vitamin a

Vitamin A refers to a group of fat‑soluble compounds that include retinol, retinal, retinyl esters, and a variety of provitamin A carotenoids such as beta‑carotene, alpha‑carotene, and beta‑cryptoxanthin. These compounds share the biological activity of all‑trans retinol, the principal form used by the body, particularly for vision and cellular differentiation processes. Vitamin A was first recognized for its role in preventing night blindness, a symptom of deficiency, and its discovery predates modern nutritional science, with early 20th‑century researchers identifying it as an essential dietary factor. In the diet, preformed vitamin A (retinol and retinyl esters) is found primarily in animal‑derived foods such as liver, fish oil, dairy products, and eggs, while provitamin A carotenoids are abundant in orange and dark green plant foods such as carrots, sweet potatoes, spinach, and kale. Unlike water‑soluble vitamins, vitamin A is absorbed along with dietary fat and stored predominantly in the liver. Because of this storage capacity, vitamin A does not need to be consumed daily in high amounts to maintain adequate status, though consistent intake ensures reserves are maintained. Retinol is critical in the visual cycle, where it is converted into retinal, a chromophore of rhodopsin, the photoreceptor pigment in rods that is essential for low‑light vision. Without sufficient vitamin A, the visual cycle is disrupted, leading to symptoms such as night blindness and, in chronic deficiency, xerophthalmia and corneal damage. Beyond vision, vitamin A modulates gene expression, supports epithelial tissue integrity throughout the body, and plays roles in immune system functioning, embryonic development, and reproductive health. The term retinol activity equivalents (RAE) reflects the differing bioactivities of food sources—one microgram of retinol activity equivalent equals one microgram of retinol or 12 micrograms of dietary beta‑carotene, highlighting the conversion efficiency from plant sources to active vitamin A forms.

Vitamin A’s biological functions span a wide range of physiological systems. The best‑characterized role is in vision: in the retina, 11‑cis retinal binds to opsin proteins to form rhodopsin, which enables the photoreceptor cells to detect photons in low light conditions. Without adequate retinal, phototransduction is impaired, leading to night blindness, a sentinel symptom of deficiency. Vitamin A also maintains the health of epithelial tissues that line the skin, eyes, respiratory, gastrointestinal, and genitourinary tracts, where it promotes cell differentiation and barrier function, limiting pathogen entry. Immune benefits of vitamin A are well documented. Retinoic acid, the active metabolite, modulates the differentiation and function of immune cells such as T lymphocytes and antigen‑presenting cells. This nutrient supports mucosal immunity by maintaining the integrity of mucous membranes and enhancing the production of secretory IgA antibodies, particularly in the gut and respiratory tracts, thereby reducing infection risk. Observational and interventional studies have shown vitamin A supplementation reduces mortality from measles and diarrhea in children in regions where deficiency is prevalent, underscoring its public health importance. Vitamin A also influences growth and reproduction. During embryogenesis, retinoic acid acts as a signaling molecule that regulates gene expression involved in organogenesis, limb development, and neural patterning. Adequate maternal vitamin A status is essential for fetal growth and development, but excessive preformed vitamin A intake during pregnancy is teratogenic. In adults, vitamin A plays roles in spermatogenesis and ovarian function. There is emerging evidence on carotenoids’ antioxidant effects, though the extent to which provitamin A carotenoids act as antioxidants in vivo is debated because their conversion to retinol and interactions with other dietary antioxidants like vitamin E influence systemic effects. Nonetheless, higher intakes of carotenoid‑rich fruits and vegetables are epidemiologically associated with lower risks of age‑related macular degeneration and certain chronic diseases, likely reflecting synergistic effects of multiple phytonutrients rather than vitamin A alone.

Vitamin A requirements vary by life stage, sex, and physiological status. Dietary guidelines express needs in retinol activity equivalents (RAE) to capture the bioavailability differences between preformed retinol and provitamin carotenoids. For adults aged 19–50 years, the RDA is 900 mcg RAE/day for men and 700 mcg RAE/day for women. These amounts are calibrated to maintain liver stores and meet metabolic demands for nearly all (97–98%) healthy individuals. Pregnant women have slightly higher requirements due to increased demands for fetal development, and lactating individuals require more to support secretion into breast milk. Infants and children have lower absolute needs. For infants 0–6 months, an adequate intake (AI) of 400 mcg RAE reflects average intake levels associated with healthy status, while older children (1–3 years, 300 mcg; 4–8 years, 400 mcg; 9–13 years, 600 mcg) require amounts proportional to growth and energy needs. Factors that influence individual needs include dietary fat intake—since absorption depends on bile and fat digestion—genetic polymorphisms affecting carotenoid conversion, and health states that alter metabolism or losses. For example, chronic infections, gastrointestinal malabsorption syndromes, and liver disease may increase requirements or reduce effective status. The RDA assumes typical diets containing a combination of animal and plant sources; individuals relying heavily on provitamin A carotenoids may need greater overall intake to achieve equivalent RAE due to conversion efficiency.

