Readers' Rating:

Rate this article

Obesity is a condition in which the relative balance between the amount of lean body mass and the amount of fat tissue has been disturbed in such a way as to present larger amounts of fat tissue than may be found normally (Brown, 1989). Usually, this excess of body fat results in a significant impairment of health from a variety of diseases, notably hypertension, atherosclerotic heart disease, and diabetes (Widmaier et al., 2004).

Long-term overeating and underexercise is the main cause of obesity in the dog, but endocrine disease and drugs can also be involved (Clutton, 1988).

The number of obese and overweight people is of growing concern in the human population (Speakman, 2004). Estimates of the incidence of obesity of dogs and cats in the United States are as high as 25% of the dog population (Armstrong and Lund, 1996), and 25 to 40% of the domestic cat population (Sloth, 1992; Scarlett et al., 1994).

It is important to distinguish between obesity and other overweight conditions. Due to the large number of dog breeds, quantitative assessment of obesity is difficult and the judgment is usually subjective. Most authors agree that the best way to assess obesity is to observe and palpate the amount of tissue overlying the rib cage.

Usually obesity is diagnosed if the animal has a mass of fat >25% of total body mass, which is associated with risk to health. While this number is somewhat arbitrary, it has passed the test of time in practice.

In contrast, ‘overweight’ is simply characterized by an excess of mass for the typically normal skeletal size. This extra mass could be bone, as in the case of particularly large-framed persons, or it could be muscle, as in the case of an animal athlete or a hard-working animal. It is unnecessary and pointless to put a non-obese animal on a weight management program (Brown, 1989).


Development of obesity

Sibley (1984) reported that obesity in dogs is developed in two phases: an initial growth phase followed by a static phase. During the initial phase energy intake exceeds utilization and the excess calories are deposited as fat. It is during this phase that the dog gains excess weight. The static phase begins when excess fat has been deposited.

Several separate feedback mechanisms reduce dietary energy intake, but since these feedback controls begin as a result of excess weight, body weight remains constant in the obese state. The amount of food required to maintain an animal in the obese state is no greater than that required for animals at normal body weights.

Sibley (1984) stated that during the initial phase, overeating is thought to be the cause of the energy imbalance, although reduced energy utilization may also play a large role.

This latter effect has been shown to occur in both man and animals on moderate to low levels of exercise, where a further reduction in activity is not associated with a reduction in food intake. A positive energy balance with subsequent obesity occurs.

The number and size of adipocytes in the body are another important factor. Adipocyte numbers can increase if obesity is initiated during growth. Once fully grown, however, an adult will retain a specific number of adipocytes throughout life. Subsequent weight gain or loss does not alter the number of fat cells, merely the size of them (Sibley, 1984; Machado, 2002).

Clutton (1988) classifies obesity as uncomplicated or complicated. Uncomplicated obesity results from overeating, and is associated with underexercise. Complicated obesity results from other causes, such as hypothyroidism.


UNCOMPLICATED OBESITY

A breakdown of the usual energy requirement for most mammals follows: 50–60% basal energy, 10–12% heat increment and 30–40% activity. In obese animals and people, the relative amount of energy spent on activity is diminished (3–5%).

The metabolic basis for uncomplicated obesity is the first law of thermodynamics: energy is neither created nor destroyed, but only transformed (Pi-Sunyer, 1988) — in this case into stored fat. Obesity results when those stores become sufficiently large. Very little surplus energy is needed on a constant daily basis to cause obesity.

In human food, for example, the standard slice of bread contains about 75 kcal. If a person eats one slice of bread per day surplus to needs for one year, that person will gain about 4.5 kg. In the case of animals, a surplus in daily energy intake as small as 1% more than required can result in a weight increase of some 25–30% by mid-adulthood (Brown, 1989).

Sibley (1984) reported that a series of factors contributes to uncomplicated obesity: age, gender, sexual integrity, and breed. Females are more likely to be overweight than males, while neutering predisposes both sexes to obesity.

Furthermore, it can be postulated that the absence of the anabolic hormone testosterone in castrated males may result in decreased amino acid deposition in muscle protein, with more energy going into fat. In the spayed female, it was suggested that high follicle-stimulating hormone (FSH) levels may have a role in causing a higher incidence of obesity. In both dogs and bitches, the tendency to become obese increases with age.

Obesity is strongly influenced by heredity. For example, human identical twins that have been separated soon after birth and raised in different households manifest strikingly similar body weights as adults (Widmaier et al., 2004). Clutton (1988) indicated that Cairn Terriers, Cocker Spaniels, Labradors and Collies are more likely to be obese than other breeds.

