Maximizing Success in the Breeding Kennel and Show Ring

Transcription

Performance Nutrition
Maximizing Success in the
Breeding Kennel and Show Ring
®
Vital Health Care and Management
of Competitive Dogs
Presented at the Iams Breeders’
Symposium Series
2002—2003 Edition
Table of Contents
Author Profiles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Joint and Leg Problems in Growing Show Dogs . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Darryl L. Millis, MS, DVM, DACVS; Jean Loonam, DVM
Nutrition for the Growing Large Breed Show Dog . . . . . . . . . . . . . . . . . . . . . . . . . . 11
Martin Coffman, DVM
The Owner Handler vs The Professional . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
George G. Alston
A Dog’s Mouth: What’s Going On? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18
Jean Hawkins, MS, DVM, DAVDC
Managing the Brood Bitch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22
Russ Kelley, MS
Nutrition and Immunology: Is There a Relationship? . . . . . . . . . . . . . . . . . . . . . . . . 29
Michael G. Hayek, PhD; Stefan P. Massimino, MS; Michael A. Ceddia, PhD
The Carbohydrate Puzzle: What’s In It for My Dog?. . . . . . . . . . . . . . . . . . . . . . . . . 35
Sean M. Murray, PhD; Gregory D. Sunvold, PhD
Copyright ©2002
The Iams Company, Dayton, OH 45414, USA
All rights reserved.
Internet address: www.iams.com
Printed in the United States of America
Item #RD0037
Cover photo: AKC Certified Pedigree reprinted with the permission of the American Kennel Club.
Photo of handler and Samoyed ©Kent and Donna Dannen, 2002.
Photo of Bernese Mountain Dog ©AKC, photo by Mary Bloom.
1
Maximizing Success in the Breeding Kennel and Show Ring—2002
Author Profiles
George G. Alston
Mr. George Alston showed his first dog in 1947 and was originally licensed as an All-Breed
Handler in 1961. During his show career, he won over 300 Best in Shows and over 1000 Group
I’s. Specials shown by him were consistently in the top rankings, which included Quaker Oats
winners, Westminster Group winners, and multiple National Specialty winners. Now retired from
handling, Mr. Alston teaches seminars where his students learn handling techniques, helpful
insights, and “secret” tips. More than 150 of his students have gone on to win (owner handled)
Specialty or All-Breed Best in Shows. Many of his students have gone on to become professional
handlers including some who started his seminars when they were showing in junior showmanship.
Mr. Alston is also the author of the best selling book, The Winning Edge: Show Ring Secrets.
Martin Coffman, DVM
Dr. Martin Coffman is a 1970 graduate of the College of Veterinary Medicine at Auburn
University. He did his undergraduate work at the University of Tennessee in Knoxville. After 30
years in private veterinary practice, Dr. Coffman is currently the Manager of Technical
Communications for The Iams Company’s Research and Development Division. He is presidentelect of the American Canine Sports Medicine Association, a member of the Society for
Theriogenology, and Auburn’s Sports Medicine Advisory Panel. He owns Briarmaster Kennels
and competes in Beagle field trials nationwide. Dr. Coffman lectures extensively to clubs and
organizations throughout the U.S.
Jean Hawkins, MS, DVM, DAVDC
Dr. Jean Hawkins received her MS and DVM from Louisiana State University in Baton Rouge.
She is a Fellow of the Academy of Veterinary Dentistry and a Diplomate of the American
Veterinary Dental College. As a dental consultant, Dr. Hawkins has had the opportunity to work
with several dental manufacturers. She has presented more than 600 hours of veterinary continuing
education both in the U.S. and internationally. She practices veterinary dentistry at Mountain
View Animal Hospital and Pet ER in Boise, Idaho.
Michael G. Hayek, PhD
Dr. Michael Hayek received a BS in Biology from Villanova University, an MS in Animal
Science and a PhD in Nutritional Science from the University of Kentucky. He was a Research
Associate at the Nutritional Immunology Laboratory at the Jean Mayer USDA Human Nutrition
Research Center on Aging at Tufts University where his research emphasis was the interaction
between nutrition and the aging immune system. Dr. Hayek is currently Director of Strategic
Research in the Research and Development Division of The Iams Company where his research
interests include geriatric nutrition, longevity, and the interaction between nutrition and the
immune response.
2
Russ L. Kelley, MS
Mr. Russ Kelley is an alumnus of Auburn University where he received his BS in Animal Science
in 1988 and his MS in Animal Science in 1998. He served on the staff of Auburn University from
1992 to 1997 as a Research Specialist in the area of Growth & Developmental Biology for the
Department of Animal & Dairy Sciences. In 1997, Mr. Kelley accepted a position with The Iams
Company as a Research Associate in the Research and Development Division. He is currently a
Research Scientist and as a member of the Strategic Research team, he provides assistance with
research efforts in the areas of reproduction and neonatal nutrition. Mr. Kelley has published
scientific papers and abstracts in peer-reviewed journals on regulatory influences of animal growth
and development.
Darryl L. Millis, MS, DVM, DACVS
Dr. Darryl Millis received his BS in Animal Science from Cornell University in 1981 and his MS
in Animal Nutrition from the University of Florida in 1983. After receiving his DVM degree from
Cornell University in 1987, he completed a small animal internship in 1988 and a surgical residency in 1991, both at Michigan State University. Dr. Millis served as an Assistant Professor of
Small Animal Surgery at Mississippi State University from 1991–1993, at which time he joined
the faculty at the University of Tennessee where he currently serves as Associate Professor of
Orthopedic Surgery and Section Head of Small Animal Surgery. His research interests include
physical therapy in small animals, osteoarthritis, and bone healing.
Sean M. Murray, PhD
Dr. Sean Murray is an alumnus of the University of Illinois where he received his BS in Animal
Science in 1992, his MS in Nutrition in 1997, and his PhD in Companion Animal Nutrition in
1999. The emphasis of his thesis research focused on glycemic and insulin responses of dogs fed
traditional versus resistant-type starches. Dr. Murray accepted a position in the Research and
Development Division of The Iams Company as a Research Nutritionist in 1999. He is currently
in charge of conducting clinical research in various areas including the nutritional management
of diabetes and obesity, as well as gastrointestinal and dental health.
3
essential. For purposes of this discussion, lameness is
defined as an alteration in the normal gait of the animal.
When evaluating a lame dog, the veterinarian should
examine the entire animal because the source of the lameness may not be orthopedic, but may involve other systems
such as the neurologic system. The lameness should be
localized to a specific area by gait analysis and palpation. At
this point, further diagnostics, such as radiographs or joint
taps, may be required to make the diagnosis. Occasionally,
advanced diagnostics, such as computerized tomography,
magnetic resonance imaging (MRI), nuclear scans, or
advanced gait analysis may be required for diagnosis.
Joint and Leg
Problems in
Growing Show
Dogs
GENERAL CAUSES OF JOINT
AND LEG PROBLEMS IN GROWING DOGS
The possible causes of lameness in young dogs may be
divided into categories: congenital, developmental, traumatic, idiopathic, infectious, nutritional/metabolic, and
neoplastic (Table 1). Congenital abnormalities are changes
that are present at birth and therefore are usually seen in
very young dogs. Developmental abnormalities occur during
the growing stages of the dog’s life and often have a genetic
basis. Traumatic injuries are common in young dogs due to
their adventurous nature and playfulness. Idiopathic abnormalities have unknown causes or origins. Orthopedic conditions are frequently associated with nutritional imbalances,
deficiencies, or excesses. Some metabolic conditions may
be related to nutritional issues, or may involve other body
systems. Infectious and neoplastic causes of lameness in
growing dogs are uncommon.
Darryl L. Millis, MS, DVM, Diplomate ACVS
Jean Loonam, DVM
College of Veterinary Medicine
University of Tennessee, Knoxville, Tennessee, USA
CONGENITAL CAUSES OF JOINT
EVALUATION OF THE GROWING DOG WITH
SUSPECTED JOINT AND LEG PROBLEMS
Forelimb
Congenital dislocation (luxation) of the shoulder is an
uncommon cause of lameness in young dogs, but is usually
seen in small breeds such as Toy Poodles, Chihuahuas, and
Pomeranians.1 The dislocation is a result of inherited weakness to the supporting structures of the shoulder joint. The
luxation is usually bilateral and the dog may only have mild
lameness. Surgery may be performed, but some animals can
learn to compensate quite well.
Congenital dislocation of the elbow is also a hereditary
disease affecting mostly small breed dogs such as Pekingnese,
Boston Terriers, Miniature Poodles, Pugs, Chihuahuas,
Miniature Pinschers, Dachshunds, and Yorkshire Terriers.
This disease has also been seen in larger breed dogs such as
Bulldogs, Basset Hounds, Akitas, Shelties, and German
Shepherd Dogs. The luxation is usually bilateral. Dogs have
varying degrees of lameness, from essentially normal to
non-weight bearing. This condition is caused by abnormal
development of the elbow joint. Most dogs require aggres-
The complete evaluation of a patient suspected to have
joint or leg problems requires knowledge of the patient profile
(age, gender, breed; also called the signalment of the patient),
a comprehensive history, and a thorough physical examination by a veterinarian knowledgeable about orthopedic
conditions. Certain breeds are afflicted more commonly than
others by a particular orthopedic condition, and knowledge
of the breed predispositions is helpful in determining the
ultimate cause of a problem. A thorough history includes how
the problem began, how it has progressed, travel history, the
presence of similar problems in siblings, parents, or grandparents, the diet, any treatments that have been applied,
and the effectiveness of the treatments.
A proper physical examination of the patient is essential to determine the source of the problem. Because most
joint and leg problems of growing dogs have some degree of
lameness, a thorough lameness and gait examination are
4
Table 1. Common joint and leg problems in growing dogs
GENERAL CATEGORY
FRONT LIMBS
HIND LIMBS
Congenital
• Shoulder dislocation
• Elbow dislocation
• Limb agenesis
• Patella dislocation
Developmental
• Osteochondritis dissecans
- Humeral head
- Medial humeral condyle
• Elbow
- Dysplasia
- Fragmented medial
coronoid process
- OCD of the medial
humeral condyle
- Ununited anconeal
process
• Osteochondritis dissecans
- Lateral femoral condyle
- Trochlear ridges of talus
• Hip dysplasia
• Legg-Calve-Perthes
disease
Traumatic
• Fractures
- Growth plate fractures
- Lateral condyle of the
humerus
- Distal radius and ulna
- Digits and metacarpals
- Joint dislocations
- Tendon and ligament
injuries
• Fractures
- Pelvis
- Femur
- Tibia and fibula
- Digits and metatarsals
- Tendon and ligament
injuries
- Joint dislocations
- Cranial cruciate
ligament injury
Idiopathic
• Panosteitis
• Hypertrophic
osteodystrophy (HOD)
• Panosteitis
• Hypertrophic
osteodystrophy (HOD)
Infectious
•
•
•
•
Septic arthritis
Osteomyelitis
Lyme disease
Rocky Mountain
Spotted Fever
• Ehrlichiosis
• Fungal infections
•
•
•
•
Nutritional and
Metabolic
• Overfeeding
• Improper nutrient ratios
• Nutritional secondary
hyperparathyroidism
• Overfeeding
• Improper nutrient ratios
• Nutritional secondary
hyperparathyroidism
Neoplasia
• Osteosarcoma
• Osteosarcoma
Septic arthritis
Osteomyelitis
Lyme disease
Rocky Mountain
Spotted Fever
• Ehrlichiosis
• Fungal infections
sive, early treatment, such as surgery, to stabilize the joint
and prevent other abnormalities, such as arthritis.
Failure of a limb to develop (limb agenesis) is a rare
congenital defect in which the bones do not develop properly. The radius is one of the more commonly affected bones
and its absence is apparent immediately after birth. Due to
the severity and difficulty in treating this disease, amputation
may be the treatment of choice.
Figure 1. Medial luxation of the patella. The small
solid arrow indicates the patella. The open arrow
shows the normal location of the patella.
intermittent lameness and an abnormal hopping or skipping gait. Patellar luxations are
graded on a scale of 1 to 4, depending on the
severity of the luxation. Surgical treatment is
recommended for symptomatic dogs to control
pain, improve gait, and prevent secondary
degenerative changes leading to arthritis. Interestingly, a
significant percentage of patients with patella luxation
develop rupture of the cranial cruciate ligament. The combination of these conditions is much more serious than
either one alone.
DEVELOPMENTAL CAUSES OF JOINT
Hind limb
Forelimb
Patellar (knee cap) dislocation is a common abnormality in toy, miniature, and some large breed dogs (Figure 1).
Medial (toward the inner surface) and lateral (toward the
outer surface) luxations occur, but medial luxation is most
common. Patellar luxation is usually a congenital disorder
that is thought to be caused by abnormal hip conformation
and a shallow patellar groove. Clinical signs are typically an
Osteochondrosis (OC) is defined as a disturbance of
the change of cartilage to bone. The cause of this disease is
not completely understood, however, it is known to be a
multifactorial disease process which includes genetic, nutritional, traumatic and vascular components. The abnormal
area of cartilage is structurally and mechanically inferior to
5
the surrounding cartilage and bone. The diseased cartilage
will often detach as a flap. The condition is then called
osteochondritis dissecans (OCD), which may cause joint
abnormalities, including synovitis (inflammed joint fluid)
joint swelling, arthritis, pain, and lameness.
Common sites of OCD in the forelimb are the head of
the top part of the arm bone and the elbow joint between
the arm and the forearm bone (medial humeral condyle).2,3
Radiographs are usually diagnostic for OCD (Figure 2).
This disease is usually managed surgically and consists of
removal of the flap and surgical removal of surrounding
abnormal tissue. Surgical intervention typically has favorable
results in the shoulder with about 90% of animals returning
to acceptable function. Success rates for elbow OCD are
less predictable.
Elbow dysplasia is an encompassing term used to
describe a group of developmental abnormalities affecting
the elbow joint of growing dogs. Included in this term are
fragmented medial coronoid process (FCP), ununited
anconeal proess (UAP), and OCD of the inside aspect of the
elbow joint surface (Figures 3–5).4,5 Some also consider
uneven (asynchronous) growth of the radius and ulna with
elbow incongruity a form of elbow dysplasia. Elbow dysplasia
is most commonly seen in large and giant breed dogs, especially in Bernese Mountain Dogs, Golden Retrievers,
Labrador Retrievers, and Rottweilers. Males are more commonly affected. Dogs with elbow dysplasia typically present
around 5–8 months of age and it is commonly seen in both
elbows. Diagnosis is based on clinical signs, signalment and
radiographs. Computerized tomography is helpful in early
cases of FCP. Depending on the specific condition, either
medical or surgical treatments may be recommended.
Medical therapy includes controlling lean body weight,
controlled exercise, monitoring pain, and non-steroidal
anti-inflammatory medications. Surgical therapy is aimed
at removing any abnormal cartilage or bone and attempting
to return the joint to more normal function. Arthroscopic
removal may have advantages over an open arthrotomy,
particularly regarding removal of FCP.
Figure 2. Osteochondritis dissecans of the caudal aspect of the head
of the humerus. The arrow indicates an area of lucency where a flap
of cartilage has broken off.
Hind Limb
Hip dysplasia (HD) is a common developmental
defect with genetic and nutritional causes.6-9 HD is more
common in large breed dogs, and nearly always involves
both sides, although one side may be more severely affected.
HD starts with slackness in the joint and partial disclocation
of the hip joints (Figure 6). This creates abnormal forces
on the joint leading to degeneration and arthritis over time.
Clinical signs include gait changes and pain. A definitive
diagnosis is made by radiographs. Early evaluation using
PennHip* may give some indication whether or not a dog
may develop hip dysplasia.8,10 Medical treatment includes
Figure 3. Fragmented medial coronoid process of the ulna. The dark
arrow indicates the region of the fragmented coronoid process (not
clearly seen). The white arrows indicate secondary arthritic changes
in the elbow joint.
weight loss or control, physical rehabilitation and controlled
exercise, nonsteroidal anti-inflammatory medications, and
disease-modifying osteoarthritis agents, such as glucosamine
and chondroitin sulfate. Surgical techniques in immature
dogs include fusing the pubic bone of the pelvis, triple
pelvic osteotomy (Figure 7), and removal of the head of
PennHip is an organized collaborative effort between of the Veterinary
School at the University of Pennsylvania, Synbiotics Corporation and
a network of more than 750 certified veterinarians.
6
Figure 4. Ununited anconeal process. The anconeal process (arrow)
has not fused with the ulna, and many secondary arthritic changes
have occurred.
Figure 6. Subluxation of both hip joints as a result of hip dysplasia.
Figure 5. Osteochondritis dissecans of the medial condyle of
the humerus. Note the dark defect indicated by the arrow which
corresponds with the area of defective ossification.
Figure 7. Triple pelvic osteotomy has been performed to improve
coverage of the head of the femur by the acetabulum.
the thigh bone (femoral head and neck ostectomy
