Calcium Supplementation Durring Growth

This is from Canine and Feline Nutrition - A Resource for Companion Animal Professionals Case, Carey & Hirakawa1995 pp 297-299

Calcium Supplementation
Supplementing a pets' diet during growth and other periods of physiological stress is a common practice. Calcium is a nutrient that is often added to a dog's diets and, less commonly, to the diets of cats. The reason most often cited for calcium supplementation relates to its essential role in normal skeletal growth and development. Supplements such as dicalcium phosphate and bone meal are added to a growing dog's diet during growth spurts or when problems such as hyperextension of the carpus or sinking of the metacarpophalangeal join occur. Some professional breeders may encourage all of their puppy buyers to routine supplement their pet's diet with calcium during the entire first year of life as a prophylactic measure. Some breeders believe that calcium supplementation is not only necessary for proper bone development but that it will also prevent the development of certain skeletal disorders. In addition, dogs' diets are occasionally supplemented with minerals during gestation and lactation. Supplemental calcium and phosphorus are believed by some to ensure healthy fetal development during pregnancy, to aid in milk production during lactation, and to prevent the onset of eclampsia after parturition. Regardless of the good intentions, there are potential risks when excessively high levels of calcium are added to an adequate and balanced diet. Excess calcium in the diet can produce deficiencies in other nutrients and has the potential for causing several serious health disorders in the dog.

Supplementation During Growth
Research has shown that normal growth in puppies can be supported by calcium intake of 0.37% available calcium or 0.6% total calcium. The Association of American Feed Control Officers (AAFCO) Nutrient Profile for Dog Food sets minimum levels for calcium of 0.8% for growth and reproduction and 0.5% for adult maintenance. The profile also mandates a maximum level of 2.5% calcium in all dog foods. This maximum level was included because published data have indicated that excess calcium during growth may contribute to abnormal skeletal development. Studies indicate that a high level of calcium in the diet is associated with the occurrence of OCD, enlarged joins, dropped hocks, splayed feet, angular limb deformities, wobbler's syndrome, and stunted growth.

In 1985 a study was undertaken with the purpose of determining the role of supplemental calcium in the occurrence of osteochondrosis in growing Great Danes. An experimental diet was formulated that met the recommendations of the 1974 National Research Council (NRC) Nutrient Requirements for Dogs. Both the control group and the experimental group received this diet throughout growth. In addition, the experimental group received calcium carbonated supplementation to achieve a level of 3.3% in the diet, which is three times the amount recommended by the NRC. Results showed that excessive calcium intake resulted in chronic hypercalcemia and hypophospatemia. Skeletal differences between the control and experimental dogs included a higher percentage of total bone volume, retarded bone maturation, retarded bone remodeling, and a decreased number of osteoclasts (bone resorption cells) in the dogs receiving calcium supplementation. This group also showed a higher incidence and severity of the cartilage irregularities associated with osteochondrosis at the distal and proximal humeral cartilages. Clinically, calcium-supplemented dogs exhibited retained cartilage cones, severe lateral deviations of the feet, and the radius curvus syndrome that was previously described by another researcher.

The mechanism through which calcium exerts these effects relates to the homeostatic control of blood calcium and phosphorus levels. Studies have shown the excessive calcium intake in young dogs results in a transient hypercalcemia and hypophosphatemia. The hormone calcitonin is secreted in response to elevated serum calcium and lowers plasma calcium to normal levels. Calcitonin produces the effects by decreasing bone resorption and retarding cartilage maturation in developing bone. The chronic suppression of bone resorption results in gradual thickening and increased density of cortical bone. In growing dogs, this change interferes with normal bone remodeling. The deposition of excessive subperiosteal bone that results may cause the clinical signs of HOD and wobbler's syndrome, and the chronic effects of calcitonin on cartilage maturation may result in the eventual detachment of the articular cartilage that is seen in OCD. Because of their rapid periods of growth and their predisposition to skeletal disorders, large and giant breeds of dogs are especially susceptible to the pathological effects of excess calcium consumption. However, it is postulated that these changes also occur in smaller breeds at a subclinical level, resulting in infrequent diagnosis of disease.

