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Skeletal Effects of Excessive Calcium Intake

Editorial comment:
Below is current research showing you should not add extra calcium to your growing dogs diet. If you are feeding a commercial kibble, regardless of quality you choose to use, the food must have, by law, the correct ratio of calcium to phosphorus in the food. When you add a pet calcium supplement to the food, that only disrupts the balance of this calcium/phosphorus ration and can over do the amount of calcium in a diet causing skeletal disease


Hormonal and Skeletal Effects of Excessive Calcium Intake
Article from PetFood Industry - Dec 20 - 2005

Hypercalcemia is prevented by decreased chief cell parathyroid hormone (PTH) release and increased C cell calcitonin (CT) release, both decreasing osteoclasia. In pups, calcium absorption increases with increased dietary calcium content, causing a rise in plasma calcium, and thus influencing calcitropic hormone secretion. However, nothing is known about the long-lasting effects after normalization of the calcium intake on calcium regulation and skeletal development.

This study was performed to measure the effect of high calcium intake (3.3% DMB) during partial weaning or until 17 weeks of age and the period thereafter with normal calcium intake until 27 weeks of age on calcium metabolism and skeletal development.
Dogs were divided into three groups of Great Danes:

Group I=1.1% Ca from 3-27 weeks of age)
Group II=3.3% Ca from 3-6 weeks then 1.1% Ca from 6-27 weeks of age;
Group III=3.3% Ca from 3-17 weeks and 1.1% from 17-27 weeks of age).
PTH (parathyroid hormone) and CT (calcitonin) release were studied following EDTA and Ca infusions at 7, 13, 19 and 26 weeks of age. Radiology of the antebrachium was performed at 9, 15, 21 and 27 weeks.

Dogs in Group II revealed pronounced C cell response still present at 13 and 19 weeks of age with radiologic signs of panosteitis, unlike the dogs in Group I.
Dogs in Group III had chief cells and C cells with reduced sensitivity to changes in plasma calcium, with severe hypoparathyroidism and hypophosphatemia with consequently rickets-like skeletal lesions with gradual, although incomplete, repair in the 17-27 weeks of age period.

Thus, high calcium intake at 3-6 weeks of age can have serious consequences for skeletal development several months later due to C cell hyperplasia and decreased PTH secretion.
High calcium intake causing hypercalcemia for a longer period of time can cause chief cell atrophy, together with hypophosphatemia and eventually under-mineralization of the growing skeleton.

Source: Schoenmakers, I, 2005. Hormonal and skeletal effects of excessive calcium intake during partial weaning and at pre-pubertal age in dogs. Abstract from Proceedings of the 2005 Nestlé Purina Nutrition Forum, St. Louis, Missouri, USA.

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