The concept that diet contributes to health has been around for almost 2 centuries. In 1826 the french lawyer and politician Jean Anthelme Brillat-Savarin coined the aphorism: “Tell me what you eat and I will tell you what you are”. A few decades later, in an essay titled Concerning Spiritualism and Materialism in 1863, the german philosopher and anthropologist Ludwig Andreas Feuerbach wrote: "man is what he eats”. Promotion of the concept in the english language awaited the publication of “You Are What You Eat: how to win and keep health with diet" by Victor Lindlahr the creator of the catabolic diet, in 1942. In 1990, even Jim Davis, the creator of Garfield, weighed in with his support for the concept.
The Carnivore Connection to Nutrition in Cats
While there are numerous papers discussing the connection between feline nutrition and health, few are as good as "The carnivore connection to nutrition in cats" by Dr. Debra L. Zoran of the College of Veterinary Medicine at Texas A&M University. In this article Dr. Zoran notes that "although cats have adjusted to most manufactured diets, the limitations of substituting animal-origin nutrients with plant-origin nutrients in foods formulated for cats are being increasingly realized.”1 In this same article Dr. Zoran points out how diets with inappropriate amounts of carbohydrates and plant based protein are likely responsible for obesity, hepatic lipidosis (fatty liver syndrome), inflammatory bowel disease and diabetes in cats.
Carbohydrates – “Junk food” for cats
Lets face it, cats are obligate carnivores. That means they have evolved to get certain nutrients from their natural diet of muscle meat, various organs and incidentals like bones. Unlike omnivorous species including dogs and man, cats simply can not produce adequate quantities of a number of amino acids (e.g., taurine). To remain healthy, cats need to consume a diet relatively high in protein. Indeed, adult cats require 2 to 3 times more protein in their diet than adults of omnivorous species.2, 3 By comparison carbohydrates represent the one component of the diet for which there is absolutely no minimum daily requirement. The function of the cat's digestive apparatus reflects their minimal utilization of carbohydrates. Cats do not produce the enzyme responsible for initiating carbohydrate digestion called amylase in their salivary glands.4, 5 In addition, cats also have low activities of intestinal and pancreatic amylase and reduced activities of the intestinal enzymes called disaccharidases, that break down carbohydrates in the small intestines.4, 5 In their natural habitat, cats consume prey high in protein with moderate amounts of fat and minimal amounts of carbohydrate; thus, they are metabolically adapted for higher metabolism of proteins and lower utilization of carbohydrates than dogs or other omnivores.1 Most commercial diets for cats are formulated with a mixture of animal- and plant-derived nutrients, most commonly in dry kibble form that requires carbohydrates for the expansion and cooking process. The unique physiologic requirements, read “obligate carnivore”, of cats makes carbohydrates in virtually any form the equivalent of "junk food" for cats.
Take away message: Cats have not evolved to eat a diet high in carbohydrates. Most cats should eat a wet food diet with limited carbohydrate content (carbohydrate < 15% on a dry-matter basis).
Obesity – When “Less is more”
While hyperthyroidism is regularly referred to as the most common endocrine disease in the cat, obesity is actually a more common endocrine (and nutritional) disorder of cats in the United States. A previous study from 1994 estimated that 25 to 33% of cats were overweight or substantially obese at that time.6 A more recent study from 2005 reported a continued increase in the incidence of obesity in cats to between 25% to 40%, depending on the study type and sources.7 The pathophysiology of obesity includes chronic hyperinsulinemia secondary to inappropriate caloric (especially carbohydrate) intake. Hyperinsulinemia leads to obesity because of insulin's potent induction of lipogenesis, the conversion of glucose into the fatty acids that ultimately become fat. The chronically elevated levels of insulin that occur with hyperinsulinemia lead to persistent lipogenesis and the ongoing production of fat. Simply put, carbohydrate intake leads to insulin release which leads to fat accumulation. Because of the association between obesity and hyperinsulinemia, obesity is actually a form of endocrine disease.
