The Guide Dog Chronicles: It’s a tumor

by Kate Chamberlin

The doctor tells me, “It’s a tumor.” The very word fills me with fear and dread; a feeling of foreboding.

“Well, if it’s one of those fatty tumors, can you Liposuction it out?” I quip, but my palms are clammy and chills permeate my insides.

“I’m not getting any fluid out,” she says aspirating the ping pong ball-sized lump, “so it’s not a cyst.”

Intellectually, I think there are two kinds of lumps: benign and malignant. The fatty tumor is usually benign and harmless. The malignant kind is cancerous and often fatal. Sometimes surgery and medication can cause the cancer to go into remission.

“It appears to be a connective tissue tumor,” the vet says lifting her face away from the microscope. “I’d like to take it out and have it biopsied.”

I have a sinking feeling that there’s something she doesn’t want to tell me, but we set a date for Future’s surgery.

I have ten days to stew about life’s ups and downs.

Future Grace is not just a beautiful Golden Retriever; she’s my friend and confidante. I know she’ll never tell my secrets and she always understands my moods. And she isn’t just a pet; she’s my guide dog and a trusted companion. We go everywhere together: San Antonio, Boston, Wegman’s for groceries, the bathroom – just everywhere. She’s a celebrity. Most people remember her name instead of mine. I’ve even been called Mrs. Future!

She’s an excellent educator. The hundreds of people we’ve met, talked with, laughed with and worked with during the past 7-1/2 years have a better understanding about guide dog teams. They’ve learned to respect the fact that when she’s in harness, she’s working and should be left to do her duty. She’s my new lease on life – my Golden Future.

The morning of her surgery dawns cold and dreary. In the vet’s office, Future is reluctant to leave me. I want to hug her and take her back home. She’d like that, too. “Future, go,” I tell her so she knows it’s okay to leave me. This tough love stuff is really rough!

Alone at home waiting for her surgery to end, I’m acutely aware of how very alone I am. There is no jangle of dog tags when I get up from my chair, no warm head resting on my lap when I sit down, and no sturdy body nudging me as I walk to the laundry room.

I pass the time by cleaning the whole house and eating the leftover Christmas cookies, nut bread and candy.

“Her surgery is over,” the vet phones me. “She’s up walking around and doing fine.”

I have time to wash and wax the kitchen floor as well as eat a tube of frozen cookie dough before my ride comes to take me to pick up Future.

“Future can’t work for seven to ten days,” the vet tells me. I feel the large bandage on Future’s left, front elbow. Was the tumor benign or malignant? The lab results won’t be in for another ten to fourteen days.

After two days of recuperation, we do obedience drills, slow walks and lots of hugging. It’s hard to keep her from licking the drain tube that sticks out of the top of the bandage.

The days pass. I’m getting more and more nervous about not hearing the lab results. Is that good news or not?

“The tumor is benign,” the vet says over the phone. “We’ll see you two in the spring for her annual check up.”

Phew! We can renew our lease on life. She is still my Golden Future.

Can Your Dog Get Mad Cow Disease?

Everyoneʼs been talking about BSE. Even Oprah. But what does it mean for you and your pets?

Now that BSE has been in the news in a big way, it’s time for Good Dog! to offer some comments. We’ve known about BSE for several years, but had vowed to ourselves to keep our mouths shut. We didn’t want to start a big scare if it was not warranted.

Well, it’s probably still not warranted, even if you’re one of our readers living in
England and feeding a British-made food.

BSE is Bovine Spongiform Encephalopathy. It’s a mystery disease that causes the brain to turn to Swiss cheese. Well, not exactly. But the brain develops holes like Swiss cheese, and begins to look like a sponge. That’s why it’s called “spongi-form.” In sheep, the disease is called scrapie. In people, it’s Creutzfeld-Jakob Disease (CJD). A similar disease also affects cats. So far, no cases of any similar diseases have been reported in dogs anywhere in the world.

We’ve been following the story in our sister publication, Dog Industry Newsletter, for several years. Judging from the response to our articles, the American pet food industry has been quite concerned.

Here in the U.S., there have been no cases of BSE reported – even after a decade-long search by the U.S. Department of Agriculture. But steps are being taken anyway, to make sure that BSE doesn’t get a toehold here, and even if it does, that it doesn’t become an epidemic. One step being taken is a long-standing ban on the importation of meat and by-products from any country with BSE. That’s handled by the U.S.D.A.’s APHIS animal and plant inspection service (the Beagle Brigade people.) APHIS is tightening their surveillance, as are the USDA’s meat inspectors at the slaughterhouses.

A few years ago, a voluntary ban on old sheep was instituted by American rendering plants. These factories take animal carcasses and body parts not used for human consumption, and use heat to make them into meat meals for use in animal feed. The ban covers older sheep, which are more likely to have scrapie. (It takes several years for scrapie and BSE to show up, so animals under the age of one year are unlikely to have the diseases.)  In addition, the renderers will only work with  sheep carcasses that come from federally-inspected meat plants.

The last major scrapie outbreak occurred in the early 1950’s in the U.S. In 1952, there was also a major outbreak in Australia and New Zealand. Those countries killed their entire flocks of sheep, and eradicated scrapie. The U.S. sheep industry didn’t go as far, and scrapie still exists here, although on a very small scale. Still, nearly all pet food manufacturers have chosen to buy lamb for their lamb and rice pet foods from scrapie-free Australia and New Zealand.

These brain diseases are still not well-understood. They’re not caused by a bacteria or a virus, but by an unusual type of protein. It’s not alive, and therefore it can’t be killed. But high heat can inactivate the protein, to a degree.

The disease can be spread by consumption of brains and spinal cords that contain the protein. It can apparently also be transmitted through blood. Six of the ten most recent British deaths from CJD were people who had worked in jobs where their blood might have come in contact with contaminated beef. The disease can also be transmitted through blood donations from people with CJD, and through growth and fertility hormones. What’s the connection with the hormones? They’re derived from corpses, and sometimes the corpses contain the protein. Five women and one man died in Australia after receiving the hormones. One scientist in Australia estimates that there could be up to 60 cases of CJD a year in Australia. Switzerland has had four to seven cases of CJD a year between 1991 and 1995, and 68 cases of BSE in 1995, 64 in 1994. No cases of BSE have been reported in the U.S.

