Meat-based diets


More than 95% of US companion animals derive their nutritional needs from a single source: processed pet food (Perry 1996). Consequently the commercial pet food industry is very big business. In 1998 US dog food sales amounted to $5.9 billion, and cat food sales to $4.7 billion. These figures represented a 25% increase from 1993. With approximately 55 million dogs and 70 million cats in 1998, each dog provided approximately $107 annually to the industry, and each cat approximately $67 (Gurkin & Fenstermacher 1999). By 2002, the US pet food industry was worth $11 billion (API 2002).

Such enormous profits are achieved by minimising the costs and maximising the palatability (desirability in terms of taste, smell, colour and texture) of the products sold. The industry uses a variety of ingenious pet food substrates to minimise its costs, some of which may pose health hazards. However, profits are maintained while consumer knowledge of such hazards remains minimal.

Encouraged by claims that 'only the highest quality ingredients are used,' consumers widely presume that quality meat products form the bulk of the commercial pet foods they feed their companion animals. Misled by advertisements displaying whole chickens, choice cuts of beef, and fresh grains, unsuspecting consumers are unaware that manufacturers have long since substituted chicken heads, feet, and intestines for whole chickens; cow brains, tongues, oesophagi, and other viscera, including diseased and even cancerous tissue, for choice cuts of beef; and grains deemed unfit for human consumption because of mould, contaminants or poor quality, and hulls and other remnants from the milling process, instead of whole grains (Perry 1996).

Up to 50% of commercial brands are comprised of ‘meat meal’ and ‘byproducts’ – industry euphemisms for assorted body parts, slaughterhouse wastes, 4-D meat (from animals who are dead, dying, diseased or disabled on arrival at the slaughterhouse), supermarket rejects, and large numbers of rendered dogs and cats euthanised in animal shelters. Old restaurant grease complete with high concentrations of dangerous free radicals and trans fatty acids; PCBs, heavy metals and other toxins, particularly from fish; bacterial, protozoal, fungal, viral, and prion contaminants, along with their associated endotoxins and mycotoxins; hormone and antibiotic residues; and dangerous preservatives; are all rendered delicious to cats and dogs by the addition of ‘digest,’ a soup of partially dissolved entrails from chickens and other animals (Gillen 2003). Pet food scientists have long since learned how to fortify a mixture of otherwise inedible scraps with artificial vitamins and minerals, preserve them to resist degradation during storage for a year or longer, add flavour enhancers and dyes to increase palatability and aesthetic appeal, and extrude the resultant mixture into whimsical shapes that appeal to the human consumer.

Not surprisingly, the health hazards intrinsic to commercial meat-based pet foods are sufficient to fill a book. Ann N. Martin’s (2003) Food Pets Die For includes a 161-page coverage of the chemicals, preservatives, hormones, pesticides, and diseased animal parts found in commercial pet food, and the illnesses each can cause. Veterinarian Dr. Wendell Belfield states: “Despite industry claims that pets live long and healthy lives on commercial pet food, we veterinarians are routinely faced with contradictory evidence in the form of sick animals. We frequently encounter acute reactions such as diarrhoea and vomiting and skin lesions. Most often, though, we are witnessing symptoms of deteriorating health, of diminished efficiency of bodily functions and organs, of kidneys failing in middle age due to excessive protein, of weakened immune systems and allergic reactions. We are seeing the cumulative effect of all those additives, toxins, lead, and the very questionable source of the natural ingredients.” (Belfield et al. 1983). As a practicing veterinarian I believe that diseases such as cancer, kidney, liver and heart failure are far more common than they should be, and that many are likely to be exacerbated or directly caused by the numerous hazardous ingredients of commercial meat-based cat and dog diets.

Potentially hazardous ingredients

Meat meal and byproducts

The proportion of ‘food’ animal carcasses not consumed by humans in the US each year has been estimated as ranging from approximately 50% (Phillips 1994) to around 20% (Pearl 1997: The US population consumes 181.2 lb of boneless meat per person per year. That consumption rate generates approximately 44 billion lb of inedible animal material that is rendered).

In 2004, Kvamme estimated that rendering produces about 50 billion pounds of fats, tallows and greases, meat and bone meal and other animal products annually in the US. Most of the meat and bone meal is used in feed supplements for animals: 43% for poultry, 23% for pet food, 13% for pigs, 10% for cattle and 11% for other uses, among them the production of feed for farmed fish. Given their higher protein needs, cat foods typically contain more meat byproducts (35-50%) than dog foods (25-40%) (Halpin et al. 1999).

The ownership of major pet food brands by multinational food production companies facilitates the recycling of animal waste products into ‘meat meal’ and ‘byproducts.’ So, what actually goes into meat meal and byproducts? Certainly not a lot of quality meat. When cattle, pigs, chickens, lambs, and other animals are slaughtered, the choice cuts of lean muscle tissue and organs prized by humans are trimmed from the carcass, leaving the bones, blood, heads, brains, noses, beaks, lungs, spleens, kidneys, livers, stomachs, intestines, ligaments, subcutaneous fat, hooves, horns and other undesirable parts for reselling as ‘byproducts’ (Perry 1996). Whole mammal bodies (cows, sheep, pigs, etc.) by the hundreds of thousands, millions of their major organs, and thousands of tons of bird flesh annually labeled as unfit for human consumption at slaughterhouses are included (Mason & Singer 1990). ‘4-D’ meat from dead, dying, diseased and disabled animals is included, and due to expensive labor costs, plastic ear tags are unlikely to be removed. Old or spoiled supermarket meat, often without removal of styrofoam packaging (which increases labor costs), is used (Gillen 2003). Veterinarian Dr. Alfred Plechner defines byproducts as “diseased tissue, pus, hair, feathers, assorted slaughterhouse rejects, and carcasses in varying stages of decomposition.” (Plechner & Zucker 1986). Even pet treats contain meat byproducts; primarily pig ears and snouts, cow hooves and tails, skins, femur bones, shark cartilage, and rabbit and deer meal (Halpin et al. 1999).

