Maximizing Success in the Breeding Kennel and Show Ring
Transcription
Maximizing Success in the Breeding Kennel and Show Ring
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. Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 AND LEG PROBLEMS IN GROWING DOGS 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 AND LEG PROBLEMS IN GROWING DOGS 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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. Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 AND LEG PROBLEMS IN GROWING DOGS 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. Maximizing Success in the Breeding Kennel and Show Ring—2002 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 AND LEG PROBLEMS IN GROWING DOGS 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 AND LEG PROBLEMS IN GROWING DOGS 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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. Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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) Maximizing Success in the Breeding Kennel and Show Ring—2002 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. Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 Photo used with permission. ©Ashbey Photography, 2002. 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. Photo used with permission. ©Ashbey Photography, 2002. 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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. Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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. Maximizing Success in the Breeding Kennel and Show Ring—2002 • 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Research and Development Division 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. Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 “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). Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Research and Development Division The Iams Company, Lewisburg, Ohio USA 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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. Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Research and Development Division The Iams Company, Lewisburg, Ohio USA 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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 Maximizing Success in the Breeding Kennel and Show Ring—2002 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. 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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. Maximizing Success in the Breeding Kennel and Show Ring—2002 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