Feeding cats for health and obesity management (Proceedings)


Cats are obligate carnivores. This statement is news to no one, and yet we often dont recognize the importance of that statement or feed them accordingly.

Feline nutrition

Cats are obligate carnivores.  This statement is news to no one, and yet we often don't recognize the importance of that statement or feed them accordingly.  While cats can use carbohydrates (CHO) as a source of metabolic energy, they have no requirement for them (nor do dogs for that matter).  But, more importantly, because cats evolved consuming prey (e.g. high protein, low to moderate fat, minimal carbohydrate), they are metabolically adapted for higher protein metabolism and lower CHO utilization.  What does that mean metabolically and nutritionally?  There are a number of specific metabolic and biochemical differences in feline physiology that are important.  For those who are interested in the specific details of these metabolic and physiologic differences in the nutritional biochemistry of cats, the reader is referred to several recent reviews on this subject.  This paper will discuss several important medical problems in cats that may be directly linked to, or may be specifically managed by, dietary manipulation.

Feline obesity

The primary reason for development of obesity in any animal is that they are consuming more energy than they are expending.  This can occur when a cat has excessive dietary intake of calories (food or treats) or when there is a reduction in energy expenditure (reduced activity, illness or injury resulting in less exercise, etc).    In indoor cats, reduced energy expenditure is a very important problem, and this is compounded by the fact that it is not easy to increase energy expenditure in cats like dogs with directed exercise.  Additionally, because many cat owners prefer to feed free choice dry food, the risk of overfeeding, even in very small amounts is very high.  In either case, the primary reason that weight gain occurs in cats is that they have a positive energy balance and this must be changed to affect weight loss.  In both dogs and cats, neutering is an important risk factor due to the hormonal changes that occur that result in changes in levels of leptin, progestins, and other hormones that result in increased appetite, and reduced energy metabolism and metabolic rate.  The key factors for prevention of obesity in neutered animals appears to be careful control of intake immediately after neutering (no free choice feeding, reduction of intake by 25% to account for the hormonal changes resulting in reduced energy needs), and close monitoring of body weight and BCS to allow adjustments in intake if needed.  In addition, because feeding our cats is a social interaction, feeding and food interaction with the cat can become a daily social interaction that can become a problem resulting in overfeeding and inappropriate food intake patterns.  It has been shown that in households where the owners are health conscious (conscious of diet and nutrition, who exercise regularly, and watch their own weight) they tend not to have obese pets (except where free choice feeding is used).  Thus, there are clearly human behavioral and “food is love” issues that have to be considered in the development of obesity, and these must be addressed for successful weight control to be achieved.

The importance of obesity as a disease

Obese humans generally do not live as long as their lean counterparts, and are much more likely to suffer from obesity-related diseases such as type II diabetes, coronary artery disease, osteoarthritis, hypertension, and some cancers.  Dogs and cats are susceptible to the same detrimental effects, including decreased longevity, and development of a variety of disorders that are associated with being obese.  In a recent study, dietary calorie restriction was clearly shown to increase longevity in a group of 24 Labrador retrievers.  In that study, the dogs in the energy restricted group were fed 75% of their counterparts, and the dogs lived an average of two years longer and had a reduced incidence of hip dysplasia, osteoarthritis and glucose intolerance.  A similar study has not be performed in cats, but there is a clear difference in morbidity in obese cats compared to their lean counterparts. 

