Vitamin A
Serum Retinol (Vitamin A)
What it is
Vitamin A refers to a family of fat-soluble retinoids — retinol (the primary circulating and storage form), retinal (the aldehyde form required for vision), and retinoic acid (the active nuclear receptor ligand that regulates gene expression) — as well as provitamin A carotenoids, primarily beta-carotene, obtained from plant sources. The body converts dietary retinol esters (from animal foods) and beta-carotene (from plants) to retinol, which is stored predominantly in the liver as retinyl esters and released into circulation bound to retinol-binding protein (RBP4). Serum retinol is the standard measure of vitamin A status in adults. The vitamin A receptor (RAR — retinoic acid receptor) is a nuclear receptor expressed in immune cells, skin, eyes, lung, and reproductive tissues, regulating the expression of hundreds of genes involved in differentiation, proliferation, and immune function. Vitamin A is essential for: dim-light and colour vision (retinal is the chromophore in rhodopsin and cone opsins); maintenance of epithelial barrier integrity across the respiratory, gastrointestinal, and urogenital tracts; immune competence (particularly innate immunity and mucosal immunity); and reproduction.
Why we measure it
Vitamin A occupies a clinically unusual position: it is one of the few micronutrients where both deficiency and toxicity are common and serious, and where supplementation without measuring can cause harm. Deficiency (rare in high-income countries but common globally) causes night blindness, xerophthalmia (corneal drying and ulceration), increased susceptibility to respiratory and gastrointestinal infections, and — at severe deficiency — total blindness. Toxicity (hypervitaminosis A) is almost exclusively caused by excess supplementation with preformed retinol, not from dietary sources or beta-carotene. Acute toxicity presents with headache, nausea, and skin changes; chronic toxicity — from sustained over-supplementation — causes liver fibrosis, bone loss (retinol directly stimulates osteoclast activity), intracranial hypertension, and in pregnancy, severe teratogenicity (causing craniofacial, cardiac, and neural tube defects). Isotretinoin (a pharmaceutical retinoid) and high-dose retinol supplements are teratogenic at doses achievable with supplementation. In the context of the Blueprint protocol, annual retinol measurement is relevant for individuals taking retinol-containing supplements (which are widespread in anti-ageing and skincare contexts), consuming large amounts of liver (one of the richest retinol sources), or using high-dose combination supplements. It provides an objective basis for supplementation decisions rather than relying on guesswork.
Why every 12 months
Annual measurement is appropriate, timed to the Blueprint Bloodwork draw. Retinol levels are relatively stable over time in individuals with consistent intake; any seasonal variation is modest for most adults. Annual measurement provides the baseline and trend data needed to confirm adequacy without excess.
What movement means
Serum retinol is reported in μmol/L or μg/dL. The standard adult reference range is approximately 1.05–3.49 μmol/L (30–100 μg/dL). Deficiency is defined as serum retinol below 0.70 μmol/L (< 20 μg/dL) by the WHO; values between 0.70 and 1.05 μmol/L are considered marginal. Toxicity risk increases substantially with sustained levels above 3.49 μmol/L (> 100 μg/dL) from supplementation.
Deficient
< 0.70 μmol/L (< 20 μg/dL)
WHO-defined deficiency. Associated with night blindness, impaired immune function, and epithelial barrier dysfunction. Clinical review and dietary assessment are appropriate. In adults in high-income countries, deficiency without a specific cause (malabsorption, strict dietary restriction, chronic liver disease) is uncommon.
WHO Vitamin A Deficiency indicators, 2009
Marginal / Low-Normal
0.70 – 1.05 μmol/L (20 – 30 μg/dL)
Marginal vitamin A status. Hepatic stores may be declining. Dietary review and, if appropriate, a low-dose vitamin A supplement or increased consumption of dietary sources (liver, oily fish, dairy, orange/yellow vegetables) is warranted.
WHO Vitamin A Deficiency indicators, 2009
Adequate
1.05 – 3.49 μmol/L (30 – 100 μg/dL)
Adequate vitamin A status. No supplementation is required on this basis. For individuals currently supplementing, continued monitoring ensures levels remain within the adequate range without approaching the upper limit.
Standard laboratory reference ranges — vary by assay method
Excess / Toxicity Risk
> 3.49 μmol/L (> 100 μg/dL)
Above the upper reference limit. At sustained levels in this range — particularly from supplemental retinol — risk of liver toxicity, bone loss, and (in pregnancy) teratogenicity increases. Supplemental retinol should be reduced or discontinued. Dietary sources alone rarely produce this level.
Penniston KL, Tanumihardjo SA, American Journal of Clinical Nutrition, 2006 — doi:10.1093/ajcn/83.2.191
In the protocol
References
- 1.
Penniston KL, Tanumihardjo SA. “The Acute and Chronic Toxic Effects of Vitamin A.” American Journal of Clinical Nutrition. 2006.
- 2.
World Health Organization. “Global Prevalence of Vitamin A Deficiency in Populations at Risk 1995–2005.” WHO Global Database on Vitamin A Deficiency. 2009.
- 3.
Ross AC, Caballero BH, Cousins RJ, Tucker KL, Ziegler TR. “Modern Nutrition in Health and Disease (11th edition) — Chapter on Vitamin A.” Lippincott Williams & Wilkins. 2014.
- 4.
Sommer A, Vyas KS. “A Global Clinical View on Vitamin A and Carotenoids.” American Journal of Clinical Nutrition. 2012.