Content uploaded by Alexander J German
Author content
All content in this area was uploaded by Alexander J German on Dec 17, 2013
Content may be subject to copyright.
The WALTHAM International Nutritional Sciences Symposia
The Growing Problem of Obesity in Dogs and Cats
1–3
Alexander J. German
4
Departm ent of Veterinary Clinical Sciences, University of Liverp ool, Small Animal Hospital, Liverpool,
L7 7EX, UK
ABSTRACT Obesity is defined as an accumulation of excessive amounts of adipose tissue in the body, and is the
most common nutritional disorder in companion animals. Obesity is usually the result of either excessive dietary
intake or inadequate energy utilization, which causes a state of positive energy balance. Numerous factors may
predispose an individual to obesity including genetics, the amount of physical activity, and the energy content of the
diet. The main medical concern of obesity relates to the many disease associations that accompany the adiposity.
Numerous studies demonstrated that obesity can have detrimental effects on the health and longevity of dogs and
cats. The problems to which obese companion animals may be predisposed include orthopedic disease, diabetes
mellitus, abnormalities in circulating lipid profiles, cardiorespiratory disease, urinary disorders, reproductive disorders,
neoplasia (mammary tumors, transitional cell carcinoma), dermatological diseases, and anesthetic complications.
The main therapeutic options for obesity in companion animals include dietary management and increasing physical
activity. Although no pharmaceutical compounds are yet licensed for weight loss in dogs and cats, it is envisaged that
such agents will be available in the future. Dietary therapy forms the cornerstone of weight management in dogs and
cats, but increasing exercise and behavioral management form useful adjuncts. There is a need to increase the
awareness of companion animal obesity as a serious medical concern within the veterinary profession. J. Nutr. 136:
1940S–1946S, 2006.
KEY WORDS:
overweight
nutrition
canine
feline
adipose tissue
Obesity is defined as an accumulation of excessive amounts of
adipose tissue in the body (1). In humans, the application of this
definition is based upon epidemiologic data, which demonstrate
increased morbidity and mortality risk with increasing body fat
mass. Criteria have been established for what constitutes
‘‘overweight’’ and what constitutes ‘‘obesity’’; such criteria are
usually based on measures of adiposity such as the BMI [weight
(kg) divided by height
2
(m)]; Caucasians, for example, are
defined as overweight when BMI is .25 kg/m
2
, and obese when
BMI exceeds 30. In contrast, one report classified cats and dogs
as overweight when their body weight is .15% above their
‘‘optimal body weight,’’ and as obese when their body weight
exceeds 30% of optimal (1). However, these criteria have not
been confirmed with rigorous epidemiologic studies, and limited
data exist on the nature of an optimal body weight.
Obesity is an escalating global problem in humans (2), and
current estimates suggest that almost two-thirds of adults in the
United States are overweight or obese (3). Studies from various
parts of the world have estimated the incidence of obesity in the
dog population to be between 22 and 40% (4). The most
recently published data come from a large study in Austr alia in
which 33.5% of dogs were classed as overweight, whereas 7.6%
were judged to be obese (4). The incidence of feline obesity is
similar (1,5,6). Most investigators agree that, as in humans, the
incidence in the pet population is increasing.
Measurement of obesity in companion animals
All measures of adiposity involve defining body composition,
or the ‘‘relative amounts of the various biological components
of the body.’’ The main conceptual division of importance is
between fat mass (FM,
5
the triglyceride component in adipose
tissue) and lean body mass (LBM) (7). Various techniques are
available to measure body composition (Table 1), and these
differ in applicability to research, referral veterinary practice,
and first-opinion practice. Whatever method is used, investi-
gators should be aware of both its precision and accuracy.
The accuracy of a test is defined as the closeness with which
1
Published in a supplement to The Journal of Nutrition. Presented as part of
The WALTHAM International Nutritional Sciences Symposium: Innovations in
Companion Animal Nutrition held in Washington DC, September 15–18, 2005. This
conference was supported by The WALTHAM Centre for Pet Nutrition and
organized in collaboration with the University of California, Davis, and Cornell
University. This publication was supported by The WALTHAM Centre for Pet
Nutrition. Guest editors for this symposium were D’Ann Finley, Francis A. Kallfelz,
James G. Morris, and Quinton R. Rogers. Guest editor disclosure: expenses for
the editors to travel to the symposium and honoraria were paid by The WALTHAM
Centre for Pet Nutrition.
2
Author disclosure: Expenses for the author to travel to the symposium and
honoraria were paid by WALTHAM.
3
Supported by grants from the Waltham Centre for Pet Nutrition, Royal Canin,
and BBSRC. A.J. German’s lectureship is currently funded by Royal Canin.
4
To whom correspondence should be addressed. E-mail: ajgerman@liv.ac.uk.
5
Abbreviations used: CLA; conjugated linoleic acid; cTSH, canine thyroid-
stimulating hormone; DM, diabetes mellitus; DXA, dual-energy X-ray absorptiom-
etry; FM, fat mass; HDL-C, HDL cholesterol; LBM, lean body mass; LIM, limb index
measurement; T3, triiodothyronine; T4, thyroxine; USMI, urethral sphincter
mechanism incompetence.
0022-3166/06 $8.00 Ó 2006 Americ an Society for Nutrition.
1940S
by on March 28, 2010 jn.nutrition.orgDownloaded from
a measurement of the variable represents its true value, whereas
precision is the ability to yield the same estimated result on
repeated analysis (irrespective of accuracy). Ideally, a test that
is both accurate and precise should be used; however, many
tests for body composition are precise but not accurate, whereas
some lack both precision and accuracy. Ot her important
aspects of a test are cost, ease of use, acceptance by vet-
erinarians and clients, and invasiveness. Currently, there is no
method that cannot be criticized; therefore, the perfect tool for
analysis does not yet exist.
Potential research techn iques include chemical analysis,
densitometry, total body water measurement, absorptiometry
[including dual-energy X-ray absorptiometry (DXA)], ultraso-
nography, electrical conductance, and advanced imaging tech-
niques (computed tomography and MRI; Table 1). In the
clinical setting, there is a need for quick, inexpensive, and
noninvasive methods of body composition measurement. The
most widely adopted quantitative procedures include measure-
ment of body weight and morphometry.