Cats are affected, too. In the past six years, 70 domestic cats have died from encephalopathy in the United Kingdom. They call it “mad cat disease” there. The speculation is that the disease was transmitted through pet food containing the remains of BSE-infected cattle.

Various countries have been taking action to protect people and pets from the BSE family of diseases. The United Kingdom’s Pet Food Manufacturers’ Association introduced a voluntary ban on what is euphemistically called “specified bovine offal” of SBO. The voluntary ban went into effect before the government introduced legislation in June of 1989. The ban on SBO in human food followed five months later.

Andrew Mackin, an animal nutritionist at Edinburgh University’s Royal Dick Veterinary College said, “It would have been safer to eat a tin of (dog food) than a beef burger in summer, 1989.” Speaking about today’s products, he said, “Pet foods are highly processed and sterilized to a very high standard.”

As for the need for a study of the problem in animals, the question of statistical significance comes up. A British Ministry of Agriculture spokesman said, “There have only been 70 cases out of a (current) cat population of 7 million. They need something like 200 cases to form a proper study and to come to any proper conclusions.” Remember, though, that those 70 cases occurred over a long period of time, and out of many millions of cats. And most of the cases occurred in older cats, who were alive before the ban on SBO.

Meanwhile, the British government is considering banning the use of all mammal protein in pet food and other animal feed. The government just rejected a plan to do a mass slaughter of all British cattle to restore confidence. But the damage has been done to the reputation of British foods abroad. Glen Brookfield, Route Managing Director for Pets Choice Ltd. said, “The problem is market forces … we spent two years penetrating the French market and just as we managed it, we’re out overnight.”

The Japanese have extended a 45-year ban on British beef imports to include pet food. “Japan has not allowed imports of beef from England, but it is possible that some beef is contained in pet food,” Agriculture Minister Ichizo Ohara told the Japanese Parliament. “We will inform the British Embassy here of the banning of all imports of beef products, including processed foods.”

Switzerland has also banned the use of meat, offal (by-products) and bone meal in animal feed. All cattle, sheep and goats more than six months old must be examined by an expert before slaughter, and all animal owners must report animals suspected of sickness to a veterinarian.

Here in the U.S., the Department of Agriculture is increasing its role in surveillance inspections for BSE. Inspectors from the Food Safety and Inspection Service will now look for any animals that show symptoms associated with BSE. There are specific procedures they’ll follow to insure that those animals are kept out of the meat or feed supply. The U.S. has not imported processed beef, or cattle, from the United Kingdom since 1989. Similar stringent restrictions on the importation of cattle and beef protect us from the possibility of BSE coming in from other countries where it is prevalent.

The USDA has examined over 2,660 suspected animals from 43 states, and hasn’t found BSE in American cattle. On March 22, the USDA held a meeting with 70 people from various international health authorities, state and public health agencies, the scientific community and industry. The goal was to discuss the situation and see what could be done to further prevent the spread of the disease.

Meanwhile, the U.S. Food and Drug Administration (FDA) is considering a ban on the use of cattle and sheep remains in cattle feed. The agency is considering whether to issue extended regulations based on an August, 1994 proposal to ban the use of goats and certain parts of sheep in animal feeds. According to the experts at the FDA we spoke with, the regulations will codify the voluntary ban on feeding ruminant by-products to other ruminants. A new proposed regulation is being drafted now. The purpose behind this regulation will be to add another layer of safety into the food supply. If there were a case of BSE, it would not be spread in animal feed, and an epidemic would be prevented. The safety factor would help protect people as well as food animals and pets.

Another safety factor involves the way meat meals are processed in the U.S. A new study shows that in Britain and other European nations, four of the 15 rendering processes used aren’t hot enough to inactivate the protein. In the U.S., renderers have always used high-temperature rendering. (In England, farmers used to feed their baby calves “greaves,” which were by-products that were not fully rendered. That practice has now been stopped.)

What does the FDA say about pet food? Dr. David Dzanis of the FDA’s Center for Veterinary Medicine says he sees little cause for concern. He told Good Dog! “There have been no reported cases of brain diseases like this in dogs, anywhere in the world. (See article below for an update.) The U.S. is currently BSE-free, and our high-temperature rendering processes would help inactivate the protein that causes BSE. Add to that the extra steps that are being taken to prevent BSE from getting into the country, and the ruminant to ruminant ban that’s being implemented voluntarily, and you’ve got a very safe pet food supply.”

Keith Hansen, Nutritionist for Merrick Petfoods (which owns its own rendering plant), concurs: “We have, without question, the safest beef supply, and the safest feed supply in the world.”

But the whole issue might become moot, sooner, rather than later. A new, simple test for BSE and similar diseases has been developed which appears to be accurate in people, cows and other animals.

Dr. Michael Harrington, of the Cali-fornia Institute of Technology in Pasadena, California, is working with scientists from the U.S. National Institutes of Health in Bethesda, Maryland. He expects to submit a paper on the new test to the peer-reviewed New England Journal of Medicine in the next few weeks.

Harrington, a native of Glasgow, Scotland, said he identified two proteins 10 years ago. These proteins are present in cases of CJD, and in the similar diseases which affect animals. His first test for the proteins, developed a decade ago, was too technologically complex for widespread use.

Dr. Harrington told the Reuters wire service, “The test has been available but no one has done it. Why is that? Because the technology is really more than hospitals and clinics will ever do. It takes about three days to do and they just don’t like the technical complexities.”

Harrington received funding a year ago to devise a simpler test. The new test uses an antibody to identify the proteins, which he has numbered 130 and 131. The same two proteins, or markers, which are extracted from spinal fluid, are also found in cows with BSE. Using the new test, a handful of technicians could test up to 2,000 cows a month.

