Despite these successes, authors have questioned the efficacy of l-thyroxine monotherapy because about 10% to 15% of patients are dissatisfied as a result of residual symptoms of hypothyroidism (1, 2), including neurocognitive impairment (3), and about 15% of patients do not achieve normal serum triiodothyronine (T3) levels (4). Studies of several animal models indicate that maintaining normal serum T3 levels is a biological priority (5). Although the clinical significance of relatively low serum T3 in humans is not well-defined (1), evidence shows that elevating serum T3 through the administration of both l-thyroxine and l-triiodothyronine has benefited some patients (6, 7). However, this has not been consistently demonstrated across trials (1). Novel findings highlight the molecular mechanisms underlying the inability of l-thyroxine monotherapy to universally normalize measures of thyroid hormone signaling (8, 9), and new evidence may lay the foundation for a role of personalized medicine (10). Understanding the historical rationale for the trend toward l-thyroxine monotherapy allows us to identify scientific and clinical targets for future trials.
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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