Thus, neither desiccated thyroid nor l-thyroxine monotherapy recreates a biochemical state of euthyroidism as defined by the serum T4:T3 ratio. l-Thyroxine and l-triiodothyronine combination therapy theoretically could be titrated to restore this measure, but such a method would be challenging because of the frequent dosing schedule needed to achieve stable serum T3 levels (5). New technology is needed to allow for steady delivery of l-thyroxine; only then would high-quality clinical trials best investigate the utility of the serum T4:T3 ratio as an outcome measure in hypothyroidism.
The thyroid uses iodine to convert T4 into freeT3. If you have hypothyroidism, you may not have an iodine deficiency per se, but your thyroid is almost certainly struggling in some way to get ahold of the iodine available to it and do what it needs to do with it. If the root cause is left unaddressed, simply increasing iodine is not always useful and at worst can be dangerous depending on how high you’re increasing your supplementation thinking if a little is good, then more will “solve” your problem.
Thyroid hormone replacement has been used for more than a century to treat hypothyroidism. Natural thyroid preparations (thyroid extract, desiccated thyroid, or thyroglobulin), which contain both thyroxine (T4) and triiodothyronine (T3), were the first pharmacologic treatments available and dominated the market for the better part of the 20th century. Dosages were adjusted to resolve symptoms and to normalize the basal metabolic rate and/or serum protein-bound iodine level, but thyrotoxic adverse effects were not uncommon. Two major developments in the 1970s led to a transition in clinical practice: 1) The development of the serum thyroid-stimulating hormone (TSH) radioimmunoassay led to the discovery that many patients were overtreated, resulting in a dramatic reduction in thyroid hormone replacement dosage, and 2) the identification of peripheral deiodinase-mediated T4-to-T3 conversion provided a physiologic means to justify l-thyroxine monotherapy, obviating concerns about inconsistencies with desiccated thyroid. Thereafter, l-thyroxine mono-therapy at doses to normalize the serum TSH became the standard of care. Since then, a subgroup of thyroid hormone–treated patients with residual symptoms of hypothyroidism despite normalization of the serum TSH has been identified. This has brought into question the inability of l-thyroxine monotherapy to universally normalize serum T3 levels. New research suggests mechanisms for the inadequacies of l-thyroxine monotherapy and highlights the possible role for personalized medicine based on deiodinase polymorphisms. Understanding the historical events that affected clinical practice trends provides invaluable insight into formulation of an approach to help all patients achieve clinical and biochemical euthyroidism.
Megan Casper, RDN, a dietitian based in New York City and the founder of Nourished Bite, points out that iodine deficiency is the leading cause of hypothyroidism worldwide. This mineral can’t be made by the body, so dietary sources like iodized salt, dairy products, seafood, seaweed, and fortified cereals are important. “Iodine is an essential nutrient in the body, and thyroid hormones are composed of iodine,” explains Rizzo. “Those lacking thyroid hormones may also be lacking iodine.”

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