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
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
Overfeeding During Growth
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
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
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
Feeding recommendations for growing dogs
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
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
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
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
weaning to half grown
50-80 % of adult weight
80 to near adult weight
- Owners should be aware of the clinical complications
- 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
- Center, S.A.(1986). Feline liver disorders and their management,
Comp Cont Ed, 8, 889-903.
- Edney, A.T.B. and Smith, P.B.(1986). Study of obesity in dogs visiting
veterinary practices in the United Kingdom, Vet Record, 118,
- 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.
- 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.
- 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.
- Hedhammer, A.(1980). Nutrition as it relates to skeletal disease, Proc
4th Kal Kan Symp, pp.41-44.
- 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.
- Joshua, J.O. (1970). The obese dog and some clinical repercussions, J
Sm Anim Pract, 11, 601-606.
- Kallfelz, F.A. and Dzanis, D.A.(1989) . Overnutrition: an epidemic problem
in pet animal practice, Vet Clin Nth Amer, Sm Anim Pract, 3,
- Krook, L., Larsson, S. and Rooney, J.R.(1960). The interrelationship
of diabetes mellitus, obesity and pyometra in the dog, Amer J Vet Res,
- Nap, R.C. (1993). Nutritional influences on the growth and skeletal
development in the dog, Thesis, Utrecht University. pp.1-144.
- 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.
- Newberne, P.M.(1966). Overnutrition on resistance of dogs to distemper
virus. Fed Proc, 25, 1701-1710.
- 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.
- Thornburg, L. P., Simpson, S. and Diglio, K. (1982). Fatty liver syndrome
in cats. J Amer Hosp Assoc, 18, 397.
- Williams, G.D. and Newberne, P.M.(1971). Decreased resistance to salmonella
infection in obese dogs, Fed Proc, 30, 572.