Morphometry. This is defined as the measurement of ‘‘form’’;
in relation to body composition analysi s, it refers to a variety of
measured parameters that are used to estimate body composi-
tion. The 3 main approaches are measurement of skin fold thick-
ness, dimensional evaluations (in which various measures of
stature are combined with weight), and body condition scores.
Dimensional evaluations. Such evaluations are usually
performed by tape measure, and a number were reported in
dogs and cats. Measurements of ‘‘length’’ (e.g., head, thorax, and
limb) are correlated with lean body components (8), whereas
measurements of girth were shown to correlate with both LBM
(8) and FM (9). Segmental limb measures and (likely) truncal
length are thought to be better measures of stature and thus
correlate best with LBM. By combining .1 measure (usually
1 that correlates with FM, and 1 correlating with LBM),
equations can be generated to predict different body compo-
nents. The best examp le of such a measure is the feline BMI
(9), where:
Body fatð%Þ5f½ðRibcage= 0 :7067Þ2LIM=0:9156g2LIM ½1:
Here, the ribcage measurement is the circumference measured
at the 9th rib, and LIM stands for the ‘‘limb index measure-
ment,’’ which is the distance between the patella and calcaneus
of the left hindlimb. All measurements are made in centime-
ters, and measurements are made with the cat in a standing
position, with the legs perpendicular to the ground and the
head upright.
Such techniques do provide a more objective measure of
body composition than body condition scoring (see below), but
problems exist when similar schemes are extrapolated to the
many breeds of dog. Despite this, a BMI has been suggested for
dogs (10).
Body condition scoring. This is a subjective, semiquanti-
tative method of evaluating body composition. A number of
schemes were devised, with a 9-point scheme being the most
widely accept ed (11,12). All systems assess visual and palpable
characteristics that correlate subcutaneous fat, abdominal fat,
and superficial musculature (e.g., ribcage, dorsal spinous pro-
cesses, and waist). A new 7-point algorithm-based approach,
specifically designed to be used by owners to assess their own
pets, was developed recently. A recent study demonstrated
good correlation between the system and body fat measure-
ments made by DXA and excellent agreement among experi-
enced operators (13). Most importantly, good agreement was
found between measurements by the experienced operators and
the owners, suggesting that the method is reliable when used
without prior training.
Causes of obesity
Although some diseases (e.g., hypothyroidism and hyper-
adrenocortism in dogs), pharmaceuticals (e.g., drug-induced
polyphagia caused by glucocorticoids and anticonvulsant drugs),
and rare genetic defects (in huma ns) can cause obesity, the
main reason for the development of obesity is having a positive
mismatch between energy intake and energy expenditure.
Therefore, either excessive dietary intake or inadequate energy
utilization can lead to a state of positive energy balance; numer-
ous factors may be involved, including genetics, the amount of
physical activity, and the energy content of the diet (1).
The effect of genetics is illustrated by recognized breed
associations in both dogs (e.g., Labrador Retriever, Cairn Terrier,
Cavalier King Charles Spaniel, Scottish Terrier, Cocker Spaniel)
and cats (e.g., D omestic Shorthair) (14,15).
Neutering is an important risk factor for obesity in both
species; many studies suggested that this is due to a decrease
in metabolic rate after neutering (16–19). However, increased
FM is usually present in neutered animals; when energy
expenditure is expressed on a lean mass basis, no difference in
metabolic rate is noted between neutered and entire individ-
uals (20–23). Alternative explanations for the effect of neuter-
ing on obesity is an alteration in feeding behavior leading to
increased food intake (17,18,21–25), and decreased activity
without a corresponding decrease in energy intake (26,27).
Gender itself is also a predisposing factor in some canine
studies, with females overrepresented (14,28). Other recognized
TABLE 1
Methods for body composition analysis in dogs and cats
Common research techniques
Chemical analysis
Densitometry
Total body water
Isotope dilution
Deuterium
Tritium
Total body potassium
Absorptiometry
Photon absorptiometry
Single-photon absorptiometry (SPA)
Dual-photon absorptiometry (DPA)
X-ray absorptiometry
Single-energy X-ray absorptiometry (SXA)
Dual-energy X-ray absorptiometry (DXA or DEXA)
Ultrasound
Subcutaneous
Visceral
Electrical impedance
Common clinical methods
Body weight
Morphometric methods (zoometry)
Body condition score
9-Point scale
5-Point scale
6-Point scale
Tape measurements
BMI
Other methods
Muscle metabolite markers
Neutron activation analysis
Electrical conductance (bioelectrical impedance)
Near infrared interactance (NIRI)
Computed tomography
MRI
1941SOBESITY IN C OMPANION ANI MALS
by on March 28, 2010 jn.nutrition.orgDownloaded from
associations in dogs include indoor lifestyle and middle age
(4,14,15). In cats, middle age and apartment dwelling are
possible risk factors (6).
Dietary factors can also lead to the development of obesity in
both species. For instance, obesity in dogs is associated with the
number of meals and snacks fed, the feeding of table scraps, and
the dog’s presence when its owners prepared or ate their own
meal (29). Interestingly, the type of diet fed (prepared pet food
vs. homemade) does not appear to predispose to obesity
(14,15,29). However, the price of the pet food does have a
notable effect, i.e., obese dogs are more likely to have been fed
inexpensive rather than more expensive foods. Further, obese
cats more commonly have a free choice of food intake (30).
Behavioral factors also play a part in the development of
obesity. For cats, possible factors involved in the development
of obesity include anxiety, depression, failure to establish a
normal feeding behavior, and failure to develop control of
satiety (31). The human-animal relationship is also of impor-
tance and was shown to be more intense in the owners of obese
cats (30). Further, misinterpretation of feline behavior on the
part of the owner is also of importance; in this regard, many
owners misread signals about the behavior of their cat asso-
ciated wth eating. In contrast to humans and dogs for whom
eating is a social function, cats do not have any inherent need
for social inter action during feeding times. When the cat
initiates contact, owners often assume that they are hungry and
are asking for food when they are not (31). Nevertheless, if food
is provided at such times, the cat soon learns that initiating
contact results in a food reward. For dogs, owner factors that
are of importance include the duration that the owner observed
the dog eating (more likely to be longer in obese dogs), interest
in pet nutrition, obesity of the owner, health consciousness of
the owner (both for their pet and themselves), and lower
income (29).