Vitamin A deficiency, though uncommon in developed nations, remains a leading cause of preventable blindness in children globally, especially in low‑income countries where diets lack sufficient vitamin A. The earliest clinical sign is night blindness (nyctalopia), reflecting compromised formation of rhodopsin in rod cells. As deficiency progresses, the conjunctiva and cornea become dry—a state called xerophthalmia—followed by Bitot’s spots, which are triangular, foamy deposits of keratin on the sclera. Without intervention, severe deficiency can lead to keratomalacia, corneal ulceration, and irreversible blindness. Globally, an estimated 250,000 to 500,000 children become blind each year due to vitamin A deficiency, with a high mortality rate among those affected. Non‑ocular symptoms include increased susceptibility to infections, particularly respiratory and diarrheal diseases, due to weakened mucosal barriers and impaired immune responses. Skin changes such as dryness, scaling, and follicular hyperkeratosis may manifest. In children, deficiency can contribute to stunted growth and delayed skeletal development due to vitamin A’s role in cellular proliferation and differentiation. Reproductive issues, including infertility and complications in pregnancy, are associated with low vitamin A status. Diagnosis involves clinical evaluation of characteristic signs and measurement of serum retinol levels. A plasma retinol concentration below 0.70 µmol/L indicates subclinical deficiency, while levels below 0.35 µmol/L signify severe deficiency with depleted liver stores. However, because serum levels may remain normal until hepatic reserves are exhausted, clinical context and dietary history complement laboratory measures. Public health approaches in regions with high deficiency prevalence include food fortification, supplementation programs for children and pregnant women, and agricultural interventions to increase access to vitamin A‑rich foods.

Vitamin A is abundant in both animal and plant foods, but the forms differ: animal foods provide preformed vitamin A (retinol and retinyl esters), which is highly bioavailable, while plant foods provide provitamin A carotenoids that the body converts to retinol. Liver from various animals is the richest source of preformed vitamin A; a 3‑ounce serving of cooked beef or lamb liver can provide thousands of micrograms of RAE, far exceeding daily requirements. Fish liver oils, such as cod liver oil, are also exceptionally rich. Eggs, dairy products like whole milk, cheese, and fortified cereals contribute moderate amounts. Among plant foods, orange and yellow vegetables such as sweet potatoes, carrots, pumpkin, and butternut squash are excellent carotenoid sources, as are dark leafy greens like spinach, collard greens, and bok choy. Colorful fruits such as cantaloupe and mango provide provitamin A carotenoids as well. Cooking plant foods and consuming them with dietary fat enhances carotenoid absorption, increasing their contribution to vitamin A status. Because of the differing bioavailability between retinol and carotenoids, diet planning should consider both sources. For individuals who avoid animal foods, larger servings of carotenoid‑rich produce and attention to dietary fat facilitate meeting requirements. Food fortification—such as adding retinyl palmitate to milks and breakfast cereals—plays a role in improving intake in some populations. Ultimately, a varied diet that includes both animal and plant sources tailored to individual preferences and needs ensures sufficient vitamin A intake.

The absorption of vitamin A depends on dietary form and concurrent intake of dietary fat. Preformed vitamin A from animal sources is absorbed with high efficiency because it is already in the retinol form. Provitamin A carotenoids from plants require enzymatic cleavage in the intestinal mucosa to yield retinol, a process influenced by factors such as food matrix and preparation. Cooking breaks down plant cell walls, improving carotenoid release and subsequent absorption. Dietary fat stimulates bile secretion and micelle formation, essential for the solubilization of vitamin A compounds; thus, consuming carotenoid‑rich vegetables with healthy fats like olive oil, avocado, or nuts increases uptake. Conversely, very low‑fat meals or conditions impairing fat digestion (e.g., cholestatic liver disease, pancreatic insufficiency, or use of fat‑binding weight‑loss drugs) reduce vitamin A absorption. Fiber and certain plant constituents may modestly inhibit absorption, but the net effect is typically outweighed by the presence of fat. Interindividual differences, including genetic polymorphisms in carotenoid cleavage enzymes, also influence the efficiency of converting carotenoids to retinol. Because absorption may vary widely, dietary recommendations are framed in retinol activity equivalents to standardize intake recommendations across food sources.

