presentation of vitamin a

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Recommended Amounts

Vitamin A is currently listed on the Nutrition Facts label measured in international units (IU). However, the Institute of Medicine lists the Recommended Dietary Allowances (RDA) of vitamin A in micrograms (mcg) of retinol activity equivalents (RAE) to account for different absorption rates of preformed vitamin A and provitamin A carotenoids. Under the Food and Drug Administration’s (FDA) new food and dietary supplement labeling regulations, as of July 2018 large companies will no longer list vitamin A as IU but as “mcg RAE.” [1]

RDA: The Recommended Dietary Allowance for adults 19 years and older is 900 mcg RAE for men (equivalent to 3,000 IU) and 700 mcg RAE for women (equivalent to 2,333 IU).
UL: The Tolerable Upper Intake Level is the maximum daily intake unlikely to cause harmful effects on health. The UL for vitamin A from retinol is 3,000 micrograms of preformed vitamin A.

Vitamin A and Health

The evidence suggests that eating a variety of foods rich in vitamin A, especially fruits and vegetables , is protective from certain diseases, though the health benefit of vitamin A supplements is less clear.

Lung Cancer: Observational studies following nonsmokers and current or former smokers have found that higher intakes of carotenoids from fruits and vegetables are associated with a lower risk of lung cancer. However, three large clinical trials did not find that supplements of beta-carotene and vitamin A helped to prevent or reduce lung cancer risk. In fact, two of those three trials actually found a significant increase in lung cancer risk among study participants taking supplements with beta-carotene or retinyl palmitate (a form of vitamin A). [1] Therefore, it is recommended that current or former smokers and workers exposed to asbestos do not use high-dose beta-carotene and retinyl palmitate supplements. Additionally, based on current evidence the U.S. Preventive Services Task Force advises against the use of beta-carotene supplements for the prevention of any cancer, stating that there is potentially greater harm in using these supplements than any suggested benefit. [2]

Prostate Cancer: Lycopene is a carotenoid that gives fruits and vegetables a pink or red hue, as in tomatoes and grapefruit. There has been interest in lycopene’s effects on cancer due to its antioxidant properties. Observational studies have noted a decreased risk of prostate cancer in men who eat high amounts of fruits and vegetables. Unfortunately, studies have not provided a clear answer specific to lycopene. Observational studies and clinical trials have shown either a protective effect of lycopene-rich foods (specifically tomatoes) or supplements, or no effect. [3] A Harvard study of more than 51,000 men from the Health Professionals Follow-up Study found a protective effect from advanced stages of prostate cancer in those with higher intakes of tomato sauce. [4] A 2015 meta-analysis of 26 studies found that higher lycopene intakes appeared protective from prostate cancer incidence. [5] However, an FDA review stated that definite conclusions about lycopene could not be made, one reason being that accurate reporting of lycopene intake is difficult due to variations in lycopene content during cooking and storage. [6] Another was that lycopene-rich foods often contain other cancer-protective compounds, so it would be difficult to isolate any health benefits to lycopene

The randomized controlled Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) trial examines the effects of the MIND diet to prevent cognitive decline. It found that higher blood levels of alpha-carotene (a form of vitamin A that includes lutein and zeaxanthin) were associated with better cognition (e.g., memory, learning, attention) in participants at risk for cognitive decline. [7] Foods contributing to higher alpha-carotene levels included fruits, and green leafy and orange vegetables.

Age-related macular degeneration (AMD) is a common painless eye condition but a leading cause of vision loss among people age 50 and older. It distorts the sharp, central vision needed to see fine details such as for reading and driving. The exact cause is unclear but oxidative stress is believed to play a role. Smokers and those with poor diets lacking fruits and vegetables have a higher risk of developing AMD. Lutein and zeaxanthin are two carotenoids with protective antioxidant effects that are found in the retina, the eye tissue that is damaged by AMD. Studies have looked to see if supplements containing lutein and zeaxanthin, as well as beta-carotene, might be useful for preventing or treating this condition. The NIH-funded Age-Related Eye Disease Studies (AREDS, AREDS2) found that daily intakes of high-dose vitamins including vitamins C and E and lutein and zeaxanthin slowed the progression of intermediate and late-stage AMD, particularly in participants who ate the lowest amounts of carotenoids. [8,9] Beta-carotene was not found to be protective.

Food Sources

Many breakfast cereals, juices, dairy products, and other foods are fortified with retinol (preformed vitamin A). Many fruits and vegetables and some supplements contain beta-carotene, lycopene, lutein, or zeaxanthin.

Leafy green vegetables ( kale , spinach, broccoli), orange and yellow vegetables (carrots, sweet potatoes , pumpkin and other winter squash , summer squash)
Red bell pepper
Cantaloupe, mango
Fortified foods

Signs of Deficiency and Toxicity

Deficiency Vitamin A deficiency is rare in Western countries but may occur. Conditions that interfere with normal digestion can lead to vitamin A malabsorption such as celiac disease, Crohn’s disease, cirrhosis, alcoholism, and cystic fibrosis. Also at risk are adults and children who eat a very limited diet due to poverty or self-restriction. Mild vitamin A deficiency may cause fatigue, susceptibility to infections, and infertility. The following are signs of a more serious deficiency.

Xerophthalmia, a severe dryness of the eye that if untreated can lead to blindness
Nyctalopia or night blindness
Irregular patches on the white of the eyes
Dry skin or hair

Toxicity Vitamin A toxicity may be more common in the U.S. than a deficiency, due to high doses of preformed vitamin A (retinol) found in some supplements. Vitamin A is also fat-soluble, meaning that any amount not immediately needed by the body is absorbed and stored in fat tissue or the liver. If too much is stored, it can become toxic. The tolerable upper intake of 3,000 mcg of preformed vitamin A, more than three times the current recommended daily level, is thought to be safe. However, there is some evidence that this much preformed vitamin A might increase the risk of bone loss, hip fracture [10-12], or some birth defects. [13] Another reason to avoid too much preformed vitamin A is that it may interfere with the beneficial actions of vitamin D . Signs of toxicity include the following.

Vision changes such as blurry sight
Nausea and vomiting
Sensitivity to bright light like sunlight

In contrast to preformed vitamin A, beta-carotene is not toxic even at high levels of intake. The body can form vitamin A from beta-carotene as needed, and there is no need to monitor intake levels as with preformed vitamin A. Therefore, it is preferable to choose a multivitamin supplement that has all or the vast majority of its vitamin A in the form of beta-carotene; many multivitamin manufacturers have already reduced the amount of preformed vitamin A in their products. However, there is no strong reason for most people to take individual high-dose beta-carotene supplements. Smokers in particular should avoid these, since some randomized trials in smokers have linked high-dose supplements with increased lung cancer risk. [14-16]

Did You Know?

Sometimes people take cod liver oil for vitamin D but may not be aware it is also very high in vitamin A, beyond the RDA at 192%, in the same synthetic form as in supplements (retinyl palmitate). So if you use cod liver oil, make sure your other supplements do not contain extra vitamin A. Other forms of fish oil supplements typically do not contain significant amounts of vitamin A, but always check the label.
Retinoids in skin creams can cause skin to become highly sensitive to bright light, so it is advised to apply vitamin A creams at night and to avoid strong sun after their use.

Vitamins and Minerals

National Institutes of Health Office of Dietary Supplements: Vitamin A Fact Sheet for Health Professionals https://ods.od.nih.gov/factsheets/VitaminA-HealthProfessional/#en24 . Accessed 6/18/2018.
U.S Preventive Services Task Force, Mangione CM, Barry MJ, Nicholson WK, Cabana M, Chelmow D, Coker TR, Davis EM, Donahue KE, Doubeni CA, Jaén CR, Kubik M, Li L, Ogedegbe G, Pbert L, Ruiz JM, Stevermer J, Wong JB. Vitamin, Mineral, and Multivitamin Supplementation to Prevent Cardiovascular Disease and Cancer: US Preventive Services Task Force Recommendation Statement. JAMA . 2022 Jun 21;327(23):2326-2333.
National Cancer Institute. Prostate Cancer, Nutrition, and Dietary Supplements (PDQ®)–Health Professional Version: Lycopene. https://cancer.gov/about-cancer/treatment/cam/hp/prostate-supplements-pdq#section/_16 . Accessed 6/18/2018.
Giovannucci, E., et al. Risk factors for prostate cancer incidence and progression in the health professionals follow-up study. Int J Cancer , 2007. 121(7): p. 1571-8.
Chen P, Zhang W, Wang X, Zhao K, Negi DS, Zhuo L, Qi M, Wang X, Zhang X. Lycopene and Risk of Prostate Cancer: A Systematic Review and Meta-Analysis. Medicine . 2015 Aug;94(33):e1260.
Kavanaugh CJ1, Trumbo PR, Ellwood KC. The U.S. Food and Drug Administration’s evidence-based review for qualified health claims: tomatoes, lycopene, and cancer. J Natl Cancer Inst . 2007 Jul 18;99(14):1074-85. Epub 2007 Jul 10.
Liu X, Dhana K, Furtado JD, Agarwal P, Aggarwal NT, Tangney C, Laranjo N, Carey V, Barnes LL, Sacks FM. Higher circulating α-carotene was associated with better cognitive function: an evaluation among the MIND trial participants. Journal of Nutritional Science . 2021;10:e64.
Age-Related Eye Disease Study Research Group. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Arch Ophthalmol . 2001;119(10):1417-1436.
Age-Related Eye Disease Study 2 Research Group. Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. JAMA . 2013 May 15;309(19):2005-15.
Feskanich D, Singh V, Willett WC, Colditz GA. Vitamin A intake and hip fractures among postmenopausal women. JAMA . 2002; 287:47-54.
Michaelsson K, Lithell H, Vessby B, Melhus H. Serum retinol levels and the risk of fracture. N Engl J Med. 2003; 348:287-94.
Penniston KL, Tanumihardjo SA. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr . 2006; 83:191-201.
Azais-Braesco V, Pascal G. Vitamin A in pregnancy: requirements and safety limits. Am J Clin Nutr . 2000; 71:1325S-33S.
Omenn GS, Goodman GE, Thornquist MD, et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med . 1996; 334:1150-5.
Albanes D, Heinonen OP, Taylor PR, et al. Alpha-tocopherol and beta-carotene supplements and lung cancer incidence in the alpha-tocopherol, beta-carotene cancer prevention study: effects of base-line characteristics and study compliance. J Natl Cancer Inst . 1996; 88:1560-70.
Virtamo J, Pietinen P, Huttunen JK, et al. Incidence of cancer and mortality following alpha-tocopherol and beta-carotene supplementation: a postintervention follow-up. JAMA . 2003; 290:476-85.
Xia Q1, Yin JJ, Wamer WG, Cherng SH, Boudreau MD, Howard PC, Yu H, Fu PP. Photoirradiation of retinyl palmitate in ethanol with ultraviolet light–formation of photodecomposition products, reactive oxygen species, and lipid peroxides. Int J Environ Res Public Health . 2006 Jun;3(2):185-90.
American Academy of Dermatology press release. Analysis finds sunscreens containing retinyl palmitate do not cause skin cancer. August 10, 2010. https://aad.org/media/news-releases/analysis-finds-sunscreens-containing-retinyl-palmitate-do-not-cause-skin-cancer . Accessed 6/25/2018.

Last reviewed March 2023

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The contents of this website are for educational purposes and are not intended to offer personal medical advice. You should seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The Nutrition Source does not recommend or endorse any products.

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The Office of Dietary Supplements (ODS) of the National Institutes of Health (NIH)

Vitamin A and Carotenoids

This is a fact sheet intended for health professionals. For a general overview, see our consumer fact sheet .

Introduction

Vitamin A is the name of a group of fat-soluble retinoids, primarily retinol and retinyl esters [ 1 , 2 ]. Vitamin A is involved in immune function, cellular communication, growth and development, and male and female reproduction [ 1-3 ]. Vitamin A supports cell growth and differentiation, playing a critical role in the normal formation and maintenance of the heart, lungs, eyes, and other organs [ 1 , 2 ]. Vitamin A is also critical for vision as an essential component of rhodopsin, the light-sensitive protein in the retina that responds to light entering the eye, and because it supports the normal differentiation and functioning of the conjunctival membranes and cornea [ 2 , 4 ].

The human diet contains two sources for vitamin A: preformed vitamin A (retinol and retinyl esters) and provitamin A carotenoids [ 1 , 5 ]. Preformed vitamin A is found in foods from animal sources, including dairy products, eggs, fish, and organ meats [ 1 , 2 ]. Provitamin A carotenoids are plant pigments that include beta-carotene, alpha-carotene, and beta-cryptoxanthin [ 1 ]. The body converts provitamin A carotenoids into vitamin A in the intestine via the beta-carotene monooxygenase type 1 BCMO1 enzyme [ 1 , 3 , 6 ], although conversion rates may have genetic variability [ 7 , 8 , 9 ]. Other carotenoids in food, such as lycopene, lutein, and zeaxanthin, are not converted into vitamin A and are referred to as non-provitamin A carotenoids; they might have other important activities not involving vitamin A formation [ 1 ].

The various forms of vitamin A are solubilized into micelles in the intestinal lumen and absorbed by duodenal mucosal cells [ 5 ]. Retinyl esters and provitamin A carotenoids are converted to retinol after uptake into the lumen (for retinyl esters) or absorption (for provitamin A carotenoids). Retinol is then oxidized to retinal and retinoic acid, the two main active vitamin A metabolites in the body [ 1 ]. Most of the body’s vitamin A is stored in the liver in the form of retinyl esters [ 1 ].

Retinol and carotenoid levels are typically measured in plasma or serum because blood samples are easy to collect [ 1 ]. However, these levels are not always reliable indicators of vitamin A status because they do not decline until vitamin A levels in the liver and other storage sites are almost depleted and because acute and chronic infections can decrease serum and plasma retinol concentrations [ 1 ]. Most vitamin A is stored in the liver, so measuring vitamin A levels in the liver is the best way to assess vitamin A adequacy [ 1 ]. In clinical studies, specialized research laboratories can measure liver vitamin A reserves indirectly using isotope-dilution or dose-response methods, in which plasma levels of retinol, a tracer surrogate, or both are measured over several days after the administration of vitamin A [ 1 ].

In clinical practice, plasma retinol levels alone can be used to document significant deficiency. A serum or plasma retinol concentration of 20 mcg/dL (0.70 micromoles/L) or less frequently reflects moderate vitamin A deficiency, and a level of 10 mcg/dL (0.35 micromoles/L) or less is considered an indicator of severe vitamin A deficiency [ 1 ].

Recommended Intakes

Intake recommendations for vitamin A and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine [ 5 ]. DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values, which vary by age and sex, include the following:

Recommended Dietary Allowance (RDA): Average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals; often used to plan nutritionally adequate diets for individuals
Adequate Intake (AI): Intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an RDA
Estimated Average Requirement (EAR): Average daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can also be used to assess the nutrient intakes of individuals
Tolerable Upper Intake Level (UL): Maximum daily intake unlikely to cause adverse health effects

RDAs for vitamin A are given as retinol activity equivalents (RAE) to account for the different bioactivities of retinol and provitamin A carotenoids, all of which are converted by the body into retinol (see Table 1). One mcg RAE is equivalent to 1 mcg retinol, 2 mcg supplemental beta-carotene, 12 mcg dietary beta-carotene, or 24 mcg dietary alpha-carotene or beta-cryptoxanthin [ 5 ].

*AI, equivalent to the mean intake of vitamin A in healthy, breastfed infants.

The units of measurement for vitamin A are now mcg RAE, but International Units (IUs) were previously used [ 10 ]. To convert IU to mcg RAE, use the following [ 11-13 ]:

1 IU retinol = 0.3 mcg RAE
1 IU supplemental beta-carotene = 0.3 mcg RAE
1 IU dietary beta-carotene = 0.05 mcg RAE
1 IU dietary alpha-carotene or beta-cryptoxanthin = 0.025 mcg RAE

RAE can only be directly converted into IUs if the sources of vitamin A are known. For example, the RDA of 900 mcg RAE for adolescent and adult men is equivalent to 3,000 IU if the food or supplement source is preformed vitamin A (retinol) or if the supplement source is beta-carotene. This RDA is also equivalent to 18,000 IU beta-carotene from food or to 36,000 IU alpha-carotene or beta-cryptoxanthin from food. Therefore, a mixed diet containing 900 mcg RAE provides between 3,000 and 36,000 IU vitamin A, depending on the foods consumed.

Sources of Vitamin A

Concentrations of preformed vitamin A are highest in liver, fish, eggs, and dairy products [ 1 ]. Most dietary provitamin A in the U.S. diet comes from leafy green vegetables, orange and yellow vegetables, tomato products, fruits, and some vegetable oils [ 1 , 5 , 14 ]. Vitamin A is routinely added to some foods, including milk and margarine [ 1 , 2 ]. Some ready-to-eat cereals are also fortified with vitamin A.

About 65% to 80% of vitamin A consumed in the United States and other high-income countries comes from preformed vitamin A, whereas provitamin A is the main form consumed in low-income countries, where diets include more plant-based foods [ 2 , 15 ]. Among U.S. children and adolescents, enriched and fortified foods account for 34%–40% of vitamin A intakes from food [ 16 ].

The body might absorb up to 75% to 100% of retinol and, in most cases, 10% to 30% of beta-carotene from foods [ 17 , 18 ]. Cooking and heat treatment can increase the bioavailability of beta-carotene from foods [ 19 ].

Table 2 lists a variety of foods and their vitamin A content per serving. The foods from animal sources in Table 2 contain primarily preformed vitamin A, the plant-based foods have provitamin A, and the foods with a mixture of ingredients from animals and plants contain both preformed vitamin A and provitamin A.

*DV = Daily Value. Food and Drug Administration (FDA) developed DVs to help consumers compare the nutrient contents of foods and dietary supplements within the context of a total diet. The DV for vitamin A is 900 mcg RAE for adults and children age 4 years and older [ 11 ], where 1 mcg RAE = 1 mcg retinol, 2 mcg beta-carotene from supplements, 12 mcg beta-carotene from foods, 24 mcg alpha-carotene, or 24 mcg beta-cryptoxanthin. FDA does not require food labels to list vitamin A content unless vitamin A has been added to the food. Foods providing 20% or more of the DV are considered to be high sources of a nutrient, but foods providing lower percentages of the DV also contribute to a healthful diet.

Dietary supplements

Vitamin A is available in stand-alone supplements and most multivitamins, often in the form of retinyl acetate, retinyl palmitate, provitamin A beta-carotene, or a combination [ 1 , 21 ]. Amounts of vitamin A in supplements vary widely, but 3,000 mcg RAE (333% of the DV) is common [ 21 ]. Multivitamins commonly have somewhat lower amounts, often 750 to 1,050 mcg RAE (83% to 117% of the DV).

The absorption of preformed vitamin A esters from dietary supplements is 70%–90%, and that of beta-carotene ranges from 8.7% to 65% [ 19 , 22 ].

Vitamin A Intakes and Status

Average daily intakes of vitamin A from foods and beverages in the United States were 682 mcg RAE for men age 20 and older and 616 mcg RAE for women in 2017–2018, according to the National Health and Nutrition Examination Survey (NHANES) [ 23 ]. For children age 2–19, mean daily intakes of vitamin A from foods and beverages ranged from 497 to 680 mcg RAE. An analysis of biochemical data from 2003–2006 NHANES data indicates that less than 1% of the U.S. population has a serum retinol level of less than 20 mcg/dL, which indicates that vitamin A deficiency is uncommon in the U.S. population [ 24 ].

Data from NHANES III, conducted from 1988 to 1994, showed that approximately 26% of the vitamin A in RAEs consumed by men and 34% of that consumed by women in the United States comes from provitamin A carotenoids [ 5 ]. The remainder comes from preformed vitamin A, mostly in the form of retinyl esters.

About 12% to 40% of the U.S. population, depending on age, uses supplements containing vitamin A [ 25 ]. Adults age 71 years or older and children younger than 9 are more likely than members of other age groups to take supplements containing vitamin A.

Vitamin A Deficiency

Frank vitamin A deficiency is rare in the United States. However, vitamin A deficiency is still common in many developing countries, often as a result of limited access to foods containing preformed vitamin A from animal-based food sources and to foods containing provitamin A carotenoids because of poverty or traditional diets [ 1 , 26 ]. A pooled analysis of population-based surveys from 138 low-income and middle-income countries found that 29% of children age 6 months to 5 years had vitamin A deficiency in 2013 [ 27 ]. Deficiency rates were highest in sub-Saharan Africa (48%) and South Asia (44%). In addition, approximately 10% to 20% of pregnant people in low-income countries have vitamin A deficiency [ 28 ].

Limited research suggests that vitamin A deficiency may also be influenced by genetic variability in conversion rates of beta-carotene to vitamin A. Certain polymorphisms in the BCMO1 gene have been found to reduce the activity of the BCMO1 enzyme in humans [ 8 , 9 ], and a study in the Philippines among 693 children and adolescents found an inverse association between vitamin A status and the A379V TT variant in the BCMO1 gene [ 7 ].

The most common clinical sign of vitamin A deficiency is xerophthalmia, which develops after plasma retinol has been low and the eye’s vitamin A reserves have become depleted. The first sign is night blindness, or the inability to see in low light or darkness as a result of low rhodopsin levels in the retina [ 1 , 27 , 28 ]. Xerophthalmia also affects the cornea and can eventually lead to permanent blindness; vitamin A deficiency is one of the top causes of preventable blindness in children [ 28 ].

Chronic vitamin A deficiency has also been associated with abnormal lung development, respiratory diseases (such as pneumonia), and an increased risk of anemia and death [ 26 , 27 , 29 ].

Another effect of chronic vitamin A deficiency is increased severity and mortality risk of infections (particularly measles and infection-associated diarrhea) [ 26 ]. In 2013, 94,500 children in low-income and middle-income countries died of diarrhea and 11,200 died of measles as a result of vitamin A deficiency [ 27 ]. More than 95% of deaths attributable to vitamin A deficiency occurred in sub-Saharan Africa and Asia, where vitamin A deficiency was responsible for 2% of all deaths in children younger than 5 years [ 27 ].

Groups at Risk of Vitamin A Inadequacy

The following groups are among those most likely to have inadequate intakes of vitamin A.

Premature infants

Preterm infants have low liver stores of vitamin A at birth, and their plasma concentrations of retinol often remain low throughout the first year of life [ 30 , 31 ]. Preterm infants with vitamin A deficiency have a higher risk of eye and chronic lung diseases [ 32 , 33 ]. However, in high-income countries, clinical vitamin A deficiency is rare in infants and occurs only in those with malabsorption disorders [ 34 ].

Infants, children, and pregnant and lactating persons in low-income and middle-income countries

Pregnant people need extra vitamin A for fetal growth and tissue maintenance and to support their own metabolism [ 35-37 ]. The breast milk of lactating people with adequate vitamin A intakes contains sufficient amounts of vitamin A to meet infants’ needs for the first 6 months of life [ 38 ]. However, in people with vitamin A deficiency, the vitamin A content of breast milk is not sufficient to maintain adequate vitamin A stores in infants who are exclusively breastfed [ 38 ].

About 190 million preschool-age children (one-third of all children in this age group), mostly in Africa and Southeast Asia, have vitamin A deficiency, according to the World Health Organization [ 27 , 39 ]. They have a higher risk of visual impairment and of illness and death from childhood infections, such as measles and infections that cause diarrheal diseases [ 1 , 39 ].

The World Health Organization estimates that 9.8 million pregnant people (15% of all pregnant people) around the world, mostly in low-income and middle-income countries, have xerophthalmia as a result of vitamin A deficiency [ 40 ].