The pathological importance of obesity
In humans, obesity is important because it increases mor-
tality risk and can predispose to a variety of diseases. Obese
humans, on average, do not live as long, and are more likely to
suffer from diseases such as type II diabetes mellitus (DM),
hypertension, coronary heart disease, certain cancers (e.g.,
breast, ovarian, prostate), osteoarthritis, respiratory disease,
and reproductive disorders. Similarly, obesity has detrimental
effects on the health and longevity of dogs and cats (Table 2),
although data are more limited. Problems to which obese
companion animals may be predisposed include orthopedic
disease, DM, abnormalities in circulating lipid profiles, cardio-
respiratory disease, urinary disorders, reproductive disorders,
neoplasia (mammary tumors, transitional cell carcinoma), derma-
tological diseases, and anesthetic complications. Human obesity
is associated with an increased risk of type II DM, cancer,
cardiac disease, hypertension, and decreased longevity (32).
Some studies do suggest an increase in morbidity in sick
patients with poorer body condition (33,34).
Clinical evaluation, physiology and anesthesia. Overall,
obesity makes clinical evaluation more difficult; techniques
that are more problematic in obese patients include physical
examination, thoracic auscultation, palpation and aspiration of
peripheral lymph nodes, abdominal palp ation, blood sampling,
cystocentesis, and diagnostic imaging (especially ultrasonogra-
phy). Anesthetic risk is reportedly increased in obese compan-
ion animals, most likely due to recognized problems with
estimation of anesthetic dose, catheter placement, and
prolonged operating time (35,36). Finally, decreased heat
tolerance and stamina were also reported in obese animals (1).
Longevity. Dietary restriction can increase longevity in
other species (37–39), and a recent prospective study con-
firmed a similar effect in dogs (40–45). Labrad or retrievers (24
pairs, 48 in total) participated in the study, and 1 dog in each
pair was randomly assigned to 1 of 2 groups (43). The dogs in
one group consumed food ad libitum, whereas the dogs in the
other group were fed 75% of the amount consumed by their
counterparts. In the energy-restricted group, the body condi-
tion score was closer to ‘‘optimal’’ (e.g., group mean 4.5/9) than
in the ad libitum feeding group (e.g., group mean 6.8/9).
Although causes of death did not differ between the 2 groups,
the lifespan was increased in the energy-restric ted group (e.g.,
median 13 y with energy restriction vs. 11.2 y with ad libitum
consumption) (45). Additional beneficial effects of feed
restriction (and thus maintenance of body condition) included
a reduced risk of hip dysplasia and osteoarthritis, and improved
glucose tolerance (40–45).
Diseases associ ated with obe sity
Endocrine and metabolic diseases. Hormonal diseases with
a reported association with obesity include DM, hypothyro id-
ism, hyperadrenocorticism, and insulinoma (1). Some condi-
tions predispose to obesity, whereas others arise more commonly
TABLE 2
Diseases reported to be associated with obesity in
companion animals
Metabolic abnormalities
Hyperlipidemia/dyslipidemia
Insulin resistance
Glucose intolerance
Metabolic syndrome
Hepatic lipidosis (cat)
Endocrinopathies
Hyperadrenocorticism
Hypothyroidism
Diabetes mellitus
Insulinoma
Hypopituitarism
Hypothalamic lesions
Orthopedic disorders
Osteoarthritis
Humeral condylar fractures
Cranial cruciate ligament rupture
Intervertebral disk disease
Cardiorespiratory disease
Tracheal collapse
Brachycephalic airway obstruction syndrome
Laryngeal paralysis
Urogenital system
Urethral sphincter mechanism incompetence
Urolithiasis (calcium oxalate)
Transitional cell carcinoma
Dystocia
Neoplasia
Mammary
Transitional cell carcinoma
Functional alterations
Joint disorders
Respiratory compromise, e.g., dyspnea
Hypertension
Dystocia
Exercise intolerance
Heat intolerance/heat stroke
Decreased immune functions
Increased anesthetic risk
Decreased lifespan
1942S SUPPLEMENT
by on March 28, 2010 jn.nutrition.orgDownloaded from
in animals that are obese. Acromegaly can lead to a generalized
increase in tissue mass, and is thus a differential diagnos is for
obesity. However, in this condition, lean tissue and bone
mineral are likely to be deposited in addition to adipose tissue.
Insulin resistance, DM, and the metabolic syndrome. Insulin
secreted by pancreatic b cells controls the uptake and use of
glucose in peripheral tissues. In humans, tissues become less
sensitive to insulin (i.e., become ‘‘insulin resistant’’) with
excessive energy intake (46), and plasma concentrations of
insulin increase in direct proportion to increasing BMI in both
men and women (47). Thus, obesity, particularly abdominal
obesity, is a major determinant of insulin resistance and
hyperinsulinemia (48). Cats most often suffer from DM, which
resembles ‘‘type II’’ DM in humans; therefore, obesity is a major
risk factor in this species (49). Indeed, it was proven
experimentally that diabetic cats have significantly lower
sensitivity to insulin than cats without DM (50). In contrast,
dogs more commonly suffer from DM resembling human type I
DM. Obesity causes insulin resistance (45), and obesity is a risk
factor for DM in this species (51). However, because type II
DM is uncommon in dogs, obesity rarely leads to overt clinical
signs of DM (52).
In humans, the metabolic syndrome was originally termed
‘‘syndrome of insulin resistance’’; in fact, it is a group of risk
factors associated with both insulin resistance and cardiovas-
cular disease (53). The main characteristics of metabolic
syndrome are as follows: 1) fasting plasma glucose . 110 mg/dL
(6.10 mmol/L); 2) visceral obesity (e.g., waist circu mference .
90 cm in women and . 102 cm in men; 3) Hypertension e.g.,
blood pressure . 130/85 mm Hg; and 4) low concentrations of
HDL cholesterol (HDL-C; ,40 mg/dL in men, , 50 mg/dL in
women).