In order to understand the role of obesity in disease development, it is necessary to first understand the role of adipose tissue in energy balance and metabolism. The expansion of adipose tissue was long thought to be simply a depot for the deposition of fatty acids (triglycerides) that occurred because of the excess energy intake.  However, research in the past decade has revealed that adipose tissue is not just a storage site, but also is responsible for production of many key hormones (e.g. leptin) involved in energy balance and a variety of other processes.  Leptin was first identified in 1994 and its discovery opened the door to a whole new world of understanding about white adipose tissue that continues to this day.  Leptin is an inhibitor of food intake – primarily through suppression of neuropeptide Y and orexin in the brain, and plays a role in the regulation energy expenditure.  In obese mice that lack leptin or have leptin resistance, appetite suppression mechanisms are non-functional and energy metabolism abnormal.  However, despite the importance of leptin in appetite suppression and energy expenditure, it is not the “silver bullet” of obesity management:  simply replacing leptin does not result in weight loss or changes in the metabolism of obese animals.   Further research in recent years has elucidated an entire list of adipokines secreted by fat cells.  These adipokines are involved in a wide variety of metabolic and physiologic, as well as inflammatory changes that are implicated in the pathophysiology of obesity.  Why did it take so long to understand the importance of fat cells in disease?  The key reason is their apparent simplicity – in histologic appearance as well as metabolically – that belied their important role in energy metabolism and as an endocrine organ.  Adipose tissue is a major secretory organ – and does not just release fatty acids during fasting – the tissue also releases a wide variety of lipid based moieties:  cholesterol, retinol, steroid hormones and prostaglandins.  However, fat cells also secrete many pro-inflammatory cytokines (e.g. tumor necrosis factor alpha was the first to be discovered), including interleukins (IL-1, IL-6, IL-10), chemokines (such as monocyte chemoattractant protein -1), proteins involved in hemostasis (platelet activator inhibitor -1) and blood pressure (angiotensinogen).  What does this mean for the obese cat?  Obesity is a metabolic disease that results in major changes in appetite control, energy expenditure, and induces a chronic, low-grade, pro-inflammatory state that may be responsible for many of the diseases associated with increased body weight.  The interested reader is directed to large number of recent reviews on this subject for additional details, as this area of research is rapidly changing as we seek to better understand obesity as a disease.

There are a number of diseases in dogs and cats are reported to be associated with obesity, including orthopedic diseases, diabetes, heart disease, abnormal circulating lipids, certain cancers, urethral sphincter mechanism incompetence, dyspnea due to compromised ability to breathe (e.g. laryngeal paralysis, brachycephalic syndrome, tracheal collapse etc), heat intolerance, decreased immune function, and dystocia to name just a few.  Further, we do not have a complete understanding of the inflammatory role of obesity hormones in our pets, and this could lead to an even greater connection between obesity and disease.


Obesity and diet   

While figures vary, recent studies indicate that greater than 35% of cats in the United States are obese.  There are a large number of factors that contribute to this problem, including sex (intact vs. neutered, male vs. female), age, activity (indoor vs. outdoor), and feeding style (meal feeding vs free choice).  Further, “it is much harder to take it off, than it is to put it on” – as we are all very aware.  One factor that is that is important to consider, both in the development of and treatment of obesity, is the role of protein in diet.  Because of the metabolic requirement for cats to utilize protein as an energy source,  higher CHO in the diet means that the diet will be lower in protein, and carb that are not immediately used for energy (e.g. via exercise or other utilization for energy) will be stored as fat.   Traditional weight loss plans include feeding an energy restricted (e.g. low fat, high CHO, high fiber) diet.  However, while these diets may result in “weight loss”, they do so to the detriment of lean body mass – the lost weight is muscle not fat.  This is important because when muscle mass is lost, metabolic rate decreases due to the catabolic signals sent to the brain – that means the cat will actually now need to eat even less to lose weight than before. This is because cats use protein for energy even in the face of other energy sources in the diet, and during weight loss when calorie intake must be severely restricted the chance for protein restriction to result in protein deficiency is increased.  Successful weight loss requires loss of adipose tissue as well as maintenance of lean body mass, as lean body mass is the driver of basal energy metabolism (loss of lean body mass is a major contributor to weight regain as appetite is not reduced and satiety not reached).   Several recent studies have evaluated use of a high protein, low CHO diet (protein 45% or higher) for weight loss in cats, and in those studies, all cats lost weight, but maintained lean body mass.  Importantly, high protein, low carbohydrate diets not only result in sustained weight loss in these cats, but also in normalization of appetite (reduced urge to eat constantly because they are satiated).   Because dry foods must be extruded (i.e. made into a biscuit), CHO are required in the cooking process, and thus, it is difficult to achieve a very low CHO diet that is dry.  Further, many of the available high protein, low CHO dry foods are NOT low calorie, so it is extremely easy to feed too much.  Too many calories, including too many protein calories, will also cause weight gain or failure to lose as well.  At this time, the best commercial diets for achieving a high protein, low CHO profile, along with controlled calories, are canned (both kitten and many adult foods are acceptable) foods. 

