Vitamin A (retinol) level
Serum retinol is the main blood measure of vitamin A. WHO counts 20 µg/dL or below as low, and US survey ranges for adults start at 31 to 36. The liver holds the level steady, so it tracks body stores only at the extremes, and infection lowers it. Both low and high levels were linked to hip fracture.
- Status
- A blood test ordered by a clinician. FDA classifies vitamin A test systems, which measure vitamin A in serum or plasma, as class I devices [1].
- Measures
- The concentration of retinol, the main form of vitamin A circulating in blood, in serum or plasma, where it travels bound to retinol-binding protein [2].
- Also called
- serum retinol, plasma retinol, retinol, vitamin A serum, vitamin A blood test, vitamin A retinol, retinol level, vitamin A level
- Tested for
- vitamin A deficiency, night blindness, dry eyes, malabsorption, liver disease, follow-up after weight loss surgery, checking a vitamin A supplement, vitamin A excess
Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on
Linked in research3
- ModerateShown in trials to cut deaths 12% in children aged 6 months to 5 years given vitamin A in countries where deficiency is common.
- ModerateLinked to more hip fractures at both high and low blood retinol in a meta-analysis of four cohorts, with no link to fractures overall.
- LimitedLimited evidence: one cohort of 29,104 Finnish men who smoked linked higher serum retinol to 17% fewer deaths, with the lowest risk near 60 to 70 µg/dL.
Reported risks0
No risks sourced yet.
Reference ranges
Each range is the one its source published, in µg/dL. Also reported in µmol/L. Where sources differ, each is shown.
World Health Organization summary of its cut-offs, 2011
Populations of adults, as cut-offs for counting how many people have low serum retinol · [2], [3], [4]
| Range | What the source calls it |
|---|---|
| below 10 µg/dL | "deficient" A doctor, immediately |
| 10 to 20 µg/dL | "low" |
| above 20 µg/dL | No name given |
WHO states that serum retinol is not useful for assessing the vitamin A status of individuals, because the liver controls it and it reflects liver stores only when they are severely depleted or extremely high. The cut-offs exist to count low values across a population. WHO's current cut-off for low serum retinol is 0.70 µmol/L or below, which it equates with 20 µg per 100 mL. The words low, for 10 to 20, and deficient, for below 10, come from a 1976 WHO meeting report that the 2011 summary cites, and WHO traces the values to a 1963 US committee. WHO states that values below 10 µg per 100 mL were associated with low liver stores and with more clinical signs of deficiency, and that the cut-off was raised to 20 in 1996 to include people who had not yet developed the clinical signs associated with severe deficiency. A later cohort paper refers to the lower cut-off as WHO's criterion for severe vitamin A deficiency [3]. The summary prints the current cut-off both as 0.70 µmol/L or below and as below 0.70 µmol/L. WHO gives no cut-off for a high result, so this block does not classify high results [2]. The factor to µmol/L on this page matches the paired values a cohort study prints, 75.62 µg/dL for 2.64 µmol/L [4].
World Health Organization summary of its cut-offs, 2011, children
Populations of children, as cut-offs for counting how many have low serum retinol · [2]
| Range | What the source calls it |
|---|---|
| below 10 µg/dL | "deficient" A doctor, immediately |
| 10 to 20 µg/dL | "low" |
| above 20 µg/dL | No name given |
The same cut-offs as for adults, with the same statement from WHO that serum retinol is not useful for assessing an individual. WHO grades vitamin A deficiency as a public health problem from the share of children aged 6 to 71 months at 0.70 µmol/L or below: 2% to 9% is mild, 10% to 19% moderate and 20% or more severe. Those words grade a population, not one child's result. WHO's table notes that these grades do not apply to infants younger than 6 months, and WHO states that infection can lower serum retinol by as much as 25% [2].
Institute of Medicine Dietary Reference Intakes report, 2001
People in the United States and Canada, as the levels the report uses to describe vitamin A status · [5]
| Range | What the source calls it |
|---|---|
| below 20 µg/dL | "vitamin A inadequacy" |
| 20 to 30.1 µg/dL | "may be marginal" |
| above 30.1 µg/dL | No name given |
The report describes a plasma retinol below 0.70 µmol/L (20 µg/dL) as a level considered to reflect vitamin A inadequacy in a population, and 0.70 to 1.05 µmol/L as a range that may be marginal for some individuals. The upper end of that range is printed in µmol/L only and is converted here by dividing by 0.0349. The report gives the median serum retinol of US adults as 48 to 63 µg/dL and states that fewer than 5% of adults, excluding pregnant women, were below 1.05 µmol/L. It notes that a low plasma retinol can also result from too little dietary protein, energy or zinc, and from infection, even when liver retinol is adequate. It gives no cut point for a high result [5].
