limit-fed dogs. Our findings confirm what has been suggested in previous studies that used fewer dogs, but that included Labrador Retrievers, Golden Retrievers, and German Shepherd Dogs."
Quite frankly, I'm puzzled by the fact that vets and PhD's keep asking me for proof that should be readily available to them. I had to e-mail this same info to the vet over on the PetCare Nutrition board here on AOL. My reading (and as a lay person, it's not as easy for me to get my hands on this stuff as it should be for a vet ) plus the advice of my veterinarian and respected breeders who have few orthopedic problems in their lines, has convinced me that puppy foods are not a good idea for large and giant breeds. So, I stand by my statement.
PS-JAVMA is the Journal of the American Veterinary Medical Assoc.
___________________________
HIP AND ELBOW DYSPLASIAS IN GOLDEN RETRIEVERS
OVERVIEW
Canine hip dysplasia (HD) is a genetic disease that is inherited in a rather complex manner because it is influenced by more than one gene. The mode of inheritance is polygenetic. It was first recorded back in the 1930s but its incidence has increased as the popularity of breeding and showing dogs has increased. Whether this is coincidence or whether there is some relationship has not been established. In a number of breeds, including Golden Retrievers, the disease is present in some degree in over 80% of individuals. Any control programme that is put in place should require that all individuals which are to be bred from have their hips scored and a score should be set above which breeding is not recommended.
Obviously the ideal situation would be to breed only with dogs that have a 0 score. However this is unacceptable as doing so would exclude most of the breed. A compromise has to be reached which will allow the retention of sufficient breeding stock but which will decrease the severity and incidence of the disease. It is up to the breed society to set standards which are acceptable for breeding. The average hip score for Golden Retrievers in Australia is 15.85 so the following criteria could be adopted as indicating suitability for breeding. If the score for any one hip is greater than 8 or if the score for any one of the 9 features listed on the score sheet is greater than 3 the dog should not be bred from. As the breed average score drops so will the score that is acceptable for breeding.
Such a control programme can be taken a step further by recording the hip status of offspring so that it can be determined which sires are tending to reduce the hip scores of their progeny.
THE SCORING SYSTEM
HIP SCORE Hip Right Left
Norberg
Angle _______________________
Subluxation _______________________
Cranial acetabular edge
_______________________
Dorsal
acetabular edge _______________________
Cranial
eff. acet. rim _______________________
Acetabular fossa _______________________
Caudal acetabular edge _______________________
Fem neck exostosis _______________________
Fem head recon touring _______________________
Total _______________________ Score ______
The 9 items listed on the scoring sheet are all details of the anatomy of the hip joint that can be seen on an x-ray film. Of these features 8 are scored out of 6 with 0 being normal. One of these, the Caudal Acetabular Edge, is scored out of 5. Therefore the worst possible score for each hip is 53 with the worst combined score being 106. The figures I have currently available show the best score for the breed is 0 and the worst 101
THE GRADING SYSTEM
There is not a direct relationship between scoring and grading which causes considerable confusion. The grading is done on the worst hip only. Because of differences in the assessment methods it is possible, though uncommon, for dog with a relatively low score to have a relatively high grade. Generally speaking it is considered acceptable to breed from dogs with grades 0, 1, 2, and 3 and not from grades 4, 5, and 6. It is probable that the grading system will stop being used sometime in the near future.
HIP DYSPLASIA
The hip joint is a ball and socket joint with the ball (femoral head) being on the proximal end of the thigh bone (femur) and the socket (acetabulum) being on the pelvis. If the hip joint is normal the ball is a neat fit in the socket. Generally all newborn puppies have normal hip joints but in those that have HD an abnormality develops during growth. The problem appears to be in the growing of the socket. For the socket to grow bigger as the dog grows requires quite a complex process because it is difficult to grow a hole. With the acetabulum this is achieved by the three bones that make up one side of the pelvis (ilium, ischium and pubis) joining at the acetabulum thus forming a complex pattern of growth zones. If the acetabulum is to develop correctly the growth rate at these different zones has to be precisely matched. If it is not, the acetabulum will become distorted so that the ball is no longer an accurate fit and this is hip dysplasia. Some recent research suggests that dogs with HD have problems with other bone growth zones but because these are mainly involving single bones they do not cause problems.
Hip dysplasia in itself does not commonly cause lameness. It only does so if it is of such a degree that the hip dislocates and this is uncommon. So many dogs, particularly younger dogs, with hip dysplasia show no signs of lameness. This combined with the fact that it is a developmental abnormality is the reason why we have to resort to assessing dogs for hip dysplasia from an X-ray taken when the dog is at least 12 months of age.
