Feeding a wolfhound puppy:
alcium content is an issue. The current recommendations is about
1% in large / giant growing puppies. The G. Dane data from the
Netherlands is over 30 yrs old and indeed the lowest level tested
was 1.5%. That does not mean that a lower level would be better.
More recent data not available to the public is suggesting that
~1% is better and safe. Personally, I feed my large breed puppy
a 1% calcium diet.
After calcium, calories are an important issue. There are several
large breed growth products out there all with the same protein
and similar calcium content, but very different caloric densities.
I always recommend the lower calories per cup to help the owner
keep the dog at a body condition score of 4 on a 9 scale. See www.purina.com, "body
Taurine is an amino acide synthesized from methionine and cysteine.
L-carnitine is a derivative of the amino acid lysine. By the very
name, carnitine (carniverous, etc.), you would suspect that L-carnitine
was first isolated from meat. Both taurine and l-carnitine are
found in animal products, especially animal heart & brain.
Both dogs and people can make their own taurine and L-carnitine.
These should be really cheap if you want to buy them. But why?
A normal dog should make all he/she needs for himself/herself.
Feeding more meat doesn't seem like a good idea, unless you keep
a spreadsheet of nutrients and can figure out how much more calcium
to feed when you feed that much more phosphorus with the meat.
If your vet were to test your dog and discover he/she is spilling massive amounts
of taurine in the urine and has low blood levels, then the vet could prescribe
taurine. It should be really cheap and I'm sure you can find a source on the
web or in maybe in a healthfood store. Priscilla
Dietary Taurine Deficiency and
Dilated Cardiomyopathy in Dogs
Dilated cardiomyopathy is a heart disease that results in an
enlarged (dilated) heart with impaired ability to contract and
Dr. Andrea Fascetti and Dr. Robert Backus check blood sample preparations
before running an assay for taurine levels.
Dilated cardiomyopathy (DCM) is one of the most common acquired
cardiovascular diseases in dogs.
In cats, a diet deficient in taurine clearly results in DCM, but
in dogs, the need for dietary taurine has not been generally recognized
because dogs are known to be able to synthesize taurine from the
sulfur amino acids cysteine and methionine.
Yet, during the past two years, veterinary nutritionist Andrea
Fascetti and her colleagues Quinton Rogers and Robert Backus documented
low plasma taurine concentrations in dogs with clinical signs of
DCM. Some animals died‹the prognosis is poor for dogs with
this disease‹while some survived when given supplemental
taurine and supportive care.
The cause of taurine deficiency in the canine DCM cases was not
readily apparent, yet the common factor was diet history. Some
of the dogs had been eating home-made diets, while others were
eating similar commercial diets‹the diets appeared sufficient
in protein and sulfur amino acid content, and had passed testing
in accordance with Association of American Feed Control Officials
(AAFCO) feeding trials for all life stages.
These cases and findings in several pilot studies suggest that
diet does affect taurine metabolism in dogs and may play a role
in the development of DCM.
Recent evidence also suggests that taurine stores and the development
of DCM may be affected not only by diet, but also by a dog's size.
There is a prevalence of DCM in families of dogs and specific breeds,
many of which are large and giant breeds.
Dr. Backus found evidence in a study of Newfoundland dogs with
taurine deficiency to support the idea that taurine metabolism
may be influenced by "metabolic" body size, which takes
into account that the amount of energy needed by the body is correlated
with total body surface area, not just body weight.
For example, calculations of metabolic body size indicate that
the caloric and protein intake per unit of body weight in a large
breed dog is actually lower than in a small breed dog.
Dr. Fascetti is currently investigating the influence of both
diet and metabolic body size on taurine metabolism in small and
large breed dogs.
Information from the studies will contribute to ongoing and subsequent
research on taurine metabolism in dogs, and will help clinicians
interpret taurine profiles to make appropriate therapeutic recommendations.
