Vitamin A: Benefits, Forms, Dosing, and Side Effects

Vitamin A is the name of a group of fat-soluble retinoids — primarily retinol and retinyl esters — that are essential for vision, immune function, cellular communication, growth, development, and reproduction [1][2]. 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]. It is also critical for vision as an essential component of rhodopsin, the light-sensitive protein in retinal rod cells that responds to light entering the eye, and because it supports the normal differentiation and functioning of the conjunctival membranes and cornea [2][3].

The human diet provides two sources of vitamin A: preformed vitamin A (retinol and retinyl esters) from animal sources — primarily liver, dairy products, eggs, and fish — and provitamin A carotenoids from plant sources, including beta-carotene, alpha-carotene, and beta-cryptoxanthin [1][4]. The body converts provitamin A carotenoids into vitamin A in the intestine via the beta-carotene monooxygenase type 1 (BCMO1) enzyme, although conversion rates have genetic variability — certain polymorphisms in the BCMO1 gene can reduce enzyme activity in humans [5][6][7]. Beta-carotene is referred to as "provitamin A" because it is converted to vitamin A based on the body's existing need, making it a safer form that reduces the risk of vitamin A overdose [1].

In the United States, vitamin A deficiency is rare — less than 1% of the population has a serum retinol level below 20 mcg/dL [8]. Globally, however, vitamin A deficiency remains a major public health problem: a pooled analysis of surveys from 138 low-income and middle-income countries found that 29% of children aged 6 months to 5 years were deficient in 2013, with the highest rates in sub-Saharan Africa (48%) and South Asia (44%) [12]. Excessive intake of preformed vitamin A poses real risks — including liver damage, birth defects, osteoporosis, and hypercalcemia — making this a nutrient where more is decidedly not better [1][14].

Table of Contents

• Overview
• Forms and Bioavailability
• Evidence for Benefits
• Recommended Dosing
• Safety and Side Effects
• Drug Interactions
• Dietary Sources
• References

Overview

Vitamin A is involved in immune function, cellular communication, growth and development, and male and female reproduction [1][2]. The various forms of vitamin A are solubilized into micelles in the intestinal lumen and absorbed by duodenal mucosal cells [4]. Retinyl esters and provitamin A carotenoids are converted to retinol after uptake, which 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].

Other carotenoids found in food — such as lycopene, lutein, and zeaxanthin — are not converted into vitamin A and are classified as non-provitamin A carotenoids, though they may have other important biological activities [1].

Average daily intakes of vitamin A from foods and beverages in the United States were 682 mcg RAE for men aged 20 and older and 616 mcg RAE for women in 2017–2018 [9]. About 65–80% of vitamin A consumed in the US and other high-income countries comes from preformed vitamin A, while provitamin A is the main form consumed in low-income countries [2][10]. About 12–40% of the US population, depending on age, uses supplements containing vitamin A [11].

Retinol and carotenoid levels are typically measured in plasma or serum, but these are not always reliable indicators of vitamin A status because they do not decline until liver and tissue stores are almost depleted [1]. Acute and chronic infections can also decrease serum retinol concentrations. In clinical practice, a serum or plasma retinol concentration of 20 mcg/dL (0.70 micromoles/L) or less reflects moderate vitamin A deficiency, and a level of 10 mcg/dL (0.35 micromoles/L) or less indicates severe deficiency [1].

Approximately 10–20% of pregnant women in low-income countries have vitamin A deficiency [13]. In 2013, an estimated 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 — more than 95% of these deaths occurred in sub-Saharan Africa and Asia [12]. 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 [12].

Forms and Bioavailability

Preformed Vitamin A (Retinol)

Preformed vitamin A is found in animal-derived foods and supplements, primarily as retinol and its ester forms:

• Retinyl palmitate — The natural form of vitamin A in fish oil and cod liver oil. It is an ester (chemical combination) of retinol and palmitic acid. The body separates the retinol and converts it to active vitamin A metabolites. Retinyl palmitate may also be produced synthetically. Approximately 55% of retinyl palmitate's molecular weight is retinol [15].
• Retinyl acetate — A synthetic form of vitamin A commonly used in supplements. Approximately 87% of retinyl acetate's molecular weight is retinol [15].
• Retinol — The alcohol form of vitamin A. Some fish-oil-based supplements list vitamin A as "retinol" or "retinol palmitate," but in practice, the form present is retinyl palmitate. Supplement labels reflect the amount of retinol activity provided regardless of the specific ester [15].

Absorption of preformed vitamin A esters from dietary supplements is 70–90% [16][17]. The body can absorb up to 75–100% of retinol from foods [16]. Labeled amounts on supplements are supposed to reflect only the amount of retinol (or retinol activity units — RAE) being provided, so consumers do not need to calculate molecular weight differences between ester forms [15].

Provitamin A Carotenoids

Beta-carotene is the most common carotenoid found in fruits and vegetables. It is an antioxidant that protects cells against damage from free radicals [1]. Rich food sources include apricots, carrots, collard greens, kale, spinach, squash, sweet peppers, and sweet potatoes [1].

