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Feline Hyperthyroidism: Overview & Nutritional Considerations

Claudia A. Kirk, DVM, PhD, DACVIM, DACVN, University of Tennessee, Knoxville

Hans S. Kooistra, DVM, PhD, DECVIM-CA, Utrecht University

J. Catharine Scott-Moncrieff, MA, MS, Vet MB, DACVIM, DECVIM, Purdue University

Karen J. Wedekind, MS, PhD, Novus International

Steven Zicker, DVM, PhD, DACVIM (LAIM), DACVN, Hill’s Pet Nutrition

This content was published originally in the Small Animal Clinical Nutrition textbook. It has been updated and provided to readers of Clinician's Brief courtesy of the Mark Morris Institute.

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Feline Hyperthyroidism: Overview & Nutritional Considerations

"I have studied many philosophers and many cats. The wisdom of cats is infinitely superior." Hippolyte Taine


The trace elements iodine and selenium are important for thyroid function. Thyroid homeostasis may not only be influenced by excessive or deficient absolute intake of iodine or selenium but also by relative historical intake of these trace elements. In addition, non-nutritive factors such as natural and synthetic exogenous thyroid disrupters affect thyroid metabolism. Finally, in addition to the nutritional and environmental influences, genetic factors influence development and progression of thyroid disorders. Despite this complexity, scientific advances have increased understanding of the factors that influence development and progression of feline hyperthyroidism, and provided information that may help to further improve treatment.

History and Prevalence

Thyroid pathology in cats has been recognized as far back as 1927, but it was not until the late 1950s to early 1960s that thyroid adenomas were first described (Clark and Meier 1958, Lucke 1964). Interestingly, clinical signs of hyperthyroidism were not documented in most of these initial pathology reports. The first clinical reports of feline hyperthyroidism were described in 1979 and 1980 in the USA (Holzworth et al 1980, Peterson et al 1979). By the early 1990s hyperthyroidism was a commonly recognized disease in the USA and UK (Broussard et al 1993, Ferguson 1993, Gerber et al 1994). Since that time, it has been recognized in multiple geographic areas throughout the world including Europe, Australia, New Zealand, South Africa, Ireland, UK, Japan, Canada, and Hong Kong (Bree et al 2018, De Wet et al 2009, McLean et al 2014).

The worldwide prevalence of feline hyperthyroidism is difficult to estimate but it has definitely increased since initial estimates. The age adjusted hospital prevalence increased from 0.61/1000 visits for the period of 1978 to 1982, to 29.64/1000 visits for the period of 1993 to 1997 (Edinboro et al 2004) Latest estimates of prevalence rates in older cats range from 3-21% (Bree et al 2017, McLean et al 2018). There appears to be geographic differences in prevalence but pathophysiologic reasons for this are poorly understood (McLean et al 2014, Stephens et al 2014).


Patient Clinical Assessment

History and Physical Examination

Hyperthyroidism is a result of excessive production and secretion of the hormones thyroxine (T4) and triiodothyronine (T3) by thyroid gland tissue. Hyperthyroidism is a disease of middle-aged and older cats and the most common feline endocrinopathy (Edinboro et al 2004, Peterson 2012). The average age at the time of diagnosis is 13 years with a range of four to 22 years. Less than 5% of cats diagnosed with this disorder are younger than 8 years of age (Scott-Moncrieff  2015). There is no sex-related predisposition, however a breed bias appears to exist with domestic shorthair and longhair cats being most frequently affected. 

Clinical signs typically include weight loss (which may progress to cachexia), polyphagia and restlessness or hyperactivity (Table 1). Weight loss is the predominant finding (98% of cases) and may be attributable to increased energy expenditure as a result of increased ATPase activity induced by the thyroid hormone excess. Polyphagia is most likely a compensatory response to increased cellular metabolism and increased energy expenditure. In a small percentage of hyperthyroid cats, appetite may be decreased or wax and wane. Decreased appetite is usually associated with weakness, muscle wasting and severe weight loss, and indicative of other concurrent illness. In such cases re-evaluation of treatment efficacy and evaluation for concurrent disease such as congestive heart failure, chronic kidney disease, neoplasia, thiamine or cobalamin deficiency, hypokalemia or inflammatory bowel disease is warranted.

The most common finding on physical examination is digital palpation of one or more discrete thyroid masses in the ventral neck. Palpation of a cervical mass is highly suggestive of, but not pathognomonic for, a thyroid lesion resulting in hyperthyroidism. Other common findings on physical examination include hyperactivity, cardiac abnormalities (tachycardia, dysrhythmias), muscle wasting, poor body condition and unkempt haircoat. Because of the multisystemic effects of hyperthyroidism, the variable clinical signs and its resemblance to many other feline diseases (Table 2), hyperthyroidism should be suspected in any aged cat with medical problems.

Table 1. Clinical manifestations associated with feline hyperthyroidism*

Table 2. Most common differential diagnoses for feline hyperthyroidism.*

Laboratory and Other Diagnostic Testing

The primary purpose of laboratory and diagnostic testing is to confirm the diagnosis of hyperthyroidism and screen for concurrent disease.

Any number of abnormalities may be present in individual cats on routine biochemical, hematologic or urinalysis evaluations, as might be expected in older cats. The most common findings are hypokalemia, increased markers of liver dysfunction (ALT, ALP, bile acids) and azotemia (Table 3). Chronic kidney disease has been estimated to be present in at least 15% of cats older than 15 years of age and thus is a common concurrent disease. Hyperthyroidism induces hyperfiltration in the kidneys, which may result in markers of renal function within the reference range despite the presence of chronic kidney disease in untreated hyperthyroid cats. Urinalysis may reveal decreased USG, which may suggest (masked) renal insufficiency, but hyperthyroidism itself may also result in dilute urine. Electrocardiography and echocardiography may reveal sinus tachycardia and evidence of left ventricular hypertrophy.  Following initial screening for concurrent disease specific diagnostics for thyroid dysfunction should be performed if thyroid disease is still suspected.

Table 3. Common abnormal diagnostic findings in cats with hyperthyroidism.

Serum Thyroid Hormone Testing

Multiple tests are available to assess thyroid function in cats. The most common tests include determination of the serum concentrations of total thyroxine (TT4) and the non-protein-bound fraction of TT4, i.e. free thyroxine (fT4). If the results of these two tests are inconclusive, additional diagnostics tests should be performed.