Centers for Disease Control and Prevention national nutrition report, 2012
The US population aged 6 years and older, as the cutoff the report used to estimate how common vitamin A deficiency is · [6]
| Range | What the source calls it |
|---|---|
| below 20 µg/dL | "deficiency" |
| 20 or above µg/dL | No name given |
The cutoff CDC applied to serum retinol measured in the US national survey of 2003 to 2006. By it, fewer than 1% of people aged 6 and older were deficient. The report uses it to estimate prevalence and does not set an upper cutoff [6].
US national survey laboratory procedure manual, 2017 to 2018, adults 20 to 39
Adults aged 20 to 39 · [7]
| Range | What the source calls it |
|---|---|
| below 31 µg/dL | No name given |
| 31 to 89 µg/dL | "reference range" |
| above 89 µg/dL | No name given |
The manual prints this as the 97.5% reference range for the US population, based on more than 8,000 specimens analyzed for the 2005 to 2006 survey. The geometric mean for this age group was 54.3 µg/dL. The range describes where results in the US fall. Its lower limit sits above the 20 µg/dL that WHO and CDC use for low or deficient, so a result below 31 is not by itself below those cut-offs [7][2][6].
US national survey laboratory procedure manual, 2017 to 2018, adults 40 to 59
Adults aged 40 to 59 · [7]
| Range | What the source calls it |
|---|---|
| below 33 µg/dL | No name given |
| 33 to 100 µg/dL | "reference range" |
| above 100 µg/dL | No name given |
From the same table of the manual, based on the 2005 to 2006 survey. The geometric mean for this age group was 58.7 µg/dL [7].
US national survey laboratory procedure manual, 2017 to 2018, adults 60 and older
Adults aged 60 and older · [7]
| Range | What the source calls it |
|---|---|
| below 36 µg/dL | No name given |
| 36 to 108 µg/dL | "reference range" |
| above 108 µg/dL | No name given |
From the same table of the manual, based on the 2005 to 2006 survey. The geometric mean for this age group was 64.4 µg/dL. The upper limit is above the 100 µg/dL at which the same manual flags a result for follow-up [7].
US national survey laboratory procedure manual, 2017 to 2018, children 6 to 11
Children aged 6 to 11 · [7]
| Range | What the source calls it |
|---|---|
| below 23 µg/dL | No name given |
| 23 to 54 µg/dL | "reference range" |
| above 54 µg/dL | No name given |
From the same table of the manual, based on the 2005 to 2006 survey. The geometric mean for this age group was 36.4 µg/dL [7].
US national survey laboratory procedure manual, 2017 to 2018, ages 12 to 19
Children and adolescents aged 12 to 19 · [7]
| Range | What the source calls it |
|---|---|
| below 29 µg/dL | No name given |
| 29 to 76 µg/dL | "reference range" |
| above 76 µg/dL | No name given |
From the same table of the manual, based on the 2005 to 2006 survey. The geometric mean for this age group was 46.5 µg/dL [7].
US national survey laboratory procedure manual, 2017 to 2018, results flagged for follow-up
Participants in the US national survey, as the levels at which the laboratory reports a result for follow-up · [7]
| Range | What the source calls it |
|---|---|
| below 20 µg/dL | "require follow-up" |
| 20 to 100 µg/dL | No name given |
| above 100 µg/dL | "require follow-up" |
Listed under the manual's heading for critical call results. The manual states that survey samples with serum vitamin A below 20 µg/dL or above 100 µg/dL are considered to require follow-up, and that such reports are forwarded to the survey physician. It gives no term for results between the two. For suspected excess the manual does not rely on retinol alone: it defines hypervitaminosis A by retinyl esters, as a retinyl ester to retinol ratio above 0.4 with retinyl palmitate of 15 µg/dL or more. Retinyl esters are a different measurement and are not placed against a result typed here [7].
How it compares with the reference method
Mixed results1
Week to week variation in one person
One small study found plasma vitamin A varied by 4.8% to 7.6% within one person from week to week, among the steadiest of the vitamins measured.
The numbers and sources
- Compared with
- The same person's results on weekly fasting draws over 22 weeks
- Effect
- Within-person variation for vitamins A, E, B1 and B2 was 4.8% to 7.6%, lower than for the other vitamins measured. Variation between people was larger than variation within a person for every vitamin, and the authors conclude that population reference intervals for vitamins are of limited value in showing deficiency or excess [14].
- Population
- 14 volunteers whom the study classed as healthy, sampled weekly for 22 weeks [14].
- Sources
- [14]
- Caveats
- Fourteen people and one laboratory. The abstract gives the range for four vitamins together and does not single out the figure for vitamin A. The study states no threshold for agreement, so the result is given as numbers only [14].
Did not match the reference method2
Infection and inflammation
Shown to read 11% to 24% lower in people with signs of infection, which can count people as deficient whose stores are adequate.