People with cystic fibrosis

Up to 90% of people with cystic fibrosis have pancreatic insufficiency, which increases their risk of vitamin A deficiency due to difficulty absorbing fat [ 1 , 41 ]. Studies in Australia and the Netherlands indicate that 2% to 13% of children and adolescents with cystic fibrosis have vitamin A deficiency [ 42 , 43 ]. As a result, standard care for cystic fibrosis includes lifelong treatment with vitamin A (daily amounts of 750 mcg RAE to 3,000 mcg RAE, depending on age, are recommended in the United States and Australia), other fat-soluble vitamins, and pancreatic enzymes [ 41 , 43 ].

Individuals with gastrointestinal disorders

Approximately one-quarter of children with Crohn’s disease and ulcerative colitis have vitamin A deficiency; adults with these disorders, especially those who have had the disorder for several years, also have a higher risk of vitamin A deficiency [ 44 , 45 ]. Although some evidence supports the use of vitamin A supplements in people with these disorders [ 46 ], other research has found that supplementation offers no benefit [ 47 ]. Some children and adults with newly diagnosed celiac disease also have vitamin A deficiency; a gluten-free diet can, but does not always, eliminate this deficiency [ 48-51 ].

Vitamin A and Health

This section focuses on three diseases and disorders in which vitamin A or carotenoids might play a role: cancer, age-related macular degeneration (AMD), and measles.

Because of its role in regulating cell growth and differentiation, several studies have examined the association between vitamin A and various types of cancer. However, the relationship between serum vitamin A levels or vitamin A supplementation and cancer risk or cancer-related death is unclear. This fact sheet does not include studies of all-trans retinoic acid, a vitamin A metabolite that is used as a drug in high doses to treat a form of leukemia [ 52 , 53 ].

Several systematic reviews and meta-analyses of observational studies have shown that higher dietary intakes of retinol, carotenoids, fruits and vegetables, or a combination are associated with a lower risk of lung cancer [ 54 ], non-Hodgkin lymphoma [ 55 ], pancreatic cancer [ 56 ], oral cavity cancer [ 57 ], laryngeal cancer [ 57 ], esophageal cancer [ 58 ], ovarian cancer [ 59 , 60 ], glioma [ 61 ], and bladder cancer [ 62 ]. However, other observational studies have found no association between intakes of different forms of vitamin A and risk of liver cancer [ 63 ], non-Hodgkin lymphoma [ 64 ], colorectal cancer [ 65 ], prostate cancer [ 65 ], or all cancers [ 66 ].

Some clinical trial evidence suggests that supplemental vitamin A might reduce the risk of certain cancers but increase the risk of other forms of cancer, cardiovascular disease morbidity and mortality, and all-cause mortality. Examples are provided below.

The Carotene and Retinol Efficacy Trial (CARET) included 18,314 male and female current and former smokers (with at least a 20 pack-year history [equivalent to smoking 1 pack per day for 20 years or 2 packs per day for 10 years, for example] of cigarette smoking) as well as some men occupationally exposed to asbestos (who also have a higher risk of lung cancer), all age 45–74 years. The study randomized participants to take supplements containing 30 mg beta-carotene plus 25,000 IU (7,500 mcg RAE) retinyl palmitate or a placebo daily for about 6 years to evaluate the potential effects on lung cancer risk [ 67 ]. The trial was ended prematurely after a mean of 4 years, partly because the supplements were unexpectedly found to have increased lung cancer risk by 28% and death from lung cancer by 46%; the supplements also increased the risk of all-cause mortality by 17%.

A subsequent study followed CARET participants for an additional 6 years after they stopped taking the study supplements [ 68 ]. During this time, the differences in lung cancer risk between the intervention and placebo groups were no longer statistically significant, with one exception: women in the intervention group had a 33% higher risk of lung cancer. In a separate analysis of CARET study data, men who took the two supplements had a 35% lower risk of nonaggressive prostate cancer during the 4-year active trial but not during the 6-year postintervention period. In contrast, men who took these two supplements in addition to another self-prescribed supplement (typically a multivitamin) had a 52% higher risk of aggressive prostate cancer during the active trial, but not during the postintervention period [ 69 ].

The Alpha-Tocopherol, Beta-Carotene (ATBC) Cancer Prevention Study also found that beta-carotene supplements increased the risk of lung cancer in smokers [ 70 ]. In this study, 29,133 male smokers age 50–69 years who smoked an average of 20.4 cigarettes a day for an average of 35.9 years took a supplement containing 50 mg/day alpha-tocopherol, 20 mg/day beta-carotene, both alpha-tocopherol and beta-carotene, or a placebo for 5–8 years. The beta-carotene supplements increased the risk of lung cancer by 18%, although they had little to no effect on the incidence of other cancers. The overall rate of death, primarily from lung cancer and ischemic heart disease, was 8% higher in participants who took beta-carotene. A subsequent study followed 25,563 of these participants for an additional 18 years [ 71 ]. During this period, participants were no longer taking the supplements, but most continued to smoke. Participants who had taken beta-carotene in the original trial did not have a higher risk of lung cancer, but they had a 20% higher risk of death due to prostate cancer.

The Age-Related Eye Disease Study 2 (AREDS2) was a 5-year randomized clinical trial with 4,203 participants age 50–85 years examining the effects on AMD of a dietary supplement containing several ingredients with or without beta-carotene (15 mg [7,500 mcg RAE]) [ 72 ]. No current smokers received the supplements containing beta-carotene. At the end of the trial, more lung cancers were discovered in the beta-carotene group than in the no beta-carotene group (23 vs. 11 cases), and 31 of the 34 affected were former smokers. In a follow-up analysis of 3,882 of the participants 5 years after the end of AREDS2 (during which they took the AREDS2 formulation containing lutein and zeaxanthin instead of beta-carotene), the increased lung cancer risk persisted, with an 82% higher risk among participants who took the supplement containing beta-carotene during the 5-year AREDS2 trial [ 73 ].

Three other clinical trials have found no relationship between taking vitamin A or beta-carotene supplements and lung cancer incidence or mortality [ 74 ]. One trial randomized 22,071 male physicians age 40–84 years to take 50 mg beta carotene on alternate days or a placebo for 12 years [ 75 ]. Eleven percent of the physicians were current smokers, and 38% were former smokers at the start of the study. The results showed no differences between the groups in number of cases of lung cancer or any malignant neoplasms or number of deaths from cancer. Another trial randomized 7,627 women (mean age 60.4 years) to take 50 mg beta-carotene on alternate days, 600 IU vitamin E on alternate days, 500 mg vitamin C daily, or a placebo for a mean of 9.4 years [ 76 ]. Fifteen percent of the women were current smokers, and 41% were former smokers at the start of the study. None of the supplements had any significant effect on total cancer incidence or cancer mortality, including from lung cancer. A third trial included 29,584 healthy men and women age 40–69 years who were living in Linxian, China, where micronutrient deficiencies are common [ 77 ]. The study randomized participants to take either a placebo or one of four vitamin and mineral combinations (including one providing retinol and zinc and another providing beta carotene, vitamin E, and selenium) for 5.25 years. The investigators followed participants for an additional 10 years after they stopped taking the supplements. The nutrient doses in the supplements were equivalent to or twice as high as U.S. recommended intakes, but the study report did not provide the exact doses. During both the intervention and follow-up periods, lung cancer death rates did not differ among the five groups, even when the investigators further analyzed the results for differences by age, sex, and smoking status.

The CARET and ATBC study results suggest that large supplemental doses of beta-carotene with or without retinyl palmitate have detrimental effects in current or former smokers and workers exposed to asbestos. However, the other studies described above that used similar vitamin A doses but had smaller proportions of current or former smokers do not raise this concern. Among nonsmokers, beta-carotene and vitamin A supplements do not appear to affect the risk of cancer.

Age-related macular degeneration

AMD is the leading cause of significant vision loss in older people [ 78 ]. AMD’s etiology involves complex interactions among genetic susceptibility, environmental factors (including exposure to oxidative stress), and normal aging [ 78 ]. Because of the role of oxidative stress in AMD pathophysiology, supplements containing carotenoids with antioxidant functions, such as beta-carotene, lutein, and zeaxanthin, might be useful for preventing or treating this condition. Lutein and zeaxanthin (which are not precursors of vitamin A), in particular, accumulate in the retina, the tissue in the eye that is damaged by AMD.

The AREDS trial found that participants with a high risk of developing advanced AMD (i.e., those who had intermediate AMD or who had advanced AMD in one eye) had a 25% lower risk of developing advanced AMD after they took a daily supplement containing beta-carotene (15 mg [7,500 mcg RAE]), vitamin E (180 mg [400 IU] dl-alpha-tocopheryl acetate), vitamin C (500 mg), zinc (80 mg), and copper (2 mg) for 5 years than participants taking a placebo [ 79 ].

The follow-up AREDS2 study confirmed the value of this supplement in reducing the progression of AMD over a median follow-up period of 5 years [ 72 ]. However, this follow-up study showed that adding lutein (10 mg) and zeaxanthin (2 mg) or omega-3 fatty acids to the formulation produced no additional benefits. Importantly, the follow-up study also revealed that beta-carotene was not a required ingredient; the original AREDS formulation without beta-carotene provided the same protective effect against developing advanced AMD.

In a more detailed analysis, participants with the lowest dietary intakes of lutein and zeaxanthin had a 26% lower risk of advanced AMD when they took a supplement containing these two carotenoids than those who did not take a supplement with these carotenoids [ 72 ]. The risk of advanced AMD was also 18% lower in participants who took the modified AREDS supplement containing lutein and zeaxanthin but not beta-carotene than in participants who took the formulation with beta-carotene but not lutein or zeaxanthin.

A subsequent study monitored dietary intakes of several nutrients in 4,504 AREDS participants and 3,738 AREDS2 participants (mean age 71 years) for a median of 10.2 years [ 80 ]. Participants in the two highest quintiles of intakes for vitamin A, beta-carotene, or lutein and zeaxanthin had a lower risk of progression to late AMD. For example, the risk of late AMD was 18% lower among those in the fifth quintile for vitamin A intake and 20% lower among those in the fourth quintile than among those in the first quintile.

At the end of the 5-year AREDS2 trial, participants were all offered the final AREDS2 formulation that included lutein and zeaxanthin in place of beta-carotene. Researchers followed up with 3,882 of these participants for an additional 5 years [ 73 ]. After 10 years, participants who had taken the AREDS2 supplement with lutein and zeaxanthin had an additional 20% reduced risk of progression to late AMD compared with those who took the supplement containing beta-carotene. This finding confirmed the benefit of replacing beta-carotene with lutein and zeaxanthin.

Individuals who have or are developing AMD should talk to their health care provider about their vitamin A intakes and the supplement formulations used in the AREDS studies.

In 2019, measles was responsible for more than 207,500 deaths around the world, mostly in young children in low-income countries [ 81 ]. A major risk factor for severe measles is vitamin A insufficiency. The World Health Organization recommends large oral doses of vitamin A for children living in areas with a high prevalence of vitamin A deficiency to prevent morbidity and mortality, including from measles [ 39 ]. Recommended doses are 30,000 mcg RAE (100,000 IU) of vitamin A once for infants age 6–11 months and 60,000 mcg RAE (200,000 IU) every 4–6 months for age 1–5 years.

In 2013, 11,200 deaths from measles were associated with vitamin A deficiency, and more than 95% of these deaths occurred in sub-Saharan Africa and south Asia. In a pooled analysis of randomized controlled trials (RCTs) within this study, vitamin A supplementation was associated with a 26% lower risk of dying from measles. However, a Cochrane Review that included six RCTs of vitamin A supplementation (15,000 mcg RAE [50,000 IU] to 60,000 mcg RAE [200,000 IU], depending on age) found that the supplementation did not affect risk of death due to measles, although it did help prevent new cases of measles [ 82 ]. These RCTs assessed the value of supplementation to prevent morbidity and mortality due to measles in a total of 19,566 children age 6 months to 5 years.

Health Risks from Excessive Vitamin A

Because vitamin A is fat soluble, the body stores excess amounts, primarily in the liver, and these levels can accumulate.

Acute vitamin A toxicity, also referred to as hypervitaminosis A, occurs within days to weeks after someone ingests one or a few very high doses (typically more than 100 times the RDA) [ 83 ]. Resulting signs and symptoms typically include severe headache, blurred vision, nausea, dizziness, aching muscles, and coordination problems. In severe cases, cerebral spinal fluid pressure can increase, leading to drowsiness and, eventually, coma and even death [ 83 ].

Chronic hypervitaminosis A (regular consumption of high doses) can cause dry skin, painful muscles and joints, fatigue, depression, and abnormal liver test results [ 83 ].

Total intakes of preformed vitamin A that exceed the UL as well as some retinoid medications used as topical therapies (such as isotretinoin, used to treat severe acne, and etretinate, a treatment for severe psoriasis) can cause congenital birth defects [ 1 ]. These birth defects can include malformations of the eye, skull, lungs, and heart [ 14 ]. Experts advise people who are or might be pregnant and those who are lactating not to take high doses (more than 3,000 mcg RAE [10,000 IU] daily) of vitamin A supplements [ 1 ].

Unlike preformed vitamin A, beta-carotene is not known to be teratogenic or lead to reproductive toxicity [ 1 ]. The most common effect of long-term, excess beta-carotene is carotenodermia, a harmless condition in which the skin becomes yellow-orange [ 3 ]. This condition can be reversed by discontinuing beta-carotene ingestion. However, the ATBC trial found that supplementation with a large amount of beta-carotene (20 mg/day), with or without 50 mg/day vitamin E, for 5–8 years increased the risk of lung cancer and mortality (mainly from lung cancer and ischemic heart disease) in male smokers [ 70 ]. The CARET trial also showed that supplementation with a large amount of beta-carotene (30 mg/day) plus 7,500 mcg RAE (25,000 IU)/day retinyl palmitate for 4–8 years in current and former smokers as well as some men occupationally exposed to asbestos increased the risk of lung cancer and death from lung cancer [ 67 ].

The FNB has not established ULs for beta-carotene and other provitamin A carotenoids [ 3 ]. However, the FNB advises against the use of beta-carotene supplements for the general population, except as a provitamin A source to prevent vitamin A deficiency.

Tolerable upper intake levels for preformed vitamin A

The FNB has established ULs for preformed vitamin A that apply to both food and supplement intakes [ 5 ]. The FNB based these ULs on the amounts associated with an increased risk of liver abnormalities in men and women, teratogenic effects, and several toxic effects in infants and children.

*These ULs apply only to products from animal sources and supplements whose vitamin A comes entirely from retinol or its ester forms, such as retinyl palmitate. However, many dietary supplements (such as multivitamins) do not provide all of their vitamin A in retinol or its ester forms. For example, the vitamin A in some supplements consists partly or entirely of beta-carotene. In such cases, the percentage of retinol or retinyl ester in the supplement should be used to determine whether an individual’s vitamin A intake exceeds the UL. For example, a supplement whose label indicates that the product contains 3,000 mcg RAE vitamin A and that 60% of this vitamin A comes from beta-carotene (and therefore 40% comes from retinol or retinyl ester) provides 1,200 mcg RAE of preformed vitamin A. That amount is above the UL for children from birth to 8 years but below the UL for older children and adults.

Interactions with Medications

Vitamin A has the potential to interact with certain medications. In addition, several types of medications might adversely affect vitamin A levels. A few examples are provided below. Individuals taking these and other medications on a regular basis should discuss their vitamin A status with their health care providers.

Orlistat (Alli, Xenical), a weight-loss treatment, can decrease the absorption of vitamin A, other fat-soluble vitamins, and beta-carotene, resulting in low plasma levels in some patients [ 84 , 85 ]. The manufacturers of Alli and Xenical recommend that patients on orlistat take a multivitamin supplement containing vitamin A and beta-carotene as well as other fat-soluble vitamins [ 86 , 87 ]. Retinoids

Several synthetic retinoids derived from vitamin A are used orally as prescription medicines. Examples include the psoriasis treatment acitretin (Soriatane) and bexarotene (Targretin), used to treat the skin effects of T-cell lymphoma. Retinoids can increase the risk of hypervitaminosis A when taken in combination with vitamin A supplements [ 85 ].

Vitamin A and Healthful Diets

The federal government’s 2020–2025 Dietary Guidelines for Americans notes that "Because foods provide an array of nutrients and other components that have benefits for health, nutritional needs should be met primarily through foods. ... In some cases, fortified foods and dietary supplements are useful when it is not possible otherwise to meet needs for one or more nutrients (e.g., during specific life stages such as pregnancy)."

The Dietary Guidelines for Americans describes a healthy eating pattern as one that