[FHO]).9,11 Surgical procedures in older dogs with secondary
osteoarthritis are limited to salvage procedures, including
total hip replacement and FHO.9
Legg-Calve-Perthe disease is seen in small and miniature dogs. The exact cause is unknown; however, genetic
and traumatic causes have been implicated. The disease
progresses to necrosis or degeneration of the femoral head.
The animal is usually lame, often after minor trauma.
Radiographs are diagnostic, showing the abnormal femoral
head. Treatment is usually performed by removing the
femoral head, a procedure called femoral head and neck
7
often have other concurrent trauma, such as chest injuries,
that must be addressed. Unique to young dogs are SalterHarris fractures, which are fractures of the area of the bone
that is growing (ie, the growth plate or physis) in skeletally
immature dogs. Growth plate fractures usually heal very well,
but the growth plate usually closes prematurely, resulting in
limb shortening, and in the case of the radius and ulna,
uneven growth, limb deformities, and partial dislocation of
the elbow and carpal joints.16 Growth plate fractures should
be reduced and stabilized as soon as possible for the best
outcome.
Fractures of the digits (toes) are fairly common in
young dogs that get their foot caught in fences or gates, or
have them stepped on. Most heal reasonably well with
splinting and rest, but occasionally surgery is necessary. Soft
tissue injuries in growing dogs occur, but should only be
diagnosed after ruling out other more serious injuries.
ostectomy. Prognosis for function after surgery is very good.
OCD is also occasionally seen in the hind leg.
Common sites include the knee joint and the hock
joint.12,13 OCD of the knee is most commonly seen in large
breed dogs such as Great Danes, Labrador and Golden
Retrievers, Newfoundlands, and German Shepherd Dogs; it
may also be seen in Akitas, Chow Chows, Boxers, Bull
Terriers, Mastiffs, and Samoyeds. Diagnosis is by clinical
signs of chronic hind limb lameness which worsens after
exercise, and seeing the lesion on radiographs. Surgical
treatment involves removing the abnormal cartilage and
the surrounding tissue. Dogs with stifle OCD may be predisposed to rupture of the cranial cruciate ligament in the
future. OCD of the hock joint is also seen in the large
breeds, but especially so in Rottweilers. One study indicated
no difference in long-term outcome between medical treatment and surgical removal of the cartilage flap in hock
OCD, but arthroscopic removal may offer some advantages
over traditional surgical removal. In general, stifle OCD
has a better prognosis than hock OCD.
Hind limb
Rupture of the cranial cruciate ligament (CrCL) is a
major cause of degenerative joint disease in the knee and is
one of the most common injuries seen in the dog (Figure 9).
Generally, rupture of the CrCL is a degenerative condition
in middle-aged to older dogs. Fortunately, this condition is
uncommon in young dogs, with the exception of
Rottweilers. If a cruciate rupture occurs in other breeds of
young dogs, it is usually secondary to trauma, such as sudden
hyperextension of the knee. Occasionally, there is a fracture
of the origin or insertion site of the cruciate ligament.
Common breeds affected with the degenerative form of CrCL
are the Akita, Labrador
Retriever, Mastiff, Rottweiler,
Staffordshire Terrier, English
Bulldog, Boxer, St Bernard,
Chesapeake Bay Retriever,
Giant Schnauzer, and Bouvier
des Flanders. Dogs with
“post-legged” conformation
are often affected, possibly
because of abnormal forces
acting on the ligament.
Diagnosis is based on clinical
signs including joint pain,
joint swelling, a firm swelling
on the inside of the joint, the
presence of a clicking sensation of the joint, and abnormal motion of the knee during
manipulation (drawer sign).
Surgical treatment is recommended in dogs with CrCL
rupture because of the devel-
TRAUMATIC CAUSES OF JOINT
Forelimb
Fractures, dislocated joints, tendon and ligament
sprains and strains, and muscle damage occur frequently in
young dogs. Numerous fractures of the canine forelimb may
occur (Figure 8).14,15 Many dogs with forelimb fractures
Figure 8. Fracture of the midshaft of the radius and ulna in a young dog. Note the open growth plates
(physes) at the ends of the long bones. These are susceptible to premature closure as a result of the trauma.
8
Danes.17 The disease is characterized by inflammation and
actual death of bone tissue with secondary microfractures of
the bone around the growth plate. It is most common in the
radius and ulna, and is also seen in the tibia and fibula. The
ends of the affected long bones are painful; the dog may
have a high fever and stop eating and drinking. Diagnosis is
made by clinical signs and radiographs. This disease may be
self-limiting, lasting several days to months. Unlike panosteitis, severe cases can have a poor prognosis with systemic
concurrent illness and long term affects on the growth
plates, with premature closure of the growth plates and
angular limb deformities. Some severely affected dogs may
have to be euthanized.
INFECTIOUS CAUSES OF JOINT
Infectious causes of lameness of the young dog are not
very common. Septic arthritis and osteomyelitis can occur in
neonatal puppies with severe systemic infections; however,
this is uncommon. Young dogs can develop septic arthritis
and osteomyelitis with bite wounds, penetrating wounds,
and trauma. Tick borne diseases such as Lyme disease, Rocky
Mountain Spotted Fever, and Ehrlichiosis, may cause lameness in young dogs, but these diseases are more commonly
seen in mature dogs. Fungal diseases, such as blastomycosis,
histoplasmosis, and coccidiodiomycosis are seen in some
parts of the country where these agents are common.
Figure 9. Secondary arthritic changes in the stifle as a result of
rupture of the cranial cruciate ligament.
opment of arthritis and the possibility of torn knee cartilage. There are several accepted techniques to stabilize the
CrCL, the most recent of which is the tibial plateau leveling osteotomy.
NUTRITIONAL AND METABOLIC CAUSES OF
JOINT AND LEG PROBLEMS IN GROWING DOGS
IDIOPATHIC CAUSES OF JOINT
Many studies have evaluated the affects of nutrition on
skeletal development in dogs. Diseases such as OCD and HD
are affected by the type and amount of diet fed to growing
dogs.6 In general, dogs are more apt to develop these conditions when fed free choice, and when fed diets high in energy
and calcium. In fact, several studies have demonstrated that
there is a lower incidence of arthritis and other joint related
problems when puppies are fed 75% of what they would
consume if food was available free choice. Perhaps the best
prevention is to breed the best to the best and hope for the
best, restrict the amount of food fed to puppies, and feed a
commercially available diet formulated for growing large
and giant breeds of dogs.
With the advent of well-formulated commercially
available diets, diseases such as nutritional secondary
hyperparathyroidism (from low calcium, high phosphorous,
or inadequate vitamin D in the diet) leading to weak bones,
skeletal deformities and pathologic fractures are rarely seen.
These diseases typically occur when feeding puppies a diet
composed mostly of meat.
Two common idiopathic causes of lameness in the forelimb and hind limb are panosteitis and hypertrophic
osteodystrophy (HOD).12,17,18 These two diseases are
labeled as idiopathic because their causes are unknown at
this time. However, rapidly growing dogs receiving high
amounts of energy and calcium appear to be predisposed to
both conditions.
Panosteitis is fairly common and can affect the midportion of any of the long bones (femur, humerus, etc).12,18
It has been reported in many breeds and in particular,
German Shepherd Dogs and Basset Hounds. It has been
suggested that panosteitis is associated with viral or bacterial
infections, stress, metabolic abnormalities, vascular abnormalities, allergic or immune-mediated diseases, parasitism,
and possibly genetic causes. The lameness may shift to
other legs and the dog usually shows pain when the affected
long bones are examined. Radiographs may show patchy
areas of increased density on the affected bones. Panosteitis
is a self-limiting disease that typically lasts several days to
weeks. Animals are usually given supportive care for pain.
Hypertrophic osteodystrophy is not a common disease,
but is seen in large and giant breed dogs, especially Great
9
NEOPLASTIC CAUSES OF JOINT AND
LEG PROBLEMS IN GROWING DOGS
Neoplasia in young growing dogs is rare. Osteosarcoma
has been reported in dogs as young as 6 months of age and
affects primarily large and giant breeds. Diagnosis is made
by clinical signs, radiographs, and biopsy (microscopic
examination) of the area. This cancer is typically seen in sites
that are “away from the elbow or toward the knee”. Treatment
consists of amputation, chemotherapy, and radiation.
REFERENCES
1. Puglisi TA. Canine humeral Joint instability—part I. Compend Cont
Educ Pract Vet 1986; 8:593-601.
2. Whitehair JG, Rudd RG. Osteochondritis dissecans of the humeral head
in dogs. Compend Contin Educ Pract Vet 1990; 12:195-204.
3. Rudd RG, Whitehair JG, Margolis JH. Results of management of
osteochondritis dissecans of the humeral head in dogs: 44 cases (1982 to
1987). J Amer Anim Hosp 1990; 26:173-178.
4. Read RA, Armstrong SJ, O ‘Keefe JD, Eger CE. Fragmentation of the
medial coronoid process of the ulna in dogs: a study of 109 cases. J Small
Anim Pract 1990; 31:330-334.
5. Padgett GA, Mostosky UV, Probst CW, Thomas MW, Krecke CF. The
inheritance of osteochondritis dissecans and fragmented coronoid
process of the elbow joint in Labrador Retrievers. J Am Anim Hosp Assoc
1995; 31:327-330.
6. Kealy RD, Lawler DF, Ballam JM, Lust G, Smith GK, Biery DN, Olsson
SE. Five-year longitudinal study on limited food consumption and
development of osteoarthritis in coxofemoral joints of dogs. J Amer Vet
Med Assoc 1997; 210:222-225.
7. Lust G. An overview of the pathogenesis of canine hip dysplasia. J Am
Vet Med Assoc 1997; 210:1443-1445.
8. Lust G, Williams AJ, Wurster-Burton N, Pijanowski GJ, Beck KA,
Rubin G, Smith GK. Joint laxity and its association with hip dysplasia in
Labrador Retrievers. Am J Vet Res 1993; 54:1990-1999.
9. Cook JL, Tomlinson JL, Constantinescu GM. Pathophysiology, diagnosis,
and treatment of canine hip dysplasia. Compend Cont Educ Pract Vet
1996; 18:853-867.
10. Smith GK, Mayhew PD, Kapatkin AS, McKelvie PJ, Shofer FS, Gregor
TP. Evaluation of risk factors for degenerative joint disease associated
with hip dysplasia in German Shepherd Dogs, Golden Retrievers,
Labrador Retrievers, and Rottweilers. J Amer Vet Med Assoc 2001;
219:1719-1724.
11. Swainson SW, Conzemius MG, Riedesel EA, Smith GK, Riley CB.
Effect of pubic symphysiodesis on pelvic development in the skeletally
immature Greyhound. Vet Surg 2000; 29:178-190.
12. Lewis DD, McCarthy RJ, Pechman RD. Diagnosis of common developmental orthopedic conditions in canine pediatric patients. Compend
Contin Educ Pract Vet 1992; 14:287-301.
13. Montgomery RD, Milton JL, Henderson RA, Hathcock JT.
Osteochondritis dissecans of the canine stifle. Compend Contin Educ
Pract Vet 1989; 11:1199-1208.
14. Muir P. Distal antebrachial fractures in toy-breed dogs. Compend Contin
Educ Pract Vet 1997; 19:137-145.
15. Rorvik AM. Risk factors for humeral condylar fractures in the dog:
a retrospective study. J Small Anim Pract 1993; 34:277-282.
16. Fox SM. Premature closure of distal radial and ulnar physes in the dog.
Part I. Pathogenesis and diagnosis. Compend Contin Educ Pract Vet 1984;
6:128-140.
17. Muir P, Dubielzig RR, Johnson KA. Hypertrophic osteodystrophy and
calvarial hyperostosis. Compend Contin Educ Pract Vet 1996; 18:143-151.
18. Muir P, Dubielzig RR, Johnson KA. Panosteitis. Compend Contin Educ
Pract Vet 1996; 18:29-33.
10
Nutrition for the
Growing Large
Breed Show Dog
While this vogue of larger breeds is understandable,
two factors have combined to increase the number of these
large breed puppies being presented to veterinary clinics for
developmental skeletal diseases. First, the large breeds in
the Working, Sporting, and Hound groups have attracted
new owners, many of which are inexperienced dog people.
While professional handlers and breeders often advise new
competitors on many areas of dog competition, nutrition,
especially the unique needs of the large breed puppy,
remains a source of confusion for many.
Secondly, these breeds have an inherently higher risk
of early-onset skeletal problems than small or medium
breeds, so developmental joint problems are more prevalent
in the puppies that many of these new competitors choose.
These two factors, plus the inordinate desire to have the
“biggest dog in town,” combine to contribute to the occurrence of skeletal and joint problems in these larger dogs.
Martin Coffman, DVM
Mature Body Weight
Research and Development Division
The Iams Company, Lewisburg, Ohio USA
INTRODUCTION
Large dogs constitute some of the most popular breeds in
the world. While this popularity may reflect renewed interest
in the field breeds, schutzen dogs, and other performancetype animals, the popularity of larger breeds is noted in the
show ring as well.
Breed differentiation can be traced back to early
domestication. From wild dogs and wolves, man noted certain characteristics in early-domesticated canids that were
useful to human survival. From sight hunting, to tracking by
scent, to pointing game, to guarding camps, dogs began to
be bred for specific purposes. Now, centuries later, the breeds
have become distinct entities that reflect these early uses,
even if societal progress has made their original function of
less importance. Many of the most useful breeds developed
by man required large body size for function. The desire to
preserve these larger breeds, and their functional structure,
has contributed to their continued popularity.
Growth Rate Comparisons
Small Breed
8–12 mo
Large Breed
12–24 mo
Medium Breed
12 mo
Age
Figure. Variation in growth rate in puppies according to breed size.
BASIC LARGE BREED PUPPY NUTRITION
Among inexperienced dog owners, there may be a lack
of knowledge about research conducted on nutrition for
large breed puppies. While most of the studies have been
conducted with Great Dane puppies, the application of the
research extends to all large breeds. For nutritional purposes,
any breed that matures at over fifty pounds is considered a
large breed.
11
Diseases like the osteochondroses, hip dysplasia, panosteitis, and even hypertrophic osteodystrophy have nutritional
influences,1,2 although genetics, trauma, and infection can
also play an important role. For example, the cause of
panosteitis appears to be a combination of factors, but it
occurs primarily in fastgrowing long bones. If
Diseases like the
we can manage the rate
osteochondroses, hip
of growth of those
bones, we may be able
dysplasia, panosteitis,
to decrease the inciand even hypertrophic
dence of panosteitis in
osteodystrophy have
growing puppies. In
nutritional influences.
addition, researchers
have documented that
increased calcium supplementation alters the accumulation of calcium in the
bones and may cause altered bony structure.3 These alterations affect the diameter of the nutrient foramen in the
bone, a small opening in the bone that allows blood vessels
to enter the marrow cavity, leading to decreased incoming
blood flow, and panosteitis may result. The osteochondroses,
hip dysplasia, and other developmental bone diseases all
have similar nutritional factors as part of their development.
The nutrients most studied in relation to developmental
skeletal problems in puppies are calcium, calories, and protein. Of these, only calcium and caloric intakes have been
documented to have a causative effect. Dietary protein levels
have no effect on the development of skeletal problems in
the growing dog when caloric intake is controlled.4 In fact;
normal protein levels are needed by growing puppies to
help develop optimal lean body mass. Elevated dietary calcium intake, either through supplementation or overfeeding
of commercial foods,
can be a causative factor
Normal protein levels
in many of these condiare needed by growing
tions.5 These associations between dietary
puppies to help develop
factors and skeletal
optimal lean body mass.
problems have led to a
large number of studies
on the nutrition of the larger breeds, and especially the
large breed puppy.6-10 These studies documented that
improper feeding during growth is associated with several
skeletal disorders in the dogs.
About 22% of dogs less than one year of age are affected
by developmental skeletal disorders and more than 90%
of these cases are influenced by nutritional factors.11 To
reiterate, two nutritional scenarios are important factors in
causing these disorders: free choice feeding of a diet leading
to consumption of excess calories and supplementation
with calcium during the growth phase of the puppy. The
onset of developmental disorders of the bones is usually
associated with the rapid growth of long bones. The most
common of these disorders are canine hip dysplasia (CHD),
osteochondrosis, and hypertrophic osteodystrophy (HOD).
Improper feeding during growth is
associated with several skeletal
disorders in the dogs.
THE DEVELOPMENTAL DISORDERS
Canine hip dysplasia is a complex biomechanical disease
of the hip joint. Typically, the surfaces of the hip joint socket
and the surface of the head of the femur are not congruent.
This results in varying degrees of laxity (looseness) in the
joint which, in turn, determines the severity of the condition.
The laxity of the joint can lead to remodeling of the joint
with resultant arthritis. Clinical signs vary from severe,
crippling lameness at a young age to no signs throughout
life. Canine hip dysplasia is caused by many factors.
Genetics are very important, as are trauma to the joints and
other environmental factors. Of these environmental factors,
diet and growth rate are very important, especially between
3 and 8 months of age. Puppies with excessive weight gain
