Most people have heard of collagen as an anti-aging cosmetic product. Collagen is the elastic protein that holds skin together. As we age, the amount and quality of collagen in our bodies starts to diminish and we can see this in our skin as it begins to wrinkle and sag.
Collagen is also found in abundance in the joints and connective tissue of the body. In fact, collagen makes up 70 to 90% of our muscles, tendons, ligaments and other joint supporting tissues. As happens in the skin, when collagen breaks down in the body, the joints become less stable, the muscles and connective tissue loosen and become more brittle, and disorders such as arthritis, degenerative disc disease, tendonitis and overuse injuries begin to occur.
The same thing happens in our dogs. They might not get the crow’s feet and turkey necks that we older humans sport, but they do suffer from age related joint and soft tissue pain due to collagen loss and degradation. Sadly, many dogs suffer from these diseases at a very young age. Breeders and lovers of large breed dogs know all too well the heartache of canine hip and elbow dysplasia. Dog owners see patellar subluxations, cruciate tears and osteochondritis dissecans (OCD) in young dogs at an alarming rate and they pay the price with expensive surgery, therapy and supplements.
Why are dogs suffering from these diseases at such a young age? Many breeders and vets are quick to say that it is due to bad genetics – so good breeders screen their dogs for these diseases before breeding, to make sure the problems are not passed down to the offspring.
The problem is, this screening hasn’t really changed the incidence of most of these diseases.
A little history . . .
Hip dysplasia was first diagnosed in dogs in 1935, although nobody seemed terribly interested at the time. Over twenty years later, the number of dogs presenting with this disease prompted the Swedish Kennel Club to become one of the first to develop a program to reduce the incidence of hip dysplasia. They believed that if German Shepherd breeders took radiographs of their dogs and only bred the dogs that did not show evidence of hip dysplasia, they could eliminate hip dysplasia. After ten years of selective breeding however, the incidence of moderate and severe cases of hip dysplasia didn’t change. Dogs that did not show radiographic evidence of hip dysplasia were still producing puppies with the disease. In one study, over two thirds of dysplastic puppies were from normal parents.
This led researchers to conclude that hip dysplasia was a polygenic disease (residing in more than one gene), meaning that the severity of the disease could be influenced by environmental factors such as diet and lifestyle. However, affected puppies are born with normal hips – the dysplastic changes are not there at birth.
Over fifty years later, despite increased testing rates, the incidence of hip dysplasia is not going down in most breeds. In fact, smaller breeds are now showing an increased susceptibility to this disease which historically was limited to larger breeds of dogs. Even in Germany, where the kennel club has very tight breeding restrictions, the incidence of hip dysplasia in German Shepherds is still 7%.
Hip dysplasia is not the only common joint disorder in dogs. Cranial cruciate tears are becoming endemic in dogs, as are luxating patellas and elbow dysplasia (two more disorders that breeders do clearances for). In the midst of this, the vets point their fingers at both breeders and purebred dogs and the breeders point their fingers at the pet owners and at each other. Surely somebody must be to blame?
A polygenic disease is one that takes the right combination of genetic susceptibility, environmental factors and dietary influences to occur. The genes are like a light switch: if a dog has a genetic susceptibility to hip dysplasia, the switch is in the ON position. Just because a dog has the gene for hip dysplasia however, does not mean he will be affected: the severity of the disease will be directly influenced by the dog’s diet and other environmental factors such as exercise level or body condition – or so the theory goes. Unfortunately, we don’t know which dogs possess and produce the genes that cause joint disease – but dog owners can change the environmental stressors.
To this point, vets and many breeders will pay lip service to things such as keeping puppies lean, not feeding them too much protein (a myth that is not proven), giving them supplements – all the usual drama. Puppy buyers usually get this well rehearsed speech when they bring their new puppy in for his vaccination. Most vets actively look for large breed puppies to show signs of hip dysplasia and are ready to step in with surgery. They blame the breeders and their purebred dogs for joint issues while, at the same time, they inject these healthy puppies with vaccines.
Is it any coincidence that even severe cases of hip dysplasia are not seen before eight weeks of age – the age at which most puppies are vaccinated? Why is it that, once again, vets are recommending expensive hip surgeries and multiple, unnecessary vaccines, while remaining oblivious to what should be obvious? Why is nobody blaming the vaccines when there are plenty of reasons to do so?
Vaccines and Joint Disorders
The Canine Health Concern’s 1997 study of 4,000 dogs showed a high number of dogs developing mobility problems shortly after they were vaccinated. Immunologist Dr. Jean Dodds has also noted similar issues: “Beyond the immediate hypersensitivity (vaccine) reactions, other acute events tend to occur 24 to 72 hours afterward, or 7 to 45 days later in a delayed type immunological response. Even more delayed adverse effects include…canine distemper antibodies in joint diseases of dogs.”
