Edinboro C.H., Scott-Moncrieff J.C. and Glickman L.T.
Thyroid, 2004. 14: p.722.
The prevalence of feline hyperthyroidism has increased dramatically since it was first reported in the late 1970s. It is now recognized as the most common endocrine disorder of cats over six years of age in the United States, Canada, New Zealand, and Great Britain, and has been observed in Europe and Australia. This disease bears histologic resemblance to toxic nodular goiter, the form of thyrotoxicosis of el- derly humans that occurs more commonly in iodine-deficient areas. Iodine concentrations of commercial cat foods vary widely. We re- viewed the historical iodine recommendations and found that in the 1970s, iodine recommendations were expressed in different units than before. If foods were supplemented at the minimum value, cats’ diets would have been iodine deficient, with concentrations at least four times lower than recommended for dogs or humans. In our case-control study of feline lifetime nutrition and health, cats that ate com- mercial cat foods without explicit iodine supplementation (according to listed ingredients) were more than four times as likely to develop hyperthyroidism, compared with cats that ate food with supplementation (odds ratio = 4.27, 95% confidence interval = 1.30, 14.01). Since the iodine recommendation for cats is undergoing revision to a concentration similar to that for humans and dogs, it is possible that clin- ically normal cats with undiagnosed thyroid hyperplasia may become overtly hyperthyroid once their diets are appropriately supple- mented with iodine. This would be analogous to the experience of iodine remediation in Europe and Africa. Humans may serve as the model for this feline disease, and the human experience may guide veterinarians and cat owners if such transient hyperthyroidism de- velops.