TT4 baseline test

Measurement of a random baseline serum TT4 concentration is extremely valuable in differentiating hyperthyroid cats from those without thyroid disease. Sensitivity and specificity have been reported at 91% and 100%, respectively (Peterson et al 2001). Serum TT4 concentrations that fall within the upper portion of the reference range (reference range typically 1.5-4.5 ug/dL) can create a diagnostic dilemma, especially when clinical signs suggest hyperthyroidism and a nodule is palpated in the ventral region of the neck. Cats with early hyperthyroidism and hyperthyroid cats with significant non-thyroidal illness may have serum TT4 concentration within the reference range and be referred to as occult hyperthyroidism (Scott-Moncrieff 2015). In these cases, repeated measurement of the serum TT4 concentration may be useful, as serum TT4 concentration fluctuates over time (Peterson et al 1987).

Additional diagnostics should be considered when basal TT4 measurement remains within the reference range but clinical signs are consistent with hyperthyroidism. Specifically, evaluation of circulating concentrations of fT4 or/and thyroid stimulating hormone (TSH), as well as the T3 suppression test, or a sodium pertechnetate thyroid scan should be considered. Cytological evaluation of a fine-needle aspiration biopsy of a mass in the ventral neck may be helpful in such cases to determine whether a cervical mass is thyroid tissue.

fT4 baseline test

Measurement of the serum fT4 concentration using an equilibrium dialysis technique is the recommendation of choice to confirm hyperthyroidism in cats with suspected hyperthyroidism but non-diagnostic serum TT4 test results (occult hyperthyroidism). Equilibrium dialysis is more expensive and time consuming than measurement of TT4 and therefore a number of commercially available assays for measurement of fT4 have been developed, which perform with reasonably good sensitivity and specificity (Peterson et al 2001, Scott-Moncrieff 2015). Unfortunately the specificity of fT4 is lower than that of TT4, with up to 20% of sick (and some clinically normal) euthyroid cats having an increased serum fT4 concentration (Peterson 2013, Scott-Moncrieff 2015). Because of the concerns with specificity, serum fT4 should always be interpreted in conjunction with TT4 measured from the same blood sample.

Serum TSH concentration

If both serum TT4 and fT4 concentrations are inconclusive and occult hyperthyroidism is still suspected, the circulating TSH concentration may be determined. In cases of hyperthyroidism, TSH secretion is suppressed. However, undetectable and low TSH concentrations have also been reported in healthy cats, resulting in very poor specificity (Peterson et al 2015a). Nonetheless, a non-suppressed circulating TSH concentration excludes feline hyperthyroidism with a sensitivity of 98% (Peterson et al 2015a).

Triiodothyronine (T3) Suppression Test

The T3 suppression test may be used to distinguish cats with a normal pituitary-thyroid axis from those with autonomous hypersecretion of thyroid hormones. The T3 suppression test is based on the theory that oral administration of T3 will suppress pituitary TSH secretion in euthyroid cats, resulting in a decrease of the circulating TT4 concentration. In contrast, pituitary TSH secretion is already suppressed in cats with hyperthyroidism because of the autonomous hypersecretion of thyroid hormones. Consequently, oral administration of T3 will not cause further TSH suppression and serum TT4 concentration will not decrease following T3 administration. In this test, T3 is administered orally three times daily for seven treatments and serum T4 concentration is determined before and 2-4 hours after the last T3 administration (Scott-Moncrieff 2015).

Sodium Pertechnetate Thyroid Scan

The sodium pertechnetate thyroid scan (i.e. thyroid scintigraphy) is used to identify functional thyroid tissue and considered the gold standard for diagnosis of (occult) hyperthyroidism (Peterson 2013, Peterson et al 2015b). Sodium pertechnetate is administered intravenously and uptake by thyroid tissue is assessed by a gamma-camera (low energy all-purpose collimator). Uptake of sodium pertechnetate and the size of functioning thyroid tissue will be greater in hyperthyroid cats than in euthyroid cats. Scintigraphy is also useful to determine unilateral vs. bilateral thyroid lobe involvement, identify ectopic thyroid tumor tissue and identify sites of metastasis in cats with thyroid carcinoma (Scott-Moncrieff 2015).


Normal Thyroid Function and Physiology


The basic histologic subunit of the thyroid gland is the spheroid thyroid follicle. The wall of the follicle is a single layer of thyroid epithelial cells which are cuboidal or flat when quiescent and columnar when active. The lumen is filled with a colloid containing a large glycoprotein called thyroglobulin (Figure 1). Within the thyroid gland, but outside of the follicle, are parafollicular cells (C cells), which secrete calcitonin in response to increased concentration of calcium in plasma (Scott-Moncrieff 2015).

Iodide, an essential building block of thyroid hormones, is actively transported from the extracellular fluid into the thyroid follicular cells. The iodide carrier, i.e. the sodium iodide symporter (NIS), located at the basal membrane of the follicular cell, co-transports sodium (Na) and iodide (I-) into the follicular cell (Figure 2). An additional thyroid cell protein, called pendrin, is thought to facilitate the apical transfer of iodide into the follicular lumen. Once within the follicular cell, iodide is rapidly oxidized in the presence of hydrogen peroxide (H2O2) to a reactive intermediate that is then incorporated into tyrosine residues of thyroglobulin. The iodination is catalyzed by the enzyme thyroid peroxidase (TPO). Iodination of the tyrosine residues of thyroglobulin result in the formation of monoiodotyrosine (MIT) and diiodotyrosine (DIT). MIT and DIT may then undergo oxidative coupling, also catalyzed by TPO, to form T4 and T3 (Figure 3), which remain bound to thyroglobulin until secretion. The iodination of thyroglobulin occurs at the apical border of the follicular cell, after which thyroglobulin is moved into the colloid by exocytosis. The lumen of the follicle acts as a storage site for thyroglobulin-bound thyroid hormones. Secretion of thyroid hormones requires that thyroglobulin is taken back into the follicular cell via pinocytosis. Lysosomal proteases then break down thyroglobulin, which results in release of T4 and T3. Finally, T4 and T3 diffuse from the follicular cell into the systemic circulation.


The thyroid gland directly produces all T4 and approximately 20% of T3 found in serum. Under normal conditions, more than 99% of thyroid hormone is bound to serum proteins (Kaptein et al 1994). The portions of T4 and T3 not associated with protein are called free thyroid hormones (fT4 and fT3). It is the free thyroid hormone concentration that determines thyroid status irrespective of the circulating total thyroid hormone concentration. The biological activity of T4 is mainly determined by peripheral metabolism to biologically active T3 or biologically inactive reverse T3 (Figure 3). In recent years several membrane carriers for transport of both T4 and T3 to the inside of the target cells have been identified. Intracellular T4 is subsequently converted to T3 via selenium deiodinase enzymes in extrathyroidal target tissues (Bianco and Kim 2006). The final destination for thyroid hormone activity is to bind to receptors for the thyroid hormones located mainly in the nucleus of peripheral tissues. The nuclear thyroid hormone receptor has a high affinity for T3 and much less for T4, which explains why T3 is considered the main biologically active thyroid hormone.

