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Reproduced below is an article from the ACCA Newsletter (Winter 1997 Issue, p20) as just one example of the quality of one regular feature ("The Doctor is In ..."). The Newsletter carries diverse reading matter; this is just a sample ....

"Risks Associated With Calcium Supplementation During Pregnancy"

By Susan Dixon DVM, Toepads Abyssinians

The Functions of Calcium

Calcium is responsible for providing structure to the skeletal system, plays a role in blood coagulation, and affects neuromuscular function. This effect of calcium on neuromuscular function is important at parturition and during the post parturient period. The main functions of calcium at the neuromuscular level include:

  1. Stimulation of muscle contraction;
  2. Maintenance of normal nerve function.

We all agree that lowered blood levels of calcium are unhealthy and may contribute to reproductive problems. So why not supplement that pregnant or lactating queen to ensure she gets all the calcium she needs? The answer lies in a complex feedback mechanism that is responsible for maintaining normal levels of blood calcium.

Three hormones are involved: parathyroid hormone, calcitonin, and cholicalciferol (vitamin D). Parathyroid hormone is the most important factor in maintaining normal calcium levels during pregnancy and lactation.

Parathyroid Hormone

There are two pairs of parathyroid glands, located adjacent to the lobes of the thyroid gland in the neck. When the blood calcium level is low (hypocalcemia), parathyroid hormone is released. Parathyroid hormone elevates blood calcium by mobilizing calcium from the bone.


Eclampsia and dystocia may both be related to low levels of blood calcium, though the mechanisms of action are different. In cases of eclampsia, the reduced amount of blood calcium causes the nervous system to become progressively more excitable. This allows the nerve fibers to discharge spontaneously, resulting in nervousness, anxiety, uncoordination, and tetany.

In certain dystocias, the absence of calcium may have a direct effect on the smooth muscle of the uterus. When calcium is not available to initiate muscle contractions, one type of primary uterine inertia may result.

Cut to the Chase

Diets that are too high in calcium result in higher blood calcium levels, so there is no need for the release of parathyroid hormone. As the pregnant queen is supplemented and maintains high calcium levels in her bloodstream, the parathyroid glands shut down. They are no longer able to respond to sudden declines in blood calcium levels.

At the time of parturition, blood calcium levels drop as the queen stops eating and begins producing milk. Since the parathyroid glands are no longer functional, the amount of calcium available for uterine contractions may be diminished, and primary uterine inertia can result.

During lactation, calcium demands are dramatically increased. Even if calcium is still supplemented in the diet, it may not be enough to balance the amount lost in the milk. The net result is lowered serum calcium, lack of parathyroid hormone, and possible eclampsia.

Calcium absorption and utilization also are affected by dietary concentrations of vitamin D and phosphorus. Commercial quality diets formulated for cats contain calcium, phosphorus, and vitamin D in the proper ratios. During the last one-third of pregnancy and throughout lactation and weaning, the best diet is a premium quality kitten food with no supplements.


  1. Too much calcium in the diet can result in a lack of parathyroid hormone.
  2. A lack of parathyroid hormone can cause hypocalcemia.
  3. Hypocalcemia can cause eclampsia and contribute to primary uterine inertia.
  4. Dietary supplementation during pregnancy and lactation can cause eclampsia and may contribute to dystocia.

Calcium supplementation: DON'T DO IT!


  1. Capen, C.C. "The Calcium Regulating Hormones: Parathyroid Hormone, Calcitonin, and Cholecalciferol." Veterinary Endocrinology and Reproduction, Lea & Febinger, 1980, pp.60-130.
  2. Carothers, M., Chew, D., & Van Gundy, T. "Disorders of the Parathyroid Gland and Calcium Metabolism." Saunders Manual of Small Animal Practice, W.B. Saunders Company, 1994, pp.229-237.