Harrington said that in the thousands of human cases he has examined using the old test and the new test, only three diagnoses were found to be inaccurate. The tests he has run on cows and other animals, while accurate in detecting spongiform encephalopathy such as BSE, have only been used on a small number of animals.

With this new test, Harrington believes that cows with BSE could be singled out. But more rigorous testing of the test is needed, according to Harrington. Once his data is published, other scientists can work with the procedure.

It’s still not known how early the two proteins appear during the development of the disease, which has a long incubation period. “But that can be evaluated once people get hold of this marker and start studying it,” Harrington said. “One can look at it experimentally and find out how early it appears in the course of the disease. Then we’ll have some idea, (if) this appears only in the established clinical syndrome in the animal or the human, or (if) it appears  before that.” In other words, will the marker be detectable ahead of the symptoms?

What does this all mean to you and your pets? Not a whole lot, at this point. Our advice is to stay calm, and to not fret. The food supply in the U.S. is quite safe right now, and even more precautions are being piled on, just in case. So all you  have do to is watch the situation and see if it changes. If you’re exceptionally concerned and have to do something, you can feed a chicken or poultry-based food. These brain diseases don’t affect any birds, including chickens or turkeys. (Then again, they don’t affect dogs, either, so why worry?)

The bottom line is that there’s no need for concern at this point. The pet food industry is watching carefully, the U.S. Department of Agriculture is watching carefully, and the Food and Drug Administration is watching carefully. So far, so good. But we’ll be watching carefully, too, and we’ll let you know if there are any further developments.

Starving cancer before it starves your dog

The idea of starving cancer before it starves your dog is an intriguing one, and the subject of much research in the last few years. These studies in dogs have led to breakthroughs in the nutritional treatment of both human and canine cancer patients.

Dr. Gregory Ogilvie, DVM is a professor at the Colorado State Univer-sity College of Veterinary Medicine and Biomedical Sciences. His research into how cancer affects nutritional needs is continuing, but has already led to some important discoveries.

Dr. Ogilvie says, “We have shown that dogs with cancer have dramatic changes in their ability to use nutrients for energy.” His early studies have determined that the energy requirements for dogs with cancer are not higher than in healthy dogs. The difference is that cancer alters the way the body uses nutrients, in effect shutting down the body so it can’t utilize its food. Those body changes continue even after the cancer is sent into remission. “Cancer changes the body and the body doesn’t recover from it even after the cancer is eliminated from the body,” Dr. Ogilvie says.

“Cancer in the body causes significant alterations in carbohydrate, protein, and lipid metabolism,” he continues. “These alterations result in decreased quality of life and decreased response to therapy. The need to reduce the lactate and insulin levels in dogs with cancer is of paramount concern to allow the body’s metabolic processes to work more efficiently to the host’s benefit.”

Glucose is the sugar the body makes from food. It’s incredibly important to the body, as it is the only nutrient which can cross the blood/brain barrier to feed the brain. Because supplying energy to the brain is the single most important function for the rest of the body, glucose production takes priority over nearly every other body function. Protein is broken down by the body into amino acids, some of which are used to make glucose. Fat gets stored for later use instead of being used for glucose production. But most of the glucose made by the body comes from digesting carbohydrates.

Cereal grains, such as corn, wheat, and barley, contain carbohydrates in the forms of sugar and starch. Digestion breaks these down to make glucose.

Immediately after a meal, high levels of glucose in the blood cause the rapid secretion of insulin, which causes the rapid uptake, storage and use of glucose by almost all tissues of the body.

That’s how things are supposed to work. With cancer patients, though, it’s different. The glucose isn’t put to work, but is instead converted to lactate. The body attempts to convert lactate back to glucose, and that requires energy. Instead of the glucose being used by the body for energy, it is diverted into this energy-draining lactate loop. Now you know why fatigue and “starvation” are major cancer symptoms.

Dr. Ogilvie’s team has determined that it’s critical to reduce the lactate and insulin levels so the dog can use the energy in the form of glucose.

Insulin levels can be controlled by feeding a food that’s relatively low in simple carbohydrates. As for protein, Dr. Ogilvie says, “Because cancer competes with the host for specific amino acids (from protein), we recommend that highly biodegradable yet modest amounts of proteins be provided to the cancer patient.”

For adequate calories, fat may be the best bet, according to Dr. Ogilvie, because there is some evidence that cancer cannot utilize fat.

He also recommends a diet containing omega-3 fatty acids, which have been demonstrated to be of value for the cancer patient. A number of studies in rodents and people have shown that omega-3 fatty acids can reduce lactate and insulin levels. The omega-3 fatty acids also have anticancer properties, including the ability to reduce or eliminate metastatic disease.

Dr. Ogilvie says that there is no commercially-available diet which is ideally suited for the cancer patient. He also says that it’s difficult to create a homemade diet which fills the bill.

Some foods that meet many of the requirements for dogs with cancer are the Eukanuba Veterinary Diets® Nutritional Recovery Formulas®. Made by The Iams Company, these have excellent flavor and are packed with energy, which encourages the sick dog to eat. But more importantly, the foods have a different composition than most, with an emphasis on protein and fat rather than carbohydrate, and high levels of omega-3 fatty acids.

Dr. Glenna E. Mauldin, DVM, MS, DACVIM and Staff Veterinarian at The Donaldson-Atwood Cancer Clinic of The Animal Medical Center of New York has also written about the best diet to feed the cancer patient. She says that “Weight loss has been shown repeatedly to be an independent determinant of prognosis in the human cancer patient. Severe debilitation and eventual death from malnourishment may result in affected individuals.”

Dr. Mauldin, in a paper titled “Feeding the Cancer Patient,” concurs with Dr. Ogilvie that it’s possible to take advantage of the differences in metabolic style that set tumor cells apart from normal tissue.

Dr. Mauldin says,“A diet high in fat and protein but relatively low in carbohydrates should selectively supply energy to the host and meet potentially increased protein requirements, while denying tumor cells the readily available carbohydrate required for continued growth. Beneficial effects have been documented in human cancer patients fed such diets, including improved weight gain, improved energy and nitrogen balance, improved preservation of body adipose stores, and decreased glucose intolerance.”