Deiodinase type 1 (D1), a selenoprotein, is located primarily in the kidneys and liver (Bianco and Kim 2006, Larsen and Berry 1995). Deiodinase I prefers rT3 as a substrate, releasing DIT; therefore, it may be important in the deactivation process of thyroid hormone. Deiodinase I also has affinity for T4, producing active T3; however, this is an order of magnitude less than the rT3 affinity. The T3 produced by the liver may be released into the general circulation to exert its biologic activity. The exact physiologic importance of deiodinase I in the liver has yet to be elucidated, but it is presumed to be mainly deactivation of thyroid hormone (Larsen and Berry 1995).

The selenoenzyme deiodinase type 2 (D2) is specific for intracellular production of T3 from T4. D2 is found in target cells including those of the brain, skin, adipose tissue, muscle and placenta (Freake and Oppenheimer 1995, Larsen and Berry 1995). Production of T3 and subsequent nuclear binding is probably the major physiologic route of thyroid hormone action and an important point of regulation (Lu and Holmgren 2009).

A third selenoenzyme, deiodinase type 3 (D3), has also been characterized. D3 has inner ring deiodinase activity and degrades T4 to rT3 and T3 to 3,3’-T2. D3 is expressed in fetal tissues and in adult brain tissue. In addition, D3 can be re-expressed under certain pathological conditions such as critical illness or in specific cancers (Peeters and Viser 2000).

Since all of the deiodinases contain selenium it is important to note that selenium deficiency may decrease expression and activity of these enzymes and thus may alter peripheral thyroid metabolism.

As a result of activation of nuclear thyroid hormone receptors, mainly by T3, target cells increase consumption and production of energy and exert endocrine effects required for normal growth and development. The exact mode of this action has yet to be elucidated; however, it is thought to involve the key enzymatic controls of carbohydrate, fat and protein metabolism. In addition, investigators have proposed a possible uncoupling of oxidative phosphorylation and modulation of Na/K-ATPase activity at the cellular membrane (Kaptein et al 1994).

Regulation of Thyroid Hormone Secretion

The thyroid gland is the site of thyroid hormone synthesis and is regulated by integration of multiple cortical substrate feedback signals as well as intrathyroidal autoregulatory mechanisms and dietary micronutrient availability (Figure 4) (Kaptein et al 1994, Scott-Moncrieff 2015). The main regulator of thyroid function is thyrotropin (TSH), a glycoprotein produced and secreted by the anterior lobe of the pituitary gland. Pituitary TSH secretion is stimulated by thyrotropin releasing hormone (TRH) and inhibited by somatostatin, both produced and secreted by the hypothalamus. Elevated circulating concentrations of thyroid hormone, primarily T3 which is produced locally by deiodination (D2) and fT3 from the systemic circulation, suppress TRH release, whereas decreased circulating thyroid hormone concentrations stimulate release of TRH. Negative feedback by T3 also occurs at the level of the pituitary anterior lobe.

Stimulation of the basolateral TSH receptor by TSH results in a cascade of events which ends in the synthesis of T4 and T3 (Figure 2). The TSH receptor is associated with G proteins, which in turn exert control on adenylate cyclase within the follicular cell. Enhanced activity of adenylate cyclase results in the generation of cAMP, which acts as a second messenger inside the follicular cell. Several key proteins involved in regulation of thyroid hormone synthesis are subject to the influence of TSH as well as iodine supply. The activity of the sodium iodide symporter (NIS), pendrin, and thyroid peroxidase are all stimulated by TSH. Long-term TSH stimulation leads to thyroid hypertrophy and hyperplasia.

There is also an intrathyroidal regulation of thyroid function which is especially important in the presence of either insufficient or excessive iodine supply. This autoregulation enables immediate adaptation to acute iodide excess that might otherwise lead to hyperthyroidism, primarily by lowering the expression of the genes encoding NIS and TPO. On the other hand, in iodine deficiency, thyroid function is increased in response to the lower iodide concentration long before the thyroid organic iodide stores (i.e., thyroglobulin) are exhausted. The thyroid also adapts to low intake of iodine by preferential synthesis of T3 rather than T4.

Schematic of the hypothalamic-pituitary-thyroid axis. Key: TRH = thyrotropin-releasing hormone, TSH = thyroid-stimulating hormone (thyrotropin), T4 = thyroxine, T3 = 3,5,3’-triiodothyronine, rT3 = reverse T3, (+) = stimulation, (–) = inhibition.
Schematic of the hypothalamic-pituitary-thyroid axis. Key: TRH = thyrotropin-releasing hormone, TSH = thyroid-stimulating hormone (thyrotropin), T4 = thyroxine, T3 = 3,5,3’-triiodothyronine, rT3 = reverse T3, (+) = stimulation, (–) = inhibition.

Figure 4 Schematic of the hypothalamic-pituitary-thyroid axis. Key: TRH = thyrotropin-releasing hormone, TSH = thyroid-stimulating hormone (thyrotropin), T4 = thyroxine, T3 = 3,5,3’-triiodothyronine, rT3 = reverse T3, (+) = stimulation, (–) = inhibition.

Figure 4 Schematic of the hypothalamic-pituitary-thyroid axis. Key: TRH = thyrotropin-releasing hormone, TSH = thyroid-stimulating hormone (thyrotropin), T4 = thyroxine, T3 = 3,5,3’-triiodothyronine, rT3 = reverse T3, (+) = stimulation, (–) = inhibition.

Iodine metabolism

Most dietary iodine is in the form of an inorganic salt of iodide. Iodine supplements are usually an iodate form that is reduced in the stomach to iodide. Iodide has high bioavailability (>90%) and is absorbed mainly in the small intestine. Enterocytes express and utilize the active transport sodium iodide symporter on the apical surface for this task. Increasing iodide in food decreases NIS expression in the enterocyte (Nicola et al 2009).

Absorbed iodide is distributed throughout the extracellular space with a half-life of approximately 10 hours. The high specific activity of NIS in the thyroid gland allows the preferential accumulation of iodide resulting in sequestration of the majority of absorbed iodide in this gland. Iodide may be concentrated to more than 40 times the concentration in plasma.

