What is vitamin A?
Vitamin A describes a group of fat-soluble metabolites that include preformed vitamin A molecules — retinols, retinals, retinyl esters, retinoic acids — and provitamin A molecules — carotenoids like beta-carotene — which are precursors that the body can convert into the other forms of vitamin A.[3][4][5] Vitamin A metabolites are involved in cell and tissue growth and in several bodily functions, including vision, bone metabolism, and immune function.[3][4]
Because they are fat soluble, vitamin A metabolites can be stored in the body (mainly in the liver) as a retinyl ester.[6][7][5][3] However, dietary intake is necessary because humans cannot synthesize vitamin A from scratch.[6][7][3][4] Humans obtain preformed vitamin A — retinols, retinals, retinyl esters, and retinoic acids — from animal products (e.g., fish, eggs, dairy, liver), and obtain provitamin A carotenoids (like beta-carotene) from plants (e.g., sweet potatoes, carrots, leafy greens); the latter can be converted to preformed vitamin A by the body.[1][5] In some countries, some foods — milk, margarine, cereals, etc. — are also fortified with vitamin A.[8][9][10][11]
Vitamin A is also taken as a dietary supplement. Such supplements typically contain preformed vitamin A (retinyl acetate or retinyl palmitate), provitamin A (beta-carotene), or a combination of both.[12] Vitamin A is also found in high levels in some fish oil supplements, such as cod liver oil, and in many multivitamins.[12]
What are vitamin A’s main benefits?
Sufficient amounts of vitamin A can be obtained through a balanced diet, but vitamin A deficiency can occur due to insufficient intake.[1][3][4] Supplementation with vitamin A is used to treat vitamin A deficiency, which is most common in malnourished infants/children living in developing countries.[1][3][4] The evidence shows that supplementation with vitamin A can improve growth, vision, and survival in malnourished infants/children[13][14][15][16][17][18] and in premature babies.[19][20] However, the precise recommendations for treating vitamin A deficiency are unclear because results are inconsistent among studies.[14][15][16][17][18][19][20]
Observational studies show that higher dietary intake of vitamin A, which includes total vitamin A intake from all sources (foods, drinks, and supplements), is associated with a reduced risk of depression.[21] However, this association is derived from cross-sectional and cohort study designs in which vitamin A intake was estimated from historical diet recall using food frequency questionnaires. This makes it difficult to prove a causal link between vitamin A intake and depression.
Besides dietary vitamin A, all-trans retinoic acid (Tretinoin) and 13-cis-retinoic acid (Isotretinoin) are types of vitamin A used in prescription drugs that are effective in treating acne.[22][23][24]
What are vitamin A’s main drawbacks?
High intakes of preformed vitamin A can cause serious side effects — symptoms include severe headache, blurred vision, nausea, dizziness, muscle aches, and problems with coordination.[1][25][26][12][27]
Excessive intakes of preformed vitamin A have been associated with an increased risk of bone problems — e.g., osteoporosis and hip fracture[28][29] — and some types of cancer, including ovarian cancer,[30] pancreatic cancer,[31] lung cancer,[32] and gastric cancer.[33] However, this evidence is derived from observational studies using cross-sectional and cohort study designs in which vitamin A intake data was estimated from historical diet recall using food frequency questionnaires. This makes it difficult to prove the causality between vitamin A intake and disease risk.
Excessive intake of preformed vitamin A during pregnancy can also cause birth defects, and excessive intake when breastfeeding can impair a child’s growth.[1][25][26][12] Therefore, high-dose supplementation with preformed vitamin A is not recommended when pregnant or lactating — consult your doctor if you are unsure.
In severe cases, excessive intake of preformed vitamin A can cause coma and death,[1][25][26][12][27] and supplementation with high doses of vitamin A has also been associated with increased mortality in well-nourished populations.[25]
There are also several drug interactions with Vitamin A, including, but not limited to, several antibiotics, some weight loss drugs (e.g., orlistat), and vitamin-A-containing drugs (e.g., isotretinoin). Always consult your doctor if you are taking over-the-counter or prescription medicines and planning to use a vitamin A supplement.
Because of the side effects and potential toxicity, there is an upper limit for total daily intake of preformed vitamin A (from food, beverages, and supplements combined):[1][2]
| Ages | Upper limit of daily intake |
|---|---|
| Birth to 12 months | 600 micrograms (mcg or µg) |
| Children 1–3 years | 600 mcg |
| Children 4–8 years | 900 mcg |
| Children 9–13 years | 1,700 mcg |
| Teens 14–18 years | 2,800 mcg |
| Adults 19 years and older | 3,000 mcg |
Unlike preformed vitamin A, high intake of beta-carotene (a provitamin A carotenoid) is not associated with serious side effects or health problems, and beta-carotene does not have an upper limit of intake. However, this does not mean that taking a higher-than-recommended dose of beta-carotene induces a greater effect.