Dr. Mauldin is currently conducting a study at The Animal Medical Center with the Eukanuba Veterinary Diet Nutritional Recovery Formula to see whether it, in fact, can starve the tumor, yet feed the dog.

References:
Mauldin, G. E. Feeding the Cancer Patient, Recent Advances in Canine and Feline Nutritional Research: Proceedings of the 1996 Iams International Nutrition Sym-posium: The Iams Company, Dayton, OH.

Ogilvie, G.K. and Moore, A.S. Managing the Veterinary Cancer Patient: A Practice Manual. Published by Veterinary Learning Systems.

Additional material supplied by Morris Animal Foundation, Englewood, CO., including January, 1997 letter from Dr. Gregory Ogilvie.

Is Your Dog Too Fat?

Here’s a diet plan both you and your dog can live with!

Dottie LaFlamme, DVM, Ph.D.

Obesity is the most common nutrition-related disease in dogs. It won’t kill your dog, but it is linked with a number of health problems. Unfortunately, most of the evidence we have concerning the links between obesity and diseases comes from other species.

Being very obese (also called gross or morbid obesity) is a definite health risk. Obesity is linked to heart disease, but it’s not likely to cause heart failure. However, it can make the stress on a weak heart worse. Obesity contributes to the pain of arthritis, due to the physical stress of the extra weight. But is being slightly overweight slightly risky? Is being moderately overweight moderately risky? We just don’t know yet.

Recognizing Obesity

It’s easy to know when your dog is grossly obese. But you probably haven’t noticed that your dog is already a little overweight. A dog who is only a little overweight will probably be ignored by the veterinarian, too. By the time most of us wake up to the fact that we have a pudgy pooch, it’s usually pretty far along. Then it takes awhile before we’re ready to take action. That’s unfortunate, as obesity is easier to prevent than treat.

You’re not alone if you haven’t realized just how fat your dog is. Recognition of obesity is one of the biggest problems of the condition. A study of the medical records of 1.5 million dogs through the Veterinary Medical Data Bank at Purdue University indicated that less than 2% of veterinary patients in the Data Bank were recognized as being obese. Compare that with two studies which showed that between 21% and 30% of 9,000 dogs seen by veterinarians should have been considered obese. Meanwhile, 54% of dog owners recognize that obesity is a problem. (Just not in their own dogs!)

The simple fact is, we don’t often recognize obesity in our own family, whether it’s in ourselves, or our dog. Maybe we’re too close to it and don’t try to critically evaluate the situation. Or maybe we just don’t want to see reality.

Most of us don’t know how much our dog weighs. It’s even tougher to know what our dog should weigh. There are no guidelines for mixed breeds, and every dog is different. Even with purebreds, there may be a range of weights listed in the breed standard which are acceptable. But then, your dog could be larger or smaller than most. Determining proper weight is just difficult to assess.

How Does Your  Dog’s Body Rate?

So, how can you tell when your dog is overweight?

While there have been systems for classifying dogs as obese, we saw the need for a new system that was both simple and accurate. We (at Ralston Purina) developed a Body Condition Scoring system. A trained pet professional such as a veterinarian or groomer can use the Body Condition Scoring (BCS) system with great accuracy. All it requires is to take a critical look and feel, and judge those observations against specific standards.

But you don’t have to be an expert to use the BCS. It helps if you can check out other dogs for comparison, though.

Here’s all you do: First, check the ribs. That’s easy. Put your hands on the dog’s sides, over the ribs, and rub over the ribs gently. You should be able to count each of the ribs. If you can’t feel and count three or four ribs (out of 13), your dog is probably overweight.

Next, look at your dog from the side. The abdomen (belly) should be tucked up in front of the back legs. Now look from above the dog. You should see a definite waist behind the dog’s ribs.

If you’re not sure if your dog is overweight, get a professional opinion.

Let’s now compare your observations to the BCS scale:

1. Emaciated.
Ribs, lumbar vertebrae (along the spine), pelvic bones and all bony prominences are visible from a distance. The dog has no discernible body fat. The dog has obviously lost not only all of his fat, but muscle, too.

2. Very Thin.
The ribs, lumbar vertebrae and pelvic bones are easily visible. No fat can be felt. Other bones are showing, but not badly. There is a minimal loss of muscle mass.

3. Thin.
The ribs can be felt easily, and may be visible. No fat can be felt. Just the tops of the vertebrae along the spine are visible. The pelvic bones are fairly prominent. The waist is easily seen from the top. The abdomen has an obvious tuck.

4. Underweight.
The ribs can be felt easily, with only a minimal covering of fat. The waist is easily seen from above. The abdominal tuck is evident.

5. Ideal.
The ribs can be felt without an excess of fat covering them. There is a thin layer of fat over the ribs, though. The waist can be observed behind the ribs when viewed from above. The abdomen is tucked up when viewed from the side.

6. Overweight.
The ribs can be felt, but there is a slight excess of fat covering them. The waist is discernible from the top of the dog, but is not prominent. The abdomen appears tucked up when viewed from the side.

7. Heavy.
The ribs can only be felt with difficulty, as they are covered with a heavy layer of fat. There are noticeable deposits of fat over the spine and at the base of the tail. The waist is absent or barely visible. The abdominal tuck may not be visible.

8. Obese.
The ribs can’t be felt because of the very heavy covering of fat. If they can be felt at all, it’s only by applying significant pressure. There are heavy fat deposits over the spine and around the base of the tail. There is no waist and no abdominal tuck. The belly may be protruding.

9. Morbid.
There are massive deposits of fat in the chest area, along the spine, and at the base of the tail. The waist and abdominal tuck are not there. There are fat deposits on the neck and legs. The abdomen is obviously protruding.

The System Checks Out

We checked the scoring system to see if different people would give the same dogs the same scores. We took 12 dogs and 6 people, and had the people evaluate the dogs twice, several days apart. The dogs had scores ranging from 2 to 8. The greatest variation between scorers was 2 units. Each person repeated his or her scores within one unit. This showed us that the system is quite accurate and reliable.