• Absorption from supplements: 8.7–65%, depending on formulation [16][17].
• Absorption from foods: In most cases, 10–30% of beta-carotene from foods is absorbed [16]. Cooking and heat treatment can increase bioavailability from foods [17].
• Oil vs. water-dissolvable forms: Beta-carotene supplements are available in oil- or water-dissolvable forms. Water-dissolvable forms raise blood beta-carotene levels more effectively than oil forms [15].
• Mineral interactions: High doses of calcium or other minerals (magnesium, zinc, ferrous iron) from supplements may decrease the absorption of beta-carotene and other carotenoids such as lycopene and astaxanthin. This is likely due to a reaction between carotenoids and divalent mineral ions, making the carotenoids less bioavailable. It is best to take beta-carotene or any carotenoid supplement at a different time of day than a supplement or meal containing large amounts of a mineral [18].

Genetic variability significantly affects conversion of beta-carotene to vitamin A. Certain polymorphisms in the BCMO1 gene reduce the activity of the BCMO1 enzyme. 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 [5]. Two common single nucleotide polymorphisms (SNPs) in the BCMO1 gene altered beta-carotene metabolism in female volunteers [6][7]. Individuals who are poor converters due to these genetic variants may have a harder time meeting vitamin A needs from plant sources alone.

Unit Conversions

Supplement labels are transitioning from International Units (IU) to micrograms of retinol activity equivalents (mcg RAE), which more accurately reflect the different bioactivities of retinol and provitamin A carotenoids [4]:

• 1 mcg RAE = 1 mcg retinol = 2 mcg supplemental beta-carotene = 12 mcg dietary beta-carotene = 24 mcg dietary alpha-carotene or beta-cryptoxanthin
• 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
• 900 mcg RAE = 3,000 IU as retinol = 6,000 IU as beta-carotene (dietary) = 18,000 IU dietary beta-carotene

A mixed diet containing 900 mcg RAE provides between 3,000 and 36,000 IU of vitamin A, depending on the proportion of preformed vitamin A versus carotenoids in foods consumed [4]. Multivitamins commonly contain 750–1,050 mcg RAE (83–117% of the Daily Value), often as retinyl acetate, retinyl palmitate, provitamin A beta-carotene, or a combination. Stand-alone vitamin A supplements may contain up to 3,000 mcg RAE (333% DV) [19].

Topical Retinoids

Naturally-occurring vitamin A derivatives — retinol, retinyl palmitate, retinyl acetate, and retinaldehyde — are common ingredients in over-the-counter skin creams, gels, and serums promoted for acne reduction or anti-aging [15]. Adapalene (the active ingredient in Differin gel), a previously prescription-only synthetic form of retinyl palmitate, is now available without a prescription at 0.1% concentration [15].

In addition to exerting antibacterial, anti-inflammatory, and antioxidant effects in the epidermis, topical retinoids may increase synthesis and inhibit degradation of collagen [20]. Evidence indicates that topical products containing at least 0.04–0.1% retinol may modestly improve skin tone and decrease the appearance of facial fine lines [21][22].

Prescription-strength topical retinoids — including tretinoin (Retin-A, Renova), isotretinoin, and alitretinoin — are used to treat acne, psoriasis, hyperkeratosis, and premature aging from UV damage [15]. Topical retinoids can cause initial skin reactions including redness, scaling, dryness, and stinging/burning, which usually lessen after 4 weeks of continued use [23]. People using topical retinoids should use caution outdoors, as exposure to sunlight, wind, or cold can cause additional skin irritation. Sunscreen and protective clothing over treated areas are recommended [23].

Although some studies have found associations between high retinol intakes and reduced bone mineral density, topical retinoids do not appear to increase blood levels of vitamin A and are not associated with fracture risk [20][24].

Cod Liver Oil and Fermented Cod Liver Oil

Cod liver oil and other fish liver oils are excellent sources of preformed vitamin A, while traditional fish oil supplements (from the oil in fish meat) are not [1]. Fermented cod liver oil, which is generally more expensive, is sometimes promoted as a more natural, superior source of vitamins A and D and omega-3 fatty acids. The fermentation process allows oil and fat-soluble vitamins to separate from the liver without heat or high pressure [15]. However, there does not appear to be any clinical evidence demonstrating that fermented cod liver oil is more beneficial than regular cod liver oil. Unlike regular cod liver oil supplements, most fermented varieties do not list specific amounts of vitamin A, D, EPA, or DHA on the label, making it impossible to know exact doses [15].

Evidence for Benefits

Vision and Eye Health

Vitamin A is essential for vision as a component of rhodopsin, the light-sensitive protein in retinal rod cells. Deficiency causes night blindness (the inability to see in low light), the most common clinical sign of vitamin A deficiency, which develops after plasma retinol has been low and the eye's vitamin A reserves become depleted [1][12][13]. Xerophthalmia (chronic vitamin A deficiency affecting the eye) can also damage the cornea and eventually lead to permanent blindness — vitamin A deficiency is one of the top causes of preventable blindness in children [13].