However, studies with animal models and human populations indicate that environmental factors, which should, in theory, be alterable, can also play important roles. Overeating in the obese-prone animal can be highly responsive to taste, but minimally responsive to the sensation of satiation. The animal may, therefore, overeat tasty food beyond physiologic requirements and undereat less appealing foods, whereas the non-obese animal will be much less selective in the types of food eaten (Sibley, 1984).

Studies conducted with rats have shown that non-obese animals became obese when fed a diet of snack foods from the supermarket (Widmaier et al., 2004). Like people, a significant number of pets become overweight, especially if they are inactive and are fed fatty or sweet snacks by well-meaning owners. Such foods contain inadequate amounts of protein, vitamins, enzymes, and other essential nutrients.

Because of a lack of the nutrients needed, the animal develops excessive cravings. The same thing can happen as a result of feeding poor quality commercial diets (Pitcairn and Pitcairn, 2005). Client-related factors also influence pet physique. Dogs owned by the elderly or the overweight, are more likely to be fat; and socioeconomic factors may also influence the incidence of canine obesity (Sibley, 1984).


COMPLICATED OBESITY

In some animals, obesity can result from disturbances in metabolism that cause an almost uncontrollable hunger that is very difficult to manage. In addition to the weight-loss program outlined below, such animals may need specific treatment to correct the underlying imbalance. Nevertheless, the role of endocrinologic disease in the incidence of canine obesity is probably minor. Diagnostic tools used to evaluate the obese dog are presented in Table 1.


Table 1. The differential diagnostic investigation in the obese dog.


Clutton (1988)


Examining hypothyroidism, Sibley (1984) concluded that it is a relatively common canine disease in which obesity frequently occurs. In one study of 62 hypothyroid dogs, 11 were diabetic. The author reported that dogs exhibited lethargy, lack of endurance, and increased sleeping. This pattern is usually accompanied by a gradual slowing of mental activity including reduced alertness and excitability, and a lack of interest in familiar activities.

The obese dog becomes lazy, but remains very alert and responsive to stimuli. A slow heart rate, reduced body temperature, and a preference for warm places are also often seen in cases of canine hypothyroidism.

Presumptive diagnosis can be confirmed by laboratory analysis of plasma T₄ concentrations. Several factors contribute to hypothyroidism, the conversion of thyroxin (T₄) into triiodothyronine (T₄), the thyroid hormone active form, being one of them. The conversion of T₄ into T₄ depends on an enzyme (deiodinase) that requires selenium as a cofactor. Edens (2001) has shown that broilers fed organic selenium (Sel-Plex®, Alltech Inc.) convert T₄ into T3 more efficiently than birds fed inorganic selenium.

Rand et al. (2004) examined diabetes mellitus in dogs and cats. They reported that there is evidence for the role of genetic and environmental factors in feline and canine diabetes.

Type 2 diabetes is the most common form of diabetes in cats. Evidence for genetic factors in feline diabetes includes the overrepresentation of Burmese cats with diabetes.

Environmental risk factors in domestic cats include advancing age, obesity, male gender, neutering, drug treatment, physical inactivity, and indoor confinement. High carbohydrate diets increase blood glucose and insulin levels and may predispose cats to obesity and diabetes. Low carbohydrate, high protein diets may help prevent diabetes in cats at risk, such as obese cats or lean cats with underlying low insulin sensitivity. Lutz and Rand (1993) indicated that obesity is a frequent concomitant problem in feline diabetes and contributes to the insulin resistance characteristic of the disease.

In a review, Atkins et al. (1988) indicated that naturally acquired canine diabetes mellitus generally is considered a disease of aged dogs, with the highest incidence observed between 5 and 12 years and median and peak ages of 8 to 9 years, respectively. Estimates revealed an incidence of 1:800. Females are afflicted approximately twice as frequently as males and an association between diabetes and obesity has been observed. There is no recognized predilection for purebred dogs, although Dachshunds, Rottweilers, Poodles, and Miniature Schnauzers have been overrepresented in some studies.

The cause of diabetes in dogs often is unknown, but the disease most commonly is associated with pancreatic necrosis secondary to chronic, relapsing exocrine pancreatitis. Other causes or concomitant conditions suspected of causing or contributing to diabetes include hereditary islet ß-cell hypoplasia, neoplastic pancreatic destruction, iatrogenic and naturally acquired endocrinopathies, obesity, and possibly, anti-islet cellular and humoral factors. It is important to point out that according to Rand et al. (2004), there are no published data showing that overt type 2 diabetes occurs in dogs or that obesity is a risk factor for canine diabetes. However, Pitcairn and Pitcairn (2005) stated that obese pets have a much harder time with this disease.

