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The following two articles were taken from the book -
about his research and experiments on hip dysplasia and vitamin C. A) HIP DYSPLASIA Increasing numbers of breeders and veterinarians are effectively warding off this dreaded puppy crippler with a very simple potion: Vitamin C. By following my suggestions in Part Three for supplementation of pregnant b###hes and growing puppies you can also put a stop to hip dysplasia among your animals. How this is possible is explained by the relationship of vitamin C, collagen and stress. Collagen, you will remember, is the intercellular cement that binds tissues, that makes tendons and ligaments strong and strengthens all other structures in the body. Good quality collagen is dependent on an ample source of vitamin C. Stress is the scourge of both man and dog. Stress undermines resistance to disease and germs in part by depleting the body's stores of water-soluble vitamins, namely vitamin C and the B-complex group. Work-stressed dogsled teams have displayed signs of scurvy, the disease that results from a vitamin deficiency. Sickness diminished when the dogs were given food containing vitamin C. Consider now the puppy, a tiny and vulnerable animal undergoing constant assault from stress: environmental and emotional stress when the puppy is separated from mother and littermates and placed in new surroundings; toxicologic stress from deworming; immunologic stress from vaccinations; physical and mental stress from conformation and obedience training; stress from cosmetic surgery such as dewclaw removal, docking of tails, and cropping of ears; stress from teething; and stress from growing. Pups of the larger breeds grow especially fast and this puts an added load of stress on their developing bodies. The chart on page 51 shows the low rank that dogs have among the animal kingdom's producers of vitamin C. For the size of the German Shepherd, Great Dane, Saint Bernard, and other large dogs, canine liver production of vitamin C is paltry. This poor production, along with the nonstop stress, results in chronic subclinical scurvy. The animal may not lapse into terminal scurvy but he will often become ill with some of the symptoms. Hypertrophic osteodystrophy (HOD or panosteidis), which was mentioned earlier, is one example. And so is hip dysplasia. Both conditions are related to deficient vitamin C and poor collagen. The big-breed pup has an extraordinary need for large amounts of vitamin C. The vitamin is needed in laying down the collagen. He needs strong ligaments and tendons to hold the bones and a heavy muscle mass in place. He gets no vitamin C in his food. If his liver doesn't produce enough, the animal is at risk, and from the worldwide incidence of hip dysplasia, it seems obvious that the liver of the domesticated dog is not up to the task. The problem is located in the area of the hip socket, where the head of the long thighbone (the femur) is shaped like a round ball and fits neatly and snugly into the concave hip socket (the acetabulum). The joint is held in place by a short, elastic, round ligament, supported by adjoining muscles. The fitting ensures rigidity and the synovial fluid between ball and socket provides lubrication for mobility. On the inner side of each leg is a tendon like muscle, called the pectineus, that connects the lower end of the thighbone to the pelvis above. When the young dog is undergoing constant stress and not producing enough vitamin C, the quality of the collagen is below par. The pectineus muscle doesn't develop as it should to keep pace with the skelatal growth. The ligaments are not enough to hold the bulk of muscle and bone in place. On the surface, all appears normal. The dog is a picture of health. The next minute he is a cripple. It can happen that fast. The dog is jumping, running, chasing a Frisbee or a tennis ball, doing what young dogs do. There is tremendous pressure -- the weight of the entire body -- on the muscles, bones, tendons, and ligaments of the rear legs each time the dog pushes off or springs. The pectineous muscle has become taut as the bones grow larger. Tension is transferred to the head of the femur in the form of an outward lateral pressure. One vigorous leap and the ball is tugged away from the natural cradle of the socket. A small gap of varying degree is created in both right and left hip joints. You now have what is medically known as congenital coxofemoral subluxation and commonly called hip dysplasia. Rapidly, from a few minutes to a few hours, the synovial fluid leaks out of the joints, causing inflammation in the adjacent tissue. There is now little or no lubrication in the joints. The rotation of the ball in the socket becomes grating and uneven. An inflammation occurs there too because of the lack of oil and irregular movements of the parts. Soon the animal is limping. With time, scar tissue and ossification build up in the gap. This is nature's way of filling the vacancy. An osteo-arthritic condition develops and contributes, I believe, a good deal of the pain. Sometimes the pain is so bad a dog will roach up his back in an attempt to alleviate the pressure on the joints. Continued activity of the animal means continued irregular wearing of the affected joints. Thus there is more inflammation, more scar tissue and ossification. The effect is to push out the head of the femur even more, a process that doesn't stop until either the animal has stopped growing or the gap has partially or totally filled. It is important to bring a young dog to the animal hospital at the