Calculating calories:  Most indoor cats do not need more than their resting energy requirement (RER) to meet their daily nutritional requirements (this is approximately 180-200 kcal/day for a 10-11 # cat).  Cats that are very obese will likely need to reduce their intake by 20-40% (or 60-80% of RER) to lose weight.  So, for a cat that is 16 lb (7.5 kg) that should weigh 11 lb (5 kg) it may require a reduction of calories to near 120-130 kcal/day.   For EXAMPLE:  canned food = 165 kcal/can, while high protein dry foods are usually > 500-600 kcal/cup – thus, it is much more difficult to reduce calories using the dry food.  The key point is this:  set a target calorie intake, then weigh the cat monthly, and adjust the amount of food based on weight loss.  The goal is for 1% weight loss per week or 3-4% per month – and if this goal is not being achieved, a reduction in calories (10-20%) must be done to meet the weight loss goals. 

Key Points

The commercially available diets lowest in CHO are canned foods.  It is important to remember that just because you are feeding a canned food, it does mean that you are feeding a high protein, low CHO diet (you must read the label) and it also doesn't mean you are feeding a high quality protein (low quality protein in foods can cause fecal odor and diarrhea due to poor digestibility).  Most cats should be fed some (50% is a starting point) canned food as part of their diet throughout their life – both to reduce the CHO in their diet, but also to better control calories (dry foods are very calorie dense), and to increase the amount of water consumed daily.   Furthermore, eating canned food is a learned behavior – if canned food is part of a kittens diet, they will more readily eat canned food as an adult (e.g. when they need canned food for urinary disease or renal disease later in life).  An important follow up point to remember about all diets is that calories count.  You cannot free choice feed most indoor cats – even with high protein, low carb diets – because if they consume too many calories (and the diabetes diets are very calorie dense) they will become or remain obese. Also, calorie control must be started when they are kittens as obesity starts in young adults due to the above mentioned issues with neutering and energy intake. 

The key point for obesity prevention (or correction) is balancing the energy intake / energy expenditure equation.  In indoor cats, where exercise is reduced by the nature of the lifestyle, energy restriction becomes paramount to obesity prevention or correction.  Energy restriction can be achieved by low fat high fiber diets, but many of these diets are not high enough in protein to preserve muscle and result in loss of muscle mass first, then eventually they will lose fat mass, resulting in an unhealthy weight loss and a strong tendency to regain weight (muscle mass loss will always increase the likelihood of yo-yo weight effects or failure of weight loss).  High protein, low carb, low fat diets are ideal for weight loss in cats because they preserve muscle mass while restricting energy sources that will induce fat loss.  However, portion control is ultimately the key to controlling energy intake – and the easiest way to achieve portion control is to feed canned food.  In cats that won't eat canned food, there are only a few high protein, low fat, low carb dry foods – but these should be selected for use in weight loss programs if at all possible.

Table 1.   Cats and nutrition:  some key nutritional differences 

  • Cats have an obligate need for protein and amino acids in their daily diet because they are unable to down regulate their urea cycle or transaminases (protein conversion to energy) as other species can in times of starvation. 

  • Cats utilize protein for energy, even in the face of large amounts of CHO in the diet

  • Taurine, arginine, methionine, cysteiine, and possibly carnitine requirements for cats are greater than non-carnivores

  • Arachidonic acid is also an essential fatty acid in cats (it is not in dogs), and is found only in fats from animal tissue

  • Cats require vitamin A and D to be present in the active form in their diet as they are unable to synthesize adequate amounts from other dietary precursors (e.g. carotenoids or vitamin D precursors in skin)

  • Cats have an increased need for many B vitamins in their diet (e.g. thiamin, pyridoxine, niacin, pantothenic acid) as they have greater metabolic needs for these vitamins and cannot synthesize or get them from other sources.

  • Salivary amylase is absent in cats, and they have greatly reduced levels of intestinal and pancreatic amylases – so CHO digestion is much less efficient.

  • Cats have fewer disaccharidases and other brush border enzymes in their small intestine designed to digest and absorb starches.

  • The small intestine of cats is much shorter than that of an equally sized omnivore – longer GI tracts are necessary for handling of complex carbohydrates.

  • Cats have greatly reduced activities of hepatic enzymes (e.g. glucokinase) designed to convert a post prandial glucose load to glycogen and thus are less able to handle this glucose load. 

  • There are no fructokinases in cats – they are unable to utilize fructose and other simple sugars.
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