Case reports of deficiency-related vision loss:

A 34-year-old woman with vitamin A deficiency due to insufficient dietary intake presented with dry eyes, vitreous floaters, light sensitivity, and peripheral vision loss, which had previously been misdiagnosed as glaucoma. Her symptoms and peripheral vision significantly improved within one week after treatment for dry eye (eye drops and tear duct plugs) and vitamin A supplementation (200,000 IU daily for two days followed by 8,000 IU per day, plus a daily multivitamin), with complete restoration of peripheral vision within 5.5 months [25].

A 60-year-old man with Crohn's disease who had undergone multiple resections developed progressive night vision loss with a very low blood level of vitamin A. He received 100,000 IU vitamin A intramuscularly for 3 days, followed by 50,000 IU daily for 2 weeks, then 25,000 IU orally per day for one year. His blood levels increased from 11 mcg/dL to 78 mcg/dL and his vision improved. However, oral supplementation was not sufficient to maintain adequate blood levels due to malabsorption, and he eventually became deficient again and required intramuscular injections [26].

A 4-year-old girl in Japan with severe vitamin A deficiency (likely caused by a diet limited to carbohydrates with no meat or vegetables) presented with conjunctival hyperemia, Bitot's spots, fragile blistering skin, leukoderma on the hands and arms, nail abnormalities, and elevated alanine aminotransferase (ALT). Her symptoms significantly improved and/or resolved, and liver enzyme levels normalized within four weeks of daily supplementation with 4,000 IU vitamin A from cod liver oil [27].

Laser eye surgery: One study demonstrated that high doses of vitamin A plus vitamin E enhanced healing rate and vision improvement after photorefractive keratectomy (PRK) laser surgery to correct near-sightedness. The dose used was 25,000 IU vitamin A (as retinyl palmitate) plus 230 mg vitamin E (as alpha tocopheryl nicotinate) [28].

Cataracts: Increased vitamin A in the diet has been associated with reduced risk of cataracts, but it is not known if the same benefit applies to vitamin A supplements [29].

Age-Related Macular Degeneration (AMD)

AMD is the leading cause of significant vision loss in older people. Its etiology involves complex interactions among genetic susceptibility, environmental factors including oxidative stress, and normal aging [30].

AREDS (Age-Related Eye Disease Study): This landmark trial found that participants at high risk of developing advanced AMD (those with intermediate AMD or advanced AMD in one eye) had a 25% lower risk of developing advanced AMD after taking a daily supplement containing beta-carotene (15 mg / 7,500 mcg RAE), vitamin E (400 IU), vitamin C (500 mg), zinc (80 mg), and copper (2 mg) for 5 years compared to placebo [31]. However, it was not known whether these benefits were attributable to a single ingredient or the combination.

AREDS2: This 5-year follow-up randomized clinical trial of 4,203 participants aged 50–85 confirmed the value of the AREDS supplement in reducing AMD progression [32]. Critically, the study showed that removing beta-carotene from the formula did not change the risk of disease progression, while substituting lutein (10 mg) and zeaxanthin (2 mg) for beta-carotene reduced disease risk. Adding omega-3 fatty acids produced no additional benefit. Participants with the lowest dietary intakes of lutein and zeaxanthin had a 26% lower risk of advanced AMD when taking a supplement containing these two carotenoids. The risk of advanced AMD was 18% lower in participants taking the modified AREDS formula with lutein and zeaxanthin but not beta-carotene, compared to those taking the formula with beta-carotene but not lutein or zeaxanthin.

10-year AREDS2 follow-up: After the 5-year trial, participants were all offered the final AREDS2 formulation with lutein and zeaxanthin replacing beta-carotene. In a follow-up analysis of 3,882 participants 5 years after the trial ended, those who had taken the supplement with lutein and zeaxanthin had an additional 20% reduced risk of progression to late AMD compared with those who had taken the supplement containing beta-carotene [33]. This confirmed the benefit of replacing beta-carotene with lutein and zeaxanthin.

Long-term dietary analysis: A study monitoring dietary intakes in 4,504 AREDS and 3,738 AREDS2 participants (mean age 71) for a median of 10.2 years found that those in the two highest quintiles of intake for vitamin A, beta-carotene, or lutein and zeaxanthin had a lower risk of progression to late AMD. 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 compared to those in the first quintile [34].

The current evidence supports lutein and zeaxanthin rather than beta-carotene as the preferred carotenoids in AMD supplement formulations.

Cancer

Because of vitamin A's role in regulating cell growth and differentiation, numerous studies have examined its relationship with various cancers. The evidence is mixed and highly dependent on the form and dose of vitamin A, smoking status, and cancer type [1].