Cancerous tissues from US slaughterhouses has been estimated as averaging fifteen million pounds a year (Mason & Singer 1990). From his experience as a veterinarian and federal meat inspector, Dr. P. F. McGargle concluded that, “feeding slaughterhouse wastes to animals increases their chances of getting cancer and other degenerative diseases... Furthermore, the increase in cancer rates corresponds to the introduction and increased use of meat meal as an animal food.” (Pitcairn & Pitcairn 1995).

Several million unwanted dogs and cats are killed in US animal shelters annually, and many of their bodies are also rendered into meat meal. Pet food manufacturers and rendering companies are understandably reluctant to publicise this use of once-loved companion animals. As reported in the San Francisco Chronicle, both the National Renderers’ Association and the executives at one plant, Modesto Tallow, denied they even used pets. Yet employees, vendors and state inspectors said they regularly observed dogs and cats rendered at both their Sacramento and Modesto plants, and the AVMA and FDA both confirmed this use of pet carcasses (Perry 1996). At Sacramento Rendering, one employee stated, “Thousands and thousands of pounds of dogs and cats are picked up and brought here every day.” A former employee confirmed, “The small animals are a big part of the company.” (Eckhouse 1990). Again because of expensive labor costs, flea collars containing toxic organophosphate insecticides are commonly not removed prior to rendering. A 1998 FDA survey also detected the euthanising solution sodium pentobarbital, which is specifically designed to kill dogs, cats and other animals and consequently used for this purpose by animal shelters, in 43 randomly selected brands and product lines of dry dog food (Anonymous undated, FDA/CVM 2002).

These ingredients are rendered together, which involves melting to separate fat-soluble from water-soluble and solid components, and removal of most of the water. While this kills bacterial contaminants, it also damages or destroys heat-vulnerable nutrients such as enzymes and vitamins (API 2002).

Largely because of the health hazards they pose, meat byproducts have been banned from British pet foods since 1990 (Peden 1999). However the use of meat meal and byproducts persists within the US despite the obvious health hazards, for reasons of profit. In 1991 a rendering plant in Greene County, N.C., paid 2.4 to 2.7 cents per pound for pig carcasses, and for poultry the going rate was 0.02 to 0.04 cents per pound (Barker & Williams 1993). With prices like these and widespread consumer ignorance of the true nature of pet food ‘byproduct’ ingredients, it is unsurprising that pet foods contain up to 50% byproduct.

Restaurant grease and other fats

Palatability of the numerous distasteful ingredients in commercial pet food is increased by spraying the dry food with a combination of refined animal fat, lard, restaurant grease, and other oils considered too rancid or inedible for human consumption. Most cats and dogs love the taste of this sprayed fat, which also acts as a binding agent to which manufacturers may add additional flavour enhancers. The odour wafting from an open bag of pet food is created by these fats (Perry 1996), and is also important to dogs and cats who rely heavily on their sense of smell.

Slaughterhouse waste, supermarket trimmings and restaurant grease are all used as fat sources, and restaurant grease in particular has become a major component of feed-grade animal fat. Deep-frying of restaurant food results in rapid oxidation, producing free radicals, trans fatty acids, and other dangerous toxins. Oil is used repeatedly, becoming increasingly contaminated. When too polluted for further restaurant use, the resultant grease may be stored in 50 gallon drums for weeks, sometimes outdoors in high temperatures, with little regard for its safety or further use. The resultant rancid product is then purchased by fat blenders who blend animal and vegetable fats together, stabilise them with powerful antioxidants to prevent further spoilage, and then sell the blended products to pet food companies. The resulting rancid, heavily preserved fats are difficult to digest and can lead to a host of animal health problems, including digestive upsets, diarrhoea, flatulence, and bad breath (Perry 1996).


The unpalatable ingredients in meat-based commercial pet foods are rendered delicious to cats and dogs by the addition of ‘digest,’ the industry euphemism for partially digested entrails. According to Small Animal Clinical Nutrition, “Digest is probably the most important factor discovered in recent years for enhancing the palatability of dry food for cats and, to a lesser degree, dogs.” (Lewis et al. 1987). In fact, digest is so effective that long-term exposure can result in behavioural symptoms of addiction, necessitating considerable patience and persistence when implementing dietary changes.

Digest is produced by controlled enzymatic degradation of the intestines, livers, lungs and miscellaneous viscera of chickens (primarily), and other animals. pH control inhibits bacterial putrefaction and promotes autolysis. The process is arrested at a state of partial digestion via the addition a strong acid (usually phosphoric). The precise enzymes and substrates used are closely guarded trade secrets. Dry pet foods receive pasteurised dried digest at 1–3% concentration for dog and 1–7% for cat food (Peden 1999), by dusting onto the finished product after tallow application, or by mixing the digest with the tallow prior to application. Digest is also added to soft-moist, soft-dry or canned formulas, via the sauce or gravy portion in the latter case (Peterson Co. date unknown).

