Vitamin A

What is vitamin A and what does it do?

Vitamin A is not a single substance but the common name for fat-soluble retinoids such as retinol and retinyl esters. NIH reports that vitamin A plays a role in immune function, cell communication, growth and development, and reproduction, and supports the normal formation and maintenance of organs such as the heart, lungs and eyes. In the eye, it is a component of rhodopsin, the protein in the retina that responds to light; it is also needed for the normal functioning of the conjunctival and corneal membranes. ^[1] EFSA also states that vitamin A is important for the maintenance of vision and for the growth and integrity of tissue cells. ^[2]

The body stores excess vitamin A mostly as retinyl esters in the liver. Thanks to this store, intake does not have to be the same every day; the same store is also the reason that excess intake can accumulate. ^[1] NHS also states that vitamin A the body does not need right away is stored, so it does not need to be taken every day. ^[4]

That a vitamin has a function in the body does not mean that taking more than the requirement would perform those functions better. This page covers separately the role of vitamin A, the results of supplementation in deficiency, and what can be expected from extra supplementation in someone with adequate levels.

How are preformed vitamin A and carotenoids distinguished?

There are two sources of vitamin A in the diet. Preformed vitamin A is retinol and retinyl esters; it is found in dairy products, eggs, fish and organ meats. Provitamin A carotenoids are plant pigments such as beta-carotene, alpha-carotene and beta-cryptoxanthin; they are converted to vitamin A in the gut by the BCMO1 enzyme, and the conversion rate can vary genetically from person to person. Other carotenoids such as lycopene, lutein and zeaxanthin are not converted to vitamin A. ^[1]

This distinction matters in practice, because the harms differ. According to NIH, beta-carotene is not known to be teratogenic or to have reproductive toxicity; when taken in excess for a long time, its most frequent effect is a reversible and harmless yellow-orange discoloration of the skin (carotenodermia). The upper limit for preformed vitamin A, on the other hand, has been set, and its risk in pregnancy requires a separate heading. ^[1]

RAE, RE and IU: how are the units read?

Because the biological activity of vitamin A varies with the source, reference values are given as retinol activity equivalents (RAE). According to the IOM conversion cited by NIH, 1 µg RAE equals 1 µg of retinol, 2 µg of beta-carotene in supplements, 12 µg of beta-carotene in foods, or 24 µg of alpha-carotene or beta-cryptoxanthin. For the international unit (IU) used on older labels, NIH gives the following conversions: ^[1]

For this reason, converting from RAE to IU can be done only if the source is known: 900 µg RAE corresponds to 3,000 IU if the source is retinol (or supplemental beta-carotene) and to 18,000 IU if it is beta-carotene in foods. ^[1] EFSA gives its reference values as retinol equivalents (RE) rather than RAE; organizations have historically used different carotenoid equivalence ratios (for example 1:6 and the IOM’s 1:12), so the numbers of the two agencies are not directly the same measure. ^[3]

How much is the daily requirement?

The recommended dietary allowances (RDA) of the US Food and Nutrition Board cited by NIH are as follows:

For infants (400 µg RAE for 0–6 months, 500 µg RAE for 7–12 months) the values are adequate intake (AI) values. ^[1] The EFSA 2015 opinion reports population reference intakes (PRI) as 750 µg for men, 650 µg for women and 700 µg for pregnant women. The values of the two agencies were set with different units (RAE/RE) and separate assessments. ^[2]

In the United Kingdom, NHS gives 700 µg RE a day for men and 600 µg for women aged 19–64 and states that all vitamin A can be met with a varied diet. ^[4] These figures are references calculated to meet the need in most healthy people; they are not the same as the amounts used in treating a deficiency, and treatment is determined by the physician.

Which foods contain it?

Preformed vitamin A is found most in liver, and also in fish, eggs and dairy products; provitamin A is found in green leafy, orange and yellow vegetables and some fruits. According to NIH, the body can absorb about 75–100% of the retinol in foods and, in most cases, 10–30% of the beta-carotene in foods; cooking and heat processing can increase the bioavailability of beta-carotene in foods. ^[1] The table of µg RAE per serving and why liver needs a separate warning are on the subpage.

Detailed guideWhich foods contain vitamin A? Serving table and liver warning→

Who gets deficiency?

NIH reports that marked vitamin A deficiency is rare in the US but still common in many developing countries. The first sign of xerophthalmia is night blindness; the cornea is also affected and it can eventually lead to permanent blindness. Conditions that impair fat absorption (cystic fibrosis, some bowel diseases), prematurity, and children and pregnant women living in regions where deficiency is common are counted among the groups at risk. ^[1] According to NIH, a serum retinol of 0.70 µmol/L (20 µg/dL) or below often reflects moderate deficiency; however, infection can lower the level, and the blood value may not fall until liver stores are depleted. ^[1] Studies in children in Türkiye and details of the thresholds are on the deficiency page.

