Hip Dysplasia and more - Page 3

Please read the last paragraph of my last entry if you don't read anything else. It should clear up the misconception that 'environment' pertains to the training field.

This, too:

You will recognize that many of these traits are features of breed type, and of course most are under direct genetic selection or are secondary to some other trait under selection. As it seems to go in the competitive show world, many of the traits on the "High Prevalence" list have become progressively more exaggerated through artificial selection - the large size gets larger, heavy bone gets heavier, a broader head gets broader. And to make matters worse, the desire for dogs that "finish" (become champions) at ever younger ages drives selection for rapid growth, which overloads the immature skeleton and muscle systems. It seems that we are trying to select against hip dysplasia at the same time as we select for many traits that increase the risk.

The factors that cause hip laxity and the development of dysplasia occur in the first few months of the puppy's life. Sometime between birth, when the cartilagenous tissues of the hip joint have the capacity to become a perfectly constructed ball and socket joint, and when the puppy is four or five months old, the soft tissues of the pelvis fail to provide the support necessary to keep the femoral head properly seated in the hip socket. As a result, the joint doesn't develop properly, then abnormal biomechanical forces exacerbated by environmental factors such as weight and inappropriate exercise begin the cycle of damage and inflammation that result in dysplasia and osteoarthritis. 

Wayne Riser showed 40 years ago that ​

In very young human and canine subjects with unstable coxofemoral joints, hip dysplasia can be prevented and the instability corrected if the congruity of the components of the hip joint is maintained and if femoral subluxation does not occur. If proper congruity cannot be maintained, the hip joint becomes malformed in a relatively short time. The changes in the bones and cartilage of the hip are thus the indirect result of failure of the soft tissues to support full congruity of the bony components of the hip.

Few genes so far analyzed directly affect osseous structures. [This is still true.] The shape of bones reflects changes by biomechanical stresses.

The spread of hip dysplasia centers around the genetic transmission and heritability of certain body size, type, conformation, movement, growth pattern, and temperament. This conclusion is based on the facts that the prevalence of hip dysplasia is approximately the same in a number of breeds with similar body characteristics and there is no gene flow between these purebred breeds. Since these facts must be respected, biomechanical and environmental factors associated with certain body conformation and size must be considered as the causes.


According to Riser, the risk factors for hip dysplasia are related to the features of a dog and its breed that result in a mismatch between the forces necessary to maintain congruency of the hip joint and the support the soft tissues are able to provide during the critical first few months of life. By the time the puppy is 6 months old, the strength of the supporting tissues and ossification of the bones should be adequate to prevent the development of hip dysplasia under normal circumstances. Prevention of hip dysplasia will come both from reducing the genetic risk factors through selection and from avoiding situations that could result in joint instability or incongruity.

The literature review and report of our work presented here have revealed a basis for optimism in controlling and reducing the prevalence of hip dysplasia in both man and animals...In children, it is basically the test for hip laxity at birth, and for the dog it is restriction of breeding only those animals with radiographically normal hips.  Both in children and dogs, hip dysplasia is, for the most part, a ‘man-made’ problem and can be controlled if man will use the tools at his disposal.

These findings uphold the validity of our two premises that (1) hip dysplasia occurs only if hip joint instability and joint incongruity are present in the young child or animal; and (2) the disease can be prevented if hip joint congruity can be maintained until ossification makes the acetabulum less plastic and the abductor muscles and supporting soft tissues become sufficiently strong and functional to prevent femoral head subluxation.


Genetic selection and management of environmental risks are both necessary to lower the frequency of hip dysplasia. For selection to be effective, we need to recognize that some of the traits that are valued as part of breed type are themselves risk factors for development of hip dysplasia. Selecting for faster growth and ever increasing size will confound efforts to produce dogs with better hips. Likewise, inadequate weight management of both puppies and adults is an environmental factor that dramatically increases the risk of developing dysplastic hips. Finally, we should use a little common sense about activities that are appropriate for puppies

Jenni78 - Not all studies come to the same conclusion as Dr. Schultz. I've looked up a bunch of them.

I included a link, the article links to Dr. Ron Schultz' notes. It's a word document that needs to be downloaded to read.
His article reads;
• Due to maternal immune interference, we must vaccinate once after 12 weeks unless you have titered the puppy to ensure he has had an individual immune response rather than maternal. Titer will tell when individual rather than maternal immunity is present.
o At 6 weeks, 50% of puppies will become immune from puppy vaccine
o At 9 weeks, 75% will become immune
o At 12 weeks, 99% will become immune

Also...from this article. Natural diet (all meat) can detrimentally affect the immune system and Vitamin E and selenium deficiency will cause a poor vaccine response. A straight meat diet causes vitamin E-selenium deficiency. The second generation was even easier to put into an E/selenium deficiency so this nutritional effect was passed on genetically.

I did some looking and found that E-selenium deficiency causes many different problems including.... Insufficient selenium intake can cause serious health problems, including Kashin-Beck disease in human beings, which is characterized by the degeneration of the articular cartilage between joints, thyroid disease and a variety of cancers. (other problems include, heart, muscle & connective tissue weakness, nerve and seizures, fertility problems). In another article, a 50lb dog requires 150 micrograms of Selenium per day, it is used up on the average of 27 hours in dogs. Too much of it is toxic.