Companion animal guardians are often also misled by insidious effects of digest. Although digest is usually just autolysed chicken entrails, some batches are considered to taste more like beef, fish or turkey, etc., than other batches. It is the type of digest added, rather than the meat content, that may determine the flavour designation on the label. Undifferentiated partially-dissolved ‘beefy’ tasting entrails might be labeled ‘Beef Stew,’ while the substitution of ‘fishy’ tasting digest may transform a can into ‘Ocean Whitefish.’

Diseased body parts

Slaughterhouse inspectors, where present, are typically provided with no more than a very few seconds to verify the freedom of each carcass from infectious diseases, parasitic infestations, and cancerous or diseased tissue. Numerous diseases exist, with the potential to adversely affect the health of consumers, whether human, dog or cat.

Because cats and dogs are not normally consumed by humans, restrictions on the use of tissues at risk of prion contamination (the cause of mad cow disease and its human equivalent, Creutzfeldt-Jacob disease), such as brain and spinal tissue, are not normally extended to pet food. The use of slaughterhouse byproducts and downed animal meat in pet food increases the risk of transmissible spongiform encephalopathies (TSEs) such as feline spongiform encephalopathy, which progressively eats away at the brain, causing a variety of neurological and systemic disorders, and eventually, death. Although at the time of writing this incurable disease had not yet been detected in dogs, the ability of TSEs to cross a number of other species barriers has been discovered fairly recently, and it is by no means inconceivable that it may at some point be discovered in dogs, as it has been in cats.

Pathogenic bacteria and other microorganisms may also be acquired during production, harvest of plant-based ingredients, processing, handling, storage, distribution or preparation for consumption, from soil, water, air, living plants, feed or fertiliser, animals, humans, sewage, processing equipment, ingredients and packaging materials. During the final stages of dry food manufacture, the product is coated with ‘digest’ and liquid fat. Although cooking during processing kills bacteria, the final product loses its sterility during the subsequent drying, fat-coating, and packaging stages of the manufacturing process. Most animal products used for food have 1000 to 10,000 bacteria per gram. The poor quality ingredients relied upon for pet food, poor sanitation, unsatisfactory heating, recontamination or poor handling and storage, all raise bacterial numbers (Strombeck date unknown).

Gastrointestinal disorders are the most common side effect of bacterial contamination. Salmonellosis is the most common illness caused by bacterial contamination of both companion animal and human-quality food. Estimates of the Salmonella contamination of the animal protein ingredients used in animal feed range from 57 to 60%; for the vegetable protein ingredients the range is 36 to 37% (Strombeck date unknown). Chicken is a common component of pet food, and as noted previously, partially-dissolved chicken entrails (‘digest’) are very commonly added as a flavour enhancer. Although the US Department of Agriculture (USDA) officially reports that 20% of all raw chickens are tainted with Salmonella, USDA studies from the late 1980s to the late 1990s illustrate that this is a gross underestimate. One of the earliest studies, conducted at a model poultry operation in Puerto Rico in 1987, put the number of contaminated birds coming out of the chill tank at 76%. When the study was repeated, the figure was 80%. USDA studies conducted in 1992 in five plants in Southeastern USA found Salmonella contamination levels averaging 58% before the chickens went into the chill tank, and 72% after their communal bath (Eisnitz 1997). Unsurprisingly, Salmonella can be cultured from the faeces of up to 30% of dogs. Many successfully cope and show no signs of disease, but others suffer potentially diarrhoea and gastrointestinal disorders (Strombeck date unknown).

Staphylococcus aureus is the second most commonly identified bacterial cause of food-borne disease, and is commonly found in contaminated meat. It may also cause gastrointestinal disturbances. Clostridium perfingens is the third most commonly identified bacterial cause of food-borne illness, and is well documented in dogs and cats. While killed during cooking, its spores are resistant to disinfectants and heat and survive to recontaminate the processed product. Pathogenic strains of Escherichia coli are often also identified as a cause of food-borne illness, and are commonly associated with faecal contamination (Strombeck date unknown).

All these bacteria may be present in low numbers within the intestines of clinically normal animals. However, large numbers, pathogenic strains or concurrent disease or stress may cause gastrointestinal disease such as diarrhoea, organ disease such as kidney disease (most of which has been assumed to be an unavoidable consequence of ageing), and nonspecific signs of illness. Bacterial numbers are also increased 100 to 1,000 times in the colons of companion animals by fermentation of high concentrations of poorly digestible cheap pet food components such as cellulose and hemicellulose fibre (Strombeck date unknown).

The toxins produced by these bacteria are of three types. Enterotoxins attach to intestinal mucosal surfaces, stimulating fluid secretion and diarrhoea. These bacteria and their toxins are usually inactivated by the heat of processing. Cytotoxins kill mucosal cells directly. Endotoxins are formed from part of the cellular structure of gram negative bacteria such as Salmonella and E. coli, and are not inactivated by processing (Strombeck date unknown). While the high-temperatures used in processing kill bacteria, they also result in bacterial disintegration, releasing more endotoxins into the host (Peden 1999).

Parasitic protozoa may also contaminate pet food. Toxoplasma gondii, for example, is the causative agent of toxoplasmosis, which may infest humans, cats and dogs. Cats are most vulnerable between the ages of two weeks and three years. Symptoms of severe infestation include breathing difficulties due to rapidly worsening pneumonia, accompanied by untreatable fever. Death usually ensues within three weeks. Reproductive failure and neonatal death may also result. Some cats carry the disease asymptomatically, but may transfer it to others. Pregnant women should take the special precautions of avoiding contact with litter boxes and using gloves when gardening, as infestations may result in congenital eye and brain damage in human babies (Peden 1999).