Regardless of the cause, obese cats have many health issues, such as development of diabetes mellitus, joint disturbances or lameness, feline lower urinary tract disease, hepatic lipidosis, and nonallergic skin conditions. While limiting calories plays an important role in the avoidance of the weight gain that leads to obesity, the form of those calories is probably even more important. Diets high in carbohydrates stimulate regular spikes in circulating insulin levels that lead to the storage of circulating fatty acids in adipose (fat) tissue. This process is a major factor in the weight gain that leads to obesity. Because protein and fat consumption lead to relatively minor fluctuations in insulin, low carbohydrate diets are optimal for avoiding weight gain and/or promoting weight loss. Canned foods are generally the best choice when seeking to provide a high-protein, low-carbohydrate diet. Dry foods tend to be energy (read calorie) dense. Also, because starch is necessary to make the kibble, dry foods tend to have greater carbohydrate concentrations (carbohydrate > 25% on a dry-matter basis).
Take away message: To avoid obesity or achieve weight loss in a cat with obesity, feed a wet food diet with limited carbohydrate content (carbohydrate < 15% on a dry-matter basis).
Diabetes – “How sweet it is”
Insulin is a very potent hormone produced by the beta cells of the pancreas. Insulin is released into the blood stream in response to increasing levels of sugar (i.e., glucose) that follow consumption of a meal, especially meals high in the complex sugars we call carbohydrates. Insulin's job is to control the level of glucose in the blood stream. Insulin's role in health is critical as excessive glucose levels, as occur with untreated diabetes mellitus, are toxic. Insulin release is triggered by increases in the glucose level in the blood. In response to increasing levels of insulin in the blood, glucose is removed from the blood stream and stored in the form of either glycogen in muscle and liver tissue, or fatty acids in adipose (fat) tissue. Elevated levels of insulin in the blood stream called hyperinsulinemia occur following the consumption of many forms of carbohydrate. Persistently elevated levels of insulin in the blood stream ultimately lead to down-regulation of the insulin receptors causing insulin resistance that if untreated often progresses to type II diabetes. Because of insulin's potent induction of fat storage, hyperinsulinemia is also a potent cause of obesity.
Very different than their omnivorous canine housemates, the majority of cats with diabetes have type 2 diabetes. This form of diabetes is highly associated with obesity frequently caused by excessive carbohydrate consumption. One recent study reported that feeding typical adult maintenance diets to cats resulted in development of greater postprandial hyperinsulinemia, even in cats with normal body weights, compared to cats consuming a high-protein diet.8 This study supported the concept that persistent hyperinsulinemia may lead to obesity in cats consuming typical maintenance (high-carbohydrate) diets.8 Another study found that high-protein, low-carbohydrate diets are highly beneficial in the management of cats with diabetes, resulting in a reduction of > 50% in the amount of insulin required in 8 of 9 cats.9 The incidence of type 2 diabetes mellitus in domestic cats appears to be rapidly increasing, in effect paralleling the epidemic of obesity and diabetes occurring in people on the traditional, high carbohydrate, western diet.10
The majority of cats with hyperthyroidism have lost weight and only a minority are obese. Never-the-less several studies have suggested that hyperthyroidism in cats may lead to long-lasting alterations of glucose tolerance and insulin secretion which may not be reversed following resolution of their thyrotoxicosis.11-13 Episodes of hyperglycemia in hyperthyroid cats are frequently secondary to stress associated hyperglycemia. Episodes of hyperglycemia in previously hyperthyroid cats, currently euthyroid (having a normal thyroid level) following treatment, may represent evidence of persistent glucose intolerance and should prompt appropriate monitoring and/or therapy. While it is generally appropriate for hyperthyroid cats to gain back the weight they had lost while thyrotoxic, efforts should be made to ensure they do not become or return to being obese as this will exacerbate their risk for developing diabetes and other obesity related chronic illnesses. The best way to control insulin release and prevent obesity in your cat is to feed it a diet high in protein and fat and low in carbohydrates.
Take away message: To minimize insulin dose requirements in diabetic cats and achieve weight loss that may actually result in remission of diabetes, feed a wet food diet with limited carbohydrate content (carbohydrate < 12% on a dry-matter basis).