Many fruits, vegetables, and dairy products are good sources of vitamin A. Some ready-to-eat breakfast cereals are fortified with vitamin A.
Beef liver contains high amounts of vitamin A. Other sources of the nutrient include eggs and some fish.
Limits foods and beverages higher in added sugars, saturated fat, and sodium.
Limits alcoholic beverages.
Stays within your daily calorie needs.
Blaner WS. Vitamin A and Provitamin A Carotenoids. In: Marriott BP, Birt DF, Stallings VA, Yates AA, eds. Present Knowledge in Nutrition. 11th ed. Cambridge, Massachusetts: Wiley-Blackwell; 2020:73-91.
Ross A. Vitamin A. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:260-77.
Carazo A, Macakova K, Matousova K, Krcmova LK, Protti M, Mladenka P. Vitamin A update: Forms, sources, kinetics, detection, function, deficiency, therapeutic use and toxicity. Nutrients 2021;13:1703. [ PubMed abstract ]
Kedishvili NY. Enzymology of retinoic acid biosynthesis and degradation. J Lipid Res. 2013 Jul;54(7):1744-60. [ PubMed abstract ]
Zumaraga MPP, Arquiza JMRA, Concepcion MA, Perlas L, Alcudia-Catalma MN, Rodriguez M. Genotype Effects on β-Carotene Conversion to Vitamin A: Implications on Reducing Vitamin A Deficiency in the Philippines. Food Nutr Bull. 2022 Mar;43(1):25-34. [ PubMed abstract ]
Lietz G, Oxley A, Leung W, Hesketh J. Single nucleotide polymorphisms upstream from the β-carotene 15,15'-monoxygenase gene influence provitamin A conversion efficiency in female volunteers. J Nutr. 2012 Jan;142(1):161S-5S. [ PubMed abstract ]
Leung WC, Hessel S, Méplan C, Flint J, Oberhauser V, Tourniaire F, Hesketh JE, von Lintig J, Lietz G. Two common single nucleotide polymorphisms in the gene encoding beta-carotene 15,15'-monoxygenase alter beta-carotene metabolism in female volunteers. FASEB J. 2009 Apr;23(4):1041-53. [ PubMed abstract ]
Dwyer J, Saldanha L, Haggans C, Potischman N, Gahche J, Thomas P, et al. Conversions of β-carotene as vitamin A in IU to vitamin A in RAE. J Nutr 2020;150:1337. [ PubMed abstract ]
Solomons NW. Vitamin A. In: Bowman B, Russell R, eds. Present Knowledge in Nutrition. 9th ed. Washington, DC: International Life Sciences Institute; 2006:157-83.
Van Loo-Bouwman CA, Naber TH, Schaafsma G. A review of vitamin A equivalency of beta-carotene in various food matrices for human consumption. Br J Nutr 2014;111:2153-66. [ PubMed abstract ]
Berner LA, Keast DR, Bailey RL, Dwyer JT. Fortified foods are major contributors to nutrient intakes in diets of US children and adolescents. J Acad Nutr Diet 2014;114:1009-22.e8. [ PubMed abstract ]
Reboul E. Absorption of vitamin A and carotenoids by the enterocyte: focus on transport proteins. Nutrients 2013;5:3563-81. [ PubMed abstract ]
Reboul E. Mechanisms of carotenoid intestinal absorption: where do we stand? Nutrients 2019;11:838. [ PubMed abstract ]
Tanumihardjo SA, Russell RM, Stephensen CB, Gannon BM, Craft NE, Haskell MJ, et al. Biomarkers of Nutrition for Development (BOND)-Vitamin A review. J Nutr 2016;146:1816S-48S. [ PubMed abstract ]
Office of Dietary Supplements, National Institutes of Health. Dietary Supplement Label Database . 2021.
Haskell MJ. The challenge to reach nutritional adequacy for vitamin A: beta-carotene bioavailability and conversion--evidence in humans. Am J Clin Nutr 2012;96:1193s-203s. [ PubMed abstract ]
Bird JK, Murphy RA, Ciappio ED, McBurney MI. Risk of deficiency in multiple concurrent micronutrients in children and adults in the United States. Nutrients 2017;9: 655. [ PubMed abstract ]
Bailey RL, Gahche JJ, Lentino CV, Dwyer JT, Engel JS, Thomas PR, et al. Dietary supplement use in the United States, 2003-2006. J Nutr 2011;141:261-6. [ PubMed abstract ]
Wiseman EM, Bar-El Dadon S, Reifen R. The vicious cycle of vitamin a deficiency: A review. Crit Rev Food Sci Nutr 2017;57:3703-14. [ PubMed abstract ]
Stevens GA, Bennett JE, Hennocq Q, Lu Y, De-Regil LM, Rogers L, et al. Trends and mortality effects of vitamin A deficiency in children in 138 low-income and middle-income countries between 1991 and 2013: a pooled analysis of population-based surveys. Lancet Glob Health 2015;3:e528-36. [ PubMed abstract ]
Bailey RL, West KP, Jr., Black RE. The epidemiology of global micronutrient deficiencies. Ann Nutr Metab 2015;66 Suppl 2:22-33. [ PubMed abstract ]
Timoneda J, Rodriguez-Fernandez L, Zaragoza R, Marin MP, Cabezuelo MT, Torres L, et al. Vitamin A deficiency and the lung. Nutrients 2018;10:1132. [ PubMed abstract ]
Schwartz E, Zelig R, Parker A, Johnson S. Vitamin A supplementation for the prevention of bronchopulmonary dysplasia in preterm infants: an update. Nutr Clin Pract 2017;32:346-53. [ PubMed abstract ]
Darlow BA, Graham PJ. Vitamin A supplementation to prevent mortality and short and long-term morbidity in very low birthweight infants. Cochrane Database Syst Rev 2007:CD000501. [ PubMed abstract ]
Rakshasbhuvankar A, Patole S, Simmer K, Pillow JJ. Enteral vitamin A for reducing severity of bronchopulmonary dysplasia in extremely preterm infants: a randomised controlled trial. BMC Pediatr 2017;17:204. [ PubMed abstract ]
Sun H, Cheng R, Wang Z. Early vitamin A supplementation improves the outcome of retinopathy of prematurity in extermely premature infants. Retina 2020;40:1176-84. [ PubMed abstract ]
Mactier H, Weaver LT. Vitamin A and preterm infants: what we know, what we don't know, and what we need to know. Arch Dis Child Fetal Neonatal Ed 2005;90:F103-8. [ PubMed abstract ]
McCauley ME, van den Broek N, Dou L, Othman M. Vitamin A supplementation during pregnancy for maternal and newborn outcomes. Cochrane Database Syst Rev 2015:Cd008666. [ PubMed abstract ]
Haider BA, Sharma R, Bhutta ZA. Neonatal vitamin A supplementation for the prevention of mortality and morbidity in term neonates in low and middle income countries. Cochrane Database Syst Rev 2017;2:Cd006980. [ PubMed abstract ]
Ota E, da Silva Lopes K, Middleton P, Flenady V, Wariki WM, Rahman MO, et al. Antenatal interventions for preventing stillbirth, fetal loss and perinatal death: an overview of Cochrane systematic reviews. Cochrane Database Syst Rev 2020;12:Cd009599. [ PubMed abstract ]
Oliveira JM, Allert R, East CE. Vitamin A supplementation for postpartum women. Cochrane Database Syst Rev 2016;3:Cd005944. [ PubMed abstract ]
World Health Organization. Global Prevalence of Vitamin A Deficiency in Populations at Risk 1995–2005: WHO Gobal Database on Vitamin A Deficiency. Geneva: World Health Organization; 2009.
de Vries JJ, Chang AB, Bonifant CM, Shevill E, Marchant JM. Vitamin A and beta (beta)-carotene supplementation for cystic fibrosis. Cochrane Database Syst Rev 2018;8:Cd006751. [ PubMed abstract ]
Rana M, Wong-See D, Katz T, Gaskin K, Whitehead B, Jaffe A, et al. Fat-soluble vitamin deficiency in children and adolescents with cystic fibrosis. J Clin Pathol 2014;67:605-8. [ PubMed abstract ]
Woestenenk JW, Broos N, Stellato RK, Arets HG, van der Ent CK, Houwen RH. Vitamin A intake and serum retinol levels in children and adolescents with cystic fibrosis. Clin Nutr 2016;35:654-9. [ PubMed abstract ]
Fabisiak N, Fabisiak A, Watala C, Fichna J. Fat-soluble vitamin deficiencies and inflammatory bowel disease: systematic review and meta-analysis. J Clin Gastroenterol 2017;51:878-89. [ PubMed abstract ]
Rempel J, Grover K, El-Matary W. Micronutrient deficiencies and anemia in children with inflammatory bowel disease. Nutrients 2021;13:236. [ PubMed abstract ]
Santucci NR, Alkhouri RH, Baker RD, Baker SS. Vitamin and zinc status pretreatment and posttreatment in patients with inflammatory bowel disease. J Pediatr Gastroenterol Nutr 2014;59:455-7. [ PubMed abstract ]
Wright JP, Mee AS, Parfitt A, Marks IN, Burns DG, Sherman M, et al. Vitamin A therapy in patients with Crohn's disease. Gastroenterology 1985;88:512-4. [ PubMed abstract ]
Tokgöz Y, Terlemez S, Karul A. Fat soluble vitamin levels in children with newly diagnosed celiac disease, a case control study. BMC Pediatr 2018;18:130. [ PubMed abstract ]
Wierdsma NJ, van Bokhorst-de van der Schueren MAE, Berkenpas M, Mulder CJJ, van Bodegraven AA. Vitamin and mineral deficiencies are highly prevalent in newly diagnosed celiac disease patients. Nutrients 2013;5:3975-92. [ PubMed abstract ]
McGrogan L, Mackinder M, Stefanowicz F, Aroutiounova M, Catchpole A, Wadsworth J, et al. Micronutrient deficiencies in children with coeliac disease; a double-edged sword of both untreated disease and treatment with gluten-free diet. Clin Nutr 2021;40:2784-90. [ PubMed abstract ]
Shepherd SJ, Gibson PR. Nutritional inadequacies of the gluten-free diet in both recently-diagnosed and long-term patients with coeliac disease. J Hum Nutr Diet 2013;26:349-58. [ PubMed abstract ]
Wang ZY, Chen Z. Acute promyelocytic leukemia: from highly fatal to highly curable. Blood 2008;111:2505-15. [ PubMed abstract ]
Lo-Coco F, Avvisati G, Vignetti M, Thiede C, Orlando SM, Iacobelli S, et al. Retinoic acid and arsenic trioxide for acute promyelocytic leukemia. N Engl J Med 2013;369:111-21. [ PubMed abstract ]
Rowles JL, 3rd, Ranard KM, Smith JW, An R, Erdman JW, Jr. Increased dietary and circulating lycopene are associated with reduced prostate cancer risk: a systematic review and meta-analysis. Prostate Cancer Prostatic Dis 2017;20:361-77. [ PubMed abstract ]
Chen F, Hu J, Liu P, Li J, Wei Z, Liu P. Carotenoid intake and risk of non-Hodgkin lymphoma: a systematic review and dose-response meta-analysis of observational studies. Ann Hematol 2017;96:957-65. [ PubMed abstract ]
Chen J, Jiang W, Shao L, Zhong D, Wu Y, Cai J. Association between intake of antioxidants and pancreatic cancer risk: a meta-analysis. International Journal of Food Sciences and Nutrition 2016;67:744-53. [ PubMed abstract ]
Leoncini E, Nedovic D, Panic N, Pastorino R, Edefonti V, Boccia S. Carotenoid intake from natural sources and head and neck cancer: a systematic review and meta-analysis of epidemiological studies. Cancer Epidemiol Biomarkers Prev 2015;24:1003-11. [ PubMed abstract ]
Li H, He P, Lin T, Guo H, Li Y, Song Y, et al. Association between plasma retinol levels and the risk of all-cause mortality in general hypertensive patients: A nested case-control study. J Clin Hypertens (Greenwich) 2020;22:906-13. [ PubMed abstract ]
Li X, Xu J. Meta-analysis of the association between dietary lycopene intake and ovarian cancer risk in postmenopausal women. Scientific reports 2014;4:4885. [ PubMed abstract ]
Wang Q, He C. Dietary vitamin A intake and the risk of ovarian cancer: a meta-analysis. Biosci Rep 2020;40. [ PubMed abstract ]
Lv W, Zhong X, Xu L, Han W. Association between dietary vitamin A Intake and the risk of glioma: evidence from a meta-analysis. Nutrients 2015;7:8897-904. [ PubMed abstract ]
Tang JE, Wang RJ, Zhong H, Yu B, Chen Y. Vitamin A and risk of bladder cancer: a meta-analysis of epidemiological studies. World J Surg Oncol 2014;12:130. [ PubMed abstract ]
Leelakanok N, D'Cunha RR, Sutamtewagul G, Schweizer ML. A systematic review and meta-analysis of the association between vitamin A intake, serum vitamin A, and risk of liver cancer. Nutr Health 2018;24:121-31. [ PubMed abstract ]
Psaltopoulou T, Ntanasis-Stathopoulos I, Tsilimigras DI, Tzanninis IG, Gavriatopoulou M, Sergentanis TN. Micronutrient intake and risk of hematological malignancies in adults: a systematic review and meta-analysis of cohort studies. Nutr Cancer 2018;70:821-39. [ PubMed abstract ]
Wang X, Yang H-H, Liu Y, Zhou Q, Chen Z-H. Lycopene consumption and risk of colorectal cancer: a meta-analysis of observational studies. Nutrition and Cancer 2016;68:1083-96. [ PubMed abstract ]
Aune D, Keum N, Giovannucci E, Fadnes LT, Boffetta P, Greenwood DC, et al. Dietary intake and blood concentrations of antioxidants and the risk of cardiovascular disease, total cancer, and all-cause mortality: a systematic review and dose-response meta-analysis of prospective studies. Am J Clin Nutr 2018;108:1069-91. [ PubMed abstract ]
Omenn GS, Goodman GE, Thornquist MD, Balmes J, Cullen MR, Glass A, et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med 1996;334:1150-5. [ PubMed abstract ]
Goodman GE, Thornquist MD, Balmes J, Cullen MR, Meyskens FL, Omenn GS, et al. The beta-carotene and retinol efficacy trial: incidence of lung cancer and cardiovascular disease mortality during 6-year follow-up after stopping β-carotene and retinol supplements. J Natl Cancer Inst 2004;96:1743-50. [ PubMed abstract ]
Neuhouser ML, Barnett MJ, Kristal AR, Ambrosone CB, King IB, Thornquist M, et al. Dietary supplement use and prostate cancer risk in the Carotene and Retinol Efficacy Trial. Cancer Epidemiol Biomarkers Prev 2009;18:2202-6. [ PubMed abstract ]
The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study Group. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med 1994;330:1029-35. [ PubMed abstract ]
Virtamo J, Taylor PR, Kontto J, Männistö S, Utriainen M, Weinstein SJ, et al. Effects of α-tocopherol and β-carotene supplementation on cancer incidence and mortality: 18-year postintervention follow-up of the Alpha-tocopherol, Beta-carotene Cancer Prevention Study. International journal of cancer 2014;135:178-85. [ PubMed abstract ]
Age-Related Eye Disease Study 2 Research Group. Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. JAMA 2013;309:2005-15. [ PubMed abstract ]
Chew EY, Clemons TE, Agron E, Domalpally A, Keenan TDL, Vitale S, Weber C, Smith DC, Christen W, for the AREDS2 Research group. Long-term outcomes of adding Lutein/Zeaxanthin and Omega-3 Fatty Acids to the AREDS Supplements on Age-Related Macular Degeneration Progression: AREDS2 Report #28. JAMA Ophthalmology. June 2, 2022. [ PubMed abstract ]
Cortes-Jofre M, Rueda JR, Asenjo-Lobos C, Madrid E, Bonfill Cosp X. Drugs for preventing lung cancer in healthy people. Cochrane Database Syst Rev 2020;3:Cd002141. [ PubMed abstract ]
Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, et al. Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease. The New England journal of medicine 1996;334:1145-9. [ PubMed abstract ]
Lin J, Cook NR, Albert C, Zaharris E, Gaziano JM, Van Denburgh M, et al. Vitamins C and E and beta carotene supplementation and cancer risk: a randomized controlled trial. J Natl Cancer Inst 2009;101:14-23. [ PubMed abstract ]
Kamangar F, Qiao YL, Yu B, Sun XD, Abnet CC, Fan JH, et al. Lung cancer chemoprevention: a randomized, double-blind trial in Linxian, China. Cancer Epidemiol Biomarkers Prev 2006;15:1562-4. [ PubMed abstract ]
Fleckenstein M, Keenan TDL, Guymer RH, Chakravarthy U, Schmitz-Valckenberg S, Klaver CC, et al. Age-related macular degeneration. Nat Rev Dis Primers 2021;7:31. [ PubMed abstract ]
Age-Related Eye Disease Study Research Group. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Arch Ophthalmol 2001;119:1417-36. [ PubMed abstract ]
Agron E, Mares J, Clemons TE, Swaroop A, Chew EY, Keenan TDL. Dietary nutrient intake and progression to late age-related macular degeneration in the Age-Related Eye Disease Studies 1 and 2. Ophthalmology 2021;128:425-42. [ PubMed abstract ]
Patel M, Lee AD, Redd SB, Clemmons NS, McNall RJ, Cohn AC, et al. Increase in measles cases - United States, January 1-April 26, 2019. MMWR Morb Mortal Wkly Rep 2019;68:402-4. [ PubMed abstract ]
Imdad A, Mayo-Wilson E, Herzer K, Bhutta ZA. Vitamin A supplementation for preventing morbidity and mortality in children from six months to five years of age. Cochrane Database Syst Rev 2017;3:Cd008524. [ PubMed abstract ]
National Institute of Diabetes and Digestive and Kidney Diseases. LiverTox: Clinical and research information on drug-induced liver injury . 2020.
Zhi J, Melia AT, Koss-Twardy SG, Arora S, Patel IH. The effect of orlistat, an inhibitor of dietary fat absorption, on the pharmacokinetics of beta-carotene in healthy volunteers. J Clin Pharmacol 1996;36:152-9. [ PubMed abstract ]
Ulbricht C, Basch E, Chao W, Conquer J, Costa D, Culwell S, et al. An evidence-based systematic review of vitamin A by the natural standard research collaboration. J Diet Suppl 2012;9:299-416. [ PubMed abstract ]

This fact sheet by the National Institutes of Health (NIH) Office of Dietary Supplements (ODS) provides information that should not take the place of medical advice. We encourage you to talk to your health care providers (doctor, registered dietitian, pharmacist, etc.) about your interest in, questions about, or use of dietary supplements and what may be best for your overall health. Any mention in this publication of a specific product or service, or recommendation from an organization or professional society, does not represent an endorsement by ODS of that product, service, or expert advice.

Updated: December 15, 2023 History of changes to this fact sheet

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Vitamin a deficiency-related disorders.

Retinol activity equivalents (RAE)
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Diseases of the skin, retinitis pigmentosa, supplements.

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Vitamin A is a generic term that refers to fat-soluble compounds found as preformed vitamin A (retinol) in animal products and as provitamin A carotenoids in fruit and vegetables . The three active forms of vitamin A in the body are retinol, retinal, and retinoic acid. (More information)
Vitamin A is involved in regulating the growth and specialization ( differentiation ) of virtually all cells in the human body. Vitamin A has important roles in embryonic development, organ formation during fetal development, normal immune functions, and eye development and vision. (More information)
Vitamin A deficiency is a major cause of preventable blindness in the world. It is most prevalent among children and women of childbearing age. Vitamin A deficiency is associated with an increased susceptibility to infections, as well as to thyroid and skin disorders. (More information)
The recommended dietary allowance ( RDA ) is 700 micrograms of retinol activity equivalents (μg RAE)/day for women and 900 μg RAE/day for men. (More information)
Vitamin A prophylaxis appears to significantly reduce childhood mortality (especially from diarrheal illnesses) in regions at high risk of vitamin A deficiency. Further, high-dose vitamin A supplementation is widely recommended for children over six months of age when they are infected with measles while malnourished, immunodeficient, or are at risk of measles complications. ( More information)
Retinoic acid and analogs are used at pharmacological doses in the treatment of acute promyelocytic leukemia and various skin diseases. (More information)
Animal food sources rich in preformed vitamin A include dairy products, fortified cereal, liver, and fish oils. Rich sources of provitamin A carotenoids include orange and green vegetables, such as sweet potato and spinach. (More information)
Overconsumption of preformed vitamin A can be highly toxic and is especially contraindicated prior to and during pregnancy as it can result in severe birth defects. The tolerable upper intake level ( UL ) for vitamin A in adults is set at 3,000 μg RAE/day. The UL does not apply to vitamin A derived from carotenoids. (More information)

Vitamin A is a generic term that encompasses a number of related compounds ( Figure 1 ). Retinol and retinyl esters are often referred to as preformed vitamin A. Retinol can be converted by the body to retinal, which can be in turn be oxidized to retinoic acid, the form of vitamin A known to regulate gene transcription . Retinol, retinal, retinoic acid, and related compounds are known as retinoids. β-Carotene and other food carotenoids that can be converted by the body into retinol are referred to as provitamin A carotenoids (see the article on Carotenoids ). Hundreds of different carotenoids are synthesized by plants, but only about 10% of them are capable of being converted to retinol (1) . The following discussion will focus mainly on preformed vitamin A compounds and retinoic acid.

Vitamin A compounds are essential fat-soluble molecules predominantly stored in the liver in the form of retinyl esters (e.g., retinyl palmitate). When appropriate, retinyl esters are hydrolyzed to generate all- trans -retinol, which binds to retinol binding protein (RBP) before being released in the bloodstream. The all- trans -retinol/RBP complex circulates bound to the protein, transthyretin, which delivers all-trans-retinol to peripheral tissues (reviewed in 2 ). Vitamin A as retinyl esters in chylomicrons was also found to have an appreciable role in delivering vitamin A to extrahepatic tissues, especially in early life (3, 4) .

Located at the back of the eye, the retina contains two main types of light-sensitive receptor cells — known as rod and cone photoreceptor cells. Photons (particles of light) that pass through the lens are sensed by the photoreceptor cells of the retina and converted to nerve impulses (electric signals) for interpretation by the brain. All- trans -retinol is transported to the retina via the circulation and accumulates in retinal pigment epithelial cells ( Figure 2 ) (5) . Here, all- trans -retinol is esterified to form a retinyl ester, which can be stored. When needed, retinyl esters are broken apart ( hydrolyzed ) and isomerized to form 11- cis -retinol, which can be oxidized to form 11- cis -retinal. 11- cis -retinal can be shuttled across the interphotoreceptor space to the rod photoreceptor cell that is specialized for vision in low-light conditions and for detection of motion. In rod cells, 11- cis -retinal binds to a protein called opsin to form the visual pigment rhodopsin (also known as visual purple). Absorption of a photon of light catalyzes the isomerization of 11- cis -retinal to all- trans -retinal that is released from the opsin molecule. This photoisomerization triggers a cascade of events, leading to the generation of a nerve impulse conveyed by the optic nerve to the brain’s visual cortex. All- trans -retinal is converted to all- trans -retinol and transported across the interstitial space to the retinal pigment epithelial cells, thereby completing the visual cycle.

A similar cycle occurs in cone cells that contain red, green, or blue opsin proteins required for the absorption of photons from the visible light spectrum (2) . Vitamin A is also essential for mammalian eye development (6) . Thus, because vitamin A is required for the normal functioning of the retina, dim-light vision, and color vision, inadequate retinol and retinal available to the retina result in impaired dark adaptation. In the severest cases of vitamin A deficiency, thinning and ulceration of the cornea leads to blindness (see Deficiency ).

Regulatory capacity of retinoic acid

In cells, all- trans -retinol can be either stored (in the form of retinyl ester) or oxidized to all- trans -retinal by alcohol dehydrogenases. In turn, retinaldehyde dehydrogenases can catalyze the conversion of all- trans -retinal into two biologically active isomers of retinoic acid (RA): all- trans -RA and 9- cis -RA. RA isomers act as hormones to affect gene expression and thereby influence numerous physiological processes. All- trans -RA and 9- cis -RA are transported to the nucleus of the cell bound to cellular retinoic acid-binding proteins (CRABP). Within the nucleus, RA isomers bind to specific nuclear receptor proteins that are ligand -dependent transcription factors . In vitro studies have indicated that both all- trans -RA and 9- cis -RA can bind to retinoic acid receptors (RARα, RARβ, and RARγ) and that 9- cis -RA can bind to retinoid X receptors (RXR) (7) . RAR and RXR subtypes form either complexes of two of the same protein (RAR/RAR and RXR/RXR homodimers ) or complexes of two different proteins (RAR/RXR heterodimers ). RAR/RXR heterodimers can bind to a regulatory DNA sequence called retinoic acid response element (RARE) located within the promoter of retinoid-responsive genes . The transcriptional activity of RAR/RXR heterodimers appears to be mainly driven by the binding of all- trans -RA to RAR.

The activation of RAR by RA binding triggers the recruitment of transcriptional coregulators to target promoters, thereby inhibiting or allowing the transcription of genes (8) . RXR also forms heterodimers with several other nuclear receptors, including thyroid hormone receptor, vitamin D receptor, steroid receptors, and peroxisome proliferator-activated receptor (PPAR) (9) . In this way, vitamin A may interact with thyroid hormone, vitamin D , steroids (e.g., estrogen ), or PPAR ligands signaling pathways and influence the transcription of a broad range of genes.

There is also evidence that RA/RAR can affect gene expression in a RARE-independent manner. For example, it was reported that RAR could interfere with TGFβ/Smad signaling pathway through direct interaction of RAR with the heterodimeric transcription factor, Smad3/Smad4. In the absence of RA, RAR was found to act as a coactivator of Smad3/Smad4-mediated transcription, while RAR agonists repressed the transcriptional activity of Smad3/Smad4 (10) . In retinoblastoma cells, RAR was also involved in RA-induced activation of signaling cascades mediated by tyrosine kinases known as phosphoinositide 3-kinase (PI3K) and leading to cell differentiation (11, 12) . RA also appeared to induce neuronal differentiation by activating ERK1/2 MAP kinase signaling pathway that phosphorylated transcription factor, CREB (cyclic AMP response element binding protein). Phosphorylated CREB can subsequently bind to the CREB response element in the promoter of genes involved in cell differentiation (13) . Also, independently of RAR, RA was found to inhibit ERK1/2 phosphorylation/activation and subsequent AP1-mediated expression of interleukin-6 in synovial cells (14) . Hence, RA can influence the expression of genes whose promoters do not contain RARE.

By regulating the expression of over 500 retinoid-responsive genes (including several genes involved in vitamin A metabolism itself), retinoic acid isomers play major roles in cellular proliferation and differentiation (i.e., cell commitment to highly specialized functions).

Regulatory capacity of retinol

In the eye and tissues like white adipose and muscle, retinol plasma membrane receptor /transporter STRA6 accepts retinol from extracellular RBP and unloads it to intracellular retinol-binding protein (CRBP). STRA6 also cooperates with lecithin:retinol acyltransferase (LRAT), an enzyme that catalyzes retinol esterification and storage, to maintain an inward concentration gradient of retinol (15) . Interestingly, retinol uptake by STRA6 was found to trigger the activation of a signaling cascade mediated by tyrosine kinases known as Janus kinases (JAK) and associated transcription factors (STAT). JAK/STAT signaling pathway regulates the expression of a wide range of cytokines , hormones , and growth factors (16) . Animal studies have reported that an increased expression of genes , such as SOCS3 by the JAK/STAT pathway, could result in the inhibition of insulin signaling. Hence, obese mice lacking LRAT or STRA6 appear to be protected from retinol/STRA6-induced insulin resistance (17, 18) .

Regulatory capacity of retinal

Apart from its role as a ligand for opsin in the visual cascade (see Visual system and eyesight ), retinal has been specifically implicated in the regulation of genes important for lipid metabolism . In humans, two types of adipose tissue have been distinguished based on their respective functions: white adipose tissue (WAT) stores fatty acids as triglycerides , and brown adipose tissue (BAT) oxidizes fatty acids to generate heat (thermogenesis). In the mitochondrial respiratory chain of brown adipose cells, the processes of electron transport and ATP production are uncoupled (dissociated) to permit the rapid production of heat from fatty acid oxidation (19) .

Retinaldehyde dehydrogenase 1 (RALDH1), which converts retinal to retinoic acid, is highly expressed in WAT but not in BAT. The suppression of RALDH1 expression in WAT can induce a thermogenic phenotype resembling that of BAT (20) . During adipocyte differentiation, the stimulation of cells with all- trans retinal has been found to activate the UCP1 gene required for thermogenesis while inhibiting genes promoting adipogenesis, such as PPARγ (20) . Retinal also appeared to regulate lipid metabolism and adiposity in bone marrow by inhibiting PPARγ/RXR heterodimer -mediated gene expression (21) . In addition, retinal was found to inhibit gluconeogenic gene expression and glucose production in the liver of mice deficient in RALDH1 (22) .

Vitamin A was initially coined "the anti-infective vitamin " because of its importance in the normal functioning of the immune system (23) . The skin and mucosal cells, lining the airways, digestive tract, and urinary tract function as a barrier and form the body's first line of defense against infection. Retinoic acid (RA) is produced by antigen -presenting cells (APCs), including macrophages and dendritic cells , found in these mucosal interfaces and associated lymph nodes. RA appears to act on dendritic cells themselves to regulate their differentiation , migration, and antigen-presenting capacity. In addition, the production of RA by APCs is required for the differentiation of naïve CD4 T- lymphocytes into induced regulatory T-lymphocytes (Tregs). Critical to the maintenance of mucosal integrity, the differentiation of Tregs is driven by all- trans -RA through RARα-mediated regulation of gene expression (see Regulation of gene expression ). Also, during inflammation , all- trans -RA/RARα signaling pathway promotes the conversion of naïve CD4 T-lymphocytes into effector T-lymphocytes — type 1 helper T-cells (Th1) — (rather than into Tregs) and induces the production of proinflammatory cytokines by effector T-lymphocytes in response to infection.

A recent meta-analysis of randomized , placebo -controlled trials found that vitamin A supplementation decreased serum concentrations of TNF-α (5 studies) and IL-6 (9 studies) but increased serum C-reactive protein (CRP) concentrations (9 studies) (24) . There is also substantial evidence to suggest that RA may help prevent the development of autoimmunity (reviewed in 25 ).