The numbers and sources
- Compared with
- Plasma retinol in people in the same studies with no raised acute phase protein
- Effect
- In a meta-analysis of 15 studies of apparently healthy people, plasma retinol was 13% lower in the incubation phase of infection, 24% lower in early convalescence and 11% lower in late convalescence than in people with no raised acute phase protein. Retinol was 25% higher in people with a normal C-reactive protein than in people with a raised one [9]. In blood samples from a hospital laboratory, median plasma vitamin A fell by more than 40% in the most inflamed group, and the authors conclude that the result can be interpreted reliably only when C-reactive protein is below 10 mg/L [11]. WHO states that clinical and subclinical infection can lower serum retinol by as much as 25% [2]. A US report explains the fall by transient decreases in retinol-binding protein and transthyretin, which carry retinol in blood, even when liver retinol is adequate [5].
- Population
- 15 studies of apparently healthy people [9]. 2,217 samples from 1,303 patients in one UK laboratory [11].
- Sources
- [9], [11], [2], [5]
- Caveats
- The meta-analysis authors ask that surveys measure C-reactive protein and alpha-1-acid glycoprotein alongside retinol so that results can be corrected [9]. A European guideline states that there is no universal adjustment for inflammation [12].
Serum retinol against liver stores
Limited evidence: the liver holds serum retinol steady across a wide range of stores, so a result above the cut-off does not show that stores are adequate.
The numbers and sources
- Compared with
- Liver vitamin A stores, estimated by retinol isotope dilution or measured in liver tissue
- Effect
- WHO states that serum retinol reflects liver vitamin A stores only when they are severely depleted, below 0.07 µmol per gram of liver, or extremely high, above 1.05 µmol per gram. Between these extremes it is homeostatically controlled and not always correlated with intake or clinical signs [2]. An expert review in the Biomarkers of Nutrition for Development series reports that Thai children with low rates of inflammation kept serum retinol above 0.7 µmol/L although their mean liver reserves, by isotope dilution, were 0.09 µmol per gram, below the 0.1 µmol per gram the review uses to define deficiency [13]. A European guideline describes serum retinol as highly specific after correction for inflammation and of questionable sensitivity against liver stores from isotope dilution [12].
- Population
- Studies summarized in an expert review and two official documents [13][2][12].
- Sources
- [2], [13], [12]
- Caveats
- Summaries by expert bodies, without a pooled estimate of sensitivity. The same control by the liver is why WHO, and the review, describe serum retinol as a measure for populations [2][13].
What studies tie it to
Linked in research3
Death in young children where deficiency is common
Shown in trials to cut deaths 12% in children aged 6 months to 5 years given vitamin A in countries where deficiency is common.
The numbers and sources
- Effect
- In a Cochrane review, vitamin A supplementation reduced deaths from any cause (RR 0.88, 95% CI 0.83 to 0.93, 19 trials, 1,202,382 children, high-certainty evidence) and deaths from diarrhea (RR 0.88, 0.79 to 0.98). It reduced night blindness (RR 0.32, 0.21 to 0.50), Bitot's spots (RR 0.42, 0.33 to 0.53) and vitamin A deficiency itself (RR 0.71, 0.65 to 0.78, 4 studies, 2,262 children). Deaths from measles and from respiratory disease did not differ [8].
- Population
- 47 studies with about 1,223,856 children in 19 countries, 30 of the studies in Asia. The mean age was about 33 months [8].
- Sources
- [8]
- Caveats
- The trials gave vitamin A to children in the community whatever their own serum retinol, so they show what supplementation did in populations with widespread deficiency. They did not test treating a child according to a measured level, and they do not describe adults or populations where deficiency is rare [8].
Death from any cause in adults
Limited evidence: one cohort of 29,104 Finnish men who smoked linked higher serum retinol to 17% fewer deaths, with the lowest risk near 60 to 70 µg/dL.
The numbers and sources
- Effect
- Over 30 years, men in the highest fifth of serum retinol had fewer deaths from any cause than men in the lowest fifth (HR 0.83, 95% CI 0.80 to 0.87), and fewer deaths from cardiovascular and respiratory disease. The relation was not a straight line. Deaths were more frequent below 483 µg/L (48.3 µg/dL), and risk was lowest at about 600 to 700 µg/L (60 to 70 µg/dL). The median at the start was 576 µg/L (57.6 µg/dL). The authors cite a US survey analysis of 16,008 people in which the middle fifths, and not the top fifth, had 18% fewer deaths than the lowest fifth [3].
- Population
- 29,104 male smokers in Finland aged 50 to 69 at entry to a cancer prevention trial, with 23,797 deaths [3].
- Sources
- [3]
- Caveats
- Observational, in men who smoked, almost none of whom had retinol in the range WHO calls low. Illness and inflammation lower serum retinol [9], so a low level may mark disease already present. No trial that raised serum retinol in adults and counted deaths was located.