Fish contaminants

Real fish are actually sometimes used in pet foods, however fish are particularly prone to bacterial and toxic contamination. Unlike other ‘food’ animals, fish typically arrive at the processing plant dead; sometimes for days. Due to the kind of bacteria and enzymes found on fish, and the effects of oxygen, fish also decompose faster than other ‘food’ animals, producing the distinctive ‘fishy’ smell of fish, which is actually one sign of spoilage (Anonymous 2001).

In a 2000 survey of human-grade fish on sale in retail outlets across the US, Consumer Reports found that although only 1% of samples were downright decomposed, 28% were on the brink of spoilage. Between 3% (based on International Commission on Microbiological Specifications for Foods) and 8% (based on Canadian government guidelines) of the samples had unacceptable levels of Escherichia coli, a potentially pathogenic bacterium most likely originating from faeces-contaminated water or unhygienic handling practices (Anonymous 2001). Fish used for pet food is, of course, of substantially poorer quality.

Oceanic pollutants are also incorporated into plankton, smaller fish, and, successively, into larger fish, concentrated at each stage by fat solubility and consequent storage of DDT, PCBs and other toxins, and by the limited ability of fish to excrete these unnatural toxins from their systems.

Mercury is released into the environment in unnatural quantities by such processes as cement manufacturing, coal-burning, and the incineration of some products. It drifts or seeps into waterways, where it is converted to methylmercury, a more toxic form that works its way up the food chain. In top-level predators, such as sharks and swordfish, methylmercury concentrations can be 10,000 to 100,000 times greater than that of the surrounding water (Anonymous 2001). A 1992 Consumer Reports survey revealed that of human-quality fish, 43% of the salmon surveyed contained PCBs, and 90% of the swordfish contained mercury (Peden 1999). In the 2000 survey, half of the swordfish samples surveyed exceeded the FDA's ‘action level’ for methylmercury of 1 part per million (ppm). In fact, the average level in all samples was 1.11 ppm (Anonymous 2001).
A study by Boyer et al. (1978) found that kittens exclusively fed a commercial red meat tuna diet for one hundred days had elevated concentrations of mercury and selenium in blood, bone, brain, kidney, liver, muscle and splenic tissue. Houpt et al. (1988) similarly found that cats fed a tuna diet had elevated tissue levels of mercury and selenium, and that these cats were less active, vocalised less, and spent more time on the floor and more time eating than cats fed commercial beef-based cat food.

Studies of children born to women routinely exposed to methylmercury in fish have found subtle but measurable changes in hearing, motor skills, and learning ability. Consequently the FDA has cautioned pregnant women or those who may become pregnant, as well as nursing mothers and young children, not to eat shark, swordfish, tilefish, or king mackerel, due to potentially hazardous levels of methylmercury (Anonymous 2001).


Major commercial meat-based brands are produced in large volumes, and stored for long periods of time, within warehouses, retailers, and homes. This predisposes to mycotoxicosis – disease caused by fungal toxins. Of these, aflatoxicosis, caused by the toxic products of Aspergillus flavus, is the most important (Peden 1999). Aflatoxins are hepatotoxic (toxic to the liver), teratogenic (cause congenital deformities), carcinogenic (cause cancer), and immunosuppressant. The most common syndrome in animals results from liver failure, and includes jaundice, blindness, circling, falling and convulsions (Blood & Studdert 1988). Vomitoxin is milder, causing inappetence, vomiting and diarrhoea (API 2002).

In 1995, Nature's Recipe pulled thousands of tons of dog food off the shelves at a cost of $20 million after consumers complained that their dogs were vomiting and losing their appetite. Vomitoxin was identified as the cause. In 1999, Doane Pet Care Company in Tennessee recalled all product shipped to Texas and Louisiana due to an aflatoxin outbreak that killed 55 dogs. Doane Pet Care Co. is the largest manufacturer of private label pet food in the US, and the second largest producer of dry pet food. The recall included Ol' Roy (Wal-Mart's brand) and 53 other brands (Peden 1999, API 2002, Bingham et al. 2004).

Antibiotics and hormones

In order to increase growth and production, while minimising feed costs, and increase the ability of intensively farmed pigs, cows and chickens to withstand the unhygienic and stressful conditions to which they are frequently subjected, US farmers routinely feed large volumes of antibiotic growth promotants to farm animals, and use hormonal injections or implants. It's been estimated that 13 million pounds of medically important antibiotics are fed annually to US farm animals to promote weight gain (Union of Concerned Scientists 2001). Partly because semi-moist food contains 25 - 50% water, antimicrobial preservatives must also be added to it (Perry 1996). These practices can result in adverse health consequences for susceptible human or animal consumers of antibiotic or hormonal residues.

Long-term exposure to low environmental levels of antibiotics also genetically selects for populations of antibiotic-resistant bacteria, some of which are pathogenic, with the potential to cause untreatable human disease. Because of these serious health concerns, antibiotic growth promotants and exogenous (externally-derived) hormones have been banned to varying levels in Europe (BBC News 1998), Australia, and other regions of the world. Their continuing use in the US violates decade-old World Health Organisation recommendations (1997). Both the American Medical Association (2001) and the American Public Health Association (1999) are also on record opposing the non-therapeutic use of antibiotics in healthy farm animals.

Their use persists in the US for reasons of profit. The National Academy of Sciences estimates that a total ban on the widespread feeding of antibiotics to farmed animals would raise the price of poultry anywhere from 1 to 2 cents per pound and the price of pork or beef maybe even 3 to 6 cents a pound, costing the average meat-eating American consumer up to $9.72 a year (NRC 1999). Meanwhile, antibiotic resistant infections every year cost US society an estimated $30 billion (Frist 1999) and, in the U.S. alone, kill 60,000 people (NIAID 2004).