Inflammatory Bowel Disease – “The Heat is On”
Dietary intolerance is an important non-immune cause of gastrointestinal tract symptoms (eg, vomiting and diarrhea) in cats. It can be caused by a variety of additives in cat foods including artificial colors, flavors and preservatives as well as the actual protein and carbohydrate sources utilized in the diet. Symptoms of dietary intolerance should be eliminated by eliminating the offending item(s) from the diet.
Unlike simple dietary intolerance, the inappropriate stimulation of the gut’s immune system can lead to the development of a clinical syndrome called inflammatory bowel disease. The gastrointestinal track has a large local immune system appropriately called the Gut Associated Lymphoid Tissue (GALT). Activation of this local immune system can lead to an influx of inflammatory white blood cells that interfere with the normal function of the bowel and lead to the clinical syndrome of inflammatory bowel disease and the associated gastrointestinal symptoms.
The immune system is designed to respond to the presence of foreign antigens, and proteins are strongly antigenic. Obviously the contents of the diet that is fed to a cat directly influence the proteins that the GALT is exposed to. In addition to the ingredients of the diet, the gut normally contains a massive number of bacterial organisms, called the intestinal microbiota, that live by feeding on the contents of the gut. These organisms have a symbiotic relationship with the host, ultimately contributing to the overall health of the host by producing an array of metabolic products including a wide variety of hormones. The content of the diet also impacts the microbiota of the gut and therefore indirectly influences the proteins that the GALT is exposed to.14-18
It is likely that IBD is triggered by an unfortunate response by the immune cells of the GALT to food or bacterial antigens within the intestines. Many commercial diets include the majority of protein in the form of plant based protein. Typical sources of the protein in both dry and canned cat foods include both corn and soy. Even grain free cat foods frequently include protein from plant sources including cassava (tapioca). Plants do not represent a significant component of the diet of the undomesticated cat and hence plant based proteins represent an evolutionarily foreign protein. Protein originating from plant sources may represent a trigger for the undesirable activation of the gut associated lymphoid tissue and contribute to the influx of inflammatory white blood cells into the bowel wall that are responsible for the symptoms of inflammatory bowel disease.
Displacement of the normal epithelial cells that line the bowel wall by this influx of inflammatory white blood cells leads to the reduced capacity of the bowel to absorb nutrients, leading to a progressive malnutrition that results in clinical weight loss. The influx of inflammatory white blood cells is also responsible for the clinical occurrence of vomiting and/or diarrhea.
Take away message: To minimize the risk of triggering the gut associated lymphoid tissue and inducing inflammatory bowel disease, feed a wet food diet with protein from all meat sources.
Dry Food – “The Good, the Bad and the Ugly”
Lets face it, dry cat foods are convenient to feed. They require virtually zero preparation or presentation time investment. Allowing your cat to free feed on dry food is much less likely to lead to ant or other pest infestation than leaving out canned food. And of course we have all heard the argument that the abrasive nature of dry food is good for dental hygiene suggesting that allowing your cat to crunch on dry kibble is the next best thing to brushing your cat’s teeth. For those concerned about feeding grains in cat food, and we should all be in this category, there are a number of brands that offer “grain-free” dry cat foods. Finally, there are many cats who really seem to enjoy dry food much more than canned food. Unfortunately, despite all of these apparent reasons to recommend them, dry cat foods are absolutely the wrong choice for virtually every cat.
The pet food business is a multi-billion dollar industry. There is a substantial economic incentive to engineer cat foods using the ingredients that will ensure that cats will keep eating them. Pet food companies use the same techniques that human snack and fast food companies use to make their products addictive for many individuals leading some to indulge in hedonic hyperphagia. As discussed in the sections on diabetes and obesity, the high carbohydrate content in most dry foods are major factors contributing to obesity and ultimately the development of type 2 diabetes. Even grain-free dry cat foods contain excessive levels of carbohydrates from sources like tapioca starch that are utilized for economic and logistic reasons. For this reason alone, dry foods do not represent a good diet for most cats.
