Most people think of collagen as an anti-aging product. You’ll find collagen in cosmetic products and in supplements because it’s the elastic protein that holds skin together.
As we age, the amount and quality of collagen in our bodies starts to diminish. That’s why we can see our skin begin to wrinkle and sag.
Collagen is also found in the joints and connective tissues of the body. In fact, collagen makes up 70 to 90% of our:
- Ligaments and other joint supporting tissues
When collagen breaks down in the body it can cause …
- The joints to become less stable
- The muscles and connective tissue loosen and become more brittle
We also see disorders such as …
- Degenerative disc disease
The same is true of collagen in your dog. And this is when you can see overuse injuries start to happen.
So your dog might not get our common crow’s feet and turkey necks …
… But he can suffer from age related joint and soft tissue pain. Sadly, many dogs suffer at a very young age when joints and tissue break down.
Breeders of large breed dogs know this young dog heartache all too well. Large breed dogs can suffer from young joint issues including:
- Canine hip and elbow dysplasia
- Patellar subluxations
- Cruciate tears
- Osteochondritis dissecans (OCD)
It’s unfortunate, but these issues in young dog’s aren’t decreasing. This leaves new owners juggling the price of expensive surgery, therapy and supplements.
So why are dogs suffering from these diseases at such a young age? Is it genetic?
Many breeders and vets are quick to blame bad genetics. That’s why good breeders screen their dogs for these diseases before breeding.
The goal of screening tests is 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 but nobody seemed interested at the time.
Over twenty years later, the number of dogs presenting with this disease was on the rise. This prompted the Swedish Kennel Club to develop a program focused on hip dysplasia.
The goal of this program was to radiograph the hips of German Shephard breeding stock. Once they knew which dogs had healthy hips, only those dogs would be bred …. and hip dysplasia would be eliminated.
But after ten years of selective breeding … the incidence of moderate and severe cases of hip dysplasia didn’t change.
Dogs without radiographic evidence of hip dysplasia were still producing puppies with dysplasia. In fact, 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. This means hip dysplasia is caused by the combined action of more than one gene.
Environmental factors like diet and lifestyle were also found to impact the severity … as some affected puppies are born with normal hips.
Over fifty years later, the incidence of hip dysplasia isn’t changing much in most breeds. Surprising when you consider the fact that breeding stock testing rates are up.
In fact, smaller breeds are now showing an increased susceptibility to this disease. And in Germany, the incidence of hip dysplasia in is still 7% in German Shepherds … despite their tight kennel club breeding restrictions.
Sadly, hip dysplasia isn’t the only common joint disorder in dogs. It’s also becoming more common to see …
- Cranial cruciate tears
- Luxating patellas *
- 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. The breeders then point their fingers at the pet owners and at each other …
…. Surely somebody must be to blame?
The truth is a polygenic disease is one that takes the right combination of the following:
- Genetic susceptibility
- Environmental factors
- Dietary influences
The genes act 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 disease severity will be directly influenced by the dog’s environmental factors.
Unfortunately, we don’t know which dogs possess and produce the genes that cause joint disease … But as dog owners we can change the environmental stressors.
To this point, vets and many breeders will pay lip service to things like:
- Keeping puppies lean
- Not feeding them too much protein (a myth that is not proven)
- Giving them a number of supplements
Puppy buyers usually get this well rehearsed speech at their first vaccine appointment. Most vets are ready to step in with surgery if they see a large breed puppy with dysplasia.
The same vets usually blame the breeders and their purebred dogs for joint issues. But they also inject these healthy puppies with vaccines that have consequence too.
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 are vets recommending expensive hip surgeries and multiple, unnecessary vaccines?
Are they 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 ran a study in 1997 that included 4,000 dogs. They found a high number of dogs developed mobility problems shortly after vaccinations.
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.”
Interestingly, the distemper vaccine was introduced in 1950. 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’s a 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”.
And here’s 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 also 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.”
Wait, autoantibodies to collagen? Vaccinated dogs developed autoantibodies to their own collagen … and nobody was worried about that?[Related: Which Vaccines Does Your Dog Need?]
The Purdue Study
A 1999 study should have connected the dots between vaccination and joint disease.
In the study, puppies were immunized with cocktail of:
- The rabies vaccine
- The usual core vaccines
- And non-core vaccines
The authors concluded that the vaccinated puppies developed autoantibodies to their own collagen. They found the same in a follow up study with dogs given only rabies the multivalent vaccine.