Excess absorbed iodide is assumed to be freely filtered without resorption by the kidneys and eliminated in urine (Trowbridge et al 1975, World Health Organization 2007). Renal iodide clearance is proposed to remain constant as a percentage of filtered iodide in plasma. This assumption results in decreased urinary iodide concentration when iodine intake is limited and an increased concentration when intake is high. However, one exception to this assumption has been suggested in that small mammals may have the ability to conserve iodide by active reabsorption from the kidney to compensate for higher GFR (Vadstrup 1993). Nonetheless, urinary iodide concentration is considered a viable assessment of iodine status in humans because of the afore-mentioned assumptions. Finally, iodine in feces appear to be derived from a constant small endogenous excretion as well as unabsorbed iodide which increases with increasing dietary iodine (Kaptein et al 1994, Kirchgessner et al 1999).

Risk Factors/Etiology/Nutritional Review

Hyperthyroidism in cats has been suggested to mimic toxic nodular goiter (Plummer’s disease) in people (Scott-Moncrieff 2015). Toxic nodular goiter represents a spectrum of disease ranging from a single hyperfunctioning nodule (toxic adenoma) to a gland with multiple areas of hyperfunctioning benign nodules, surrounded by inactive follicular tissue. In cats, a small percentage, around 1-3%, of tumors have been suggested to be carcinoma at time of diagnosis, however, in long-standing hyperthyroidism the prevalence of carcinoma may increase to up to 20% (Peterson and Broome 2015b, Peterson et al 2015c).

A disease entity comparable to Grave’s disease in humans, in which TSH-receptor antibodies stimulate the thyroid, has not been observed in cats. Several lines of evidence to date indicate that in hyperthyroid cats the level of dysfunction is restricted to the follicular cell. Cells from hyperthyroid cats have been shown to function autonomously when transplanted into nude mice (Peter et al 1987, 1991). The loss of inhibitory control results in excessive thyroid hormone production and hyperplasia. Analysis of the TSH receptor for somatic mutations has revealed that the feline TSH receptor has many similar mutations to those observed in human toxic nodular goiter (Palos-Paz et al 2008, Watson et al 2005). Some of these mutations are in a region which imparts a “gain of function” activity to the receptor which may contribute to the autonomous stimulation of the follicular cell (Watson et al 2005). Furthermore, mutations in the gene that encodes for G proteins associated with the TSH receptor may result in autonomous hyperfunction of the follicular cell (Peeters et al. 2004).

Overexpression of the c-ras oncogene in areas of nodular follicular hyperplasia in feline thyroid glands suggests that mutations in this oncogene may also play a role in the etiopathogenesis of hyperthyroidism in cats (Merryman et al 1999). In normal cells, activation of the ras protein leads to mitosis. Mutations of the ras oncogene result in mutated ras proteins, which are not subject to the normal cellular feedback mechanisms which prevent uncontrolled mitosis (Palos-Paz et al 2008). Finally, altered expression of G proteins involved in the signal transduction pathway which stimulates growth and differentiation of thyroid cells has also been identified in adenomatous thyroid glands obtained from hyperthyroid cats (Hammer et al 2000, Ward et al 2005, 2010). Decreased inhibitory G protein expression creates a relative increase in stimulatory G protein expression, which may promote unregulated mitogenesis and thyroid hormone production in hyperthyroid cells. 

Although the clinical and pathological aspects of feline hyperthyroidism have been well characterized, the etiology of hyperthyroidism remains largely undetermined. A variety of factors have been associated with an increased risk of hyperthyroidism in cats including: ingestion of canned foods (Edinboro et al 2004 , Kass et al 1999, Martin et al 2000, Peterson 2012, Scarlett et al 1988); specific flavors of canned foods (Martin et al 2000), specifically fish and giblets/liver flavors; increased variety of canned foods vs single source (Oliczak et al 2005); exposure to flea sprays, insecticides and herbicides (Scarlett et al 1994, Gerber et al 1994); and use of cat litter (Wakeling et al 2009). Because of the strong association with specific food forms, ingredients, or environmental contaminants, one of the preferred hypotheses for etiology is the deleterious effect of one or more of these factors caused by either nutritional deficiencies or excesses, or by the presence of thyroid disrupting compounds in the environment, drinking water or food (Table 4). It should be noted that a review of available published data concluded that there is not enough information to fully support either of these two major hypotheses (Van Hoek et al 2014). The following sections contain more detailed information on the support for hypotheses on the etiology of feline hyperthyroidism.

Table 4. Potential goitrogenic factors in foods and the environment.*

Iodine and disease

Both deficient and excessive iodine intake have long been associated with thyroid dysfunction. Approximately 30% of the world human population experiences insufficient iodine intake. An early clinical sign of iodine deficiency includes enlargement of the thyroid gland (endemic goiter), attributable to the loss of feedback inhibition to the TRH-TSH-thyroid axis resulting in thyroid hyperplasia. Insufficient iodine intake in people may be presumed when concentrations of iodine in urine fall below 100 µg/mL (de Benoist et al 2008). Most commercially prepared cat foods contain adequate amounts of iodine, with measured levels being highly variable, ranging from three to 100 times recommended amounts (Edinboro et al 2013, Johnson et al 1992, Mumma et al 1986). However, a general decreasing trend in iodine content in pet foods from 1980 to current has been suggested as an etiological factor in feline hyperthyroidism (Peterson 2012).

Supplementation of iodine to previously long-standing iodine-deficient human beings may result in iodine-induced hyperthyroidism (Jod-Basedow syndrome) (Fradkin and Wolff 1983). This is presumed to be attributable to long-standing stimulation of the thyroid under conditions of iodine deficiency and resultant hyperplasia with autonomy. The supplementation of iodine, even at normal quantities, subsequently results in hyperthyroidism. This phenomenon has been observed in many areas of the world where iodine fortification programs have been introduced (Kohn 1976).

In contrast to iodine-induced hyperthyroidism it is also possible to induce transient or permanent hypothyroidism and goiter with excessive iodine supplementation (Trowbridge et al 1975). High intake of iodine appears to inhibit the ability of iodide to be bound to tyrosine, e.g. by suppressing the activity of TPO, and thus result in decreased circulating thyroid hormone concentrations. Subsequently, serum TSH concentration is increased and thyroid hyperplasia may ensue. Many individuals may undergo this “escape” phenomenon (Wolfe-Chaikoff syndrome) and some susceptible individuals (0-10% of the human population) may develop permanent hypothyroidism. Prior to the development of effective antithyroid drugs, high concentrations of iodine were sometimes used to treat hyperthyroidism.