Hydration is a major factor in feline health. Cats have a less sensitive response to thirst and dehydration than dogs or other omnivores, and they adjust their water intake to the dry-matter content of their diet rather than the moisture content.19 This means that cats eating commercial dry foods will consume approximately half the amount of water (in their diet and through drinking), compared with cats eating canned foods.2 Feeding canned foods increases both water intake and urine volume. This increased water intake benefits cats in 2 important ways. First, the increased urine volume that accompanies a wet food diet decreases the concentration of crystal-forming minerals in the urine and reduces the risk of developing bladder stones and obstructive uropathy (i.e., blocked tom-cat syndrome). Second, as cats age their kidney function gradually declines leading to the production of more dilute urine. The inability to maximally concentrate their urine leads to increased volumes of urine water loss and is a factor in inducing dehydration. The increase in water intake from a wet food diet is important to avoid dehydration and worsening of chronic kidney disease in older cats.
Well, at least the abrasive nature of dry cat foods is going to ensure that my cat won’t suffer from dental disease, right? Actually the development of dental disease probably has relatively little to do with the form of the food (dry vs wet) and a lot more to do with the sugar content. Everyone remembers their mother telling them that if they ate too many sweets their teeth would rot out of their mouths. Well mom was not alone in her concern about your consumption of sweets. The relationship of diet to dental caries (cavities) risk was suspected as early as the fourth century B.C., when Aristotle hypothesized that dental caries were caused by consumption of sweet figs, which stuck to the teeth.20 Indeed there is convincing evidence, collectively from human intervention studies, epidemiological studies, animal studies and experimental studies, for an association between the amount and frequency of free sugar intake and dental caries.21
Dietary carbohydrates represent a readily available source of the sugars that nourish the bacteria that live in our mouths and produce the acids that contribute to dental decay. As it turns out, dental caries simply do not develop in the absence of fermentable carbohydrates in the diet.
Take away message: To avoid inappropriate carbohydrate intake, optimize hydration for kidney health and reduce the risk of dental disease, feed a wet food diet with limited carbohydrate content (carbohydrate < 15% on a dry-matter basis).
Prescription Diets – Not necessarily “What the doctor ordered”!
Since the early 1980’s Donald Strombeck, DVM, PhD (Professor Emeritus, University of California, Davis, School of Veterinary Medicine, and honorary member of the College of Veterinary Internal Medicine) recognized the direct link between many of our dogs’ and cats’ gastrointestinal problems and the commercial diets they were being fed. In the first edition of his book entitled “Home-Prepared Dog & Cat Diets: the Healthful Alternative” Strombeck acknowledged that many cases of diarrhea in pets are directly related to the contamination of the diets with bacteria or inadequate cooking of those diets with significant carbohydrate content. Copies of the 1st edition of Stombeck’s book are still available from sources like Amazon and Google, but the contents of that book have also been made available online at Dr. Stombeck’s web site.
While many cats may become ill eating commercial cat foods contaminated with bacteria or containing inadequately cooked carbohydrates, these cats represent the minority of cats harmed by eating commercial diets. Most commercially available cat foods cause problems in the cats that eat them due to their use of improper ingredients including their reliance on excessive carbohydrate content, their use of plant based proteins and the marginal dehydration induced by feeding dry diets.
Only a relatively small subset of pet food companies produce “prescription” diets. These diets are intended to be prescribed by a licensed veterinarian as they have been formulated to address specific medical needs including urinary tract stones, inflammatory bowel disease and diabetes, to name a few. The irony here is that a large percentage of the problems these prescription diets are designed to address actually develop in the first place because of the inappropriate ingredients and formulations used in standard cat food diets, including those produced by the prescription diet companies.
Clearly the prescription diet manufacturers have a vested interest in suggesting the source of the problems experienced by the cats that develop urinary track stones or diabetes are unique to the cats themselves, rather than recognizing that the source of the problem is the standard diets that they produce. Even worse, the prescription diet manufacturers have focused on metabolic methods to overcome the symptoms that the original commercial diets caused without addressing the real nutritional needs of the cat.
An example of the wrong choices made by the prescription diet industry can be found in the way they attempted to deal with the problem of feline urinary track health. In the 1980s, when cats developed uroliths (either bladder stones or urethral plugs) they were predominantly composed of a combination of minerals called struvite (i.e., magnesium ammonium phosphate). The root cause of these uroliths was simply the inadequate water intake of cats eating a dry food diet. Rather than recognize that feeding dry food to cats can have negative consequences like inducing bladder stones, the pet food industry responded by developing prescription diets designed to acidify the urine and dissolve or prevent the formation of these kinds of stones.
