Bonny Canteen 2020; 1: 165-178.
Anton C. Beynen
Copper in dog food
Copper is a co-factor of enzymes that catalyse reactions involved in energy production, free-radical
detoxification and the synthesis of neurotransmitters and structural proteins. Superoxide
dismutase, the enzyme that converts potentially harmful superoxide into harmless oxygen, holds
copper in its cuprous (reduced) state, which transforms into the cupric (oxidized) state during the
reaction. The role of copper as co-factor of various enzymes reflects its essentiality in animals and
man. Clearly, sufficient dietary, available copper is indispensable for normal body metabolism and
prevention of diseases. At the same time, the body requires strict control to prevent excessive,
toxic accumulation of copper in the liver, which acts as copper-storage site.
Deficiency of copper becomes noticeable only after its reserve in the liver is depleted. In Beagle
puppies fed a copper-deficient diet, blood copper began to fall after two weeks. Two-and-half
months later, pigmented hair of face and head lost its color and became grey. Another month
later, some puppies showed backward bending of the toe-tip bones. Development of lameness in
copper-deficient puppies has also been reported. Experimental copper deficiency in adult dogs has
not been described.
In individual dogs of some breeds, excessive copper accumulation in the liver is an inherited
disease. Very high copper amounts in the liver cause clinical signs: lack of appetite, inactivity and
weight loss, followed by liver failure associated with fluid accumulation in the abdomen and brain
dysfunction. The liver of affected dogs appears limited in its ability to secrete copper with bile into
the intestine so that it reaches the feces via gut contents. Inherited copper toxicosis has been
described for Bedlington Terriers and Labrador Retrievers, while a hereditary background is
suspected in several other breeds (1). In dogs with clinical or non-clinical copper toxicosis a copper-
restricted diet may either reduce the existing quantity of liver copper or curb further accumulation.
Copper in commercial dog food comes with most of its ingredients and also as supplemental
copper in various chemical forms. The total amount of copper in those foods, according to
chemical analysis, is normally higher than the recommended amount for adult dogs (5.4 mg
copper/kg dry food). However, some home-prepared dog foods had a calculated total copper
content that is much lower. Despite that, overt copper deficiency appears undescribed for dogs fed
Requirement and supply
The US National Research Council has set the recommended copper allowances for growing puppies
after weaning, and for adult dogs, at 0.66 and 0.36 mg/MJ metabolizable energy (2, Note 1). These
copper amounts correspond with 9.9 and 5.4 mg/kg dry food (1.5 MJ/100 g) and with 3.3 and 1.8
mg/kg wet food (0.5 MJ/100 g). The recommended allowance for puppies (0.66 mg/MJ) is based on
two studies (3, 4, see below). The copper allowance for adult dogs is a factorial estimate (Note 2).
Minimal copper requirements have not been proposed (2).
Five articles, published in the period of 2012 to 2018, report the analysed levels of total copper in
complete dry dog foods (5-9, Note 3). For 183 dry foods, the mean concentration and range were
18.0 and 7.6- 47.0 mg/kg dietary dry matter (ddm). For 6 wet foods (8, Note 3) the mean
concentration and range were 25.7 and 10.0- 45.6 mg/kg ddm. The lowest value (7.6 mg copper/kg
ddm) may not cause deficiency symptoms in puppies (see under Copper deficiency).
Within the EU, the maximum, legal limit for total copper in dog food is 28 mg/kg ddm, and named
copper compounds are authorized as additives (10). Complete, industrially produced dogs foods are
supplemented with copper. Forms of added copper are copper sulfate, cupric sulfate, chelated
copper sulfate, copper oxide, copper amino-acid chelate, cupric chelate of glycine, copper-
Putting the practice of copper supplementation in perspective, a dry dog food comprising 30%
poultry by-product meal, 50% corn and 20% copper-free ingredients, contains 3.0 mg copper/kg
(about 0.2 mg/MJ, Note 4). The food provides less than 60% of the copper allowance for adult dogs.