Evidence exists for a genetic basis and altered immune response in the pathogenesis of canine diabetes. At least 50% of diabetic dogs have type 1 diabetes based on present evidence of immune destruction of ß-cells. Extensive pancreatic damage likely from chronic pancreatitis, causes approximately 28% of canine diabetes cases. Environmental factors such as feeding of high-fat diets are potentially associated with pancreatitis and likely play a role in the development of pancreatitis in diabetic dogs. Diabetes diagnosed in a bitch during either pregnancy or diestrus is comparable to human gestational diabetes (Rand et al., 2004).

Traditional diabetes treatment consists of strictly regulating sugar intake and using daily injections of insulin. Pitcairn and Pitcairn (2005) suggest several more dietary guidelines:

• Restrict feeding to canned food fed once a day, about 12 h after insulin is given (when its activity is highest).

• Feed the diabetic dog fresh and raw natural food diet two or three meals during the day, rather than one large one.

• Avoid the soft, moist dog foods that are very high in carbohydrates.

• Use glucose tolerance factor (GTF), a natural chromium (+3)-containing substance found in yeast such as Bio-Chrome™ (Alltech Inc.). As GTF is the cofactor for insulin, adequate amounts can assist the body in using blood glucose more effectively.

The authors point out that they always recommend supplementing the natural food diet with this element. They also recommend yeast to diabetic pets. Possible roles for organic selenium (e.g., Sel-Plex®) or nucleotides and inositol (e.g., NuPro®) are yet to be explored.

• Supplementation of vitamin E (25 IU to 200 IU/d) is recommended, because it reduces the need for insulin.

• A regular exercise program is recommended, as it reduces insulin needs. Note that an erratic exercise pattern can destabilize insulin needs, thus exercise regularity is important.

In more severe cases of diabetes, Pitcairn and Pitcairn (2005) recommend further reducing the stress placed on the pancreas by strict avoidance of foods that contain sugar as well as keeping fat intake low (because the pancreas produces a number of enzymes particularly involved in breakdown of fat).

Data from poultry indicate an important role of selenium in the integrity of the pancreas, which produces lipase (Leeson and Summers, 2001). Organic selenium (Sel-Plex®) is better retained in several organs in the body (Surai, 2002) than is selenium from inorganic sources. Because improved selenium retention occurs in the pancreas, it can be hypothesized that Sel-Plex® may play an indirect role in improving diabetic animal condition.

Cats, being natural carnivores, will sometimes recover from diabetes if they are fed large amounts of fresh meat and avoid significant amounts of grain and vegetables (small amounts OK). A diet of mostly meat with a pinch of bone meal added to each meal can make a huge improvement in diabetic condition after just for a few weeks (Pitcairn and Pitcairn, 2005).


The consequences of obesity

Excessive body fat results in a series of consequences affecting several bodily organs. Edney and Smith (1986) concluded that only grossly obese dogs are prone to circulatory disease, and that age is more important in influencing the incidence of cardiovascular disease in the moderately obese dog. Fatty infiltration of the myocardium is said to occur in the obese dog (Sibley, 1984), and causes a reduction in ventricular performance and predisposes to dysrhythmias (Albrink, 1971). Furthermore, respiratory problems (Fadell et al., 1962), secondary polycythemia (Fisher et al., 1975) and locomotor pathology (Sibley, 1984) have been linked to obesity.


Managing obese pets

Management of obese pets calls for elimination of excess fat, which strains the heart, makes circulation sluggish, seriously complicates other disorders, and probably contributes to a shortened life span. Attempts to overcome one’s genetic legacy are difficult to sustain, so although most calorie-restricted diets are successful in the short term, they are usually unsuccessful in the long term (Speakman, 2004).

It should be remembered that an energy deficit of over 7500 kcal is required to lose 1 kg fat. Even in medium-sized dogs, 1 kg can represent a fairly high proportion of body weight. Initial weight loss will, therefore, not be as dramatic as in humans.

According to Pitcairn and Pitcairn (2005), the basic weight-loss program for pets involves three principles:

1. Increase activity levels. Take the dog for daily walks and runs. Encourage the cat to play. Increased activity raises the metabolic rate and burns calories faster. Exercise has proven to be a valuable element in any weight loss program. The exercise itself utilizes calories, although relatively few, and usually does not stimulate appetite in obese individuals. More importantly, exercise partly offsets the tendency for metabolic rate to decline during long-term caloric restriction and weight loss. Also, the combination of exercise and diet causes the animal to lose a relatively larger proportion of fat to protein than with diet alone. Care must be taken, however, if the obesity is complicated by congestive heart failure or skeletal problems.

