Overfeeding of dogs and cats is a common practice. Most pet owners know that prolonged overfeeding results in obesity, which predisposes animals to a number of clinical conditions. However, the potentially damaging effects of overfeeding young, growing dogs, particularly of the larger breeds, are less well known. In this article we examine the problems associated with obesity and the complications which may arise from overfeeding during growth.


A wide range of conditions tend to affect obese dogs and cats more than animals of normal body weight. Some of these are obvious, but owners often need reminding that obesity is a serious risk to the health and quality of life of their pets.

Orthopaedic problems are probably the most important pathological effect of obesity in dogs. In a U.K. study, between 28% and 44% of dogs visiting veterinary clinics were recorded as overtly obese. About 25% of the obese dogs had orthopaedic problems, whereas 10% of all dogs seen in a variety of veterinary practices had orthopaedic problems.² The abnormal stress imposed by excess weight on the major weight-bearing joints, especially the stifles and elbows, is an important factor in the aetiology of canine osteoarthritis.⁸

Respiratory difficulties may occur in obese dogs.⁸ This may be due to narrowing of the airway by fatty deposits in the tissues surrounding the larynx and pharynx.
Diabetes mellitus and obesity and have been closely linked in humans, dogs and cats.^10,14

Surgical risk, both on a physiological and technical level, is increased in obese animals.

The risk of infectious diseases may be higher in obese dogs than in individuals of normal bodyweight.^13,16

Liver disease may be a serious consequence of obesity, particularly in cats.¹ Feline Hepatic Lipidosis deserves a specific mention. This syndrome is unique to cats, and is characterised by extreme accumulation of fats within hepatocytes, resulting in severe liver dysfunction. Obese cats are predisposed to this condition, often after some form of trauma or illness, which causes a sudden loss of appetite from which the cat never recovers.¹⁵

In young animals, unlike adults, excessive energy intake not only causes an increase in fat deposition, but also a more rapid rate of growth. If the diet supplies sufficient amounts of specific nutrients, such as protein and essential fatty acids, the amount of energy regulates the rate of growth within the animal's genetic potential.³

In large and giant breed dogs, overnutrition results in excess body weight and overloading of the juvenile skeleton. Overfeeding during the phase of rapid growth after weaning is linked to a variety of multi-factorial skeletal diseases including osteochondrosis, hip dysplasia, hypertrophic dystrophy and wobbler syndrome.^6,7

A high protein diet (30% on a dry matter basis) does not increase the frequency or severity of skeletal abnormalities in giant breed dogs. So the excess weight during the period of rapid growth, rather than the protein content of the diet, is probably the factor which alters skeletal development.¹² Contrary to the belief of many breeders and owners, high protein intake does not affect the final height and body weight of dogs, although dogs fed a low protein diet (14.6% of dry matter) tend to have lower body weights at 13 to15 weeks of age than dogs fed a normal diet, reflecting the marginal nature of their diet.¹²

The skeletal abnormalities listed above are seldom diagnosed in dogs of small and miniature breeds or in cats, possibly due to the reduced weight-bearing stresses on the skeleton. However all owners of young dogs and cats should be aware of the severe clinical effects which may result from oversupplementation of the diet with the fat-soluble vitamins A and D, as they may accumulate in the body. Hypervitaminosis A can develop after prolonged intake of raw liver or fish liver oils, and causes severe skeletal abnormalities. Supplementation of a commercial petfood with a vitamin additive can result in giving 100 times the normal requirement of vitamin A.⁹ Extra supplementation with vitamin D can cause increased calcium and phosphate absorption, with deleterious effects on skeletal development and kidney function.

Excess calcium intake may also cause damage to the growing skeleton. When the calcium content of the diet is increased, and all other nutrients are provided in normal amounts, the incidence of osteochondrosis and other skeletal abnormalities, such as retained cartilage core, radius curvus syndrome and stunted growth, increases.⁴ Skeletal problems have been induced by feeding as little as three times the recommended intake of calcium.⁵ For example, a 35 kg Great Dane puppy, eating 2700 kcal/day of a complete and balanced diet (1.2g calcium/ 400kcal) gets about 8g calcium per day. The maximum recommended calcium intake (AAFCO)for this pup is 7.1g/1000kcal, equivalent to 19.1g. So 27g (about 5 teaspoonsful) of powdered calcium carbonate (containing 4.0g calcium/10g) added to the diet could produce a dangerous excess of dietary calcium.

The mechanism by which excess dietary calcium alters normal bone development is thought to involve changes in bone remodelling.¹¹ High calcium intake results in excess calcium being deposited in the skeleton and reduces intestinal absorption of calcium. This triggers compensatory increases in plasma phosphorus levels, due to the actions of the calciotropic hormones. The hyperphosphataemia depresses the activity of the osteoclasts, which are important for bone remodelling during growth. The excess calcium deposited in the skeleton, coupled with slower bone turnover results in pathological changes in skeletal development, particularly affecting endochondral ossification.