The previous discussion reveals that thyroid status and response to changes in iodine intake depend on current thyroid follicle status (autonomous vs regulated) as well as nutrient intake history (deficient or adequate). Increased iodine intake may result in hyperthyroidism in the case of previous deficiency with induced hyperplasia (iodine-induced hyperthyroidism). Conversely, excess supplementation of iodine in normal and some hyperthyroid cases can paradoxically inhibit thyroid production for a short while or, in some sensitive individuals, permanently. It has been suggested that deficient or excessive iodine intake in homemade or poorly formulated cat foods may also be goitrogenic (Scarlett et al 1994).

Iodine requirement in cats

Evaluation of the effect of dietary iodine on iodine balance and thyroid function in cats has been difficult to assess, mainly attributable to the few number of actual feeding studies performed (Edinboro et al 2010). In order to interpret the impact of the iodine status on the development of thyroid disease, consensus must be reached on dietary requirements of iodine.  Four key factors need to be met in order to determine a definitive nutrient requirement estimate (Baker 1986) including: 1) evaluation of a sufficiently wide enough range of intakes to define both a linear and plateau response curve, 2) use of appropriate and sensitive biomarkers for assessing nutrient status, 3) sufficiently long enough period to allow for adaptation, and 4) use of a nutritionally balanced diet with only the nutrient in question varying between treatments. A number of studies have suggested minimum iodine (I) recommendations for the cat approximating 2-4 mg I/kg diet (Scott et al 1961, Smith 1996, Ranz et al 2002, Meyer and Heckőtter 1986), but these studies failed to meet one or more of the criteria listed above.

Nonetheless, based on the above studies the National Research Council (NRC, 2006) of the United States currently recommends an allowance for food iodine content of 1400 μg/kg or 35 μg/kg-bodyweight0.67 for adult cats at maintenance. This was a 4 fold increase over the recommendation of 350 μg/kg food for kittens suggested in the 1986 NRC. Current recommendations from the Association of American Feed Control Officials (AAFCO) suggests 600 μg I/kg food for adult cats at maintenance (2018). The Fédération Européenne de l’Industrie des Aliments pour Animaux Familiers (FEDIAF 2018) suggests 1300 to 1700 μg I per kg food for adult cats at maintenance.

The most recent iodine requirement study suggests that a value of approximately 460 μg I/kg should be the dietary value for cat foods (Wedekind et al 2010). This estimate was based on break-point analysis of the ratio of thyroid to salivary gland technetium 99 uptake via scintigraphy (T:S ratio) regressed against iodine intake at 7 different levels of inclusion (Figure 5). The x value for the breakpoint corresponded to a dietary intake of 0.46 mg I/kg diet and the Y value corresponded to 1.43 T:S ratio. T:S ratio > 1.66 is considered a positive test for hyperthyroid disease (Henrikson et al 2005). The two lowest food I concentrations resulted in T:S ratios that exceeded 1.66 whereas the five other treatments (food iodine concentrations ranging between 0.46 mg I/kg food to 9.2 mg I/kg food) had T:S ratios that were not different from each other and were below the 1.66 threshold. In addition, there was good agreement between the iodine requirement estimate determined via T:S ratio with other biomarkers of iodine status suggested for human evaluation, urine iodine concentration and iodine balance data, which yielded iodine requirement estimates of 460 and 440 μg I/kg diet, respectively. Multiple parameters in this feline study yielded remarkably similar iodine requirement estimates which suggest robustness and validity of the estimates obtained.

It is important to compare nutrient requirements or recommendations between species, because numerous nutrients (e.g., amino acids, trace minerals and vitamins) show remarkable similarity in metabolism and physiology. When the index of iodine status is based on thyroidal uptake (eg, radioiodine uptake or pertechnetate scintigraphy), there is close agreement across species. The NRC minimum requirement for iodine in dogs was based on a radioiodine uptake study (Belshaw et al 1975). Significant changes in radioiodine metabolism occurred between 90 and 140 µg/day, suggesting dietary iodine intakes below 140 µg/day were insufficient to maintain normal iodine thyroid kinetics metabolism (140 µg/day was equivalent to 560 μg I/kg diet). This estimate is similar to the iodine requirement estimate derived for cats (460 μg I/kg diet; Wedekind et al 2010). In humans, the recommended dietary allowance for iodine (DRI 2001) is 150 µg/day which on a metabolic equivalent basis equates to 510 μg I/kg food for the cat. When all of the iodine recommendations are compared across species it would appear that the NRC recommendation for the cat is an unusually large requirement (Zicker and Schoenherr 2012). Extrapolation of published dietary iodine requirements scaled across species by body weight would yield a hypothetical dietary inclusion value of 220 μg/kg for cats.

When the index of iodine status is based on minimum iodine concentration needed to avoid appearance of clinical signs (e.g. thyroid hypertrophy, poor hair coat, TT4 reduction, increased TSH, decreased weight gain or food consumption), the iodine requirement estimate is lower. For example, the iodine requirement for the rat (NRC 1994) and pig (NRC 1998); 150 and 140 μg I/kg diet, respectively) was determined based on minimum level of iodine to prevent thyroid hypertrophy. The safety of the 460 μg I/kg diet requirement estimate based on thyroidal uptake can be further supported based on absence of clinical signs at lower iodine intakes. There were no negative clinical consequences observed at the lowest iodine concentration tested (170 μg I/kg diet); no clinical signs of iodine deficiency (eg, thyroid hypertrophy, poor hair coat, decreased bodyweight and/or food intake, myxedema or lethargy) and there were no changes in thyroid hormone concentrations. Note that this lower level is also in close agreement with the NRC iodine requirements listed for poultry (NRC 1994), rat and pig (140, 150, and 140 μg I/kg diet, respectively). As long as iodine intake is maintained above an iodine threshold of 50 µg/day in people (metabolic equivalent for cats = 180 μg I/kg diet), normal iodine metabolism is maintained without risk of goiter or clinical signs of deficiency (Delange and Ermans 1991). This finding that 180 μg I/kg diet may be a critical threshold for the cat is supported by the fact that after one year duration, even at the lowest iodine intake evaluated (170 μg I/kg diet), low iodine intake had no effect on food intake, body weight or thyroid hormone profiles and no clinical signs such as goiter or poor hair coat observed in the study. Use of scintigraphy data is preferred over use of a marker that indicates deficiency because of the importance of identifying a biomarker that occurs in advance of clinical signs.  This similarity in agreement between cats and other species (dog, human, rat, pig) regarding the iodine requirement (regardless of whether the index is based on optimal thyroidal update or minimum concentration needed to prevent appearance of clinical signs) suggests that the current NRC (2006) recommendation for cats is an over-estimation when Wedekind et al. (2010) is considered.