Additional features may include systemic inflammation,
prothrombotic state, and increased oxidant stress (54). Further,
in ;20% of cases of metabolic syndrome, there is concurrent
pancreatic b-cell dysfunction leading to DM (53). Some of
these criteria were applied to dogs, an d this species is often used
as a model for human metabolic syndrome (55).
Hypothyroidism and thyroid function. Although hypothyroid-
ism is co mmonly cited as an underlying cause for obesity, such
cases are the exception rather than the rule. The prevalence of
hypothyroidism in dogs is estimated at 0.2%, with less than half
of these dog s reported to be obese (56). In contrast, the
proportion of dogs that are obese is much greater (25–40%) (4).
Hypothyroidism is extremely rare in cats. Thus, although hypo-
thyroidism should always be considered, it is rarely the reason
for obesity. Obesity itself has a subtle, but likely clinically
insignificant effect on thyroid function (57); obese dogs had
higher concentrations of both total thyroxine (T4) and total
triiodothyronine (T3) than nonobese controls, although such
concentrations remained within the reference range and other
parameters [e.g., free T4, canine thyroid-stimulating hormone
(cTSH), TSH stimulation test] did not differ. Further, weight
loss caused significant decreases in total T3 and cTSH. Thus,
although obesity and subsequent weight restriction may have
some effects on energy balance and thyroid homeostasis, such
changes are unlikely to affect the interpretation of thyroid
function tests.
Hyperlipidemia and dyslipidemia. Limited data exist for
dogs with naturally occurring obesity, and most information was
derived from experimental studies. Published data suggest that
lipid alterations can occur in obese dogs, with increases in
cholesterol, triglycerides, and phospholipids all noted, albeit
often not exceeding the upper limit of the ref erence range (58–
60). M aking laboratory dogs obese by feeding a hyperenergetic
diet was shown to increase plasma nonesterified fatty acid and
triglyceride concentrations by increasing concentrations of
VLDL and HDL, while decreasing those of HDL-C (59). Such
changes were associated with insulin resistance and, interest-
ingly, were also described in insulin-resistant humans. Whether
lipid alterations account for the increased incidence of
pancreatitis in obese dogs requires further studies (61). Thus,
additional work is warranted to assess further the significance of
lipid abno rmalities in dogs.
Orthopedic disorders. Obesity is a major risk factor for
orthopedic diseases in companion animals, especially dogs. An
increased incidence of both traumatic and degenerative ortho-
pedic disorders was reported (14,62). One study reported body
weight to be a predisposing factor in humeral condylar frac-
tures, cranial cruciate ligament rupture, and intervertebral disc
disease in cocker spaniels (63). A recent study in boxers re-
ported a link between neutering and hip dysplasia (64);
although the effect of obesity was not assessed directly in that
study, this association was attributed to an increased incidence
of obesity in neutered dogs. Further, a number of studies
highlighted the association between obesity and the develop-
ment of oste oarthritis (41,42), whereas weight reduction can
lead to a substantial improvement in the degree of lameness in
dogs with hip osteoarthritis (65).
Cardiorespiratory disease and hypertension. Obesity can
have a profound effect on respiratory system function. Most
notably, obesity is an important risk factor for the development
of tracheal collapse in small dogs (66). Obesity can exacerbate
heatstroke in dogs; other respiratory diseases that can be
exacerbated by obesity include laryngeal paralysis and brach-
ycephalic airway obstruction syndrome. Obesity can also affect
cardiac function; increased body weight can result in effects on
cardiac rhythm and increased left ventricular volume, blood
pressure, and plasma volume. The effect of obesity on
hypertension is controver sial in dogs. One study suggested
that obesity was significantly associated with hypertension, but
its effect was only minor (67). In contrast, many experimental
studies utilized the obese dog as a model for the pathogenesis of
hypertension and insulin resistance (68). Obesity may also be
associated with portal vein thrombosis (69) and myocardial
hypoxia (70).
Urinary tract and reproductive disorders. There is evi-
dence from experimental dogs that the onset of obesity is
associated with histologic changes in the kidney, most notably
an increase in Bowma n’s space (as a result of expansion of the
Bowman’s cap sule), increased mesangial matrix, thickening of
glomerular and tubular basement membranes, and an increased
number of dividing cells per glomerulu s (71). Functional
changes were noted in the same study and included increases in
plasma renin concentrations, insulin concentrations, mean
arterial pressure, and plasma renal flow. As a consequence, the
authors speculated that these changes, if prolonged, could
predispose to more severe glomerular and renal injury. An as-
sociation between obesity and some cases of urethral sphincter
mechanism incompet ence (USMI) was reported. Obesity is not
the only risk factor, with ovariohysterectomy (and consequent
lack of sex hormones) itself also playing a major role.
Nevertheless, the effect of obesity is clear in some dogs that
become incontinent only when they become obese. Further,
weight reduction in overweight dogs with USMI can often be
all that is required for continence to be restored. The
mechanisms that predispose obese animals to USMI are not
known, although it was suggested that the effect is purely
mechanical, e.g., increased retroperitoneal fat leading to caudal
displacement of the bladde r (72). The risk of developing
calcium oxalate urolithiasis is also reported to be increased in
obese dogs (73). Finally, obese animal s are reported to suffer
1943SOBESITY IN C OMPANION ANI MALS
by on March 28, 2010 jn.nutrition.orgDownloaded from
from an increased risk of dystocia, likely related to excess
adipose tissue in and around the birth canal (14,74,75).
Neoplasia. In humans, obesity predisposes to a number of
different types of cancer; the International Agency for Research
on Cancer found a signific ant link between obesity and cancers
of the female breast (postmenopausal), colon/rectum, kidney
(renal cell), and esophagus (47). It is estimated that, if this link
is entirely causal, 1 in 7 cancer deaths in both men and women
in the United States might be the direct result of being
overweight or obese (47). Breast cancer is the most common
form of cancer among women (76), and obesity was shown
consistently to increase rates of breast cancer in postmenopau-
sal women by 30–50% (48). An association between mammary
carcinoma and obesity was also reported in some (74) but not
all (77,78) canine reports. Overweight dogs were also reported
to have an increased risk of developing transitional cell
carcinoma of the bladder (79).