In order to minimise the degradation of commercial brands produced in large volumes and stored for potentially lengthy periods, and because most pet foods contain large percentages of added fat, manufacturers place a heavy reliance on preservatives, some of which are so toxic they are banned from human food. Two-thirds of the pet food manufactured in the US contains synthetic preservatives added by the manufacturer, and of the remaining third, 90% includes ingredients already stabilised by synthetic preservatives (Perry 1996).

Preservatives commonly used include propylene glycol, which is known to cause illness in dogs; propyl gallate, which is suspected of causing liver damage; butylated hydroxyanisole, which causes liver damage, metabolic stress, foetal abnormality, and serum cholesterol increase; sodium nitrite, which may be metabolised into powerful carcinogenic compounds; and ethoxyquin, which is banned from human food and suspected of causing severe health problems in some dogs (Pitcairn & Pitcairn 1995).

Ethoxyquin (EQ) was developed by Monsanto in the 1950s and first used as a rubber stabiliser. It has also proven effective as an insecticide, pesticide, fungicide and herbicide. It was originally permitted in feeds as a stabiliser for alfalfa, clover, and grasses fed to livestock, at 150 ppm (0.015% or 4.8 oz. per ton). Although never intended under the original permit, and despite the very large digestive and metabolic differences between companion animals and livestock, because pet food falls under the legal category of animal feed, EQ is added to it (Peden 1999 & 2004).

FDA officials clearly recognised EQ as a poisonous substance and permitted minuscule amounts in feedstuff only because it was the cheapest and most powerful preservative available. FDA and Monsanto researchers originally stated that EQ degraded at around 160 to 190 C, so that when a product containing EQ was cooked, the EQ simply disappeared. Later research demonstrated that it didn't disappear, instead mutating into oxidised EQ. The FDA progressively allowed increased EQ in pet foods, because, in accordance with its primarily role in protecting human health, its attention was primarily on ‘food,’ rather than companion animals. Today, virtually all dog food is preserved with EQ in some way, although it’s absent from labels because it’s added earlier at the rendering plant. There have been no long term studies of EQ toxicity in dogs or cats, but some breeders relate that reproductive and dermatological disorders disappear when foods containing EQ are removed from the diet (Peden 1999 & 2004).

Butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) are used to prevent fats, oils, and fat-containing foods from becoming rancid, and BHA or BHT is often also added to food packaging materials. In fact, the use of BHA is near universal, despite its proven or suspected causative role in liver damage, behaviour problems, and brain defects. Researchers have reported that BHA in the diet of pregnant mice results in brain enzyme changes in their offspring, including a 50% decreased activity in brain cholinesterase, which could affect the normal sequence of neurological development in young animals. BHA and BHT also affect the animals' sleep, levels of aggression, and weight (Steinman 1990). Unfortunately for growing pets, Hills Science Diet includes BHA in their puppy and kitten, as well as adult formulations (Peden 1999). Yet despite its hazards, BHA may not even reliably fulfil its intended role. According to Eastman Chemical Products, “BHA and/or BHT are not found to provide significant improvement in the stability of vegetable oils.” (Jacobsen 1972).

Sodium nitrite, often used as a colouring agent, fixative, and preservative, has the ability to combine with natural stomach and food chemicals to create nitrosamines, which are powerful carcinogens (Perry 1996). In fact, sodium nitrite is so dangerous that the FDA attempted to ban it in the 1980s, but failed due to powerful lobbying from food manufacturers, who make widespread use of its colouring and preservative properties (Peden 1999).


Rendering involves melting to separate fat-soluble from water-soluble and solid components, and extrusion uses a heat and pressure system to ‘puff’ dry foods into nuggets or kibbles (API 2002). The heating, freezing, dehydrating, canning, extruding, pelleting and baking that occurs during the processing of commercial meat-based pet food subjects sensitive nutrients such as enzymes and vitamins to temperatures, pressures and chemical treatments which markedly impair their biological activity, and hence their nutritional value. Consequently the final product must be fortified with vitamins and minerals. Despite this, 7 – 12% of pet foods analysed by US state agriculture departments failed chemical analyses for guaranteed nutrients (Perry 1996).

Enzymes, which assist in the digestion of most other nutrients, and hence play a very important role, are also the most vulnerable to heat or pH-induced denaturation (molecular unraveling). Biochemist Edward Howell states that enzymes are “completely destroyed by 2 or 3 minutes of boiling in water. Furthermore, they are destroyed to the extent of 100 percent in baking, broiling, frying, stewing, canning; and 80 to 95 percent by the customary one-half hour pasteurization period at 145 degrees F. The extreme heat liability of enzymes renders the food intake highly enzyme deficient and this deficiency is communicated to the organism. I make these statements only after several years of intensive study of the subject and believe them to be essentially correct.” (Howell 1980).

From 1932 to 1942 Dr. Francis Pottenger conducted a feed­ing experiment involving 900 cats, to determine the effects of fresh as opposed to cooked food. His carefully documented work, most recently published in 1983 as Pottenger’s Cats, fills a 126 page book with charts and photos. Pottenger found that those cats eating cooked food were “irritable, tormented by vermin and intes­tinal parasites, suffered skin lesions, allergies, heart, kidney and liver problems, bad eyesight, infections of glands, joint and nervous disorders.” The raw food group suffered none of these ailments. The food in both groups, although essentially the same, was cooked for one group and uncooked for the other (Pottenger 1983). Despite its age, Pottenger’s carefully documented study clearly illustrates the nutritional and health advantages of fresh foods.