It cannot be decided whether or not adult dogs develop copper deficiency when feeding them for
longer duration on the unsupplemented food (cf. Note 2), but it would be imprudent to do so.
The amount of copper supply has been calculated for various types of home-prepared foods for
dogs: bone and raw food (BARF) rations (11), maintenance diets (12-14) and diets recommended for
dogs with cancer (15). For 431 recipes, the mean and range of total copper concentrations were 5.4
and 0.5 -124 mg/kg ddm (Note 5). Thus, some of the recipes may not furnish adequate amounts of
At a meeting in 1951, Baxter (16) communicated the following: “Puppies (5 to 6 weeks old) were
placed on a purified diet containing approximately 1 μg. of copper per gram of (dry) food, and
demineralized water. After 1 to 2 months, about two-thirds of the animals developed lameness. The
lameness was accompanied by severe anemia, graying and poor condition of the hair, thickening and
scaling of the skin and sometimes poor growth. Litter-mates on the same diet with added copper (10
μg/gm.) remained entirely normal.” Details of the study were published two years later (17, Note 6).
Zentek et al. (3, 18) also studied the impact of copper deficiency in growing dogs. Beagle puppies,
aged 7 weeks, and with prior access to their mother’s milk only (Note 7), were weaned onto a
semipurified diet (Note 8) without (1.2 mg Cu/kg ddm) or with added copper sulfate (14.1 mg Cu/kg
ddm). Average baseline body weights of the puppies fed the low- (n = 6) and high-copper diet (n = 4)
were 1.95 and 1.80 kg. The dogs were fed restricted amounts of food so that energy intake was
similar for the two groups. At the age of six months, food intakes for the control and copper-
deficient dogs were 25.3 and 24.5 g ddm/kg body weight.day. Intermediate and final body weights
are not reported, but it is mentioned that copper intake did not significantly affect the development
of body weight.
The dogs were kept in a copper-free environment. After feeding the diets for two weeks, plasma
copper and ceruloplasmin concentrations began to fall in the copper-deficient dogs. After three
months, pigmented hair of face and head lost its color and became grey. At that stage, plasma
copper concentrations in the control and deficient dogs were about 10 and 1 μmol/l. Hemoglobin
and packed-cell volume were lower in the copper-deficient dogs, but only after the low-copper diet
had been fed for two months (cf. Note 6). At the end of the experiment, after the four-month
feeding period, liver copper concentrations were 221 and 17 mg/kg hepatic dry matter (hdm) (Note
9). Hair copper concentrations were 14 and 4 mg/kg dry matter for the control and copper-deficient
A study published in abstract form (4) concerns growing puppies (breed and number per treatment
not mentioned) fed a canned diet containing 0.26, 0.45 or 0.65 mg Cu/MJ from copper sulfate, or
0.41 or 1.12 mg Cu/MJ from copper oxide. Diet composition and total dietary copper contents are
unreported. Serum copper fell rapidly in puppies fed 0.41 mg Cu/MJ from copper oxide, which was
followed by a decrease in blood hemoglobin. The authors stated that 0.65 mg Cu/MJ from copper
sulfate was required to maintain serum copper at initial levels, while 0.45 mg/MJ was required to
prevent anemia. The US National Research Council deduced that 0.65 mg copper/MJ may be taken
as a dietary recommended allowance for the growing puppy (2).
Copper deficiency caused disorders of bone development in mongrel (17) and Beagle (18) puppies.
In weanling Great Dane puppies, copper deficiency was induced by oral administration of
ammonium tetra-thiomolybdate (TTM), an inhibitor of copper absorption (19, see under Anti-copper
treatment, Note 10). The authors concluded that copper deficiency caused a reduction in the
number of active osteoblasts, leading to osteoporosis. It cannot be excluded that TTM had a direct
effect or indirect effects on bone development, in addition to induction of copper deficiency.