Interesting. The distemper vaccine was introduced in 1950 and just a few years later, the breed clubs suddenly felt the need to start doing hip clearances on breeding stock. There is no cause and effect here but the temporal relationship is fairly noteworthy.
Vaccination has been implicated in cases of polyarthritis in dogs. Here is an interesting passage from the Veterinary Products Committee (VPC) Working Group on Feline and Canine Vaccination.
“Occasional self-limiting cases of immune-based arthritis in dogs have been reported usually following primary vaccination, and recently, four young adult dogs of different breeds have been reported to develop an idiopathic polyarthritis three to 15 days after multivalent vaccination. Immune-mediated polyarthritis and systemic disease including amyloidosis has been reported in Akita dogs following modified live vaccination. Hypertrophic osteodystrophy (HOD), in some cases associated with juvenile cellulitis, has been reported following vaccination, mainly in Weimaraners, and it has been suggested that canine distemper virus may be involved. There is also some evidence that canine distemper virus (and possibly vaccines) may be involved in canine rheumatoid-like arthritis through the formation of immune complexes”.
Here is the predictable part: “…the immunological basis of such reactions is unclear, and it is possible that such apparent associations with vaccination may be due to coincident disease development, particularly in young animals”.
That sure would be a heck of a coincidence. Catherine O’Driscoll sheds more light on the relationship.
“A paper appearing in the British Veterinary Journal states that dogs with rheumatoid arthritis showed higher anti-heat shock protein antibody levels in their sera and synovial fluids compared to control dogs. There was a significant correlation between anti HSP65 and antibodies to canine distemper virus, and the paper discussed the relevance of the presence of canine distemper virus within the joints. Since vaccines inject modified live distemper virus into the dog, this research should be of concern. Shed attenuated live vaccine might also be considered in this regard. And it’s worth noting that the high antibody titers to distemper that we are so pleased with might also play a role in our dogs’ decreasing mobility. Rheumatoid arthritis is, of course an autoimmune condition in which there is inflammation of joints and progressive erosion of cartilage and bone, which reflects the autoantibodies to collagen found in the Purdue study.”
Autoantibodies to collagen? Vaccinated dogs developed autoantibodies to their own collagen and nobody was worried about that?
The Purdue Study
In 1999, a one of a kind study was performed that should have connected the dots between vaccination and joint disease (Hogenesch H, Azcona-Olivera J, Scott-Montcrieff C, Snyder PW, Glickman LT. Vaccine-induced autoimmunity in the dog. Adv Med Vet 1999;41:733-747). In this study, puppies were immunized with the rabies vaccine and the usual cocktail of core and non-core vaccines. The authors concluded that the vaccinated but not the unvaccinated puppies developed autoantibodies to their own collagen. The authors noted and reproduced similar findings in a followup study in dogs that were given just the rabies vaccine and just the multivalent vaccine.
The vaccinated dogs in this study were literally destroying their own collagen (as well as their own DNA and other important substances), and nobody thought “aha, maybe this is why our dogs are being hit so hard with joint disease and we can’t breed it out of them.” Instead, the researchers discontinued the study when the puppies were 22 weeks of age and, over a decade later, nobody has viewed these results as a serious threat to canine (or human) health.
Why is it that vets and researchers can claim purebred dogs and genetics are to blame for these joint disorders when this shining beacon is aimed squarely on vaccination, especially the distemper shot?
Collagen and Joint Disease
In a 1989 study, Bari et al found autoimmunity to collagen in 72.4% of dogs with rheumatoid arthritis, 88% of dogs with infective arthritis and 52% of dogs with osteoarthritis. Dogs with cruciate disease also showed significantly increased levels of autoantibodies. They also had higher levels of anti-collagen antibodies in the synovial fluid (the fluid that surrounds joints). They concluded that anti-collagen complexes were present in all joint disorders.
The presence of these anti-collagen antibodies, just like those noted in the vaccinated dogs in the Purdue study, can actually predict cruciate tears. In dogs with cruciate tears in one leg, studies show elevated anti-collagen antibodies in the other leg which predicted future tears. When multiple joints were tested, higher levels of autoantibodies were found in stifle joints that were eventually torn than in other joints of the body (DeBruin et al, 2007). These autoantibodies have also been found in the joints of dogs suffering from arthritis that is not secondary to cruciate tears (Niebauer et al, 1987).
Duke University Medical Center researchers led by Kyle Allen found that collagen deficient mice prematurely developed common and chronic musculoskeletal disorders while the wild-type mice did not. “We observed a pattern of behavioral changes in the collagen deficient mice that suggests a relationship to (osteoarthritis and de- generative disc disease),” said Allen, who noted the collagen deficient mice also had elevated levels of knee and intervertebral disc structural changes.
Collagen and Joint Integrity
Collagen is concentrated mostly in weight supporting tissues, basically cartilage and bones. Collagen is also concentrated in high percentages in the parts of the body transmitting strength, such as tendons. Collagen not only protects joint cartilage, it is also what protects tendons and ligaments against tears.