Regression of thyroid:salivary (T:S) ratio on iodine intake (µg I/d) at wk 51.  A breakpoint was determined using a model involving two linear splines with no plateau.  Each point represents an average of 6 cats with one exception; trt 4 represents means of 5 cats.  The X and Y coordinates for the inflection point determined for T:S ratio were 21.8 µg l/d and 1.2, respectively (Wedekind et al. 2010).
Regression of thyroid:salivary (T:S) ratio on iodine intake (µg I/d) at wk 51.  A breakpoint was determined using a model involving two linear splines with no plateau.  Each point represents an average of 6 cats with one exception; trt 4 represents means of 5 cats.  The X and Y coordinates for the inflection point determined for T:S ratio were 21.8 µg l/d and 1.2, respectively (Wedekind et al. 2010).

Figure 5 Regression of thyroid:salivary (T:S) ratio on iodine intake (µg I/d) at wk 51.  A breakpoint was determined using a model involving two linear splines with no plateau.  Each point represents an average of 6 cats with one exception; trt 4 represents means of 5 cats.  The X and Y coordinates for the inflection point determined for T:S ratio were 21.8 µg l/d and 1.2, respectively (Wedekind et al. 2010).

Figure 5 Regression of thyroid:salivary (T:S) ratio on iodine intake (µg I/d) at wk 51.  A breakpoint was determined using a model involving two linear splines with no plateau.  Each point represents an average of 6 cats with one exception; trt 4 represents means of 5 cats.  The X and Y coordinates for the inflection point determined for T:S ratio were 21.8 µg l/d and 1.2, respectively (Wedekind et al. 2010).

Influence of variable iodine intake in cats

Extreme variation in iodine intake has been suggested as a potential “trigger” for conversion of a normal functioning follicular cell to a follicular cell with autonomous function.  To determine the effect of short-term variable iodine intake on cat thyroid status, dietary iodine at low (102 μg/kg dry matter), medium (2221 µg/kg dry matter), and high (13769 μg/kg dry matter) concentrations were assessed in 2-week feeding trials compared to a control diet (approximately 2200 μg/kg dry matter, mixture of canned and dry food). In addition, a 5-month feeding trial with high (21142 μg/kg dry matter) and low (112 μg/kg dry matter) concentrations were fed to assess longer term effects of iodine (Kyle et al 1994, Tartellin and Ford 1994). The 2-week duration feeding trials led the authors to conclude that increasing iodine intake over baseline control resulted in decreased circulating concentrations of fT4. This may be attributable to the Wolff-Chaikoff effect. It is of interest to note that the control iodine concentration was substantially higher than what is recommended by Wedekind (2010) and different ingredients were used between control and canned formulas to achieve desired iodine content. Thus, results may have been attributable to other factors than just iodine concentration of the food. The longer 5-month feeding period of high and low iodine concentration foods revealed no effect on circulating thyroid hormone concentrations and is consistent with the data from Wedekind (2010). In summary, it appears that short-term variations in iodine intake may significantly alter circulating concentrations of fT4, although the concentrations were generally within historical normal ranges reported for fT4 (Skinner 1998). Other evidence that variable iodine intake may induce hyperthyroidism includes the findings that iodine content of foods for adult cats is highly variable and cats on a variety of canned foods are at higher risk than cats on a single flavor (Oliczak et al 2005, Peterson 2012). This may fit well with findings in human populations where previous iodine intake may influence subsequent thyroid response in both positive and negative ways. The possibility that strong variation in ingested iodine may affect thyroid hormone production needs to be evaluated more fully in long-term prospective studies.

Safety and utilization of low iodine intake in cats

Management of feline hyperthyroidism with iodine-restricted food (150 μg/kg to 280 μg/kg) has recently been established as a viable treatment modality (Carney et al 2016, Melendez et al 2011a, 2011b, Van der Kooij et al 2014, Yu et al 2011). A food containing 200 μg I/kg food has been shown to decrease the circulating thyroid hormone concentration into the reference range for 83% of cats within 6 months of start of trial (Carney et al 2016, Hui et al 2015). In addition, a 2-year study in healthy cats (Paetau-Robinson et al 2018) feeding foods with either 200 μg I/kg vs 3200 μg I/kg food revealed no differences in markers of health status or thyroid function over the course of the study. Based on these studies it appears that feeding levels of iodine down to 200 μg/kg, and possibly lower, are not deleterious to healthy cats for an intermediate length of time and may serve as a method to help decrease circulating TT4 concentrations in hyperthyroid cats.


Selenium is a cofactor for several enzymes in the metabolism of thyroid hormone and intuitively would be a nutrient of concern. Both the highly variable content of selenium and the presence of high selenium concentrations in feline wet foods, have led to the hypothesis of selenium involvement in the development of hyperthyroidism (Simcock et al 2005, Zicker et al 2010). Selenium deficiency has been hypothesized to decrease activity of the deiodinases and thus may impair conversion of T4 to T3, resulting in loss of feedback inhibition. Kittens fed foods with a low selenium content had increased circulating TT4 concentrations and it was also shown that TT3 was positively correlated to serum selenium (Wedekind et al 2003, Wedekind et al 2004, Yu et al 2002 ). However, in another study in which selenium concentrations were assessed in euthyroid and hyperthyroid cats from the same geographic region no difference in selenium status was noted between the two groups (Foster et al, 2001). Interestingly, serum selenium has been found to be approximately 5 times higher in cats than other species (Zicker et al 2010).

To investigate the possible effects of selenium excess, in a prospective study, selenium was added to dry food resulting in a final level of 1250 μg/kg compared to 800 μg/kg in control food. There was an increase in physical activity in treatment group cats (Hooper et al 2018). However, a wet food with selenium content at the control level of 800 μg/kg was also associated with increased physical activity compared with the 800 μg/kg selenium dry food, leading to the hypothesis that increased dietary water intake may have been a causal factor in the observed increased physical activity. No difference was found between any of the foods for thyroid or other general health measures (Hooper et al 2018).

In additional studies, thyroid:salivary (T:S) ratio, as measured by Tc99m scintigraphy, increased linearly (P < 0.05) with increasing Se intakea T:S ratio > 1.55 was measured in cats with highest intakes of selenium and is a suggestive standard for hyperthyroid disease.  However, T3 suppression test and iodothyronines confirmed these cats were not hyperthyroid. Finally, although not a cat study, it has been shown in a dose titration study in dogs that increased selenium intake resulted in changes that mirror thyroid hormone changes observed in hyperthyroid cats (Zicker et al 2010).