Miscellaneous disorders. Obese animals were reported to
be at increased risk of certain dermatologic disorders. Diffuse
scale is commonly observed (especially in cats), most likely due
to a reduced ability to groom efficiently. Animals that are
severely obese can develop pressure sores. Decreased immune
function has also been documented, with obese dogs showing
less resistance to the development of infections (80,81).
Treatment of obesity
In humans, current therapeutic options for obesity include
dietary management, exerc ise, psychological and behavioral
modification, drug therapy, and surgery. Many of these options
are available for companion animals, although it is not ethically
justifiable to consider surgical approaches. Further, to date,
there are no pharmaceutical compou nds licensed for weight loss
in dogs and cats. Dietary therapy forms the cornerstone to
weight management in dogs and cats, but increasing exercise
and behavioral management comprise useful adjuncts.
Dietary management. It is recommended that the weight
reduction protocol be tailor ed toward the individual patient.
Although total energy restriction (starvation) successfully leads
to weight loss, it has the disadvantages of causing excessive
protein (and thus lean body mass) loss and requiring hospital-
ization for proper monitoring (1). Therefore, it is preferable to
use purpose-formulated weight reduction diets, which generally
are restricted in fat and energy, while being supplemented in
protein and micronutrients. Protein supplementation is impor-
tant because the amount of lean tissue lost is minimized even
though the weightloss is not more rapid (82,83). Supplementation
of micronutrients ensures that deficiency states do not arise
(84,85).
Additional dietary factors that may be of ben efit for weight
loss include
L-carnitine supplementation (to maintain lean
mass), conjugated linoleic acid (CLA), and the use of high-fiber
diets (to provide satiety).
L-Carnitine is an amino acid that is synthesized de novo in
the liver and kidneys from lysine and methionine in the
presence of ascorbate. Dietary supplementation of
L-carnitine
improves nitrogen retention, increasing lean mass and reducing
fat mass (86). Incorporation of
L-carnitine at a level of 50–300
ppm, in weight reduction diets, was shown to reduce lean tissue
loss during weight loss (86,87). Possible mechanisms for this
protective effect on lean tissue include enhancing fatty acid
oxidation and energy availability for protein synthesis during
times of need.
CLA is a family of fatty acid isomers derived from linoleic
acid. Various studies in experimental animals suggested that it
has an antiadipogenic effect; proposed mechanisms include
inhibition of stearoyl-CoA desaturase activity, which limits the
synthesis of monounsaturated fatty acids for triglyceride
synthesis, and suppression of elongation and desaturation of
fatty acids into long-chain fatty acids (86). At present, data on
the use of CLA as an antiobesity agent in humans and cats are
conflicting, with the most recent data suggesting the lack of a
significant effect (88,89). Therefore, more information is
required before its use can be recommended. There is also
controversy concernin g the effect of fiber satiety; some reports
suggested that feeding up to 12–16% of dry matter as dietary
fiber has no effect (90–92), whereas other work demonstrated
appetite suppression when 21% of the diet was consumed as
dietary fiber (93).
Lifestyle management. Increasing physical activity is a
useful adjunct to dietary therapy; when used in combination
with dietary therapy, it promotes fat loss (94) and may assist in
lean tissue preservation (95). There is also some evidence that
exercise may help prevent the rapid regain in weight that can
occur after successful weight loss (94). The exact program must
be tailored to the individual and take into account any
concurrent medical concerns. Suitable exercise strategies in
dogs include lead walking, swimming, hydrotherapy, and
treadmills. Exercise in cats can be encouraged by increasing
play activity, using cat toys (e.g., fishing rod toys), motorized
units, and feeding toys. Cats can also be encouraged to ‘‘work’’ for
their food by moving the food bowl between rooms before
feeding, or by the use of feeding toys.
Monitoring of weight loss. In addition to the above
strategies, it is essential that the whole weight reduction
regimen be supervised. This is labor intensive, requires some
degree of expertise and training in owner co unseling, and often
requires a dedicated member of staff. Nevertheless, in the
author’s opinion, correct monitoring is the single most impor-
tant component of the weight loss strategy. A recent study
demonstrated that weight loss is more successful if an organized
strategy is followed with regu lar weigh-in sessions (96). It is
essential to continue to monitor body weight after the ideal
weight has been achieved to ensure that weight that was lost is
not regained; as with humans, a rebound effect was demon-
strated after weight loss in dogs (97).
Summary
Obesity is a growing concern in companion animals, and the
increasing incidence appears to be mirroring the trend observed
in humans. The main medical concern of obesity relates to the
many disease associations that accompany the adiposity. There
is a need to increase awareness within the veterinary profession
that obesity in companion animals is a serious medical concern.
ACKNOWLEDGMENTS
The author thanks Vivien Ryan and Shelley Holden for assistance
with manuscript preparation.
LITERATURE CITED
1. Burkholder WJ, Toll PW. Obesity. In: Hand MS, Thatcher CD, Reimillard
RL, Roudebush P, Morris ML, Novotny BJ, editors. Small animal clinical nutrition,
4th edition. Topeka, KS: Mark Morris Institute. 2000; p. 401–30.
2. Kopelman PG. Obesity as a medical problem. Nature. 2000;404:635–43.
3. Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in
obesity among US adults, 1999–2000. J Am Med Assoc. 2002:288:1723–1727.
4. McGreevy PD, Thomson PC, Pride C, Fawcett A, Grassi T, Jones B.
Prevalence of obesity in dogs examined by Australian veterinary practices and the
risk factors involved. Vet Rec. 2005;156:695–707.
5. Armstrong PJ, Lund EM. Changes in body composition and energy
balance with aging. Vet Clin Nutr. 1996;3:83–7.
1944S SUPPLEMENT
by on March 28, 2010 jn.nutrition.orgDownloaded from
6. Scarlett JM, Donoghue S, Saidla J, Wills J. Overweight cats: prevalence
and risk factors. Int J Obes Relat Metab Disord. 1994;18:S22–8.