One group of investigators examined the effects of excess dietary calcium and endogenous vitamin D formation on the calcitonin-producing cells of the thyroid gland. Growing beagles were given 2.3 grams of supplemental calcium per day and exposed to direct sunlight. After 70 days, the thyroid glands of the supplemented dogs contained significantly increased proportions of calcitonin-producing C-cells and decreased proportions of thyroid follicles, compared with those of control dogs. The authors of the study concluded that high dietary calcium intake cause thyroid C-cell hyperplasia, which would suggest the occurrence of chronic hypercacitoninism in these dogs. Additionally, examination by electron microscope of the thyroid C-cells of dogs fed excess calories, protein, and calcium showed that these cells were releasing larger amounts of calcitonin than were in the C-cells of dogs fed restricted diets. Under the influence of calciotropic hormones (calcitonin), excess calcium is routed largely to the skeleton, and resorption of mineral from bone also decreases.

A complicating factor involved in calcium nutrition for growing dogs is that they do not appear to have a mechanism that will protect them from absorbing large amounts of calcium when there are excessive levels in the diet. Dietary calcium is absorbed across the intestinal epithelium through either active transport or passive diffusion. The active transport mechanism is saturable, carrier-mediated, and depends on the animal’s vitamin D status. The second mechanism is nonsturable, diffusional transfer that is directly dependent on the concentration of available calcium in the intestinal lumen. Studies of humans and laboratory animals have shown that nonsaturable passive diffusion is the predominant pathway for calcium absorption in neonates and young animals. In adults, the percentage of calcium that is absorbed from the diet varies between 10% and 90%, depending on the food, calcium content of the diet, and the physiological state of the animal.

A study with growing dogs found that 45% of dietary calcium was absorbed when a normal level of calcium was fed (1.1% of the diet dry matter). The percent of calcium absorption increased to 80% when the level of calcium was decreased to 0.55%. However, when the calcium level was increased to 3.3%, 45% of the calcium was still absorbed. As a result, calcium balance was significantly more positive in the dogs fed a high level of mineral compared with the dogs that were fed either normal or low levels. Mineral content of cortical and cancellous bone was greater in the high-calcium dogs and there was decreased bone turnover and remodeling of the skeleton. As dogs age and reach maturity, they appear to be able to adapt to high calcium intakes by decreasing the proportion that is absorbed. Therefore young dogs are especially susceptible to the adverse effects of high dietary calcium because of their inability to decrease calcium absorption in response to excess levels in the diet.

Diets containing excessively high amounts of calcium are also capable of causing a relative zinc deficiency in dogs. High levels of calcium and other minerals, such as iron and copper, interfere with zinc absorption, possibly through competition for absorption sites or by acting as intestinal ligands. Although adult animals can be affected, these effects have been most frequently observed in growing dogs. A controlled study found that puppies fed balanced diets containing excess supplemental calcium developed zinc deficiency within 2 to 3 months. Clinical signs included impaired growth rate, anorexia, conjunctivitis, asnd the development of a dull, coarse hair coat. Desquamating skin lesions that are characteristic of zinc deficiency were also observed on the abdomen and extremities. Clinical cases of zinc deficiency have also been reported. Three separate litters of puppies developed zinc-responsive dermatosis when fed diets containing two or three times the NRC requirement for calcium. When supplemented with oral zinc, all puppies showed dramatic improvement with in 7 – 10 days.

Studies with growing dogs indicate that adding excess amounts of calcium or calcium-containing foods to a balanced diet can contribute to the development of the skeletal disorders that owners are attempting to prevent. This practice may also lead to subclinical or clinical zinc deficiency. If a growing dog is fed an appropriate amount of a high-quality pet food that is formulated for growth, supplementation with calcium is unnecessary and contraindicated. If a pet owner is feeding their pet a food that appears to contain inadequate or unavailable levels of calcium, switching the dog to an adequate commercial diet is safer than attempting to correct the imbalance in the poor diet through supplementation.