The vaccinated dogs in this study were literally destroying their own collagen … and their own DNA and other important substances!
And yet 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.
So why blame purebred dogs and genetics 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
- 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 their joint fluids. This data concluded that anti-collagen complexes were present in all joint disorders.
The presence of these anti-collagen antibodies can actually predict cruciate tears. A study found elevated anti-collagen antibodies in the “good” knee of dog’s who had the other knee tear.
When multiple joints were tested … the stifle joints always tested high for autoantibodies (DeBruin et al, 2007). These autoantibodies have also been found in arthritic joints (Niebauer et al, 1987).
Duke University Medical Center researchers found 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)”
The collagen deficient mice had knee and intervertebral disc structural changes.
Collagen and Joint Integrity
Collagen is most concentrated in weight supporting tissues, including cartilage and bones. It’s also in high percentages in the parts of the body transmitting strength, such as tendons.
Collagen not only protects joint cartilage, but also tendons and ligaments against tears.
The elastic property of collagen gives ligaments a tiny bit of stretch. This allows the joint ligament to be able to hold tension without tearing. Just as bridges and high rise buildings need a tiny bit of give in them to weather high winds and earthquakes.
Collagen is also important for the integrity of joint surfaces. There’s a thin layer of tissue surrounding the cartilage on the surface of joints. This layer is known as the pericellular matrix (PCM).
The PCM, collagen and other cartilage cells form a barrier layer in the joint. But when collagen is disrupted the changes in mechanical forces can lead to degenerative changes.
What Science Has To Say About Collagen And Joints
Leonidas Alexopoulos studied the relationship between collagen and osteoarthritis at Duke University. The results were presented 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.”
A Closer Look At The Many Factors
Vets and breeders are both on a similar path. They know that joint disorders are caused by a variety of factors. And yes, genetics probably do play a role.
But let’s not forget that it could be a result of the cumulative damage.
When we look at the puppies’ parents and grandparents suffer through:
- Repeated vaccination
- Highly processed diets
It becomes clear to see how these effects can add up. On top of that, the Purdue study showed that the dogs developed autoantibodies to their own DNA.
Perhaps vaccinated breeding dogs are passing along damaged DNA and that is a part of the picture.
Vets and researchers repeatedly stating there’s no cause and effect relationship. In fact, they request that further studies be done before vaccines are related to joint disease.
Sadly, as we wait for those magical studies, vets continue to vaccinate every three years. Some vaccinate even more frequently, with vaccines known to last at least seven years.
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,Dr. Ronald Schultz vaccinated puppies with one dose of distemper vaccine.Four hours later he placed in a room with distemper-infected dogs. What he found was that all of the puppies were protected against distemper.
This bears repeating.
Dr. Ronald Schultz is a leading canine immunologist. 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.[Related: What Your Vet Doesn’t Know About Distemper Could Harm Your Dog]
Collagen And Too Many Vaccinations
So it should be obvious that it only takes one distemper vaccine to protect a puppy from distemper for life.
But why then does the average dog get vaccinated for distemper at:
- 8 weeks
- 12 weeks
- 16 weeks
- 1 year
- 4 years
- 7 years
- 10 years
Hopefully your dog is lucky enough to have lived through this unnecessary and dangerous onslaught of vaccines. But will your vet recommend that he’s vaccinated again at thirteen and sixteen?
That’s nine shots of a virus known to be permanently effective within hours of the very first vaccine!
It’s no wonder joint disease is on the rise in dogs ..especially in purebred dogs. They’re the most aggressively vaccinated subset.[Related: How To Detox Your Dog]
It’s Time For Change
Clearly, more research needs to be done in this area. We also need more acknowledgement of the unwanted adverse effects caused by vaccines.
This long list of joint and collagen related changes is a significant problem for dogs. I’m not saying don’t vaccinate for distemper altogether, although that is a viable option. I’m suggesting that we stop the madness of unnecessarily over vaccinating dogs.
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 research and analysis are not all that necessary when it comes to giving more vaccines. Doesn’t it make you wonder why more research put on the hot seat when we ask for less? It seems that common sense goes out the window on this one.
What’ll it take before vets start taking this research seriously and stop over-vaccinating?