How does vitamin A work?
When ingested, beta-carotene, a provitamin A carotenoid, is converted in the gastrointestinal system into a retinal form of vitamin A, which can be subsequently converted into retinol, retinoic acid, or retinyl ester forms of vitamin A.[5][3][6][7] Retinyl esters are the storage form of vitamin A, and are primarily stored in the liver.[5][3][6]
The metabolism of vitamin A is complex: there are many interconvertible forms, and each has a different role.[6][3][12][7] For example, different types of retinols, retinals, and retinyl esters are precursor molecules to the synthesis of rhodopsin, a pigment involved in vision;[3] retinols can act as cofactors in several enzymatic processes;[12] and retinoic acids directly regulate gene expression while also regulating vitamin A metabolism by, for example, modifying the intestinal absorption of beta-carotene.[3]
What are other names for Vitamin A
- retinol
- retinal
- retinoic acid
- tretinoin
- beta-carotene
- Retinyl ester
- all-trans retinoic acid
- 13-cis-retinoic acid
Dosage information
Recommended intake is similar between males and females, except during pregnancy and lactation when vitamin A requirements are elevated. The recommended dietary allowances (RDA) are:[1][2]
| Ages | Recommended daily intake |
|---|---|
| Birth to 6 months | 400 micrograms (mcg, or µg) |
| Infants 7–12 months | 500 mcg |
| Children 1–3 years | 300 mcg |
| Children 4–8 years | 400 mcg |
| Children 9–13 years | 600 mcg |
| Teen males 14–18 years | 900 mcg |
| Teen females 14–18 years | 700 mcg |
| Teen females, pregnant | 750 mcg |
| Teen females, breastfeeding | 1,200 mcg |
| Adult males | 900 mcg |
| Adult females | 700 mcg |
| Adult females, pregnant | 770 mcg |
| Adult females, breastfeeding | 1,300 mcg |
Due to potential toxicity, the upper limit of total daily intake of preformed vitamin A (from food, beverages, and supplements combined) is as follows:[1][2]
| Ages | Upper limit of daily intake |
|---|---|
| Birth to 12 months | 600 mcg |
| Children 1–3 years | 600 mcg |
| Children 4–8 years | 900 mcg |
| Children 9–13 years | 1,700 mcg |
| Teens 14–18 years | 2,800 mcg |
| Adults 19 years and older | 3,000 mcg |
Examine Database: Vitamin A
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Frequently asked questions
Vitamin A describes a group of fat-soluble metabolites that include preformed vitamin A molecules — retinols, retinals, retinyl esters, retinoic acids — and provitamin A molecules — carotenoids like beta-carotene — which are precursors that the body can convert into the other forms of vitamin A.[3][4][5] Vitamin A metabolites are involved in cell and tissue growth and in several bodily functions, including vision, bone metabolism, and immune function.[3][4]
Because they are fat soluble, vitamin A metabolites can be stored in the body (mainly in the liver) as a retinyl ester.[6][7][5][3] However, dietary intake is necessary because humans cannot synthesize vitamin A from scratch.[6][7][3][4] Humans obtain preformed vitamin A — retinols, retinals, retinyl esters, and retinoic acids — from animal products (e.g., fish, eggs, dairy, liver), and obtain provitamin A carotenoids (like beta-carotene) from plants (e.g., sweet potatoes, carrots, leafy greens); the latter can be converted to preformed vitamin A by the body.[1][5] In some countries, some foods — milk, margarine, cereals, etc. — are also fortified with vitamin A.[8][9][10][11]
Vitamin A is also taken as a dietary supplement. Such supplements typically contain preformed vitamin A (retinyl acetate or retinyl palmitate), provitamin A (beta-carotene), or a combination of both.[12] Vitamin A is also found in high levels in some fish oil supplements, such as cod liver oil, and in many multivitamins.[12]
Inadequate dietary intake of vitamin A — either preformed vitamin A molecules or provitamin A molecules, like beta-carotene — is the primary cause of vitamin A deficiency.[1][3][4] Common signs and symptoms of Vitamin A deficiency include damage to the skin, vision problems under dim light conditions (night blindness), and poor immune system function.[1][3][34] Vitamin A deficiency during pregnancy can also cause birth defects in babies and growth impairments in children.[1][4][34]
In developing countries, vitamin A deficiency increases the risk of respiratory infections and diarrhea and increases the risk of dying from such conditions.[1][3] Vitamin A deficiency also leads to xerophthalmia — a condition that damages the eyes and is the leading cause of blindness in developing countries.[35][1][34]
This variety of outcomes caused by vitamin A deficiency arises because the many forms of vitamin A have diverse functions in the body.[1][3]
Due to the many approaches by which vitamin A status has been assessed, there is large variability in the prevalence estimates for vitamin A deficiency.[36][37] However, vitamin A deficiency is most common in infants/children living in low- and middle-income countries,[1][3][4] in whom prevalence of vitamin A deficiency is approximately 30%.[38][37]