We also determined the BCS, body weight and percent over the ideal weight for 39 dogs, both before and after weight loss. We found that the BCS and the body weight correlated with the percent overweight for large and small breed dogs of both sexes.

We found, too, that each change in the BCS score was associated with approximately 11.5% change in the dog’s body weight. This does vary, though, by breed. In smaller dogs, each category represents a larger percentage change in body weight.

Ethoxyquin: You Be The Judge

 The Scientific Data and How To Understand It

In the last section we discussed both sides of the ethoxyquin controversy. The breeders said the preservative is responsible for skin problems, kidney problems, and litters born with birth defects or stillborn. The dog food manufacturers and Monsanto, maker of ethoxyquin, claim the stuff is safe, but offered no solid evidence. We concluded that more scientific study was necessary.

Then we found it. The report that provides the answer to the question of ethoxyquin’s safety.

Ethoxyquin is an antioxidant. It keeps fats from spoiling, and has been used in dog foods and animal feeds for over thirty years. As the protein content in a dog food increases, so does the need for fat (so the protein can be assimilated). Incorporation of fat into a diet means preservatives are needed, which usually means either a combination of BHA and BHT, or ethoxyquin.

Ethoxyquin is used as a preservative in chicken, horse, cattle, and pig feeds, as well as dog and cat food. It is also used to preserve the ingredients of many animal feeds, including fish meal and rendered fats like poultry fat. Further, it is used as a preservative for certain dehydrated for-age crops such as alfalfa. It is also used in paprika and chili powder to preserve the red color.

To Interpret, You Must First Understand

We’re about to provide you with the scientific data you need to make your own decision about the safety of ethoxyquin. But first, you need to know how to interpret it. So here’s a review of scientific methods, and a crash course in understanding the meaning of scientific research.

The goal of scientific research is to explain, predict, and/or control phenomena. The goal is based on the assumption that all events in the universe are orderly and that their effects have discoverable causes.

Progress towards this goal involves the acquisition of knowledge and the development and testing of theories or hypotheses. The existence of a viable theory greatly enhances and facilitates scientific progress. This is so especially when com-pared to other sources of knowledge such as experience, anecdotes, inductive and deductive reasoning.

Of all the sources of knowledge, the scientific method is undoubtedly the most efficient and reliable. Let’s compare these different methods.

The problems of using experience and anecdotal information as a method of understanding is best illustrated by a story about Aristotle.

One day the great philosopher Aristotle caught a fly. He carefully counted and recounted the number of legs on the fly. From this study, he concluded that flies have 5 legs. At that time, no one questioned the great wisdom of Aristotle. For many years to come, his findings were uncritically accepted as the truth. As it happened, though, the fly Aristotle had caught was missing a leg. Whether you believe this story or not, it shows the limitations of relying on personal experiences and anecdotes as an authority or source of knowledge. Stories you hear “through the grapevine” or from someone’s experience may contain a germ of truth, but will not be “reliable” in the scientific meaning of the word – the same result occurs every time an experiment is conducted.

Inductive and deductive reasoning also have their limitations when used as a single source of knowledge.

Inductive reasoning involves the formulations of generalizations based on an observation of a limited number of specific events. For example: Every dog book contains a chapter on canine nutrition. Therefore, all dog books contain a chapter on canine nutrition.

Deductive reasoning, on the other hand, involves the reverse process: arriving at specific conclusions based on generalizations. For example: All dog books contain a chapter on canine first aid. This book is a dog book. Therefore, this book contains a chapter on canine first aid. (Does it?)

None of these approaches are entirely satisfactory. However, when used together, as integral components of scientific research, they can be very effective. The scientific method involves induction of hypotheses based on observation, deduction of the implications of the hypotheses, the testing of the implication, and confirmation or disconfirmation of the hypotheses.

The scientific method is a very orderly process entailing a number of sequential steps: recognition and definition of a problem, formulation of a hypothesis, collection of data, confirmation or disconfirmation of the hypothesis.

These steps can be applied informally to everyday situations to determine such things as which route to take to this week-end’s dog show … the best time to go to the bank drive-in window … the best crate to purchase. The more formal application of scientific methodologies to solutions is what scientific research is all about.

Scientific research is the formal, systematic application of an experimental method to the study of problems. Basic scientific research is conducted for the purpose of theory development and refinement. Applied scientific research is conducted for the purpose of testing or applying a theory and evaluating its usefulness in solving a particular problem.
In other words, basic research pro-vides the theory that produces a possible solution to the problem. Applied research provides the data to support or disprove the theory, guide revision of the theory, or suggest the development of a new theory.
The experimental method is the only method of research which really tests a hy-pothesis in a cause-and-effect relationship. It represents the most valid approach we have to solving scientific questions, both practical and theoretical, and to advancing human knowledge.
In all experimental studies, the researcher manipulates the independent variable (who gets what; which group of subjects get which treatments) and controls other relevant variables, observing the effects on one or more dependent variables. The effects on the dependent variables are measured.

The independent variable is also referred to as the cause or the experimental variable. It is the activity or characteristic believed to make a difference. Generally, all other factors will be held equal or constant, so a cause and effect relationship can be established.

The effect is seen as the dependent variable. The dependent variable is the outcome of the experiment which is dependent upon the independent variable. It is measured by an analytical test or method to produce reliable data. When conducted properly, the experimental variable is demanding and most productive. It produces the soundest evidence concerning hypothesized cause/effect relationships. The findings of an experiment permit predictions to be made about the cause and effect relationship.

Analytical testing and methodologies are used to ensure the reliability and validity of each measurement of the dependent variable. Reliability is the degree to which a test consistently measures what it is supposed to measure. You might call it the degree of trustworthiness or dependability. The higher the reliability of a test, the more reliable the data.

Validity is the degree to which a test measures what it is supposed to measure. Many people think that a test is either valid or not valid. The truth is, a test may be valid for a particular purpose or experiment, but not for another. The question is not “Is it valid?”, but valid for what and for whom?

