Dysplasia & Vitamin C
between Type I Collagen deficiency and joint dysplasia – esp. young dogs !!
1998, Article about Joint Dysplasia by Dr. Wendell O. Belfield
I t may interest breeders
and fanciers of the larger breeds of dogs, the winds of time are changing the
concept of canine hip dysplasia (CHD). In the May, 1997 issue of the Journal of
the American Veterinary Medical Association, were two papers discussing a new
outlook on CHD.
The first paper, "Onset of epiphyseal mineralization and growth plate closure
in radiographically normal and dysplastic Labrador Retrievers," was a
collaboration of seven researchers/educators at the veterinary schoool at
Cornell University. The results of this study is as follows.
"There were 26 radiographically normal left and right hip joints. Onset of
mineralization of the proximal femoral epipysis and of the right proximal tibial
epiphysis was significantly later in dysplastic than in radiographically normal
puppies. The left femoral capital growth plates closed significantly later in
dysplastic than radiographically normal joints, but other differences in growth
plate closure were not detected."
"Clinical Implications -- Endochondral ossification may be abnormal in dogs
with CHD. The disease appears to affect multiple joints, even though it is most
evident clinically in the hip joint."
The second paper was presented 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.
"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. To test this hypothesis, a study was
performed on 19 mature dogs (14 with radiographic evidence of CHD) and 10
Greyhounds (9 with radiographically normal hip joint conformation). Joint
capsules were harvested from all dogs, and the ration of type-III:I collagen in
each capsule was calculated. The mean ratio was significantly higher in dogs
from breeds with a high prevalence of hip dysplasia (1:0.161) than in Greyhounds
(1:0.100; P=0.005); however, within each group of dogs, there was no difference
in ratio between dogs with normal and dysplastic hips. A high collagen type-III:I
ratio indicates a weak joint capsule, because strength requires type-I collagen.
Therefore, 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
For over twenty years I have asked the "experts" to describe the lesion of
the dysplastic hip joint; at the cell level; the pathology involved, if you
will. I was delighted to read these reports because they give hope that this
disease can be prevented be it genetic or nutritional.
In October, 1976 I published a paper, "Chronic Subclinical Scurvy and Canine
Hip Dysplasia" published in Veterinary Medicine/Small Animal Clinician." My
conclusion was as follows:
"In large breeds of dogs, hip dysplasia, long considered an inherited birth
defect, may be an easily controlled biochemical condition. The lesion in hip
dysplasia appears to be merely poor-quality, low-strength collagen in the
affected ligaments, caused by too little ascorbate for proper synthesis and
maintenance of collagen. In eight litters from dysplastic German Shepard parents
or parents that had produced dysplastic offsprings, there were no signs of hip
dysplasia when the bitches were given mega doses of ascorbate during pregnancy
and the pups were kept on a similar regimen until they reached young adulthood."
Though my observation was made more than twenty years ago, it was rejected by
most researchers and educators. As the analogy made by Dr. Madsen in children
with congenital hip joint dislocation, my analogy was drawn from a book by John
Lind describing the pathology in the hip joints of scarbutic cadavers, the book
was "A Treatise on Scurvy" published in 1753.
My elation over these publications was short lived as I began to recall the
numbers of beautiful canines that had been euthanized over the past two decades.
The number of breed-lines that are now extinct. This was a canine genocide. It
has taken more than fifty years, after CHD was first reported, for the "experts"
to describe the lesion of the disease; how long will it take them to offer a
solution, another half century?
Now that CHD is a systemic condition we can get on with the business of
saving these canines from this crippling disease. Lets begin eliminating some
myths that have prevailed over the past fifty years. Unilateral CHD, does not
exist. One normal hip and the other subluxted is not CHD this is simply an
injury. Since the experts recognize that all joints can be involved in slow
mineralization why then one hip will remain normal. Since collagen synthesis is
involved in CHD, another systemic problem, why will one hip and not the other be
involved. CHD must be in both hip joints. The next issue, is CHD an inherited
disease? I have never been a proponent of this concept. To me, it has always
been a biochemical problem. Regardless if CHD is genetic or not, it does have
systemic implications which means it can be prevented and controlled; I have had
success in this area for more than twenty years.
The 1990's have brought forth scores of research publications from around the
world on the subject of collagen synthesis and its relationship to nutrition and
nutritional supplementation. These publications are not by veterinarians and do
not appear in veterinary journals. It does require those who are seeking broader
knowledge go beyond the limits of veterinary medicine. As a contributing author
to a recent textbook, "Complementary and Alternative Veterinary Medicine:
Principles and Practice" all of my literature research into collagen synthesis
orginated from biochemist at medical teaching institutions and other research
facilities other than veterinary research facilities.
Much to my surprise, many veterinary practioners are not aware of these
recent publications on these new observations of CHD. Does this mean that some
canines are still being euthanized? We have known about CHD since 1945, and the
"experts" have failed to solve this problem. To fail only gives rise to a new
beginning and a fresh approach to new concepts.
