Vitamin A

Vitamin A is a fat-soluble vitamin with two distinct dietary forms — preformed vitamin A (retinol and its esters), found in animal foods, and provitamin A carotenoids (particularly beta-carotene), found in orange, yellow, and dark green plant foods. The body converts carotenoids into active vitamin A, but at a low and variable efficiency. As a fat-soluble vitamin, vitamin A is stored in the liver — in well-nourished adults, often enough to last many months or more — which means deficiency develops slowly and excess builds up over time. Both extremes are clinically significant: vitamin A deficiency is the leading preventable cause of blindness in children worldwide, and vitamin A toxicity is one of the most serious vitamin toxicities, with documented risks of birth defects and liver damage from sustained excess.

Key Mechanisms

The visual cycle — retinal and night vision:

The retina contains two types of light-sensing cells: rods (for dim light and peripheral vision) and cones (for color and detail). Rod cells contain rhodopsin — the protein opsin bound to 11-cis-retinal, a form of vitamin A. When light strikes rhodopsin:

1. 11-cis-retinal changes shape to all-trans-retinal — a structural change that activates opsin
2. This triggers a signaling cascade that generates the nerve signal perceived as light
3. All-trans-retinal separates from opsin and is converted back to all-trans-retinol
4. It must then be converted back to 11-cis-retinal to restore working rhodopsin

This regeneration cycle depends on a steady supply of vitamin A. When vitamin A is deficient, rhodopsin can’t be regenerated quickly enough after light exposure, and the ability to adapt to low light fails — producing the first and most characteristic symptom: night blindness.

Retinoic acid as a gene regulator:

Retinoic acid — the most active form of vitamin A — doesn’t work like most vitamins. It acts more like a hormone: it enters the cell nucleus and binds to nuclear receptors — retinoic acid receptors (RARα, β, γ), which work in partnership with retinoid X receptors (RXRα, β, γ). These receptor pairs bind to specific stretches of DNA called retinoic acid response elements, directly switching hundreds of genes on or off. Those genes control:

• Cell differentiation and growth — including the maturation of immune cells, the cells lining the body’s surfaces, and reproductive cells
• Embryonic development — limb patterning, organ formation, and nervous system development; retinoic acid is one of the most powerful signaling molecules in embryonic development
• Skin cell turnover — the basis of retinoid skincare and acne treatments
• Immune cell development, including T cells, and the function of natural killer cells
• Maintenance of the mucous membranes lining the respiratory, digestive, and urinary tracts

This gene-regulating role is why vitamin A is essential for life, and why both deficiency and excess have such wide-ranging effects throughout the body.

Retinol-binding protein (RBP4) and zinc dependency:

Vitamin A is stored in the liver as retinyl esters. When tissues need it, it’s released as retinol bound to retinol-binding protein 4 (RBP4), which travels in the blood together with a second protein, transthyretin. Making RBP4 depends on zinc: without enough zinc, the liver can’t release vitamin A to the rest of the body effectively — even when its stores are adequate. That’s why zinc deficiency can cause signs of vitamin A deficiency, including night blindness, that don’t fully respond to vitamin A alone, and why zinc and vitamin A status are best considered together.

Beta-Carotene Conversion — A Nuance Worth Understanding

Carotenoids in plant foods are much less potent than preformed vitamin A. The official conversion ratio is 12:1 — 12µg of beta-carotene from food provides 1µg of retinol activity equivalents (RAE). For other provitamin A carotenoids in food (alpha-carotene and beta-cryptoxanthin), the ratio is 24:1. Beta-carotene in supplements, dissolved in oil, is absorbed far better, at about 2:1.

Modern food tables expressed in µg RAE — including the figures on this page — already account for these conversion ratios. Older figures in international units (IU), still found on some labels and websites, used more generous conversion assumptions and an older daily value, which made plant foods look far richer in vitamin A. For example, older figures put baked sweet potato at over 380% of the daily value per 100g; based on RAE and today’s daily value, it’s 107%.

Several factors affect how much vitamin A you actually get from carotenoids:

• Fat intake: carotenoids are fat-soluble and need fat in the same meal to be absorbed well. A carotenoid-rich salad with an oil-based dressing provides substantially more than the same salad with a fat-free dressing.
• Raw vs cooked: cooking softens plant cell walls and releases carotenoids, so cooked carrots, for example, provide more absorbable beta-carotene than raw ones.
• Genetics: common variations in the BCMO1 gene, which makes the enzyme that converts beta-carotene, can reduce conversion substantially — by roughly a third to more than two-thirds in some studies — making some people “poor converters.”