The copper allowance for adult dogs is founded on net copper absorption of 30% (2, Note 2). In the
study on copper deficiency in Beagle puppies (18), apparent copper absorption after 4 months on
the copper-sufficient and -deficient diets was 28 and 50% (Note 11), pointing to up-regulation of the
efficiency of copper absorption in the deficient state (see below). Indirect evidence as described
above, suggests that copper from copper sulfate is absorbed more efficiently by puppies than that
from copper oxide (4).
Copper absorption in dogs is affected by the composition of the diet. As dietary protein source, soy
protein reduced copper absorption when compared with wheat gluten, curd or greaves (20). Corn
gluten versus lung, tripe or meat increased apparent copper absorption (21). Dietary lactose or raw
potato starch instead of gelatinized starch reduced apparent copper absorption (22). High calcium
intake may not influence apparent copper absorption in adult dogs (Note 12).
Zentek (23) compared dry diets with 55% of either greaves meal, soy-protein isolate or corn gluten,
35% rice, 2% soybean oil, 3% cellulose and 5% vitamin-mineral mixture without copper. Distilled
water served as drinking water. Analysed copper contents of the diets were 6.9, 9.6 and 9.6 mg/kg
ddm. In four adult dogs, average copper intakes/fecal excretions were 125/127, 178/188 and
182/171 μg/kg body weight.day (bw.d). Apparent copper absorption for the corn-gluten diet was 6%
of intake, but for the other two diets copper balance was negative. In dogs fed commercial,
complete foods, negative copper balances have also been found (24). By comparison, negative zinc
balances in dogs have been commonly measured (25).
Absorption of dietary copper is conceptualized as follows (26). Cuprous copper (Cu+) is taken up by
CTR1, a high affinity copper transporter in the apical membrane of enterocytes. Prior to uptake by
CTR1, dietary cupric copper (Cu2+) has to be reduced. The copper chaperone, antioxidant-1 (ATOX1),
shuttles copper from CTR1 to ATP7A (copper-transporting ATPase), which exports copper into the
portal blood. Copper binds to albumin or α2-macroglobulin in the blood and is transported to the
liver. There, copper is loaded by another copper-transporting ATPase onto ceruloplasmin for
systemic circulation and delivery to tissues. The amount of CTR1 probably is down- and up-regulated
by high and low cellular copper levels (26).
Dietary copper sources that bypass CTR1 may escape from homeostatic down-regulation of copper
absorption (cf. 25). Possibly, copper chelates cross the mucosa via passive transport or carrier
systems for their organic moiety. Should that happen, then copper could accumulate in liver and
other tissues, possibly disturbing normal metabolism or even leading to toxicity.
For adult dogs in a dynamic steady state of maintenance with constant amount of body copper, the
influx and efflux of copper are identical. Copper influx equals apparent (net) absorption of copper.
The efflux is represented by the sum of fecal and urinary excretion, and the losses with skin, nails
and hair. On a daily basis, the last three lost amounts are very small (Note 2) so that in essence net
copper absorption is tantamount to urinary copper excretion. Regulation of body-copper
homeostasis may be exerted by adapting absorption (see under Copper absorption) and by biliary
excretion of copper (see below).
The Beagles puppies described above were fed diets containing either 14.1 or 1.2 mg copper/kg ddm
(18). At the age of 5-6 months, the copper-sufficient animals excreted 270 and 34 μg copper/kg bw.d
with feces and urine (feces:urine = 89:11). For the copper-deficient dogs the amounts were 16 and
22 μg/kg bw.d (feces:urine = 42:58). The deficient animals had an increased percentage of apparent
copper absorption (see under Copper absorption), reflecting increased absorption efficiency and/or
decreased biliary secretion. Nevertheless, the dogs became depleted of body copper.