Detailed guideVitamin A deficiency: night blindness, risk groups and serum retinol→

Why does vitamin A need attention in pregnancy?

Vitamin A is necessary in pregnancy (RDA 770 µg RAE at ages 19–50), but high amounts of preformed vitamin A have been associated with birth defects. ^[1] The most frequently cited evidence is the prospective observational study of Rothman and colleagues following 22,748 pregnant women in the US. The rate of defects of cranial neural crest origin in the babies of those taking more than 15,000 IU a day of preformed vitamin A from food and supplements was 3.5 times higher (95% CI 1.7–7.3) than in those taking 5,000 IU or less a day. Among those taking more than 10,000 IU a day from supplements alone, the ratio was 4.8 (2.2–10.5); the authors observed a threshold at about 10,000 IU/day for supplements and reported that the increase was mostly concentrated in those with high intake before the seventh week of pregnancy. The study is observational; intake was asked about through an interview on the first three months of pregnancy. ^[5]

Official agencies therefore warn in the same direction:

• NIH: According to NIH, experts recommend that people who are or could be pregnant and people who are breastfeeding not take vitamin A supplements above 3,000 µg RAE (10,000 IU) a day; preformed vitamin A intake above the upper limit and some retinoid medicines (NIH’s example: isotretinoin, used for severe acne) can also lead to birth defects, including malformations of the eye, skull, lungs and heart. ^[1]
• EFSA 2024: The critical effect on which the preformed vitamin A UL is based is teratogenicity; the UL is 3,000 µg RE/day for adults, including pregnant, breastfeeding and women of childbearing age. EFSA recommends that women who are pregnant or planning pregnancy not consume liver products; it states that the European population is not expected to exceed the UL if it eats liver and organ meats once a month or less often. ^[3]
• NHS: Liver or liver products (for example liver pâté) should not be eaten in pregnancy. ^[4]

Retinoid medicines (such as isotretinoin) are a separate source of risk and are prescription drugs. Beta-carotene is not known to be teratogenic. ^[1]

Vitamin A excess and the upper limit

Because fat-soluble vitamin A can accumulate, excess is possible. NIH defines acute toxicity (hypervitaminosis A) as the picture seen, typically at more than 100 times the RDA, after one or a few very high doses within days or weeks; symptoms are severe headache, blurred vision, nausea, dizziness, muscle pain and impaired coordination; in severe cases cerebrospinal fluid pressure may rise, and drowsiness, coma and death may occur. In chronic excess (regular high intake), dry skin, muscle and joint pain, fatigue, depression and impaired liver tests are reported. ^[1]

The upper limits (UL) cited by NIH apply only to preformed vitamin A (animal foods and supplements made of retinol or its esters); no UL has been set for beta-carotene:

NIH explains with an example that, if part of the vitamin A on a label comes from beta-carotene, only the retinol/retinyl ester share should be counted when comparing with the upper limit: a supplement stated to contain 3,000 µg RAE, of which 60% is beta-carotene, provides 1,200 µg RAE of preformed vitamin A. ^[1] EFSA’s 2024 opinion keeps the adult UL at 3,000 µg RE/day; ULs by age group range from 600 µg RE/day in infants (4–11 months) to 2,600 µg RE/day at ages 15–17. For beta-carotene, lung cancer was chosen as the critical effect; no UL was set because a dose-response relationship could not be derived. ^[3]

How is the relation to bone and hip fracture interpreted?

The EFSA 2024 opinion reports that the EU Scientific Committee on Food (SCF, 2002) recommended that postmenopausal women not exceed 1,500 µg RE a day, that this recommendation was based on two prospective observational studies (Melhus 1998; Feskanich 2002) in which the risk of hip fracture rose above this level, and that the SCF reported uncertainty about causality. EFSA re-examined the topic with a systematic review and, noting that factors such as diet and medicine use were only partly adjusted for in observational studies and that the evidence diverged, concluded that causality could not be established between intake in the 1,000–3,000 µg RE/day range and fracture risk; it also stated that there was no new evidence supporting a relation between intake of ≤3,000 µg RE/day and impaired bone health. ^[3] NHS is more cautious: it says there is research that average intake above 1.5 mg (1,500 µg) a day over many years may make bones prone to fracture, and for postmenopausal women and older men it recommends a limit of 1.5 mg/day total from food and supplements and not eating liver pâté more than once a week. ^[4] The message of the two agencies differs; the basis is observational data and causality has not been established.

Why are beta-carotene supplements a problem for smokers?