Both vitamin A excess and deficiency are known to cause birth defects. Retinoid signaling begins soon after the early phase of embryonic development known as gastrulation. During fetal development, RA is critical for the development of organs, including the heart, eyes, ears, lungs, as well as other limbs and visceral organs. Vitamin A has been implicated in fetal lung maturation (2) . Vitamin A status is lower in preterm newborns than in full-term infants (26) . There is some evidence to suggest that vitamin A supplementation may help reduce the incidence of chronic lung disease and mortality in preterm newborns (see Disease Prevention ). Retinoid signaling is also involved in the expression of many proteins of the extracellular matrix (ECM; material surrounding cells), including collagen , laminin, and proteoglycans (27) . Vitamin A deficiency may then result in alterations of the ECM composition, thus disrupting organ morphology and function (reviewed in 27 ).

Red blood cell production (erythropoiesis)

Red blood cells ( erythrocytes ), like all blood cells, are derived from pluripotent stem cells in the bone marrow. Studies involving in vitro culture systems have suggested a role for retinoids in stem cell commitment and differentiation to the red blood cell lineage. Retinoids might also regulate apoptosis (programmed cell death) of red blood cell precursors (erythropoietic progenitor cells) (28) . However, whether retinoids regulate erythropoiesis in vivo has not been established. Yet, vitamin A supplementation in vitamin A deficient-individuals has been shown to increase hemoglobin concentrations. Additionally, vitamin A appears to facilitate the mobilization of iron from storage sites to the developing red blood cell for incorporation into hemoglobin, the oxygen carrier in red blood cells (28, 29) .

Zinc deficiency is thought to interfere with vitamin A metabolism in several ways (30) : (1) zinc deficiency results in decreased synthesis of retinol-binding protein (RBP), which transports retinol through the circulation to peripheral tissues and protects the organism against potential toxicity of retinol; (2) zinc deficiency results in decreased activity of the enzyme that releases retinol from its storage form, retinyl palmitate, in the liver; and (3) zinc is required for the enzyme that converts retinol into retinal (31) . The health consequences of zinc deficiency on vitamin A nutritional status in humans are yet to be defined (30) .

Vitamin A deficiency often coexists with iron deficiency and may exacerbate iron deficiency anemia by altering iron metabolism (28) . Vitamin A supplementation has beneficial effects on iron deficiency anemia and improves iron nutritional status among children and pregnant women (28, 29 , 32) . The combination of supplemental vitamin A and iron seems to reduce anemia more effectively than either supplemental iron or vitamin A alone (33) . Moreover, studies in rats have shown that vitamin A deficiency interferes with erythropoiesis (34) and iron deficiency also alters plasma and liver levels of vitamin A (35, 36) .

Vitamin A deficiency usually results from inadequate intakes of vitamin A from animal products (as preformed vitamin A) and fruit and vegetables (as provitamin A carotenoids). In developing countries, vitamin A deficiency and associated disorders predominantly affect children and women of reproductive age. Other individuals at risk of vitamin A deficiency are those with poor absorption of lipids due to impaired pancreatic or biliary secretion and those with inflammatory bowel diseases , such as Crohn’s disease and celiac disease (2) .

Subclinical vitamin A deficiency is often defined by serum retinol concentrations lower than 0.70 μmol/L (20 μg/dL). In severe vitamin A deficiency, vitamin A body stores are depleted and serum retinol concentrations fall below 0.35 μmol/L (10 μg/dL). Other biomarkers have been calibrated to assess vitamin A nutritional status (reviewed in 37 ). Of note, the World Health Organization considers vitamin A deficiency in a population to be a moderate public health problem when the prevalence of low serum retinol (<0.70 μmol/L) among children ages 6-71 months is at least 10% but less than 20% and a severe public health problem when the prevalence is 20% or greater (38) .

Disease of the eye and blindness

With an estimated 250,000 to 500,000 children becoming blind annually, vitamin A deficiency constitutes the leading preventable cause of blindness in low- and middle-income nations (39) . The earliest symptom of vitamin A deficiency is impaired dark adaptation known as night blindness or nyctalopia. The next clinical stage is the occurrence of abnormal changes in the conjunctiva (corner of the eye), manifested by the presence of Bitot's spots. Severe or prolonged vitamin A deficiency eventually results in a condition called xerophthalmia (Greek for dry eye), characterized by changes in the cells of the cornea (clear covering of the eye) that ultimately result in corneal ulcers, scarring, and blindness (40) . Immediate administration of 200,000 international units (IU; 60 mg RAE) of vitamin A for two consecutive days is required to prevent blinding xerophthalmia (40) .

There is an estimated 19.1 million pregnant women worldwide (especially in Sub-Saharan Africa, Southeast Asia, and Central America) with vitamin A deficiency and over half of them are affected by night blindness (41) . The prevalence of vitamin A deficiency and night blindness is especially high during the third trimester of pregnancy due to accelerated fetal growth. Prenatal vitamin A supplementation lowers the risk of maternal night blindness (42) . Approximately 190 million preschool-age children have low serum retinol concentrations (<0.70 μmol/L), with 5.2 million suffering from night blindness. Moreover, half of the children affected by severe vitamin A deficiency-induced blinding xerophthalmia are estimated to die within a year of becoming blind (41) . The World Health Organization (WHO) and the United Nations Children’s Fund (UNICEF) promote vitamin A supplementation as a public health intervention to reduce child mortality in areas and populations where vitamin A deficiency is prevalent (see the section on Childhood morbidity and mortality ) (43) .

Susceptibility to infectious diseases

Infectious diseases have been associated with depletion of vitamin A hepatic reserves (already limited in vitamin A-deficient subjects), reduced serum retinol concentrations, and increased loss of vitamin A in the urine (41) . Infection with the measles virus was found to precipitate conjunctival and corneal damage, leading to blindness in children with poor vitamin A status (44) . Conversely, vitamin A deficiency can be considered a nutritionally acquired immunodeficiency disease (45) . Even children who are only mildly deficient in vitamin A have a higher incidence of respiratory complications and diarrhea, as well as a higher rate of mortality from measles infection compared to children consuming sufficient vitamin A (46) . Because vitamin A supplementation may decrease both the severity and incidence of measles complications in developing countries (see Disease Prevention ), WHO recommends that children aged at least one year receive 200,000 IU of vitamin A (60 mg RAE) for two consecutive days in addition to standard treatment when they are infected with measles virus and live in areas of vitamin A deficiency (47) .

A prospective cohort study , conducted in 2,774 Colombian children (ages, 5-12 years old) followed for a median 128 days, also reported an inverse relationship between plasma retinol concentrations and rates of diarrhea with vomiting and cough with fever, the latter being a strong predictor of influenza infection (flu) (48) . A review of five randomized , placebo -controlled studies that included 7,528 HIV -positive pregnant or breast-feeding women found no substantial benefit of vitamin A supplementation in reducing the mother-to-child transmission of HIV (49) . One early observational study found that HIV-infected women who were vitamin A deficient were three to four times more likely to transmit HIV to their infants (50) . Yet, no trial to date has provided any information on potential adverse effects of vitamin A supplementation on mother-to-child HIV transmission (51) .

Thyroid dysfunction

In North and West Africa, vitamin A deficiency and iodine deficiency induced- goiter can coexist in up to 50% of children. The response to iodine prophylaxis in iodine-deficient populations appears to depend on various nutritional factors, including vitamin A status (52, 53) . Vitamin A deficiency in animal models was found to interfere with the pituitary - thyroid axis by (1) increasing the synthesis and secretion of thyroid-stimulating hormone (TSH) by the pituitary gland, (2) increasing the size of the thyroid gland, (3) reducing iodine uptake by the thyroid gland and impairing the synthesis and iodination of thyroglobulin, and (4) increasing circulating concentrations of thyroid hormones (reviewed in 54, 55 ). A cross-sectional study of 138 children with concurrent vitamin A and iodine deficiencies found that the severity of vitamin A deficiency was associated with higher risk of goiter and higher concentrations of circulating TSH and thyroid hormones (53) . These children received iodine-enriched salt with either vitamin A (200,000 IU [60 mg RAE] at baseline and 5 months) or placebo in a randomized , double-blind , 10-month trial. This vitamin A supplementation significantly decreased TSH concentration and thyroid volume compared to placebo (53) . In another trial, supplementation of vitamin A to iodine-deficient children had no additional effect to iodine on thyroid status compared to placebo, but vitamin A supplementation alone (without iodine) reduced the volume of the thyroid gland, as well as TSH and thyroglobulin concentrations (56) .

Other disorders

Phrynoderma or follicular hyperkeratosis is a skin condition characterized by an excessive production of keratin in hair follicles. The lesions first appear on the extremities, shoulders, and buttocks and may spread over the entire body in the severest cases (57) . While vitamin A deficiency may contribute to the occurrence of phrynoderma, the condition has been strongly associated with multiple nutritional deficiencies and is considered a sign of general malnutrition. A rare case of esophagitis ( inflammation of the esophagus ) has been attributed to hyperkeratosis secondary to vitamin A deficiency (58) .

Also, vitamin A deficiency affects iron mobilization, impairs hemoglobin synthesis , and precipitates iron deficiency anemia that is only alleviated with supplementation of both vitamin A and iron (see Nutrient interactions ) (28) .

The Recommended Dietary Allowance (RDA)

Retinol activity equivalents (rae).

Vitamin A can be obtained from food as preformed vitamin A in animal products or as provitamin A carotenoids in fruit and vegetables (see Food sources ). Yet, while preformed vitamin A is effectively absorbed, stored, and hydrolyzed to form retinol, provitamin A carotenoids like β-carotene are less easily digested and absorbed, and must be converted to retinol and other retinoids by the body after uptake into the small intestine. The efficiency of conversion of provitamin A carotenes into retinol is highly variable, depending on factors such as food matrix, food preparation, and one’s digestive and absorptive capacities (59) .

The most recent international standard of measure for vitamin A is retinol activity equivalents (RAE), which represent vitamin A activity as retinol. It has been determined that 2 micrograms (μg) of β-carotene in oil provided as a supplement could be converted by the body to 1 μg of retinol giving it an RAE ratio of 2:1. However, 12 μg of β-carotene from food are required to provide the body with 1 μg of retinol, giving dietary β-carotene an RAE ratio of 12:1. Other provitamin A carotenoids in food are less easily absorbed than β-carotene, resulting in RAE ratios of 24:1. RAE ratios are shown in Table 1 (60) .

Determination of the RDA

The RDA for vitamin A was revised by the Food and Nutrition Board of the US National Academy of Medicine in 2001. The RDA is based on the Estimated Average Requirement ( EAR ), which is defined as the biological requirement for 50% of the population. The RDA is the recommended intake needed by nearly all of the population to ensure adequate hepatic stores of vitamin A in the body (20 μg/g for four months if the person consumes a vitamin A-deficient diet) to support normal reproductive function, immune function, gene expression , and vision (for details of calculations, see 60 ). Table 2 lists the RDA values in micrograms (μg) of Retinol Activity Equivalents (RAE) per day.

Disease Prevention

Preterm infants are born with inadequate body stores of vitamin A, placing them at risk of developing diseases of the eye and the respiratory and gastrointestinal tracts. About one-third of preterm infants born between 22 and 28 weeks of gestation develop bronchopulmonary dysplasia (BPD), a chronic lung disease that can be fatal or result in life-long morbidities in survivors. A few randomized controlled trials have investigated the effect of postnatal vitamin A administration on the incidence of BPD and the risk of mortality in very low birth weight infants (VLBW; ≤1,500 g) requiring respiratory support (61-63) . In the largest, multicenter, randomized, blinded, placebo -controlled trial that enrolled 807 extremely low birth weight (ELBW; ≤1,000 g) preterm newborns, the intramuscular administration of 5,000 IU (1,500 μg RAE) of vitamin A three times a week for four weeks significantly, though modestly, reduced the risk of BPD or death at 36 weeks’ postmenstrual age (gestational age plus chronological age) (62) . While vitamin A supplementation was included in some neonatal programs after this trial (64) , a national shortage in vitamin A supply that has affected US neonatal intensive care units since 2010 has led to a significant reduction in the use of vitamin A supplementation in premature newborns (401-1,000 g at birth) with respiratory failure (65, 66) . However, a retrospective analysis of US nationwide data from 6,210 preterm infants born between 2010 and 2012 found that a reduction in vitamin A prophylaxis from 27.2% to 2.1% during the same period had no significant impact on the incidence of BPD or death before hospital discharge (66) . A Cochrane review that pooled six randomized controlled trials in VLBW (≤1,500 g) or premature (less than 32 weeks' gestation) infants found vitamin A administration (5 trials of intramuscular administration and one trial or oral administration) only slightly reduced the risk of chronic lung disease or death at 28 days post birth ( RR , 0.93; 95% CI , 0.88-0.99) (67) .

In a retrospective study, the nonrandomized use of vitamin A supplementation with inhaled nitric oxide (iNO) was found to result in a lower incidence of BPD (but not mortality) compared to iNO therapy alone in preterm newborns with a birth weight of 750-999 g (68) . Neurodevelopment index scores at one year of age were also improved in the vitamin A group of newborns weighing 500-749 g at birth. Yet, caution is advised with the interpretation of the results, especially because the trial was not designed to assess the effect of vitamin A. In Germany, a large, multicenter, randomized study — the NeoVitaA trial — is underway to explore the effect of high-dose oral vitamin A (5,000 IU/kg/day) for 28 days on the incidence of BPD and mortality at 36 weeks' postmenstrual age (69, 70) .

While high doses of vitamin A during early pregnancy can cause birth defects (see Safety ), vitamin A supplementation during late pregnancy may improve maternal and fetal vitamin A status (71) . However, it is not known whether vitamin A supplementation during pregnancy might reduce BPD incidence in infants.

Childhood morbidity and mortality

A 2022 Cochrane review and meta-analysis of randomized controlled trials evaluating the preventive effect of vitamin A on childhood mortality indicated that high-dose vitamin A supplementation in children ages 6 to 59 months reduced all-cause mortality by 12% (19 studies) and diarrhea-specific mortality by 12% (9 studies) (72) . However, vitamin A administration in this age group had no preventive effect on mortality from respiratory disease (9 studies), measles (6 studies), or meningitis (3 studies). However, in this pooled analysis, vitamin A supplementation reduced the incidence of diarrhea by 15% (15 studies), measles by 50% (6 studies), Bitot’s spots by 58% (5 studies) and night blindness by 68% (2 studies) but had no effect on the incidence of respiratory disease (72) .

Current WHO policy recommends vitamin A supplementation at routine vaccination contacts in children after six months of age living in regions at high risk of vitamin A deficiency (73) . Supplementation with high doses of vitamin A — 100,000 IU (30 mg RAE) for infants 6 to 11 months of age and 200,000 IU (60 mg RAE) for children 12 to 59 months of age — is thought to provide adequate protection for up to six months (74) . See the WHO website for the current guidelines. Because beneficial effects are lacking, WHO does not recommend vitamin A supplementation in the neonatal period (in the 28 days following birth) (75) or in children under 6 months of age (reviewed in 76 ) to prevent infant morbidity and mortality.

There is some concern that vitamin A supplementation may interfere with vaccine effectiveness in young children. The timing of vitamin A interventions needs to be further examined in relation to the timing of vaccinations in order to maximize their benefits. Future studies should also examine whether the effects of vitamin A supplementation are modified by sex (75) , as observed in at least one randomized controlled trial (77) .

Complications from measles infection

An earlier meta-analysis of seven randomized controlled trials examining specifically the role of vitamin A supplementation in 2,069 children with measles found no overall reduction on the risk of mortality (78) . Yet, the pooled analysis of four studies that reported the age distribution of participants found an 83% lower risk of mortality with two doses of 200,000 IU (60 mg RAE) of vitamin A in children younger than two years. In addition, the pooled analysis of three studies indicated a 67% reduction in the risk of pneumonia -led mortality (78) . Similar to WHO and UNICEF guidelines, the American Academy of Pediatrics recommends vitamin A supplementation for children over six months of age when they are infected with measles while malnourished, immunodeficient, or are at risk of measles complications or vitamin A deficiency disorders (79) . Although measles infection has been associated with vitamin A deficiency and blindness, there is currently no evidence to suggest that vitamin A supplementation reduces the risk of blindness in children infected with measles (80) .

Studies in cell culture and animal models have documented the capacity for natural and synthetic retinoids to reduce carcinogenesis significantly in skin, breast, liver, colon , prostate , and other sites. However, the results of human studies examining the relationship between the consumption of preformed vitamin A and cancer do not currently suggest that consuming vitamin A at intakes greater than the RDA benefit in the prevention of cancer (2) .

Lung cancer

The results of the β-Carotene And Retinol Efficacy Trial (CARET) suggested that high-dose supplementation of preformed vitamin A and β-carotene should be avoided in people at high risk for lung cancer (81) . In the CARET study, about 9,000 people (smokers and people with asbestos exposure) were assigned a daily regimen of 25,000 IU (7,500 μg RAE) of retinyl palmitate and 30 mg of β-carotene, while a similar number of people were assigned a placebo . After four years of follow-up, the incidence of lung cancer was 28% higher in the supplemented group compared to the placebo group; however, the incidence was not different six years after the intervention ended (82) . A possible explanation for an increase in lung cancer is that the oxidative environment of the lung, created by smoke or asbestos exposure, could give rise to unusual carotenoid cleavage products, which might promote carcinogenesis (83) . Interestingly, a case-control study that included 749 lung cancer cases and 679 controls from the CARET trial found a significant association between lung cancer risk reduction and high vitamin D intakes (≥400 IU/day) in individuals who received the active CARET supplements or in those with vitamin A intakes equal to or greater than 1,500 μg RAE/day (84) . Further, a meta-analysis of four randomized controlled trials , including a total of 202,924 participants at low risk of lung cancer, indicated that supplementation with retinol and/or β-carotene had no significant effect on lung cancer incidence (85) . While an inverse association has been observed between blood retinol concentration and lung cancer incidence in a dose-response meta-analysis of eight prospective cohort studies (86) , randomized controlled trials have not shown that preformed vitamin A (e.g., retinol) lowers the risk of lung cancer.

Disease Treatment

Retinoids may be used at pharmacological doses to treat several conditions, including, acute promyelocytic leukemia , retinitis pigmentosa, and various skin diseases. It is important to note that treatment with high doses of natural or synthetic retinoids overrides the body's own control mechanisms; therefore, retinoid therapies are associated with potential side effects and toxicities. Additionally, all of the retinoid compounds have been found to cause fetal deformations. Thus, women who have a chance of becoming pregnant should avoid treatment with these medications. Retinoids tend to be very long acting: side effects and birth defects have been reported to occur months after discontinuing retinoid therapy (2) . The retinoids discussed below are prescription drugs and should not be used without medical supervision.

Normal differentiation of myeloid stem cells in the bone marrow gives rise to platelets , red blood cells, and white blood cells (also called leukocytes ) that are important for the immune response. Altered differentiation of myeloid cells can result in the proliferation of immature white blood cells, giving rise to leukemia . Reciprocal chromosome translocations involving the promyelocytic leukemia ( PML ) gene and the gene coding for retinoic acid receptor α (RARα) lead to a specific type of acute myeloid leukemia called acute promyelocytic leukemia (APL). The fusion protein PML/RARα represses transcription by binding to RARE in the promoter of retinoid-responsive genes involved in hematopoietic cell differentiation. Gene repression by PML/RARα is achieved by the recruitment of several chromatin modifiers, including histone deacetylases (HDACs) and DNA methyltransferases (DNMTs). Contrary to RARα wild-type receptor, PML/RARα appears to be insensitive to physiological concentrations of retinoic acid (RA) such that only treatments with high doses of all- trans -RA can restore normal differentiation and lead to significant improvements and complete remission in some APL patients (87) . Combination therapy with arsenic trioxide (or chemotherapy) improves long-term remission (reviewed in 88 ).

More information on APL treatment can be found on the Leukemia & Lymphoma Society website .

Both natural and synthetic retinoids have been used as pharmacologic agents to treat disorders of the skin. Acitretin is a synthetic retinoid that has been FDA-approved for the treatment for psoriasis (89, 90) . Topical tretinoin (all- trans -retinoic acid) and oral isotretinoin (13- cis -retinoic acid) have been used successfully to treat mild-to-severe acne vulgaris (91, 92) . Retinoids exhibit anti-inflammatory properties and regulate the proliferation and differentiation of skin epithelial cells, as well as the production of sebum . Use of pharmacological doses of retinoids (especially oral isotretinoin) by pregnant women causes birth defects and is therefore contraindicated prior to and during pregnancy (see Safety in pregnancy ).

For more information on the use of retinoids in the management of acne, see the article on Vitamin A and Skin Health .

Retinitis pigmentosa (RP) affects approximately 1.5 million people worldwide and is a leading cause of inherited blindness. RP describes a broad spectrum of genetic disorders that result in the progressive loss of photoreceptor cells (rods and cones) in the retina of the eye (93) . While at least 45 loci have been associated with RP, mutations in the rhodopsin gene ( RHO ), the usherin gene ( USH2A ), and the RP GTPase regulator gene ( RPGR ) account for about 30% of all RP cases (94) .

Early symptoms of RP include impaired dark adaptation and night blindness, followed by the progressive loss of peripheral and central vision over time (94) . The results of a randomized controlled trial in 601 patients with common forms of RP indicated that supplementation with 4,500 μg RAE/day of retinyl palmitate significantly slowed the loss of retinal function over a period of four to six years (95) . In contrast, supplementation with 400 IU/day of vitamin E ( dl -α-tocopherol) modestly but significantly increased the loss of retinal function, suggesting that patients with common forms of RP may benefit from long-term vitamin A supplementation but should avoid high-dose vitamin E supplementation. Up to 12 years of follow-up in these patients did not reveal any signs of liver toxicity as a result of excess vitamin A intake (96) . Because neither children nor adults affected by less common forms of RP were included in the trial, no formal recommendation about vitamins A and E could be made (94) . Evidence of a beneficial effect of vitamin A supplementation on the progression of RP is lacking, as concluded in a 2020 Cochrane review (97) . Nevertheless, use of high-dose vitamin A supplementation in RP would require close medical supervision and must be discontinued if there is a possibility of pregnancy (see Safety ).

Food sources

Free retinol is not generally found in food. Retinyl esters (including retinyl palmitate) are the storage form of retinol in animals and thus the main precursors of retinol in food from animals. Plants contain carotenoids , some of which are precursors for vitamin A (e.g., α-carotene, β-carotene, and β-cryptoxanthin). Yellow- and orange-colored vegetables contain significant quantities of carotenoids. Green vegetables also contain carotenoids, though yellow-to-red pigments are masked by the green pigment of chlorophyll (1) . Additionally, certain foods, including milk, margarines, and breakfast cereals, may be fortified with retinyl esters or β-carotene (2) .

Table 3 lists a number of good food sources of vitamin A, including fruit and vegetables, along with their vitamin A content. The retinol activity is indicated in micrograms of retinol activity equivalents (μg RAE). For information on this unit of measurement, see the section on RAE . In addition, use the USDA’s FoodData Central database to check foods for their content of carotenoids without vitamin A activity, such as lycopene, lutein, and zeaxanthin.

Vitamin A international units (IUs)

In the past, vitamin A was listed on food and supplement labels in international units instead of μg RAE ('μg' on labels). In contrast to RAE, the number of IUs of vitamin A does not reflect the bioavailability of vitamin A from different food sources. Conversion rates between IUs and μg RAE are as follows:

1 IU of retinol is equivalent to 0.3 μg RAE
1 IU of supplemental β-carotene is equivalent to 0.3 μg RAE
1 IU of dietary β-carotene is equivalent to 0.05 μg RAE
1 IU of α-carotene or β-cryptoxanthin to 0.025 μg RAE

Table 3 lists some foods rich in vitamin A; the amounts of preformed vitamin A (retinol) and the RAE, which account for bioavailability, are both listed.