Associated diseases

Diseases described in the scientific literature following long-term maintenance of cats and dogs on commercial meat-based diets include kidney, liver, heart, neurologic, visual, neuromuscular and skin diseases, bleeding disorders, birth defects, immunocompromisation and infectious diseases (Dow et al. 1989, DiBartola et al. 1993, Strieker et al. 1996 and Freytag et al. 2003; see Appendices). Some of these findings are described below.

Additionally, after examining and treating many thousands of animals over more than a decade as a practicing veterinarian, I’ve become convinced that rates of diseases such as cancer, kidney and liver disease, are far higher than would occur naturally. I believe that many cases are probably exacerbated or directly caused by long-term exposure to the numerous hazardous ingredients of meat-based diets. Kidney disease, for example, is one of the top three killers of companion animals, and may be exacerbated by the extra load placed on the kidneys by the high protein content (Di Bartola et al. 1993) and poor quality ingredients of many meat-based commercial diets. Left untreated, kidney disease may result in the systemic buildup of toxins, leading to uraemic poisoning, appetite loss, vomiting, neurological disorders, and death.

Kidney, liver, neurologic, neuromuscular and infectious diseases

In the Journal of the American Veterinary Medical Association in 1989, Dow and colleagues published the results of a retrospective review of serum biochemical data from 501 cats over a three year period from 1984 to 1987. 37% (186/501) suffered from abnormally low potassium levels (hypokalaemia). Within the group of 186 hypokalaemic cats, 48% (89/186) had elevated cholesterol levels, 47% (88/186) had elevated blood glucose levels, 46% (86/186) had high serum urea nitrogen concentrations, 43% (73/186) had high chlorine levels, and 39% (73/186) had high serum creatinine concentrations. Kidney disease (specifically, chronic renal failure), liver disease, viral or bacterial infections, and neurologic or neuromuscular disease were all statistically significantly associated (p < 0.05) with the occurrence of hypokalaemia. Cats with severe hypokalaemia were 3.5 times more likely to have chronic renal failure than cats with less severe hypokalaemia.

Additionally, DiBartola and colleagues also published the results of a two year study of ten cats maintained on a commercial diet in the Journal of the American Veterinary Medical Association in 1993. 50% (5/10) developed inflammation and scaring of the kidneys (specifically, lymphoplasmacytic interstitial nephritis and interstitial fibrosis).

Heart disease, neurological dysfunction, visual disturbances and immunocompromisation

In Science in 1987, Pion and colleagues demonstrated low plasma taurine concentrations associated with echocardiographic (ultrasonographic) evidence of myocardial (heart muscle) failure in 21 cats fed commercial meat-based cat foods. At that time thousands of pet cats died annually from the heart muscle disease dilated cardiomyopathy.

Deficiency of the amino acid taurine may also result in retinal atrophy, causing visual deficits, developmental deficits of the visual cortex and cerebellum, reproductive failure and thromboembolism. Normal growth, immune and neurological function are all dependent on adequate taurine levels (National Research Council 1986, Palackal et al. 1986, Blood & Studdert 1988, Baker & Czarnecki-Maulden 1991, Peden 1999 & Gray 2004). Pion and colleagues demonstrated that oral supplementation with taurine reversed the disease, and consequently most meat-based and vegetarian pet foods are now supplemented with synthetic taurine.

The amino acid L-Carnitine is of potential importance to dogs at risk of dilated cardiomyopathy. This potentially fatal disease affects about 2% of all dogs, appearing mostly in large and giant breeds. A small percentage of these lack sufficient cardiac L-Carnitine, which is normally removed during processing, and not supplemented due to cost (Porreca 1995).

Bleeding disorders

In the Journal of Small Animal Practice, Strieker and colleagues (1996) demonstrated clinical signs of vitamin K deficiency in cats fed two commercial canned diets high in salmon or tuna. Some of the queens and kittens died, while survivors had increased blood clotting times. Necropsies revealed bleeding in the liver and intestines.

Skin diseases

In the Journal of the American Veterinary Medical Association in 1988, Sousa and colleagues examined 13 dogs with skin disease, described as a crusting dermatosis of the mucotaneous junctions around the mouth and eyes, pressure points such as elbows, and trunk. The disease was similar to that which has previously been called canine dry pyoderma, but is now known to be a zinc-responsive dermatosis. All of the dogs had been fed nutritionally inadequate commercial dry dog foods, and the skin diseases of all 13 resolved completely after their diets were changed to one that met the National Research Council's nutritional recommendations.

Birth defects

High concentrations of retinoids (vitamin A derivatives) occur in some commercial cat food formulations as a result of the use of animal liver as an ingredient. In the Journal of Animal Physiology and Animal Nutrition, Freytag and colleagues (2003) published their study of 397 kittens from 97 litters of queens fed high retinoid diets. They demonstrated that high retinoid concentrations may cause birth defects in kittens, namely cleft palate, cranioschisis (defects in closure of the bones of the skull, fatally exposing the brain), foreshortened mandible (lower jaw), stenotic colon (strictures in the large intestine), cardiac enlargement, and agenesis (failure of development) of the spinal cord and small intestine.

Premium brands

While organically farmed animals may avoid hormones and antibiotics, and while extensively farmed animals may avoid the worst excesses of cruelty suffered by intensively farmed animals, investigations of ‘free range’ or similar farms repeatedly reveal that conditions on many such farms remain far from humane or natural, and that the animals still undergo considerable suffering. And even animals from the best farms still have to endure the violent, frightening and potentially painful experience of death at a modern slaughterhouse, normally at a very premature stage of life.