during this period have a higher frequency of serious
changes in the hip joint and resultant degenerative changes
in that joint than pups that grow at a slower rate.1,9
The osteochondroses, one of which is osteochondritis
dissecans (OCD) are characterized by minute disruptions in
the maturation of cartilage. While these conditions can
occur at multiple points in the skeleton, the most important
12
locations are the shoulder, stifle, hock, and elbow.
Osteochondrosis can lead to an acutely inflamed joint or
degenerative joint disease involving the cartilage surface.
Osteochondritis dissecans occurs when a tiny divot-like
flap of cartilage separates from the underlying bone exposing
the bone to joint fluid. While many factors like age, gender,
and breed are incriminated in OCD, excess weight gain and
supplementation with calcium have received the most
attention from a nutritional standpoint.12,13 Breeds that
commonly exhibit OCD include Great Danes, Labrador
Retrievers, Newfoundlands, and Rottweilers.12
Hypertrophic osteodystrophy also occurs primarily in
large and giant breeds and is characterized by excessive
bone deposits and retarded bone resorption near the distal
radius, ulna, and tibia. As the disease progresses, soft tissue
damage occurs around the large bony deposits. Pain and
swelling with concurrent lameness and fever are common.
needed to provide the energy for a show dog’s optimal performance might not be the same as the optimal nutrition
for large breed puppies. Thus the question arises, when is it
best to begin feeding the higher calorie levels associated
with performance dog foods and discontinue feeding the
special diet for large breed puppies. For example, a puppy
owner wants to begin showing her 6-month-old German
Wirehaired Pointer, which she also plans on using for hunting
tests and obedience events. Training is beginning in
earnest, so when does she need to begin feeding a diet that
is more suitable for hard-working dogs?
Ideally, the puppy will stay on a diet designed for large
breeds until at least 12 months, when the incidence of
developmental skeletal disease diminishes substantially. Due
to the increased caloric needs of dogs in training, it may be
advisable to increase the quantity of the large breed diet fed
during the intervening period between 6 and 12 months of
age. As the amount of the food increases, however, the total
calcium intake increases too. Therefore, careful evaluations
of the puppy on a monthly basis are in order to ensure that
optimal body weight and growth rate are being maintained.
WHAT TO RECOMMEND
As breeders, ideally, we are aware of the latest research
to better guide purchasers of puppies or beginning competitors in dog sports. Application of current research dictates
the following nutritional recommendations for large breed
puppies (Table):
1. Do not supplement diets with additional calcium
2. Choose a diet with moderate calcium levels
3. Choose a diet with moderate calorie levels
4. Choose a diet that has normal protein levels
WHEN SHOULD WE BEGIN
PERFORMANCE FEEDING
Successful exhibitors know that nutrition is an important
tool in conditioning the show dog. The type of nutrition
Table. Summary of protein, energy, and calcium effects on skeletal development and nutritional recommendations
Nutrient
Nutritional
Recommendation
Effect of Nutrient Level on Skeletal Development
Low
Medium
High
Protein
Growth rate if
nutrient deficiency
Normal growth
Normal growth
26%
Energy
Growth rate if
nutrient deficiency
Normal growth
Growth rate
Skeletal
abnormalities
14%
Growth rate
Bone mineral
Bone strength
Gait abnormalities
Bone mineral
Bone strength
Gait abnormalities
HOD
Good conformation
Calcium
13
Bone mineral
Bone strength
Gait abnormalities
HOD
Poor conformation
0.80%
(1.2:1 Ca:P ratio)
Each case, such as this one, must be evaluated individually to encourage a healthy bodyweight and minimize risks
of developmental joint and bone disease. At 12 months of
age, a typical dog in training or preparation for the show
ring would benefit from the change to a more nutrientdense diet. However, puppies not being conditioned for
competition would likely benefit from the special large
breed diet for an additional six months.
CONCLUSION
Managing the growth rate of growing large breed puppies requires careful attention to the nutritional needs of
each individual pup. Optimal calcium and calorie intake
must be maintained, not only as the puppy grows, but also
as it enters intense training. Protein levels in the food
should be sufficient to maintain normal muscle growth. The
timing of change to performance foods for hard training
should be evaluated on a case-by-case basis.
REFERENCES
1. Goodman SA, Montgomery RD, Fitch RB, Hathcock JT, Lauten SD,
Cox NR, Kincaid SA, Rumph PF, Brawner WR, Baker, HJ, Lepine AJ,
Reinhart GA. Serial orthopedic examinations of growing Great Dane
puppies fed three diets varying in calcium and phosphorous. In: Reinhart
GA, Carey DP, eds. Recent Advances in Canine and Feline Nutrition, Vol.
II: 1998 Iams Nutrition Symposium Proceedings. Wilmington OH: Orange
Frazer Press, 1998; 3-12.
2. Nap RC. Nutritional influences on growth and skeletal development in
the dog [thesis]. Utrecht, The Netherlands: Utrecht University; 1993.
3. Hazewinkel H. Etiology and pathogenesis of OCD, ED, HOD, in
Proceedings. Large Breed Health Care Symposium, Venice, Italy; 2001.
4. Nap R. Effects of dietary protein levels on skeletal development in large
breed dogs, in Proceedings. Large Breed Health Care Symposium, Venice,
Italy; 2001.
5. Hazewinkel H. Influences of chronic calcium excess on the skeleton of
growing Great Danes. J Am Anim Hosp Assoc 1985; 21: 377-391.
6. Richardson DC, Zentek J. Nutrition and osteochondrosis. Vet Clin North
Am Small Anim Pract 1998; 28:115-135.
7. Sunvold GD, Bouchard GF. The glycemic response to dietary starch. In:
Reinhart GA, Carey DP, ed. Recent Advances in Canine and Feline
Nutrition, Vol. II: 1998 Iams Nutrition Symposium Proceedings.
Wilmington OH: Orange Frazer Press, 1998; 123-131.
8. Johnson JA, Austin C, Breuer GJ. Incidence of canine appendicular
musculoskeletal disorders in 16 veterinary teaching hospitals from 19801989. J Vet Comp Orthop Trauma 1994; 7:56-59.
9. Crenshaw TD. Nutritional effects on bone strength in the growing
canine. In: Reinhart GA, Carey DP, ed. Recent Advances in Canine and
Feline Nutrition, Vol. II: 1998 Iams Nutrition Symposium Proceedings.
Wilmington OH: Orange Frazer Press, 1998; 29-40.
10. Hedhammer A, Wu F, Krook L, et al. Overnutrition and skeletal disease—an experimental study in growing Great Dane dogs. Cornell Vet
1974; 64:1-159.
11. Lavelle RB. The effect of the overfeeding of a balanced complete commercial diet to a group of growing Great Danes. In: Burger IH, Rivers
JPW, eds. Nutrition of the Dog and Cat. Cambridge UK: Cambridge Univ
Press, 1989; 303-316.
12. Slater MR, Scarlett JM, Kaderly RE, et al. Breed, gender, and age risk
factors for canine osteochondritis dessicans. J Vet Com Orthop Trauma
1991; 4:100-106.
13. Slater MR, Scarlett JM, Donoughue S, Kaderly RE, Bonnett BN,
Cockshutt J, Erb HN. Diet and exercise as potential risk factors for
osteochondritis dessicans in dogs. Am J Vet Res 1992; 53:2119-2124.
14
The Owner
Handler vs
The Professional
Photo used with permission. ©Ashbey Photography, 2002.
George G. Alston
First you have to take the word can’t out of your
vocabulary. It is a terrible word. You have to stop listening
to all those people who say, “The amateur can’t beat the
Professional”. That is hog wash. So many owner handlers
have been successful over the years. They have won many
Best in Shows, Best in Specialty, number One in their Group
or number One All Breed. Here are a few tips and thoughts.
Cary, North Carolina USA
WHAT THE JUDGE SEES IS WHAT YOU GET
A judge can only judge what is presented in the ring.
The American Kennel Club allows a judge 2 minutes per
dog. After passing out ribbons and marking their book that
leaves them about 11⁄2 minutes per dog. The judge cannot
assume. He or she has to judge what they see. If you do not
present what the judge wants to see you will lose. You must
learn to present the dog as efficiently as possible in the least
amount of time. It takes work, practice, and dedication.
When the judge comes to the end of the class and tries to
make a decision, if the professional handler has his dog set
up right and the owner handler has his set up wrong, who
wins? The professional will, 9 times out of 10. Yet the owner
handler will stand there and complain that the professional
always wins.
Amateurs have a great advantage, if they would use it
to their benefit. They usually have only one dog to show, so
they have the time to train that dog, condition it, learn
about its strong and weak points, and practice showing
under all kinds of circumstances. Therefore, when they go
into the ring, there should be no surprises.
The professional must handle a great many dogs in the
course of a day—some of them the handler may not know
very well, yet that handler is expected to make each one
look good. Who has the advantage under those conditions?
The amateur of course.
The amateur often has an advantage over the professional because a judge is going to be more forgiving if an
INTRODUCTION
Showing dogs is the only sport that, by the payment of an
entry fee and with no training whatsoever, you can compete
directly with a professional. There is no other organized
sport in which you can do that.
The amateur owner handler is competing against someone who makes his or her livelihood from showing dogs.
The owner handler is competing with a professional who
has dedicated his or her life to this sport and who has spent
many years in apprenticeship learning the trade. Yet the
amateur will compete in the same arena for the same awards
without special training.
In order to do this successfully, you have to have the
same dedication. You have to do something every day, 365
days a year, to improve your skill, knowledge, and abilities.
The professional is doing all this and more. How are you to
beat them if you don’t work at it?
15
amateur makes a mistake, sets up a dog imperfectly, or gaits
awkwardly. If the dog is worthy, the judge will give the
amateur every opportunity. The judges will not forgive the
professional as easily.
I don’t care about it.” If the owner handler doesn’t seem to
care about the dog, why should the judge!
Consider a collector of fine china and porcelain. When
you go to visit the collection, the owner grabs a beer mug
from the shelf and says, “I got this at the local saloon.” You
will notice there is no particular care taken in handling this
piece of china. “But this one,” the collector says, reaching
for another piece, “is very rare and beautiful. See the lines
and the translucent quality.” This porcelain is held gently
with the fingertips. It is presented to you with the greatest
care so you can admire its value.
When you present your dog to the judge, you must take
as much care as that collector did with the china. The more
you use your fingertips instead of your hands, both on the
dog and the leash, the better the presentation will be.
This concept of the handler as an artist, collector, and
caretaker of the dog will often make the difference between
being able to present a dog consistently at its best and winning, or losing to the competition who may be showing a
dog not as good as yours.
Anyone can handle a dog. But it takes great skill to
present one so that the judge thinks this is the greatest
specimen of the breed that they have ever seen and they are
honored to have it in their ring.
THE HANDLER AS AN ARTIST
When you are in the ring showing a dog, you are an
artist. You are creating a picture, usually an unnatural picture, because you will be emphasizing the dog’s assets. Work
with the good points. You are trying to sell a picture to the
judge. In order to create a picture that you want with that
dog, you must know both its good points and faults. You
must have studied your dog both standing and gaiting so
you are familiar with all of its parts.
The difference between the the artist and the handler
is that when an artist creates a work, such as a sculpture, it
is done once and it is done for all time. They never have to
do that piece again. If an artist makes a painting or an
engraving, they can make prints of that, but they never
have to go back and create the original work of art again.
Nor could they.
When you show a dog, you must create the same picture of that dog every time it is shown. Every time you stack
a dog, it must look the same. Every time you gait a dog, it
must look the same, and be as perfect a picture as you can
make it.
Remember consistency. Amateurs often walk into the
ring and stack their dog very well the first time. But the
next time, maybe three minutes later, its feet are going in
four different directions. It does not take magic to stack and
gait perfectly and consistently every time. It does take work
and patience.
You must practice showing off the dog’s good points so
that the judge sees what you want to be seen. A lot of owner
handlers attempt to hide the dog’s faults. This is a big mistake. When you try to hide faults you just bring attention
to them. If God could not fix them, then how can you? Set
the faulty part up then leave it alone.
Just as an artist creates an illusion on canvas or paper,
the handler creates an illusion for the judge. Professionals
know how to show to the judge those points they want the
judge to see. You must practice in order to create the picture
you want to present to the judge. Work in front of a mirror
to see what the judge sees. Look at and admire the good
points, stay away from the faults. The judge will tend to follow your eyes to see what you are looking at and then the
judge will see what you want them to see.
As an artist takes pride in their work, you must take
pride in presenting your dog as if it were the best animal you
have ever seen and you are doing the judges a favor to allow
them to put their hands on this valuable animal.
Exhibitors who manhandle their dogs, pulling them
around, grabbing them by the muzzle, or yanking them here
and there project the feeling “This is just another dog and
THE PSYCHOLOGY OF THE SHOW RING
The sport of showing dogs is 80% mental and 20%
physical. You can beat yourself before you ever step into the
show ring.
In the past 20 years there has been a lot of information
gathered about the use of psychology in sports. Football
teams have their own sports psychologists who are hired to
motivate the players into a winning attitude. Basically, the
whole concept is to have a positive outlook, to think you
are going to win and that you are going to play the best
game of your life. This is also used by professional golfers,
tennis players, race car drivers, professional horsemen, etc.
16
The Power of the Mind
dog on that particular day under the unique circumstances
in that ring.
Most amateurs stand outside the ring and talk. Their
dogs are out at the end of the lead looking terrible. Then
when they take their dog in the ring and lose, they complain
that the judge only puts up professionals.
The power of the mind is a wonderful thing. It is as
important when you are showing a dog as it is in any
endeavor. You must believe in your dog before you ever
undertake the job of showing. Then you must transfer that
belief so that your dog thinks it is the greatest dog that ever
walked. In order to take advantage of positive psychology,
you must mentally prepare every step of the way up to and
into the ring.
TUNNEL VISION
When you bring your dog up to the ring, you must have
tunnel vision. Your total concentration is on your dog. Shut
out the world. Spend your time reading your dog. What is
he reacting to? How does he feel today? Is he up and happy
or low and dragging? How can you compensate for those
subtle changes in attitude and mood that can mean the difference between winning and losing in tough competition?
Also, you have to concentrate on reading your dog the
whole time you are in the ring. When you do this you will
see that the dog is ever changing and you will have to adapt
to the situation.
WIDE-ANGLE VISION
While you are concentrating with tunnel vision on
your dog, at the same time you also have to be aware of
everything that is going on around you and how it will
affect your dog’s performance. You must have wide-angle
vision in order to evaluate the competition and to ward off
any dangers that might threaten your dog. You must see that
dog coming at yours and be quick to react. You must see the
person walking in a daze who may trip or fall over your dog.
You can’t do that if you’re chatting with neighbors or paying
attention to other things.
Wide-angle vision means something else, too. It means
sizing up the competition before you go into the ring or
within 30 seconds after. You have to know every dog in that
ring and how it compares to yours. How do your dog’s
strengths and weaknesses compare to the others? You have to
know this in order to present your dog to its best advantage.
You also have to be constantly reading the competition to
see if they make any mistakes or have a change of attitude so
you can take advantage of them. Also you must be reading
the judge. A judge will, unknown to them, give clues about
likes and dislikes of the dogs they are judging. Sometimes
this can help you.
Prior to going to a show you should sit down for about 10
minutes a day, close your eyes and put yourself into situations
that could get you into trouble. For instance, what will you
do when a handler runs up on you in the ring? What will
you do if your dog breaks stride, or the tent falls down, or
you trip on the baby gates and fall down? What would you
do if your dog won’t put up his ears, or gets too excited, or
not excited enough?
Whatever the situation, if you have the problem solved
in advance, then you will know how to respond to it. You
must solve all of these potential problems mentally before you
go into the ring. That takes concentration, not only the night
before, but right up until the time you walk into the ring.