In healthy, female dogs (n = 5) with a balloon catheter inserted into their bladder, urinary copper
excretion was 3 μg/kg bw.d (27). In dogs (n = 20) equipped with a temporary biliary fistula, copper
secreted with bile amounted to 95 μg/kg bw.d (27). The dogs were fed a commercial dry food
containing 19.2 mg copper/kg. When compared with the puppies (18), calculated, daily urinary
copper excretion is very low, which might relate to the catheterization procedure. Calculated daily
biliary copper secretion may also differ from the rate in the intact body.
At dietary copper concentration of 19.2 mg/kg (27), a food intake of 16.7 g/kg bw.d and 30%
apparent (net) absorption (Note 2), intake, absorption and fecal excretion of copper are 321 and 96
and 225 μg/kg bw.d. The magnitude of net copper absorption is similar to that of biliary copper
secretion. However, 30% apparent (net) absorption may be at the high end (see under Copper
absorption). Copper is assumed to appear in bile as unabsorbable complex (28) so that there is no
entero-hepatic cycling. At steady state, true copper absorption corresponds with the sum of biliary
copper secretion, urinary excretion, endogenous fecal copper and losses with skin, nails and hair.
The copper concentration in bile of healthy dogs (n = 20) was 209 μmol/l (27) which is about 17
times higher than that in plasma. It appears that copper reaches the bile against a concentration
ingredient, pointing to an active transport mechanism for biliary secretion of copper in dogs. Copper
is thought (1, 29) to enter the hepatocyte via CTR1 as membrane copper transporter, and is
delivered by a copper-chaperone protein (ATOX1) to copper-transporting P-type ATPase (ATP7B)
which conveys copper further to either ceruloplasmin for secretion into the circulation or to
lysosomes. The lysosomes may store copper or facilitate its transport to bile canaliculi for biliary
Hepatic copper accumulation
The liver is the main storage organ for surplus copper in dogs. The concentration of liver copper is
not only a measure of the reserve in relation to long-term, average daily copper intake, but is also an
index of pathological copper accumulation. In the puppies fed a copper-adequate diet, liver copper
was 13 times higher than in their counterparts fed a copper-deficient diet (18). Bedlington Terriers
and Labrador Retrievers with inherited, clinical copper toxicosis on average had 24 and 6 times more
liver copper than their normal counterparts, with individual animals having a 52- and 11-fold
increase (30, 31).
In Bedlington Terriers with copper-storage disease, copper absorption was unchanged, but biliary
excretion was diminished, when compared with controls (27). In Alaskan Malamutes with dwarfism,
aged 26 weeks, liver copper was elevated two to four fold (32), while copper absorption was
diminished (33), likely in response to hepatic copper accumulation. In Labrador Retrievers with high
(933 mg copper/kg hdm; n = 6) versus normal liver copper (354 mg/kg hdm; n = 5) urinary copper
excretion was 18% lower (34), conforming to down-regulation of copper absorption. However,
sample size was limited and copper contents of the dogs’ diets were unreported.
In 55 Labrador Retrievers, 44 of them being first degree relatives to dogs diagnosed with copper-
associated hepatitis, the relationship between copper content of their habitual diet and hepatic
copper concentration has been computed (5). Each dog was fed the same brand and type of
commercial, dry diet for at least one year. Dietary and liver copper ranged between 7.6 and 23.6
mg/kg ddm and between ± 100 and ± 3500 mg/kg hdm. The presented scatter plot illustrates that
the variation in dietary copper explained only a minor percentage of the variation in ln-transformed
liver copper. Perhaps, copper toxicosis in Labrador Retrievers relates to diminished biliary copper
Treatment of copper toxicosis in dogs aims at decoppering by inducing a negative copper balance. To
that end, copper intake may be restricted and/or fecal copper excretion may be increased by oral
administration of copper chelators such as D-penicillamine, TTM or zinc salts (1). D-pencillamine
binds copper and the complex is excreted into urine. TTM mainly forms an unavailable complex with
copper in the intestine. Zinc may interfere with the transport of copper from the apical to
basolateral membrane of enterocytes (25).
