The following two articles were taken from the book "How to Have a Healthier Dog" by Dr. Wendell. O. Belfield D.V.M., about his research and experiments on hip dysplasia and vitamin C.


Symptoms: An affliction of puppyhood marked by the rather sudden appearance of limping, several hours after vigorous activity. Lameness in the rear legs, and usually one leg is favored. The dog may be in pain and may whimper as it walks. It may drag itself up from the lying position. Appetite and activity often decline. Five to six months of age is the critical period, although general incidence ranges from three months to two years. Common to larger breeds but can strike smaller breeds as well.

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 bitches 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 inflammation down. After a time, however, the drugs lose their effect. Such prolonged treatment in fact may be inviting more trouble. Aspirin is known to destroy huge quantities of vitamin C. Steroid therapy can cause a potassium deficiency, water retention and high blood pressure over the long haul. It can also interfere with collagen production. I have seen dogs become lethargic and develop poor hair coats after prolonged use of steroids. The effect of either of these approaches is to invite a deterioration of the immune system and collagen quality. It has been found in humans that vitamin C supplementation can prevent or reverse the disturbances created by extended usage of steroid drugs.

In my practice I will put the dysplastic dog on a good dose of vitamin C and all the other vitamins and minerals. Vitamin C has analgesic powers. It makes the animal more comfortable. High doses of vitamin C have been determined to ease the pain and swelling of human sufferers of osteo-arthritis. The other nutrients will support the animal in many ways. One of them is to prevent the arthritic condition from advancing due to any possible vitamin or mineral deficiency.

Many veterinarians today will suggest to a dog owner at this stage that the animal undergo a pectinectomy, a surgical procedure I pioneered in 1968. The operation entails snipping the pectineus muscle, which is as taut as a piano wire. This procedure eliminates the outward tension of the head of the femur. It also eliminates some of the pain and the limp, depending on how far the osteo-arthritis has developed. There is no technique, however, to restore the ball and socket to its pre-dysplastic state, because inflammation has occurred and calcified scar tissue and even bone tissue have begun filling up the socket.


The reigning myth - which unfortunately still clouds much of veterinary thinking 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 bitch or their sire had produced dysplastic puppies. If you were a breeder and word got out that your bitch 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 responsible, he believed, and it should be simple to breed away from this gene so you wouldn't have the problem anymore.

The veterinary and dog world jumped on the genetic bandwagon and everybody began trying to breed out the recessive genes. But it was apparently still there, as prevalent as ever, no matter what anybody did.

One Swedish doctor X-rayed army dogs and concluded that dysplastic animals produce 10 percent more dysplastic puppies than non-dysplastic animals. More recently, some of the authorities who championed the genetic argument for years are slowly doing an about-face and talking about hip dysplasia being a biochemical problem. Out of this transformation came one of the most unusual statements I ever heard. A university specialist, a die-hard supporter of the genetic theory, now felt the problem as he saw it was 42 percent genetic! A 1973 report from Australia talked in terms of 25 percent.

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 bitch 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 bitch 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 Eye Dog standard. The bitch was bred and immediately placed on 2000 milligrams daily of sodium ascorbate, no difficulties were reported. The pregnancy proceeded uneventfully and the dog whelped much faster than usual. This, as I mentioned earlier, is one of the benefits of vitamin C during pregnancy. The dog produced eight normal pups, who in turn were placed on 50-100 milligrams daily of liquid vitamin C during early puppyhood. When the puppies were weaned, the liquid was replaced with powdered vitamin C providing 500 milligrams daily. This dose was maintained until the animals were four months of age. At that time the dosage was increased to 1000 milligrams daily, then gradually to 2000 milligrams over the next couple of months and kept at that level throughout the growth period.

Since those early days I have adjusted the amount of vitamin C I recommend for growing puppies, especially for young animals put under stress conditions such as training programs or work. See the chart for weaned puppies in Chapter 13 for precise dosages.

The original shepherd bitch was bred three different times, and out of thirty puppies there was not a single case of hip dysplasia.

During a five-year period, I similarly monitored two other bitches. At the end there was a total of eight different litters where both mother and puppies were supplemented with vitamin C. In each case, one or both of the parents were dysplastic or had previously produced dysplastic puppies. Through all eight litters, not one puppy showed any dysplasia as determined by X-rays.

One of the litters I worked with belonged to a breeder friend who raised tracking German Shepherds, dogs trained for mountain rescue work. The woman had one particularly handsome and fertile female, who unfortunately had grade-three hip dysplasia. She bred the bitch twice to two different OFA-certified males and both times half the litter developed hip dysplasia. She didn't want to breed the dog any more because she said she didn't want to bring any more cripples into the world. I badgered her into trying the vitamin C experiment and breeding the animal again.

We went to a third OFA-certified male because neither of the previous two were available. The bitch was bred and eleven puppies were whelped. The woman sold the offspring after they were weaned and provided the new owners with a supply of vitamin C for each animal. A stipulation of the sale was that the new owners had to supplement the puppies with vitamin C and bring them in for X-rays when the animals were between eighteen months and two years of age. The time passed. The x-rays were taken. To my delight, I found eleven pairs of perfect hips. I took the pictures over to a veterinarian at a Seeing Eye Dog center and showed them to him. He looked first at the X-rays of the bitch and said that at the center they would either have neutered the animal or put her to sleep. He looked at the X-rays of the OFA-certified father and praised the hips. Then he began looking at the X-rays of the puppies, and as he got to the end he was amazed. It was hard for him to believe that these eleven dogs came out of the dysplastic bitch who previously had produced dysplastic litters.

In 1976, I published an article in a leading veterinary magazine about vitamin C and hip dysplasia and, like most new ideas that tend to explode popular theories, my hypothesis came in for much criticism. But eventually I began receiving very positive feedback, particularly from breeders. Some of them told me that the program with vitamin C was so successful that when they sell their puppies, they incorporate into their sales agreements a clause stating that the pups are guaranteed dysplastic-free only if they are kept on the prescribed regimen of vitamin C.

In bygone years, breeders were reluctant to admit they had a hip dysplasia problem. It could affect their business. Now, people were admitting for all to hear: Yes, I had hip dysplasia in my kennels but I don't have it anymore. A Great Dane breeder in Australia wrote a letter to a veterinary journal proclaiming he had controlled his hip dysplasia problem by feeding vitamin C daily. A breeder of Saint Bernards in Seattle reports similarly he has totally eliminated hip dysplasia. I hear from other veterinarians who have tried the vitamin C approach that they too are overcoming the problem. What I am observing with my own clients and hearing from others convinces me that hip dysplasia is preventable with vitamin C. For me, the problem is solved!

The idea is to prevent hip dysplasia if you can, rather than to look for ways to help a limping dog in pain that already has the condition.

Remember that pet food manufacturers believe that dogs produce sufficient vitamin C and so they don't fortify their food with vitamin C. Remember that a dog may not produce enough vitamin C to cope with stress and excess lead levels in his diet. This is particularly true of the fast-growing, large breed puppies. You need to bolster their ability to produce good collagen that is needed for strong ligaments and tendons. You need to supplement.

Carefully follow the prevention plan. If your bitch is being bred, start her on the vitamins and minerals immediately. If you have to purchase a young puppy, start the animal on supplements without delay.

If it is too late and your animal is limping, he should still be taking plenty of vitamin C for its pain-killing and other beneficial powers. The regular preventive dosages, as I have outlined in the charts in Part Three, will be helpful to your dog.

Hip dysplasia is a problem that has anguished dog owners and breeders for years. The day has come that it no longer has to affect you and your dog.