Soy isoflavones and quercetin

Soy isoflavonoids and quercetin have also been suggested as dietary ingredients that may influence the development of abnormal thyroid function (Ralph et al  2007, Scott-Moncrieff 2015). Soybean is a potential dietary goitrogen that is commonly used as a high quality vegetable protein in commercial cat foods where it is usually higher in dry formulations compared to wet (Court and Freeman 2002, White et al 2004). The goitrogenic effect of soybeans has been attributed to an inhibitory effect of the soy isoflavones, genistein and daidzein, on thyroid peroxidase (TPO), an enzyme essential to thyroid hormone synthesis (Doerge and Sheehan 1992, Divi et al 1997). Soy isoflavones may also interfere with deiodinases, resulting in inhibition of T3 production (Peterson 2012). Genistein and daidzein have been detected and measured in pet foods in New Zealand and the USA (Bell et al 2006, Court and Freeman 2002). Short-term administration of dietary soy isoflavones, at levels much higher than found in commercial foods, to healthy cats has been demonstrated to result in a modest increase in serum TT4 and free T4 concentrations relative to serum T3 concentrations (White et al 2004). Finally, quercetin, a flavonoid, is capable of stimulating mitogenesis in a cell-culture line from hyperthyroid cats (Ralph et al 2007).

Endocrine disruptors

Exogenous organic compounds that are similar in structure to thyroid hormone may interfere with normal thyroid hormone metabolism. These compounds are used in a variety of environmental applications such as flame retardants, can liners, and plastic drinking bottles and may persist in the environment for long periods of time. The disruptors implicated most include bisphenols, polychlorinated biphenyls (PCB) and polybrominated diphenyl ester (PBDE) compounds.

Bisphenol A is contained in the chemical linings of canned foods, which may be released into the food matrix during cooking (Edinboro et al 2004, Kang and Kondo 2002). Bisphenol A reduces binding of T3 to the thyroid receptor and interferes with the intracellular signal transduction in rats (Moriyama et al, 2002). The compound has been detected in canned cat foods (Kang and Kondo 2002), but at concentrations well below safety levels set for human foods. Concentrations of bisphenol A have not been reported in cats with hyperthyroidism (Van Hoek et al 2014).

PCB and PBDE have both been suggested as causative agents for feline hyperthyroidism. Multiple studies have documented higher concentrations of PBDE in serum of cats compared to  humans from the same environment (Guo et al 2016, Norrgran et al 2015, Walter et al 2017), suggesting that cats may be bioaccumulators of these endocrine disruptors. The common use, up to 1979 (PCB) and beyond (PBDE), of these endocrine disruptors may therefore have led to high tissue concentrations in cats, which may play a role in the development of hyperthyroidism. Indeed, circulating concentrations of PBDEs and PCBs have been determined to be higher in hyperthyroid cats compared to euthyroid cats, with PCBs concentrations being statistically significantly higher in hyperthyroid cats. In addition, PBDE concentrations in serum of feral cats were found to be significantly lower than in indoor cats suggesting that the house environment was the source of exposure, which coincides with studies that suggest an increased risk of hyperthyroidism in indoor cats (Guo et al 2016, Mensching et al 2012, Norrgran et al 2017). A study in wild bobcats revealed increased concentrations of next generation PBDEs, raising concern of bioaccumulation of endocrine disruptors in mammalian food chains (Boyles et al 2017). Although the associations mentioned above do not prove that endocrine disruptors are the cause of feline hyperthyroidism, they should certainly be taken into consideration when thinking about the etiology of feline hyperthyroidism.

Key Nutritional Factors

The key nutritional factors (KNF) for an appropriate food for cats with hyperthyroidism include water, energy, protein and select minerals which are discussed in more detail below. Whether nutrition is being used as the primary modality of treatment or support for other modalities does not change the initial KNF recommendations, except for the recommended iodine content (Table 5). Following initial recommendations, if hyperthyroidism is well controlled by way of non-nutritional therapy and no health abnormalities are revealed, it may be appropriate to reassess the initial KNF recommendations.

Table 5. Key nutritional factors for hyperthyroid cats.*


Cats with hyperthyroidism often exhibit polydipsia and polyuria. Therefore, fresh, clean water should be available at all times.


Uncompensated hyperthyroid cats have an increased metabolic rate and are typically in an energy-deficit state. Interestingly, only 1/3 of untreated hyperthyroid cats are reported underweight whereas the remainder have a history of previous weight loss but still were assessed to have adequate body condition score (Peterson 2016). Hyperthyroid cats may also have decreased fat stores because of their catabolic state.

Primary emphasis should be directed at regulation of hyperthyroidism through medical, surgical or nutritional therapy. Adequate treatment of hyperthyroidism should result in equilibration of energy requirements to what is expected for age and physiologic status.

Provision of daily energy requirement (DER) at the calculated ideal body weight of the patient should result in return to normal body weight if the primary disease process is controlled. DER: neutered cats = 1.2 x Resting energy requirement, intact cats = 1.4 x Resting energy requirement.  Recommended levels of dietary fat, on a dry matter basis, are suggested to be between 15-30% for foods for hyperthyroid cats, energy density should be between 4000-4700 kcal ME/kg of food. If response to weight gain appears refractory, or severe wasting of body mass is present, the fat and energy content of foods may be increased to achieve higher caloric intake to achieve ideal weight.


Hyperthyroid cats are in a hypercatabolic state and may exhibit signs of protein wasting and deficiency.  Approximately 75% of untreated cats exhibit muscle loss yet surprisingly almost half were still found to be below an ideal normal muscle mass following successful treatment (Peterson et al 2016). When muscle mass of treated cats was analyzed with respect to age category, an influence of age was found with older cats having more muscle loss. It is possible that sarcopenia attributable to aging may be a confounding process for muscle mass restoration in hyperthyroid cats.  Protein requirements for untreated hyperthyroid cats or cats in the remission phase of treatment have not been determined.

Since hyperthyroidism is frequently associated with renal failure, a complete evaluation of renal function should be performed prior to recommending a food nutrient profile (Forrester et al 2010). Symmetric dimethyl arginine (SDMA) has been shown to be a new specific predictor of azotemia, however, sensitivity of the test is low in cats with hyperthyroidism (Peterson et al 2018). Since impaired renal function may be masked by hyperthyroidism, a conservative approach to protein recommendations is suggested, even with a normal SDMA. This approach makes the assumption that appropriate treatment of hyperthyroidism should alleviate muscle wasting and allow for adequate protein intake to restore muscle mass. Supplementation of protein in great excess of adequacy should not be considered until hyperthyroidism is controlled and a new renal GFR set point is reached and the true extent of renal compromise is better understood. Initially, dry matter protein levels of 30-40% are adequate, unless renal function is compromised. If renal disease is suspected it is recommended to decrease protein content to 28-35%. True protein digestibility should be greater than 85%.


