Canine Hip Dysplasia – Frequently Misunderstood

Canine Hip Dysplasia

Frequently Misunderstood!

 

You will see that this topic is one that I wish for everyone,  especially dog breeders to really research out for  yourselves and be convinced in your minds.  Please don’t take my word for it or anyone else’s word for it for that matter.  Look at all sides, ponder what you read and learn- be convicted or convinced in your mind.

CHD (Canine Hip Dysplasia) is a condition that is frequently misunderstood.

  • Why is this condition thought to be mainly genetic?
  • Is it preventable?
  • After all these years, has it been bred out of dogs by ethical breeders to any extent?
  • If not, why not?

Are you asking yourself the same questions?

While the exact cause of canine hip dysplasia is said to be unknown,  it is still widely believed to be mainly genetic in the dog world.  In human science, however, hip dysplasia is more often said to be “developmental”.

Why the discrepancy when veterinary medicine continues to teach that dogs are so similar to humans in so many ways?  In the human medicine world, it is pretty well known that  hip dysplasia develops around the time of birth, shortly after birth, or even during childhood.

How much is really genetics?  How much may be epigenetic?  Developmental? Environmental?

“The hip joints of all dogs are normal at birth. The joints continue to develop normally as long as full congruity is maintained between the acetabulum and the femoral head… The acetabular rims are stimulated to grow by mild traction applied by the joint capsule and gluteal muscles attached along their dorsal borders, and from pressure by the femoral heads upon the articular surfaces… The morphologic characteristics of the complex hip structure show that biomechanics behavior is the prime influence in the growth of this joint.” (Wayne Riser 1985)

“Canine hip dysplasia is a complex disease. It is a concentration of factors from a pool of genetic weaknesses and environmental stresses that fall into a programmed pattern of progressive remodeling and degenerative joint disease. The degree of involvement varies from minute changes in bone structure to total destruction of the hip joint. Investigators have searched intensively for genetic, chemical, and metabolic defects, but the cause has remained obscure.

Hip dysplasia affects humans and all other domestic mammals. In humans, 1.3 children in 1000 are affected. In dogs the prevalence may run over 50% in large dogs if control measures have not been practiced. Few data are available on the prevalence of hip dysplasia in other mammals, but it is thought to be low. The disease is undoubtedly rare in undomesticated animals.” (Hip Dysplasia chapter 83 Wayne H. Riser, W. Harker Rhodes, and Charles D. Newton) http://cal.vet.upenn.edu/projects/saortho/chapter_83/83mast.htm

Are you interested in knowing even more facts and having more thoughts to ponder?  The following is a very informative article written by Dr. John Symes.

 

 

Hip Dysplasia
by Dr. Symes

Please note that all comments and/or emphasis on some of his views are mine and will be in bold, purple colored font.

I have had plans to write a major paper on this frequently misunderstood topic for quite some time. Unfortunately, the need to write about an ever-increasing number of life-threatening health issues prevented this from happening before now. But as misconceptions go, this is a high-priority item.

Hip dysplasia is not a “genetic malformation of the hip socket”, as commonly thought, but rather a weakness in the ligaments that support the hip joint. This allows the ball of this ball-in-socket joint to bang away at the joint surface, preventing the socket from forming properly. In other words, the instability created by weak supportive ligaments keeps the body from being able to manufacture a deep, smooth hip socket for the ball to fit snuggly into, resulting in the flattening of the acetabulum (hip socket) and a squaring of the femoral head (the ball). The sockets are shallow because of repetitive trauma to the developing bone (micro-fractures), which prevents the weight-bearing surface of the hip joint from forming properly. These changes worsen drastically as the cartilage covering of the joint wears away and bone-on-bone contact occurs, leaving them with the characteristic signs of the osteoarthritis we see in radiographs of affective dogs.

This may sound like a radical idea but there have been veterinary studies that strongly suggest this for years and years, beginning with those done by orthopedic surgeons and radiologists who developed a technique for measuring joint laxity in Labradors. They took 2 sets of X rays of the hip, one with the ball forced deeply into the socket and one with the ball distracted as much as possible, measuring the differential and trying to use those measurements as a predictor hip dysplasia in the individual.

Why would this be valid? Because the degree of laxity tells us how strong or weak the ligaments surrounding the hip joint might be, which would in turn determine the instability of that joint as the dog grows into maturity. Did all dogs with significant joint laxity go on to become dysplastic? No. Some managed to recover when their muscles developed and the joints stabilized. But others developed radiographic signs of dysplasia as late as 2 years of age, long after the hip sockets were fully formed. Where is that “genetic malformation of the hip socket”in these cases? What criteria do we use in evaluating these cases? We look at how well the hips are seated in the socket? What determines that? The tightness of the ligaments and joint capsule does as much as the depth of the socket. Some of the femoral heads are not anywhere near the socket, appearing to be floating in space on the X ray of these crippled dogs. Loose ligaments.

Imagine a large breed dog, such as a Lab or Saint Bernard, with lax hip joint ligaments as they grow and develop. Imagine the stress and strain this would place on the cartilage of the hip socket as that large or giant breed puppy clumsily runs, slips and slides while chasing the ball or walking across the kitchen floor. Now imagine the same scenario in a more sure-footed cat or toy breed.

