Medeiros, Davidson, and Jenkins, Proceedings of the Society for Experimental Biology and Medicine,
203:262-273, 1993, are to be complemented on their timely Minireview on cardiomyopathy related to consumption of a diet inadequate in copper. It was also gratifying to see the inclusion of a tentative working model to explain the events leading to cardiac failure in copper deficiency. However, the Minireview and the model have a basic flaw which should be addressed. The purpose of a review is to provide a historical account of all of the relevant experiments related to the specific topic of the review. A more difficult step is to attempt to make “sense” out of all of the information, and the inclusion of a hypothetical model is a bonus and provides food for thought. The Minireview by Medeiros et al. nearly provided an excellent historical account of all of the relevant references, with the exception of the exclusion of data that have been generated over the past decade at the Human Nutrition Research Center in Beltsville, MD. This is not necessarily a trivial comment because consideration of the excluded information forces one to reconsider the model proposed by Mederios et al. We have shown repeatedly for over a decade that if you provide male weanling rats with a diet that is deficient in copper and contains sucrose or fructose as its carbohydrate, the rats develop cardiac lesions, hypertrophy, altered biochemical function, and pathology as described by Medeiros et al. However, this outcome occurs only under specific dietary conditions. The carbohydrate of the diet must contain sucrose or fructose. If the carbohydrate of the diet is starch and the diet is deficient in copper, organ copper concentrations will be low and the activity of copper-dependent enzymes will be low or nondetectable, but there will be only mild cardiac lesions, mild hypertrophy, little pathology, and the rats can eat the copper-deficient diet indefinitely without death by hemothorax or aneurysms.