A major ethical disadvantage of some premium brands is that unlike lesser brands, which rely heavily on byproducts of the farming and slaughter industries, some premium brands use animals killed specifically for pet food, thereby providing far greater financial support for these industries.


Meat-based companion animal diets provide a vast industrial dumping ground for slaughterhouse waste products, 4-D meat (from animals who are dead, dying, diseased or disabled on arrival at the slaughterhouse), old or spoiled supermarket meat, large numbers of rendered dogs and cats from animal shelters, sometimes with detectable levels of euthanising solution, old restaurant grease, complete with high concentrations of dangerous free radicals and trans fatty acids, and damaged or spoiled fish, sometimes with dangerous levels of mercury, PCBs and other toxins. The combined results are rendered so delicious to cats and dogs by the addition of ‘digest’ – a soup of partially dissolved entrails from chickens and other animals – that more than 95% of US companion animals subsist primarily on commercial meat-based diets (Perry 1996), generating in excess of $11 billion annually for the US pet food industry (API 2002).

The pathogenic bacteria, protozoa, fungi, viruses and prions, and their associated endotoxins and mycotoxins, and the hormone and antibiotic residues and potentially dangerous preservatives common to commercial meat-based diets, also present important hazards to the health of our companion animals.

Diseases described in the scientific literature following long-term maintenance of cats and dogs on meat-based diets include kidney, liver, heart, neurologic, visual, neuromuscular and skin diseases, bleeding disorders, birth defects, immunocompromisation and infectious diseases (Dow et al. 1989, DiBartola et al. 1993, Strieker et al. 1996 and Freytag et al. 2003). As a practicing veterinarian I believe that diseases such as cancer, kidney, liver and heart failure are far more common than they should be, and that many are likely to be exacerbated or directly caused by the numerous hazardous ingredients of commercial meat-based cat and dog diets. Kidney disease, for example, is one of the top three killers of companion animals, and is exacerbated by the extra load placed on the kidneys by the high protein content (Di Bartola et al. 1993) and poor quality ingredients of many meat-based diets. Left untreated, kidney disease may result in the systemic buildup of toxins, leading to loss of appetite, uraemic poisoning, vomiting, neurological disorders, and death. The serious and potentially-fatal disease of hyperthyroidism in cats first surfaced in the 1970s, when canned food products appeared on the market, and may be related to excessive dietary iodine levels (Smith 1993).

Our widespread reliance on meat-based diets causes enormous suffering, ill-health and premature deaths for literally billions of ‘food’ and companion animals annually. A range of healthy vegetarian alternatives are available, however. Vegetarian canine and feline diets are explored elsewhere in this website.