7. Burkholder WJ. Precision and practicality of methods assessing body
composition of dogs and cats. Comp Cont Educ Pract. 2001;23:1–10.
8. Stanton CA, Hama DW, Johnson DE, Fettman MJ. Bioelectrical imped-
ance and zoometry for body composition analysis in domestic cats. Am J Vet Res.
1992;53:251–7.
9. Hawthorne A, Butterwick RB. Predicting the body composition of cats:
development of a zoometric measurement for estimation of percentage body fat in
cats [abstract]. J Vet Intern Med. 2000;14:365.
10. Pendergrass PB, Bartley CM, Nagy F, Ream LJ, Stuhlman R. A rapid
method for determining normal weights of medium-to-large mongrel dogs. J Small
Anim Pract. 1983;24:269–76.
11. Laflamme DP. Development and validation of a body condition score
system for dogs. Canine Pract. 1997;22:10–5.
12. Laflamme DP. Development and validation of a body condition score
system for cats: a clinical tool. Feline Pract. 1997:25:13–18.
13. German AJ, Holden SL, Moxham G, Holmes K, Hackett R, Rawlings J. A
simple, reliable tool for owner s to assess the body condition of their dog or cat.
J Nutr. 2006:136:2031S–3S.
14. Edney AT, Smith PM. Study of obesity in dogs visiting veterinary practices
in the United Kingdom. Vet Rec. 1986;118:391–6.
15. Mason E. Obesity in pet dogs. Vet Rec. 1970; 86:612–6.
16. Root MV, Johnston SD, Olson PN. Effect of prepuberal and postpuberal
gonadectomy on heat production measured by indirect calorimetry in male and
female domestic cats. Am J Vet Res. 1996;57:371–4.
17. Harper EJ, Stack DM, Watson TDG, Moxham G. Effect of feeding
regimens on body weight, composition and condition score in cats following
ovariohysterectomy. J Small Anim Pract. 2001;42:433–8.
18. Flynn MF, Hardie EM, Armstrong PJ. Effect of ovariohysterectom y on
maintenance energy requirements in cats. J Am Vet Med Assoc. 1996;209:1572–81.
19. Hoenig M, Ferguson DC. Effects of neutering on hormonal concentrations
and energy requirements in cats. Am J Vet Med Res. 2002;63:634–9.
20. Fettman MJ, Stanton CA, Banks LL. Effects of neutering on body weight,
metabolic rate and glucose tolerance in domestic cats. Res Vet Sci. 1997;62:
131–6.
21. Kanchuk ML, Backus RC, Calvert CC, Morris JG, Rogers QR. Weight gain
in gonadectomized normal and lipoprotein lipase-deficient male domestic cats
results from increased food intake and not decreased energy expenditure. J Nutr.
2003;133:1866–74.
22. Martin L, Siliart B, Dumon H, Backus R, Biourge V, Nguyen P. Leptin,
body fat content and energy expenditure in intact and gonadectomized adult cats:
a preliminary study. J Anim Physiol Anim Nutr (Berl). 2001;85:195–9.
23. Nguyen PG, Dumon HJ, Siliart BS, Backus R, Biourge V. Effects of dietary
fat and energy on body weight and composition after gonadectomy in cats. Am J
Vet Res. 2004;65:1708–13.
24. Goggin JM, Schryver HF, Hintz HF. The effect of ad libitum feeding and
caloric dilution on the domestic cat’s ability to maintain energy balance. Feline
Pract. 1993:21:7–11.
25. Houpt KA, Hintz HF. Obesity in dogs. Canine Pract. 1978;5:54–8.
26. Hart BL, Barrett RE. Effects of castration on fighting, roaming and urine
spraying in adult male cats. J Am Vet Med Assoc. 1973;163:290–2.
27. Houpt KA, Coren B, Hintz HF, Hildernrandt JE. Effect of sex and
reproductive status on sucrose preference, food intake, and body weight of dogs.
J Am Vet Med Assoc. 1979;174:1083–5.
28. Krook L, Larsson S, Rooney JR. The interrelationship of diabetes mellitus,
obesity, and pyometra in the dog. Am J Vet Res. 1960;21:120–4.
29. Kienzle E, Bergler R, Mandernach A. Comparison of the feeding
behaviour of the man-animal relationship in owners of normal and obese dogs.
J Nutr. 1998;128:2779S–82.
30. Kienzle E, Berger R, Ziegler D, Unshelm J. The human-animal relation-
ship and overfeeding in cats [abstract]. Compendium on Continuing Education for
the Practicing Veterinarian. 2000;23:73.
31. Heath S. Behaviour problems and welfare. In: Rochlitz I, editor. The
welfare of cats. Animal welfare, Vol. 3. London: Springer, 2005; p. 91–118.
32. Kolonin MG, Saha PK, Chan L, Pasquani R, Arap W. Reversal of obesity
by targeted ablation of adipose tissue. Nat Med. 2004;10:625–32.
33. Doria-Rose VP, Scarlett JM. Mortality rates and causes of death among
emaciated cats. J Am Vet Med Assoc. 2000;216:347–51.
34. Scarlett JM, Donoghue S. Associations between body condition and
disease in cats. J Am Vet Med Assoc. 1998;212:1725–31.
35. Clutton RE. The medical implications of canine obesity and their relevance
to anaesthesia. Br Vet J. 1988;144:21–8.
36. Van Goethem BE, Rosenweldt KW. Kirpensteijn J. Monopolar versus
bipolar electrocoagulation in canine laparoscopic ovariectomy: a nonrandomized
prospective, clinical trial. Vet Surg. 2003;32:464–70.
37. Weindruch R, Walford RL. The retardation of aging and disease by dietary
restriction. Springfield (IL): Charles C. Thomas Publishers; 1988.
38. McCay CM, Crowell MF, Maynard LA. The effect of retarded growth upon
the length of life span and upon the ultimate body size. J Nutr. 1935;10:63–79.
39. Lane MA, Black A, Ingram DK, Roth GS. Calorie restriction in non-
human primates: implications for age-related disease risk. Anti-Aging Med. 1998;1:
315–26.