Dr. Fascetti hopes these studies will increase veterinarian and
client awareness in order to prevent diet-related DCM and to improve
the life expectancy of dogs afflicted with the disease.
Dr. Fascetti and her colleagues are carrying out a variety of
investigations to find out how diet composition affects taurine
metabolism in dogs, and how taurine deficiency may play a role
in the development of DCM, particularly in large-breed dogs.
Dr. Fascetti and her clinical nutrition resident, Dr. Sean Delaney,
have begun a scientific survey to determine normal ranges for plasma
and whole blood taurine concentrations in dogs‹reference
ranges for taurine concentrations in cats are known, yet healthy
ranges in dogs have not been determined. Understanding normal ranges
for taurine is essential to understanding the factors that affect
taurine metabolism in dogs and the link between taurine deficiency
and DCM. Blood samples will be collected from client-owned animals
along with each dog's age, breed, weight and other measurements,
medical history and a complete diet history. The effect of metabolic
body size and diet on the taurine
levels will be determined.
Last year Dr. Backus found diet-associated taurine deficiency
and cardiac insufficiency in more than half of a group of 21 privately
owned Newfoundland dogs, which excreted extraordinary amounts of
taurine in their urine. Drs. Backus and Fascetti are now planning
a larger project to estimate the prevalence of a possible widespread
taurine deficiency in the Newfoundland breed. Non-invasive clinical
tests and feeding trials will determine if taurine deficiency in
Newfoundlands might result from 1) a reduction in protein digestibility,
2) a diminished capacity to synthesize taurine from sulfur amino
acids, or 3) loss of taurine in urine. Pedigree analysis may reveal
a genetic basis for taurine deficiency.
Another breed susceptible to DCM is the Doberman pinscher. In
a three year project funded by the Doberman Pinscher Foundation
of America, Royal Canin, Morris Animal Foundation and the CCAH,
graduate student Dr. Cristina Torres is working on developing a
taurine-deficient adult dog model that can be used to further study
DCM in humans and animals. Dogs in the study are given purified
diets and monitored for taurine concentrations and cardiac changes.
Upon depletion of taurine, the dogs are supplemented with taurine
until their physiology returns to normal. The study investigates
possible causes for taurine deficiency and will determine the quantities
of dietary taurine and sulfur amino acids needed to prevent DCM
in purified and commercial diets.
Department of Veterinary Clinical Sciences, Graduate School of
Veterinary Medicine, Hokkaido University, Sapporo, Japan.
OBJECTIVE: To determine whether dogs given garlic extract developed
hemolytic anemia and to establish the hematologic characteristics
induced experimentally by intragastric administration of garlic
extract. ANIMALS: 8 healthy adult mixed-breed dogs. PROCEDURE:
4 dogs were given 1.25 ml of garlic extract/kg of body weight (5
g of whole garlic/kg) intragastrically once a day for 7 days. The
remaining 4 control dogs received water instead of garlic extract.
Complete blood counts were performed, and methemoglobin and erythrocyte-reduced
glutathione concentrations, percentage of erythrocytes with Heinz
bodies, and percentage of eccentrocytes were determined before
and for 30 days after administration of the first dose of garlic
extract. Ultrastructural analysis of eccentrocytes was performed.
RESULTS: Compared with initial values, erythrocyte count, Hct,
and hemoglobin concentration decreased to a minimum value on days
9 to 11 in dogs given garlic extract. Heinz body formation, an
increase in erythrocyte-reduced glutathione concentration, and
eccentrocytes were also detected in these dogs. However, no dog
developed hemolytic anemia. CONCLUSIONS AND CLINICAL RELEVANCE:
The constituents of garlic have the potential to oxidize erythrocyte
membranes and hemoglobin, inducing hemolysis associated with the
appearance of eccentrocytes in dogs. Thus, foods containing garlic
should not be fed to dogs. Eccentrocytosis appears to be a major
diagnostic feature of garlic-induced hemolysis in dogs.
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