The night before a show lie in bed and think about the
competition. If you have been going to shows on a regular
basis, you’ll have an idea of the dogs you will be competing
against. You should know the strong and weak points of
every dog in the ring, and if you don’t know them in
advance of getting to the show, stand at ringside and watch
them as they come up to the class.
In addition to solving all the possible problems in your
head, you must visualize the picture you want to make with
your dog. Imagine in your mind exactly how you will show
your dog so that it makes a perfect picture for the judge. If
you know your dog well you will not have to put your hands
on it in order to create the mental picture as you prepare for
the competition. Prior to going in to the ring most good
professional handlers will seem to be “off in space”, but they
are not. They are thinking about the best way to show their
SUMMARY
This article just begins to touch on the owner/amateur
handler vs. the professional handler. I hope some of these
things will help you in your quest to show winning dogs.
Remember, you can do it!
This article reprinted, with permission, from The Winning Edge: Show Ring
Secrets by George Alston and Connie Vanacore, Howell Book House, New York.
17
A Dog’s Mouth:
What’s Going
On?
Figure 1. Example of good, healthy teeth and gums;
no periodontal disease present.
Tartar (Calculus)
If plaque is not removed every day, it begins to mineralize into tartar (calculus) in a day or two. Saliva always
moistens the mouth. The two largest salivary gland duct
openings are over the upper back cheek teeth. Saliva contains
dissolved calcium. The calcium hardens in the plaque to
form the calculus. Calculus is hard and cannot be removed
by brushing or even with hard kibble. The heaviest build-up
of calculus is usually over the upper cheek teeth. Calculus
should be removed using an ultrasonic scaler at a veterinary
clinic with the patient asleep and on gas anesthesia (that is,
an endotracheal tube should be in place).
After initial scaling, hand instruments are used to
locate and clean any periodontal pockets. The pockets can
then be treated with Doxirobe™ (Pharmacia Animal
Health), a bioabsorbable polymer which encourages tissue
reattachment and helps control infection. The teeth should
be polished with fine or flour polishing paste or pumice.
(Kitchen-type cleaners are too coarse and have undesirable
chemicals; besides, most dogs cannot be rotated at 3000 to
5000 rpm around your hand to polish the teeth!). Hand
scaling in an awake animal cannot detect periodontal pockets
and gives one a false sense of security regarding the dental
health of the patient.
Jean Hawkins, MS, DVM, Diplomate AVDC
Mountain View Animal Hospital and Pet ER
Boise, Idaho USA
INTRODUCTION
“Doggie breath is normal.” NOT! Bad breath caused by
periodontal disease is the most preventable disease in the
world! It takes work, planning, and perseverance but the
control of periodontal disease results in healthier dogs
(Figure 1).
PHASES OF PERIODONTAL DISEASE:
GINGIVITIS AND PERIODONTITIS
A DOG’S BREATH AND PERIODONTAL DISEASE
Mouth odor caused by periodontal (dental) disease is
preventable in most cases and controllable in dogs with a
normal immune system. Periodontal disease is an infection
of the tissues and bone surrounding the teeth. Periodontal
disease is the most common infectious (but not contagious)
disease in the world that affects both man and other animals.1
Periodontal disease has two distinct phases: gingivitis
and periodontitis.2 Gingivitis is completely reversible with
thorough teeth cleaning and polishing and daily home care.
No soft tissue or bone loss has occurred in gingivitis.
Inflammation of the soft tissue is present and the gums
bleed easily. As gingivitis becomes more chronic, the gums
may thicken and not seem to bleed as readily (Figure 2).
Periodontitis is an irreversible, but usually controllable
phase of periodontal disease (Figure 3). The inflammation
of the soft tissue moves down into the gingival sulcus causing
attachment and bone loss. The gingival sulcus is a little
Plaque
Periodontal disease is the result of plaque-ladened
teeth. Plaque is a soft coating of germs (bacteria) and oral
debris. Plaque can be removed by brushing.
18
moat that surrounds each tooth. (It is where the popcorn
husks get stuck!) Periodontitis is controllable with regular
professional cleaning as often as needed for that particular
patient, and daily home care.
Tissue recession and bone loss are somewhat repairable,
but require intensive, expensive veterinary periodontal
therapy and regular re-treatment (every 6–9 months) under
anesthesia. Meticulous home care is necessary to maintain
attachment gain. Here, prevention is certainly important.
Attachment and bone loss mean eventual tooth loss. This
can occur in small breeds and brachycephalic breeds by two
years of age. Lower front (incisor) teeth are affected most in
brachycephalic breeds. There may not be much bone in the
area anyway, which increases the risk of early tooth loss.
Upper incisors seem to be affected earlier in small breeds
with a scissors occlusion (Figure 4). Stomatitis, an inflammation of the gums, occasionally accompanies periodontal
disease (Figure 5).
Figure 2. Gingivitis is present in this dog’s mouth.
WHEN DOES PERIODONTAL DISEASE BEGIN?
The adult size, breed, food, and home care all have an
affect on when periodontal disease begins (Table 1). The
gingivitis phase begins at two or three years of age in
Beagles. The periodontitis phase in Beagles begins at four to
six years of age. Daily toothbrushing, feeding a diet such as
Eukanuba®, which is designed to significantly reduce calculus
formation, and regular dental prophylaxis by your veterinarian are essential for healthy teeth and gums in most dogs.
Figure 3. Early signs of periodontitis.
Breed Predisposition
Certain breeds are predisposed to developing periodontal
disease at an early age. Brachycephalic head types usually
have crowded cheek teeth in the upper arch. Breeds with
moustaches and beards tend to trap food and moisture in
the facial hair, so bacteria abound inside and outside the
mouth. Breeds with long, thin muzzles often have food
trapped in the cheek area speeding calculus formation.
Dogs kenneled in crowded or unsanitary conditions will
sometimes have severe periodontal disease caused by filth.
In general, the smaller the adult size of the breed, the earlier
the onset of periodontal disease. The teeth are usually more
crowded, eliminating the self-cleaning effect of the tooth
design in small breeds, which traps food and facilitates
plaque and calculus accumulation.
Retained deciduous teeth contribute to dental disease
and malpositioned teeth in the adult. Deciduous teeth
should be removed as soon as the corresponding adult tooth
is visible.
Figure 4. Severe periodontal disease.
WHAT CAN BREEDERS DO?
What can you as breeders do to improve the dental
health of your kennel animals? Begin “brushing” your puppies’ teeth as soon as the teeth erupt. Prevention plays an
Figure 5. Severe periodontal disease with stomatitis.
19
Table 1.
(This procedure is similar to a “hot wax” treatment on your
car.) ProVSeal™ home care “wax” is applied twice weekly to
the outside of all upper teeth with a finger or an applicator.
All home care is more easily accomplished by holding
the muzzle closed with one hand and applying the home
care product (wax, tooth brush, gel application) with the
other. The ProVSeal™ makes other home care much more
effective in my experience.
Dogs at Risk for Developing Periodontal Disease
• Dogs that weigh less than 10 pounds
• Dogs with short noses, such as Pekingnese, Boston Terriers,
English Bulldogs, etc.)
• Dogs with long slender noses such as Dachshunds, Poodles,
Shetland Sheepdogs
• Dogs with other diseases such as diabetes mellitus, thyroid
problems or heart disease
DIET AND DENTAL DISEASE
• Dogs with excess hair or skin around the face
One of the most logical ways to promote dental health
is food. Everyone is going to feed their dogs. Hard kibble is
preferable to soft food or food mixed with water. Calculus
accumulation is typically less with dry food. Some foods are
formulated to help control plaque and tartar buildup. It is best
to select a food that has been shown to reduce tartar buildup.
• Dogs who do not have their teeth brushed every day
essential role in young animals. Examine each mouth of
adult dogs and schedule breeding animals with the heaviest
calculus and most inflamed gums for a thorough dental
cleaning and polishing at your veterinarian’s clinic as soon
as possible. Larger litters may result when dental disease is
not present and the uterine wall is less thickened. Certainly
pups will benefit from having moms with cleaner mouths to
tend to them. Progressing then to the younger dogs for
more preventive care will decrease their risk of developing
periodontitis.
From strictly a financial standpoint, retired dogs logically could be considered the “least important”. However,
that is not always the case. Sometimes these dogs are your
best friends! A lot can be done dentally to improve the
quality of life of older dogs. In those cases when a dog will
be adopted out, a good option would be to place the dog
with a person who agrees to have appropriate professional
veterinary dental care as often as needed (every 6–12
months, usually) and provide daily home dental care.
Ask your veterinarian about the availability of dental
x-rays and the treatment of periodontal pockets. Also ask the
vet to probe for the presence of inapparent oronasal fistulas
(IONF: a hole between the mouth and nose on the hard
palate side of the upper canine tooth; the tooth is still in
place and usually not loose). These usually occur in dogs
that are less than 20 pounds and between 4 and 5 years old.
There may be occasional nasal discharge, sneezing, and
constant nose licking. An IONF is usually found during the
dental cleaning using a periodontal probe. Extraction is
generally the end result; however, if found early and treated
often, closure of the IONF is possible.
ANYTHING ELSE?
Good housekeeping practices such as washing food and
water bowls in hot soapy water daily, washing long muzzle
hair weekly, and keeping the kennel areas clean are essential.
As much home care as possible, especially for dogs that
have had soft tissue, bone, and possibly tooth loss is very
important. Training puppies to have their muzzles handled
and introducing home care at an early age can prevent
much of the periodontal disease we see from ever occurring.
A soft-bristled child’s or adult’s toothbrush or a special pet
toothbrush, fingerbrush or swab all work (Table 2). Always
Table 2.
Tips for Brushing Phido’s Forty-two Teeth
• Begin by handling his face and muzzle gently.
• Never risk getting bitten while trying to brush your dog’s teeth.
• Use lots of patience and praise; it’s training!
• Work slowly, you have the rest of his life to teach him this “trick”.
• Hold the muzzle closed.
SOMETHING NEW
• Gently introduce the toothbrush inside the mouth.
A huge improvement can be seen in reducing calculus
reformation following a dental cleaning by applying
ProVSeal™ (KBA, Los Angeles, CA) hydrophobic “dental
wax”. The professional wax is applied by a veterinarian to
all clean dry tooth surfaces in the anesthetized patient
while the wax is very warm to assure thorough coating.
• Brush just one tooth for a few days until he gets the idea.
• Brush just the outside of all upper teeth, next.
• Brush as many other areas of the mouth as possible later.
• Brush your dog’s teeth daily, if possible.
20
feel the toothbrush bristles, however, as some are sharp and
will scratch the gums.
Beginning home care in the puppy stage (hold the muzzle
closed with one hand and apply home care treatment with
the other) will keep you “flippin’ those lips” and helping to
keep those pearlies white for years to come!
Eukanuba is a registered trademark of The Iams Company.
Eukanuba Dental Defense System is a trademark of The Iams Company.
REFERENCES
1. Page RC, Schroeder HE. Periodontitis in man and other animals:
A comparative review. Basel, Switzerland: Kargor, 1982.
2. Loe H. The gingival index, the plaque index, and the retention index
systems. J Periodontal 1967; 38:610-616.
21
A visit to the veterinarian for a physical examination is
important. Every brood bitch should be current on all vaccinations and free from infections and parasites prior to
breeding.
It is also a good idea to request documentation of
health status on the potential sire, regardless of source.
While relatively uncommon today, Brucella canis remains a
serious threat and can destroy years of efforts.
Managing the
Brood Bitch
The Importance of Body Condition
The breeder should ensure that the bitch is in good
physical condition. Like all dogs, the breeding bitch should
receive daily exercise and be maintained on a diet that
matches energy needs relative to energy output. The breeder
should strive to condition the bitch to possess evident muscle
tone with a slight degree of body fat. This type of body condition will help promote a healthy endocrine system, which
is so critical to the success of the reproductive process. If
the bitch is too thin, there is an increased risk that she will
produce a small litter or have problems during lactation,
provided that she conceives. Should the bitch be over conditioned, there is an increased risk of dystocia (prolonged or
difficult labor). Either case is not worth the risk.
If the bitch’s body condition is not optimal, it would be
wise not to breed her during the current cycle; instead,
begin to properly condition her over the next several
months so she will be ready for breeding during her next
cycle. If the bitch meets all of the criteria that you have
established for your breeding kennel, then move forward
with the breeding. The only real management change you
will need to do at that time is to transition the bitch to a
high-density diet recommended for pregnancy and lactation.
Russ Kelley, MS
The Iams Company, Lewisburg, Ohio, USA
INTRODUCTION
Reproductive success in the bitch should be defined as
the generation and weaning of an adequate size litter of
healthy viable puppies reflecting the genetic potential of
both the dam and sire, while preserving the health of the
dam. To achieve this goal, the breeder needs to not only
select the proper breeding stock, but also to develop a sound
management plan. While the basis of the program must be
applicable to an entire kennel, it must also have some degree
of flexibility to meet the needs of each individual bitch.
NUTRITIONAL SUPPORT DURING
PREGNANCY AND LACTATION
PRE-BREEDING
Proper management of the brood bitch does not begin
at breeding. Just as one must prepare a dog for competition,
one should also prepare the bitch for the reproductive
process. Before the upcoming cycle, the breeder should take
every precaution to ensure that the bitch is in ideal health.
Nutrition is one of the most critical components related
to a competitive animal’s performance. The same is true for
the reproducing bitch. In fact, outside an animal’s genetics,
nutrition is probably the single most important component
22
to a successful breeding program. Unfortunately, many
breeders fail to appreciate the nutritional demands placed
on the bitch during pregnancy and lactation. Much as an
umbrella protects us during a rainstorm, optimal nutrition
will help protect the bitch and her pups from the various
metabolic and environmental stresses that will occur during
the high-stress periods of pregnancy and lactation (Figure 1).
During the reproductive process, a bitch’s diet must
support three areas: 1) her body maintenance, 2) the growth
of her reproductive tissues, and 3) the growth and development of her offspring (Figure 2). However, the requirement
and nutrient priority is not equal between the areas.
Once the bitch’s body “recognizes” the pregnancy, the
developing puppies will have the highest nutrient drain on
her body’s resources, followed by her reproductive tissues;
maintaining her own condition will become her body’s lowest
priority.
A key component to remember is that unlike the bitch,
the developing pups have two nutrient sources—the bitch’s
diet and the bitch’s body (Figure 2). Should the bitch’s diet
fail to meet the required nutrient levels, she will respond by
sacrificing her own body condition. Her body will begin
mobilizing nutrients from fat, muscle, and skeletal tissue in
order to meet the demands of the pups and her reproductive
tissues. In extreme cases, her only solution may be to reduce
the demand by decreasing the number of offspring or by
completely aborting the pregnancy.
To what extent the bitch is able to offset nutrient
shortfalls remains unclear. However, since deficiencies in
maternal nutrition in other species have now been associated with adult disorders in the offspring,1 it is critical that
the breeder make all attempts to supply optimal maternal
nutrition.
Environmental
Stress
Gestational
Stress
Lactation
Stress
NUTRITIONAL
MANAGEMENT
Maternal
Health
Figure 1.
Neonatal
Health
OPEN
Diet
Maintenance
Maintenance
Diet
Reproductive
Tissues
Body
Tissues
Developing or
Nursing Offspring
PREGNANT
Figure 2. Utilization of dietary nutrients by the brood bitch.
NUTRITIONAL REQUIREMENTS OF THE BITCH
Research studies conducted in the 1950’s provided some
of the earliest insight into the specialized nutritional
requirements for the reproducing bitch.2,3 Diets known to be
sufficient for canine growth and maintenance were found
to be inadequate for reproduction. However, since these
studies were conducted 50 years ago, it is doubtful that any
current growth formula would be insufficient for reproduction. While this thought is comforting, a diet that is merely
“sufficient” should not be the goal. Sufficiency does not
equate to optimal nutrition. Sufficiency simply means the
bitch is able to complete the reproductive process.
More recent observations 4 conclude that the stress
associated with reproduction would manifest even the
smallest of nutrient inadequacies in diets assumed to be