The association of carotenoid-rich foods with lower lung cancer risk in observational studies led to supplements being tried in randomized trials; the result was unexpected. In the ATBC trial, 29,133 male smokers aged 50–69 in Finland were followed for 5–8 years to receive 20 mg/day of beta-carotene, 50 mg of alpha-tocopherol, both or placebo; in those who took beta-carotene, lung cancer incidence was 18% higher (95% CI 3–36) and total mortality was 8% higher. ^[6] In CARET, among 18,314 smokers, former smokers and people exposed to asbestos, those who took 30 mg/day of beta-carotene plus 25,000 IU of retinyl palmitate had an RR of 1.28 (1.04–1.57) for lung cancer and an RR of 1.17 (1.03–1.33) for all-cause mortality over a mean follow-up of 4 years, and the trial was stopped 21 months earlier than planned. ^[7] NIH also reports that in the AREDS2 eye trial, in which a beta-carotene-containing formula was not given to smokers, more lung cancer was detected in those who took the beta-carotene-containing formula (23 versus 11 cases; 31 of the 34 cases were in former smokers). ^[1]

NIH also reports that other studies testing similar doses in communities with fewer smokers did not show this risk, and that beta-carotene and vitamin A supplements do not appear to affect cancer risk in nonsmokers. ^[1] EFSA 2024 states that smokers should avoid food supplements containing beta-carotene, that beta-carotene supplementation in the general population should be limited to meeting vitamin A requirements only, and that there is no indication that beta-carotene from food is associated with harmful effects. ^[3]

How well evidenced is the benefit of vitamin A supplementation?

Benefit depends on whether there is a deficiency. Deficiency leads to night blindness and xerophthalmia; in children aged 6 months–5 years, supplementation has reduced deaths in large trials. The Cochrane 2022 review examined synthetic vitamin A supplementation in community-dwelling children aged 6 months–5 years (47 trials in 19 countries, about 1,223,856 children; children in hospital and with disease, food fortification and beta-carotene trials were excluded). For all-cause mortality the RR was 0.88 in 19 trials (0.83–0.93; high certainty), for diarrhea-related mortality RR 0.88 (0.79–0.98; high certainty); no difference was shown for measles-related mortality (RR 0.88; 0.69–1.11; low certainty). The risk of vomiting in the first 48 hours increased (RR 1.97; 1.44–2.69). ^[8] These results are for children in the low- and middle-income countries where most trials were conducted; NIH states that marked vitamin A deficiency is rare in the US and still common in many developing countries. For a healthy adult in Türkiye, a benefit of supplementation for infection, skin or cancer has not been shown by these data. ^[1]

Detailed guideVitamin A benefits: evidence for vision, immunity, skin and cancer→

Skin, acne and retinoid medicines

Although the words “retinol” and “retinoid” often appear in skin care, vitamin A supplements and prescription retinoid medicines are not the same thing. NIH’s health section covers cancer, macular degeneration and measles; results of oral vitamin A supplements for skin or acne are not included there. Among the prescription retinoids NIH gives as examples, isotretinoin (severe acne) and etretinate (severe psoriasis) are associated with birth defects; preformed vitamin A intake above the upper limit is also cited with the same risk. ^[1]

With which medicines does it interact?

NIH reports that orlistat can reduce absorption of vitamin A, other fat-soluble vitamins and beta-carotene, leading to low blood levels in some patients. Oral retinoid medicines (for example acitretin and bexarotene) can increase the risk of hypervitaminosis A when taken together with vitamin A supplements. ^[1] NIH gives these as “a few examples”; the list is not exhaustive. In people who use regular medicines, supplements are also included in the physician’s or pharmacist’s assessment.

Common misunderstandings about vitamin A

• “Eating carrots causes vitamin A excess.” No UL has been set for beta-carotene; the most frequent effect of long-term excess intake is reversible skin discoloration (carotenodermia). The problem of excess comes mainly from preformed vitamin A (supplements, liver). ^[1]
• “Liver is the healthiest food and should be eaten often.” NHS says that eating liver more than once a week can lead to too much vitamin A intake and that liver should be avoided entirely in pregnancy. ^[4]
• “Vitamin A supplementation is necessarily beneficial for children.” The reduction in deaths in Cochrane comes from community trials in children aged 6 months–5 years, mostly done in Asia; the result cannot be transferred as is to every child. ^[8]
• “Beta-carotene is antioxidant protection for smokers.” ATBC and CARET showed the opposite. ^[6]

Summary of the evidence

This guide does not recommend a daily or weekly personal dose. If pregnancy, liver disease, retinoid medicine use or a high-dose product is involved, the decision is made with a physician or pharmacist together with the product label.