Observational evidence for reduced risk: 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 lower risks of lung cancer [35], non-Hodgkin lymphoma [36], pancreatic cancer [37], oral cavity and laryngeal cancer [38], esophageal cancer [39], ovarian cancer [40][41], glioma [42], and bladder cancer [43]. However, other observational studies have found no association between intakes of different forms of vitamin A and risk of liver cancer [44], non-Hodgkin lymphoma [45], colorectal cancer [46], prostate cancer [46], or all cancers combined [47].

Melanoma (skin cancer): A large study found that adults aged 50–76 taking vitamin A supplements had a 40% lower risk of developing melanoma over an average of 6 years compared to those not supplementing. The protective effect was strongest and most statistically significant in women. The effect was observed only among people taking 4,000 IU or more of vitamin A (as retinol) daily. Melanoma risk reduction was greater for the head and limbs (areas with greater sun exposure) than for the trunk. There was no association between melanoma risk and intake of carotenoids or vitamin A from foods [48].

Squamous cell carcinoma: A study tracking more than 120,000 men and women over approximately 27 years found that adults with the highest intakes of vitamin A (about 21,691 IU daily, as retinol and carotenoids including beta-carotene) had a 17% lower risk of squamous cell carcinoma compared to those with the lowest intakes (about 6,808 IU daily). However, the benefit was largely driven by dietary rather than supplemental intake — higher intakes of vitamin A from foods alone were associated with a 14% decrease in cancer risk [49].

Breast cancer: Population studies suggest that vitamin A (both preformed and beta-carotene) might reduce the risk of breast cancer, but these results require confirmation from interventional studies [50].

Negative results: Vitamin A together with beta-carotene has not been found to prevent colorectal, esophageal, pancreatic, or stomach cancers. Vitamin A alone does not appear to prevent ovarian cancer [1].

Beta-Carotene Supplementation and Lung Cancer Risk in Smokers

The most important finding in vitamin A and cancer research is the consistently harmful effect of high-dose beta-carotene supplementation in smokers and asbestos-exposed workers.

CARET (Carotene and Retinol Efficacy Trial): This trial enrolled 18,314 male and female current and former smokers (with at least a 20 pack-year history) and some men occupationally exposed to asbestos, all aged 45–74. Participants were randomized to take 30 mg beta-carotene plus 25,000 IU (7,500 mcg RAE) retinyl palmitate or placebo daily. The trial was ended prematurely after a mean of 4 years because the supplements unexpectedly increased lung cancer risk by 28%, death from lung cancer by 46%, and all-cause mortality by 17% [51]. In a subsequent 6-year follow-up after stopping supplements, differences in lung cancer risk were no longer statistically significant, except that women in the intervention group had a 33% higher risk of lung cancer [52]. In a separate analysis, men who took the two supplements had a 35% lower risk of nonaggressive prostate cancer during the active trial, but men who additionally took self-prescribed supplements (typically a multivitamin) had a 52% higher risk of aggressive prostate cancer during the active trial [53].

ATBC (Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study): This study enrolled 29,133 male smokers aged 50–69 who smoked an average of 20.4 cigarettes per day for an average of 35.9 years. Participants were randomized to take 50 mg/day alpha-tocopherol, 20 mg/day beta-carotene, both, or placebo for 5–8 years. Beta-carotene supplementation increased lung cancer risk by 18% and the overall rate of death (primarily from lung cancer and ischemic heart disease) by 8% [54]. In an 18-year post-trial follow-up of 25,563 participants, the increased lung cancer risk was no longer present, but participants who had taken beta-carotene during the trial had a 20% higher risk of death due to prostate cancer [55].

AREDS2 lung cancer finding: Among the 4,203 AREDS2 participants, no current smokers received beta-carotene supplements. At the end of the 5-year trial, more lung cancers were found 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 5 years later, the increased lung cancer risk persisted — an 82% higher risk among participants who had taken beta-carotene during the trial [33].

Negative results in non-smokers: Three other clinical trials found no relationship between vitamin A or beta-carotene supplementation and lung cancer incidence or mortality in populations with smaller proportions of smokers [56]. The Physicians' Health Study randomized 22,071 male physicians aged 40–84 (11% current smokers, 38% former smokers) to take 50 mg beta-carotene on alternate days or placebo for 12 years — no differences were found [57]. A trial of 7,627 women (mean age 60.4, 15% current smokers, 41% former smokers) found no significant effect of 50 mg beta-carotene on alternate days over 9.4 years [58]. The Linxian, China trial of 29,584 men and women aged 40–69 found no difference in lung cancer death rates with vitamin/mineral combinations over 5.25 years plus 10 years of follow-up [59].

Overall assessment: The CARET and ATBC results indicate that large supplemental doses of beta-carotene have detrimental effects in current or former smokers and workers exposed to asbestos. The USPSTF (2022) advises against beta-carotene supplements for preventing cancer or cardiovascular disease among healthy adults [60]. Among nonsmokers, beta-carotene and vitamin A supplements do not appear to affect cancer risk. Long-term retinol supplementation has been independently associated with increased lung cancer risk in the VITAL study [61].