A pound of; 70/30% ground beef, dark meat chicken have 61 micrograms, beef liver has 550 micrograms, salmon 510 micrograms.

Meats typically doesn't have vitamin E - Diets high in fat omega-3 and Vitamin C will increase the tocopherol (Vitamin E) requirements in the diet.

The results showed that meat, with the exception of chicken thigh, is not an important supplier of vitamin E, not even from animals fed a vitamin E enriched diet. Still looking for E requirements for dogs.

100 grams Beef liver has .63 milligrams, 100 grams of chicken thigh with skin has .27 milligrams, Egg yolks have 2.58 miligrams.

According to the NRC, the recommended allowance for maintenance, reproduction and growth of dogs, should be satisfied by 20 IU vitamin E/kg diet (3300 kcal ME), 1.1 IU/kg BW for pregnancy and 1.2 IU/kg BW for growth.

• Vitamin E: 1 IU is the biological equivalent of about 0.67 mg d-alpha-tocopherol, or 0.9 mg of dl-alpha-tocopherol.
   

  Let's say that I have a soft gel capsule that contains 500 IU of Vitamin E as retinol. To convert this to mcg, using the information above, I would multiply it by 0.67:

  500 × 0.67 = 355 mcg.

I cannot find info about bone or bone meal.

https://ndb.nal.usda.gov/ndb/search/list

Exactly, Joan. The inheritance is not so simple as a "bad gene," rather, a type of conformation, predisposition to certain other factors, etc. Correlation is being seen as causation.

Sitasmom, I am aware of other studies, but none that seemed as concrete as what Dr. Schultz has done since the 60's and 70's- I assume you've seen the video interview he did with Dr. Becker where he chuckles that it's being treated as "new" information that there is no scientific basis for annual revaccination?

https://www.youtube.com/watch?v=L1Xd5ghnlJ4

Beetree, thanks for another thought-provoking contribution. Don't know what we'd do without you.

I looked at the OFA statistics by dog breed, and the "type", and "size" doesn't be a determining factor...
http://www.ofa.org/stats_hip.html

Since 1974, some breeds have improved a great deal, while others haven't.

I agree that our dogs are over vaccinated, every year is just too much, as for me, after the puppy shots, mine get them every 3 years.
I also do not give regular shots within several weeks of rabies. It's probably too much, but significantly reduces the load.

Joan, can you confirm that you are 100 percent agreeing with Jenni? I certainly did not draw that conclusion with my own readings of your information.

I strongly feel there is a denial of breeder responsibility and blaming of the victim in the dog that shows hip dysplasia. I didn't think you were in that frame of mind, rather that there is genetic component responsible in a type, and therefore something able to be selected for in breeding. The joints as they grow and mature also respond by changes seen, to certain environmental factors and those are what set the stage for hip dysplasia.

And then there are those dogs being born with bone and socket deficiencies, too. The one's needing the femor removals to be without pain. Those can't be ignored as being influenced by environmental causes.

It shouldn't be about deflecting (breeder) responsibilty and blaming the victim with generalities of (pet) ownership.

I certainly remember Blitzen writing often how this problem was addressed and improved in a different breed than the GSD through screening and selective breeding.

 

Sit as, it is the size of the 'breed' of dog, but the genetic muscularity of the dogs within the breed. Plus how the puppies are raised, from birth onward. Please go to this link, halfway down the page are two short videos of a litter of newborn greyhound puppies and a litter of newborn burnese mtdog...the comparison of the litters and the surface they are on should help you understand what the whole article is talking about.

http://www.instituteofcaninebiology.org/blog/how-do-hips-become-dysplastic

Beetree: Joan, can you confirm that you are 100 percent agreeing with Jenni? I certainly did not draw that conclusion with my own readings of your information.


Bee, where did I state I'm 100% in agreement with Jen.?

I believe what is stated in the article I posted, multiple ways in an attempt to get readers to 'READ' the article.
I am no where saying the breeder doesn't have responsibly for litters they produce. How puppies are raised from birth till they are eight weeks, as the article states; the first 8 weeks are the most critical in hip formation. Giving instruction to new owners and hoping that the instructions are followed, especially not to overfeed, is all that can be done once the pup has gone home.
I know first hand what happens when puppies are overfed and grown too fast in first eight weeks. Do over with a repeat breeding and following proper protocol as outlined in this article produced tremendously positive results.

I have also changed my selection of breeding dogs for the lighter boned, dryer type of dogs instead of the more popular 'big bone' loose skinned, big ol' bucket heads. When people tell me they are looking for that type of gsd, I give them suggestions of other kennels.

BTW, bee, if HD was due to HD gene, decades of ofa to select breeding stock would have had a great oimpact on reduction of occurance. But it has not.

No puppy is born needing an FHO, Beetree. That happens during DEVELOPMENT. Why, is the question.

Guess what, beetree? Different breeds have different heritable disorders. Just because one breed can reduce HD via selective breeding doesn't mean it's that easy in another. Obviously, we've tried that. We're in the same place we were before (which is really not that bad, relatively speaking, if you look at the breeds most affected by HD).