Vitamin A deficiency on purely plant-based diets is uncommon where diets are varied, but it’s possible — particularly in poor converters, people with fat malabsorption, or those eating a low-fat diet low in carotenoid-rich foods.

Vitamin A RDA (Recommended Dietary Allowance)

Values are in µg RAE (retinol activity equivalents). Older labels and supplements may use IU, and the conversion depends on the form: 1 IU of retinol = 0.3µg RAE; 1 IU of supplemental beta-carotene = 0.15µg RAE; and 1 IU of beta-carotene from food = 0.05µg RAE.

* Adequate Intake (AI) for infants. Source: US National Academies, via the NIH Office of Dietary Supplements. The daily value used on food labels is 900µg RAE.

ODA (Optimal Daily Allowance)

Meet the RDA — about 700–900µg RAE for most adults — mainly from food, with a good share from carotenoid-rich plants. There’s no good evidence that intakes above the RDA improve health, and with vitamin A, more can do harm: in some large observational studies, long-term intakes of preformed vitamin A above roughly 1,500µg a day were linked with lower bone density and a higher risk of hip fracture. So keep preformed vitamin A from supplements and fortified foods modest, and well below the 3,000µg upper limit. Beta-carotene and other carotenoids from food don’t carry this risk and can be eaten freely.

Found In (per 100g, as µg RAE)

Preformed vitamin A (retinol) sources:

Provitamin A (carotenoid) sources:

Note: liver values vary with the animal’s own diet and vitamin A status. Cod liver oil is shown per 100g for comparison — a teaspoon (about 4.5g) provides roughly 1,350µg RAE, though modern products vary, so check the label.

Liver deserves a specific caution: a single 100g serving of braised lamb liver provides about 7,490µg RAE — two and a half times the 3,000µg daily upper limit — and duck liver even more. An occasional serving is fine for most adults, because the limit applies to long-term daily intake, but liver shouldn’t be eaten every day. During pregnancy, UK health guidance advises avoiding liver and liver products altogether because of the risk of birth defects from excess preformed vitamin A.

Vitamin A Helps With

• Night vision and adaptation to low light, through the visual cycle
• Maintaining mucous membranes — respiratory, digestive, urinary, and reproductive tracts
• Immune cell development and function, including T cells and natural killer cells
• Skin cell turnover and the integrity of the body’s surface linings
• Embryonic development — limb formation, organ development, and the nervous system
• Reproductive health — sperm production and the development of ovarian follicles
• Normal bone remodeling, alongside vitamins D and K
• Antioxidant protection (from beta-carotene and other carotenoids specifically)
• Regulating gene expression through retinoic acid receptors

Vitamin A for Athletes and Active People

Vitamin A matters for athletes mainly through immune function and the integrity of the body’s protective barriers — as with most vitamins, getting enough is what counts, not taking extra.

Immune protection during heavy training: retinoic acid helps regulate the development of T cells and supports natural killer cell activity. Very heavy training can temporarily weaken immune defenses, and adequate vitamin A supports the mucous membranes of the airways and gut — the first line of defense against infection.

Skin and barrier health: vitamin A maintains the skin and other surface linings, which is relevant in contact sports and shared training environments where skin infections spread. Good hygiene matters far more for preventing those infections, though — vitamin A simply needs to be adequate.

Muscle repair: retinoic acid receptors are present in skeletal muscle, and laboratory research suggests vitamin A signaling plays a role in how muscle stem cells (satellite cells) develop during repair. This is a background role — there’s no evidence that extra vitamin A improves muscle growth or performance.

Vision: adequate vitamin A is needed for normal vision, especially in low light. Beyond correcting a deficiency, extra vitamin A doesn’t improve vision or reaction time.

Supplement stacking risk: athletes taking several supplements — a multivitamin, fortified protein products, and especially cod liver oil — can unknowingly add up preformed vitamin A from several sources. Cod liver oil is particularly high in it, while most standard fish oils contain little. It’s worth adding up your total preformed vitamin A from all supplements.