With dogs that have HD the ball is not a neat fit in the socket so the joint is subject to excessive wear and tear. This excessive wear and tear results in the development of degenerative joint disease (arthritis). It is the arthritis that causes the lameness. Other factors can impact of the degree of wear and tear the joint is subjected to. The two main ones are the weight of the dog and the amount and type of exercise the dog takes. Obviously the heavier the dog the more stress is put on the hip joint so large heavy dogs are more likely to become lame because of hip dysplasia than small light ones. Dogs that get a lot of exercise at fast gaits such as galloping behind a car or bicycle and dogs that do a lot of jumping or turning and stopping such as when fetching balls or sticks stress the hip joints and are therefore more likely to become lame. A normal hip joint can sustain these sorts of stresses without developing arthritis. So the age at which a dog with HD shows signs of lameness and the severity of the lameness is influenced by an inherited component. That is the degree of developmental abnormality of the joint. Then there is the environmental influence which is the degree of stress the joint is subjected to.
OUTCOMES
Now addressing the question of how successful the hip dysplasia control programme can be. Progress will be painfully slow for a reason. If only those dogs with a 0 score were bred from there would be a rapid decline in the incidence of hip dysplasia as has been demonstrated by some experimental breeding programmes carried out in Sweden. This approach, however, is socially unacceptable as it would eliminate a large percentage of animals from breeding. As a compromise is reached which acknowledges that dogs with some degree of hip dysplasia can be included in a breeding programme the control scheme is slowed but control is much better than allowing the disease to become even more widely distributed.
ELBOW DYSPLASIA
Elbow dysplasia is a disease with a high inherited component, which primarily affects intermediate and large breed dogs. The incidence in Golden Retrievers is not as high as in some other breeds. Typically, both elbows are affected. However, unilateral elbow dysplasia is not uncommon.
The elbow joint is formed by three bones (radius, ulna, and humerus) which must all grow synchronously and fit perfectly. The radius and ulna are paired bones with the radius being the main weight bearing bone. The normal elbow joint is characterized by a smooth transition from the ulnar articular surface to the radial surface. In a dysplastic elbow the edge of the ulnar surface lies above the level of the adjoining radius, creating a step between the radius and ulna and causing incongruity of the joint. The height of the step may vary from barely noticeable to 4 mm or more. When this occurs the weight bearing force on the ulna is increased, resulting in excessive pressure on the medial coronoid process. This leads to fragmentation of the coronoid process. This usually occurs between 5 and 7 months of age. A superficial to deeply grooved "kissing lesion" is often present on the humeral articular surface opposite the fragment. A cartilage flap or OCD (osteochondritis dissecans) lesion may also develop. Secondary arthritis becomes evident at 6-7 months. Compensatory adjustments during growth may occur in some dogs, tending to minimize unequal growth rates between the three bones and moving the ulna distally to better conform to the radius. . If the ulnar surface lies below the radial one, excessive force is then placed on the anconeal process at the top of the ulnar articular surface. This force will cause a failure of ossification, leading to an ununited anconeal process.
CLINICAL SIGNS
Affected dogs are frequently lame or have an abnormal gait. The gait is often characterized by excessive paddling or flipping of the front feet. The animal may either hold the elbows out or tucked in and often stands with the feet rotated outward. Many sit or lie down much of the time, or play for shorter periods of time than other dogs of comparable age. They are often described as quiet or even lazy. Frequently, they are stiff when rising and tire easily. Exercise typically makes the lameness worse. In dogs with bilateral elbow dysplasia, the lameness may seem intermittent or shift from one front leg to the other. When both front legs hurt, dogs do not limp constantly. Rather, they shift weight off their elbows by altering their gait and stance. These dogs will only "limp" when one elbow is more painful than the other. On examination, manipulation of the elbow is often resisted. Swelling and crepitus (grating) may be palpated. The swelling may be worse after exercise. In some cases, the joint will be thickened. Muscle atrophy may also be present.
DIAGNOSIS
The routine monitoring for the presence of elbow dysplasia is carried out from a lateral x-ray of the flexed elbow joint taken when the dog is over 12 months of age. Correct radiograph technique is critical for making the diagnosis. The grade is derived by measuring the amount of new bone that has developed as a result of arthritis. Unlike the grading systems for hip dysplasia the system for elbow dysplasia is used internationally.
ADVICE
It is generally considered that dogs with grade 3 elbow dysplasia should not be used for breeding and that dogs with grade 2 should be considered a serious risk
Reference: World Small Animal Veterinary Association web site
If there are any questions address them to me at wyburn@netserv.net.au
R S Wyburn BVMS, DVR, PhD, FACVSc, MRCVS