There are two basic requirements for any experiment. First, the method should lead to decisions regarding the reliability of the analytical data. Second, the decisions should be related to the purposes for which the analyses are being done.

The final judgement regarding the reliability of the data and validity of the analytical test or method is made on the basis of one question: Have consistently precise and accurate short and long-term biochemical data been provided?

An experiment should end with decisions regarding not only the analytical significance of the data but also the significance of the control data. Control samples must be analyzed and handled in the same rigorous way as the experimental samples. Data from both control and experimental samples reflect changes which occur in the analytic test itself. With two sources of data – control and experimental – the researcher can select the most effective method of analyzing the data to arrive at a reliable and valid conclusion.

Back to Ethoxyquin

Now that you know what to look for in an experiment, and how the scientific method works, we can ask the big question about ethoxyquin. Do we have consistently precise and accurate biochemical data, both short and long-term, on the toxico-logical effects of ethoxyquin to determine its safety?

The answer is yes, we have the data to determine its long- and short-term safety. But don’t take our word on it. Armed with the preceding basic lesson in scientific research, you can draw your own conclusions based on the information and data which follows.

Many articles published by others on ethoxyquin informed you that so-and-so did a scientific literature search to see if there were any adverse effects on animals. So and so’s findings were that no adverse effects were found. Other articles stated that someone else found evidence that ethoxyquin may be beneficial as an anticancer agent … and some said the FDA says it’s safe, therefore it must be safe. Yet other articles mention that ethoxyquin, when fed at extremely high dosages, showed it may have a cancer-causing potential. One article even went as far as discussing ethoxyquin’s effects on slowing down the aging process.

Quite frankly, that information is all well and good, but it doesn’t provide you with the information you need to know. None of the statements you just read are relevant to the question at hand: Is there precise scientific data on the toxicological effects which determines the safety of ethoxyquin?

Research on the carcinogenic potential of ethoxyquin, where it is fed well in excess of the toxic level, has nothing to do with determining the safety range of the substance. Research on anticancer properties of ethoxyquin has nothing to do with it either. Nor does anyone’s opinion on ethoxyquin’s safety really matter. All this information is nice to have, but it does not answer the question. Nor does it provide you with the hard-core scientific data that you need to make your own decision.

In order to answer the question you must review the published scientific studies relevant to the question of toxicity. If a study is not relevant, then it has no business being discussed as other than supplemental materials. It should not be used as part of your decision making process, nor in your conclusion. Unfortunately, until now there has not been any pertinent research available for you to look at.

When looking at literature and data, you’ll want to separate it into three basic categories. The first is studies which con-tribute useful information on ethoxyquin’s toxicity. This is the information you’ll need to determine how safe or unsafe ethoxyquin is in your dog’s diet.

The second category of studies are those examined and judged to be inappropriate for use in developing a database. These may be poorly conducted studies, or just plain irrelevant to the question at hand.

The third category is standard reference materials relating to the reliability and validity of analytical tests and methods. These allow you to determine whether the methods used to analyze the experimental results fall under the category of frequently used, reliable and valid tests.

In the following pages we will provide you with the relevant data on the toxicity of ethoxyquin. All of this information falls within the realm of “good scientific research.” The analytical methods and data are reliable, repeatable and valid. We have eliminated the irrelevant or invalid studies from this discussion.

Our telling you what we think is no different from any other “expert,” and we are certainly not going to be an Aristotle claiming that flies have five, not six legs. We encourage you to read on, and make your own conclusions.

Where the Information Is  From … And Why No One Told You About It Before!

At the beginning of this article, we mentioned ethoxyquin’s use in dog and cat food, plus chicken, horse and pig feeds, paprika and chili powder. There’s one other use of ethoxyquin: as a scald control on apples and pears. Many have misunderstood this use, calling it a pesticide. But that’s not true.

Commercially sold apples and pears, like much fruit, are picked “green” – before they ripen. The fruit is hard, and is better at surviving the bumping around on the way to the marketplace.

When fruit ripens, it goes through an oxidizing process which gives off ethane gas. The ethane gas speeds ripening. If the ripening occurs too soon, the fruit develops brown spots, also called scald.

Drench the fruit with an antioxidant, and the ripening process slows down, preventing those unsightly brown spots. That’s why ethoxyquin (e.g. 3000 parts per million – ppm – for 2 to 3 minutes) is used. By the time it reaches your store, there is no more than 3 ppm. on the fruit. (Alternatively, wax used on apples, and paper used for shipping pears and apples, will contain ethoxyquin to slow the ripening process.)

It was this use of ethoxyquin which led us to information most dog food companies didn’t know about, and neither Monsanto nor the Food and Drug Administration pointed us to-ward. You see, because of this agricultural use, ethoxyquin is regulated as a pesticide, even though it isn’t really used as a pesticide. The federal agency which keeps a tight rein on pesticides is the Environmental Protection Agency (EPA), and that’s where we found all of the following information.

The EPA took over pesticide regulation from the U.S. Department of Agriculture, and routinely reviews applications for registration of new pesticides. Traditionally, a new pesticide would be reviewed application by application, each independently. This way the pesticide could be judged safe or not for each use.

This method left little opportunity to combine information into a “big picture” of the safety of a particular chemical. So the EPA revised their procedures to look at the overall safety of each chemical, as well as the individual uses.

The EPA and Congress also spotted another problem: many pesticides had been registered before the advent of modern scientific methods, and were being sold and used without any current assurance of their human and environmental safety. Ethoxyquin was one such product, having been invented in the 1920’s.

Congress mandated that the EPA re-register all previously registered products, and required that the database for each be brought up to current standards. The new procedure is called the Registration Standard.

The Registration Standard contains all the information on a particular product:. This includes its active ingredients, current uses, conditions and requirements for registration, existing and future products which contain the active ingredient, all required scientific data. Also included is a discussion on compliance with government standards on toxicity, composition, labeling, packaging and the reliability of the data.

In 1981 the EPA put together the Registration Standard for ethoxyquin.