However, since the introduction of these stone dissolving diets in the early 1980’s the frequency of a different kind of kidney and bladder stone, namely calcium oxalate stones has increased more than 50 times. (Thats not 50% put 50 times.) This dramatic increase in the incidence of calcium oxalate stones is directly attributable to cats eating dry food diets designed to acidify their urine. The fact that struvite crystals dissolve in a acid environment and calcium oxalate precipitates from solution into crystals that become stones in the same environment means that feeding these diets just substitutes one problem for another. The real solution is to feed wet food diets which result in an increase in water intake as well as urine volume. The larger volume of more dilute urine produced by cats eating a wet food diet generally prevents either type of crystal from developing in sufficient quantity to become clinically important.
There are numerous other examples of the veterinary prescription diet industry just getting it wrong including the use of dry prescription diets with a high carbohydrate (= fermentable sugar) content for control of dental disease and my personal favorite, iodine deficient diets for the control of the elevated thyroid hormone levels in cats with thyroid adenomas causing hyperthyroidism.
Take away message: Consider the value of feeding meat based diets with low carbohydrate and relatively high water content as a potential alternative to “prescription” diets designed to achieve similar results.
What should I feed my hyperthyroid cat?
Few medical conditions impact feline health more than hyperthyroidism. Indeed hyperthyroidism has been reported to be the most common endocrine disease of the cat since shortly following its initial description in 1979.22 More recent reports suggest the disease currently affects upwards of 10% of the geriatric cat population.23 While no clear causative relationships have been identified, numerous reports have suggested weak correlations between various elements of the diet and the development of hyperthyroidism.23-27 Unfortunately these relatively weak correlations not only fail to prove causation but prevent us from making specific dietary recommendations that will prevent the development of hyperthyroidism in cats. Never-the-less, the shear number of cats developing hyperthyroidism makes the question, “What should I feed my hyperthyroid cat?” an important one to address.
Cats with hyperthyroidism share some unique physiologic challenges. The hypermetabolic state induced by the sustained elevation in circulating thyroid hormone levels (i.e., thyrotoxicosis) that persists in hyperthyroid cats induces a progressive weight loss and muscle wasting. Dietary recommendations for hyperthyroid cats must take into consideration the importance of adequate calories and protein to offset these challenges. The most commonly reported symptom of hyperthyroidism in cats is weight loss that occurs despite a good appetite. The nature of cats unique metabolic needs as obligate carnivores means that this weight loss comes with the added symptom of muscle wasting. Despite the increase in food consumption that virtually always accompanies hyperthyroidism, these cats are simply unable to meet their daily caloric and protein intake needs. Hyperthyroid cats need high calorie and high protein diets to reduce the rate of weight loss and muscle wasting that accompanies the disease.
Thyroxine (the major hormone produced by the thyroid gland) is one of numerous counter-regulatory or anti-insulin hormones. As such it’s effects are opposite to those of insulin. This means it tends to promote an increase in circulating blood glucose by promoting glycogenolysis (the release of stored glucose in muscle and liver into the bloodstream), gluconeogenesis (the production of glucose from fatty acids), and other catabolic processes. Other counter-regulatory hormones that similarly contribute to increasing circulating glucose levels include glucagon, epinephrine, cortisol and growth hormone. As a result of the counter-regulatory effect of thyroid hormones, cats with hyperthyroidism frequently develop glucose intolerance and insulin resistance. Previous research has shown that hyperthyroidism in cats may lead to long-lasting alterations of glucose tolerance and insulin secretion which may not be reversed following resolution of the thyrotoxicosis.13 For this reason cats with hyperthyroidism are at an increased risk for developing diabetes mellitus. These cats should be fed a diet low (< 15% on a dry mater basis) in carbohydrate content. Furthermore, weight gain following resolution or control of hyperthyroidism should be managed to avoid development of obesity as this also contributes to the progression from insulin resistance to overt diabetes.