complete. These dietary inadequacies may not be severe
enough to stop the bitch from reproducing; however, they
most likely will prevent her from performing at her genetic
potential.
Essential and Non-Essential Nutrients
In a broad sense, dietary nutrients are defined as essential
and non-essential. Essential nutrients cannot be adequately
produced by the body to meet the animal’s requirement
and, therefore, must be obtained from the diet. Essential
nutrients would include the essential amino acids and essential fatty acids, as well as various minerals and vitamins.
Conversely, non-essential nutrients can be supplied
either from the diet or they can be produced by the body
should the diet fail to supply sufficient quantities. However,
this concept does not hold true for the developing offspring.
Puppies—whether embryonic, fetal or nursing—are
dependent upon the bitch to supply all the nutrients they
need. Because many of the metabolic pathways to produce
23
non-essential nutrients are not functional until late neonatal life, all of their nutrients are in a sense “essential”.
This is not to imply, however, that the best course is
simply switching to a diet that contains the highest available nutrient content (protein or energy or both) or using
various dietary supplements to enhance a food. Excessnutrition can be as detrimental as nutrient deficiencies.
Excess dietary energy often contributes to increased pup
morbidity and excessive maternal weight gain, which dramatically increases the chance of difficult labor. The use of
dietary supplements can supply excessive amounts of nutrients such as minerals, thus altering the balanced nutritional
matrix of the diet.
The key to optimal nutrition is supplying a food that
has a balanced nutrient profile at levels that meet the animal’s need. As Mosier5 stated in 1977, “only by feeding well
managed balanced diets can the health of an individual be
maximized”. The individual nutritional components of a
diet should be considered, including not only the level of
protein, fat, carbohydrate, vitamins and minerals, but also
the type of protein and fat and the ratio of nutrients, such
as protein to fat.
(milk). During early and mid gestation (first 5 weeks), the
energy requirements of the bitch are approximately equal to
maintenance (Figure 3).6 However, this does not mean
that the bitch should be fed a “maintenance” diet. The
maintenance recommendation relates only to the daily
energy requirement.6
As mentioned earlier, the bitch must also supply the
developing offspring with the nutrients they need to grow
and develop. Because of this, we recommend that a bitch be
switched, prior to breeding, to a nutrient dense formula that
is less dependent on carbohydrates (< than 35% of the calories) to ensure that the protein and fatty acid requirements
of the puppies are met (Table 1).
Prior to Breeding
Approximately two weeks prior to breeding, the bitch
should be transitioned (if necessary) from her maintenance
diet to a diet comprised of at least 28% highly digestible
animal-based protein and 18% fat. The fat portion of the
diet should be balanced for fatty acid content to supply an
omega-6 to omega-3 fatty acid ratio in the range of 5:1 to
10:1.
Findings from a recent study conducted by The Iams
Company that compared three diets demonstrated the positive benefits of feeding a diet with the optimal fatty acid
ratio (5:1 to 10:1 omega-6 to omega-3 fatty acids).7 When
fed throughout the reproductive cycle, this type of diet
resulted in fewer misconceptions, a reduced number of stillbirths and more consistent-sized litters from breeding to
breeding (Figure 4).7 The exact amount of food required
will vary depending on breed and metabolic rate, however
the level of intake should be closely monitored to target a
caloric intake similar to maintenance levels, thus avoiding
over-feeding the bitch (Table 1).
WHAT SHOULD I FEED?
% Maintenance Requirement
Owners and handlers of competitive dogs generally
have higher performance expectations than the average dog
owner, making this question a little easier to answer. They
have first-hand experience in the positive results that feeding
a performance formula can provide. For the breeding bitch,
the same logic must be applied, only to a higher extent.
Again you may ask, “What should I feed?” Select a
commercially available premium food manufacturered by a
reputable company, formulated using animal-based protein
sources, and recommended for gestation and
lactation. While there are many “home based”
diet recipes circulating, it is extremely difficult
300
to achieve a complete and balanced diet using
these recipes. These diets can often be deficient
250
(or unbalanced) in vitamins, minerals, or other
nutrients and are undefined with regard to
200
amino acid and fatty acid levels. They may also
300%
150
vary over time because of inconsistent ingredi200%
250%
ent supply. Commercial formulas offer distinct
100
advantages by allowing the breeder to feed a
150%
200%
product of known nutrient content and type
50
proven to support the reproductive process.
Maintenance
125%
Most competitive dogs during active sea0
1 2 3 4 5 6 7 8 9 1 2 3 4 5 6 7 8
sons will require around 125–150% of their
Whelp Lactation (Wks)
Wean
Gestation (Wks)
maintenance nutrition needs compared to noncompetitive dogs. However, the nutritional
requirements for the pregnant or lactating bitch
Figure 3. Estimated energy requirements of the pregnant and lactating bitch relative to
are not constant. Her requirement levels are
maintenance. Adapted from Lepine AJ. Feeding managemnet of the reproductive cycle,
influenced by the stage of the reproductive cycle
in Proceedings. Canine Reproductive Health Symposium at the 1997 North American
Veterinary Conference; 27-29.
as well as her litter size and genetic ability
24
Table 1. Effect of diet matrix on daily nutrient intake a
Metabolizable
Energy (kcal/day)
Protein
(g/day)
Fat
(g/day)
Carbohydrate
(g/day)
Total Intake
(g/day)
Maintenance
Formula
1143
78.4
48.3
108.6
279.0
High Density
Formula
1143
88.3
57.2
80.1
257.8
a Based on the average analysis of Eukanuba® Adult Maintenance Formula, guaranteed to contain 25% protein and 16% fat compared to Eukanuba® Premium Performance Formula,
guaranteed to contain 30% protein and 20% fat.
During Pregnancy
During the first 5 weeks of pregnancy, the breeder
should continue to feed the bitch the above mentioned diet
matrix at maintenance levels (Figure 3; energy basis). It is
possible that a change in the bitch’s appetite may be
observed at approximately 3 weeks post-breeding; her
appetite may first decrease, followed by a dramatic increase.
However, this may not indicate that the bitch is being
overfed or underfed. Because the bitch’s body begins to
“recognize” pregnancy and embryonic implantation, these
appetite changes may be triggered. It is very important that
the bitch be maintained on her normal routine during this
period to prevent any undue stress, which could be detrimental to the pregnancy.
At approximately 5 weeks post-breeding, the food
intake of the bitch should be increased slightly each day to
achieve a 50% increase in energy by the end of week 6
(Figure 3).7 For example, if the bitch is consuming 1,000
calories/day for maintenance, by the end of week 6 she
should be consuming approximately 1,500 calories/day.
There are two reasons for the needed increase. The first
is to meet the increased nutrient demands of the fetal puppies
as their growth rate dramatically accelerates (Figure 5). In
fact, the fetal puppy body weight will increase approximately 1200% during the last 3 weeks of pregnancy!8
Secondly, the caloric increase is needed to help the bitch
boost the energy stores (body fat) that she will need during
lactation (Figure 6).
It will be necessary to closely monitor the bitch for
weight gain during the later stages of gestation to ensure
that she is gaining sufficient weight. It is impossible to give
an exact percentage of weight that a bitch should gain since
the increase will vary greatly from breed to breed, even
within similar adult sizes. For instance, one would expect a
Labrador Retriever to gain more weight (as a percentage)
than an English Setter since they typically give birth to
larger litters. However, a good rule of thumb would be to
target a 25% weight gain in the bitch by the end of week 8
(day 56) post-breeding.
0.7
0.6
*denotes significant difference due to diet, P<.05
γ denotes significant difference due to parity, P<.05
0.5
∗,γ
0.4
∗,γ
0.3
∗
∗
∗
2
3
4
0.2
0.1
1
n6:3 Ratio=20:1
5
n6:3 Ratio=5:1
Kelley, 2000
Figure 4. Effect of dietary fatty acids and parity on still-birth number.
300
Weight (grams)
250
200
150
100
50
0
26
30
34
40
44
48
52
56
60
Gestational Age (days)
Figure 5. Fetal puppy body weight (grams) plotted
throughout pregnancy.
25
this management practice is not possible, offer the food free
choice. The general target would be to achieve approximately 200% of maintenance by the end of week 2 of lactation
and 250–300% by the end of week 3 (Figure 3).6 The rule
of thumb for weeks 4 and 5 of lactation would be 300% of
maintenance; however, this figure may be as high as 500%
in heavy milking bitches or bitches with large litters. Weeks
4 and 5 are typically peak lacation, the time when the bitch
will be producing the greatest amount of milk. Some of the
best bitches may utilize as much as 8,000 calories per day
(estimated) during this time, thus it is practically impossible
for these bitches to consume enough calories to meet these
needs. This tremendous energy requirement is why is it so
important for the bitch to gain the proper amount of weight
during late pregnancy. The added weight (body fat) that the
bitch acquires during late pregnancy (Figure 6) will be mobilized during this timeframe to offset the energy deficiency.
Late Lactation. Nutritional management during late
lactation is dependent upon what age the breeder plans to
wean the litter. The vast majority of breeders decide to wean
between 6 and 8 weeks of age, although some will start as
early as 5 weeks and some may extend the nursing period to
as long as 10 weeks; the latter is certainly the exception.
There is no perfect age for weaning and each litter should be
managed individually. The final decision should be based on
how well the puppies are eating and drinking. While it is
impossible to force the puppies to accept the new practice,
there are management practices that the breeder can use to
help promote the weaning process.
After 35 days of lactation, the amount of food offered
to the bitch can be reduced to around 250% of maintenance
levels with additional decreases each day until the bitch is
being fed around 125% of maintenance levels at the desired
weaning time (Figure 3).6 The decrease in food intake will
result in decreased milk production, thus stimulating the
puppies to seek an alternative nutrient source.
During this period, it is critical that the puppies be
offered a wet gruel (ground kibble and water). Remember
that the bitch’s milk is also the puppies’ source of water, so
water should also accessible by the puppies. Gruel can be
prepared by mixing some of the bitch’s formula (preferably
a performance or growth formula) with warm water.
Alternatively, there are specially designed formulas for the
weaning process. Eukanuba® Weaning Formula is a nutritionally balanced, calorie-dense formula that has been preground to allow easy mixing with warm water. Initially, the
gruel should be semi-liquid (65–70% water) where the puppies can easily lap the mixture. The percentage of solids can
be increased as the puppies grow more accustomed to the
routine. It is also helpful to begin to add a few whole kibbles
in the bowl after a week or so. This will help the puppies
become familiar with the food texture and by 6 to 7 weeks
of age most puppies will freely consume dry kibbles. Once
the puppies have mastered the art of eating and drinking,
they are ready to be weaned.
Relative Percentage
140
120
100
80
60
40
G0
G14 G28 G42 G56
P0
P14 P28 P42 P56
Physiological Period
Desirable
Undesirable
Figure 6. Effect of pregnancy and lactation on maternal body fat stores.
WHAT TO FEED DURING LACTATION
Nutritional management through the lactation period
is even more difficult than during pregnancy. However, the
same recommendation holds true—provide the bitch with
“balanced nutrition.” The breeder must consider numerous
factors when developing a management program for lactation. How many puppies is the bitch nursing? What is the
bitch’s normal metabolic rate? What is the nutrient density of
the chosen diet? What stage of lactation is she at? These are
all questions that the breeder must take into consideration.
Although each bitch must be handled individually, there
are some guidelines that a breeder may find helpful.
Early Lactation. Most bitches have depressed
appetites for the first few days following whelping. This is
perfectly normal and should not be a concern unless the
behavior continues longer than 3 days or if she is displaying
other heath concerns (putrid discharge, fever). Should the
bitch’s appetite remain depressed for more than 3 days, or if
she is displaying other heath concerns it is advisable to seek
immediate medical attention.
First and foremost, ensure that the bitch has free access
to water. Remember that milk is composed of approximately
78% water, making one of the keys to good milk production
an adequate water supply. While the bitch’s body can offset
the other nutrients needed for colostrum and milk production, she cannot offset a lack of water. Generally speaking,
most bitches’ appetites have returned to normal by day 4 or
5 post-whelping with a targeted intake around 150% of
maintenance through the first week of lactation (Figure 3).6
Mid-Lactation. Provided the bitch is carrying a typical
size litter, the breeder should try daily to slowly increase the
amount of food offered from days 8 through 30 of lactation
(Figure 3).6 Offering numerous (4–6) meals per day often
gives better results as opposed to offering two large meals. If
26
MATERNAL NUTRIENT DEPLETION
diet to the bitch for at least 3 weeks after weaning. The
amount of diet required should be dictated by the physical
condition of the bitch—the worse her physical condition,
the greater the amount of food that should be supplied. A key
point to remember is that the bitch cannot fully recover if
the amount of nutrients supplied only meets her maintenance requirement.
It is important for the breeder to remember that management of the bitch is not over once she has weaned her
litter. Each bitch should be carefully examined to determine
her physical condition after weaning. While not necessary,
it is advisable to have your veterinarian perform a physical
exam. The desired outcome is for the bitch’s body condition
to be identical to her condition before breeding.
Unfortuantely, in most cases, this does not happen.
The reproductive process is one of the most demanding
metabolic periods of a bitch’s adult life. Because of this,
some bitches (most, but not all) will undergo a physiological
condition termed “maternal nutrient depletion”. Although
this condition occurs naturally, it should still be a concern
for the breeder. An easy way to visualize this condition is to
imagine the bitch’s body as a reservoir, the bitch’s diet as
the streams and rivers that supply water to the reservoir and
the puppies as the floodgates. As long as the supply of water
coming into the reservoir equals the amount of water being
released through the floodgates, then the water level
remains at normal levels. However, should the amount of
water leaving the reservoir exceed the amount being supplied
by the streams and rivers, the water level in the reservoir
will fall. This is exactly what happens to certain nutrients
during reproduction.
There are several examples of maternal nutrient depletion. One of the most common is the loss of body fat during
lactation (Figure 6). All breeders have observed bitches
that increase the amount of body fat that they carry during
the latter stages of pregnancy. This increased fat will be
mobilized during peak lactation to serve as an “energy
buffer” and ensure quality milk production. Normally this
type of nutrient depletion is not a big concern since the
bitch has increased her body’s supply of this nutrient.
However, in some cases, the demand may still exceed the
bitch’s nutrient deposits, resulting in an animal that is in
poor condition (Figure 6; Undesirable).
Another type of nutrient depletion that should concern breeders relates to the essential nutrients. To date,
there is only limited information available on the absolute
nutritional requirement levels of essential nutrients during
pregnancy and lactation. For the non-essential nutrients
there is less of a risk because hopefully the bitch’s body will
be able to offset the shortage by increasing production of
those nutrients. However, essential dietary nutrients are a
different situation.
As the term “essential” implies, these are nutrients that
the bitch cannot produce (or cannot produce in sufficient
levels) and must be supplied in the diet. When the diet fails
to meet the combined requirements of the bitch and her
offspring, she must resort to mobilizing her tissues (bone
and muscle) to meet the demands of the puppies and her
most critical systems (Figure 7). For this reason, it is recommended that the breeder continue to provide the same
A
B
Figure 7. The bitch (A) appears to be thriving and has obviously
successfully nursed three healthy pups. A full view of her body
condition (B), however, reveals that she has sacrificed her own body
reserves due to a lack of nutrients sufficient to maintain her high
energy needs during lactation.
DIETARY SUPPLEMENTS
The use of dietary supplements for the gestating bitch
has been the topic of many debates. Numerous publications
have hinted at the benefits of nutrient supplementation.3,4,9
Some of the most commonly mentioned nutrients include
protein, calcium, and vitamins. In practice, the only reason
to utilize dietary supplements is when the diet fails to supply