Measles

In 2023, measles was responsible for about 107,500 deaths worldwide, mostly in young children in low-income countries [62][63]. Vitamin A deficiency is a risk factor for severe measles [12].

A 2022 Cochrane Review of six clinical trials enrolling 19,566 children aged 6 months to 5 years in low- and middle-income countries found that vitamin A supplementation reduced the risk of new measles cases by 50%. Vitamin A doses ranged from 15,000 mcg RAE (50,000 IU) to 60,000 mcg RAE (200,000 IU) depending on age, administered as a single dose or every 4–6 months. However, the same review found that vitamin A supplementation did not affect the risk of death due to measles, based on six trials in a total of 1,088,261 children [65].

Current treatment guidelines (American Academy of Pediatrics Red Book 2024–2027; CDC Yellow Book 2024) recommend the following for children with acute measles, under medical supervision [64]:

• Infants < 6 months: 50,000 IU once daily for 2 days
• Infants 6–11 months: 100,000 IU once daily for 2 days
• Children ≥ 12 months: 200,000 IU once daily for 2 days
• Children with clinical signs of vitamin A deficiency: an additional age-specific dose 2–4 weeks after the first round

Autism Spectrum Disorder (ASD)

A small study of children aged 4–6 in China with an autism spectrum disorder found that they had significantly lower blood levels of retinol compared to children without ASD (average 0.54 µmol/L vs. 0.82 µmol/L). The children with ASD were given a single large dose of vitamin A (200,000 IU). Six months later, average blood retinol levels had increased to 0.79 µmol/L and significant improvements were noted on the overall childhood autism rating scale (CARS) score, including relating to people, adaptation to change, anxiety, and verbal and non-verbal communication. Blood serotonin levels — previously elevated in the ASD group — significantly decreased after supplementation [66]. However, the study lacked a placebo control group, making it impossible to attribute the improvements solely to vitamin A.

A US study found that children with ASDs aged 4–8 consumed, on average, less than the recommended daily intake of vitamin A, while younger children tended to consume excessive amounts above the Tolerable Upper Intake Level [67].

Aging Skin

A study among 60 adults (average age 60, mostly women) in Italy found that taking 50,000 IU (15,000 mcg RAE) of vitamin A plus 50 mg of vitamin E daily for 12 weeks while also applying a topical gel (0.02% retinoic acid and 4% glycolic acid) improved overall skin appearance slightly more than applying the gel alone (3.8 vs. 2.8 points on a 0–30 scale). The supplement group showed greater improvements in skin elasticity, roughness, pigmentation, and pores, though it was not reported whether these differences were statistically significant [68]. The vitamin A dose used (approximately 17–21 times the RDA and five times the UL for adults) may not be safe for general use.

Acne

A review of evidence from several older studies (1943–1981) suggested that supplementation with high-dose vitamin A (36,000–500,000 IU or 10,800–150,000 mcg RAE — approximately 3–50 times the UL) daily for 1–7 months might be beneficial for acne management [69]. However, the most recent placebo-controlled study among those reviewed showed that 150,000 IU of vitamin A daily for 12 weeks did not significantly improve acne compared to placebo [70].

Erythropoietic Porphyria and Sun Sensitivity

Beta-carotene has specifically been used to reduce sensitivity to sunlight in people with erythropoietic porphyria, a genetic condition [1]. Beta-carotene may also provide modest protection from sunburn in sun-sensitive individuals at a daily dose of 25 mg (6,250 mcg RAE or 41,666 IU). However, beta-carotene supplements are unlikely to protect the general population from sunburn and do not reduce the risk of skin cancer from sun exposure [15].

Other Potential Benefits of Beta-Carotene

Limited human research suggests that beta-carotene might prevent exercise-induced asthma, lessen symptoms of oral leukoplakia, slow the progression of osteoarthritis, and improve exercise ability and muscle strength in older people [1]. Although population research has linked dietary intake of beta-carotene with reduced risk of breast cancer and ovarian cancer in postmenopausal women, experts advise against the use of beta-carotene supplements for preventing cancer or cardiovascular disease among healthy adults, as the potential harms outweigh the risks [60].

Recommended Dosing

Recommended Dietary Allowances (RDA)

The Food and Nutrition Board at the National Academies of Sciences provides the following RDAs for vitamin A as retinol activity equivalents (RAE) [4]:

Age Group	Male	Female	Pregnancy	Lactation
Birth to 6 months*	400 mcg RAE	400 mcg RAE	—	—
7–12 months*	500 mcg RAE	500 mcg RAE	—	—
1–3 years	300 mcg RAE	300 mcg RAE	—	—
4–8 years	400 mcg RAE	400 mcg RAE	—	—
9–13 years	600 mcg RAE	600 mcg RAE	—	—
14–18 years	900 mcg RAE	700 mcg RAE	750 mcg RAE	1,200 mcg RAE
19–50 years	900 mcg RAE	700 mcg RAE	770 mcg RAE	1,300 mcg RAE
51+ years	900 mcg RAE	700 mcg RAE	—	—

*Adequate Intake (AI), equivalent to the mean intake in healthy breastfed infants. In IU equivalents: 900 mcg RAE = 3,000 IU as retinol or 6,000 IU as beta-carotene for males aged 14 and older. For females aged 14 and older, 700 mcg RAE = 2,333 IU as retinol [15].