The principal forms of preformed vitamin A in supplements are retinyl palmitate and retinyl acetate. β-Carotene is also a common source of vitamin A in supplements, and many supplements provide a combination of retinol and β-carotene (98) . If a percentage of the total vitamin A content of a supplement comes from β-carotene, this information may be included in the Supplement Facts label under vitamin A. While many multivitamins available in the US contain the daily value of 900 μg RAE of vitamin A, some may provide up to 1,500 μg RAE from preformed vitamin A, which is substantially more than the current RDA for vitamin A.

The condition caused by vitamin A toxicity is called hypervitaminosis A. It is caused by overconsumption of preformed vitamin A, not carotenoids . Preformed vitamin A is rapidly absorbed and slowly cleared from the body. Therefore, toxicity from preformed vitamin A may result acutely from high-dose exposure over a short period of time or chronically from a much lower intake (2) . Acute vitamin A toxicity is relatively rare, and symptoms include nausea, headache, fatigue, loss of appetite, dizziness, dry skin, desquamation, and cerebral edema. Signs of chronic toxicity include dry itchy skin, desquamation, anorexia, weight loss, headache, cerebral edema , enlarged liver, enlarged spleen, anemia , and bone and joint pain. Also, symptoms of vitamin A toxicity in infants include bulging fontanels. Severe cases of hypervitaminosis A may result in liver damage, hemorrhage , and coma. Generally, signs of toxicity are associated with long-term consumption of vitamin A in excess of 10 times the RDA (8,000-10,000 μg RAE/day). However, more research is necessary to determine if subclinical vitamin A toxicity is a concern in certain populations (99) . There is evidence that some populations may be more susceptible to toxicity at lower doses, including the elderly, chronic alcohol users, and some people with a genetic predisposition to high cholesterol (100) . In January 2001, the Food and Nutrition Board of the US National Academy of Medicine set the tolerable upper level ( UL ) of vitamin A intake for adults at 3,000 μg RAE/day of preformed vitamin A (60) .

Safety in pregnancy

Although normal fetal development requires sufficient vitamin A intake, consumption of excess preformed vitamin A (such as retinol) during early pregnancy is known to cause birth defects, mainly of the cardiovascular and central nervous systems (101) . No increase in the risk of vitamin A-associated birth defects has been observed at doses of preformed vitamin A from supplements below 3,000 μg RAE/day (60) . Of note, in 2011, the World Health Organization (WHO) recommended vitamin A supplementation (up to 3,000 μg RAE/day or 7,500 μg RAE/week) during pregnancy in areas with high prevalence of vitamin A deficiency for the prevention of blindness (102) . In industrialized countries, pregnant or potentially pregnant women should monitor their intake of vitamin A from fortified food and food naturally high in preformed vitamin A (e.g., liver) and avoid taking daily multivitamin supplements that contain more than 1,500 μg RAE of vitamin A. There is no evidence that consumption of vitamin A from β-carotene might increase the risk of birth defects.

The synthetic derivative of retinol, isotretinoin, is known to cause serious birth defects and should not be taken during pregnancy or if there is a possibility of becoming pregnant (91) . Tretinoin (all- trans -retinoic acid), another retinol derivative, is prescribed as a topical preparation that is applied to the skin. Although percutaneous absorption of topical tretinoin is minimal, its use during pregnancy is not recommended (103) .

Do high intakes of vitamin A increase the risk of osteoporosis?

Results from some prospective studies have suggested that long-term intakes of preformed vitamin A in excess of 1,500 μg RAE/day are associated with reduced bone mineral density (BMD) and increased risk of osteoporotic fracture in older adults (104-106) . However, other investigators failed to observe such detrimental effects on BMD and/or fracture risk (107-110) . A meta-analysis of four prospective studies, including nearly 183,000 participants over 40 years of age, found that highest versus lowest quintiles of retinol (preformed vitamin A) intake significantly increased the risk of hip fracture (111) . A 2017 meta-analysis found similar results, and additionally, did not find higher retinol intakes to be associated with an increased risk of total fracture (112) . Only excess intakes of retinol, not β-carotene, have been associated with adverse effects on bone health. The earlier meta-analysis indicated a U-shaped relationship between circulating retinol and risk of hip fracture, suggesting that both elevated and reduced retinol concentrations in the blood were associated with an increased risk of hip fracture (111) . It is important to note that the available data on retinol intake and bone fracture come from observational studies , not randomized controlled trials .

To date, limited experimental data have suggested that vitamin A (as all- trans -retinoic acid) may affect the development of bone-remodeling cells and stimulate bone matrix degradation ( resorption ) (reviewed in 113 ). Vitamin A may also interfere with the ability of vitamin D to maintain calcium balance (114) . In the large Women’s Health Initiative prospective study, the highest versus lowest quintile of retinol intake (≥1,426 μg/day vs. <474 μg/day) was found to be significantly associated with increased risk of fracture only in women with the lowest vitamin D intakes (≤440 IU/day) (115) .

It is advisable for older individuals to consume multivitamin supplements that contain no more than 750 μg of preformed vitamin A (usually labeled vitamin A acetate or vitamin A palmitate) and no more than 750 μg RAE of additional vitamin A as β-carotene.

Chronic alcohol consumption results in depletion of liver stores of vitamin A and may contribute to alcohol-induced liver damage ( cirrhosis ) (116) . However, the liver toxicity of preformed vitamin A (retinol) is enhanced by chronic alcohol consumption, thus narrowing the therapeutic window for vitamin A supplementation in alcoholics (116) . Oral contraceptives that contain estrogen and progestin increase retinol binding protein (RBP) synthesis by the liver, increasing the export of all- trans -retinol/RBP complex to the circulation. Whether this increases the dietary requirement of vitamin A is not known. Also, the use of cholesterol -lowering medications (like cholestyramine and colestipol), as well as orlistat, mineral oil, and the fat substitute, olestra, which interfere with fat absorption, may affect the absorption of fat-soluble vitamins, including vitamin A (98) . Further, intake of large doses of vitamin A may decrease the absorption of vitamin K . Retinoids or retinoid analogs , including acitretin, all- trans -retinoic acid, bexarotene, etretinate, and isotretinoin, should not be used in combination with single-nutrient vitamin A supplements , because they may increase the risk of vitamin A toxicity (98) .

Linus Pauling Institute Recommendation

The RDA for vitamin A (700 μg RAE/day for women and 900 μg RAE/day for men) is sufficient to support normal gene expression , immune function, and vision. However, following the Linus Pauling Institute’s recommendation to take a multivitamin/mineral supplement daily could supply as much as 1,500 μg RAE/day of vitamin A as retinol, the amount that has been associated with adverse effects on bone health in older adults. For this reason, we recommend taking a multivitamin/mineral supplement that provides no more than 750 μg RAE of preformed vitamin A (usually labeled vitamin A acetate or vitamin A palmitate) and no more than 750 μg RAE of additional vitamin A as β-carotene. High potency vitamin A supplements should not be used without medical supervision due to the risk of toxicity.

Older adults (>50 years)

Presently, there is little evidence that the requirement for vitamin A in older adults differs from that of younger adults. Additionally, vitamin A toxicity may occur at lower doses in older adults than in younger adults. Further, data from observational studies suggested an inverse association between intakes of preformed vitamin A in excess of 1,500 μg RAE day and risk of hip fracture in older people (see Safety ). Yet, following the Linus Pauling Institute’s recommendation to take a multivitamin/mineral supplement daily could supply as much as 1,500 μg RAE/day of retinol, the amount that has been associated with adverse effects on bone health in older adults in some studies. For this reason, the Linus Pauling Institute recommends taking a multivitamin/mineral supplement that provides no more than 750 μg RAE of preformed vitamin A (usually labeled vitamin A acetate or vitamin A palmitate) and no more than 750 μg RAE of additional vitamin A as β-carotene. As for all age groups, high potency vitamin A supplements should not be used without medical supervision due to the risk of toxicity.

Originally written in 2000 by: Jane Higdon, Ph.D. Linus Pauling Institute Oregon State University

Updated in December 2003 by: Jane Higdon, Ph.D. Linus Pauling Institute Oregon State University

Updated in November 2007 by: Victoria J. Drake, Ph.D. Linus Pauling Institute Oregon State University

Updated in January 2015: Barbara Delage, Ph.D. Linus Pauling Institute Oregon State University

Updated in January 2024 by: Victoria J. Drake, Ph.D. Linus Pauling Institute Oregon State University

Reviewed in February 2024 by: A. Catharine Ross, Ph.D. Professor of Nutrition, Texas A&M University Professor of Nutrition Emeritus, The Pennsylvania State University

1. Groff JL. Advanced Nutrition and Human Metabolism. 2 nd ed. St. Paul: West Publishing; 1995.

2. Ross AC. Vitamin A. In: Ross A, Caballero B, Cousins R, Tucker K, Ziegler T, eds. Modern Nutrition in Health and Disease. 11 th ed: Lippincott Williams & Wilkins; 2014:260-277.

3. Tan L, Green MH, Ross AC. Vitamin A kinetics in neonatal rats vs. adult rats: comparisons from model-based compartmental analysis. J Nutr. 2015; 145(3):403-10. (PubMed)

4. Tan L, Wray AE, Green MH, Ross AC. Compartmental modeling of whole-body vitamin A kinetics in unsupplemented and vitamin A-retinoic acid-supplemented neonatal rats. J Lipid Res. 2014;55(8):1738-1749. (PubMed)

5. Zhong M, Kawaguchi R, Ter-Stepanian M, Kassai M, Sun H. Vitamin A transport and the transmembrane pore in the cell-surface receptor for plasma retinol binding protein. PLoS One. 2013;8(11):e73838. (PubMed)

6. See AW, Clagett-Dame M. The temporal requirement for vitamin A in the developing eye: mechanism of action in optic fissure closure and new roles for the vitamin in regulating cell proliferation and adhesion in the embryonic retina. Dev Biol. 2009;325(1):94-105. (PubMed)

7. Theodosiou M, Laudet V, Schubert M. From carrot to clinic: an overview of the retinoic acid signaling pathway. Cell Mol Life Sci. 2010;67(9):1423-1445. (PubMed)

8. Lefebvre P, Martin PJ, Flajollet S, Dedieu S, Billaut X, Lefebvre B. Transcriptional activities of retinoic acid receptors. Vitam Horm. 2005;70:199-264. (PubMed)

9. Amann PM, Eichmuller SB, Schmidt J, Bazhin AV. Regulation of gene expression by retinoids. Curr Med Chem. 2011;18(9):1405-1412. (PubMed)

10. Pendaries V, Verrecchia F, Michel S, Mauviel A. Retinoic acid receptors interfere with the TGF-beta/Smad signaling pathway in a ligand-specific manner. Oncogene. 2003;22(50):8212-8220. (PubMed)

11. Masia S, Alvarez S, de Lera AR, Barettino D. Rapid, nongenomic actions of retinoic acid on phosphatidylinositol-3-kinase signaling pathway mediated by the retinoic acid receptor. Mol Endocrinol. 2007;21(10):2391-2402. (PubMed)

12. Qiao J, Paul P, Lee S, et al. PI3K/AKT and ERK regulate retinoic acid-induced neuroblastoma cellular differentiation. Biochem Biophys Res Commun. 2012;424(3):421-426. (PubMed)

13. Canon E, Cosgaya JM, Scsucova S, Aranda A. Rapid effects of retinoic acid on CREB and ERK phosphorylation in neuronal cells. Mol Biol Cell. 2004;15(12):5583-5592. (PubMed)

14. Kirchmeyer M, Koufany M, Sebillaud S, Netter P, Jouzeau JY, Bianchi A. All-trans retinoic acid suppresses interleukin-6 expression in interleukin-1-stimulated synovial fibroblasts by inhibition of ERK1/2 pathway independently of RAR activation. Arthritis Res Ther. 2008;10(6):R141. (PubMed)

15. Amengual J, Golczak M, Palczewski K, von Lintig J. Lecithin:retinol acyltransferase is critical for cellular uptake of vitamin A from serum retinol-binding protein. J Biol Chem. 2012;287(29):24216-24227. (PubMed)

16. Noy N. Signaling by retinol and its serum binding protein. Prostaglandins Leukot Essent Fatty Acids. 2015; 93:3-7. (PubMed)

17. Berry DC, Jacobs H, Marwarha G, et al. The STRA6 receptor is essential for retinol-binding protein-induced insulin resistance but not for maintaining vitamin A homeostasis in tissues other than the eye. J Biol Chem. 2013;288(34):24528-24539. (PubMed)

18. Marwarha G, Berry DC, Croniger CM, Noy N. The retinol esterifying enzyme LRAT supports cell signaling by retinol-binding protein and its receptor STRA6. FASEB J. 2014;28(1):26-34. (PubMed)

19. Farmer SR. Molecular determinants of brown adipocyte formation and function. Genes Dev. 2008;22(10):1269-1275. (PubMed)

20. Kiefer FW, Vernochet C, O'Brien P, et al. Retinaldehyde dehydrogenase 1 regulates a thermogenic program in white adipose tissue. Nat Med. 2012;18(6):918-925. (PubMed)

21. Nallamshetty S, Le PT, Wang H, et al. Retinaldehyde dehydrogenase 1 deficiency inhibits PPARgamma-mediated bone loss and marrow adiposity. Bone. 2014;67:281-291. (PubMed)

22. Kiefer FW, Orasanu G, Nallamshetty S, et al. Retinaldehyde dehydrogenase 1 coordinates hepatic gluconeogenesis and lipid metabolism. Endocrinology. 2012;153(7):3089-3099. (PubMed)

23. Green HN, Mellanby E. Vitamin A as an anti-infective agent. Br Med J. 1928;2(3537):691-696. (PubMed)

24. Gholizadeh M, Basafa Roodi P, Abaj F, et al. Influence of vitamin A supplementation on inflammatory biomarkers in adults: a systematic review and meta-analysis of randomized clinical trials. Sci Rep. 2022;12(1):21384. (PubMed)

25. Raverdeau M, Mills KH. Modulation of T cell and innate immune responses by retinoic acid. J Immunol. 2014;192(7):2953-2958. (PubMed)

26. Spears K, Cheney C, Zerzan J. Low plasma retinol concentrations increase the risk of developing bronchopulmonary dysplasia and long-term respiratory disability in very-low-birth-weight infants. Am J Clin Nutr. 2004;80(6):1589-1594. (PubMed)

27. Barber T, Esteban-Pretel G, Marin MP, Timoneda J. Vitamin A deficiency and alterations in the extracellular matrix. Nutrients. 2014;6(11):4984-5017. (PubMed)

28. Semba RD, Bloem MW. The anemia of vitamin A deficiency: epidemiology and pathogenesis. Eur J Clin Nutr. 2002;56(4):271-281. (PubMed)

29. Allen LH. Iron supplements: scientific issues concerning efficacy and implications for research and programs. J Nutr. 2002;132(4 Suppl):813S-819S. (PubMed)

30. Christian P, West KP, Jr. Interactions between zinc and vitamin A: an update. Am J Clin Nutr. 1998;68(2 Suppl):435S-441S. (PubMed)

31. Auld DS, Bergman T. Medium- and short-chain dehydrogenase/reductase gene and protein families : The role of zinc for alcohol dehydrogenase structure and function. Cell Mol Life Sci. 2008;65(24):3961-3970. (PubMed)

32. da Cunha MSB, Campos Hankins NA, Arruda SF. Effect of vitamin A supplementation on iron status in humans: A systematic review and meta-analysis. Crit Rev Food Sci Nutr. 2019;59(11):1767-1781. (PubMed)

33. Suharno D, West CE, Muhilal, Karyadi D, Hautvast JG. Supplementation with vitamin A and iron for nutritional anaemia in pregnant women in West Java, Indonesia. Lancet. 1993;342(8883):1325-1328. (PubMed)

34. da Cunha MS, Siqueira EM, Trindade LS, Arruda SF. Vitamin A deficiency modulates iron metabolism via ineffective erythropoiesis. J Nutr Biochem. 2014;25(10):1035-1044. (PubMed)

35. Jang JT, Green JB, Beard JL, Green MH. Kinetic analysis shows that iron deficiency decreases liver vitamin A mobilization in rats. J Nutr. 2000;130(5):1291-1296. (PubMed)

36. Rosales FJ, Jang JT, Pinero DJ, Erikson KM, Beard JL, Ross AC. Iron deficiency in young rats alters the distribution of vitamin A between plasma and liver and between hepatic retinol and retinyl esters. J Nutr. 1999;129(6):1223-1228. (PubMed)

37. Tanumihardjo SA. Biological evidence to define a vitamin A deficiency cutoff using total liver vitamin A reserves. Exp Biol Med (Maywood). 2021;246(9):1045-1053. (PubMed)

38. World Health Organization. Serum retinol concentrations for determining the prevalence of vitamin A deficiency in populations. Vitamin and Mineral Nutrition Information System. Geneva, 2011. https://www.who.int/publications/i/item/WHO-NMH-NHD-MNM-11.3 . Accessed 1/25/2024.

39. Underwood BA, Arthur P. The contribution of vitamin A to public health. Faseb J. 1996;10(9):1040-1048. (PubMed)

40. Solomons NW. Vitamin A. In: Erdman JJ, Macdonald I, Zeisel S, eds. Present Knowledge in Nutrition. 10 th ed: John Wiley & Sons, Ltd.; 2012:149-184.

41. Sherwin JC, Reacher MH, Dean WH, Ngondi J. Epidemiology of vitamin A deficiency and xerophthalmia in at-risk populations. Trans R Soc Trop Med Hyg. 2012;106(4):205-214. (PubMed)

42. McCauley ME, van den Broek N, Dou L, Othman M. Vitamin A supplementation during pregnancy for maternal and newborn outcomes. Cochrane Database Syst Rev. 2015;2015(10):CD008666. (PubMed)

43. World Health Organization. Guideline: Vitamin A supplementation in infants and children 6–59 months of age. Geneva, 2011. Available at: https://www.who.int/publications/i/item/9789241501767 . Accessed 1/19/24.

44. Gilbert C, Awan H. Blindness in children. BMJ. 2003;327(7418):760-761. (PubMed)

45. Semba RD. Vitamin A and human immunodeficiency virus infection. Proc Nutr Soc. 1997;56(1B):459-469. (PubMed)

46. Field CJ, Johnson IR, Schley PD. Nutrients and their role in host resistance to infection. J Leukoc Biol. 2002;71(1):16-32. (PubMed)

47. World Health Organization, UNICEF, IVACG Task Force. Vitamin A supplements: a guide to their use in the treatment and prevention of vitamin A deficiency and xerophthalmia . Geneva: World Health Organization; 1997.

48. Thornton KA, Mora-Plazas M, Marin C, Villamor E. Vitamin A deficiency is associated with gastrointestinal and respiratory morbidity in school-age children. J Nutr. 2014;144(4):496-503. (PubMed)

49. Wiysonge CS, Shey M, Kongnyuy EJ, Sterne JA, Brocklehurst P. Vitamin A supplementation for reducing the risk of mother-to-child transmission of HIV infection. Cochrane Database Syst Rev. 2011(1):CD003648. (PubMed)

50. Semba RD, Miotti PG, Chiphangwi JD, et al. Maternal vitamin A deficiency and mother-to-child transmission of HIV-1. Lancet. 1994;343(8913):1593-1597. (PubMed)

51. Wiysonge CS, Ndze VN, Kongnyuy EJ, Shey MS. Vitamin A supplements for reducing mother-to-child HIV transmission. Cochrane Database Syst Rev. 2017;9(9):CD003648. (PubMed)

52. Zimmermann MB, Adou P, Torresani T, Zeder C, Hurrell RF. Effect of oral iodized oil on thyroid size and thyroid hormone metabolism in children with concurrent selenium and iodine deficiency. Eur J Clin Nutr. 2000;54(3):209-213. (PubMed)

53. Zimmermann MB, Wegmuller R, Zeder C, Chaouki N, Torresani T. The effects of vitamin A deficiency and vitamin A supplementation on thyroid function in goitrous children. J Clin Endocrinol Metab. 2004;89(11):5441-5447. (PubMed)

54. Zimmermann MB. Interactions of vitamin A and iodine deficiencies: effects on the pituitary-thyroid axis. Int J Vitam Nutr Res. 2007;77(3):236-240. (PubMed)

55. Capriello S, Stramazzo I, Bagaglini MF, Brusca N, Virili C, Centanni M. The relationship between thyroid disorders and vitamin A.: A narrative minireview. Front Endocrinol (Lausanne). 2022;13:968215. (PubMed)

56. Zimmermann MB, Jooste PL, Mabapa NS, et al. Vitamin A supplementation in iodine-deficient African children decreases thyrotropin stimulation of the thyroid and reduces the goiter rate. Am J Clin Nutr. 2007;86(4):1040-1044. (PubMed)

57. Maronn M, Allen DM, Esterly NB. Phrynoderma: a manifestation of vitamin A deficiency?... The rest of the story. Pediatr Dermatol. 2005;22(1):60-63. (PubMed)

58. Herring W, Nowicki MJ, Jones JK. An uncommon cause of esophagitis. Answer to the clinical challenges and images in GI question: image 1: esophageal hyperkeratosis secondary to vitamin A deficiency. Gastroenterology. 2010;139(2):e6-7. (PubMed)

59. Weber D, Grune T. The contribution of beta-carotene to vitamin A supply of humans. Mol Nutr Food Res. 2012;56(2):251-258. (PubMed)

60. Food and Nutrition Board, Institute of Medicine. Vitamin A. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington D.C.: National Academy Press; 2001:65-126. (National Academy Press)

61. Ravishankar C, Nafday S, Green RS, et al. A trial of vitamin A therapy to facilitate ductal closure in premature infants. J Pediatr. 2003;143(5):644-648. (PubMed)

62. Tyson JE, Wright LL, Oh W, et al. Vitamin A supplementation for extremely-low-birth-weight infants. National Institute of Child Health and Human Development Neonatal Research Network. N Engl J Med. 1999;340(25):1962-1968. (PubMed)

63. Wardle SP, Hughes A, Chen S, Shaw NJ. Randomised controlled trial of oral vitamin A supplementation in preterm infants to prevent chronic lung disease. Arch Dis Child Fetal Neonatal Ed. 2001;84(1):F9-F13. (PubMed)

64. Ambalavanan N, Kennedy K, Tyson J, Carlo WA. Survey of vitamin A supplementation for extremely-low-birth-weight infants: is clinical practice consistent with the evidence? J Pediatr. 2004;145(3):304-307. (PubMed)

65. Laughon MM. Vitamin A shortage and risk of bronchopulmonary dysplasia. JAMA Pediatr. 2014;168(11):995-996. (PubMed)

66. Tolia VN, Murthy K, McKinley PS, Bennett MM, Clark RH. The effect of the national shortage of vitamin a on death or chronic lung disease in extremely low-birth-weight infants. JAMA Pediatr. 2014;168(11):1039-1044. (PubMed)

67. Darlow BA, Graham PJ, Rojas-Reyes MX. Vitamin A supplementation to prevent mortality and short- and long-term morbidity in very low birth weight infants. Cochrane Database Syst Rev. 2016;2016(8):CD000501. (PubMed)

68. Gadhia MM, Cutter GR, Abman SH, Kinsella JP. Effects of early inhaled nitric oxide therapy and vitamin A supplementation on the risk for bronchopulmonary dysplasia in premature newborns with respiratory failure. J Pediatr. 2014;164(4):744-748. (PubMed)

69. Meyer S, Gortner L, NeoVita ATI. Early postnatal additional high-dose oral vitamin A supplementation versus placebo for 28 days for preventing bronchopulmonary dysplasia or death in extremely low birth weight infants. Neonatology. 2014;105(3):182-188. (PubMed)

70. Meyer S, Gortner L, NeoVita ATi. Up-date on the NeoVitaA Trial: Obstacles, challenges, perspectives, and local experiences. Wien Med Wochenschr. 2017;167(11-12):264-270. (PubMed)

71. Babu TA, Sharmila V. Vitamin A supplementation in late pregnancy can decrease the incidence of bronchopulmonary dysplasia in newborns. J Matern Fetal Neonatal Med. 2010;23(12):1468-1469. (PubMed)

72. 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 Syst Rev. 2022;3(3):CD008524. (PubMed)

73. World Health Organization. Essential Programme on Immunization. Vitamin A supplementation. https://www.who.int/teams/immunization-vaccines-and-biologicals/essential-programme-on-immunization/integration/linking-with-other-health-interventions/vitamin-a . Accessed 1/25/24.