Fracture
Linked to more hip fractures at both high and low blood retinol in a meta-analysis of four cohorts, with no link to fractures overall.
The numbers and sources
- Effect
- In a meta-analysis of prospective studies, both high and low blood retinol went with more hip fractures (RR 1.87, 95% CI 1.31 to 2.65, and RR 1.56, 1.09 to 2.22), in a U-shaped relation. The risk of all fractures taken together did not differ by blood retinol [10]. In one of the cohorts, Swedish men in the highest fifth of serum retinol (above 75.62 µg/dL) had a rate ratio of 1.64 (1.12 to 2.41) for any fracture and 2.47 (1.15 to 5.28) for hip fracture against the middle fifth (62.16 to 67.60 µg/dL). Men above the 99th percentile (103.12 µg/dL) had about seven times the fracture risk of men with lower levels [4].
- Population
- 8,725 participants in four prospective studies of blood retinol [10]. 2,322 men aged 49 to 51 at enrollment, followed for 30 years, with 266 fractures [4].
- Sources
- [10], [4]
- Caveats
- Observational, from four cohorts. The Swedish cohort measured retinol once, at about age 50, in men only [4].
Sources
- US Food and Drug Administration. 21 CFR 862.1805, Vitamin A test system. Electronic Code of Federal Regulations. https://www.ecfr.gov/current/title-21/section-862.1805
- World Health Organization. Serum retinol concentrations for determining the prevalence of vitamin A deficiency in populations. Vitamin and Mineral Nutrition Information System. Geneva: World Health Organization, 2011. WHO/NMH/NHD/MNM/11.3. https://iris.who.int/handle/10665/85859
- Huang J, Weinstein SJ, Yu K, et al. Association between serum retinol and overall and cause-specific mortality in a 30-year prospective cohort study. Nature Communications. 2021. https://doi.org/10.1038/s41467-021-26639-4
- Michaëlsson K, Lithell H, Vessby B, Melhus H. Serum Retinol Levels and the Risk of Fracture. New England Journal of Medicine. 2003. https://doi.org/10.1056/NEJMoa021171
- Institute of Medicine, Panel on Micronutrients. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academies Press. 2001. https://doi.org/10.17226/10026
- Centers for Disease Control and Prevention, National Center for Environmental Health. Second National Report on Biochemical Indicators of Diet and Nutrition in the U.S. Population, Executive Summary. 2012. https://www.cdc.gov/nutrition-report/media/Second-Nutrition-Report-Exec-Summary.pdf
- Centers for Disease Control and Prevention, National Center for Health Statistics. National Health and Nutrition Examination Survey 2017-2018 Laboratory Procedure Manual: Vitamins A, E, and carotenoids, serum or plasma, liquid chromatography. Performed by the Nutritional Biomarkers Branch, Division of Laboratory Sciences, National Center for Environmental Health. https://wwwn.cdc.gov/nchs/data/nhanes/public/2017/labmethods/VITAEC-J-MET-508.pdf
- Imdad A, Mayo-Wilson E, Haykal MR, et al. Vitamin A supplementation for preventing morbidity and mortality in children from six months to five years of age. Cochrane Database of Systematic Reviews. 2022. https://doi.org/10.1002/14651858.CD008524.pub4
- Thurnham DI, McCabe GP, Northrop-Clewes CA, Nestel P. Effects of subclinical infection on plasma retinol concentrations and assessment of prevalence of vitamin A deficiency: meta-analysis. The Lancet. 2003. https://doi.org/10.1016/S0140-6736(03)15099-4
- Wu AM, Huang CQ, Lin ZK, et al. The Relationship Between Vitamin A and Risk of Fracture: Meta-Analysis of Prospective Studies. Journal of Bone and Mineral Research. 2014. https://doi.org/10.1002/jbmr.2237
- Duncan A, Talwar D, McMillan DC, et al. Quantitative data on the magnitude of the systemic inflammatory response and its effect on micronutrient status based on plasma measurements. The American Journal of Clinical Nutrition. 2012. https://doi.org/10.3945/ajcn.111.023812
- Berger MM, Shenkin A, Schweinlin A, et al. ESPEN micronutrient guideline. Clinical Nutrition. 2022. https://doi.org/10.1016/j.clnu.2022.02.015
- Tanumihardjo SA, Russell RM, Stephensen CB, et al. Biomarkers of Nutrition for Development (BOND): Vitamin A Review. The Journal of Nutrition. 2016. https://doi.org/10.3945/jn.115.229708
- Talwar DK, Azharuddin MK, Williamson C, et al. Biological Variation of Vitamins in Blood of Healthy Individuals. Clinical Chemistry. 2005. https://doi.org/10.1373/clinchem.2005.056374