Avoid food with dry matter fiber levels greater than 5% in patients with poor body condition as this would just dilute the caloric intake and perhaps decrease palatability of the food as well.

Other Nutritional Factors


Because hyperthyroidism may result in changes of circulating concentrations of macrominerals (i.e., phosphate, potassium, sodium, calcium), it is best to avoid foods with excess (all-purpose or growth foods) or extremely restricted macromineral levels. Because hyperthyroidism may present with concurrent renal disease, special attention should be paid to the phosphorus level of the food. If renal disease is suspected phosphorus levels should be controlled at recommended levels of 0.3-0.6% dry matter basis (Forrester 2010).  In cases where renal disease is unlikely, care should still be exercised to assure phosphorus levels are appropriate for mature adult cats (0.5-0.7% dry matter) in light of the increased incidence of renal disease in this age group and the potential for masked renal disease. Decreased sodium chloride intake may benefit some cases in which hypertension and cardiac disease are primary problems (Roudebush and Keene 2010). Foods between 0.2 to 0.4% sodium, on a dry matter basis should suffice in most cases.

Trace Minerals

Generally, foods that meet AAFCO allowances of trace minerals for maintenance are adequate for hyperthyroid cats with the exception of iodine for cats being treated with restricted iodine foods. Nonetheless, specific attention should be given to selenium and iodine as some commercial products have been shown historically to vary greatly in these mineral contents. As discussed previously, strong variation in iodine or selenium intake may play a role in the development of thyroid disease in animals.

It is recommended that content of selenium meet AAFCO minimum recommendations of 300 μg/kg food no matter which modality of treatment is being utilized. No safe upper limit for cats has been established for selenium in cats by AAFCO but it is suggested an upper limit of 1250 μg/kg food be used regardless of treatment modality. Interestingly, it has been suggested by FEDIAF to set a limit for selenium of 568 μg/kg food, however a recent report revealed up to 76% of wet foods from the UK exceeded this limit (Davies et al 2017). Iodine content for non-restricted iodine foods should be in the range of 600-9000 μg/kg as suggested by AAFCO.

Iodine-restricted foods for the management of feline hyperthyroidism

Cats with hyperthyroidism have been shown to return to euthyroid state when fed an iodine-restricted food (170-280 μg I/kg) and this modality is currently used in the management of feline hyperthyroidism (Carney et al 2016, Melendez et al 2011a, 2011b, Yu et al 2011). Foods with iodine content between 170 to 280 μg/kg, depending on the caloric density, have been utilized to not only decrease thyroid hormone concentrations in cats with spontaneously occurring disease (Melendez et al 2011 a, 2011b) but actually return them to a euthyroid state in up to 83% of cases managed with a 200 μg I/kg food long term (Hui et al 2015). Concerns with sole source feeding of iodine-restricted foods for the remainder of the cat’s lifespan, palatability, and dietary fatigue (see next section) should be discussed thoroughly with owners to ensure optimal success.

Feeding and Treatment Plan for Hyperthyroid Cats

The success of management of abnormalities associated with hyperthyroidism depends to a great degree on the effectiveness of treatment for the primary disease. Four modes of treatment are generally accepted for hyperthyroidism in cats: 1) long-term antithyroid medication, 2) surgical thyroidectomy, 3) radioactive iodine, and 4) iodine-restricted food (Carney et al 2016, Melendez et al 2011 a, b, Peterson et al 1983). The least invasive of these modalities is dietary management but this modality does come with some special management issues. Even though compliance with feeding of exclusively iodine-restricted food is sometimes a challenge, many cats voluntarily eat iodine-restricted food every day in order to meet daily energy requirements.

Assess and Select the Food

Initial foods for hyperthyroid cats treated by any modality should be selected which meet the guidelines suggested in Table 5.  These KNFs assume age demographics, possible impact of trace mineral effects on thyroid metabolism and potential of underlying renal disease (Forrester 2010). Attention to iodine content is important when utilizing nutrition as primary compared to a support therapy for other modalities of treatment (Table 5).

Identify any discrepancies between the recommended levels of KNFs and current intake. If discrepancies exist, consider selecting a food that more closely matches the KNF targets in Table 5. If nutritional therapy is chosen as the sole source of intervention, recommendation of the level of iodine listed for treatment should be referenced from the KNFs in Table 5.

Assess and Determine the Feeding Method

It may not be necessary to change the feeding method when feline hyperthyroidism is not managed with iodine-restricted food. In general, provision of the daily energy requirement with free access over a 24 hour period is adequate.  If multiple cats exist in the household it would be ideal to offer the affected animal a separate secure feeding location from others so intake can be assessed.

If changing to dietary management of hyperthyroidism a transition period of 1 to 2 weeks from current food to iodine-restricted food is recommended to optimize acceptance. It may be necessary to use low iodine food inducements or enrichment (feeding toys) in cases where initial intake wanes after a period of adequate intake on low iodine foods.  Feeding of affected individuals in a secure location is recommended to assess intake.  Intake of low iodine foods to healthy cats has not been shown to result in adverse effects and should not be a concern if cross feeding is observed in this population.  Finally, it has been hypothesized that long term management of hyperthyroidism by pharmaceutic or nutritional therapy may lead to increased risk of carcinoma compared to other modalities which are considered curative in action however current information remains inconclusive (Peterson and Broome 2012).


During the convalescent period, monitor response to therapy and assess if protein and energy intake are adequate with respect to renal function. The response to treatment may be assessed by owner observation of clinical signs, bimonthly body weight charting and monitoring of food intake, findings on physical examination, blood work, and measurement of serum TT4 concentration. Return to normal activity, body condition and appearance, and normal serum TT4 concentration indicate a successful response to treatment.  If all assessment parameters are within normal ranges after reaching euthyroidism, and body weight/muscle mass still lags one may consider changing foods, if not using iodine restricted therapy, to achieve a more desirable endpoint.  Foods with KNFs for middle age to mature adult cats may be considered at this point (Gross et al 2010). Before instituting dietary changes it is important to make sure that renal function and blood pressure have been evaluated to rule out cardiac and renal disease, so that foods containing appropriate levels of sodium and phosphorus may be recommended.

Treatment or dietary recommendation may be inadequate if clinical signs persist, body weight and body condition remain poor and serum TT4 concentration remains increased. Adjustments in the treatment regimen and problems with owner compliance should be considered if the response to treatment is inadequate, especially if dietary or pharmaceutical treatment has been instituted. Remnants of hyperfunctioning thyroid tissue should be considered if thyroidectomy was performed or radioactive iodine-131 was administered and serum TT4 concentration is still elevated.

aHill’s Pet Nutrition, Inc. Topeka KS; unpublished data.


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