first sign of limping. Many people will wait weeks before acting, hoping
the limp is only a temporary thing. The delay only allows the arthritic
condition to progress. Hip dysplasia can be diagnosed only through X-ray. The
degree of severity, that is the extent of joint separation, is defined through a
numbering system from zero to five. Zero means good, flawless hips. Five means
the worst has happened. I have one set of pictures on my office wall of the
worst case of grade-five hips I ever saw. Both joints had separated so far that
the entire bowl of the acetabulum had filled solid with bony tissue. The damage,
once done, is permanent. Many animals are put to sleep. Many vets will
tell the owner there is nothing that can be done except to put the animal
on aspirin or cortico-steroid drugs. This will keep the pain and B) VITAMIN C VERSUS THE GENETIC THEORY OF HIP DYSPLASIA The reigning myth -
which unfortunately still clouds much of veterinary hinking to this day - is
that hip dysplasia is an inherited condition. A limping, dysplastic dog, so the
reasoning goes, begets other limping, dysplastic dogs. The protocol calls for
drastic action: Destroy the dysplastic puppies or have them neutered, so there
is no possibility to pass on dysplastic genes. I know of breeders who, even
before the X-ray was dry, would ask the vet to put the dog down. So severe has
been the stigma, they were afraid to let it be known that their b###h or
their sire had produced dysplastic puppies. If you were a breeder and word
got out that your b###h was giving dysplastic puppies, you couldn't sell
the offspring. You quickly and quietly brought afflicted dogs to the vet
and had them put away. When hip dysplasia was involved, people talked in
whispers. Behind this proprietary stealth is a residue of heartache. Many
breeders would provide a guarantee when they sold a puppy. If the dog turned up
lame and was found to be dysplastic, they would give you another dog. But it
doesn't take long to develop an attachment to a puppy, and I have seen
many a grown-up sitting and crying over a young dog that was put to sleep. The
story of hip dysplasia is written in tears. An East Coast veterinarian connected
to the Seeing Eye Dog-program says that animals with zero-, one-, and two-
degree hip dysplasia can be approved for training. Dogs with three degree hips
are not to be trained. They are neutered "to keep them from
producing" and are handed over to individuals for pets. The four- and
five- degree dogs "have to be put to sleep", according to this
veterinarian. Furthermore, he recommends that only zero-rated dogs be allowed to
breed and reproduce. Over the years I would hear of something like one hundred
dysplastic puppies being put to sleep every year in the San Jose area alone.
There probably were many more I wasn't aware of. Projected over the
nation, there must be thousands of Saint-Bernards, German Shepherds, Great
Danes, Great Pyrenees, and other large dogs that are destroyed each year
because of the genetic concept. Personally, I refuse to euthanize any animal I
feel can be helped, and most of these animals can be helped. The first medical
observer of canine hip dysplasia was Dr. Gerry Schnelle, a radiologist at the
Angell Memorial Animal Hospital in Boston. He published a paper in 1945
theorizing that this condition was genetically based and suggested
sterilization of all pups in a dysplastic litter. A recessive gene was In the sixties, the Orthopedic Foundation for Animals (OFA) came into
existence, an organization established to gather data on dysplastic dogs
and to issue certificates to non-dysplastic animals. It was hoped this
would facilitate selective breeding and help eliminate the problem. An
individual had his animal X-rayed at the pet hospital. Then he submitted the
film and a $10 fee to OFA. The X-ray was reviewed and if the animal was found to
have flawless hips, the owner was issued an OFA certificate. In an era of
general acceptance of the genetic theory, possession of such a certificate
greatly enhanced the marketability of a stud and breeding b###h and their
offspring. I was never able to find a genetic pattern. I saw males and females
certified by OFA produce dysplastic pups and dysplastic parents produce normal
offspring. My own experience was telling me that the genetic theory was
wrong. In 1968, an interesting paper was published examining hip dysplasia
from the cellular level. The article focused on the involvement of the
pectineus muscle, that suffers from a state of atrophy in potentially
dysplastic puppies. The vitamin C-collagen connection may be responsible, I
suspected. I then set out to test my hunch. It wasn't difficult to find
breeders willing to cooperate in an experiment. Enough of them came to my
office angry and frustrated over their hip dysplasia problem, which OFA
certification was not helping at all. My idea was to fortify the b###h and
the newborn puppies with vitamin C. I hoped in this manner to prevent hip
dysplasia by building stronger collagen. The first animal in the experiment was
a two year old German Shepherd with grade three hips. She should have been
neutered, according to the Seeing |
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