the needed amount of a given nutrient. However, the theory
of supplementation is often much easier than putting it into
practice.
The majority of currently available commercial foods
are formulated to provide a balanced supply of nutrients—
27
“balanced” being the key word. A critical point to remember
is that nothing can be added to or taken away from a diet
without affecting the overall nutrient profile.
Also remember that few supplements are “pure” sources
of a given nutrient. For example, cottage cheese (for calcium)
and liver (for protein) are two commonly used supplements
fed to the breeding bitch. However, since neither of these
supplements is composed of a single nutrient, the net result
supplies more than just the desired nutrient. For example,
both cottage cheese and liver add large quantities of phosphorus. In fact, cottage cheese adds more phosphorus than
calcium, the targeted nutrient (Table 2). If cottage cheese
is added to a balanced commercial diet, the overall calcium
to phosphorus ratio will be altered. While the intention is
good, it is important not to confuse an increase in the level
of nutrition required with a need to change the diet profile.
tion may require years to understand, the actual practice of
providing nutrition can be summarized fairly simply, feed the
appropriate amount of a diet that meets the animals needs. While
this practice still requires the breeder to make evaluations
as to what and how much diet will be fed, it does eliminate
questions such as what mix of products and/or supplements
must be utilized.
Based on our efforts in the area of canine reproduction,
a good starting point for the breeder would be to identify a
diet that contains at least 28% highly digestible animalbased protein, 18% fat, and the optimal balance of omega-6
and omega-3 fatty acids (5:10 to 10:1). The benefits of feeding a diet of this type include increased conception rate,
increased live births, and more consistent maternal productivity.7
While nutrition is only one component of bitch management, it is one of the most (if not the most) important.
Thus by providing the proper nutrition, the breeder has
taken a great step forward in achieving a successful breeding
program.
Eukanuba is a registered trademark of The Iams Company.
REFERENCES
1. Godfrey KM, Barker DJ. Fetal nutrition and adult disease. Am J Clin
Nutr 2000; 71(5 Suppl): 1344S-1352S.
2. Campbell JE,Phillips PH. Reproduction studies in dogs. J Nutr 1952; 47:
621-629.
3. Ontko JA, Phillips PH. Reproduction and lactation studies with bitches
fed semipurified diets. J Nutr 1957; 65: 211-218.
4. Collins DR. The reproducing bitch. In: The Collins Guide to Dog
Nutrition. 6th edition. New York: Howell Book House, 1987; 231-236.
5. Mosier JE. Nutritional recommendations for gestation and lactation in
the dog. Vet Clin N Am 1977; 7:683-692.
6. Lepine AJ. Feeding management of the reproductive cycle, in
Proceedings. Canine Reproductive Health, The North American
Veterinary Conference. 1997: 27-29.
7. Kelley RL. Canine Reproduction: What should we expect? In: Reinhart
GA, Carey DP, eds. Recent Advances in Canine and Feline Nutrition,
Volume III. Wilmington, OH: Orange Frazier Press, 2000; 225-242.
8. Evans HE. Reproduction and Prenatal Development. In: Evans, H.E. &
Christensen, G.C., eds. Miller’s Anatomy of the Dog, 2nd edition, W.B.
Saunders Company, Philadelphia, PA. 1979: 13-77.
9. Moser E. Feeding to optimize canine reproduction efficiency. Prob Vet
Med 1992; 4:545-550.
The bitch does require that nutrient intake be
increased during the later stages of pregnancy and lactation;
however, the increase does not mean that the diet profile
should be altered. It is critical to remember that during
these periods, the bitch will be consuming a greater volume
of food, which will increase her nutrient intake while still
maintaining dietary balance (Table 2).
CONCLUSIONS
Feeding your bitch does not have to be complicated.
While the science associated with nutrition and reproduc-
Table 2. Effect of dietary supplements on the nutrient balance of a commercial diet*
A LT E R E D N U T R I E N T L E V E L B Y A D D I T I O N O F
Nutrient
Protein (g)
Fat (g)
Calcium (mg)
Phosphorus (mg)
Ca:P (ratio)
Amount of Nutrient Provided By
Feeding 300 grams of Dry Diet*
93
63
3500
2900
1.2:1
1/ 2
cup
Cottage Cheese
106
67.5
3563
3080
1.15:1
3 oz.
Beef Liver
100 g
Extra Dry Diet
115
67
3509
3305
1.05:1
*Based on the average analysis of Eukanuba® Premium Performance, guaranteed to contain 30% protein, 20% fat, and 4452 kcal metabolizable energy (ME).
28
124
84
4700
3850
1.2:1
OVERVIEW OF THE IMMUNE SYSTEM
The immune system is an intricate network of specialized
and interacting organs, tissues, cells, and chemicals. All dogs
have various mechanisms to protect against invading disease
agents (pathogens), ranging from non-specific barriers to
specific defenses.
Immunity can be classified as either innate or acquired
(Figure 1). Puppies are born with innate immunity, which
consists of non-specific barriers, and cellular and chemical
defense mechanisms. Non-specific physical barriers, such as
skin and mucous membranes, protect against the initial
entry of pathogens such as bacteria, viruses, and parasites.
However, once those barriers are overcome, a functional
immune system is required to mount a specific response to
clear the infection and protect the dog.
Nutrition and
Immunology:
Is There a
Relationship?
The Immune System
Innate
Michael G. Hayek, PhD
Stefan P. Massimino, MS
Michael A. Ceddia, PhD
Acquired
physical barriers
natural killer cells
macrophages
Cell-mediated
T & B cells
Humoral
antibody-mediated
Figure 1. Classifications of immunity.
Cellular and chemical defenses rely heavily on detection
of the difference between invading microorganisms (called
pathogens) and what is considered “self” or part of the individual’s body. When these pathogens are detected, enzymes
that digest bacterial cell walls are activated and cells that
recognize these invading microorganisms and destroy them
are deployed. This response is specific to the invading
organism and does not require priming (no lag time), but is
slow and usually not sufficient to clear the pathogen once it
has become established. Rather, it serves to contain the
infection until the next level of defense, known as acquired
immunity, develops.
Acquired immunity is a much more complex system
that can rapidly develop a specific response against invading
pathogens. It can be divided into either cell-mediated or
humoral immunity. Cell-mediated immunity includes the
interaction of macrophages, B cells and T cells. These cells
work together to generate an immune response by recognizing
pathogens. Through cell to cell interactions and release of
soluble immune mediators, production of additional T and
B cells occurs. These cells are then responsible for sustaining
INTRODUCTION
Altering the immune system through diet is an evergrowing area in pet food nutrition. Much work in this area has
now been conducted, and this research has shown justification for a ‘cradle-to-grave’ mentality. By this, we mean that
nutrition has been shown to play a beneficial role with the
immune system in nearly every lifestage of the dog, from
birth to death. Dogs can specifically benefit from a stronger
immune system. Fewer days missed due to illness, and an
overall healthier dog are just two benefits for an adult dog,
but there are benefits for both puppy and senior dogs as well.
A puppy’s immune system is immature and still developing,
while senior dogs experience an age-associated decline in
their functional immune system. Keeping dogs productive
and active into their golden years, or just happy and healthy
as retired family pets, is another way that nutrition’s effect
on the immune system can help these dogs.
29
the immune response, destroying the invading pathogen
and infected cells, and terminating the immune response
once the infection has been cleared. Some cells, known as
memory cells, survive so that in the event of another attack
by the same pathogen, the immune system is able to
respond much more rapidly and vigorously.
Humoral immunity is also commonly referred to as the
antibody-mediated immune response. When an invading
pathogen has been recognized, pathogen-specific B cells
proliferate and are transformed into antibody-secreting
cells. Antibodies are blood-borne immune proteins that are
able to bind specifically with infected cells, as well as free
microorganisms, which leads to their destruction. As with
T cells, memory B cells remain after the infection to produce
specific antibodies if the same pathogen is detected.
contain higher levels of polyunsaturated fatty acids making
them more susceptible to oxidative damage. This might be
one way in which immune cells try naturally to protect
themselves from damage from free radicals.
Supplementation with vitamin E has been reported to
increase lymphocyte proliferation and antibody production
in several species.3 Interleukin-2 production (a pro-inflammatory soluble immune mediator) and the delayed-type
hypersensitivity response (an excellent determination of the
cellular immune response; DTH) have also been reported
to be elevated with vitamin E supplementation in older
rodents and senior humans. Lastly, prostaglandin (PG) E2
production (an immune-suppressing compound) was significantly decreased in rodents after vitamin E supplementation.
Beta-Carotene. Beta-carotene belongs to a family of
antioxidants called carotenoids. Carotenoids are naturally
occurring plant pigments that have been suggested to play
important roles in modulating immunity and health of animals. Studies have shown that beta-carotene supplementation is able to affect both specific as well as nonspecific cellular defenses.4,5 Iams-sponsored studies have revealed that
beta-carotene is effectively absorbed in dogs and can affect
the canine immune system.6-8 Studies in dogs have shown
that beta-carotene supplementation results in increased antibody levels, an increased DTH response, modified immune
cell numbers, and increased T and B cell proliferation
responses. Feeding beta-carotene has also been shown to
improve various measures of immune function in senior, as
well as young adult dogs.9
Lutein. Lutein is another naturally occurring
carotenoid antioxidant found abundantly in plants and
microorganisms. Unlike beta-carotene, lutein cannot function
as a precusor for vitamin A synthesis (it cannot be used to
make vitamin A in the body). However, like beta-carotene,
lutein functions as an antioxidant protecting cell membranes
from oxidative damage.
In dogs, lutein can be absorbed from the diet and taken
up by lymphocytes.10 Lutein supplementation in dogs has
resulted in increased cell-mediated immune responses, such
NUTRITION AND IMMUNE FUNCTION
Interactions between nutrition and immunity have
been well-documented.1 Diets deficient in protein, energy,
minerals, vitamins, and essential fatty acids have long been
known to impair immunity. More recently, supplementation
with nutrients above and beyond minimum required levels
has been reported to be successful in improving health and
immune function in a wide range of species, including dogs.
Specific nutrients that have attracted special interest
for these purposes are antioxidants and fatty acids.
Antioxidants are thought to benefit immune function by
their effects on free radicals. Free radicals are chemically
reactive compounds that are produced daily in the body as a
result of aerobic (oxygen-requiring) metabolism and normal
immune system functioning. Therefore, free radical production is not only normal, but required as a consequence of
having to breathe oxygen. However, if free radical accumulation is not controlled, it can damage healthy cells. The
membranes that surround the various cells of the body are
primary targets for free radical damage.
Immune cells are especially susceptible to this free radical
damage because their cell membranes contain high levels of
polyunsaturated fatty acids, which are more easily damaged.
The body has several systems in place to combat these free
radicals, including antioxidant enzyme systems and various
endogenous factors.
Another alternative to these internal antioxidants are
the various diet-derived antioxidants including vitamin E,
beta-carotene, and lutein.
Vitamin E. Vitamin E is a term used to encompass a
group of potent, chemically similar antioxidants. One form
of vitamin E, alpha-tocopherol, is most abundant in the
body, has the highest biological activity, and reverses vitamin E-deficiency symptoms. In cells, vitamin E contributes
to cell membrane stability, regulates cell membrane fluidity,
and protects cellular components from oxidative damage.2
Immune cells possess a higher vitamin E level than other
cells, and as previously mentioned, these cells coincidentally
30
as the delayed-type hypersensitivity and lymphocyte proliferation after only 6 weeks. In addition, humoral immunity
as measured by elevated antibody levels, was also increased
in dogs with lutein supplementation.11
Taken together, the above studies show that the antioxidant nutrients vitamin E, beta-carotene, and lutein have
a positive influence on the immune system. Also noted in
these studies is that these nutrients interact with different
parts of the immune system. Therefore, incorporating a
combination of these nutrients will have a stronger effect
on the overall immune system than one nutrient alone.
Dietary Fat. Dietary fat has also been reported to modulate immune function. Historically it was thought that
high-fat diets were responsible for suppressing the immune
response.12 However, work conducted within the last 10 to
15 years has shown that the type of fat in the diet plays an
even larger role in modulating immunity. Omega-3 fatty
acids exert their influence on the immune response by their
ability to be incorporated into the cell membrane and act
as substrates for eicosanoid metabolism. This results in the
production of eicosanoids with lower inflammatory potential than those eicosanoids produced by the omega-6 fatty
acid series.13 Indeed, the 2-series prostaglandins, 2-series
thromboxanes, and 4-series leukotrienes that are generated
from the omega-6 fatty acid arachidonic acid, have been
characterized as proinflammatory, proaggregatory, and
thrombotic. This is in contrast to the 3-series prostaglandins,
3-series thromboxanes, and 5-series leukotrienes that are
generated from the omega-3 fatty acid eicosapentanoic
acid, which has been characterized as anti-inflammatory,
anti-thrombotic, and vasodilatory. The ultimate goal of
nutritional immunology is to regulate all these modifiable
components of the immune system through nutrition, to
bring about the desired response.
Immunity
Birth
Age
Figure 2. Maturation and decline curve of the immune system
in puppies.
to possess lymphocyte populations similar to that of healthy
adult dogs.
Unfortunately, puppy losses do occur during growth and
development and mainly during specific times, including in
utero, at birth, immediately after birth, and immediately
after weaning. Losses during this postweaning period are
typically the result of disease brought on by a compromised
immune system. Therefore, a stronger immune system as
early as possible can help puppies grow and develop into
healthy adult dogs.
A recent Iams-sponsored study14 showed that puppies
weaned (6 weeks of age) on a diet supplemented with the
antioxidants vitamin E, beta-carotene, and lutein had higher
levels of T cell activation (Figure 3) at 14 and 22 weeks of
age when compared to their age-matched controls (puppies
weaned on a diet containing standard vitamin E levels and no
added lutein or beta-carotene). This effect was also seen for
B cell activation (Figure 4). Puppies fed the antioxidantsupplemented diet also were seen to produce higher antibody
IMMUNITY IN THE PUPPY
When puppies are born, they emerge from a sterile
environment (the uterus) to become exposed to a host of
microorganisms, all of which are potentially pathogenic.
Unfortunately, the immune system is not fully functional
and developed for some time after birth. As a result, newborn
puppies are especially vulnerable to infection in the first
few weeks of life and require immune assistance in order to
survive. This assistance is provided by the bitch, by transfer
of immune cells and components through the colostrum
and milk which immediately confers some level of immune
protection for the newborn. This transfer of immunity from
dam to newborn is very important for the newborn’s survival.
The immune system then requires time to develop to its
fully functional capacity (Figure 2). Both the distribution of
immune cell types and their responses have been reported
to change as puppies grow and develop. T cell populations
are significantly smaller and their proliferation response to
stimulation is less in puppies, compared with that in adult
dogs. Only by 16 weeks of age, puppies have been reported
31
250
300
Control Diet
Antioxidant-supplemented Diet
Immune-cell Activity Index (%)
Immune-cell Activity Index (%)
300
200
150
100
50
250
Control Diet
Antioxidant-supplemented Diet
200
150
100
50
0
0
6 Weeks
14 Weeks
6 Weeks
22 Weeks
14 Weeks
22 Weeks
Age
Age
Figure 4. B cell activity is increased in puppies fed a diet with a specific
antioxidant package.
Figure 3. T cell activity is increased in puppies fed a diet with a specific
antioxidant package.
levels to specific vaccines such as distemper, parvovirus,
and parainfluenza (Figure 5).
To summarize, puppies can benefit from a boost in
immune function since they possess a lower level of
immune response when compared with adult dogs. During
this vulnerable period, puppies are at a higher risk for developing disease. Previous research in adult dogs, as well as
other species, shows that nutritional supplementation can
influence immune function. This study showed that in puppies, dietary supplementation with antioxidants can
improve both cell-mediated (T and B cell response) and
humoral immune function (antibody production) which
enhances the responses necessary to protect puppies against
infectious disease.