Chronic kidney disease (CKD) affects even more cats than hyperthyroidism. The prevalence of CKD has been reported to be between 7.7% for cats over 10 years of age and 30% for cats over 15 years of age.28-30 The prevalence of CKD in hyperthyroid cats has been reported to be between 14 and 49%.31-39 The increase in prevalence of CKD in hyperthyroid cats compared to cats without hyperthyroidism supports a potential damaging effect of hyperthyroidism on the kidney. While there are undoubtedly aspects of hyperthyroidism that contribute to damaging the kidneys, a large number of hyperthyroid cats have chronic kidney disease simply because both diseases are common in older cats. Never-the-less the high prevalence of CKD in hyperthyroid cats points out the importance of managing these cats with their kidney function in mind.40 Toward that end, diets inherently high in moisture which promote hydration are immensely valuable. As described above, dry cat foods have little to recommend them other than convenience.
While feeding an appropriate diet to your hyperthyroid cat is an important step in their management, the most important factor in their recovery is achieving an adequate control of their elevated thyroid hormone levels. While this is possible using chronic medical management with methimazole, it is best achieved with curative therapies like radioiodine or surgery.
Take away message: To avoid obesity or diabetes, as well as support good kidney health with adequate hydration, feed a wet food diet with limited carbohydrate content (carbohydrate < 15% on a dry-matter basis).
Pet Food Recalls
Unless we invest in the effort to produce, process and prepare our own food, we are all susceptible to the potential missteps of the food industry. Likewise, if we don't produce, process and prepare our pets’ food they are similarly susceptible to a variety of hazards. It takes many steps to get food into our pets’ food dishes and contamination can occur at any stage of the process. The causes of foodborne illness include contamination with various bacteria, viruses, parasites, toxins, metals, and prions. Due to the limited variety common in our pets’ diets, food related illness can also result from misformulations resulting in diets deficient in essential nutrients like vitamins.
In a previous study evaluating food-related illness and death in the United States. the authors estimated that foodborne diseases were responsible for approximately 76 million illnesses, 325,000 hospitalizations, and 5,000 deaths in the United States each year.41 Reports describing food-related illness and death in pets in the United States are relatively few in number. The massive food recall that occurred in 2007 due to adulteration of dog and cat food with the industrial chemicals melamine and cyanuric acid exposed the many deficiencies in the pet food recall process and ultimately lead to congressional attention and passage of the Food and Drug Administration Amendment Act (FDAAA) of 2007. Melamine and cyanuric acid contamination tainted over 53 million cans or pouches of dog and cat food across the USA and Canada. The manufacturer of these pet foods, Menu Foods, Inc. ultimately initiated a recall involving over 100 brands of dog and cat foods.42
Take away message: Pet owners need to maintain a constant vigilance for symptoms that may be related to the foods they feed their pets. Consider consulting references that report current pet food recalls regularly.
1. Zoran D.L., The Carnivore Connection to Nutrition in Cats. J Am Vet Med Assoc, 2002. 221(11): p. 1559-67.
2. Kirk C.A., Debraekeleer J. and Armstrong P.J., Normal Cats, in Small Animal Clinical Nutrition, M.S. Hand, C.D. Thatcher, and R.L. Remillard, Editors. 2000, WB Saunders Company: Philadelphia. p. 291-351.
3. Morris J.G., Idiosyncratic Nutrient Requirements of Cats Appear to Be Diet-Induced Evolutionary Adaptations. Nutr Res Rev, 2002. 15(1): p. 153-68.
4. Kienzle E., Carbohydrate Metabolism of the Cat 1. Activity of Amylase in the Gastrointestinal Tract of the Cat1. Journal of Animal Physiology and Animal Nutrition, 1993. 69(1-5): p. 92-101.
5. Kienzle E., Carbohydrate Metabolism of the Cat 2. Digestion of Starch1. Journal of Animal Physiology and Animal Nutrition, 1993. 69(1-5): p. 102-114.
6. Scarlett J.M., Donoghue S., Saidla J., et al., Overweight Cats: Prevalence and Risk Factors. Int J Obes Relat Metab Disord, 1994. 18 Suppl 1: p. S22-8.