Tolerable Upper Intake Levels (UL) for Preformed Vitamin A

ULs apply only to preformed vitamin A (retinol and retinyl esters) from supplements, fortified foods, and animal sources — not to vitamin A from beta-carotene or other carotenoids [4]:

Age Group	UL (mcg RAE)	UL (IU as retinol)
Birth to 12 months	600 mcg	2,000 IU
1–3 years	600 mcg	2,000 IU
4–8 years	900 mcg	3,000 IU
9–13 years	1,700 mcg	5,666 IU
14–18 years	2,800 mcg	9,333 IU
19+ years (incl. pregnancy, lactation)	3,000 mcg	10,000 IU

Many supplements provide vitamin A partly or entirely from beta-carotene. In such cases, only the retinol/retinyl ester portion should be considered when assessing whether intake exceeds the UL. No UL has been established for beta-carotene, but the Food and Nutrition Board advises against beta-carotene supplementation for the general population, except as a provitamin A source to prevent deficiency [71].

Specific Therapeutic Doses

• Post-PRK laser eye surgery: 25,000 IU vitamin A (as retinyl palmitate) (7,500 mcg RAE) plus 230 mg vitamin E daily — requires medical supervision [28].
• Melanoma risk reduction: Supplemental vitamin A ≥ 4,000 IU per day (as retinol) was associated with reduced melanoma risk in one large observational study (effect significant in women) [48].
• Sunburn protection (beta-carotene): 25 mg beta-carotene daily (6,250 mcg RAE or 41,666 IU) for sun-sensitive individuals; not effective for the general population [15].
• Measles treatment in children: Age-specific high doses (50,000–200,000 IU) for 2 days under medical supervision [64].
• Cystic fibrosis: Lifelong supplementation at 750–3,000 mcg RAE per day depending on age, alongside other fat-soluble vitamins and pancreatic enzymes [72][73].

Beta-Carotene from Diet

Beta-carotene supplements are generally not recommended for most people because dietary beta-carotene is abundantly available from food sources. Experts recommend five daily servings of fruits and vegetables, which may provide 6–8 mg of beta-carotene (1,250–2,000 mcg RAE) [15]. A long-term study found the risk of dying during the study period (approximately 14 years) was lowest when blood serum beta-carotene levels were above the bottom 20% of the population (i.e., above 0.13 micromol/L) but did not change significantly when levels were further increased [74].

Safety and Side Effects

Preformed Vitamin A Toxicity

Because vitamin A is fat-soluble, excess amounts accumulate primarily in the liver.

Acute toxicity (hypervitaminosis A): Occurs within days to weeks after ingestion of one or a few very high doses (typically more than 100 times the RDA, approximately 70,000–90,000 mcg). Symptoms include severe headache, blurred vision, nausea, vertigo, muscle aches, coordination problems, skin peeling, and hair loss. In severe cases, increased cerebral spinal fluid pressure can lead to drowsiness, coma, and death [14][75].

Chronic toxicity: Results from taking high doses (7,000–9,000 mcg or more, approximately 10 times the RDA) over months to years. Symptoms include dry skin, cracking at the corners of the mouth, gum inflammation, muscle and joint pain, fatigue, cognitive difficulties, depression, and abnormal liver test results [14][75].

Liver damage: High doses of vitamin A (typically 40,000 IU or about 12,000 mcg per day or more) can cause liver damage. People with liver problems should consult their physician before using vitamin A supplements. Vitamin A can also increase the risk of liver damage when taken with prescription drugs that cause liver damage as a side effect [14].

Hypercalcemia: High intakes of retinol can cause excessive calcium in the blood, possibly through effects on bone metabolism (stimulation of bone resorption and inhibition of bone formation) and effects on vitamin D receptors and parathyroid hormone [76][77]. Symptoms include fatigue, muscular pain, constipation, headache, irritability, confusion, and weakness. People with chronic kidney disease, older adults, and children may be at highest risk [78]. In one case, a 69-year-old woman developed mild hypercalcemia with chronic fatigue, nausea, and constipation four months after beginning 7,500 mcg (25,000 IU) of vitamin A daily; her calcium levels normalized within one month of stopping vitamin A [79].

Uric acid: A study among US adults aged 20+ found that those with higher blood vitamin A levels (≥73.93 mcg/dL) had higher blood uric acid levels (5.92 mg/dL) compared to those with lower vitamin A levels (≤47.1 mcg/dL; uric acid 4.81 mg/dL), though levels remained within the normal range [80].