We were taught in veterinary school that the breeds of dogs over 40 lbs were the most likely to develop hip dysplasia. This has proven to be true, although I have rarely seen cases of dysplasia in cats and small breeds. In stark contrast, nearly all St. Bernards are dysplastic and the malady is incredibly common in numerous large breeds of dogs; the same breeds of dogs that develop other juvenile bone diseases, including OCD of the shoulder and ununited anconeal or coronoid processes of the elbow. Think there is some stress on the elbows of a rambunctious German Shepherd or Rottie puppy?

All of these maladies are a failure of collagen, the building block of our entire skeletal system, which serves as elastic in our connective tissue. Collagen makes up approximately 30% of the protein in our body and is the protein matrix for ligaments, tendons, cartilage, bones, organs, and even blood vessels. Failure of collagen to form properly can have catastrophic results, including skeletal abnormalities, polycystic organ syndromes (e.g. liver, kidneys), and severe vascular syndromes (e.g. aortic aneurysm). A quick study of Ehlers-Danlos Syndrome and Marfan Syndrome tells us most of what we need to know. These run in families just as most collagen disorders (and cancer) run in breeds of dogs. There are “genetics”involved but the truth is much more than skin deep. Food intolerance also runs through families, with 40% of first degree relatives born to a celiac developing the condition. Interestingly, we were taught that if two OFA certified, hip dysplasia-free dogs were bred together, up to 40% of their litter (this exact same percentage) could be born with dysplasia. This is not a coincidence.         (Read  about the link between vaccines, joint issues and collagen HERE )

The first clue of how to combat this epidemic comes when we grasp the importance of nutrition in the development of our entire body. One of the most important components of collagen is ascorbic acid – good old vitamin C. Without adequate levels of this essential vitamin, we develop scurvy; a horrible condition marked by bleeding gums, open sores, pathological fractures, and death if not treated properly. This follows a combination of collagen and immune failure, all resulting from inadequate vitamin C intake.

In the human, where is the vitamin C absorbed? It is absorbed by the small intestine where most nutrients are picked up by the delicate villi of the bowel lining; those same villi that are damaged by the  foods of gluten grains (wheat, barley, rye), dairy, soy and corn. Could celiac disease lead to weakened collagen and hypermobile joints? Most definitely! This is a major problem among celiac youngsters.  (Celiac is a human disorder however, we know that dog’s being carnivores are not designed to eat or digest grains, dairy or soy in the first place and along with eating dead, nutritionally void processed pet food, is certainly a major underlying cause – whether the dog is truly celiac or not)

But what about dogs? We were taught that dogs and cats are not dependent upon dietary vitamin C because they possess the ability to make their own ascorbic acid in their liver. This is true partly. Yes, we were told this in veterinary school but the details of how they do this were never explained to us. Vitamin C is made from glucose in a four step, enzyme-driven process taking place in the liver, that amazing organ that our colleagues practicing Eastern medicine call the center of our medical universe. They are only off by a matter of inches. Why do I boldly state that as fact? Because the liver is completely dependent upon the nutrients coming out of the small intestine, thus making the small bowel the true center of our vast biological galaxy.

Now imagine a dog or a cat being fed a grain-based diet (wheat, barley, corn, rice) laced with soy and dairy. This is the composition of numerous commercial dry kibbles. What if they suffer from a food intolerance (no doubt about it, being carnivore they would be naturally intolerant of not only gluten due to the lack of enzymes to digest it) to one or more of those proteins in the way that celiacs do to gluten? This happens much more frequently than we’ve even imagined. And, yes, they will fail to absorb the proper amounts of calcium, iron, iodine, trace minerals, proteins, fats, sugars and vitamin C just like as the gluten intolerant individual does when their villi are damaged. This can ultimately lead us into every medical condition known to man, especially when we understand essential body functions, including the immune system and enzyme-driven activities in the liver (e.g. vitamin C and protein production).

Enzyme systems are made up of proteins and cofactors, the latter being vitamins (e.g. B complex), minerals, and other enzymes. An enzyme system must have adequate cofactors to operate properly. Back to the production of vitamin C: What if the dog is not receiving adequate vitamins and minerals in their diet or is malabsorbing those that are in the diet due to food intolerance? (Again, no doubt at all that being carnivores they are NOT absorbing or receiving adequate nutrition) The enzyme systems will eventually fail, including the four that are involved in the conversion of glucose to vitamin C. This is not hard to imagine. So, is the dog truly independent of dietary vitamin C as we have assumed for years? Perhaps so, if it is getting a biologically appropriate, non-offending diet that provides all of the substrates it needs to perform this vital task. (However, many nutritionists believe that the dog gets vitamin C in their natural diet to augment what they make in their liver. This would open another avenue for “subclinical scurvy” in the dog, as the food intolerant pet fails to absorb the vitamin C that is commonly added to many commercial pet foods (just in case).