Vitamin A Deficiency

Deficiency risk is higher in:

• Young children and pregnant women in low-income countries with limited access to animal foods and carotenoid-rich produce — the WHO estimates that around 190 million preschool-age children have low vitamin A levels, and vitamin A deficiency is the leading preventable cause of childhood blindness worldwide
• People with fat malabsorption — such as from celiac disease, Crohn’s disease, cystic fibrosis, pancreatic conditions, or some types of weight-loss surgery — which impairs absorption of all fat-soluble vitamins
• People with zinc deficiency — which reduces RBP4 production, so vitamin A can’t be released from the liver effectively
• People with heavy, long-term alcohol use — alcohol interferes with vitamin A metabolism and depletes liver stores, while also making the liver more vulnerable to vitamin A toxicity
• People on strict plant-based diets low in carotenoid-rich vegetables, particularly poor converters

Xerophthalmia — the progression to blindness:

Vitamin A deficiency causes xerophthalmia — progressive drying and damage to the eye — in a predictable sequence:

1. Night blindness (nyctalopia): the first symptom, usually reversible with treatment
2. Conjunctival xerosis: the white of the eye becomes dry and thickened
3. Bitot’s spots: foamy, whitish patches on the white of the eye
4. Corneal xerosis: the cornea becomes dry and hazy
5. Corneal ulceration and keratomalacia: the cornea softens, ulcerates, and may perforate — causing irreversible blindness
6. Corneal scarring: permanent damage to the eye

Vitamin A supplementation programs for young children in deficient regions are among the most cost-effective health interventions known. Children aged 6–59 months receive high-dose vitamin A — 100,000 IU for infants aged 6–11 months and 200,000 IU for children aged 1–5 years — every 4–6 months. Cochrane reviews have found these programs reduce child deaths from all causes by about 12–24%, largely by reducing deaths from diarrhea and measles.

General symptoms of vitamin A deficiency:

• Night blindness — difficulty seeing in dim light
• Dry, rough skin
• Follicular hyperkeratosis — rough, goosebump-like bumps, particularly on the arms and thighs
• More frequent and severe respiratory and digestive infections
• Poor wound healing
• Poor growth in children
• Impaired fertility

Excessive Doses of Vitamin A

Upper limit (UL) for preformed vitamin A: 3,000µg RAE (10,000 IU) a day for adults, including during pregnancy and breastfeeding. The limits are much lower for children:

The upper limits apply to preformed vitamin A (retinol) only, not to beta-carotene and other carotenoids. Source: US National Academies, via the NIH Office of Dietary Supplements.

Vitamin A toxicity is one of the most serious vitamin toxicities, because excess builds up in the liver over time and can affect many body systems.

Acute toxicity: from a single very large dose. The famous historical example is Arctic explorers who ate polar bear liver and developed severe headache, drowsiness, nausea, vomiting, and later widespread peeling of the skin. In samples analyzed by the Norwegian researcher Kaare Rodahl in the 1940s, polar bear liver contained about 18,000–27,000 IU of vitamin A per gram — so a single meal could deliver millions of IU. The amount varies between bears, which may explain why some explorers ate it without ill effects.

Chronic toxicity: from long-term intake above the upper limit:

• Liver damage and fibrosis: vitamin A is stored in the liver’s stellate cells, and chronic excess activates them to produce scar tissue
• Bone loss: excess retinol stimulates the cells that break down bone and appears to interfere with vitamin D‘s effects, increasing fracture risk — and, as noted above, observational studies have linked even moderately high long-term intakes with lower bone density
• Raised pressure inside the skull (pseudotumor cerebri): causing persistent headaches, visual disturbances, and swelling of the optic nerve
• Dry, cracking skin; hair loss; brittle nails
• Fatigue, irritability, and bone and joint pain

Birth defects: excess preformed vitamin A is a known cause of birth defects. In one large study, women who took more than 10,000 IU (3,000µg RAE) a day of preformed vitamin A from supplements in early pregnancy had a higher risk of babies with malformations of the face, heart, and nervous system. The synthetic retinoid isotretinoin (Accutane, Roaccutane) requires strict pregnancy prevention programs for the same reason.

Important distinction: beta-carotene from food doesn’t cause vitamin A toxicity — the body converts less of it when vitamin A stores are adequate. Very high intakes can cause carotenemia, a harmless yellow-orange tint to the skin, most visible on the palms and soles, which fades when intake falls.

Beta-carotene supplement caution: in two large trials in smokers and asbestos-exposed workers — the ATBC trial (20mg of beta-carotene a day) and the CARET trial (30mg a day, combined with retinyl palmitate) — high-dose beta-carotene supplements significantly increased lung cancer risk. This doesn’t apply to carotenoids from food, but smokers and former smokers should avoid high-dose beta-carotene supplements.