A Minor Use Chemical

In its review, the EPA classified ethoxyquin as a “minor use” chemical. This means that in the preceding five years, less than 30,000 pounds of the chemical’s active ingredient were used in formulated products.

Data Required

The EPA required data on the physical and chemical properties as well as acute toxicity for all ethoxyquin products. We’ll explain these in more detail later.

Results of tests were required for the technical grade of ethoxyquin (95% pure active ingredient) and the emulsifiable concentrate (a liquid concentrate to be diluted) which comes in 52.2%, 59.0%, 65.5% and 70% ethoxyquin concentrations. In this article we’ll use the data for the technical grade of ethoxyquin – the 95% pure chemical. Data for the emulsifiable concentrate reflect similar findings.

Manufacturers and formulators of ethoxyquin products supplied data on ethoxyquin’s chemistry, residue chemistry, and toxicology. Data was also required for other ingredients in the formulation, active or not, which constitute 0.1% of the product by weight. This allows for a good evaluation of the toxicity of the ingredient up for registration, and helps to complete the “big picture.”
All data was reviewed to insure that it met the EPA’s standard of scientific methodology. Most met the standards, but some studies were thrown out. The information in this article came from studies which met the standards.

Toxicology

When a chemical is submitted for registration for use on food, each of the fol-lowing kinds of studies must be submitted:

1. Chronic Feeding. A two-year feeding study is done using rats. Controlled amounts of the chemical are fed to the rats, and an autopsy is done at the end of the study to determine the effects.

2. Cancer. Oncogenicity studies are required from each of two suitable species of mammal. For ethoxyquin, rats were used in this test to see if the material causes tumors.

3. Teratogenicity testing, performed in two species of mammals, is designed to see whether the chemical causes abortion or reabsorption of the fetus. Two species are tested because some mammals will reabsorb the fetus, others are more likely to abort.

4. Reproduction. A two-generation reproduction study was required, preferably in the rat. This tests litter size, the survival rate of babies, growth, and liveborn vs. stillborn.

5. Mutagenicity. Tests are conducted to see if cells are damaged or mutated. Other tests are checked to see whether the DNA has been changed or damaged.

6. Metabolism. A general test to see how the chemical is metabolized in one mammalian species. The purified substance is labeled with radioactive material and followed through the animal’s system. Monitoring is done to see what organs it visits on its journey through the body.

Other studies are required, such as Acute Inhalation Toxicity, Skin Sensitization, and Subchronic Oral Toxicity. We’ll take each of these one by one and explain them, then look at what the study of ethoxyquin found.

One of the purposes of these studies is to determine at what level the chemical causes illness. Just about every substance will cause some problem, if given in high quantity.

Long-Term Feeding Studies

One chronic, or long-term feeding study, preferably in rats, is required to check for toxicity – to see whether the substance is toxic, and if so, in what amounts.

The EPA reviewed eight studies on rats and chickens, where technical grade, 95% pure ethoxyquin was fed daily in concentrations ranging from 62 ppm to 15,000 ppm, for a period ranging from 50 weeks to 2 years.

(Where appropriate, we’ve converted all measurements into parts per million (ppm) a unit of concentration, for easy comparison. The maximum concentration allowed in finished animal foods is 150 ppm, and far less is generally used. No matter how much food is consumed, the ppm – the relative amount of ethoxyquin – will remain the same.)

Wilson (et al) found that rats receiving 2000 ppm of ethoxyquin for over 200 days had problems. When autopsied, male rats had lesions in the kidneys, whereas females had none.

At the end of the study (715 days total) rats given this high dose exhibited a transient depression in growth rates. Instead of showing steady growth, they would grow sporadically. Male rats had lesions in the kidneys, livers and thyroids. Females had no lesions.

Obviously, 2000 ppm caused problems for the male rats. But the study also tested the 620 ppm concentration of ethoxyquin. There were no observable effects. A study by De Eds (et al) confirmed that there was no observable effect on rats at 620 ppm.

Panner and Packer did a two year feeding trial with rats, with the control rats being given 100 ppm of ethoxyquin, and the experimental rats 15,000 ppm. Only 11% of the rats fed the 15,000 ppm survived the entire two years. The high level of ethoxyquin caused both visible and microscopic changes in the livers.

Rudra (et al) reported that 5000 ppm of ethoxyquin fed to weanling (just weaned) male rats for 500 days, causes a slowing in weight gain, and severe kidney damage.

Colorado A&M University reported the effects of 75 ppm and 750 ppm fed to chickens for 70 weeks. They found no effect on growth of the breeding flock.

Gassner (et al) also did a 70 week chicken study, feeding 7.5 ppm, 75 ppm, and 750 ppm in the diet. They found no significant effects on mortality, growth, feed consumption, livability, egg production, fertility of eggs or hatchability which could be ascribed to the ethoxyquin.

What does this mean? From this data, one might assume that if your dog were to get several thousand parts per million of ethoxyquin in the diet, liver, kidney and thyroid problems might occur. But the reality is that your dog, on any commercial dog food, is getting as little as 10 ppm and as much as 100 ppm. Even at seven times the amount, one would not expect any illness.

Tumor Formation

The EPA found only one oncogenicity study discussing the presence of tumors and ethoxyquin. In rats fed 62 ppm and 2000 ppm for 715 days, an occasional tumor was found at day 700. The EPA found fault with this study because 700 days is a long time for a rat to live, and rats that age commonly have tumors. Further, the study didn’t link ethoxyquin to the tumors, and didn’t describe the relationship between tumors and the dose level.

Acute Oral Toxicity: How Much Ethoxyquin is Lethal?

One scientific number to look for is the LD50. The LD50 is the median (av-erage) dose which killed 50% of the test animals in the study.

The LD50 for ethoxyquin indicates that the amount required to be fed to cause damage is very high – 21 times the normal usage. The LD50 in rats is 3,150 ppm (Kellman, G.Y., 1965).
In mice the LD50 is 3000 ppm (Kell-man, G.Y., 1965) and in chickens the LD50 is 8000 to 10,000 ppm (Colorado Agricultural Research Foundation, 1951.) We have not found any studies which determine the LD50 in dogs, probably because no one is willing to do a study which intentionally kills dogs.