Some conditions also increase a person’s risk of developing vitamin A deficiency. These include chronic alcohol intake, liver cirrhosis, intestinal absorption disorders like Crohn’s disease, and conditions that affect the exocrine pancreas (e.g., chronic pancreatitis).[39]
Retinol binding protein 4 (RBP4) is a carrier protein that transports retinol (preformed vitamin A) in the blood from the liver to other tissues.[44] Single-nucleotide polymorphisms (variants) in the gene that codes for the RBP4 protein appear to be associated with retinol concentrations in the blood[45] and the risk of some conditions, including childhood obesity,[46] coronary artery disease,[47] insulin resistance,[48] gestational diabetes,[49] and type 2 diabetes.[50][51][52] The concentration of RBP4 protein in the blood has also been shown to be associated with the risk of gestational diabetes and type 2 diabetes.[53][54][55][42] However, while experiments using genetic mouse models support some of these associations,[44][56] further clinical studies are needed to fully understand whether RBP4 plays a causal role in human disease.
Sufficient amounts of vitamin A can be obtained through a balanced diet, but vitamin A deficiency can occur due to insufficient intake.[1][3][4] Supplementation with vitamin A is used to treat vitamin A deficiency, which is most common in malnourished infants/children living in developing countries.[1][3][4] The evidence shows that supplementation with vitamin A can improve growth, vision, and survival in malnourished infants/children[13][14][15][16][17][18] and in premature babies.[19][20] However, the precise recommendations for treating vitamin A deficiency are unclear because results are inconsistent among studies.[14][15][16][17][18][19][20]
Observational studies show that higher dietary intake of vitamin A, which includes total vitamin A intake from all sources (foods, drinks, and supplements), is associated with a reduced risk of depression.[21] However, this association is derived from cross-sectional and cohort study designs in which vitamin A intake was estimated from historical diet recall using food frequency questionnaires. This makes it difficult to prove a causal link between vitamin A intake and depression.
Besides dietary vitamin A, all-trans retinoic acid (Tretinoin) and 13-cis-retinoic acid (Isotretinoin) are types of vitamin A used in prescription drugs that are effective in treating acne.[22][23][24]
Tretinoin and isotretinoin are prescription drugs used to treat acne.[22][23][24] They contain types of vitamin A — all-trans retinoic acid (tretinoin) and 13-cis-retinoic acid (isotretinoin) — and can have serious side effects, particularly in the skin.[57][58] Furthermore, isotretinoin is not advised for use in pregnant or lactating women because it can cause severe birth defects and growth defects.[58] Some evidence also shows that isotretinoin use is associated with an increased risk of depression and suicide in people with acne.[59][60][61][62] However, this association is not shown in all studies,[63][64] and the causal link is unclear because acne is independently associated with these mental health conditions,[65][60][61][66][67][68] and because some evidence suggests that other underlying mood disorders in people with acne (e.g., bipolar disorder) may play a role.[66][62][68]
Beta-carotene is a pigment found in plants like sweet potatoes, carrots, leafy greens, etc.[5] It is also available as a dietary supplement. Because beta-carotene is a provitamin A carotenoid, it is converted to vitamin A in the intestine when ingested.[5]
Observational studies show that higher dietary intake of beta-carotene is associated with improved cognitive function[69] and a lower incidence of depression,[21] osteoporosis,[70] and bone fractures.[71] Observational studies also show that a higher beta-carotene concentration in the blood is associated with improved cognitive function[69] and a lower incidence of metabolic syndrome.[72] However, these studies use cross-sectional or cohort study designs, and beta-carotene intake data is estimated from food frequency questionnaires. Furthermore, randomized controlled trials examining many of these outcomes are lacking, making it difficult to draw firm conclusions. That said, evidence from randomized controlled trials shows that supplementation with beta-carotene has no beneficial effect on cognitive function,[69] nor does it have any effect on the risk of cardiovascular disease, the risk of cancer, or associated mortality.[73][74][75] Some evidence even shows that supplementation with beta-carotene might increase the risk of lung cancer, particularly in smokers.[74][75] Consequently, the causal effects of beta-carotene intake on disease risk/prevention are mixed, and high-quality dose-response randomized controlled trials will be needed before firm conclusions can be made.