Types of Vitamin A

• Retinol (retinyl palmitate / retinyl acetate): the preformed vitamin A used in supplements and fortified foods. Retinyl palmitate is the most common, stable form, and retinyl acetate is also widely used. These are the forms that can build up and cause toxicity, so doses need care.
• Retinal (retinaldehyde): the aldehyde form and the working molecule of the visual cycle. It isn’t usually sold as a supplement, but it’s used in some skincare products.
• Retinoic acid (tretinoin, all-trans-retinoic acid): the most active form. It’s used medically as a prescription skin treatment for acne and sun damage (tretinoin) and as a treatment for a type of leukemia (acute promyelocytic leukemia). It’s regulated as a medicine, not sold as a supplement.
• Beta-carotene: the most common provitamin A supplement and widely used in multivitamins. Safe at food-like doses, but high-dose supplements carry risks for smokers (see above).
• Mixed carotenoids: alpha-carotene, beta-cryptoxanthin, lycopene, lutein, and zeaxanthin. Only some of these (alpha-carotene and beta-cryptoxanthin) can be converted to vitamin A; lycopene, lutein, and zeaxanthin can’t, but they have antioxidant and eye-health roles of their own.

Which form for your goal:

How to Take Vitamin A

Take it with fat: vitamin A is fat-soluble, so supplements are best taken with a meal that contains some fat.

Add up your total intake: preformed vitamin A from several sources — multivitamins, cod liver oil, fortified foods, and separate vitamin A supplements — can add up past the upper limit without you realizing. Check labels for µg RAE (or convert from IU) and total them before adding another supplement.

Pregnancy: avoid high-dose preformed vitamin A supplements, and choose a prenatal supplement with little or no preformed vitamin A — beta-carotene is a safe alternative. Get the rest from a varied diet, including carotenoid-rich vegetables, and follow your national guidance on liver (in the UK, avoid it altogether during pregnancy).

Treating deficiency: higher-dose vitamin A to correct a diagnosed deficiency should be done under medical supervision, especially during pregnancy.

Cod liver oil users: cod liver oil is very high in both vitamin A and vitamin D. Traditional cod liver oil provides roughly 1,350µg RAE per teaspoon and about 4,000µg RAE per tablespoon — above the adult upper limit — though many modern products contain less. Check your product’s label and count it in your daily total.

Interactions

Alcohol increases the risk of liver damage from vitamin A — both are processed by some of the same liver enzymes, and heavy drinking depletes the liver’s vitamin A stores while making the liver more sensitive to vitamin A’s toxic effects. Cholestyramine (a cholesterol-lowering resin) and mineral oil (a laxative) reduce vitamin A absorption, and orlistat (a fat-absorption blocker) reduces absorption of all fat-soluble vitamins. Retinoid medicines such as isotretinoin and acitretin should never be combined with vitamin A supplements without medical supervision, because the effects add up.

Synergy

• Works with zinc, which is needed to make RBP4 and release vitamin A from the liver — the two are closely linked.
• Works with vitamins D and K in normal bone metabolism — though excess vitamin A works against vitamin D in bone.
• Works with iron — vitamin A helps the body mobilize stored iron for making red blood cells, and in populations where both are lacking, adding vitamin A can improve the response to iron.
• Vitamin E helps protect vitamin A from oxidation.
• Works with zinc and vitamin C in wound healing and immune function.

Antagonistic Interactions

High intakes of preformed vitamin A can work against vitamin D in bone, increasing fracture risk.

Alcohol increases vitamin A’s toxic effects on the liver.

Food values: USDA FoodData Central — fish oil, cod liver (SR Legacy, FDC ID 173577); duck liver, raw (SR Legacy, 174467); lamb liver, braised (SR Legacy, 172532); butter, salted (SR Legacy, 173410); cheddar cheese (Foundation Foods, 328637); egg, hard-boiled (SR Legacy, 173424); Atlantic salmon, farmed, cooked (SR Legacy, 175168); sweet potato, baked (SR Legacy, 168483); carrots, boiled (SR Legacy, 170394); pumpkin, canned (SR Legacy, 168450); butternut squash, baked (SR Legacy, 169296); spinach, boiled (SR Legacy, 168463). RDA and upper limits from the US National Academies, via the NIH Office of Dietary Supplements. % Daily Values use the FDA’s current Daily Value of 900µg RAE.