  • American Medical Association (AMA) House of Delegates Annual Meeting. Resolution 508 - Antimicrobial Use and Resistance. 2001.
  • American Public Health Association (APHA). Policy Number 99081. 1999.
  • Anonymous. Undated. Your pet's dog food could be dangerous., accessed 12 Aug. 2004.
  • Anonymous. America's fish: fair or foul? Consumer Reports. 2001., accessed 29 Jul. 2004.
  • Animal Protection Institute (API). What is REALLY in your pet's food?: you may not want to know. Revised 29 Jan. 2002. WJRT-TV/DT., accessed 17 May 2004.
  • Baker DH, Czarnecki-Maulden GL. Comparative nutrition of dogs and cats. Annu Rev Nutr 1991; 11: 239-263.
  • Barker J. & Williams H. Greene County Animal Mortality Collection Ramp. NC, US: North Carolina Cooperative Extension Service. 1993.
  • BBC News. 14 Dec. 1998.
  • Belfield, Wendell O. & Zucker, M. Very Healthy Cat Book. New York, NY, US: McGraw-Hill Book Company. 31. 1983.
  • Bingham AK, Huebner HJ, Phillips TD, Bauer JE. Identification and reduction of urinary aflatoxin metabolites in dogs. Food Chem Toxicol. 2004; 42(11): 1851-1858.
  • Blood D. and Studdert V. Bailliere’s Comprehensive Veterinary Dictionary. London: Bailliere Tindall. 1988.
  • Boyer CI Jr, Andrews EJ, deLahunta A, Bache CA, Gutenman WH, Lisk DJ. Accumulation of mercury and selenium in tissues of kittens fed commercial cat food. Cornell Vet 1978; 68(3): 365-374.
  • DiBartola SP, Buffington CA, Chew DJ, McLoughlin MA, Sparks RA. Development of chronic renal disease in cats fed a commercial diet. J Am Vet Med Assoc 1993; 202(5): 744-751.
  • Dow SW, Fettman MJ, Curtis CR, LeCouteur RA. Hypokalemia in cats: 186 cases (1984-1987). J Am Vet Med Assoc 1989; 194(11): 1604-1608.
  • Eckhouse J. How dogs and cats get recycled into pet food. San Francisco Chronicle. 1990; Feb 19.
  • Eisnitz G. Slaughterhouse. Amherst, NY: Prometheus Books. 1997. 175.
  • Food and Drug Administration/Center for Veterinary Medicine (FDA/CVM). 2002. Report on the risk from pentobarbital in dog food., accessed 12 Aug. 2004.
  • Freytag TL, Liu SM, Rogers QR, Morris JG. Teratogenic effects of chronic ingestion of high levels of vitamin A in cats. J Anim Physiol Anim Nutr (Berl) 2003; 87(1-2): 42-51.
  • Frist, US Senator Bill, in a hearing of the Subcommittee on Public Health to examine the problem of and potential solutions for the problem of antimicrobial resistance. Feb. 1999.
  • Gillen J. Obligate Carnivore. Seattle, WA: Stein Hoist Books. 2003.
  • Gray, Christina M.; Sellon, Rance K.; Freeman, Lisa M. Nutritional Adequacy of Two Vegan Diets for Cats. JAVMA 2004;225(11):1670-1675.
  • Gurkin A., Fenstermacher, S. Petfood Report. Mt. Morris, IL, US: Watt Trade Press. 1999.
  • Halpin K., Sullivan J., Bradfield R., Liu, Q. By-products usage: results from a survey of major petfood manufacturers. Petfood Industry. 1999 May – Jun;37-40.
  • Houpt KA, Essick LA, Shaw EB, Alo DK, Gilmartin JE, Gutenmann WH, Littman CB, Lisk DJ. A tuna fish diet influences cat behavior. J Toxicol Environ Health. 1988;24(2):161-72.
  • Howell E. Food Enzymes for Health & Longevity. Woodstock Valley, CT: Omangod Press. xx. 1980.
  • Jacobson, M. Eater’s Digest. Garden City, NY, US: Doubleday & Co. Inc. 1972:86-87.
  • Kvamme J. SRM skirmish. Petfood Industry. 2004 Mar;46(3):4,52.
  • Lewis L., Morris M., Hand M. Small Animal Clinical Nutrition. (3rd Edn). Topeka, KS, US: Mark Morris Associates. 1987:2-3.
  • Martin A. Food Pets Die For: Shocking Facts About Pet Food. (2nd Edn). Troutdale, OR, US: NewSage Press. 2003.
  • Mason J, Singer P. Animal Factories. New York, NY, US: Harmony Books. 1990.
  • National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIAID). The problem of antibiotic resistance., accessed Apr. 2004.
  • National Research Council. Nutrient requirements of cats. Washington, DC: National Academy Press, 1986.
  • National Research Council (NRC). Chapter 7: Costs of eliminating subtherapeutic use of antibiotics. In The Use of Drugs in Food Animals: Benefits and Risk. Washington, D.C., US: National Academy Press. 1999:179.
  • Palackal T, Moretz R, Wisniewski H, Sturman J. Abnormal visual cortex development in the kitten associated with maternal dietary taurine deprivation. J Neurosci Res. 1986;15(2):223-239.
  • Pion PD, Kittleson MD, Rogers QR, Morris JG. Science. Myocardial failure in cats associated with low plasma taurine: a reversible cardiomyopathy. Science 1987 Aug 14;237(4816):764-8.
  • Pearl G. Personal communication. Fats and Proteins Research Foundation, Inc., Bloomington, IL. 1997. In Halpin K., Sullivan J., Bradfield R., Liu, Q. By-products usage: results from a survey of major petfood manufacturers. Petfood Industry. 1999 May – Jun:37-40.
  • Peden J. Vegetarian Cats & Dogs. 3rd Edn. Troy, MT, US: Harbingers of a New Age. 1999.
  • Peden J. Personal communication to Andrew Knight re: ethoxyquin. 2004.
  • Perry T. What's really for dinner?: the truth about commercial pet food. The Animals' Agenda. 1996. Nov. - Dec., accessed 2004.
  • Peterson Co. Product Specifications. Date unknown. Peterson Co. is a large distributor of liquid enzymatic digests to the pet food industry.
  • Phillips T. Rendered products guide: fats, animal proteins and quality criteria. Petfood Industry. 1994. Jan. – Feb.:12 - 21.
  • Pitcairn R., Pitcairn S. Dr. Pitcairn’s Complete Guide to Natural Health for Dogs & Cats. Emmaus, PA, US: Rodale Press. 1995:16.
  • Plechner A., Zucker, M. Pet Allergies. Inglewood, CA, US: Very Healthy Enterprises. 1986:13.
  • Porreca K. Personal letter to James Peden re: Interview of University of California (Davis), North Carolina State University, and University of Guelph researchers investigating the connection between dilated cardiomyopathy and diet. 1995 Mar. 17.
  • Pottenger F.M. Jr. Pottenger’s Cats. La mesa, CA, US: Price-Pottenger Nutrition Foundation. 1983.
  • Smith C.A. Research roundup: changes and challenges in feline nutrition. J Am Vet Med Assoc. 1993;203:1395-1400.
  • Sousa CA, Stannard AA, Ihrke PJ, Reinke SI, Schmeitzel LP. Dermatosis associated with feeding generic dog food: 13 cases (1981-1982). J Am Vet Med Assoc. 1988 Mar 1;192(5):676-80.
  • Steinman D. Diet for a Poisoned Planet. New York, NY, US: Ballantine Books. 1990:355.
  • Strieker MJ, Morris JG, Feldman BF, Rogers QR. Vitamin K deficiency in cats fed commercial fish-based diets. J Small Anim Pract. 1996 Jul;37(7):322-6.
  • Strombeck D. The question of bacteria in processed pet foods. Excerpted from Home Prepared Dog & Cat Diets, The Healthful Alternative. Date unknown., accessed 29 Jul. 2004.
  • Union of Concerned Scientists. Hogging it: Estimates of antimicrobial abuse in livestock. Jan. 2001.
  • World Health Organization (WHO). The Medical Impact of the Use of Antimicrobials in Food Animals: Report of a WHO Meeting, Berlin, Germany, 13-17 October 1997., accessed 12 Aug. 2004.

Appendix: studies

A sizeable body of studies published in the biomedical literature illustrate the hazardous ingredients sometimes found within meat-based pet food, and the diseases that may be associated with long-term maintenance on such diets.