Hair loss: A person on dialysis taking a multivitamin with 5,000 IU of vitamin A experienced gradually increasing hair loss (blood vitamin A at 140 mcg/dL, normal range 20–80 mcg/dL), which subsided within one month of stopping the supplement [81]. Two cases of hair loss were reported in adults with diabetes taking 50,000 IU daily [82].

Bone health: There is evidence that excessive retinol intake (more than 1,500–3,000 mcg or 5,000–10,000 IU daily) may increase the risk of osteoporosis and hip fractures [14]. A study in Sweden among 175 women aged 28–74 found that dietary retinol intakes above 1,500 mcg per day were associated with a 10% reduction in femoral neck bone mineral density and 14% reduction in lumbar spine bone mineral density compared to intakes below 500 mcg per day [83]. However, a much larger Danish population study found no increased fracture risk with oral or injected retinoids, even at very high doses (>14,000 mcg per day) [24].

Mortality: A Cochrane review of clinical studies found a small increase in mortality associated with higher-dose vitamin A supplements [84]. A long-term study found that the risk of dying was lowest at blood vitamin A levels at or above 1.82 micromol/L, but for those in the top 20% (≥2.44 micromol/L), mortality risk was higher than at moderate levels [74].

Birth Defects (Teratogenicity)

Preformed vitamin A in modestly excessive doses can cause birth defects including malformations of the eye, skull, lungs, and heart [1][14]. Experts advise women who are or might be pregnant not to take more than 3,000 mcg RAE (10,000 IU) daily of preformed vitamin A supplements [1].

The March of Dimes recommends that pregnant women should not use a multivitamin or prenatal supplement containing more than 1,500 mcg (5,000 IU) of preformed vitamin A (such as retinyl palmitate), and should minimize consumption of liver [15]. The European Food Safety Authority (EFSA) advises pregnant or planning-to-conceive women to completely avoid foods with high retinol content, including animal liver (approximately 17,270 mcg retinol per 3.5 oz), offal (approximately 20,260 mcg per 3.5 oz), and liver-based spreads (5,357 mcg per 3.5 oz) [85]. The UK NHS advises pregnant women to avoid any supplements containing vitamin A as retinol, including cod liver oil [86].

Unlike preformed vitamin A, beta-carotene is not known to be teratogenic or cause reproductive toxicity [1][71]. US prenatal vitamins tend to provide vitamin A as beta-carotene or at least 50% as beta-carotene. Experts advise pregnant women to avoid topical retinoids based on isolated case reports [87].

Beta-Carotene Risks

Lung cancer in smokers: Smokers and people exposed to asbestos should avoid beta-carotene supplements. Daily intake of 20 mg (33,333 IU) or more may increase the risk of lung cancer and prostate cancer in these groups. Among smokers, taking beta-carotene at these doses also increases the risk of strokes and death from heart disease [88]. Eating foods rich in beta-carotene does not have these effects.

Carotenodermia: High doses of beta-carotene can cause the skin to turn yellow-orange, a harmless condition reversible by reducing intake [71].

Mortality: A Cochrane review found a slight (5%) but statistically significant increase in mortality associated with beta-carotene supplementation and concluded that current evidence does not support beta-carotene supplements in the general population [84].

Children

Children are more at risk than adults for vitamin A overdoses. Vitamin A-containing products should be stored away from children, and dosing directions followed carefully. When possible, beta-carotene-containing products should be chosen for children as they are safer [15].

Drug Interactions

Retinoid Medications

Avoid taking vitamin A supplements with prescription medications in the retinoid family, as the combination increases the risk of toxicity and hypervitaminosis A. Retinoid drugs include isotretinoin (Accutane), tazarotene (Avage), tretinoin (Renova, Retin-A), acitretin (Soriatane), bexarotene (Targretin), and etretinate (Tegison) [15][89].

Orlistat (Alli, Xenical)

Orlistat, 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 [90][91]. 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 [92][93].

Hepatotoxic Medications

Vitamin A can increase the risk of liver damage when taken with prescription drugs that can cause liver damage as a side effect. Patients should have their medications reviewed by a physician or pharmacist before using vitamin A supplements [14].

Dietary Sources

Preformed vitamin A concentrations are highest in liver, fish, eggs, and dairy products. Most dietary provitamin A comes from leafy green vegetables, orange and yellow vegetables, tomato products, fruits, and some vegetable oils [1][4]. Vitamin A is routinely added to some foods including milk and margarine [1][2]. Among US children and adolescents, enriched and fortified foods account for 34–40% of vitamin A intakes from food [94].

