Zinc & Selenium
Zinc & Selenium
What it is
Zinc is an essential trace mineral that serves as a structural or catalytic component of over 300 enzymes, including carbonic anhydrase, superoxide dismutase (antioxidant), alkaline phosphatase, and enzymes involved in DNA synthesis and repair. Zinc is also a structural component of approximately 2,700 transcription factors (zinc finger proteins) — making it critical for gene expression regulation. Dietary zinc is obtained from animal products (particularly red meat, shellfish, and poultry), with plant-based zinc having lower bioavailability due to phytate binding. Selenium is an essential micronutrient incorporated into selenoproteins through the unique amino acid selenocysteine. The most important selenoproteins include the glutathione peroxidase family (GPx1–4, neutralising hydrogen peroxide and lipid hydroperoxides), thioredoxin reductase (maintaining intracellular redox balance), and iodothyronine deiodinase types 1 and 2 (converting the prohormone T4 to active T3 in thyroid and peripheral tissues). Dietary selenium is obtained from foods grown in selenium-rich soils — Brazil nuts are the richest known source — and dietary selenium content is highly variable geographically, reflecting soil composition rather than dietary choices alone. Both zinc and selenium exhibit U-shaped relationships with health outcomes: deficiency causes distinct clinical harm, and excess — from over-supplementation — causes toxicity.
Why we measure it
Zinc deficiency impairs virtually every arm of the immune response — reducing T-cell and natural killer cell function, impairing neutrophil activity, and reducing antibody production. In males, zinc is required for Leydig cell testosterone synthesis and for spermatogenesis; zinc deficiency is associated with significantly reduced testosterone and impaired sperm quality. Zinc also plays a direct role in wound healing, taste and smell function, and skin barrier integrity. Selenium deficiency impairs thyroid hormone metabolism by reducing iodothyronine deiodinase activity — reducing the peripheral conversion of T4 to active T3, potentially contributing to hypothyroid symptoms even when TSH is normal. At the population level, selenium status is inversely associated with thyroid volume and the risk of autoimmune thyroid disease (Hashimoto's thyroiditis and Graves' disease). Selenium deficiency is also associated with increased oxidative stress and has been linked in prospective studies to increased cancer risk — particularly for cancers of the prostate, colorectal, and lung. However, selenium toxicity (selenosis) from excessive supplementation causes hair and nail loss, neurological symptoms, and gastrointestinal disturbance — a real risk in people who supplement without measuring. The same over-supplementation risk applies to zinc (which at high doses competitively inhibits copper absorption, causing copper deficiency). This is precisely why measurement matters more than blanket high-dose supplementation.
Why every 6 months
Serum zinc is reasonably stable across the day when measured in a fasting state; selenium (measured as serum or plasma selenium) reflects intake over weeks to months. The six-month interval provides sufficient resolution to assess the impact of dietary changes or supplementation on both markers and to detect slow-developing deficiency or excess.
What movement means
Both zinc and selenium reference ranges vary by laboratory and assay method. Serum zinc is typically reported in μmol/L or μg/dL; serum selenium in μmol/L or μg/L. The ranges below are approximate adult reference values.
Zinc — Deficient
< 10.7 μmol/L (< 70 μg/dL)
Associated with impaired immune function, reduced testosterone in males, poor wound healing, and dermatitis. Dietary review and supplementation (zinc glycinate or citrate; avoid zinc oxide) are appropriate. Copper should be co-monitored with zinc supplementation.
Standard laboratory reference ranges — vary by assay method
Zinc — Normal
10.7 – 17.9 μmol/L (70 – 117 μg/dL)
Within the adult reference range. Phytate-rich plant-based diets may require monitoring even when intake appears adequate due to reduced bioavailability.
Standard laboratory reference ranges — vary by assay method
Selenium — Deficient
< 0.85 μmol/L (< 67 μg/L)
Associated with impaired thyroid hormone conversion, elevated oxidative stress, reduced immune function, and — at severe deficiency — cardiomyopathy (Keshan disease, endemic in low-selenium regions). Supplementation with selenium (selenomethionine preferred) is appropriate, with re-testing to confirm repletion.
Thomson CD, European Journal of Clinical Nutrition, 2004 — doi:10.1038/sj.ejcn.1601977
Selenium — Normal
0.85 – 1.90 μmol/L (67 – 150 μg/L)
Within the adult reference range. Optimal levels for selenoprotein activity are in the upper portion of this range. Values above 1.90 μmol/L suggest adequate intake; values above 2.5 μmol/L from supplementation warrant dose reduction.
Thomson CD, European Journal of Clinical Nutrition, 2004 — doi:10.1038/sj.ejcn.1601977
In the protocol
References
- 1.
Prasad AS. “Zinc in Human Health: Effect of Zinc on Immune Cells.” Molecular Medicine. 2008.
- 2.
Thomson CD. “Selenium and Iodine Intakes and Status in New Zealand and Australia.” British Journal of Nutrition. 2004.
- 3.
Ventura M, Melo M, Carrilho F. “Selenium and Thyroid Disease: From Pathophysiology to Treatment.” International Journal of Endocrinology. 2017.
- 4.
Rayman MP. “Selenium and Human Health.” The Lancet. 2012.