74. World Health Organization. Guideline - Vitamin A supplementation for infants and children 6-59 months of age - Guideline . Geneva 2011. Available at: https://www.who.int/publications/i/item/9789241501767 . Accessed 2/23/2024.

75. World Health Organization. Guideline - Neonatal vitamin A supplementation Geneva 2011. Available at: https://iris.who.int/bitstream/handle/10665/44626/9789241501798_eng.pdf?sequence=1 . Accessed 2/23/2024.

76. Benn CS, Bale C, Sommerfelt H, Friis H, Aaby P. Hypothesis: Vitamin A supplementation and childhood mortality: amplification of the non-specific effects of vaccines? Int J Epidemiol. 2003;32(5):822-828. (PubMed)

77. Fisker AB, Bale C, Rodrigues A, et al. High-dose vitamin A with vaccination after 6 months of age: a randomized trial. Pediatrics. 2014;134(3):e739-748. (PubMed)

78. Huiming Y, Chaomin W, Meng M. Vitamin A for treating measles in children. Cochrane Database Syst Rev. 2005(4):CD001479. (PubMed)

79. American Academy of Pediatrics Committee on Infectious Diseases: Vitamin A treatment of measles. Pediatrics. 1993;91(5):1014-1015. (PubMed)

80. Bello S, Meremikwu MM, Ejemot-Nwadiaro RI, Oduwole O. Routine vitamin A supplementation for the prevention of blindness due to measles infection in children. Cochrane Database Syst Rev. 2016;2016(8):CD007719. (PubMed)

81. Omenn GS, Goodman GE, Thornquist MD, et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med. 1996;334(18):1150-1155. (PubMed)

82. Goodman GE, Thornquist MD, Balmes J, et al. The Beta-Carotene and Retinol Efficacy Trial: incidence of lung cancer and cardiovascular disease mortality during 6-year follow-up after stopping beta-carotene and retinol supplements. J Natl Cancer Inst. 2004;96(23):1743-1750. (PubMed)

83. Palozza P, Simone R, Mele MC. Interplay of carotenoids with cigarette smoking: implications in lung cancer. Curr Med Chem. 2008;15(9):844-854. (PubMed)

84. Cheng TY, Goodman GE, Thornquist MD, et al. Estimated intake of vitamin D and its interaction with vitamin A on lung cancer risk among smokers. Int J Cancer. 2014;135(9):2135-2145. (PubMed)

85. Cortes-Jofre M, Rueda JR, Corsini-Munoz G, Fonseca-Cortes C, Caraballoso M, Bonfill Cosp X. Drugs for preventing lung cancer in healthy people. Cochrane Database Syst Rev. 2012;10:CD002141. (PubMed)

86. Abar L, Vieira AR, Aune D, et al. Blood concentrations of carotenoids and retinol and lung cancer risk: an update of the WCRF-AICR systematic review of published prospective studies. Cancer Med. 2016;5(8):2069-2083. (PubMed)

87. Lo-Coco F, Avvisati G, Vignetti M, et al. Retinoic acid and arsenic trioxide for acute promyelocytic leukemia. N Engl J Med. 2013;369(2):111-121. (PubMed)

88. Yilmaz M, Kantarjian H, Ravandi F. Acute promyelocytic leukemia current treatment algorithms. Blood Cancer J. 2021;11(6):123. (PubMed)

89. Booij MT, Van De Kerkhof PC. Acitretin revisited in the era of biologics. J Dermatolog Treat. 2011;22(2):86-89. (PubMed)

90. Armstrong AW, Read C. Pathophysiology, clinical presentation, and treatment of psoriasis: a review. JAMA. 2020;323(19):1945-1960. (PubMed)

91. Orfanos CE, Zouboulis CC. Oral retinoids in the treatment of seborrhoea and acne. Dermatology. 1998;196(1):140-147. (PubMed)

92. Thielitz A, Gollnick H. Topical retinoids in acne vulgaris: update on efficacy and safety. Am J Clin Dermatol. 2008;9(6):369-381. (PubMed)

93. Vishwanathan R, Johnson EJ. Eye disease. In: Erdman JJ, Macdonald I, Zeisel S, eds. Present Knowledge in Nutrition. 10 th ed: John Wiley & Sons, Ltd; 2012:939-981.

94. Hartong DT, Berson EL, Dryja TP. Retinitis pigmentosa. Lancet. 2006;368(9549):1795-1809. (PubMed)

95. Berson EL, Rosner B, Sandberg MA, et al. A randomized trial of vitamin A and vitamin E supplementation for retinitis pigmentosa. Arch Ophthalmol. 1993;111(6):761-772. (PubMed)

96. Sibulesky L, Hayes KC, Pronczuk A, Weigel-DiFranco C, Rosner B, Berson EL. Safety of <7500 RE (<25000 IU) vitamin A daily in adults with retinitis pigmentosa. Am J Clin Nutr. 1999;69(4):656-663. (PubMed)

97. Schwartz SG, Wang X, Chavis P, Kuriyan AE, Abariga SA. Vitamin A and fish oils for preventing the progression of retinitis pigmentosa. Cochrane Database Syst Rev. 2020;6(6):CD008428. (PubMed)

98. Hendler SS, Rorvik DR, eds. PDR for Nutritional Supplements. 2 nd ed: Thomson Reuters; 2008.

99. Penniston KL, Tanumihardjo SA. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr. 2006;83(2):191-201. (PubMed)

100. Russell RM. The vitamin A spectrum: from deficiency to toxicity. Am J Clin Nutr. 2000;71(4):878-884. (PubMed)

101. Bastos Maia S, Rolland Souza AS, Costa Caminha MF, et al. Vitamin A and pregnancy: a narrative review. Nutrients. 2019;11(3):681. (PubMed)

102. World Health Organization Organization. Guideline - Vitamin A supplementation in pregnant women . Geneva 2011.

103. Bozzo P, Chua-Gocheco A, Einarson A. Safety of skin care products during pregnancy. Can Fam Physician. 2011;57(6):665-667. (PubMed)

104. Michaelsson K, Lithell H, Vessby B, Melhus H. Serum retinol levels and the risk of fracture. N Engl J Med. 2003;348(4):287-294. (PubMed)

105. Promislow JH, Goodman-Gruen D, Slymen DJ, Barrett-Connor E. Retinol intake and bone mineral density in the elderly: the Rancho Bernardo Study. J Bone Miner Res. 2002;17(8):1349-1358. (PubMed)

106. Feskanich D, Singh V, Willett WC, Colditz GA. Vitamin A intake and hip fractures among postmenopausal women. JAMA. 2002;287(1):47-54. (PubMed)

107. Rejnmark L, Vestergaard P, Charles P, et al. No effect of vitamin A intake on bone mineral density and fracture risk in perimenopausal women. Osteoporos Int. 2004;15(11):872-880. (PubMed)

108. Sowers MF, Wallace RB. Retinol, supplemental vitamin A and bone status. J Clin Epidemiol. 1990;43(7):693-699. (PubMed)

109. Ballew C, Galuska D, Gillespie C. High serum retinyl esters are not associated with reduced bone mineral density in the Third National Health And Nutrition Examination Survey, 1988-1994. J Bone Miner Res. 2001;16(12):2306-2312. (PubMed)

110. de Jonge EA, Kiefte-de Jong JC, Campos-Obando N, et al. Dietary vitamin A intake and bone health in the elderly: the Rotterdam Study. Eur J Clin Nutr. 2015;69(12):1360-1368. (PubMed)

111. Wu AM, Huang CQ, Lin ZK, et al. The relationship between vitamin A and risk of fracture: meta-analysis of prospective studies. J Bone Miner Res. 2014;29(9):2032-2039. (PubMed)

112. Zhang X, Zhang R, Moore JB, et al. The effect of vitamin A on fracture risk: a meta-analysis of cohort studies. Int J Environ Res Public Health. 2017;14(9):1043. (PubMed)

113. Conaway HH, Henning P, Lerner UH. Vitamin A metabolism, action, and role in skeletal homeostasis. Endocr Rev. 2013;34(6):766-797. (PubMed)

114. Johansson S, Melhus H. Vitamin A antagonizes calcium response to vitamin D in man. J Bone Miner Res. 2001;16(10):1899-1905. (PubMed)

115. Caire-Juvera G, Ritenbaugh C, Wactawski-Wende J, Snetselaar LG, Chen Z. Vitamin A and retinol intakes and the risk of fractures among participants of the Women's Health Initiative Observational Study. Am J Clin Nutr. 2009;89(1):323-330. (PubMed)

116. Lieber CS. Relationships between nutrition, alcohol use, and liver disease. Alcohol Res Health. 2003;27(3):220-231. (PubMed)

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Micronutrient Inadequacies
Other Nutrients
Dietary Factors
Food and Beverages
Life Stages
Health and Disease

The Linus Pauling Institute's Micronutrient Information Center provides scientific information on the health aspects of dietary factors and supplements, food, and beverages for the general public. The information is made available with the understanding that the author and publisher are not providing medical, psychological, or nutritional counseling services on this site. The information should not be used in place of a consultation with a competent health care or nutrition professional.

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What Are Vitamin A and Carotenoids, and What Do They Do?

Side Effects

Precautions

Interactions

Similar Supplements

Sources & What to Look For

Frequently Asked Questions

Vitamin A is an essential nutrient, meaning we can't make it in our bodies and must get it from an outside source to stay healthy. There are two sources of vitamin A: preformed vitamin A and carotenoids.

Vitamin A is a fat-soluble nutrient requiring fat for it to be effectively absorbed in the digestive tract. Vitamin A is stored in the liver.

Vitamin A is essential for the health of the following:

Epithelia (surface tissue, like skin)
The immune system
Growth and development
Reproductive health

This article will discuss what you should know about vitamin A, including its potential uses, safety, and more.

Dietary supplements are not regulated like drugs in the United States. They can cause interactions with medications or have other safety concerns.

For this reason, it’s important to be aware of what to look for when choosing a supplement , such as third-party testing, potential drug interactions, and more.

Supplement Facts

Active Ingredient(s) : Vitamin A
Alternate Names(s) : Vitamin A, retinol, fat-soluble vitamins, fat-loving vitamins, essential vitamins, preformed vitamin A, carotenoids, provitamin A carotenoids
Legal Status : Substances added to food, nutrient found in food, dietary supplement
Suggested Dose : May vary based on age, sex, and medical condition
Safety Considerations : Possible side effects, interactions, and special considerations for children, pregnancy, and breastfeeding

What Are Some Effects of Vitamin A on Health?

Supplement use should be individualized and vetted by a healthcare professional, such as a registered dietitian nutritionist (RD or RDN), pharmacist, or healthcare provider. No supplement is intended to treat, cure, or prevent disease.

While more extensive research is necessary in regard to effectiveness, people use vitamin A or carotenoids for various health conditions.

Research for the effects of vitamin A and carotenoids on health is most robust for the following conditions:

Age-related macular degeneration (AMD)
Vitamin A deficiency (low vitamin A)

Catherine Falls Commercial / Getty Images

Age-Related Macular Degeneration

AMD is a vision-threatening condition that tends to affect people over 50—including older adults over 65.

In AMD, blood leaks into the macula , which is the center of the retina in the back of the eye. The macula helps you see fine details.

In a clinical trial, study participants who took more vitamin A, beta-carotene, or lutein and zeaxanthin had a lower likelihood of worsening AMD when compared to participants who took less vitamin A and/or these carotenoids.

Since vitamin A toxicity is possible, however, speak with a healthcare provider before taking this vitamin.

Moreover, there is an AREDS2 supplement that decreases the risk of worsening AMD. But the most current AREDS2 supplement contains no vitamin A or provitamin A carotenoid—like beta-carotene.

A few systematic reviews and meta-analyses suggested a lower risk of several different cancers with higher dietary amounts of the following:

Carotenoids
Fruits and vegetables
Combination of the above

Results from some studies, however, didn't find a relationship between different forms of vitamin A and cancer risk.

There were also a few large and long-term studies that showed beta-carotene supplements with or without retinyl palmitate (a preformed vitamin A) had harmful effects—like lung cancer —on specific groups of people.

This includes people who currently or formerly smoked and people who had exposure to asbestos .

In other studies, these adverse effects were not seen, but these studies contained smaller groups of people who currently or formerly smoked.

Based on these articles, the evidence regarding the relationship between vitamin A and cancer is mixed.

There is a possible relationship between vitamin A deficiency (low vitamin A) and a higher risk of death from infections such as measles. Measles is a highly contagious and severe viral infection, which is preventable with a vaccine .

Results from a systematic review showed vitamin A supplementation reduced the number of new measles cases in children. Interestingly, however, vitamin A supplementation didn't affect the number of deaths from measles.

Vitamin A supplementation generally decreased the risk of morbidity and mortality in children. Morbidity is the state of having a medical condition, and mortality is death.

Data supported the continued use of vitamin A supplements in children younger than 5 at risk for low vitamin A. But additional clinical trials are still necessary to study vitamin A doses and various ways vitamin A is given.

Vitamin A Deficiency

While rare in the United States, it is possible to have a vitamin A deficiency.

However, low vitamin A levels in developing countries are more common—especially in pregnant and breastfeeding people. Infants—particularly preterm infants—and children are also at a higher risk.

Low vitamin A levels may occur in people who eat certain traditional diets that contain few foods with vitamin A. People in developing countries may also have difficulties accessing foods with vitamin A or provitamin A carotenoids.

Low vitamin A is also more likely with certain groups of people or in people with certain medical conditions.

What Causes a Vitamin A Deficiency?

Potential causes of vitamin A deficiency also include:

Cystic fibrosis (CF) : CF is a medical condition that runs in families. CF affects the lungs , pancreas, and other organs. Because people with CF are more likely to have pancreatic problems, they also have problems absorbing vitamin A into the bloodstream. For this reason, there is a higher likelihood of vitamin A deficiency.
Digestive system conditions : People with certain digestive system conditions have a higher risk of vitamin A deficiency. Examples of these digestive system conditions include inflammatory bowel disease (IBD) and celiac disease .

Am I Getting Enough Vitamin A?

If you live in the United States, you're likely getting enough vitamin A.

However, if you're living in a developing country where access to vitamin A-containing foods is difficult, there's a chance you may not be not getting enough vitamin A.

If you have a vitamin A deficiency, short-term symptoms may include:

Night blindness
Trouble seeing in environments with low lighting

Long-term or worsening vitamin A deficiency symptoms may include:

Abnormal lung development
High risk of anemia
Irreversible (permanent) blindness
Lung conditions, such as pneumonia
Severe infections, especially from measles or infection-related diarrhea

If you suspect that you're experiencing a vitamin A deficiency or if any of your symptoms feel life-threatening, call 911 and get medical help right away.

What Are the Side Effects of Vitamin A?

As with many medications and natural products, vitamin A supplements may have side effects.

Additionally, vitamin A is a fat-soluble vitamin. The body stores excess amounts, primarily in the liver. These levels can accumulate over time, potentially increasing the possibility of toxicity.

Common Side Effects

Common side effects of vitamin A may include:

Appetite changes

Severe Side Effects

Severe side effects are possible, especially from vitamin A toxicity. Examples of serious side effects may include:

Severe allergic reaction : A severe allergic reaction is a serious side effect possible with any medication or natural product. If you're having a severe allergic reaction , symptoms may include breathing difficulties, itchiness, and rash.
Brain swelling : Too much vitamin A might cause some brain swelling. Symptoms of brain swelling may include vision changes, seizures , and memory problems.
Cancer : Vitamin A might have harmful effects—like lung cancer—on specific groups of people, such as people who currently or formerly smoked and people who had asbestos exposure.
Liver problems : There are reports of liver problems above the upper limit (UL)—the maximum amount not likely to pose harm—of daily vitamin A. If you have worsening liver function, symptoms may include upper right-sided stomach discomfort, dark urine, and yellowing of the eyes or skin.
Bone problems : Large amounts of vitamin A might cause bone pain and decrease bone mineral density (BMD). BMD measures the strength and thickness (density or mass) of your bones. And low BMD increases your osteoporosis (weak and brittle bones) and bone fracture (break) risk.
Negative effects on the unborn fetus : If a pregnant person takes too much vitamin A—or even uses skin products with retinol—adverse effects can happen to the unborn fetus.

If you're having a severe allergic reaction or if any of your symptoms feel life-threatening, call 911 and get medical help right away.

A healthcare provider may advise against your taking vitamin A if any of the following applies to you:

Severe allergic reaction : Avoid vitamin A if you have a known allergy to it or its ingredients or parts. If you need clarification on whether it's safe, ask a registered dietitian, pharmacist, or healthcare provider for more information.
Pregnancy : There are recommended daily allowances (RDAs) for vitamin A from different sources—like foods and supplements—for pregnant people. However, harmful effects on your unborn fetus are more likely above the following daily UL—14 to 18 years: 2,800 micrograms (mcg), 19 years and over: 3,000 mcg. Contact a healthcare provider to discuss the benefits and risks.
Breastfeeding : There are RDAs of vitamin A for breastfeeding people. However, harmful effects for you or your child are more likely above the following daily ULs for vitamin A—2,800 mcg (14 to 18 years) to 3,000 mcg (19+ years). Reach out to a healthcare provider to discuss the benefits and risks. The healthcare provider may also help you know more about your vitamin A needs.
Adults over 65 : Some older adults may have a higher likelihood of medication side effects. Discuss your vitamin A use with your healthcare provider.
Children : Children have different vitamin A needs compared to adults. Harmful effects for you or your child are more likely above the following daily ULs for vitamin A—600 mcg (birth to 3 years), 900 mcg (4 to 8 years), 1,700 mcg (9 to 13 years), and 2,800 mcg (14 to 18 years). Talk with your child's healthcare provider about giving your child vitamin A.
Age-related macular degeneration (AMD) : A clinical trial showed that study participants who took more vitamin A, beta-carotene, or lutein and zeaxanthin had a lower likelihood of worsening AMD—when compared to participants who took less vitamin A and/or these carotenoids. The most current AREDS2 supplement for AMD doesn't contain vitamin A or beta-carotene. If you have AMD, contact a healthcare provider to discuss your options before taking vitamin A or beta-carotene.
Tobacco use or asbestos exposure : Studies suggest beta-carotene with or without retinyl palmitate (a preformed vitamin A) had harmful effects—like lung cancer—on people who currently or formerly used tobacco and people who had asbestos exposure. Therefore, talk with a healthcare provider before trying vitamin A or beta-carotene—especially if you smoke cigarettes or have in the past, or have had asbestos exposure.
Lung cancer : Beta-carotene with or without retinyl palmitate might increase the risk of harmful effects—like lung cancer—on specific groups of people, such as people who currently or formerly smoked and people who had asbestos exposure. If you have these risk factors or already have lung cancer, healthcare providers may recommend against vitamin A or beta-carotene.
Liver problems : Above the daily upper limit (UL) of vitamin A, there are reports of liver problems. If you already have liver problems, healthcare providers may want to closely monitor you and make any necessary medication adjustments.
Osteoporosis : Large amounts of vitamin A may decrease bone mineral density. And this may increase your risk of osteoporosis (weak and brittle bones) and bone fracture (break). If you have osteoporosis, healthcare providers may want to closely monitor you and make any necessary medication adjustments.

Dosage: How Much Vitamin A Do I Need?

Always speak with a healthcare provider before taking a supplement to ensure that the supplement and dosage are appropriate for your individual needs.

The Recommended Dietary Allowance (RDA) is the daily amount of vitamins or minerals needed.

RDAs may vary based on age, sex, pregnancy, and breastfeeding status.

Upper limits (ULs) are the maximum amounts of a vitamin or mineral people should ingest daily. Amounts ingested above the daily UL may produce side effects or toxicity.

The following includes information about different populations' RDAs and ULs.

In children with a high risk of vitamin A deficiency in developing countries, the recommended dosages for vitamin A are:

Infants between 6 and 11 months : 100,000 international units (IU) or 30,000 micrograms (mcg) of retinol activity equivalents (RAE) as a onetime dose
Children between 1 and 5 years old : 200,000 IU or 60,000 mcg RAE every 4 to 6 months

For these children, vitamin A supplementation might lower the risk of morbidity and mortality . Additional clinical trials are still necessary to study different vitamin A doses and various ways vitamin A is given.

If you plan to use vitamin A, follow a healthcare provider's recommendations or product label instructions.

Vitamin A Toxicity

If you take too much vitamin A, toxicity is possible. Generally, the recommended daily amounts of vitamin A from different sources—like foods and supplements—are based on age, sex, pregnancy, and breastfeeding status.

Once you're older than 18, the upper limit (UL) for animal-based foods and vitamin A supplements is around 3,000 mcg daily.

If you accidentally took too much vitamin A, overdose symptoms are likely similar to vitamin A's potential and serious side effects. This may include the following:

Bone problems : Too much vitamin A may cause bone pain and decrease your bone mineral density (BMD). So, over time, large amounts of vitamin A may increase your risk of osteoporosis (weak and brittle bones) and bone fracture (break).
Brain swelling : High amounts of vitamin A might cause some brain swelling. Symptoms may include headaches, nausea or vomiting , vision changes, seizures, and memory problems.
Cancer : Vitamin A might have harmful effects—like lung cancer—on certain groups of people, such as people who currently or formerly smoked and people who had asbestos exposure.
Liver problems : There are reports of liver problems with vitamin A over the daily upper limit. Symptoms of worsening liver function may include upper right-sided stomach pain, dark urine, and yellowing of the eyes or skin.
Negative effects on the unborn fetus : Above the UL for daily vitamin A, there are reports of negative effects on the unborn fetus.

If you think you took too much vitamin A or suspect you are experiencing life-threatening side effects, seek immediate medical attention.

Does Vitamin A Interact With Medications or Other Dietary Supplements?

Limited information about possible vitamin A interactions with medications or other dietary supplements exists.

Possible interactions include the following:

Medications or supplements that affect fat absorption : Vitamin A is a fat-soluble vitamin, meaning it needs some fat to be absorbed into the bloodstream. Therefore, medications or supplements that affect fat absorption will likely affect vitamin A's absorption into your bloodstream. Examples of these medications may include Xenical (orlistat) for weight loss and Questran (cholestyramine) for cholesterol .
Retinoids : Retinoids are vitamin A-based medications. For this reason, combining vitamin A with retinoids may increase the likelihood of vitamin A toxicity and side effects. An example of a retinoid medication may include Soriatane (acitretin) for certain skin conditions, such as psoriasis .

It is essential to carefully read a supplement's ingredients list and nutrition facts panel to know which ingredients and how much of each ingredient is included.

Please review this supplement label with a healthcare provider to discuss potential interactions with foods, other supplements, and medications.

Vitamin A may affect health, such as supporting eye health and limiting the severity of infections. So, other potentially similar supplements may include the following:

AREDS2 supplements : AREDS2 supplements may slow down the worsening of a vision-threatening eye condition called age-related macular degeneration (AMD).
Vitamin C : Routinely taking vitamin C may help relieve your cold symptoms.

Only combine multiple natural products once you first talk with a healthcare provider, pharmacist, or registered dietitian nutritionist (RD or RDN) . Checking in can help you avoid possible harmful interactions and side effects and ensure you're giving these supplements a fair trial at appropriate doses.