2. Resist the temptation to feed extra snacks and treats. At most, an obese but begging pet ought to receive only modest amounts of the following: lean meat, carrots or other vegetables, apples, and raw bones.

3. Feed a highly nutritious, low-fat, high bulk diet that provides about two-thirds of the calories needed to maintain the animal’s ideal weight. Although low in fat, it must be high in protein, enzymes, vitamins and minerals. Include plenty of bran or vegetables to help fill the stomach and minimize begging. This type of diet helps the animal lose weight gradually and safely, while ensuring sufficient basic nutrients. A daily vitamin-mineral pet supplement should be included in the diet.


References

Albrink, M.J. 1971. Cecil-Loeb Textbook of Medicine (P.B. Beeson ad W. McDermott, eds). 13th ed. W.B. Saunders, London, pp. 1452.

Armstrong, P.J. and E.M. Lund. 1996. Changes in body composition and energy balance with aging. Vet. Clin. Nutr. 3:83-87.

Atkins, C.E., P.M. LeCompte, H.P. Chin, J.R. Hill, C.L. Ownby and M.S. Brownfield. 1988. Morphologic and immunocytochemical study of young dogs with diabetes mellitus associated with pancreatic islet hypoplasia. Am. J. Vet. Res. 49:1577-1581.

Brown, R.G. 1989. Dealing with canine obesity. Can. Vet. J. 30:973-975.

Clutton, R.E. 1988. The medical implications of canine obesity and their relevance to anesthesia. Br. Vet. J. 144:21-28.

Edens, F. 2001. Involvement of Sel-Plex® in physiological stability and performance of broiler chickens. In: Science and Technology in the Feed Industry. Proceedings of Alltech’s 17th Annual Symposium (T.P. Lyons and K.A Jacques, eds). Nottingham University Press, UK, pp. 349-376.

Edney, A.T.B. and P.M. Smith. 1986. Study of obesity in dogs visiting veterinary practices in the United Kingdom. Vet. Rec. 118:391-396.

Fadell, E., J. Richman, A.D., W.W. Ward and J.R. Hendon. 1962. Canine obesity. New England J. Med. 266:861.

Fisher, A., T.D. Waterhouse and A.P. Adams. 1975. Secondary polycythaemia. Anaesthesia 30:633-637.

Leeson, S. and J.D. Summers. 2001. Nutrition of the Chicken. 4th ed. University Books, Guelph, Canadá, pp. 482.

Lutz, T.A and J.S. Rand. 1993. A review of new developments in Type 2 diabetes in human beings and cats. Br. Vet. J. 149:527-536.

Machado, C.R. 2002. Crescimento do Tecido Adiposo. In: Fisiologia Aviária-Frangos de corte (M. Macari, R.L. Furlan and E. Gonzales, eds). Second ed. Funep/FAPESP, Jaboticabal, Brazil, pp. 299-311.

Pi-Sunyer, X. 1988 . Obesity. In: Modern Nutrition in Health and Disease (M.E. Shils and V.R. Young,eds). 7th ed. Philadelphia: Lea & Febiger, pp. 795-816.

Pitcairn, R.H. and S.H. Pitcairn. 2005. Natural Health for Dogs and Cats. 3rd ed. Rodale, USA, pp.466.

Rand, J.S., L.M. Fleeman, H.A Farrow, D.J. Appleton and R. Lederer. 2004. Canine and feline diabetes mellitus: Nature or nurture? J. Nutr. 134:2072S-2080S.

Scarlett, J.M., S. Donoghue, J. Saidia and J. Wills. 1994. Overweight cats: prevalence and risk factors. Int. J. Obes. Realt. Metab. Disord. 18(Suppl. 1):S22-S28.

Sibley, K.W. 1984. Diagnosis and management of the overweight dog. Br. Vet. J. 140:124- 131.

Sloth, C. 1992. Practical management of obesity in dogs and cats. J. Small Anim. Pract. 33:178-182.

Speakman, J. 2004. Obesity: The integrated roles of environment and genetics. J. Nutr. 134:2090S-2105S.

Surai, P. 2002. Natural Antioxidants in Avian Nutrition and Reproduction. 1st ed. Nottingham University Press, UK, pp. 615.

Widmaier, E.P., H. Raff and K.T. Strang. 2004. Human Physiology. 9th ed. McGraw Hill. Boston, USA, pp. 825.

Readers' Rating:

Rate this article