A number of studies have shown that puppies should not be fed to achieve the maximum possible rate of growth. With large and giant breeds, the aim is to achieve growth rates which allow proper development without increased risk of skeletal abnormalities or obesity. The optimum growth rate is probably the average for the breed. It should be emphasised to owners that lower growth rates do not affect mature body size, but merely increase the age at which dogs reach their mature body size.

Controlled intake of food during growth is preferable to ad libitum feeding. If puppies are fed a complete and balanced food, which has been trialled according to the AAFCO lifestage feeding protocol for growing dogs, dietary supplementation with vitamins and minerals is rarely necessary.

To calculate the correct amount to feed, calculate the metabolisable energy requirement of the dog (see Table). Once this figure is known, (expressed as kcal/day), divide it by the ME content of the diet (kcal/100g) to give the number of grams of food per day. The food should be divided into several meals per day and meal times restricted to 20 minutes.

Of course it must always be remembered that there can be up to 25 per cent variation in the energy requirements of individual dogs from the average, so adjustment up or down should be made to suit the individual dog's requirements, based on its condition, previous growth rate and activity level.

Daily amount of food (g) = ME requirement

ME content of the diet

ME requirement = a × 125 × Bodyweight ^0.75

Using the following values of a to adjust for the stage of growth:
2.0 weaning to half grown

1.5 50-80 % of adult weight

1.2 80 to near adult weight

• Owners should be aware of the clinical complications of obesity
• Overfeeding puppies of giant breeds is linked to skeletal abnormalities
• Supplements of vitamin A and D and calcium can be deleterious to puppies fed complete and balanced pet foods
• Puppies should be given sufficient food to achieve average growth rates

1. Center, S.A.(1986). Feline liver disorders and their management, Comp Cont Ed, 8, 889-903.
   
2. Edney, A.T.B. and Smith, P.B.(1986). Study of obesity in dogs visiting veterinary practices in the United Kingdom, Vet Record, 118, 391-396.
   
3. Grondalen, J. and Hedhammer, A.(1982). Nutrition of the rapidly growing dog with special reference to skeletal disease, In Nutrition and Behaviour in Dogs and Cats (ed. R.S. Anderson), pp.81-88. Pergamon, Oxford.
   
4. Hazewinkel, H.A.W. (1989). Calcium metabolism and skeletal development in dogs, In Nutrition of the Dog and Cat, (ed. I.H. Burger and J.P.W. Rivers), pp. 293-302. Cambridge University Press, Cambridge.
   
5. Hazewinkel, H.A.W., Goedegebuure, S.A., Poulos, P.W. and Wolvekamp, W.T.C. (1985). The influences of chronic calcium excess on the skeletal development of growing Great Danes, J Amer Vet Hosp Assoc, 21, 377-391.
   
6. Hedhammer, A.(1980). Nutrition as it relates to skeletal disease, Proc 4th Kal Kan Symp, pp.41-44.
   
7. Hedhammer, A., Wu, F., Krook, L, Schryver, H.F., de Lahunta, A., Whalen, J.P., Kallfelz, F.A., Nunez, E.A., Hintz, H.F., Sheffey, B.E. and Ryan, G.D. (1974). Over-nutrition and skeletal disease. An experimental study in growing Great Dane dogs, Cornell Vet, 64, suppl.5, 1-160.
   
8. Joshua, J.O. (1970). The obese dog and some clinical repercussions, J Sm Anim Pract, 11, 601-606.
   
9. Kallfelz, F.A. and Dzanis, D.A.(1989) . Overnutrition: an epidemic problem in pet animal practice, Vet Clin Nth Amer, Sm Anim Pract, 3, 433-436.
   
10. Krook, L., Larsson, S. and Rooney, J.R.(1960). The interrelationship of diabetes mellitus, obesity and pyometra in the dog, Amer J Vet Res, 21, 120-124.
    
11. Nap, R.C. (1993). Nutritional influences on the growth and skeletal development in the dog, Thesis, Utrecht University. pp.1-144.
    
12. Nap, R.C., Hazewinkel, H.A.W., Voorhout, G., Van den Bron, W.E., Goedegebuure, S.A. and Van'T Kloosters, A. (1991). Growth and skeletal development in Great Dane pups fed different levels of protein intake, J Nutr, 121:s107-s113.
    
13. Newberne, P.M.(1966). Overnutrition on resistance of dogs to distemper virus. Fed Proc, 25, 1701-1710.
    
14. Panciera, D.L., Thomas, C.B., Eicker, S.W. and Atkins, C.E. (1990). Epizootiologic patterns of diabetes mellitus in cats: 333 cases (1980-1986), J Amer Vet Med Assoc, 197, 1504-1508.
    
15. Thornburg, L. P., Simpson, S. and Diglio, K. (1982). Fatty liver syndrome in cats. J Amer Hosp Assoc, 18, 397.
    
16. Williams, G.D. and Newberne, P.M.(1971). Decreased resistance to salmonella infection in obese dogs, Fed Proc, 30, 572.