The elastic property of collagen gives ligaments a tiny bit of stretch so that if the joint that ligament supports is stressed, the ligament can withhold the tension without tearing. Just as bridges and high rise buildings need a tiny bit of give in them to weather high winds and earthquakes, ligaments need the elastic properties of collagen to bear shearing forces within the joints.
Collagen is also important for the integrity of joint surfaces. There is a thin layer of tissue surrounding the cartilage on the surface of joints called the pericellular matrix (PCM). Together with collagen and other cartilage cells, the PCM forms a barrier between the cells and the rest of the cartilage tissue. When collagen is disrupted in joints, the changes in mechanical forces on the cells can lead to degenerative changes.
Leonidas Alexopoulos studied the relationship between collagen and osteoarthritis at Duke University and presented the results at the 51th annual scientific meeting of the Orthopedic Research Society in Washington, DC. Alexopoulos explains: ““When we analyzed the PCM of mice unable to produce type VI collagen, we found that the chondrons (joint surface structures) in these mice were much softer and the joints did not respond well to mechanical pressures. The joint looked as if osteoarthritis had developed.”
In May, 1997, a paper was presented in the Journal of the American Veterinary Medical Association by Jens Sejer Madsen, Ph.D., D.V.M. from the Small Animal Hospital, Department of Clinical Studies, Royal Veterinary and Agricultural University, Frederiksberg C, Denmark. This study shows how collagen can be related to hip dysplasia.
“Mechanical strength of the joint capsule is related to its collagen content and composition. In children with congenital hip joint dislocation, the collagen composition of the joint capsule has been shown to be abnormal. Thus, it is reasonable to hypothesize that laxity of the hip joint in dogs may be related to the collagen composition of the capsule…results of the study support the hypothesis that a change in collagen composition may contribute to hip joint laxity in dogs with a predisposition to CHD.”
The vets and breeders are right in that hip dysplasia and other joint disorders are caused by a variety of environmental and nutritional factors. Genetics probably do play a role, although it could have something to do with the cumulative damage the puppies’ parents and grandparents suffer through repeated vaccination, highly processed diets, antibiotics and toxins. On top of that, the Purdue study showed that vaccinated dogs develop autoantibodies to their own DNA; perhaps vaccinated breeding dogs are passing along damaged DNA and that is a part of the picture.
Meanwhile, the vets and researchers repeatedly state there is no cause and effect relationship and that further studies will have to be done before vaccines can be implicated in joint disease. While we wait for those magical studies, vets continue to vaccinate every three years, or even more frequently, with vaccines that were shown to last at least seven years over thirty years ago.
In the case of distemper, one of the vaccines repeatedly vindicated in joint disease, puppies develop titers within hours of their first distemper vaccination. In his study at the University of Wisconsin- Madison, Dr. Ronald Schultz vaccinated puppies with one dose of distemper vaccine just four hours prior to being placed in a room with distemper-infected dogs. All of the puppies were protected against distemper in this challenge study.
What your vet doesn’t know, but you need to know about distemper. Click Here!
This bears repeating. Dr. Ronald Schultz, the leading canine immunologist, publishes a study in which every single puppy is protected within hours of the very first vaccination. Thirty years prior to this, he determined that core vaccines (including distemper) last at least seven years, and most likely for the life of the dog. So it should be pretty obvious that it only takes one distemper vaccine to protect a puppy from distemper for life.
Why then does the average dog get vaccinated for distemper at:
? 8 weeks
? 12 weeks
? 16 weeks
? 1 year
? 4 years
? 7 years
And if he is lucky enough to have lived through this unnecessary and dangerous onslaught – thirteen and sixteen years of age?
Nine shots of the same virus that is shown to be permanently effective within hours of the very first vaccine is considered a minimal vaccine schedule by most veterinarians – many other dogs receive 15 or more shots of distemper! It is no wonder that joint disease is on the rise in dogs, especially in the most aggressively vaccinated subset: purebred dogs.
Clearly, more research needs to be done in this area but somebody should at least pay attention to the growing list of unwanted and adverse effects caused by vaccines. There is a growing list of joint and collagen related changes that occur after vaccination and they are implicated in joint disease which has become a significant problem in today’s dog population. I’m not saying stop vaccination for distemper altogether (although that is a viable option), but at the very least, stop the madness of unnecessarily vaccinating dogs for distemper over, and over, and over, and over again. Isn’t there enough research to make vets just a little bit concerned about potential damage from the eight or more distemper vaccines that go into dogs?
It seems that in-depth research and analysis are not all that necessary when it comes to giving more vaccines but when it comes to giving less, research is suddenly put on the hot seat and common sense goes out the window. What will it take before vets start taking this research seriously and stop vaccinating dogs unnecessarily?