The epiphany comes when we grasp the prenatal effects of this degenerative process. I like to remind people that we and our pets are born fully formed, just incompletely developed. Every ligament, tendon, bone and organ is in place at birth. These elements simply have to grow and mature as our bodies reach adulthood. Imagine what happens if the initial building blocks for these critical structures are inadequate or absent during the initial construction. It would be like building a house out of faulty lumbar or defective bricks or laying a sub-par foundation under a two story house. The first major storm that comes along could do immeasurable harm to the structure. In fact, it could come apart at the seams.

The first evidence of failure in the poorly constructed individual is often found in the skeletal system of large dogs for the reasons mentioned above. The stress put on the frames of rapidly growing large breeds can be tremendous. But we also have certain breeds that we call chondrodysplastic, a bit of med-speak that basically means – messed up cartilage. This is an example of genetic engineering at its worst as man created the flat-faced, squatty body dogs that make up this class- the English Bulldog, Shih Tzu, Lhasa, Bassett hound, Dachshund, and others. I love these breeds as much as the next veterinarian but our forefathers made some serious blunders in making dogs look the way they wanted them to appear, especially the first two.

The Bulldog and Shi Tzu suffer from collagen problems within the first months of life in the form of “cherry eye”, a weakness in the cartilage that gives the third eyelid shape and supports a lymph gland it contains. Their bent legs, deviated septum, congested throats, elongated palates and back problems are often overshadowed by their horrible skin allergies and ear infections, signs that the damage is being done to the intestinal lining by the “big 4″foods. (and from vaccination damage) I have not met many English Bulldogs or Shih Tzus that did not have major skin or ear problems before I put them on hypoallergenic (grain free) diets. They also tend to develop Demodectic mange – a sign that their immune system can’t handle the mites that nearly all dogs have in their skin, passed on to them by their mother. This points directly to the malnutrition that results from the damage taking place in the center of their galaxy.

Then we have the intermediate chondrodysplastics; the Cocker, Poodle, Schnauzer, Westie, Jack Russell, Cavalier, and others. These breeds often develop collapsing trachea syndrome, intervertebral Disc syndrome and heart valve problems, all  involving collagen. Tragically, 50% of Cavies develops acute mitral valve prolapse at 5 years of age with 90% having died from congestive heart failure by age 10. Why does this particular collagen failure wait 5-10 years to show up, knowing that heart valves are flopping back and forth at the rate of 60-200 beats per minute?

Interestingly, this valvular demise occurs right around the time that the Cockers are rupturing their (left) cruciate ligaments, the Dachshunds are blowing discs, the Labs are developing lower back issues, the Dobies are dying of cardiomyopathy, and the Rottie, German Shepherd, Irish Wolfhound and Irish setter are dying from bone cancer? That’s a whole other paper but here’s a hint: It involves the residential organisms that have taken up residence in the collagen (e.g. viruses and mycoplasma). Another clue is the spike in other autoimmune diseases taking place in other breeds during this time period.

The lesson to be learned is that all of these tragedies are related events. The body is one big orchestra and the conductor is the immune system. Once we start playing out of key, the conductor goes to work. We get out of tune early in life by eating the wrong things and not eating the right things. (and compromising the immune system with vaccinations and toxic drugs) Those are two different insults. The cascade of events that follows is predictable. We just have to have an ear for the music. And, once again, this symphony starts long before our offspring are even born.

We know what we have to do to reverse this dangerous trend. It is not a requirement that we solve more mysteries or uncover more secrets in order to achieve optimal health, even after sinking into the abyss as I have done. Do we need to name every virus or bacteria that is involved in our man-made dilemma. After all, they are simply reacting (adapting) to our every insult. No, the solution is amazingly simple: We must consume biologically appropriate, non-offending foods and feed our pets in the same manner, starting with the prenatal period and continuing through adulthood, and into our twilight years. If we do this alone, medical miracles will occur. (and cease with all the toxic Rx medications and vaccinations)

Here’s the parting shot and the takeaway message: We can and will eliminate hip dysplasia in the dog by feeding the soon-to-be pregnant female a healthy, non-damaging diet before she is bred and throughout her gestation. Of course, the puppy diets must follow suit. We have already proven this in individuals with a history of producing dysplastic puppies. The results have been amazing, yet as predictable as rain on the horizon. I believe down to my socks that this would also be true of innumerable other collagen disorders, the likes of which are mentioned above.

We’ve all heard the expression “Garbage in, garbage out“ a perfect summation for any article that deals with the intricate functions of these incredible machines we call our body, including one written about a “genetic condition” – hip dysplasia.

 

More References for your own research:

 

http://belfield.com/canine-hip-dysplasia-chd/

http://cal.vet.upenn.edu/projects/saortho/chapter_83/83mast.htm

http://www.stanfordchildrens.org/en/topic/default?id=developmental-dysplasia-of-the-hip-ddh-90-P02755

http://www.instituteofcaninebiology.org/blog/the-10-most-important-things-to-know-about-canine-hip-dysplasia

http://dogtorj.com/appetizers/newest-appetizers/hip-dysplasia/

http://dogtorj.com/hip-dysplasia-its-not-what-youve-been-told/