Retinol (Vitamin A) Unit Converter
Retinol (Vitamin A) Unit Converter
Convert serum retinol between µg/dL, µmol/L, µg/L and nmol/L, with the WHO deficiency thresholds. Serum retinol is not dietary vitamin A activity: the IU and RAE factors used for intake do not apply to a blood concentration, and confusing the two is the commonest error made with this analyte.
Serum retinol converter
Mass ⇄ molarSerum retinol 55 µg/dL
Formula and conversion factor
µg/dL = µmol/L × 28.65
nmol/L = µg/dL × 34.91
These apply to SERUM RETINOL only
- 0.03491
- derived from the molecular weight of retinol, 286.45 g/mol. One µg/dL is 10 µg/L, which is 10 ÷ 286.45 = 0.03491 µmol/L
- the cross-check
- WHO puts subclinical deficiency at below 0.70 µmol/L and severe deficiency at below 0.35; the NIH Office of Dietary Supplements gives the same two thresholds as 20 and 10 µg/dL. 20 × 0.03491 = 0.698 and 10 × 0.03491 = 0.349, so the factor reproduces two independently published pairs
- IU
- a unit of dietary vitamin A activity, not of blood concentration. 1 IU of retinol is 0.3 µg RAE. It cannot be applied to a serum result, and a serum retinol has no IU value
- µg RAE
- retinol activity equivalents, the unit of dietary intake. 1 µg RAE = 1 µg retinol = 2 µg supplemental beta-carotene = 12 µg dietary beta-carotene = 24 µg dietary alpha-carotene or beta-cryptoxanthin. These factors describe absorption and bioconversion in the gut and have nothing to do with converting a plasma concentration
- why the confusion is so common
- both quantities are called vitamin A and both are quoted in micrograms. One is how much a person ate; the other is what is circulating bound to retinol-binding protein. No arithmetic connects them
Worked example
Serum retinol 55 µg/dL
55 × 0.03491 = 1.92 µmol/L
= 550 µg/L = 1,920 nmol/L
Within the adult reference interval of 32.5–78.0 µg/dL (1.13–2.72 µmol/L)
Well above the WHO deficiency threshold of 0.70 µmol/L, which is 20 µg/dL
This patient's dietary intake in µg RAE cannot be inferred from any of these numbers
Deficiency thresholds in both units
| µmol/L | µg/dL | |
|---|---|---|
| WHO: subclinical vitamin A deficiency | < 0.70 | < 20 |
| WHO: severe vitamin A deficiency | < 0.35 | < 10 |
| Adult reference interval (Mayo) | 1.13 – 2.72 | 32.5 – 78.0 |
| 0 to 6 years reference interval (Mayo) | 0.39 – 2.26 | 11.3 – 64.7 |
Serum retinol against dietary vitamin A — two different quantities
| Serum retinol | Dietary vitamin A | |
|---|---|---|
| What it is | The concentration circulating bound to retinol-binding protein and transthyretin | How much vitamin A activity was eaten or supplemented |
| Units | µg/dL, µmol/L, µg/L, nmol/L | µg RAE, IU, mg |
| Conversion | × 0.03491 from µg/dL to µmol/L, from the molecular weight | 1 µg RAE = 1 µg retinol = 12 µg dietary beta-carotene; 1 IU retinol = 0.3 µg RAE |
| What changes it | Liver stores near exhaustion, inflammation, protein-energy malnutrition, zinc deficiency, liver disease | What the person ate and absorbed |
| Can one be derived from the other | No | No |
Why a low retinol is not automatically deficiency
| Finding | What to do |
|---|---|
| Low retinol, CRP or AGP raised | Retinol falls in the acute phase response. Repeat once the inflammation has settled, or adjust for it — the BRINDA regression correction lowered estimated deficiency prevalence by 6 to 22 percentage points in surveys of preschool children |
| Low retinol, no inflammation, poor intake or malabsorption | Consistent with deficiency. Cystic fibrosis, cholestasis, pancreatic insufficiency, coeliac disease and bariatric surgery are the usual malabsorptive causes |
| Low retinol, adequate intake, low albumin or transthyretin | Retinol travels bound to retinol-binding protein and transthyretin; protein-energy malnutrition and liver disease lower the carrier and with it the measured retinol |
| Normal retinol, night blindness or xerophthalmia | Trust the eye. Hepatic release holds serum retinol steady until stores are nearly gone, so a normal concentration does not exclude deficiency |
What a serum retinol measures, and what it does not
Retinol is C20H30O, molecular weight 286.45, and the conversion from µg/dL to µmol/L is the molecular weight and nothing else: 10 µg per litre divided by 286.45 g/mol gives 0.03491 µmol/L per µg/dL. The factor is worth checking against something other than itself, and two published pairs oblige. The World Health Organization defines subclinical vitamin A deficiency as a serum or plasma retinol below 0.70 µmol/L and severe deficiency as below 0.35 µmol/L; the NIH Office of Dietary Supplements gives the same two cut-offs as 20 µg/dL and 10 µg/dL. Twenty times 0.03491 is 0.698 and ten times is 0.349. The ladder is right.