Two Bedlington Terriers and two West Highland White Terriers with mean hepatic copper levels of
5550 and 1595 mg/kg hdm were orally administered zinc acetate (35). The initial dose was 200 mg
zinc/day (84 mg zinc/MJ), followed by lower doses to maintain plasma zinc below 150 μmol/l. The
intakes of copper and zinc with the diet are not reported. After two years, liver copper was
decreased by 65%. At the start, 3 of the 4 dogs had histologically determined hepatitis, which was
absent after zinc administration.
Labrador Retrievers with high liver copper were subjected to dietary treatment (36). The dogs, which
had relatives with copper-associated, chronic hepatitis (31), were fed a commercial, low-copper
canned food (4.8 mg copper and 102 mg zinc/kg ddm; ± 0.3 mg copper and 5.8 mg zinc/MJ) and
either a placebo (n=12) or zinc gluconate (± 65 mg zinc/MJ; n=9) as supplement. After 8 months, the
medians of initial liver copper (720 and 770 mg/kg hdm) had dropped by 56% in both groups. At the
start of diet intervention, one third of the dogs had histologically-diagnosed chronic hepatitis, the
severity remaining unchanged.
Labrador Retrievers with inherited copper-associated hepatitis (n = 16) had been effectively treated
with D-penicillamine. Then, they were fed a commercial veterinary hepatic diet low in copper and
high in zinc for a median time period of 19.1 months (37). The diet contained 0.31 mg copper and
15.4 mg zinc/MJ. Overall baseline liver copper was 273 mg/kg hdm (n = 16), which was increased to
536 mg/kg hdm (n = 11) after 18 months on the dietetic food. During the study period, dietary
treatment maintained liver copper below 800 mg/kg hdm liver in 12 dogs.
Client-owned Labrador Retrievers with subclinical hepatic copper accumulation (n = 28), were also
fed the veterinary hepatic diet with 0.31 mg copper and 15.4 mg zinc/MJ (38). The test animals were
related to dogs previously diagnosed with clinical copper-associated hepatitis. On average, baseline
liver copper concentration was 925 mg/kg hdm (n = 28). After about 13 months, liver copper had
fallen to 482 mg/kg hdm (n = 12). The authors stated that in responders (15/28), mean hepatic
copper had decreased from 710 to 343 mg/kg hdm after a median period of 7.1 months.
In individual dogs of some breeds, copper accumulation in the liver is an inherited disease. For those
dogs, normal dietary copper levels (cf. Note 3) are too high. They should be fed a copper-restricted
diet. A dietary copper level somewhat below the recommended allowance of 0.36 mg/MJ is
practically achievable (cf. 37, 38) and preferred in dogs with risk of hepatic copper accumulation.
For healthy dogs, copper toxicosis due to long-term, high intake of copper has not been described. A
dog given 165 mg copper/kg bw in the form of copper sulfate caused vomiting and, four hours later,
death (39). Total plasma copper rose from 16 to 143 μmol/l within 40 minutes. A single meal of 250
g dry food that provides 2475 mg copper to a 15-kg dog would have to contain as much as 9900 mg
The European Petfood Industry (FEDIAF) has set the minimum recommended amount of copper at
0.43 and 0.50 mg/MJ for adult dogs with maintenance energy requirements of 110 and 95 kcal/kg0.75
(40). The American Association of Feed Control Officials (AAFCO) recommends a minimum dietary
copper content of 0.44 mg/MJ for adult dogs (41).