Is Ethoxyquin Toxic if Inhaled?

The EPA requires one acute inhalation toxicity test with the albino rat. Rats were exposed for 6 hours to 1750 ppm of 95% pure ethoxyquin and observed for 14 days. An autopsy revealed no visible damage, no ill effects.

Skin Sensitivity

Allergies often show up in skin sensitivity. The EPA requires an interdermal test in one species of mammal, preferably the guinea pig. Ethoxyquin was injected under the skin. The guinea pigs showed no sensitivity, no allergic reaction.

Short Term Feeding Studies

The EPA requires at least one sub-chronic oral toxicity test – a short-term feeding test – in two species of mammal. Eleven studies of this kind were analyzed by the EPA. Seven looked at ethoxyquin and rats, three used chickens, and one checked the effects of ethoxyquin on lambs.

Whanger (et al) found that 500 mg of purified ethoxyquin, fed three times a week to lambs, exceeded the LD50 – lambs died. Unlike the other studies discussed in the EPA report, Whanger fed straight ethoxyquin. When the dosage was cut back to 250 mg three times a week, there were no deaths.

Colorado A&M University fed Monsanto’s Santoquin® brand of ethoxyquin to chickens for 12 weeks, at levels ranging from 150 to 15,000 ppm of the diet. There were no effects on body weight, feed consumption, or livability, and the liver, spleen, kidney, thyroid and testes remained normal.

Conclusions of the EPA

“Ethoxyquin as described in the standard may be registered for sale, distribution, reformulation and use in the United States.” Based on all of the scientific data on ethoxyquin from the worldwide scientific literature as of 1980, plus the data submitted by the registrants through the time of the standard’s publication in 1981, the “Agency finds that none of the risk criteria found in section 162.11(a) of Title 40 of the U.S. Code of Federal Regulations have been met or exceeded by ethoxyquin, and that ethoxyquin does not appear to cause an unreasonable adverse effect with proper label directions and precautions.”

In other words, ethoxyquin exceeded all safety standards of the law. The EPA considers ethoxyquin a low toxicity chemical, and very safe.

The maximum level allowed by the EPA is 3 parts per million of ethoxyquin residue in or on apples and pears. The FDA allows a maximum of 150 ppm in finished animal feeds and dehydrated forage; most dog food contains far less.

The difference in the regulated amounts has more to do with the purpose for which ethoxyquin is being used. It takes far less ethoxyquin to prevent bruising of fruit than to keep fats from going rancid.

References

Colorado Ag. Research Foundation (1958). Chronic Toxicity of the antioxidant 6-ethoxy-2,2,4-trimethyl-1,2, dihydroquinoline.

Gassner, F.X.; Buss, E.C.; Hopwood, M.L.; Thompson, C.R. (1960). Effect of feeding 1,2, dihydro-6-ethoxy-2,2,4, trimethylquinoline to chickens. Poultry Science 39:524-533.

Gordon, R.S.; Machlin, L.J. (1952). Determination of minimum dietary level of Santoquin® which produces no more than .1ppm residue in dog and monkey liver: Ratio to greatest possible human consumption of Santoquin and calculation of safety factors. EPA Registration Standard MRID#00001932.

Hadley, K.G. (1965). Summary of Test Residues From Ethoxyquin Treated Pear Wrap. EPA Registration Standard MRID#000002198.

Hanzal, R.F. (1955) Chronic Oral Administration in Dogs: Metabolic Studies. Hanzal Laboratories. EPA Registration Standard MRID#000001925.

Jung, H.D. (1975). Professional dermatoses in agriculture of agricultural and industrial district of Neubrandenburg, East Germany. Deutsch Gesundheistwesen 30, 39: 1540-1543.

Kahl, R; Netter, K.J. (1977). Ethoxyquinas an inducer and inhibitor of Phenobarbital-type cytochrome P-450 in rat liver microsomes. Toxicology and Applied Pharmacology 40(3):473-483.

Kellman, G.Y. (1965). Comparative Toxicity of Santoflex AW and acetoaniline. Crude and Vulcanized Rubber I:24(3):40-41.

Koziak, B; Sesevick, L. (1971). Eczema produced by contact with poultry feed mixtures. Occupational Medicine 23(7):240-244.

Netter, K.J.; Kahl, R.; Elcomb, C.R. (1978). Significance of induction phenomena. Archives of Toxicology, Supplement (1):85-99.

Parke, D.V.; Rahim, A.; Walker, P. a) (1973). Reversibility of hepatic changes caused by Ethoxyquin. Biochemical Society Transactions 1(6):1316-1319.

b) (1974). Biochemical Pharmacology 23(13): 1871-1876.

c) (1974) Inhibition of rat hepatic microsomal enzymes by Ethoxyquin. Biochemical Pharmacology 23(24): 3385-3394.

Pascal, G. (1974). Physiological and metabolic effects of antioxidant food additives. World Review of Nutrition and Dietetics. 19: 237-299.

Rudra, D.N.; Dickerson, J.W.T.; Walker, R. (1975). Long-term studies and some antioxidants in the rat. Journal of the Science of Food and Agriculture. 25(8): 1049-1050.

Takahashi, O.; Hiraga, K. (1978). The relationship between hemorrhage induced Butylated hydroxytoluene and its antioxidant properties or structural characteristics. Toxicology and Applied Pharmacology. 46 (3): 811-814.

Wilson, R.H.; De Eds, F. (1959). Toxicity studies on the antioxidant 6-Ethoxy-1, 2-dihy-dro-2, 2, 4-trimethyl-quinoline. Journal of Agricultural and Food Chemistry. 7 (3): 203-206.

Wilson, R.H.; Thomas, J.O.; Thompson, C.R.; Launer, H.F.; Kohler, C.O. (1959). Absorption, metabolism and excretion of the antioxidant 6-ethoxy-1, 2-dihydro-2, 2, 4-trimethyl-quinoline. Journal of Agricultural and Food Chemistry 7(3): 206-209.