7. Lund E.M., Armstrong P.J., Kirk C.A., et al., Prevalence and Risk Factors for Obesity in Adult Cats from Private Us Veterinary Practices. Int J Appl Res Vet, 2005. 3(2): p. 88-96.
8. Hoenig M., Alexander S. and Pazak H. Effect of a High- and Low- Protein Diet on Glucose Metabolism and Lipids in the Cat in Conference Proceedings Purina Nutritional Forum. 2000: p. 98-99.
9. Frank G., Anderson W., Pazak H., et al., Use of a High-Protein Diet in the Management of Feline Diabetes Mellitus. Vet Ther, 2001. 2(3): p. 238-46.
10. Wolongevicz D.M., Zhu L., Pencina M.J., et al., Diet Quality and Obesity in Women: The Framingham Nutrition Studies. Br J Nutr, 2010. 103(8): p. 1223-9.
11. Hoenig M. and Ferguson D.C., Impairment of Glucose Tolerance in Hyperthyroid Cats. J Endocrinol, 1989. 121(2): p. 249-51.
12. Hoenig M., Peterson M.E. and Ferguson D.C. Glucose Intolerance in Spontaneous Hyperthyroid Cats in Scientific Proceedings (Abstract) American College of Veterinary Internal Medicine. 1990.
13. Hoenig M., Peterson M.E. and Ferguson D.C., Glucose Tolerance and Insulin Secretion in Spontaneously Hyperthyroid Cats. Res Vet Sci, 1992. 53(3): p. 338-41.
14. Backus R.C., Puryear L.M., Crouse B.A., et al., Breath Hydrogen Concentrations of Cats Given Commercial Canned and Extruded Diets Indicate Gastrointestinal Microbial Activity Vary with Diet Type. J Nutr, 2002. 132(6 Suppl 2): p. 1763S-6S.
15. Ugarte C., Guilford W.G., Markwell P., et al., Carbohydrate Malabsorption Is a Feature of Feline Inflammatory Bowel Disease but Does Not Increase Clinical Gastrointestinal Signs. J Nutr, 2004. 134(8 Suppl): p. 2068s-2071s.
16. Inness V.L., Mccartney A.L., Khoo C., et al., Molecular Characterisation of the Gut Microflora of Healthy and Inflammatory Bowel Disease Cats Using Fluorescence in Situ Hybridisation with Special Reference to Desulfovibrio Spp. J Anim Physiol Anim Nutr (Berl), 2007. 91(1-2): p. 48-53.
17. Janeczko S., Atwater D., Bogel E., et al., The Relationship of Mucosal Bacteria to Duodenal Histopathology, Cytokine Mrna, and Clinical Disease Activity in Cats with Inflammatory Bowel Disease. Veterinary microbiology, 2008. 128(1-2): p. 178-93.
18. Lubbs D.C., Vester B.M., Fastinger N.D., et al., Dietary Protein Concentration Affects Intestinal Microbiota of Adult Cats: A Study Using Dgge and Qpcr to Evaluate Differences in Microbial Populations in the Feline Gastrointestinal Tract. J Anim Physiol Anim Nutr (Berl), 2009. 93(1): p. 113-21.
19. Anderson R.S., Water Balance in the Dog and Cat. Journal of Small Animal Practice, 1982. 23(9): p. 588-598.
20. Forster E.S., The Works of Aristotle. Problemata. Vol. VII. 1927, London: Oxford University Press.
21. Moynihan P. and Petersen P.E., Diet, Nutrition and the Prevention of Dental Diseases. Public Health Nutr, 2004. 7(1A): p. 201-26.
22. Peterson M.E., Johnson J.G. and Andrews L.K. Spontaneous Hyperthyroidism in the Cat. in Conference Proceedings American College of Veterinary Internal Medicine. 1979. Seattle: p. 108.
23. De Wet C.S., Mooney C.T., Thompson P.N., et al., Prevalence of and Risk Factors for Feline Hyperthyroidism in Hong Kong. J Feline Med Surg, 2008: p. 1-7.