The text of the US National Research Council (1) reads: “By extrapolating from factorial data on
mineral requirements of pregnant and lactating bitches, the RA (recommended allowance) for
maintenance can be estimated at 0.1 mg Cu.kg BW-1.d-1 (0.2 mg.kg BW-0.75.d-1), assuming an apparent
bioavailability of Cu of 30 percent (Meyer, 1984; Meyer et al., 1985a). A diet containing 1.5 mg Cu
per 1,000 kcal ME (metabolizable energy) would provide this amount to a 15-kg adult dog
consuming 1,000 kcal ME.d-1.” The estimate of 30% net copper absorption seems rather high for
adult dogs (23, Note 12).
Kienzle (42) has estimated the endogenous copper losses in dogs. Fecal, urinary and cutaneous
losses were rated at 0.015, 0.015 and 0.001 mg/kg body weight (bw) per day. When assuming a net
copper absorption of 30%, a 15-kg adult dog would require 1.55 mg dietary copper per day (15 x
0.031 x 100/30). At an energy intake of 1,000 kcal/day (4.184 MJ/day), the copper requirement is
0.37 mg/MJ. The so-called inevitable losses with feces and urine have been estimated by
extrapolation of fecal and urinary excretions to zero copper intake (42).
With regard to the published data on copper contents of dog foods (5-9) the following assumptions
were made: the foods were complete (5, 7, 8); the results are expressed as mg/kg dry matter (8).
Results presented as mg/1000 kcal (5, 7) were converted into mg/kg dry matter holding 4000 kcal.
The methods used for copper analysis were atomic absorption spectroscopy (5), inductively coupled
plasma atomic emission spectroscopy (7) and inductively coupled plasma mass spectrometry
analysis (6, 8, 9).
Analysed total copper (mg/kg dry matter) in dog foods
Dry dog foods
7.6 – 23.6
7.7 – 18.0
9.2 – 36.0
14.7 – 17.0
11.0 – 47.0
15.0 – 30.2
7.6 – 47.0
Wet dog foods
10.0 – 45.6
Reference 9 concerns 20 adult and 6 puppy foods. References 7 and 8 explicitly mentioned the use of
adult foods only. *Median
Poultry by-product meal has been reported to contain 6.99 mg copper/kg (43). The copper
concentration in six whole-kernel corn samples from six different locations was on average 1.88
mg/kg, with a range of 1.74 to 1.99 mg/kg (44).
Calculated† total copper contents (mg/kg dry matter) of home-made dog foods
Type of food
0.8 – 26.3
0.5 – 22.9^
0.9 – 26.0
0.7 – 66.9
1.6 – 123.7
0.5 – 123.7
The original data were converted into mg copper/kg dry matter representing 4000 kcal/16.736 MJ.
The reports used four different units: percentage of the recommended allowance (6 mg/4000 kcal) as
set by the National Research Council (11), mg/kg (12), mg/1000 kcal (13), mg/MJ (14) or mg/Mcal
(15). †The copper values provided by reference 12 are not calculated, but based on analysis of pooled
subsamples for one-week feeding periods of the home-prepared diets. The method of copper analysis
is not mentioned. *Median; ^The range was reductively estimated as mean minus one and plus two
reported standard deviations.
The paper on the BARF diets (11) subjoined that low-copper rations were of the same ration type as
low-zinc rations and usually also deficient in zinc and iodine. Low-zinc rations usually consisted of
meat with only small amounts of bone and without either offal, zinc-containing supplements or nuts.
Mongrel puppies aged 3-5 weeks were divided into two comparable groups and fed the
experimental diets (17). In each experiment, control animals were fed the deficient diet with copper
added. In 11 experiments, purified diets were used. The diets consisted of 20% casein, 55.7%
sucrose, 19% vegetable shortening, 1% corn oil, 4% salt mixture, 0.3% choline and added vitamins.
The calculated energy content of the diets is 1.97 MJ/100 g. In experiments 12 and 13, raw- and
dried-milk diets were used.