Most individuals meeting their daily needs through a balanced diet do not require vitamin A supplements; however, supplementation may be appropriate in specific situations. Populations at risk of deficiency—such as individuals in low‑income regions with limited access to vitamin A‑rich foods, those with malabsorption syndromes, or people with liver or pancreatic disorders—may benefit from targeted supplementation under medical supervision. In settings with high deficiency prevalence, public health programs often provide high‑dose vitamin A supplements to young children and pregnant women to reduce morbidity and mortality from infectious diseases. Supplements come in preformed retinol forms or as carotenoid precursors; retinol forms directly raise vitamin A status, while carotenoid supplements contribute indirectly. In practice, beta‑carotene supplements are generally considered safer regarding toxicity risk because conversion is regulated by body needs, whereas preformed vitamin A can accumulate and reach toxic levels if taken excessively. Before starting supplementation, individuals should consult a healthcare professional, as excessive intake—especially of preformed vitamin A—can cause toxicity, particularly in pregnancy where teratogenic effects are a concern. Supplements are often included in multivitamins or specific vitamin A formulations; third‑party testing for quality assurance is recommended. For those taking medications that affect fat absorption or liver function, professional guidance ensures that supplementation is both safe and effective. Ultimately, a food‑first approach is encouraged, with supplements reserved for clinical indications or public health strategies.

Because vitamin A is fat‑soluble, excess amounts are stored in liver and adipose tissues, and chronic intake above the tolerable upper intake level can lead to toxicity—hypervitaminosis A. The established adult UL of 3,000 mcg RAE/day is based on evidence showing adverse effects above this level. Symptoms of chronic toxicity include headache, nausea, dizziness, dry skin, hair loss, bone and joint pain, and hepatotoxicity. Severe cases may result in intracranial hypertension, cognitive disturbances, and, rarely, death. Pregnant individuals are particularly susceptible to teratogenic effects from excess preformed vitamin A, including craniofacial and cardiac malformations. Because provitamin A carotenoids are converted to retinol in a regulated manner, high intake of carotenoid‑rich plant foods does not pose the same toxicity risk; their excess is reflected in benign carotenemia, a reversible yellowing of the skin without systemic toxicity. Acute toxicity can occur after ingesting very high doses in a short period, whereas chronic toxicity arises from long‑term overconsumption of supplements containing preformed vitamin A. Clinical management involves discontinuing excessive intake and monitoring liver function and symptoms. Awareness of the UL and careful consideration of total vitamin A intake—dietary and supplemental—helps prevent toxicity while ensuring adequacy.

Vitamin A supplements can interact with certain medications, altering drug effectiveness or increasing adverse effects. Oral retinoids, such as isotretinoin and etretinate used for severe acne and psoriasis, share metabolic pathways with vitamin A; concurrent intake of high‑dose supplemental vitamin A can elevate systemic retinoid levels and increase toxicity risk. Anticoagulant therapy with warfarin may be affected by high vitamin A doses, potentially increasing bleeding risk through mechanisms that may involve vitamin K antagonism and effects on prothrombin, particularly at intakes above the upper limit. Weight‑loss medications like orlistat can reduce the absorption of fat‑soluble vitamins, including vitamin A; spacing vitamin A supplementation at least two hours before or after orlistat may mitigate this effect. Other interactions have been reported with tetracycline antibiotics and alcohol, which may exacerbate hepatotoxicity in the setting of high vitamin A intake. Patients should disclose all supplements to healthcare providers to avoid interactions and ensure appropriate monitoring, especially when taking medications with narrow therapeutic indices.

Common Forms: retinyl palmitate, retinyl acetate, beta‑carotene

Typical Doses: 700–900 mcg RAE for adults; higher for pregnancy/lactation under guidance

When to Take: with meals containing fat to enhance absorption

Best Form: preformed retinol (retinyl esters) with dietary fat

⚠️ Interactions: orlistat (may reduce absorption), warfarin (bleeding risk with high vitamin A), retinoid medications (additive toxicity)