24. Edinboro C.H., Scott-Moncrieff J.C. and Glickman L.T., Environmental Risk Factors for Feline Hyperthyroidism: Pet Cats as Potential Sentinels for Public Health. Thyroid, 2004. 14: p. 759.
25. Olczak J., Jones B.R., Pfeiffer D.U., et al., Multivariate Analysis of Risk Factors for Feline Hyperthyroidism in New Zealand. N Z Vet J, 2005. 53(1): p. 53-8.
26. Wakeling J., Everard A., Brodbelt D., et al., Risk Factors for Feline Hyperthyroidism in the UK. J Small Anim Pract, 2009. 50(8): p. 406-14.
27. Peterson M., Hyperthyroidism in Cats: What's Causing This Epidemic of Thyroid Disease and Can We Prevent It? J Feline Med Surg, 2012. 14(11): p. 804-18.
28. Dibartola S.P., Rutgers H.C., Zack P.M., et al., Clinicopathologic Findings Associated with Chronic Renal Disease in Cats: 74 Cases (1973-1984). J Am Vet Med Assoc, 1987. 190(9): p. 1196-202.
29. Krawiec D.R. and Gelberg H.B., Chronic Renal Disease in Cats, in Current Veterinary Therapy X, R.W. Kirk, Editor. 1989, W. B. Saunders Company. p. 1170-1173.
30. Lulich J.P., Osborne C.A., O’Brien T.D., et al., Feline Renal Failure—Questions, Answers, Questions. Compen Contin Educ Pract Vet., 1992. 14: p. 127.
31. Graves T.K., Olivier N.B., Nachreiner R.F., et al., Changes in Renal Function Associated with Treatment of Hyperthyroidism in Cats. Am J Vet Res, 1994. 55(12): p. 1745-9.
32. Broussard J.D., Peterson M.E. and Fox P.R., Changes in Clinical and Laboratory Findings in Cats with Hyperthyroidism from 1983 to 1993. J Am Vet Med Assoc, 1995. 206(3): p. 302-5.
33. Adams W.H., Daniel G.B., Legendre A.M., et al., Changes in Renal Function in Cats Following Treatment of Hyperthyroidism Using 131I. Vet Radiol Ultrasound, 1997. 38(3): p. 231-8.
34. Becker T.J., Graves T.K., Kruger J.M., et al., Effects of Methimazole on Renal Function in Cats with Hyperthyroidism. J Am Anim Hosp Assoc, 2000. 36(3): p. 215-23.
35. Bucknell D.G., Feline Hyperthyroidism: Spectrum of Clinical Presentions and Response to Carbimazole Therapy. Aust Vet J, 2000. 78(7): p. 462-5.
36. Slater M.R., Geller S. and Rogers K., Long-Term Health and Predictors of Survival for Hyperthyroid Cats Treated with Iodine 131. J Vet Intern Med, 2001. 15(1): p. 47-51.
37. Milner R.J., Channell C.D., Levy J.K., et al., Survival Times for Cats with Hyperthyroidism Treated with Iodine 131, Methimazole, or Both: 167 Cases (1996-2003). J Am Vet Med Assoc, 2006. 228(4): p. 559-63.
38. Boag A.K., Neiger R., Slater L., et al., Changes in the Glomerular Filtration Rate of 27 Cats with Hyperthyroidism after Treatment with Radioactive Iodine. Vet Rec, 2007. 161(21): p. 711-5.
39. Riensche M.R., Graves T.K. and Schaeffer D.J., An Investigation of Predictors of Renal Insufficiency Following Treatment of Hyperthyroidism in Cats. Journal of Feline Medicine & Surgery, 2008. 10(2): p. 160-166.
40. Broome M.R., Treatment of Hyperthyroidism and Concurrent Renal Disease, in August’s Consultations in Feline Internal Medicine, S.E. Little, Editor. 2015, Elsevier: Philadelphia, PA.
41. Mead, P.S., et al., Food-related illness and death in the United States. Emerg Infect Dis, 1999. 5(5): p. 607-25.
42. Rumbeiha, W. and J. Morrison, A Review of Class I and Class II Pet Food Recalls Involving Chemical Contaminants from 1996 to 2008. Journal of Medical Toxicology, 2011. 7(1): p. 60-66.