The purified diets contained about 1 mg copper/kg dietary dry matter (ddm), and so did the milk
diets. In the course of the experiments, copper contents of the control diets were increased, from 8
to 15 and then 30 mg/kg in order to raise serum copper levels of the control dogs. The source of
added copper is not reported. Lumped together, dietary calcium and phosphorus contents were 0.66
and 0.59% on a dry-weight basis.
There were 19 control and 27 copper-deficient dogs. After periods of 2 to 4 months on the copper-
deficient diets, 19 animals had developed lameness or deformities of the extremities.
Hyperextension of the wrist joints was a prominent feature in some experiments. Nine dogs showed
obvious fractures of the limb bones. Graying of hair was seen in 19 copper-deficient dogs. In all
cases, the control animals appeared normal.
Mean plasma copper concentrations and ranges were 13 and 8-17 μmol/l for the controls, and 4 and
3-6 μmol/l for the test dogs. Liver copper levels were 124 (89-159, n = 6) and 7 (3-11, n =8) mg/kg
hepatic dry matter (hdm) in control and test animals. The data are reported on the basis of fresh-
liver weight; it is assumed that fresh liver dog liver contains 27% dry matter (45). Hematocrit values
were about 45 and 28% in copper-sufficient and –deficient dogs.
Bitch milk contains on average 0.34 mg copper/100 g (42). The calculated energy content of bitch
milk (8.4% protein, 10.3% fat, 3.3% lactose, 23.6% dry matter) is 0.58 MJ metabolizable energy/100 g
so that the copper content equals 0.59 mg/MJ or 14.4 mg/kg dry matter.
The experimental diets consisted of 38% casein, 5% skim-milk powder, 36% lard, 17% glucose, 4%
cellulose and an additional mineral/vitamin supply (18). The calculated energy content is 2.32
The liver copper data are reported on the basis of fat-free dry matter (18). It is assumed that liver
contained 10% fat on a dry-matter basis (45).
Ingested and absorbed ammonium tetra-thiomolybdate (TTM) acts as copper chelator that forms a
complex with copper in the intestinal contents, plasma and liver. Weanling Great Dane pups were
fed a diet consisting of 25% canned and 75% dry food (19). At 9 weeks of age, 5 animals were daily
given a TTM solution (50 mg/ml) per os. The dose rate of TTM was initially 6 mg/kg body weight,
which was increased over 8 weeks to 12 mg/kg. After 8 weeks of treatment, group-mean liver
copper concentrations in the two groups were 229 and 95 mg/kg, presumably kg hdm. Based on
histologic, chemical and densitometric bone measurements, the authors concluded that TTM-
induced copper deficiency caused osteoporosis as a result from a reduction in the number of active
At the age of 5-6 months, food intakes of the puppies on the copper-sufficient and -deficient diets
were 26.5 and 26.7 g dietary dry matter/kg body weight.day (bw.d), which equaled 0.374 and 0.032
mg copper/kg bw.d (18). Fecal excretion was 0.270 and 0.016 mg/kg bw.d. Thus, on the copper-
sufficient and -deficient diets, apparent copper absorption was 27.8 and 50.0% of intake.
Three adult female and male Beagles (body weights 7.5- 16.5 kg) were fed a low- and high-calcium
diet according to a cross-over design with feeding periods of two weeks (Beynen AC, Yu S,
unpublished study, 1994). The composition of the control diet has been described elsewhere (46),
except that the diets contained 0.1% chromium oxide, added at the expense of gelatinized corn
starch. The test diet was formulated by replacing equal amounts of corn starch and glucose by 2.5%
CaCO3. Added copper (6.35 mg/kg) was in the form of copper sulfate. The analysed concentrations of
calcium and copper in the dry control and tests diets were 0.99 and 1.80%, and 14 and 15 mg/kg.
During the last week of each feeding period, feces of individual dogs were collected quantitatively.
During the feces-collection intervals, group-mean (n = 6) copper intakes with the low- and high-
calcium diets were 3.85 and 4.13 mg/dog.day. The fecal copper excretions for the two diets were
3.49 and 3.68 mg/dog.day. Thus, high versus low calcium intake probably did not influence copper
absorption. Average apparent copper absorption was 10% of intake.