40. Kealy RD, Olsson SE, Monti KL, Lawler DF, Biery DN, Helms RW, Lust G,
Smith GK.. Effects of limited food consumption on the incidence of hip dysplasia in
growing dogs. J Am Vet Med Assoc. 1992;201:857–63.
41. 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 Am Vet Med Assoc. 1997;210:222–5.
42. Kealy RD, Lawler DF, Ballam JM, Lust G, Biery DN, Smith GK, Mantz SL.
Evaluation of the effect of limited food consumption on radiographic evidence of
osteoarthritis in dogs. J Am Vet Med Assoc. 2000;217:1678–80.
43. Kealy RD, Lawler DF, Ballam JM, Mantz SL, Biery DN, Greeley EH, Lust
G, Segre M, Smith GK, Stowe HD. Effects of diet restriction on life span and age-
related changes in dogs. J Am Vet Med Assoc. 2002;220:1315–20.
44. Larson BT, Lawler DF, Spitznagel EL, Kealy RD. Improved glucose
tolerance with lifetime restrict ion favorably affects disease and survival in dogs.
J Nutr. 2003;133:2887–92.
45. Lawler DF, Evans RH, Larson BT, Spitznagel EL, Ellersieck MR, Kealy
RD. Influence of lifetime food restriction on causes, time, and predictors of death in
dogs. J Am Vet Med Assoc. 2005;226:225–31.
46. Pittas AG, Joseph NA, Greenberg AS. Adipocytokines and insulin
resistance. J Clin Endocrinol Metab. 2004;89:447–52.
47. Calle EE. Thun MJ Obesity and cancer. Oncogene. 2004;23:6365–78.
48. Arner P. The adipocyte in insulin resistance: key molecules and the
impact of the thiazolidinediones. Trends Endocrinol Metab. 2003;14:137–45.
49. Nelson RW, Himsel CA, Feldman EC, Bottoms GD. Glucose tolerance and
insulin response in normal weight and obese cats. Am J Vet Res. 1990;51:1357–62.
50. Feldhahn JR, Rand JS, Martin G. Insulin sensitivity in normal and diabetic
cats. J Feline Med Surg. 1999;1:107–15.
51. Klinkenberg H, Sallander MH, Hedhammar A
˚
, Feeding, exercise, and
weight identified as risk factors in canine diabetes mellitus. J. Nutr. 2006;136:1985S–
8S.
52. Rand JS, Fleeman LM, Farrow HA. Canine and feline diabetes mellitus:
nature or nurture? J Nutr. 2004;134:2072S–80.
53. Vega GL. Obesity and the metabolic syndrome. Minerva Endocrinol.
2004;29:47–54.
54. Hawkins MA. Markers of increased cardiovascular risk: are we measuring
the most appropriate parameters? Obes Res. 2004;12:107S–14S.
55. Kim SP, Ellmerer M, Van Citters GW, Bergman RN. Primacy of hepa tic
insulin resist ance in the development of the metabolic syndrome induced by an
isocaloric moderate-fat diet in the dog. Diabetes. 2003;52:2453–60.
56. Scott-Moncrief JCR, Guptill-Yoran L. Hypothyroidism. In: Ettinger, SJ,
Feldman EC editors. Textbook of veterinary internal medicine. 5th edition.
Philadelphia: WB Saunders; 2000. p. 1419–28.
57. Daminet S, Jeusette I, Duchateau L, Diez M, VandeMaele I, DeRick A.
Evaluation of thyroid function in obese dogs and in dogs undergoing a weight loss
protocol. J Am Vet Med Assoc Ser A Physiol Pathol Clin Med. 2003;50:213–8.
58. Chikamune T, Katamoto H, Nomura K, Ohashi F. Serum lipid and
lipoprotein concentration in obese dogs. J Vet Med Sci. 1995;57:595–8.
59. Bailhache E, Ouguerram K, Gayet C, Krempf M, Siliart B, Magot T,
Nguyen P. An insulin-resistant hypertriglyceridaemic normotensive obese dog
model: assessment of insulin resistance by the euglycaemic hyperinsulinaemic
clamp in combination with the stable isotope technique. J Anim Physiol Anim Nutr
(Berl). 2003;87:86–95.
60. Diez M, Michaux C, Jeusette I, Baldwin P, Istasse L, Biourge V. Evolution
of blood parameters during weight loss in experimental obese Beagle dogs. J Anim
Physiol Anim Nutr (Berl). 2004;88:166–71.
61. Hess RS, Kass PH, Shofer FS, Van Winkle TJ, Washabau RJ. Evaluation
of risk factors for fatal acute pancreatitis in dogs. J Am Vet Med Assoc. 1999;214:
46–51.
62. 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 Am Vet Med Assoc. 2001;219:1719–24.
63. Brown DC, Coz emius MG, Shofer FS. Body weight as a predisposing
factor for humeral condylar fractures, cranial cruciate rupture and intervertebral
disc disease in Cocker Spaniels. Vet Comp Orthop Traumatol. 1996;9:75–8.
64. van Hagen MA, Ducro BJ, van den Broek J, Knol BW. Incidence, risk
factors, and hereditability estimates of hind limb lameness caused by hip dysplasia
in a birth cohort of boxers. Am J Vet Res. 2005;66:307–12.
65. Impellizeri JA, Tetrick MA, Muir P. Effect of weight reduction on clinical signs
of lameness in dogs with hip osteoarthritis. J Am Vet Med Assoc. 2000;216:1089–91.
66. White RAS, Williams JM. Tracheal collapse in the dog—is there really a
role for surgery? A survey of 100 cases. J Small Anim Pract. 1994;35:191–6.
67. Bodey AR, Mitchell AR. Epidemiological study of blood pressure in
domestic dogs. J Small Anim Pract. 1996;37:116–25.
68. Truett AA, Borne AT, Monteiro MP, West DB. Composition of dietary fat
affects blood pressure and insulin responses to dietary obesity in the dog. Obes
Res. 1998;6:137–46.
69. Van Winkle TJ, Bruce E. Thrombosis of the portal vein in eleven dogs. Vet
Pathol. 1993;30:28–35.
70. Baba E, Arakawa A. Myocardial hypoxia in an obese beagle. Vet Med Sm
Anim Clin. 1984;79:788–91.
