Zinc, Selenium and Thyroid Hormone Conversion

Exploring the cofactor roles of zinc and selenium in thyroid hormone synthesis and deiodinase enzyme function

Iodine and Thyroid Hormone Synthesis

Thyroid hormones—thyroxine (T4) and triiodothyronine (T3)—contain iodine atoms essential for their biological activity. The thyroid gland actively concentrates iodine and incorporates it into tyrosine residues on thyroglobulin protein, producing iodotyrosines that are coupled to form T4 and T3. Adequate dietary iodine is the foundation for thyroid hormone synthesis; deficiency directly impairs hormone production and is the leading preventable cause of hypothyroidism globally.

Selenium and Deiodinase Enzymes

Beyond iodine, selenium serves as a critical cofactor in selenoprotein synthesis, particularly the deiodinase enzymes (types 1, 2, and 3) that regulate thyroid hormone metabolism. Type 1 deiodinase (D1), found primarily in liver and kidney, catalyzes the conversion of T4 to T3—the more metabolically active form. Type 2 deiodinase (D2), present in brain, pituitary, and adipose tissue, also generates T3 locally within target tissues. Type 3 deiodinase (D3) inactivates thyroid hormones by converting T4 to reverse T3 and T3 to diiodothyronine.

Selenium deficiency impairs deiodinase function, reducing the conversion of T4 to T3 and limiting thyroid hormone bioavailability. Research documents that selenium supplementation in deficient individuals can improve thyroid function and antibody-mediated autoimmune thyroiditis markers. However, effects of selenium supplementation in replete populations remain less clear.

Zinc in Thyroid Function

Zinc functions as a cofactor in multiple enzymes involved in thyroid hormone metabolism and immune regulation. Zinc is required for the synthesis and function of zinc finger transcription factors that regulate thyroid peroxidase and thyroglobulin expression. Additionally, zinc plays a role in T cell-mediated immunity, affecting the autoimmune responses that can target the thyroid gland.

Zinc deficiency has been associated with reduced T4 and T3 levels and impaired immune responses that may increase susceptibility to autoimmune thyroid disease. Conversely, adequate zinc status supports optimal thyroid function and immune regulation. The interplay between zinc and other micronutrients in thyroid axis regulation reflects the integrative nature of endocrine control.

Interactions and Overall Micronutrient Status

Zinc and selenium do not function in isolation. The thyroid axis also requires adequate iron, copper, and vitamin B12 for optimal function. Zinc and iron compete for absorption in the intestine; imbalances in either can impair thyroid hormone metabolism. Copper is required for proper iron metabolism and ceruloplasmin synthesis, which supports thyroid peroxidase function.

Practical Considerations

Cross-sectional studies document associations between micronutrient status and thyroid hormone levels in various populations. Controlled trials in micronutrient-deficient individuals demonstrate improvements in thyroid function with repletion. However, supplementation of these micronutrients in replete, healthy populations has shown more limited benefits. Individual assessment of micronutrient status and professional guidance are important for personalized approaches to thyroid health.

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