Antibody Production Index
20
Day 7 post-vaccination
Day 21 post-vaccination
15
10
5
0
-5
Distemper
Parvovirus
Parainfluenza
EXERCISE AND IMMUNITY
Once puppies have successfully grown into young adult
dogs they may undergo a variety of stressful situations. These
may include stresses of travel, competing in the show ring
or participating in exercise during sporting events. The
effect of exercise on immunity is a stress situation that has
recently received research attention. Although exercise in
the long term is beneficial (lower percent body fat, higher
percent lean body mass, improved cardiovascular system),
acute levels of exercise produce short, but intense bursts of
oxidative products such as free radicals. Increased levels of
free radicals have been theorized to suppress various parameters of immune function. Indeed, many studies in the field
of exercise immunology have reported fluctuations with
immune cell numbers and function.
Natural killer cells are part of the innate immune system,
and as such act as the first barrier of defense against pathogens
that breach the body’s physical barriers. These cells are
Figure 5. Antibody production improves when puppies are fed a diet
with a specific antioxidant package.
involved in the early response to viral infection and tumor
growth. Natural killer cell cytotoxic activity increases
acutely and proportionately with exercise intensity, and
then returns to resting levels soon after brief to moderate
exercise.15,16 However, it continues to decline and remains
below resting levels for up to 6 hours following intense and
prolonged exercise.17
Neutrophils, which are also known as polymorphonuclear leukocytes, represent 50 to 60% of the total circulating
leukocytes and also constitute part of the first line of
defense against infectious agents. Once an inflammatory
response is initiated, neutrophils are the first cells to be
recruited to sites of infection or injury. Their targets include
32
bacteria, fungi, protozoa, viruses, virally infected cells, and
tumor cells. Studies have suggested that although acute
exercise stimulates neutrophil function, prolonged periods
of intense exercise are associated with downregulation of
neutrophil function.18
Macrophages are a first line of defense against
pathogens and malignancies by nature of their phagocytic,
cytotoxic, and intercellular killing capacities. Ceddia and
Woods demonstrated that exhaustive exercise suppressed
macrophage function for up to 24 hours post-exercise.19
This suppression in macrophage function was due to the
inability of macrophages to degrade athogens.20
Lymphocytes are also influenced by exercise. Lymphocyte
stimulation has been reported to be particularly sensitive to
exercise-induced changes. Brief, moderate exercise has little effect (it may actually slightly stimulate lymphocyte
activation), but intense or prolonged exercise suppresses
the proliferative response for up to 3 hours.17 The effect of
intensive exercise on oxidative stress was examined in sled
dogs. Several studies have examined the levels of oxidative
stress markers released in the blood of sled dogs during a
three day exercise bout (15–20 mile race per day for three
days).21-23 During this exercise period the authors noted
increases in serum uric acid, isoprostane levels,22 serum 7,
8-dihydro-8-oxo-2’deoxyguanosine, and an increase in the
lag time of in vitro oxidation of lipoprotein particles.23
These results indicate an increase in free radical production
due to the exercise regime.
Due to the increase in oxidative stress noted in the sled
dog, it was of interest to determine if there is an effect on the
immune system similar to that reported in other species.7 In
this study, 62 trained sled dogs were randomized to either a
sedentary (n=22) or exercised group (n=21) or an exercised
group receiving supplemental antioxidants (n=19). All
dogs were fed a commercially available diet containing 35%
protein, 30.8% fat, 23.1% carbohydrates, and an omega-6
to omega-3 fatty acid ratio of 5.9:1. Antioxidant supplementation consisted of 1 biscuit per day containing 21.6 mg
beta-carotene and 18.4 mg lutein as well as 400 IU of
alpha-tocopherol in the form of a softgel capsule.
Similar to observations in other species, several immune
indices were altered due to the 3-day exercise session. The
proportion of blood neutrophils were increased while the
proportion of lymphocytes, eosinophils, and monocytes
were decreased. Also a decrease in lymphocyte activity and
alterations in the proportions of T cells and B cells were
noted. Lastly, exercise resulted in an increase in the blood
levels of acute phase proteins indicating that the exercise
resulted in a generalized inflammatory response.
Supplementation with antioxidants resulted in a normalization of the acute phase proteins as well as the proportions
of certain T cells and B cells. These data demonstrate that
supplementation with antioxidants result in alleviating
some of the effects of exercise on the immune response.
AGING AND IMMUNITY
The dysregulation in immune function is a well-documented consequence of aging. This can lead to an increased
incidence of morbidity (illness) and mortality (death).
Cell-mediated immunity is clearly the component of the
immune system most adversely affected with advancing age,
primarily T cells. Age-related T cell immunity dysfunction
has been implicated as the cause of many chronic degenerative diseases in elderly humans, including arthritis, cancer,
autoimmune diseases, and increased susceptibility to infectious diseases.
There are many theories that have been put forth to try
and explain the mechanism(s) responsible for this decline,
but no one theory can fully account for all the changes
observed. The free radical theory of aging is particularly
interesting. This theory is based on the premise that a single
common process, modifiable by genetics and environmental
factors, is responsible for the aging and death of all living
things. Proposed by Harmon in 1956,24 this theory suggests
that aging is caused by free radical reactions and accumulation of reactive oxygen by-products.
As explained previously in this chapter, free radical
production and accumulation can have several damaging
effects on various cells, including those of the immune system.
Therefore, much research with aging animals has been
done looking at dietary antioxidants as a means of reducing
free radical reactions and accumulation.
Senior dogs have been reported to show a decreased
immune system response compared to younger dogs (Figure
6). Older dogs also differ in the make up of their immune
system compared to younger dogs. Based on these observations, the aging process results in a dysregulation of the
immune response in dogs too, as is similar with other
species. Studies recently conducted by Iams have reported
benefits from feeding senior dogs a diet supplemented with
beta-carotene (Figure 6).
CONCLUSION
In conclusion, there is ample evidence to warrant
nutritional support of the immune system through all walks of
life. There are not only issues with immune function through
growth and development in the puppy and through decline
in the senior dog, there are also issues that arise during certain conditions such as exercise. Studies have reported that
nutrition, especially antioxidant supplementation, can help
in all these scenarios. However, it is important to realize
some of the dynamics behind antioxidant supplementation.
Studies have shown a dose-response with antioxidants
like vitamin E and beta-carotene. At very high and very low
levels, these antioxidants lose their effectiveness. There
appears to be an optimal level for these compounds as far as
immune function is concerned. Eukanuba™ dog foods are
formulated with important antioxidants, such as vitamin E.
33
REFERENCES
Antibody Production Index
In summary, antioxidants such as vitamin E, betacarotene, and lutein can improve several markers of
immune function, thereby
lowering the risk for infectious
disease and ultimately helping
100
the dog to remain productive
and stay healthy from puppy75
hood into senior years.
50
1. Gershwin ME, German BJ,
Keen CL, eds. Nutrition and
25
Immunology; Principles and
Practice. Totowa, NJ: Humana
Press, 2000.
0
2. Coquette A, Vray B, Vanderpas J.
Young
Senior
Young Dogs
Senior Dogs
Senior Dogs + beta-carotene
Role of vitamin E in the protecImmune response declines
Immune-cell activity is restored in senior dogs
tion of the resident macrophage
in senior dogs
fed diets containing ß-carotene
membrane against oxidative
damage. Arch Int Physiol Biochim
1986; 94:S29-S34.
Figure 6. Immune response in senior dogs and response to diet containing ß-carotene.
3. Meydani SN, Hayek, MG.
Vitamin E and the immune
14. Massimino SP, Daristotle L, Ceddia MA, Hayek, MG. The influence of
response. In: Chandra RK, ed. Proceedings of the International Congress on
diet on the puppy’s developing immune system, in Proceedings. Canine
Nutrition and Immunity. St. John’s, Newfoundland, Canada: ARTS
Reproduction and Neonatal Health. Tufts Animal Expo 2001, 15-19.
Biomedical Publishers and Distributors, 1992; 105-128.
15. Nielsen HB, Secher NH, Christensen NJ, Pedersen BK. Lymphocytes
4. Chew BP. Vitamin A and ß-carotene on host defense. Symposium:
and NK cell activity during repeated bouts of maximal exercise. Am J
Immune function: Relationship of nutrition and disease control. J Dairy
Physiol 1996; 271:1 (Pt 2) R222-7.
Sci 1987; 70:2732-2743.
16. Nieman DC, Miller AR, Henson DA, Warren BJ, Gusewitch G,
5. Chew BP. Role of carotenoids in immune response. Symposium on
Johnson RL, Davis JM, Butterworth DE, Nehlsen-Cannarella SL. Effects
“Antioxidants, Immune Response and Animal Function.” J Dairy Sci
of high- vs moderate-intensity exercise on natural killer cell activity.
1993;76:2804-2811.
Med Sci Sports Exerc 1993; 25:1126-1134.
6. Chew BP, Park JS, Wong TS, Weng B, Kim HW, Byrne KM, Hayek MG,
17. Nieman DC, Simandle S, Henson DA, Warren BJ, Suttles J, Davis JM,
Reinhart GA. Importance of beta-carotene nutrition in the dog and cat:
Buckley KS, Ahle JC, Butterworth DE, Fagoaga OR. Lymphocyte prolifUptake and immunity. In: Reinhart GA, Carey DP, eds. Recent Advances
erative response to 2.5 hours of running. Int J Sports Med 1995; 16:404in Canine and Feline Nutrition, Vol II: 1998 Iams Nutrition Symposium
409.
Proceedings. Wilmington, OH: Orange Frazer Press, 1998; 513-533.
18. Pyne DB, Baker MS, Fricker PA, McDonald WA, Telford RD,
7. Chew BP, Park JS, Kim HW, Wong TS, Cerveny C, Park HJ, Baskin CR,
Weidemann MJ. Effects of an intensive 12-wk training program by elite
Hinchcliff KW, Swenson RA, Reinhart GA, Burr JR, Hayek, MG.
swimmers on neutrophil oxidative activity. Med Sci Sports Exerc 1995;
Effects of heavy exercise and the role of dietary antioxidants in immune
27:536-542.
response in the Alaska sled dog. In: Reinhart GA, Carey DP, eds. Recent
19. Ceddia MA, Wood JA. Exercise suppresses macrophage antigen
Advances in Canine and Feline Nutrition, Vol II: 2000 Iams Nutrition
presentation. J Appl Physiol 1999; 87:2253-2258.
Symposium Proceedings. Wilmington, OH: Orange Frazer Press, 2000;
20. Ceddia MA, Voss EW, Woods JA. Intracellular mechanisms responsible
531-539.
for exercise-induced suppression of macrophage antigen presentation.
8. Chew BP, Park JS, Weng BC, Wong TS, Hayek MG, Reinhart GA.
J Appl Physiol 2000; 88:804-810.
Dietary ß-carotene is taken up by blood plasma leukocytes in dogs.
21. Hinchcliff KW, Reinhart GA, DiSilvestro R, Reynolds A, Blostein-Fujii
J Nutr 2000; 130:1788-1791.
A, Swenson RA. Oxidant stress in sled dogs subjected to repetitive
9. Kearns RJ, Loos KM, Chew BP, Massimino S, Burr JR, Hayek MG. The
endurance exercise. Am J Vet Res 2000; 61:512-517.
effect of age and dietary ß-carotene on immunological parameters in the
22. Hinchcliff KW, Piercy RJ, Baskin CR, DiSilvestro RA, Reinhart GA,
dog. In: Reinhart GA, Carey DP, eds. Recent Advances in Canine and
Hayek MG, Chew BP. Oxidant stress, oxidative damage and antioxidants:
Feline Nutrition. Vol III. 2000 Iams Nutrition Symposium Proceedings.
Review and studies in Alaskan sled dogs. In: Reinhart GA, Carey DP,
Wilmington, OH: Orange Frazer Press, 2000; 389-401.
eds. Recent Advances in Canine and Feline Nutrition, Vol II: 2000 Iams
10. Chew BP, Wong TS, Park JS, Weng B, Cha N, Kim HW, Byrne KM,
Nutrition Symposium Proceedings. Wilmington, OH: Orange Frazer Press,
Hayek MG, Reinhart GA. The role of dietary lutein in the dog and cat.
2000; 517-530.
In: Reinhart GA, Carey DP, eds. Recent Advances in Canine and Feline
23. Baskin CR, Hinchcliff KW, DiSilvestro RA, Reinhart GA, Hayek MG,
Nutrition, Vol II: 1998 Iams Nutrition Symposium Proceedings.
Chew BP, Burr JR, Swenson RA. Effects of dietary supplementation on
Wilmington, OH: Orange Frazer Press, 1998; 547-554.
oxidative damage and resistance to oxidative damage during prolonged
11. Kim HW, Chew BP, Wong TS, Park SJ, Weng BB, Byrne KM, Hayek
exercise in sled dogs. Am J Vet Res 2000; 61:886-891.
MG, Reinhart GA. Dietary lutein stimulates immune response in the
24. Harmon D. Aging: A theory based on free radical and radiation therapy.
canine. Vet Immunol Immunopathol 2000; 74:315-327.
J Gerontol 1956; 11:298-300.
12. Vitale JJ, Broitman SA. Lipids and immune function. Cancer Res 1981;
41:3706-3710.
13. Reinhart GA. Review of dietary omega-3 fatty acids and dietary influences
on tissue concentration. In: Carey DP, Norton SA, Bolser SM, eds. Recent
Advances in Canine and Feline Nutrition: Proceedings from the 1996 Iams
Nutrition Symposium. Wilmington, OH: Orange Frazer Press, 1996; 235-242.
34
CLASSIFICATION OF CARBOHYDRATES
Carbohydrates are divided into two categories: simple
and complex carbohydrates. Simple carbohydrates are often
referred to as “simple sugars” due to being made up of one
or two sugar molecules. These sugars require little or no
digestive breakdown and are readily absorbed from the small
intestine. Some examples include fructose (fruit sugar),
sucrose (table sugar) and lactose (milk sugar). Complex carbohydrates are also made up of the simple sugars but are
strung together to form much longer and more complex
chains that do require additional breakdown by intestinal
enzymes before they are absorbed and utilized by the dog.
Some examples of complex carbohydrates include starches
such as whole grains and potatoes.
The Carbohydrate
Puzzle: What’s in
It for My Dog?
Sean M. Murray, PhD
Gregory D. Sunvold, PhD
WHAT IS STARCH?
Starch is simply the multiple linked chains of glucose
that plants have effectively compacted together to store as
energy for growth and production of seeds, such as cereal
grains. For years, nutritionists have known that the starch,
and more specifically, the glucose stored in these grains is a
readily available source of energy for dogs. Records of dogs
being fed carbohydrates date back to the late 1770’s when
they were typically fed vegetables as a dietary staple.1
Today, canine diets contain starch, derived predominantly
from cereal grains, which are incorporated through the use
of extrusion technology.
Starch is abundant in the seeds of cereal grains and tubers
(potatoes) and represents up to 70–80% of a grain’s dry
matter. It plays an important role (Figure 1) in the nutritive
value of diets consumed by dogs since it is the primary
source of energy for many body functions and is necessary
for the synthesis and metabolism of other nutrients. Some
examples include the use of glucose, derived from starch, as
the only source of fuel used by the brain and red blood cells
to maintain proper function. In addition, not only does
starch provide an excellent source of metabolizable energy
to the animal, but it also influences the way products are
INTRODUCTION
Carbohydrates are the largest class of organic compounds
found in nature, mainly as components of plant material.
Plants capture the sun’s radiant energy and store it as carbohydrates. These plants and the grains they provide are
then utilized as key components of dietary formulations for
dogs. However, when ranked with other major ingredients
that supply protein and fat, carbohydrates are generally
considered the least important and are often regarded as the
“filler ingredient”. To the contrary, carbohydrates do not
just provide “bulk” in the diet, instead they provide an
excellent source of metabolizable energy for dogs. Thus, the
puzzle surrounding the use of carbohydrates in dog diets
centers on understanding how various carbohydrate sources
impact blood sugar levels—to provide either quick or sustained energy—in addition to providing the most beneficial
responses of the blood sugar levels for dogs in various life
stages and lifestyles.
35
IMPORTANCE OF STARCH IN CANINE DIETS
Primary source of energy
for many body functions
Necessary for synthesis and
metabolism of other nutrients
Influences the way diets
are manufactured
• Locomotion
• Metabolized to produce
energy for cells
• Gives diets their kibbled
shape
• Used to synthesize steroid
hormones and fatty acids
• Provides diet texture
• Only source usable by the
brain and red blood cells
Importance of Insulin
Insulin is a hormone secreted by the
pancreas in response to elevated blood levels
of glucose. The magnitude of the insulin
response is directly proportional to the level
of glucose present in the bloodstream.
Hence, the more glucose present in the blood will result in
greater levels of insulin being released. Insulin promotes the
efficient storage and use of glucose molecules by controlling
their transport across cell membranes. Insulin acts as the
key that unlocks the cell and permits glucose to enter and
be metabolized (Figure 2). Therefore, just as in the case of
glucose, a dog’s post-meal insulin level is strongly influenced by digestion and absorption of the starch contained
in its diet.
• Helps evenly distribute
micronutrients
Figure 1.
manufactured by providing for proper expansion and cohesion of dietary ingredients to form kibbled and different
textured diets.
METABOLIZING STARCH TO GLUCOSE
On average, 30 to 60% of metabolic calories in a commercially available diet come from dietary starch. While