Summer, 2000, by Dr. Wendell O.
Arthritis is probably
one of the most common incapacitating diseases known to man and beast. It
is not serious enough to cause death but can cause extreme pain and discomfort.
In medical vernacular-"itis" at the end of a word indicates
inflammation, thereby arthritis indicates inflammation of a joint. However,
there are exceptions to the rule; in other words there are instances when an
arthritis is not one involving inflammation.
Because of this the pathologists have placed this condition in categories;
non-inflammation (arthrosis, osteoarthrosis), and inflammation (arthritis,
osteoarthritis). As time moves forward so does our knowledge and technology.
Because of this progress, we in the profession are able to better isolate and
identify many different types of arthritises, which leads to better therapies
and preventions. The types discussed in this article will be limited to those
seen in my practice.
Osteoarthritis is by far the most common. This type of
arthritis is seen in every case of canine hip dysplasia, the crippling disease
affecting the young of the large and giant breeds. In hip dysplasia, the head of
the femur separates from the hip socket and after a period of time, nature
attempts to fill the gap left by the separation with bone tissue. This bone
tissue is rough and the movement of the head of the femur over this rough
surface is extremely painful. Bear in mind, the two surfaces of a joint must be
very smooth and lubricated with a fluid called synovial fluid. In the case of
hip dysplasia this is lacking. This, articulation causes a great deal of pain
and discomfort in one or both hind limbs.
Osteochondritis dissecans is a type of arthritis affecting the
cartilage surface of the upper arm (humerus). There may be one or more areas
that undergo degeneration (necrosis) causing lameness to the young dogs of the
large and giant breeds. This condition is seen in animals a year and younger,
and is manifested by limping in the affected forelimb. Most animals will outgrow
the condition if strenuous activities are curtailed for a few weeks. "Numerous
theories have been propose, suggesting that the cause of osteochondritis may
involve biochemical, nutritional, hormonal and hereditary factors." These
theories are quoted directly from the textbook.
Legg-Calve-Perthes' disease is characterized by a flattening of
the femoral head. This condition almost always occurs in canine hip dysplasia,
but can and will occur as a separate entity. This condition occurs as a result
of cartilage necrosis (death),
In recent years the veterinary profession has been moving in the direction of
specialization. This has resulted in veterinary orthopedics. These specialists,
with their expertise and technology. have been able to aid the practitioner in
making a more positive diagnosis. In other words, we have more descriptive names
for the different bone and joint diseases. To date, most of the therapies to
eliminate the bone and joint problems seems to be some sort of surgery. Though
some theories have been put forth about nutrition, the textbook fails to offer a
nutritional solution or other preventive measures.
Osteoarthritis, osteochondritis and Legg-Calve-Perthes' are all very common
crippling diseases that are occurring daily to our pets because we as
veterinarians, do not understand the role good nutrition plays in preventing
In recent years, since the advent of glucosamine and condroitin, the tendency
in veterinary medicine, has been to treat the existing condition. These two
natural substances have eliminated, to some extent, the administration of
steroids, which have multiple adverse side effects. Like many therapies, there
are those patients that will not respond favorably, only to have the condition
persist throughout their entire lives.
All three of these crippling diseases can be prevented through preventive
protocols. Collagen synthesis is essential for osteogenesis and chondrogenesis
the formation of bone and cartilage respectively. Bone and cartilage are not as
dependent on mineral intake as much as collagen synthesis. With poor collagen
synthesis there is minimal matrix for minerals to be deposited. Most often,
extreme amounts of minerals like calcium are being administered with the intent
to develop strong bones, only to have patients develop other biochemical
problems, such as unwanted calcium deposits in other parts of the body.
A preventive protocol I have used successfully my
practice for a quarter of a century consist of Mega C Plus and hydrolyzed
protein (Mega C Drops). This preventive regimen begins with the pregnant
mother and continues in the pups through nine months of age. This
protocol is discussed more scientifically in my chapter, "Orthomolecular
Medicine In Veterinary Practice", in the textbook, "Complementary And
Alternative Veterinary Medicine:Principles And Practice", published by Mosby.
thirty-seven years of practicing small animal medicine, developing new and
effective preventive protocols for the prevention of diseases was less taxing
than promoting my concept of prevention to veterinarians and animal breeders and
fanciers. Should there be a pathological condition indigenous to a specific
breed, is it not preferable to prevent the occurrence rather than to attempt
(Mega C cannot
be imported into New Zealand because the levels of vitamin are too high.
However, slow release GNLD Threshold Vitamin C can be used).
Wendell O. Belfield
Hip Dysplasia (CHD),
a crippling disease
of the coxofemoral joint (hip), was first observed and reported in 1945 by the
late Dr. Gary Schnelle. Dr. Schnelle was the staff radiologist at Angels
Memorial Hospital at Boston, Massachusetts and reported his observations in The
North American Veterinarian Journal and termed the condition "Congenital
Coxofemoral Subluxation". Though "congenital", by definition, means "existing at
birth but not hereditary", Schnelle theorized the cause to be a recessive gene.