The important distinction on this page is not between units but between quantities. Dietary vitamin A is measured in retinol activity equivalents and, historically, in international units, and the factors for those are bioconversion factors: one µg RAE is one µg of retinol, two µg of supplemental beta-carotene, twelve µg of dietary beta-carotene or twenty-four µg of dietary alpha-carotene or beta-cryptoxanthin, and one IU of retinol is 0.3 µg RAE. Those numbers describe how much of what was eaten becomes usable vitamin A in the body. They are not concentrations, they do not apply to blood, and no arithmetic converts a serum retinol into an intake or an intake into a serum retinol. Both are called vitamin A and both are quoted in micrograms, which is why the error is so easy to make and so easy to miss once made.
Interpretation has a second trap, and it is the reason this page will not let a low value stand unqualified. Serum retinol is homeostatically controlled: the liver holds the circulating concentration steady by releasing retinol bound to retinol-binding protein, and it goes on doing so until hepatic stores are nearly exhausted. So a normal retinol does not prove adequate stores, and clinical deficiency — night blindness, conjunctival xerosis, Bitot spots — can coexist with a concentration inside the reference interval. In the other direction, retinol and retinol-binding protein are negative acute phase reactants and fall during infection and inflammation. The BRINDA project found that correcting retinol for C-reactive protein and alpha-1-acid glycoprotein by regression lowered the estimated prevalence of deficiency by between 6 and 22 percentage points across surveys of preschool children. Those coefficients are survey-specific and are not reproduced here as a formula; the actionable version is simpler. Measure CRP and AGP alongside retinol, and do not diagnose deficiency from a low retinol in an inflamed patient.
Other things lower it without deficiency. Retinol circulates bound to retinol-binding protein, itself carried by transthyretin, so protein-energy malnutrition, liver disease and nephrotic syndrome lower the measured concentration by lowering the carrier. Zinc deficiency impairs synthesis of retinol-binding protein and can produce a low retinol that will not correct with vitamin A until the zinc is replaced. True malabsorptive deficiency is seen in cystic fibrosis, cholestatic liver disease, pancreatic insufficiency, coeliac disease and after bariatric surgery.
At the top of the scale there is no threshold to publish. Mayo Clinic Laboratories states there is no widely accepted serum vitamin A level associated with toxicity; hypervitaminosis A is a clinical diagnosis supported by intake history, and where a laboratory can measure them it is the retinyl esters, not retinol, that indicate excess. This page therefore gives an upper reference limit and no toxic level, because there is not one to give.
Frequently asked questions
How do I convert serum retinol from µg/dL to µmol/L?
Multiply by 0.03491, a factor derived from the molecular weight of retinol, 286.45 g/mol. A retinol of 55 µg/dL is 1.92 µmol/L. Going the other way, multiply µmol/L by 28.65.
Can I convert serum retinol to IU or to µg RAE?
No, and this is the single most common mistake made with vitamin A. IU and µg RAE are units of dietary intake, related to each other by bioconversion factors — 1 IU of retinol is 0.3 µg RAE, and 12 µg of dietary beta-carotene is 1 µg RAE. A serum concentration is a different quantity altogether and has no IU value.
What retinol level defines vitamin A deficiency?
WHO defines subclinical deficiency as a serum or plasma retinol below 0.70 µmol/L (20 µg/dL) and severe deficiency as below 0.35 µmol/L (10 µg/dL), in children and adults. These are also used as population indicators: a prevalence above 20% in preschool children marks a severe public health problem.
Does a low serum retinol always mean vitamin A deficiency?
No. Retinol is a negative acute phase reactant and falls during infection and inflammation, so check a CRP and an alpha-1-acid glycoprotein before concluding anything. Low albumin or transthyretin, liver disease and zinc deficiency also lower it by lowering the carrier protein rather than by depleting stores.
Does a normal serum retinol rule out deficiency?
No. The liver holds the circulating concentration constant until its stores are nearly exhausted, so serum retinol is insensitive to moderate depletion. If the eye signs are there — night blindness, conjunctival xerosis, Bitot spots — treat the patient rather than the number.
What retinol level is toxic?
There is no widely accepted serum concentration that defines toxicity. Hypervitaminosis A is diagnosed on the clinical picture and the intake history, and where available it is the retinyl esters rather than retinol that indicate excess.
Related calculators
References
- World Health Organization. Serum retinol concentrations for determining the prevalence of vitamin A deficiency in populations. WHO, Geneva. Deficiency <0.70 µmol/L; severe deficiency <0.35 µmol/L.
- National Institutes of Health, Office of Dietary Supplements. Vitamin A and Carotenoids: Fact Sheet for Health Professionals. Deficiency thresholds 20 and 10 µg/dL; 1 µg RAE = 1 µg retinol = 12 µg dietary beta-carotene; 1 IU retinol = 0.3 µg RAE.
- Larson LM, Guo J, Williams AM, et al. Approaches to assess vitamin A status in settings of inflammation: Biomarkers Reflecting Inflammation and Nutritional Determinants of Anemia (BRINDA) project. Nutrients. 2018;10(8):1100.
- Mayo Clinic Laboratories. Vitamin A, Serum (VITA), test 42357: adults 32.5–78.0 mcg/dL; no widely accepted serum level associated with toxicity.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.