Kastenmayer et al. (47) measured copper absorption in adult Beagles employing the stable isotope
of copper. The dogs were fed a kibbled food containing 14.5 mg copper/kg dry matter. 65Cu as
sulfate was added to a single meal and feces were collected quantitatively for 5 days. Based on 250 g
food intake with the isotope-containing meal, mean (n = 15) copper absorption was 23%. Copper
absorption efficiency as measured with a stable (or radioactive) isotope of copper concerns its
carrier, but is not representative for total dietary copper.
Van Wyk et al. (48) have tested whether the bone changes seen in dogs with copper deficiency (17)
were secondary to anemia and bone-marrow hyperplasia. Dogs were maintained on diets sufficient
in copper, but with inadequate amounts of iron. With comparable degrees of anemia produced by
copper or iron deficiency, the changes in red-cell size and hemoglobin content were much greater in
iron deficiency. Bone marrow changes also differed between copper and iron deficiency. It was
concluded that the anemias of iron and copper deficiency are different. In essence, the anemia
produced by copper deficiency in dogs is normocytic and normochromic, whereas it is microcytic and
hypochromic in iron deficiency.
Hartley et al. (49) reported that all but one of a litter of 8 five-month-old German Shepherd pups on
a raw-meat diet, died in the space of two weeks, with enlarged thyroids, bony changes and low liver
copper. The diet was supplemented with tri-calcium phosphate. Liver samples from two cases were
analysed for copper, the outcomes being as low as 4.1 and 5.3 mg/kg hdm. Copper and calcium
contents of the diet are not reported. The authors suggested that the skeletal lesions in the affected
dogs were due to a copper deficiency. They surmised that copper in the diet was unavailable as a
result of excess supplementary phosphate.
The diet of the pups consisted of raw beef or horse meat ad libitum and a pint of milk per pup per
day. At the age of 3-4 months, when they had reached about half of their adult body weight (17 kg),
the pups may have consumed 9.1 MJ metabolizable energy per day. That amount of energy is
equivalent to 939 g beef meat and 473 g cow milk, which may have contained 1.97 mg copper (1.88
+ 0.09) or 0.22 mg/MJ. That amount is 33% of the recommended allowance for puppies and explains
the low copper concentration in liver. Skeletal lesions have been observed (17, 18) at dietary copper
levels of 0.05 mg/MJ. It is uncertain whether a diet with 0.22 mg copper/MJ as the only
incompleteness produces bone changes. There is no evidence that high phosphate intake reduces
copper absorption in dogs.
A series of sudden deaths in Samoyed pups occurred in a breeding kennel (50). In two examined
pups anemia was present, but not characterized (cf. Note 14). In one pup, liver copper concentration
was found to be only 5.8 mg/kg hdm. The deaths were limited to one group of full sibs. The author
concluded that adequate copper was available to the dogs and suggested that some heritable defect
in copper metabolism was involved.
A case report shows that a Bedlington Terrier with copper-storage disease had developed copper
deficiency after 8 years of copper chelation (51). Penicillamine was prescribed initially, but because
of adverse gastrointestinal effects, trientine was substituted (cf. 1). A prescription diet low in copper
(3.45 mg/kg ddm) and distilled water were also given.
A 7-years-old Border Collie with cachexia, jaundice and ascites was euthanized and subsequently
found to have a liver copper content of 4460 mg/kg hdm (52). The histopathological changes were
consistent with copper-induced hepatitis. The dog had lived on a farm and used to eat significant
quantities of commercial, dry calf feed with 13 mg added copper/kg ddm (cf. Note 3). The title of the
case report reads “Possible nutritionally induced copper-associated chronic hepatitis in two dogs”.
The copper content of the whole diet of the first dog is unknown and the second dog was not
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