71. Henegar JR, Bigler SA, Henegar LK, Tyag S, Hall JE. Functional and
structural changes in the kidney in the early stages of obesity. J Am Soc Nephrol.
2001;12:1211–7.
72. Holt PE. Studies on the control of urinary continence in the bitch [PhD
thesis]. Bristol (UK): University of Bristol; 1987.
73. Lekcharoensuk C, Lulich JP, Osborne CA, Pusoonothornthum R, Allen
TA, Koehler LA, Urlich LK, Carpenter KA, Swanson LL. Patient and environmental
1945SOBESITY IN C OMPANION ANI MALS
by on March 28, 2010 jn.nutrition.orgDownloaded from
factors associated with calcium oxalate urolithiasis in dogs. J Am Vet Med Assoc.
2000;217:515–9.
74. Sonnenschein EG, Glickman LT, Goldschmidt MH, McKee LJ. Body
conformation, diet, and risk of breas t cancer in pet dogs: a case-control study. Am
J Epidemiol. 1991;133:694–703.
75. Glickman LT, Sonnenschein EG, Glickman NW, Donoghue S, Goldschmidt
MH. Pattern of diet and obesity in female adult pet dogs. Vet Clin Nutr. 1995;2:6–13.
76. Spencer E, Key T. Obesity and cancers of the endometrium and breast.
Prog. Obes Res. 2003;9:668–71.
77. Perez Alenza MD, Rutteman GR, Pena L, Beynen AC, Cuesta P. Relation
between habitual diet and canine mammary tumors in a case-control study. J Vet
Intern Med. 1998;12:132–9.
78. Perez Alenza MD, Pena L, del Castillo N, Nieto AI. Factors influencing the
incidence and prognosis of canine mammary tumours. J Small Anim Pract.
2000;41:287–91.
79. Glickman LT, Schofer FS, McKee LJ, Reif JS, Goldschmidt MH.
Epidemiologic study of insecticide exposure, obesity, risk of bladder cancer in
household dogs. J Toxicol Environ Health. 1989;28:407–14.
80. Williams GD, Newberne PM. Decreased resistance to Salmonella
infection in obese dogs [abstract]. Fed Proc. 1971;30:572.
81. Fiser RH, Beisel WR, Rollins JB. Decreased resistance against infectious
canine hepatitis in dogs fed a high-fat ration. Am J Vet Res. 1972;33:713–19.
82. Diez M, Nguyen P, Jeusette I, Devois C, Istasse L, Biourge V. Weight
loss in obese dogs: evaluation of a high-protein, low-carbohydrate diet. J Nutr.
2002;132:1685S–7.
83. Blanchard G, Nguyen P, Gayet C, Leriche I, Siliart B, Paragon BM. Rapid
weight loss with a high-protein low-energy diet allows the recovery of ideal body
composition and insulin sensitivity in obese dogs. J Nutr. 2004;134:2148S–50.
84. Fisler JS. Cardiac effects of starvation and semi-starvation diets: safety
and mechanisms of action. Am J Clin Nutr. 1992;56:230S–4.
85. Weinsier RL, Wadden TA, Ritenbaugh C, Harrison GG, Johnson FS,
Wilmore JH. Recommended therapeutic guidelines for professional weight control
programs. Am J Clin Nutr. 1984;40:865–72.
86. MacIntosh MK. Nutrients and compounds affecting body composition and
metabolism. Compendium on Continuing Education for the Practicing Veterinarian.
2001;23:18–28.
87. Heo K, Odle J, Han IK, Cho W, Seo S, van Heugten E, Pilkington DH.
Dietary
L-carnitine improves nitrogen utilization in growing pigs fed low-energy, fat-
containing diets. J Nutr. 2000;130:1809–14.
88. Desroches S, Chouinard PY, Galibois I, Corneau L, Delisle J, Lamarche
B, Couture P, Bergeron N. Lack of effect of dietary conjugated linoleic acids
naturally incorporated into butter on the lipid profile and body composition of
overweight and obese men. Am J Clin Nutr. 2005;82:309–19.
89. Leray V, Dumon H, Martin L, Siliart B, Sergheraert R, Biourge V, Nguyen
P. No effect of conjugated linoleic acid or garcinia cambogia on fat-free mass and
energy expenditure in normal cats. J Nutr. 2006;136:1982S–4S.
90. Fahey GC, Merchen NR, Corbin JE, Hamilton AK, Serbe KA, Lewis SM,
Hirakawa DA. Dietary fiber for dogs: I. Effect of graded levels of dietary beet pulp
on nutrient intake, digestibility, metabolizable energy and digesta mean retention
time. J Anim Sci. 1990;68:4221–8.
91. Fahey GC, Merchen NR, Corbin JE, Hamilton AK, Serbe KA,
Hirakawa DA. Dietary fiber for dogs: II. Iso-total dietary fiber (TDF) additions of
divergent fiber sources to dog diets and effects of nutrient intake, digestibility,
metabolizable energy and digesta mean retention time. J Anim Sci. 1990;68:
4229–35.
92. Butterwick RF, Markwell PJ. Effect of level and source of dietary fiber on
food intake in the dog. J Nutr. 1994;124:2695S–700S.
93. Jewell DE, Toll PW. Effect of fiber on food intake in dogs. Vet Clin Nutr.
1996;3:115–8.
94. Van Dale D, Sarris WHM. Repetitive weight loss and weight reduction,
resting metabolic rate, and lipolytic activity before and after exercise and/or diet
treatment. Am J Clin Nutr. 1989;49:409–16.
95. Phinney SD. Exercise during and after very low calorie dieting. Am J Clin
Nutr. 1992;56:190S–4.
96. Yaissle JE, Holloway C, Buffington CAT. Evaluation of owner education
as a component of obesity treatment programs for dogs. J Am Vet Med Assoc.
2004;224:1932–5.
97. Laflamme DP, Kuhlman G. The effect of weight loss regimen on
subsequent weight maintenance in dogs. Nutr Res. 1995;15:1019–28.
1946S SUPPLEMENT
by on March 28, 2010 jn.nutrition.orgDownloaded from