several starch sources are available for use in developing
canine diets, not all starch sources are alike. In general, all
starches require further breakdown or degradation to their
basic building block—glucose. However, some starch
sources do contain more complex carbohydrates than others
and, in essence, contain more potentially available glucose.
Some starch sources may also require additional digestion
time or require specific enzymes in the digestive process in
order to make the glucose available. The ability to do this
is achieved through a process by which digestive enzymes
break apart the chemical bonds that once linked multiple
glucose molecules together to form starch.
In dogs, the main enzymes that orchestrate the breakdown of starch are the alpha amylases. These enzymes are
secreted in the saliva and from the pancreas, adhere to the
large starch molecules, and continue to break up the starch
into more simple sugars. Ultimately, the process results in
the production of glucose that will be used as the major fuel
source of all cells in the dog’s body. Several other digestive
enzymes exist that are important, as well as specific, to
metabolizing a multitude of other carbohydrates in the dog.
These enzymes will also be vital to the process of deriving
glucose from many other simple and complex carbohydrates
from the time your dog matures from a puppy to a beloved
senior companion.
CELL
GLUCOSE
INS
ULI
N
Figure 2. Insulin acts as the key that unlocks the cell and permits
glucose to enter and be metabolized.
AFTER MEAL GLUCOSE
AND INSULIN RESPONSE
The nutritional importance of the “after meal” glucose
and insulin response to different sources of carbohydrates is
gaining greater awareness. In dogs, the body’s ability to control glucose may be impaired in a number of life stages or
conditions. Diabetes, obesity, gestation, and aging are
examples of such life stages or conditions.
One of the primary concerns with overweight pets is
abnormal glucose metabolism, since obesity and poor glucose
metabolism are highly correlated. Animals with impaired
Importance of Glucose
Metabolizing starch to glucose is important since glucose
is the chief end product of starch digestion, as well as the
primary metabolic fuel for cells in the body.
Glucose is readily absorbed in the small
intestine, is transported via blood vessels,
and is found circulating in the bloodstream
to provide tissues with needed fuel. The rate
of starch digestion and absorption is directly
responsible for the rise in blood glucose
immediately following a meal. Thus, choosing the appropriate source of starch will
have a substantial effect on a dog’s blood
sugar status.
36
the lowest glycemic index when compared to other starch
sources such as corn, wheat, rice, and millet.12 These findings
suggest that the source of starch influences the glucose and
insulin response to food in simple-stomached animals and
humans.
glucose control have difficulty storing blood glucose, and
glucose levels remain higher for longer periods of time than
in normal individuals. Therefore, to reestablish a state of
normalcy more quickly in these individuals, diets that minimize the glucose response after a meal should be sought.
It was originally believed that complex carbohydrates
(starches) would result in lower glucose surges because their
digestion rate is slower than simple carbohydrates.2 However,
a number of studies evaluating the after meal glucose and
insulin responses to both simple and complex carbohydrate
foods have contradicted this assumption.2-6 For instance, in
some cases complex carbohydrates result in comparable
blood sugar and insulin responses to simple carbohydrates.3,4,6 After a meal, blood glucose surges appear to be
regulated by several factors in the diet such as the chemical
nature of carbohydrates,7,8 protein, fat,9 dietary fiber,10 and
the type of food processing.11
Studying Starch Source in Canine Diets
Recognizing that carbohydrates are a significant portion
of the daily diet of dogs, The Iams Company designed a
study to evaluate the blood sugar response of diets containing
corn, wheat, barley, rice, or sorghum as a chief source of
energy in 30 weight stable, clinically normal, adult dogs.
The dogs were housed individually according to approved
Animal Welfare Act standards. All procedures were reviewed
and approved by the Institutional Animal Care and Use
Committee and the dogs were treated humanely and ethically during the entire study period.
Each testing period lasted a minimum of 2 weeks and a
blood sugar response test was performed at the end of each
testing period. During the first study, the dogs were randomized into 1 of 5 dietary treatment groups of 6 animals
each. The dogs were re-randomized and assigned to a different experimental diet for the second period. Immediately
following the collection of 2 baseline blood samples
approximately 10 minutes apart, the dogs were fed an
amount of food based on their body weight and allowed a
maximum of 15 minutes to eat the experimental diets. Time
0 corresponded to the end of the food intake. The blood
samples were collected at 10, 20, 30, 45, 60, 120, 180, and
240 minutes after the food was consumed. The extracted
plasma was assayed for glucose and insulin.
During the stabilization period, dogs were fed their
respective maintenance diet. The daily food intake was
adjusted for each animal during this period to stabilize body
weights. The five experimental diets were formulated to
contain a similar starch content so that blood sugar response
was not influenced by differences in carbohydrate intake.
Evaluation of the carbohydrate sources in a complete diet
matrix was also a consideration. To achieve this, protein
levels needed to vary considerably while fat levels were at
similar levels. The concentrations of the following nutrients
were consistent across all diets: 32% protein, 10% fat, and
30% starch.
The different cereal sources were corn, wheat, barley,
rice, and sorghum. The experimental diets were processed
similarly with each starch source consisting of whole grain
without the hull. Supplementation of micronutrients was
held constant among diets since certain vitamins17,18 and
minerals19,20 have been shown to alter signs of glycemic status. Individual daily feed allowances were based on the stabilization period intake. Glucose and insulin levels were
analyzed using standard laboratory methods accepted by
nutritionists.21 The results of glucose and insulin assays
from the two baseline samples were averaged and reported
as one baseline value (also called the area under the curve,
or AUC).
In humans, the different sources of starch have been
ranked comparatively based on blood sugar response.12,13
The resulting “glycemic index” utilized white bread as the
standard and all other foods were ranked accordingly.14
These efforts have resulted in the publication of an international table of the glycemic index summarizing hundreds
of separate entries. The glycemic index and dietary levels of
carbohydrates have been used to explain approximately
90% of the reason for differences in glucose and insulin
responses to a meal.15 This evaluation of a starch’s influence
on blood glucose and insulin is important to determine its
influence on glucose response. No such glycemic index has
been developed for animals.
DOES STARCH SOURCE MATTER?
The source of starch affects the blood sugar response in
a clinically relevant manner. For instance, the consumption
of a diet using whole sorghum significantly reduces plasma
glucose peak levels and percent of glycemic response in diabetics when compared to consumption of dehulled
sorghum, wheat, and rice recipes.16 In humans, barley had
37
Study Results
Study Conclusions
Results of the study are summarized in Table 1. The
rice diet resulted in higher glucose levels from 20 to 180
minutes after eating and also the greatest average glucose and
after meal peak (Figure 3). The sorghum diet had consistently lower after meal plasma glucose levels than the other
diets between 20 and 60 minutes and the glucose levels
gradually increased for the remainder of the time points.
The sorghum diet also resulted in the lowest average glucose
levels (Figure 3). The glucose response to corn, wheat, and
barley were intermediate to sorghum and rice with corn
tending to yield the lowest glucose response of the three
diets. The rice diet had a significant increase in blood
insulin levels at 45- and 60-minute time points over all
other experimental diets. The rice diet also resulted in a
higher average insulin level, and insulin peak (Figure 4).
Conversely, the barley diet resulted in the lowest plasma
insulin levels from 20 minutes to 240 minutes and the lowest
insulin response. The corn, wheat, and sorghum diets were
generally intermediate for most insulin response criteria.
This study showed that the rice-based diet increased
the blood sugar response after a meal and resulted in significantly higher post-meal glucose and insulin responses.
Sorghum generally resulted in
the lowest post-meal glucose
The source of
response while barley resulted
starch influences
in the lowest post-meal
insulin response. These findthe glucose and
ings suggest that the source
insulin response in
of starch influences the gludogs after a meal.
cose and insulin response in
dogs after a meal.
DIETARY RECOMMENDATIONS
So what exactly is in it for your dogs? It’s simple—
Eukanuba® and Iams® diets contain the appropriate types of
carbohydrates that help your dog achieve optimum blood
sugar and insulin levels. Iams carbohydrate research has
Table 1. Summary of a study evaluating the effect of starch source in canine diets
STARCH SOURCE
STUDY RESULTS
PRACTICAL APPLICATION
Rice
•
•
•
•
•
•
Higher glucose levels
Greatest average glucose
Greatest after meal peak
Increase in blood insulin levels
Higher average insulin level
Higher insulin peak
• Rice-based diets increase the blood sugar response after a
meal and result in significantly higher post-meal glucose and
insulin responses
• Used judiciously, rice may be effective in diets specifically
formulated to provide a combination of quick and sustained
energy for performance dogs
• Rice should not be used as the main carbohydrate source in
a diet formulated for animals with poor glucose control,
such as diabetes and obesity
Sorghum
•
•
•
•
Lower after meal plasma glucose levels
Gradually increased glucose levels
Lowest average glucose level
Intermediate insulin response
• Sorghum diets result in the lowest post-meal glucose
response
• Dietary recommendations for improving glucose control in
dogs should include sorghum.
Corn
• Intermediate glucose response vs rice
• Intermediate insulin response vs rice
• Lowest glucose response vs wheat and barley
• Corn when used with sorghum, barley or both will help to
achieve a more even glycemic response
Wheat
• Intermediate glucose response vs rice
• Intermediate insulin response vs rice
• Wheat is not as effective as corn in leveling glucose
• May be used as secondary starch source along with
appropriate levels of sorghum and barley
Barley
• Intermediate glucose response
• Lowest plasma insulin levels
• Lowest insulin response
• barley resulted in the lowest post-meal insulin response
• Dietary recommendations for improving glycemic (glucose
and insulin) control in dogs should include barley
Combined carbohydrate
sources
• Corn
• Rice
• Sorghum
In the case of extreme energy needs, a combination of corn,
rice, and grain sorghum can provide highly active/very athletic
dogs with rapidly available energy for exertion, while helping
them maintain adequate body weight and condition in adverse
environments
38
Glucose (mg/dl)
94
14
Glucose Average
92
12
90
10
88
8
86
6
84
4
82
2
80
Corn
Wheat
Barley
Rice
Insulin Average
0
Sorghum
Test Diets
Test Diets
Figure 3. Average after meal glucose response for each starch-based diet
evaluated (Average = average of baseline, 10, 20, 60, 120, 180, and
240-minute samples) in dogs.
Figure 4. Average after meal insulin response for each starch-based diet
evaluated (Average = average of baseline, 10, 20, 30, 45, 60, 120, 180,
and 240-minute samples) in dogs.
shown that some products are best formulated using a combination of carbohydrate sources to fit the special nutritional
requirements of your dog during specific life stages and lifestyles. Iams uses carbohydrate sources such as grain sorghum,
corn, and barley that are all highly digestible, which means
your dog’s body will metabolize a high percentage of each
for energy. What’s unique about the carbohydrate sources
used in Eukanuba® and Iams® dog foods is the slow breakdown that results in moderate, stable blood glucose and
insulin levels after a meal. By minimizing blood glucose,
diets containing such a blend supply sustained energy.
Therefore, dietary recommendations for improving glucose control in your dog should include feeding diets that
contain grain sorghum, corn and barley. It should be noted
that in the case of extreme energy needs a combination of
highly available carbohydrate sources (corn, rice, grain
sorghum) can provide highly active/very athletic dogs with
more rapidly available energy for exertion and can help
them maintain adequate body weight and condition in
adverse environments. However, rice as the main source of
carbohydrate in a canine diet is not recommended for those
animals with poor glucose control, such as dogs that suffer
from diabetes or obesity.
Finally, you as dog owners can now solve the carbohydrate puzzle by completing the last piece—Help enhance
the health and well being of your dog by providing them
with Eukanuba® and Iams® diets that contain the appropriate carbohydrate sources to achieve optimal glucose control.
Copyright 2002, Kent and Donna Dannen.
REFERENCES
1. McCay, CM. Nutrition of the dog. Ithaca NY: Comstock Publishing
Company, 1949.
2. Jenkins DJA, Wolever TMS, Jenkins Al, Josse RG, Wong GS. The
response to carbohydrate foods. Lancet 1984; 388-391.
3. Blaak EE, Saris WHM. Health aspects of various digestible carbohydrates.
Nutrition Res 1995; 15:1547-1573.
4. Reavan GM. Effects of differences in and amount and kind of dietary
carbohydrate on plasma glucose and insulin responses in man. Am J Clin
Nutr 1979; 32:2568-2578.
5. Crapo PA, Insel RDJ, Sperlind M, Kolterman OG. Comparison of serum
glucose, insulin, and glucagon responses to different types of complex
carbohydrate in noninsulin-dependent diabetic patients. Am J Clin Nutr
1981; 34:184-190.
6. Dunnigan MG, Fyfe T, McKiddie MT, Crosbie SM. The effects of
isocaloric exchange of dietary starch and sucrose on glucose tolerance,
plasma insulin and serum lipids in man. Clin Sci 1970; 38:1-9.
Eukanuba and Iams are registered trademarks of The Iams Company.
39
7. Behall KM, Schofield DJ, Yuhaniak I, Canary J. Diets containing high
amylose vs amylopectin starch: Effect on metabolic variables in human
subjects. Am J Clin Nutr 1989; 49:337-344.
8. Goddard MS, Young G, Marcus R. The effect of amylose content on
insulin and glucose responses to ingested rice. Am J Clin Nutr 1984;
42:495-503.
9. Nguyen P, Dumon H, Buttin P, Martin L, Gouro AS. Composition of
meal influences changes in postprandial incremental glucose and insulin
in healthy dogs. J Nutr 1994; 2707S-2711S.
10. Nishimune T, Yakushiji T, Sumimoto T, Taguchi S, Konishi Y, Nakahara
S, Ichikawa T, Kunita N. Glycemic response and fiber content of some
foods. Am J Clin Nutr 1991; 54:414-419.
11. Holste LC, Nelson RW, Feldman EC, Bottoms GD. Effect of dry, soft
moist, and canned dog foods on postprandial blood glucose and insulin
concentrations in healthy dogs. Am J Vet Res 1989; 50:984-989.
12. Powell KF, Miller JB. International tables of Glycemic index. Am J Clin
Nutr 1995; 62:871S-893S.
13. Jenkins DJA, Wolever TMS, Taylor RH, Baker H. Fielden H, Baldwin
JM, Bowling AC, Newman HC, Jenkins AL, Goff DV. Glycemic index
of foods: A physiological basis for carbohydrate exchange. Am J Clin
Nutr 1981; 34:362-366.
14. Jenkins DJA, Wolever TMS, Jenkins AL, Thorne MJ, Lee R. Kalmosky
J, Reichert R, Wong GS. The glycaemic index of foods tested in diabetic
patients: A new basis for carbohydrate exchange favouring the use of
legumes. Diabetologia 1983; 24:257-264.
15. Wolever TMS, Colognesi C. Prediction of glucose and insulin responses
of normal subjects after consuming mixed meals varying in energy, protein, fat, carbohydrate and glycemic index. J Nutr 1996; 126:2807-2812.
16. Lakshmi KB, Vimala V. Hypoglycemic effect of selected sorghum recipes.
Nutr Res 1996; 16:1651-1658.
17. Ceriello A, Giugliano D, Quatraro A, Donzella C, Dipalo G, Lefebvre
PJ. Vitamin E reduction of protein glycosylation in diabetics: New
prospect for prevention of diabetic complications. Diabetes Care 1991;
14:68-72.
18. Jain SK, McVie R, Jaramillo JJ, Palmer M, Smith T. Effect of modest
vitamin E supplementation on blood glycated hemoglobin and triglyceride
levels and red cell indices in type 1 diabetic patients. J Amer Coll Nutr
1996; 15:458-461.
19. Burn J-F, Guintrant-Hugret R,Fons C, Carvajal J, Fedou C, Fussellier M,
Bardet L, Orsetti A. Effects of oral zinc gluconate on glucose effectiveness and insulin sensitivity in humans. Biol Trace Element Res 1995;
47:385-391.
20. Thompson KH, Godin DV, Micronutrients and antioxidants in the
progression of diabetes. Nutr Res 1995; 15:1377-1410.
21. SAS User’s guide: Statistics. Cary NC: SAS Institute Inc, 1989.
40
Innovative Research in Dog and Cat Nutrition
®
®
Makers of Eukanuba® and Iams®
premium dog and cat foods, and
veterinary exclusive canine and
feline Eukanuba Veterinary Diets®
7250 Poe Avenue
Dayton, OH 45414 USA
1-800-535-VETS (8387)
www.iams.com

Maximizing Success in the Breeding Kennel and Show Ring

Transcription

Similar documents

Kennel stationery

Costa Blanca News. - hospital veterinario JG

Nothing to do - Rabbit Welfare Association

Wiltshire View - One Man and His Gundogs

Monday 9th of November PC Andy Price and PC Alan Wood visit

How does my dog see?

Solutions to Jumping Problems Consults

Dew Claw Explanation Best - Canine Sports Productions

Newsletter JULY 2016 - Bleakholt Animal Sanctuary

the night I followed the dog