Sources of Vitamin A & What to Look For

There are several sources of vitamin A, but health nutrition guidelines typically place more importance on food sources to improve the diet.

Although food sources are preferable, there is still a place for supplements for people with nutrient absorption problems.

This may happen to people in certain age groups or with certain medical conditions.

What Foods Have Vitamin A?

Generally, there are two sources of vitamin A—preformed vitamin A and provitamin A carotenoids.

Preformed vitamin A—like retinol—is naturally available in various animal-based foods, such as the following:

Dairy (milk) products

The provitamin A carotenoids are also naturally available in food—but plant-based products. And your body can change these carotenoids into vitamin A. These foods include the following:

Sweet potatoes
Corn (not the white variety)
Red palm oil
Buriti palm oil

Vitamin A is a fat-soluble, essential vitamin for several normal bodily functions. Your body needs fat to absorb it.

Vitamin A deficiency in the United States is rare. However, vitamin A may have some potential effects on health, such as age-related macular degeneration, cancer, and measles.

Some of the evidence for vitamin A is mixed. And some studies showed that vitamin A or beta-carotene (a provitamin A carotenoid) supplements might have harmful effects in certain groups of people. Vitamin A and beta-carotene supplements tend to have a much higher concentration of these nutrients than foods. Try to get vitamin A and beta-carotene from food sources instead of supplements unless your healthcare provider advises differently.

It's essential to ensure the diagnosis and treatment of your medical conditions are completed on time. Avoid self-diagnosing and/or self-treating conditions that may be potentially serious. Involving an RD or RDN, pharmacist, or healthcare provider before taking vitamin A to help you safely achieve your health goals.

Vitamin A is a fat-soluble vitamin. It's also an essential vitamin because it's necessary for a number of normal bodily functions.

Vitamin A plays several essential parts in your body, such as your eyesight and immune system (the body's defense system). It's also essential for normal growth, development, and reproductive health. Moreover, vitamin A affects your heart, lungs, and other organs.

Vitamin A supplements are available in a few different dosage forms—with capsules being the most common.

Gilbert C. What is vitamin A and why do we need it? Community Eye Health . 2013;26(84):65.

PubChem. Retinol .

National Institutes of Health. Vitamin A and carotenoids - fact sheet for health professionals .

National Institutes of Health: Office of Dietary Supplements. Dietary supplement label database: vitamin A .

Food and Drug Administration. Substances added to food (formerly EAFUS) : vitamin A .

United States Department of Agriculture. FoodData Central: vitamin A .

American Academy of Ophthalmology. What is macular degeneration? .

Agrón E, Mares J, Clemons TE, et al. Dietary nutrient intake and progression to late age-related macular degeneration in the Age-Related Eye Disease Studies 1 and 2 . Ophthalmology . 2021;128(3):425-442. doi: 10.1016%2Fj.ophtha.2020.08.018

Chew EY, Clemons TE, Agrón E, et al. Long-term outcomes of adding lutein/zeaxanthin and ω-3 fatty acids to the AREDS supplements on age-related macular degeneration progression: AREDS2 report 28 . JAMA Ophthalmology . 2022;140(7):692-698. doi: 10.1001/jamaophthalmol.2022.1640

National Eye Institute. AREDS/AREDS frequently asked questions .

Rowles JL 3rd, Ranard KM, Smith JW, et al. Increased dietary and circulating lycopene are associated with reduced prostate cancer risk: a systematic review and meta-analysis . Prostate Cancer Prostatic Dis . 2017;20(4):361-377. doi:10.1038/pcan.2017.25

Chen F, Hu J, Liu P, et al. Carotenoid intake and risk of non-Hodgkin lymphoma: a systematic review and dose-response meta-analysis of observational studies . Ann Hematol . 2017;96(6):957-965. doi:10.1007/s00277-016-2898-1

Chen J, Jiang W, Shao L, et al. Association between intake of antioxidants and pancreatic cancer risk: a meta-analysis . Int J Food Sci Nutr . 2016;67(7):744-53. doi:10.1080/09637486.2016.1197892

Leoncini E, Nedovic D, Panic N, et al. Carotenoid intake from natural sources and head and neck cancer: a systematic review and meta-analysis of epidemiological studies . Cancer Epidemiol Biomarkers Prev . 2015;24(7):1003-11. doi:10.1158/1055-9965.EPI-15-0053

Li H, He P, Lin T, et al. Association between plasma retinol levels and the risk of all-cause mortality in general hypertensive patients: A nested case-control study . J Clin Hypertens (Greenwich) . 2020;22(5):906-913. doi:10.1111/jch.13866

Li X, Xu J. Meta-analysis of the association between dietary lycopene intake and ovarian cancer risk in postmenopausal women . Sci Rep . 2014;4:4885. doi:10.1038/srep04885

Wang Q, He C. Dietary vitamin A intake and the risk of ovarian cancer: a meta-analysis . Biosci Rep . 2020;40(4):BSR20193979. doi:10.1042/BSR20193979

Lv W, Zhong X, Xu L, et al. Association between dietary vitamin A intake and the risk of glioma: evidence from a meta-analysis . Nutrients . 2015;7(11):8897-904. doi:10.3390/nu7115438

Tang JE, Wang RJ, Zhong H, et al. Vitamin A and risk of bladder cancer: a meta-analysis of epidemiological studies . World J Surg Oncol . 2014;12:130. doi:10.1186/1477-7819-12-130

Leelakanok N, D'Cunha RR, Sutamtewagul G, et al. A systematic review and meta-analysis of the association between vitamin A intake, serum vitamin A, and risk of liver cancer . Nutr Health . 2018;24(2):121-131. doi:10.1177/0260106018777170

Psaltopoulou T, Ntanasis-Stathopoulos I, Tsilimigras DI, et al. Micronutrient intake and risk of hematological malignancies in adults: a systematic review and meta-analysis of cohort studies . Nutr Cancer . 2018;70(6):821-839. doi:10.1080/01635581.2018.1490444

Wang X, Yang HH, Liu Y, et al. Lycopene consumption and risk of colorectal cancer: a meta-analysis of observational studies . Nutr Cancer . 2016;68(7):1083-96. doi:10.1080/01635581.2016.1206579

Aune D, Keum N, Giovannucci E, et al. Dietary intake and blood concentrations of antioxidants and the risk of cardiovascular disease, total cancer, and all-cause mortality: a systematic review and dose-response meta-analysis of prospective studies . Am J Clin Nutr . 2018;108(5):1069-1091. doi:10.1093/ajcn/nqy097

Omenn GS, Goodman GE, Thornquist MD, et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease . N Engl J Med . 1996;334:1150-1155. doi:10.1056/NEJM199605023341802

Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers . N Engl J Med . 1994;330(15):1029-35. doi:10.1056/NEJM199404143301501.

Age-Related Eye Disease Study 2 Research Group. Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial . JAMA . 2013;309(19):2005-15. doi:10.1001/jama.2013.4997

Hennekens CH, Buring JE, Manson JE, et al. Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease . N Engl J Med . 1996;334(18):1145-9. doi:10.1056/NEJM199605023341801

Lin J, Cook NR, Albert C, et al. Vitamins C and E and beta carotene supplementation and cancer risk: a randomized controlled trial . J Natl Cancer Inst . 2009;101(1):14-23. doi:10.1093/jnci/djn438

Kamangar F, Qiao YL, Yu B, et al. Lung cancer chemoprevention: a randomized, double-blind trial in Linxian, China . Cancer Epidemiol Biomarkers Prev . 2006;15(8):1562-4. doi:10.1158/1055-9965.EPI-06-0316

Benn CS, Aaby P, Arts RJW, et al. An enigma: why vitamin A supplementation does not always reduce mortality even though vitamin A deficiency is associated with increased mortality . International Journal of Epidemiology . 2015;44(3):906-918. doi: 10.1093/ije/dyv117

World Health Organization. Measles .

Imdad A, Mayo-Wilson E, Herzer K, 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 . 2017;3:CD008524. doi: 10.1002/14651858.CD008524.pub3

Debelo H, Novotny JA, Ferruzzi MG. Vitamin A . Adv Nutr . 2017;8(6):992-994. doi:10.3945/an.116.014720

National Institutes of Diabetes and Digestive and Kidney Diseases. LiverTox: Clinical and research information on drug-induced liver injury .

MedlinePlus. Bone density scan .

MedlinePlus. Bone density .

National Center for Complementary and Integrative Health. 5 things to know about dietary supplements for eye conditions .

National Center for Complementary and Integrative Health. 5 tips: natural products for the flu and colds: What does the science say? .

Lentjes MAH. The balance between food and dietary supplements in the general population . Proc Nutr Soc . 2019;78(1):97-109. doi:10.1017%2FS0029665118002525

By Ross Phan, PharmD, BCACP, BCGP, BCPS Ross is a writer for Verywell with years of experience practicing pharmacy in various settings. She is also a board-certified clinical pharmacist and the founder of Off Script Consults.

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Health Encyclopedia

Other name(s):.

b-carotene, beta-carotene, retinol, vitamin A-1

General description

Vitamin A is also called retinol. It was the first substance isolated in the group called vitamins. It is 1 of 4 fat-soluble vitamins. This means it can dissolve in fats and oils. It’s found in animal products. Fat-soluble vitamins are stored in the body. They can build up to toxic levels if you take too much of them.

Precursors of vitamin A exist in plants. They’re called carotenoids. These are fat soluble but nontoxic, even in large quantities. The best-known carotenoid is beta-carotene. Both retinoids and carotenoids are good antioxidants.

Vitamin A is part of the reproductive process. It helps with the growth of sperm. It also helps with the growth of a baby in the womb. But high doses of vitamin A and synthetic retinols may lead to problems with growth in the womb. It may also lead to birth defects. Vitamin A seems to help the growing tissues in a baby in the womb. It also helps the placenta form during pregnancy.

Vitamin A is an important factor in growth throughout life. Vitamin A helps grow and maintain epithelial tissues. These include mucous membranes, the lining of the gastrointestinal tract, lungs, bladder, urinary tract, vagina, cornea, and skin. Vitamin A also helps the growth of bones and teeth.

Vitamin A prevents drying of the skin. This may protect the body from infectious diseases. It also helps maintain the immune system.

Vitamin A is also needed for night vision. Retinol (a vitamin A metabolite) combines with opsin (a pigment in the retina of the eye) to form rhodopsin. This is a chemical that helps with night vision.

Medically valid uses

Vitamin A helps with the reproductive process, growth, and development. It also keeps eyes and skin healthy and acts as an antioxidant.

Vitamin A supplements may reduce the risk for certain types of cancer. Vitamin A influences cell development. It also increases the activity of immune-system cells. This could make it valuable in the fight against cancer, especially skin, lung, bladder, and breast cancer.

Unproven claims

There may be benefits that have not yet been proven through research.

Vitamin A may prevent some types of cancer and acne. It may also help treat psoriasis. It’s also claimed to help treat dry or wrinkled skin. It may also protect against the effects of pollution and prevent respiratory tract infections. Vitamin A may aid in healing sunburns. It’s also been used to treat kidney stones, inflammatory bowel disease, and deafness.

Vitamin A has been called the anti-infection vitamin because of its role in helping the body fight bacterial, parasitic, and viral infections.

Recommended intake

Vitamin A is measured in Retinol Activity Equivalents (RAE) to account for the different bioactivities of retinol and provitamin A carotenoids. The RDA is the recommended dietary allowance.

Vitamin A was previously listed on labels in international units (IUs). Under new FDA labeling rules, vitamin A will be listed in mcg RAE and not IUs. This change took effect in 2020 and 2021. An RAE can't be directly converted into an IU if you don't know the source of vitamin A. Conversion rates between mcg RAE and IU are:

1 IU retinol = 0.3 mcg RAE

1 IU beta-carotene from dietary supplements = 0.15 mcg RAE

1 IU beta-carotene from food = 0.05 mcg RAE

1 IU alpha-carotene or beta-cryptoxanthin = 0.025 mcg RAE

*Adequate intake (AI). This is based on the average intake in healthy, breastfed infants.

Smaller people need less vitamin A than larger people do. In most cases, women need less than men, except during pregnancy and while breastfeeding.

Vitamin A is stable at room temperature. It doesn’t need to be refrigerated. Cooking, freezing, or canning vegetables and fruits doesn’t destroy much vitamin A. But you shouldn’t freeze vitamin A tablets and capsules. Vitamin A is also stable in light.

A poor diet with not enough vitamin A can increase your need for vitamin A. So can diets containing large amounts of snack foods containing the fat substitute olestra.

Malabsorption syndromes that cause excess fat in the stool (steatorrhea) may deplete all 4 fat-soluble vitamins: A, D, E, and K. There are many types of malabsorption syndromes. These include:

Lactose intolerance

Tropical and nontropical sprue

Celiac disease

Cystic fibrosis

Ulcerative colitis

Crohn's disease

Steatorrhea can also be caused by removal of all or part of the pancreas.

You may need more vitamin A if you have any of these:

A fever that lasts

Hyperthermia

Ongoing use of mineral oil

Hyperthyroidism

An early sign of vitamin A deficiency is night blindness. This may start with less ability to see at night or in the dark. The time for your eyes to adjust to the dark increases. Over time, you lose the ability to see at night.

Vitamin A deficiency also causes conjunctival dryness. This starts with a dry feeling in your eyes. The eyelid linings also become dry and rough. Then the cornea dries out. It becomes wrinkled and cloudy. Scarring then occurs. This causes permanent changes. It leads to blindness.

Skin changes are another sign of too little vitamin A. The skin becomes dry and rough. This is seen over the shoulders, buttocks, and the opposite side of a joint of the arms and legs. Little bumps may show up around the base of each hair. This causes a sandpaper-like feel to the skin.

Mucous membranes may also change. This may affect the lining of the urinary tract. This may cause burning and bleeding with urination. The lining of the vagina may also get dry and inflamed.

Retinol is used to treat vitamin A deficiency. In many undeveloped countries, vitamin A deficiency is common. Because vitamin A can be stored in the body, large doses can be given to children (and some adults) only 2 or 3 times a year. This is done to prevent xerophthalmia. This is a condition that leads to blindness. Vitamin A deficiency is rare in the U.S. When it occurs, it’s usually due to malabsorption caused by other diseases.

Side effects, toxicity, and interactions

Vitamin A in the form of beta-carotene is considered safe. It doesn’t appear to be toxic in large doses. But high doses over a long period of time can lead to carotenemia. In this condition, your skin becomes yellowish orange.

Too much vitamin A may increase the risk for hip fracture in women.

Vitamin A overdose in the form of retinoids from animal sources can be toxic. The conditions of overdose (hypervitaminosis) are divided into two groups: acute and chronic. These are then split into infant and adult.

Children are more sensitive than adults to overdoses of vitamin A. The symptoms of an acute overdose in an infant or child include:

Nausea and vomiting

Extreme sleepiness

Bulging soft spot (fontanel) on the top of the baby's head

Pseudotumor cerebri. This condition increases pressure around the brain, bulging of the optic disc in the back of the eye, paralysis, or change in function of some of the cranial nerves. This is seen after the soft spot has closed over and the sutures fused.

The symptoms of a chronic overdose in a baby or child include:

Loss of appetite

Slowed weight gain

Irritability

Hair loss (alopecia)

Skin changes, such as dryness, roughness, and cracks in the corners of the mouth

In adults, symptoms of an acute overdose may include:

Double vision

The signs of a chronic overdose in adults include:

Skin changes, such as dryness, roughness, and cracks in the lips and corners of the mouth

Increased pressure around the brain that may cause symptoms like a brain tumor

You shouldn’t take vitamin A supplements if you’re allergic to vitamin A.

You shouldn’t take very high doses of vitamin A during pregnancy. This is because high doses may cause malformations in your baby growing in the womb.

Mineral oil, cholestyramine, and foods containing olestra may interfere with the absorption of vitamin A. Orlistat, a medicine for weight loss, has been shown to decrease absorption of beta-carotene and vitamin E. Whether orlistat has the same effect on vitamin A is unknown.

You shouldn’t take vitamin A supplements if you’re taking isotretinoin, acitretin, or etretinate.

If you’re using topical ointments that are in the retinoid family, ask your healthcare provider if it’s safe for you to take vitamin A supplements.

Taking tetracycline with high doses of vitamin A may cause benign intracranial hypertension. You shouldn’t take this medicine with vitamin A.

Oral birth control pills increase the levels of vitamin A in your body. For this reason, you may not need vitamin A supplements.

Warfarin (Coumadin) is used to slow blood clotting. Large amounts of vitamin A can also slow blood clotting. Taking vitamin A along with warfarin can increase the chances of bruising and bleeding. Have your blood checked regularly. The dose of your warfarin might need to be changed.

Medical Reviewers:

Brittany Poulson MDA RDN CD CDE
Heather M Trevino BSN RNC
Rita Sather RN
Ask a Medical Librarian Make an Appointment Physicians & Services Pediatric Gastroenterology/Nutrition at Golisano Children's Hospital

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Continuing Education Activity

Vitamin A plays a crucial role in regulating various physiological processes of the body and maintaining vision and immune system function to support skin health and cell growth. Although vitamin A is essential for the body, excessive intake can pose various adverse effects, disrupting the body's equilibrium and overall well-being. Vitamin A toxicity, also known as hypervitaminosis A, can result from either the excessive consumption of vitamin A and related compounds or its topical application. This activity describes the causes, evaluation, management, treatment, and prevention of vitamin A toxicity, emphasizing the essential role of the interprofessional healthcare team in enhancing care for affected patients.

Identify the risk factors associated with excessive vitamin A intake, considering dietary sources, supplements, and medication history.
Assess laboratory findings, including serum vitamin A levels, liver function tests, lipid profiles, and hematological parameters, to diagnose and monitor vitamin A toxicity in patients.
Select and recommend appropriate treatment modalities, alternative therapies, or supplements to patients based on the severity and presentation of vitamin A toxicity.
Coordinate with the interprofessional healthcare team to guide pregnant women about safe vitamin A use during pregnancy and prevent teratogenic malformations.
Introduction

Vitamin A is essential for maintaining the body's vision, cell division, reproduction, and immune function. Vitamin A belongs to the category of lipid-soluble compounds called retinoic acids. Beta-carotene is the most well-known form of 2 clinically significant forms of vitamin A: preformed vitamin A and provitamin A carotenoids. Mammals metabolize carotenoids into active vitamin A. Preformed vitamin A encompasses metabolically active compounds such as retinol, retinal, retinoic acid, and retinyl esters. Although essential for overall health, excessive consumption of preformed vitamin A can lead to acute and chronic toxicity. The condition characterized by elevated levels of vitamin A in the body is referred to as hypervitaminosis A. Vitamin A, also known as teratogen, is capable of causing severe malformations. This article comprehensively reviews the prevention, presentation, laboratory findings, and treatment of the 3 recognized syndromes of vitamin A toxicity: acute, chronic, and teratogenic.

Hypervitaminosis A is relatively uncommon and usually arises from excessive supplementation or medication usage. The primary cause of toxicity is the consumption of substantial quantities of vitamin A through dietary supplements and foods. This usually occurs when individuals consume high doses of vitamin A without proper medical supervision. Most diets contain a combination of preformed vitamin A and provitamin A carotenoids. Preformed vitamin A is derived from animal sources and is found in egg yolks, butter, chicken, beef, organ meats, fish, fish oils, and fortified foods. [1] Preformed vitamin A is readily absorbed in the small intestine and subsequently stored in the liver. Therefore, excessive intake of dietary preformed vitamin A from animal-based sources and supplements can contribute to the risk of toxicity.

Provitamin A carotenoids, such as beta-carotene, are plant pigments that the body converts into active vitamin A. These carotenoids are plentiful in leafy greens and vibrantly colored vegetables and fruits, including carrots, sweet potatoes, and papayas. [2] The absorption of provitamin A is variable and subject to feedback regulation, making it unlikely to lead to toxicity with excessive intake. [3] Certain dermatological medications, such as isotretinoin, contain analogs of vitamin A. Prolonged or excessive usage of these medications can lead to an accumulation of vitamin A stores, resulting in hypervitaminosis A, toxicity, and teratogenic effects.

The recommended daily allowance (RDA) for vitamin A is measured in retinol activity equivalents (RAE) to account for the different bioactivities of retinol and provitamin A carotenoids. Notably, 1 RAE is equivalent to 1 mcg of retinol or 3 International units (IU).

The RDA for vitamin A is as follows:

700 RAE for adult women
900 RAE for adult men
750 to 770 RAE for pregnant women
1200 to 1300 RAE for lactating women

The tolerable upper intake levels (UL) for vitamin A have been established to prevent toxicity. The UL of vitamin A for adults is 3000 RAE per day, including preformed vitamin A from foods and supplements and the amount that can be converted from plant-based sources such as beta-carotene. The consumption of preformed vitamin A from dietary supplements in developed countries frequently surpasses the RDA. [4]

Epidemiology

Few published reports of vitamin A toxicity have been published, with fewer than 10 cases per year documented from 1976 to 1987. [5] Infants and children are at a higher risk of toxicity due to their smaller body size and reduced tolerance for high doses. [6] Accidental ingestion of vitamin A supplements by children is a common cause of acute toxicity. There is no substantial difference in the occurrence of vitamin A toxicity between males and females. However, pregnant women are at risk if they take high doses of vitamin supplements.

Excessive supplement intake typically occurs in developed countries when individuals exceed the RDA. [4] Supplementation programs have been implemented in regions where vitamin deficiency is a significant public health concern. Moreover, toxicity can arise if dosing guidelines are not carefully followed. [7] [8] Populations heavily reliant on liver-based food sources rich in vitamin A, such as polar bear liver and chicken liver, face an increased risk of vitamin A toxicity. However, only rare cases of this phenomenon are reported in the published literature, and it is not considered a significant public health concern. [9] [10] [11]

Pathophysiology

The symptoms of systemic vitamin A toxicity vary depending on the severity and duration of excessive intake. The 3 recognized syndromes of vitamin A toxicity are acute, chronic, and teratogenic.

Acute systemic vitamin A toxicity typically arises when an individual consumes over 100,000 RAE within a short period, often from supplements or high-dose medications. The toxicity symptoms include nausea, vomiting, headache, dizziness, irritability, blurred vision, and muscular incoordination. Acute toxicity is rare and is more likely to occur after consuming synthetic forms of vitamin A, such as the retinoid medication isotretinoin. Mucocutaneous effects include cheilitis and dryness of lips and oral, ophthalmic, and nasal mucosa. The suggested mechanism involves decreased sebum production, reduced epidermal thickness, and altered barrier function. Additional cutaneous effects include dry skin, pruritus, peeling of the palms and soles, and fissuring of the fingertips. Higher doses of vitamin A may lead to telogen effluvium. Severe cases may manifest with bone pain and increased intracranial pressure.

Chronic vitamin A toxicity is associated with prolonged ingestion of excessive vitamin A, typically exceeding 8000 RAE per day. This condition can develop after consuming substantial quantities of animal-based foods rich in preformed vitamin A, such as liver, or through the prolonged use of high-dose vitamin A supplements. [12] The toxicity symptoms include dry, cracked skin, hair loss, brittle nails, fatigue, loss of appetite, bone and joint pain, and hepatomegaly. Chronic retinoid toxicity affects various organ systems. Bone-related effects include bone spurs, calcinosis, and bone resorption, leading to hypercalcemia, osteoporosis, and hip fractures. [13] [14] Central nervous system effects include headache, nausea, and vomiting.

Pseudotumor cerebri syndrome has been associated with vitamin A toxicity. [15] Hypothyroidism, reversible upon discontinuation of therapy, was observed in 40% of patients during clinical trials for cutaneous T-cell lymphoma with bexarotene, a derivative of vitamin A. [16] Reversible renal dysfunction with elevated serum creatinine has been observed after etretinate use, but not after isotretinoin use. [17] Etretinate, a psoriasis medication, is no longer prescribed in most countries because of its teratogenic effects.

