Goitrogenic compounds

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Goitrogenic compounds have a proven association with the development of feline hyperthyroidism[1].

Goitrogenic compounds contributing to feline hyperthyroidism including phthalates, resorcinol, isoflavones, polyphenols (plasticized bisphenol A - BPA) and PCBs, found in food, drinking water, household cleaners and polluted air[2]. Extensive studies have shown that consumption of more than 50% of the diet containing canned food was associated with a higher risk of hyperthyroidism in cats, and the relative risk increased the longer the cats remained on the diet. In addition, cats that ate food from pop-top cans also had an elevated risk compared with those fed from a can which required a can-opener[3].

Goitrogenic compounds in the food and the environment generally reduce the efficiency of thyroid hormone synthesis by the thyroid gland, increasing TSH secretion secondarily and leading to thyroidal enlargement. Aside form iodine, most cat foods contain relatively high levels of goitrogenic compounds such as phthalates[4]. Cats may be exposed to many other goitrogenic compounds either in diets (particularly fish-containing diets) or the environment, which could contribute to the development of thyroid adenomas.

Isoflavones inhibit 5'-deioinase activity, and polyphenolic soy isoflavones, in particular, genistein and daidzein, have been identified in almost 60% of cat foods tested[5]. In particular, virtually all dry and semi-moist cat foods contain soy protein with more than 11 μg/g of isoflavones, levels adequate to interfere with thyroid function (August, 2006). Additionally, these isoflavones tend to be biologically inert within the cat's body and are retained for significantly long periods of time, thus having an accumulative effect.

Cats have a relatively slow capacity for glucuronidation, the metabolic pathway responsible for metabolizing many goitrogenic compounds. Autoantibodies have been suggested as a risk factor for the development of hyperthyroidism, but have not been proven to exist in hyperthyroid cats[6].

A genetic basis for hyperthyroidism also has been suggested. Decreased expression of a G-protein in adenomatous thyroid glands of some hyperthyroid cats has been shown to reduce the negative inhibition of the cAMP cascade in thyroid cells. This leads to autonomous growth of the thyroid and the hypersecretion of thyroxine. The results of one study indicated that over-expression of the c-ras oncogene in hyperthyroid cats was highly associated with areas of nodular follicular hyperplasia and adenomas of the thyroid glands. Currently, the role of this hypothesis in the pathogenesis of hyperthyroidism is unclear[7].

It appears prudent to reassess dietary protocols in cat's diagnosed with hyperthyroidism, and determine the care-givers interest and momentum in adoption a more natural diet to minimise goitrogenic exposure. The use of chelation therapy, a common alternative medical procedure in humans for removal of heavy metals and chemicals, has been suggested anecdotally, but never been reported.

References

  1. August, JR (2006) Consultations in feline internal medicine. Vopl 5. Elsevier Saunders, USA. pp:211-212
  2. Martin, KM et al (2000) Evaluation of dietary and environmental risk factors for hyperthyroidism in cats. J Am Vet Med Assoc 217:853-856
  3. Edinboro, CH et al (2004) Epidemiological study of relationships between consumption of commercial canned food and risk of hyperthyroidism in cats. J Am Vet Med Assoc 224(6):879-886
  4. Mumma, RO et al (1986) Toxic and preventive constituents in pet foods. Am J Vet Res 47(7):1633-1637
  5. Court, MH & Freeman, LM (2002) Identification and concentrations of soy isoflavones in commercial cat foods. Am J Vet Res 63(2):181-185
  6. Nguyen, LQ et al (2002) Cloning of the cat TSH receptor and evidence against autoimmune etiology of feline hyperthyroidism. Endocrinology 143(2):395-402
  7. Kennedy, RL & Thoday, KL (1998) Autoantibodies in feline hyperthyroidism. Res Vet Sci 45:300-306