Today, this condition is associated with the large breeds of canines, however
Schnelle's initial observations were in the smaller breeds i.e., cocker
spaniels, terriers, etc..
During the 1960's, Dr. Wayne Riser, a veterinary pathologist, collaborated with
a geneticist and postulated the concept that CHD was "polygenetic with
environmental overtones" and during this time frame, the term "Canine Hip
Dysplasia" was born. There has been a string of professionals who have
perpetuated the heredity theory even until the present. We have been encouraged
to breed selectively, alter, and in some cases, euthanize the afflicted canines.
This is what the veterinary experts have been insisting the dog breeders and
fanciers do to prevent CHD for the past fifty-two years. Is it possible we have
been on the wrong track for more than a half century? One authority, of a
veterinary teaching institution in a personal correspondence to the author,
admitted the "experts" have failed to solve the CHD problem.
In 1976, The author published his observations ("Chronic Subclinical Scurvy and
Canine Hip Dysplasia") in his small animal practice through the administration
of vitamin C to prevent CHD. Whether this concept has been accepted or not it
has sparked controversy, and has some veterinarians reassessing the archaic
heredity theory. There are two unanswered relevant questions the "experts" have
failed to answer to prove the heredity theory.
1. What is the action of the gene/genes, how do they create the disease?
2. How does the veterinary practitioner differentiate between a hip subluxation
due to trauma (injury) from true CHD?
Since the mid 1970's, the author has been successful in preventing CHD through
the administration of nutritional supplements to the pregnant female and within
hours of birth to the newborn.
As earlier presented, the first canines observed with CHD were the smaller
breeds; yet today the larger canines are most affected. The reason for this
phenomenon is that the present day dog food is considerably more nutritious than
that being fed in the 1940's, i.e., more attention is now being given to
nutritional requirements. The requirements that have been established over the
past four decades have eliminated the CHD problem in the smaller breeds but
these requirements are not adequate for the large and giant breeds. One cannot
expect the nutritional requirements for a Chihuahua be the same for that of a
Great Dane. When these large and giant breeds of canines are adequately
subsidized through nutritional supplementation, the condition is prevented.
CHD must be more specifically defined. At the present, any abnormality in the
coxofemoral joint is considered hip dysplasia. The first photograph shows a dog
who was diagnosed with unilateral dysplasia. No consideration was given to the
history of this patient. The fact of the matter is, this subluxation was due to
a falling bail of hay impacting the right pelvic region. Bitches often sit on
their new born causing subluxations which are not manifested for some weeks
later when the pups begin to walk. For this reason the author, in his practice,
does not diagnose or recognize "unilateral" hip dysplasia.
The second photograph is without a doubt CHD. Both hips are subluxated with
accompanying osteoarthritis. The problem of CHD is directly associated with
collagen synthesis. Inadequate collagen synthesis will adversely affect
osteogenesis (development and formation of bone), chondrogenesis (development
and formation of cartilage), and myogenesis (develop and formation of muscle).
These three physiological processes are dependent on good collagen synthesis
which is dependent on good nutrition.
Research biochemists, during the 90's, have established the involvement of good
nutrition for good collagen synthesis. This supports the author's concept set
forth in 1976 that CHD is nutritionally related rather than hereditary. If it
can be established that these alleged genes, in fact, inhibit bone, cartilage,
and muscle formation, then it would be possible to control dysplasia through
nutritional supplementation. Some genetic tendencies can be overridden by other
factors, such as nutritional supplementation. The bottom line is, if CHD can be
prevented be it hereditary or nutritional there is more to gain than to lose
with the nutritional concept.
The author has developed a nutritional protocol for the prevention and control
of CHD. The protocol begins with the pregnant bitch. To ensure a healthy
pregnancy, the female is administered Mega C Plus. This supplement will aid in
the maintenance of a good pregnancy and a healthy litter. This vitamin/mineral
compound will enhance immune function and most importantly, aid in the synthesis
of collagen while the pups are developing in utero. After the birth of the
litter, Mega C Drops (pediatric formula) is administered to each pup within two
hours and is continued through weaning. Mega C Drops is a formula containing
hydrolyzed protein (collagen), vitamin C as sodium ascorbate, plus other
essential nutrients that enhances collagen synthesis. Post weaning, the pups are
placed on a Mega C Plus regimen through two years of age.
The author discusses CHD, at the cell level, in the forthcoming textbook
"Complementary and Alternative Veterinary Medicine: Practices and Principle"
Mosby. There has been extensive research in recent years concerning collagen
synthesis by many renown biochemists that supports the author's nutritional
concept. This new textbook is targeting veterinary practitioners and educators
and will be available September, 1997.
(Mega C cannot
be imported into New Zealand because the levels of vitamin are too high.
However, slow release GNLD Threshold Vitamin C can be used).