Hypertriglyceridemia is the most common laboratory abnormality associated with oral retinoid use. Triglyceride, low-density lipoprotein, and total cholesterol levels increase in many patients using bexarotene, isotretinoin, etretinate, and acitretin. [18] [19] Elevated serum transaminases may also occur with oral retinoid usage, more often with etretinate or acitretin compared to isotretinoin and bexarotene. These levels typically show an increase within 2 to 8 weeks after the initiation of therapy, followed by normalization over the subsequent 2 to 4 weeks. Prolonged liver damage can include fibrosis and cirrhosis. [20] No definitive causal association has been established between isotretinoin and depression, psychosis, or suicide attempts, although such a link had been previously suggested. [21]

The teratogenic effects of vitamin A intake were first discovered in animal studies during the 1950s. Subsequently, extensive research has been conducted to elucidate the underlying causes of the effects. [22] Excessive vitamin A consumption during pregnancy has been associated with various congenital malformations in humans. The disabilities associated with this condition include abnormalities in the central nervous system, such as microcephaly and hydrocephalus; cardiac issues, such as transposition of the great vessels; craniofacial deformities, such as cleft lip and palate; limb abnormalities; and urinary tract disorders. [5] [3]

Vitamin A is critical for regulating gene expression and guiding cell differentiation during embryonic development. The embryo is particularly susceptible to the teratogenic effects of excessive amounts of vitamin A during the first trimester, which is a phase marked by rapid organogenesis. Teratogenic effects are primarily associated with high doses of retinoid medications such as isotretinoin rather than dietary sources of vitamin A. A minimum safe dose of oral retinoids during pregnancy has not been established. Isotretinoin is estimated to increase the risk of fetal malformations by 25-fold. [5] The mechanism is believed to be linked to a toxic effect on neural crest cells, possibly affecting the regulation of axial patterning in the embryo via the expression of the homeobox gene Hoxb-1 . [23]

Pregnant women should refrain from using oral retinoid medications and excessive vitamin A supplements to mitigate the risk of vitamin A-related malformations. They should consult healthcare professionals and prenatal care providers to ensure proper prenatal nutrition and avoid drugs or supplements that are contraindicated during pregnancy. Prescribers should only recommend oral retinoids to women of childbearing age who are not pregnant and use reliable birth control methods to prevent the potential risk of vitamin A-related teratogenic effects.

Histopathology

Hypervitaminosis A affects multiple organ systems of the body and can damage the liver, bones, central nervous system, and skin. The specific histopathological findings differ based on the severity and duration of the toxicity, some of which are listed below.

Liver: Hepatic steatosis, hepatocellular injury, and fibrosis with collagen deposits

Bone: Osteoporosis and thickening of cortical bone

Central nervous system: Pseudotumor cerebri and cerebral edema

Skin: Exfoliative dermatitis and epidermal hyperplasia [24] [25]

Toxicokinetics

The toxicokinetics of vitamin A toxicity involve its absorption, distribution, metabolism, and elimination from the body.

Absorption: Dietary vitamin A is sourced from 2 main categories: preformed vitamin A, including retinol and retinyl esters, which are found in animal-derived products and supplemented foods, and provitamin A carotenoids present in fruits and vegetables. High-fat meals enhance the absorption of vitamin A in the small intestine.

Distribution: After absorption, vitamin A is transported to the liver, where it is stored as retinyl esters. From there, it is released into the bloodstream bound to retinol-binding protein (RBP) and transthyretin. These carrier proteins help transport vitamin A to target tissues, including the eyes, skin, and other organs.

Metabolism: Retinol is converted into its active forms, retinal and retinoic acid, within target tissues. Lecithin retinol acyltransferase (LRAT) is the enzyme responsible for catalyzing retinoid esterification for storage in the liver. [26] Cellular RBP assists LRAT in regulating retinoid uptake and metabolism. These 2 proteins are essential in the metabolism of retinoids, which may be responsible for the toxic effects of vitamin A.

Elimination: Fat-soluble vitamin A and its metabolites are primarily excreted through bile and feces, with only a small portion being eliminated in the urine.

History and Physical

The medical history will likely reveal excessive consumption of vitamin A-rich foods, supplements, or oral retinoid medications. Symptoms include blurred vision, headaches, dry skin, hair loss, fatigue, and bone pain. Typical physical examination findings may include dryness of the conjunctiva and mucous membranes, scaly skin, alopecia, papilledema, bone tenderness, and hepatomegaly.

Patients with a history of using topical vitamin A derivatives will likely exhibit localized skin peeling and erythema, but systemic signs and symptoms are not expected.

A patient's history and physical examination findings guide the selection of diagnostic studies. Patients with persistent headaches while taking vitamin A medications should be evaluated for increased intracranial pressure and pseudotumor cerebri syndrome.

Laboratory findings obtained during assessing patients with vitamin A toxicity can reveal several abnormalities, a few of which are mentioned below.

Serum vitamin A levels: The serum vitamin A levels exceed 80 mcg/dL.

Liver function tests: Elevated levels of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP) indicate potential hepatic damage or inflammation.

Serum lipids: Increased levels of triglycerides and cholesterol are observed.

Hematological abnormalities: The identified abnormalities in the blood include leukocytosis, thrombocytopenia, and anemia.

Bone markers: Increased levels of ALP are associated with bone turnover.

Renal function: Elevations of blood urea nitrogen and creatinine occur.

Electrolyte imbalances: Alterations in electrolyte levels, such as sodium, potassium, and calcium occur.

Some patients require laboratory testing to monitor their condition. Individuals taking isotretinoin should undergo regular lipid level checks. [27] Elevations in liver enzymes are usually mild and reversible, although ALT and AST may need to be monitored based on the dosage and any comorbidities the patient may have. [28]

Women of childbearing age must have 2 negative pregnancy tests, conducted 30 days apart, before initiating isotretinoin treatment. Additional testing during and immediately after discontinuing the treatment is also necessary. [29]

Free T4 should be monitored both before and during treatment with bexarotene. [30] In addition, baseline fasting serum lipid levels should be measured at treatment initiation and then every 1 to 2 weeks during therapy until they stabilize.

Patients with a history of kidney disease and undergoing etretinate therapy should regularly monitor their renal function throughout the treatment course. [17]

Treatment / Management

The treatment of systemic vitamin A toxicity includes discontinuing vitamin A intake, providing supportive care, and managing patient symptoms.

The management of skin irritation caused by topical retinoids involves reducing the volume and frequency of applications while increasing the use of emollients. Patients can be reassured that this adverse effect will likely improve with the continued use of the skincare products.

Acute retinoid toxicity is rare, but in documented cases, recovery is typically rapid upon discontinuation of the medication. [31] The sources of excess vitamin A intake, including dietary supplements and medications, must be identified as a primary step. Furthermore, healthcare professionals should recommend avoiding foods rich in preformed vitamin A to patients, such as liver and fortified products, until the toxicity resolves.

Supportive care involves close monitoring of the patient's condition, including vital signs and overall health status. Severe cases may necessitate hospital admission. Hypotension can be managed with fluid administration, and hypercalcemia can be treated with calcitonin and corticosteroids. When there is evidence of hepatic damage, liver function tests can assess the extent of the injury and guide further management decisions.

Patients with dry or peeling skin are advised to use moisturizers or emollients to alleviate discomfort and facilitate skin healing. For patients experiencing dry eyes, artificial tears and lubricating eye drops, including those containing methylcellulose, can be beneficial.

The treatment of medication-induced chronic toxicity depends on the specific drug and its adverse effects. In cases where oral retinoids can lead to an elevation of the fasting triglyceride level to 800 mcg/dL or higher, options such as discontinuation, dose reduction, or the addition of lipid-lowering medication can be considered to prevent pancreatitis. Milder elevations can be monitored or treated similarly.

Patients experiencing toxicity from bexarotene can consider using a statin or fibrate concurrently to manage retinoid-induced hyperlipidemia and lower the risk of pancreatitis. Therapy may need to be discontinued if values remain elevated despite intervention and exceed 3 times the upper limit of normal. [32]

Patients diagnosed with pseudotumor cerebri syndrome should discontinue using vitamin A medications and might need acetazolamide to lower the intracranial pressure. [15]

Teratogenic malformations result in permanent damage, and the necessary supportive or surgical care varies based on the affected organ system.

Differential Diagnosis

When assessing the differential diagnosis of hypervitaminosis A, it is crucial to exclude other conditions that might manifest with similar symptoms, some of which are listed below.

Acute liver injury: Viral hepatitis, alcohol use, or drug toxicity.

Hypercalcemia: Hyperparathyroidism, malignancy, or excessive calcium and vitamin D intake.

Hypothyroidism: Primary thyroid disorders or medications.

Chronic renal failure: Diabetes, hypertension, glomerulonephritis, or polycystic kidney disease.

Central nervous system: Headache, nausea, and vomiting may be symptoms of pseudotumor cerebri and are not always caused by vitamin A toxicity.

Dermatological conditions: Exfoliative dermatitis and other skin conditions.

Nonspecific symptoms: The nonspecific symptoms, including skin rashes, joint pain, fatigue, and renal and liver abnormalities, can also indicate conditions such as systemic lupus erythematosus and may not solely point to vitamin A toxicity.

The prognosis of hypervitaminosis A depends on the severity of the condition and the duration of exposure to high levels of vitamin A. In most patients who discontinue the source of excess vitamin A, toxicity symptoms gradually reverse, and complete recovery is expected. Symptoms such as dry skin, headache, and nausea typically improve within a few weeks or months with no long-term complications.

However, severe cases can have serious consequences. Prolonged and excessive vitamin A intake can result in significant organ damage, including the liver, bones, central nervous system, and skin. Liver fibrosis or cirrhosis may be irreversible. Bone abnormalities, such as reduced bone density or fractures, may persist even after discontinuing vitamin A intake. In cases of pseudotumor cerebri, visual impairment may be permanent. The prognosis depends on the extent of organ damage and the promptness of medical intervention.

Complications

Complications of vitamin A toxicity include those listed below.

Acute toxicity: Nausea, vomiting, headache, dizziness, irritability, blurred vision, and intracranial hypertension

Chronic toxicity: Dry, itchy skin, hair loss, bone and joint pain, fatigue, anorexia, and weight loss

Teratogenic effects: Craniofacial abnormalities, central nervous system malformations, and cardiovascular malformations

Hepatic toxicity: Hepatomegaly, elevated liver enzymes, jaundice, fibrosis, and cirrhosis

Skeletal abnormalities: Increased bone resorption, decreased bone formation, osteoporosis, fractures, and bone pain

Hematological disturbances: Leukocytosis, anemia, and thrombocytopenia

Central nervous system: Pseudotumor cerebri, with symptoms of headache, visual disturbances, and papilledema

Deterrence and Patient Education

Patient education regarding vitamin A toxicity is a shared responsibility among healthcare professionals, including physicians, advanced care practitioners, registered dietitians, nurses, and pharmacists. The significance of maintaining a balanced diet that includes essential vitamins and minerals is emphasized during routine medical appointments. Information regarding dietary sources of vitamin A, such as liver, fish, eggs, dairy products, and colorful fruits and vegetables, is provided to patients. Clinicians should advise patients about their recommended daily vitamin A intake according to their age, sex, and overall health.

Pharmacists provide information about both over-the-counter and prescription drugs containing vitamin A or its derivatives, including retinoids. They can elucidate the proper usage and potential adverse effects of these medications, underscoring the significance of adhering to the recommended dosage and treatment duration.

Obstetricians and other clinicians responsible for caring for women of childbearing age are responsible for educating them about the risks associated with excessive vitamin A intake from supplements or medications during pregnancy and the potential for teratogenic effects.

If clinicians suspect toxicity, they should communicate the possible complications to patients and recommend discontinuing sources of vitamin A. This may involve dietary modifications and adjustments to medication and supplement usage.

Pearls and Other Issues

Teratogenicity is the most significant adverse effect of vitamin A toxicity. To mitigate this risk, patients should be counseled to avoid consuming more than the recommended amount of supplemental vitamin A during pregnancy. Most other adverse effects, such as skin irritation, dryness, and increased intracranial pressure, typically resolve when vitamin A intake or application is reduced or discontinued. Elevated triglycerides, cholesterol, or transaminases generally show improvement even with the continued use of the medication. Nevertheless, these levels should be closely monitored, and treatment should be discontinued if elevations persist or worsen.

Enhancing Healthcare Team Outcomes

Many individuals regularly consume substantial amounts of vitamins and supplements, often assuming they are safe due to their over-the-counter availability. However, poison control centers receive thousands of calls yearly related to vitamin overdoses and potential toxicity. An interprofessional team can collaborate to educate the public about these risks.

Healthcare professionals, including physicians, nurses, and pharmacists, must possess a comprehensive skill set to address vitamin A toxicity effectively. Pharmacists are critical in disseminating vitamin safety information to the public, advocating for a balanced, healthy diet over supplement reliance. They also instruct consumers about the vitamin A content in both over-the-counter and prescription medications. The nursing staff encourages patients to consume a healthy diet and refrain from taking vitamin A supplements unless advised by their medical provider. Primary care physicians should collaborate with nurses and pharmacists to ensure that patients maintain safe levels of vitamin A intake from dietary sources, supplements, and medications.

Pregnancy is an absolute contraindication for isotretinoin therapy. Despite this, patients may still take other retinoid medications and supplements that have teratogenic effects. The nursing and medical staff, along with obstetricians and clinicians, are responsible for obtaining and coordinating patients' medication history, ensuring thorough documentation and periodic review of all medications, vitamins, and supplements. Patients should be informed about the teratogenic risks associated with excessive vitamin A intake and provided with guidance on the maximum recommended dosages during pregnancy.

By combining these skills, strategic approaches, shared responsibilities, effective communication, and seamless care coordination, healthcare professionals can deliver patient-centered care, optimize outcomes, enhance patient safety, and improve overall interprofessional team performance when managing vitamin A toxicity.

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Disclosure: Jazmine Olson declares no relevant financial relationships with ineligible companies.

Disclosure: Muhammad Atif Ameer declares no relevant financial relationships with ineligible companies.

Disclosure: Amandeep Goyal declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Cite this Page Olson JM, Ameer MA, Goyal A. Vitamin A Toxicity. [Updated 2023 Sep 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Vitamin A (overview, Introduction, sources, types, RDA, deficiency and health issues)<br>Vitamin A is a vital fat-soluble vitamin essential for vision, immune function, skin health, and growth. It is found in animal-based foods and colorful fruits/vegetables. Deficiency leads to vision problems, weak immunity, and growth issues. Excessive intake can cause toxicity. Balance in intake is crucial for overall well-being.<br>https://www.icfitnessclub.com/diploma-in-personal-trainer-course/

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Vitamin A Introduction, Functions, RDA, Deficiency By IC Fitness Club – An Institute of Fitness Science

Introduction • Vitamin A is a vital and essential fat-soluble vitamin that plays a critical role in maintaining overall health and well-being. It belongs to a group of organic compounds that includes retinol, retinal, and retinoic acid. These compounds are crucial for several physiological functions within the human body. www.icfitnessclub.com

Sources of Vitamin A Vitamin A can be obtained from two main sources: • Preformed Vitamin A: This type of Vitamin A is found in animal-based foods such as liver, fish oil, dairy products, and eggs. • Provitamin A Carotenoids: These are found in colourful fruits and vegetables like carrots, sweet potatoes, spinach, and mangoes. The body can convert these carotenoids into Vitamin A. www.icfitnessclub.com

Functions & Role of Vitamin A • Vision: Retinal, one form of Vitamin A, is a key component of the visual pigments in the eyes. It plays a vital role in converting light into nerve signals, allowing us to see in low-light conditions and maintain good vision. • Immune Support: Vitamin A is essential for a robust immune system. It helps in the development and proper functioning of white blood cells, which are crucial for fighting off infections and diseases. • Skin Health: Another form of Vitamin A, retinoic acid, is well-known for its benefits in promoting healthy skin. It supports cell turnover, helps maintain skin integrity, and is used in various skincare products for its rejuvenating properties. • Growth and Development: Vitamin A is crucial for the proper growth and development of children. It is necessary for the development of bones, teeth, and soft tissues. • Antioxidant Properties: Vitamin A acts as an antioxidant, protecting the body against damage caused by free radicals, which can lead to various chronic diseases and premature aging. www.icfitnessclub.com

Deficiency and Toxicity: • Vitamin A deficiency can result from inadequate dietary intake and can lead to several health issues, such as night blindness, dry eyes, impaired immunity, and growth problems. www.icfitnessclub.com

Recommended Intake • The recommended daily intake of Vitamin A varies based on age, gender, and life stage. The average Intake is 700mcg/day for adults. It is essential to follow the recommended guidelines to maintain a proper balance of this crucial vitamin in the body. In conclusion, Vitamin A is a multifunctional nutrient that is indispensable for various bodily processes, including vision, immunity, and skin health. A balanced diet rich in Vitamin A sources is crucial to ensure optimal health and prevent deficiency or toxicity-related issues. www.icfitnessclub.com

Conclusion • In conclusion, Vitamin A is a multifunctional nutrient that is indispensable for various bodily processes, including vision, immunity, and skin health. A balanced diet rich in Vitamin A sources is crucial to ensure optimal health and prevent deficiency or toxicity-related issues. www.icfitnessclub.com

Thank You! By IC Fitness Club – An Institute of Fitness Science www.icfitnessclub.com

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COMMENTS

Overview of vitamin A
Vitamin A is a subclass of a family of lipid-soluble compounds referred to as retinoic acids. These consist of four isoprenoid units joined in a head-to-tail fashion. There are two main forms of vitamin A: provitamin A carotenoids (beta-carotene and others) and preformed vitamin A. Provitamin A carotenoids are found in plants.
Vitamin A
Vitamin A. It's only a semi-myth that eating carrots will help you see in the dark. A carrot's main nutrient, beta-carotene (responsible for this root vegetable's characteristic orange color), is a precursor to vitamin A and helps your eyes to adjust in dim conditions. Vitamin A can't give you superpowers of night vision or cure your ...
Vitamin A: What It Is and How Much You Need
Vitamin A is good for supporting healthy fetal growth and development and beyond, as well as: 1. Maintains healthy vision. One of vitamin A's most important roles is to preserve and maintain ...
Vitamin A Update: Forms, Sources, Kinetics, Detection, Function
Vitamin A is a group of vital micronutrients widely present in the human diet. Animal-based products are a rich source of the retinyl ester form of the vitamin, while vegetables and fruits contain carotenoids, most of which are provitamin A. Vitamin A plays a key role in the correct functioning of multiple physiological functions.
Vitamin A Deficiency
Vitamin A is a fat-soluble vitamin essential in cell development, metabolism, immune competency, vision, and reproductive functions.[1][2] Vitamin A deficiency (VAD) is a highly prevalent health concern associated with substantial morbidity and mortality, mostly affecting young children in impoverished regions throughout the world. Insufficient intake of absorption leads to deficiency and ...
Vitamin A and Carotenoids
This is a fact sheet intended for health professionals. For a general overview, see our consumer fact sheet.. Introduction. Vitamin A is the name of a group of fat-soluble retinoids, primarily retinol and retinyl esters [1,2].Vitamin A is involved in immune function, cellular communication, growth and development, and male and female reproduction []. ...
Vitamin A
Vitamin A is a generic term that refers to fat-soluble compounds found as preformed vitamin A (retinol) in animal products and as provitamin A carotenoids in fruit and vegetables. The three active forms of vitamin A in the body are retinol, retinal, and retinoic acid. ... Armstrong AW, Read C. Pathophysiology, clinical presentation, and ...
Vitamin A
Definition. Vitamin A is a fat-soluble vitamin, a category that also includes vitamins D, E and K. The vitamin encompasses several chemically related naturally occurring compounds or metabolites, i.e., vitamers, that all contain a β-ionone ring. The primary dietary form is retinol, which may have a fatty acid molecule attached, creating a retinyl ester, when stored in the liver.
Vitamin A: Everything You Need To Know
There are two sources of vitamin A: preformed vitamin A and carotenoids. Vitamin A is a fat-soluble nutrient requiring fat for it to be effectively absorbed in the digestive tract. Vitamin A is stored in the liver. Vitamin A is essential for the health of the following: Epithelia (surface tissue, like skin) The eyes.
Vitamin A Deficiency: Causes, Symptoms, Treatment & Prevention
Vitamin A is a vitamin that plays an important role in your vision. While vitamin A deficiency is rare in the United States, it can cause severe complications such as vision loss, skin issues and immune system problems. It's important to eat a diet that includes foods that have vitamin A, such as meat, dairy, dark leafy greens, and yellow or ...
Vitamin A
Vitamin A is an important factor in growth throughout life. Vitamin A helps grow and maintain epithelial tissues. These include mucous membranes, the lining of the gastrointestinal tract, lungs, bladder, urinary tract, vagina, cornea, and skin. Vitamin A also helps the growth of bones and teeth. Vitamin A prevents drying of the skin.
Vitamin A: Introduction
Sign up here and try our FREE content: http://lectur.io/freecontentyt If you're an medical educator or faculty member, visit: http://lectur.io/medytb2u T...
Vitamin A Deficiency Clinical Presentation
Subclinical forms of vitamin A deficiency (VAD) may not cause any symptoms, but the risk of developing respiratory and diarrheal infections is increased, the growth rate is decreased, and bone development is slowed. Patients may have a recent history of increased infections, infertility secondary to impaired spermatogenesis, or recent ...
Vitamin A
Vitamin A is important for normal vision, gene expression, reproduction, embryonic development, growth, and immune function. There are a variety of foods rich in vitamin A and provitamin A carotenoids that are available to North Americans. Thus, current dietary patterns appear to provide sufficient vitamin A to prevent deficiency symptoms such as night blindness. The Estimated Average ...
Vitamin A: Structure, Properties, Functions, and Deficiency
Cycle diagram. 2. Other Biochemical Functions. Vitamin A is necessary for the maintenance of normal epithelium and skin.; Retinoic acid is found to have an important role in glycoprotein synthesis.; Retinoyl phosphate acts as a donor of oligosaccharide units across the lipid bilayer of the cell.; Retinol acts as a steroid hormone in controlling the expression of certain genes.
The Role of Vitamin A in Retinal Diseases
The liver is the main storage organ of vitamin A in the body, as up to 80% of vitamin A in the body is stored there [ 2, 13, 28, 30, 31 ]. When needed, retinyl esters are hydrolysed into retinol. Its mobilisation to extrahepatic tissues requires retinol-binding protein (RBP4), the main vitamin A carrier in the blood.
PPT
Presentation Transcript. Vitamin A. Retinoids Precursors of vitamin A 1- Retinol It is found in animal tissues as a retinyl ester with long-chain fatty acids. 2- Retinal The aldhyde derived from the oxidation of retinol. Retinol and retinal can be interconverted. 3- Retinoicacid The acidderived from retinal.
Vitamin A Toxicity
Vitamin A is essential for maintaining the body's vision, cell division, reproduction, and immune function. Vitamin A belongs to the category of lipid-soluble compounds called retinoic acids. Beta-carotene is the most well-known form of 2 clinically significant forms of vitamin A: preformed vitamin A and provitamin A carotenoids. Mammals metabolize carotenoids into active vitamin A. Preformed ...
PPT
Presentation Transcript. Introduction • Vitamin A is a vital and essential fat-soluble vitamin that plays a critical role in maintaining overall health and well-being. It belongs to a group of organic compounds that includes retinol, retinal, and retinoic acid. These compounds are crucial for several physiological functions within the human ...

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