High intakes of preformed vitamin A can cause serious side effects — symptoms include severe headache, blurred vision, nausea, dizziness, muscle aches, and problems with coordination.[1][25][26][12][27]
Excessive intakes of preformed vitamin A have been associated with an increased risk of bone problems — e.g., osteoporosis and hip fracture[28][29] — and some types of cancer, including ovarian cancer,[30] pancreatic cancer,[31] lung cancer,[32] and gastric cancer.[33] However, this evidence is derived from observational studies using cross-sectional and cohort study designs in which vitamin A intake data was estimated from historical diet recall using food frequency questionnaires. This makes it difficult to prove the causality between vitamin A intake and disease risk.
Excessive intake of preformed vitamin A during pregnancy can also cause birth defects, and excessive intake when breastfeeding can impair a child’s growth.[1][25][26][12] Therefore, high-dose supplementation with preformed vitamin A is not recommended when pregnant or lactating — consult your doctor if you are unsure.
In severe cases, excessive intake of preformed vitamin A can cause coma and death,[1][25][26][12][27] and supplementation with high doses of vitamin A has also been associated with increased mortality in well-nourished populations.[25]
There are also several drug interactions with Vitamin A, including, but not limited to, several antibiotics, some weight loss drugs (e.g., orlistat), and vitamin-A-containing drugs (e.g., isotretinoin). Always consult your doctor if you are taking over-the-counter or prescription medicines and planning to use a vitamin A supplement.
Because of the side effects and potential toxicity, there is an upper limit for total daily intake of preformed vitamin A (from food, beverages, and supplements combined):[1][2]
| Ages | Upper limit of daily intake |
|---|---|
| Birth to 12 months | 600 micrograms (mcg or µg) |
| Children 1–3 years | 600 mcg |
| Children 4–8 years | 900 mcg |
| Children 9–13 years | 1,700 mcg |
| Teens 14–18 years | 2,800 mcg |
| Adults 19 years and older | 3,000 mcg |
Unlike preformed vitamin A, high intake of beta-carotene (a provitamin A carotenoid) is not associated with serious side effects or health problems, and beta-carotene does not have an upper limit of intake. However, this does not mean that taking a higher-than-recommended dose of beta-carotene induces a greater effect.
Observational studies find that vitamin A status, as measured by serum concentrations of retinol, retinoic acid, or retinyl esters, is associated with several health conditions. For example, lower serum vitamin A concentrations are found in people with asthma compared to healthy controls,[40] and low serum vitamin A concentrations are associated with a greater risk of stroke.[41] Other studies find complicated relationships. For example, a U-shaped relationship exists between vitamin A status and the risk of hip fracture: both lower-than-normal and higher-than-normal serum concentrations are correlated with a greater risk of fracture.[28] Furthermore, vitamin A status has been associated with cardiometabolic diseases like cardiovascular disease, obesity, and type 2 diabetes, but the direction of association varies depending on which vitamin A metabolite is measured.[42]
Consequently, it is difficult to determine causality from such observations. Furthermore, the measurement of vitamin A metabolites in the blood is not a good biomarker for bodily vitamin A stores or dietary intake.[3][4][5][6][7] The better approach is the retinol isotope dilution method, which is considered the gold standard since it correlates strongly with liver stores and indicates vitamin A status in deficiency and in excess.[43] However, this method is not used in the above-described observational studies. Therefore, further research, ideally with dose-response and/or randomized controlled trial designs, is needed to clarify the causal effect of vitamin A status on health conditions.
When ingested, beta-carotene, a provitamin A carotenoid, is converted in the gastrointestinal system into a retinal form of vitamin A, which can be subsequently converted into retinol, retinoic acid, or retinyl ester forms of vitamin A.[5][3][6][7] Retinyl esters are the storage form of vitamin A, and are primarily stored in the liver.[5][3][6]
The metabolism of vitamin A is complex: there are many interconvertible forms, and each has a different role.[6][3][12][7] For example, different types of retinols, retinals, and retinyl esters are precursor molecules to the synthesis of rhodopsin, a pigment involved in vision;[3] retinols can act as cofactors in several enzymatic processes;[12] and retinoic acids directly regulate gene expression while also regulating vitamin A metabolism by, for example, modifying the intestinal absorption of beta-carotene.[3]
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References
Examine Database References
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