Food	mcg RAE per serving	% Daily Value
Beef liver, pan fried, 3 oz	6,582	731%
Sweet potato, baked in skin, 1 whole	1,403	156%
Spinach, frozen, boiled, ½ cup	573	64%
Pumpkin pie, commercially prepared, 1 piece	488	54%
Carrots, raw, ½ cup	459	51%
Herring, Atlantic, pickled, 3 oz	219	24%
Ice cream, French vanilla, soft serve, ⅔ cup	185	21%
Milk, skim, with added vitamin A and D, 1 cup	149	17%
Cantaloupe, raw, ½ cup	135	15%
Cheese, ricotta, part skim, ½ cup	133	15%
Sweet red peppers, raw, ½ cup	117	13%
Mangos, raw, 1 whole	112	12%
Fortified breakfast cereals, 1 serving	90	10%
Egg, hard boiled, 1 large	75	8%
Black-eyed peas, boiled, 1 cup	66	7%
Dried apricots, 5 pieces	63	7%
Broccoli, boiled, ½ cup	60	7%
Salmon, sockeye, cooked, 3 oz	59	7%
Tomato juice, canned, ¾ cup	42	5%
Yogurt, plain, low fat, 1 cup	32	4%
Tuna, light, canned in oil, drained, 3 oz	20	2%

*DV for vitamin A is 900 mcg RAE for adults and children age 4+ [4].

Groups at Risk of Vitamin A Inadequacy

Premature infants: Preterm infants have low liver stores of vitamin A at birth, and plasma concentrations often remain low throughout the first year of life. Those with vitamin A deficiency have a higher risk of eye and chronic lung diseases [95][96][97].

People with cystic fibrosis: Up to 90% of people with cystic fibrosis have pancreatic insufficiency, increasing their risk of vitamin A deficiency. Studies indicate that 2–13% of children and adolescents with cystic fibrosis have vitamin A deficiency. Standard care includes lifelong vitamin A supplementation at 750–3,000 mcg RAE per day depending on age [72][73].

People with Crohn's disease and inflammatory bowel disease: Approximately one-quarter of children with Crohn's disease and ulcerative colitis have vitamin A deficiency [103][104]. A study among 61 children and adolescents with IBD (including 40 with Crohn's disease) found that supplementation with a daily multivitamin providing 1,000 IU of vitamin A for one year normalized blood levels in all deficient participants [102].

People with celiac disease: Some children and adults with newly diagnosed celiac disease have vitamin A deficiency. A gluten-free diet can — but does not always — eliminate the deficiency [105][106][107][108].

Infants and children in low-income countries: Approximately 190 million preschool-age children (one-third of all children in this age group), mostly in Africa and Southeast Asia, have vitamin A deficiency [1][12][98]. The World Health Organization estimates that 9.8 million pregnant women (15% worldwide) have xerophthalmia from vitamin A deficiency [99].

References

1. Blaner WS. Vitamin A and Provitamin A Carotenoids. In: Marriott BP, Birt DF, Stallings VA, Yates AA, eds. Present Knowledge in Nutrition. 11th ed. Wiley-Blackwell; 2020:73-91.

2. Ross A. Vitamin A. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Lippincott Williams & Wilkins; 2014:260-77.

3. Carazo A, et al. Vitamin A update: Forms, sources, kinetics, detection, function, deficiency, therapeutic use and toxicity. Nutrients 2021;13:1703. PubMed

4. Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academy Press; 2001.

5. Zumaraga MPP, et al. Genotype effects on β-carotene conversion to vitamin A. Food Nutr Bull 2022;43(1):25-34. PubMed

6. Lietz G, et al. Single nucleotide polymorphisms upstream from the β-carotene 15,15'-monoxygenase gene influence provitamin A conversion efficiency. J Nutr 2012;142(1):161S-5S. PubMed

7. Leung WC, et al. Two common SNPs in the gene encoding beta-carotene 15,15'-monoxygenase alter beta-carotene metabolism. FASEB J 2009;23(4):1041-53. PubMed

8. Bird JK, et al. Risk of deficiency in multiple concurrent micronutrients in the United States. Nutrients 2017;9:655. PubMed

9. U.S. Department of Agriculture, Agricultural Research Service. What We Eat in America, 2017-2018. 2021.

10. Bailey RL, West KP Jr, Black RE. The epidemiology of global micronutrient deficiencies. Ann Nutr Metab 2015;66(Suppl 2):22-33. PubMed

11. Bailey RL, et al. Dietary supplement use in the United States, 2003-2006. J Nutr 2011;141:261-6. PubMed

12. Stevens GA, et al. Trends and mortality effects of vitamin A deficiency in children in 138 low-income and middle-income countries. Lancet Glob Health 2015;3:e528-36. PubMed

13. Bailey RL, West KP Jr, Black RE. The epidemiology of global micronutrient deficiencies. Ann Nutr Metab 2015;66(Suppl 2):22-33. PubMed

14. National Institute of Diabetes and Digestive and Kidney Diseases. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. 2020.

15. ConsumerLab. Vitamin A review — ConsumerTips and What It Is sections. ConsumerLab

16. Reboul E. Absorption of vitamin A and carotenoids by the enterocyte. Nutrients 2013;5:3563-81. PubMed

17. Reboul E. Mechanisms of carotenoid intestinal absorption. Nutrients 2019;11:838. PubMed

18. Corte-Real J, et al. Food Chem 2016; Borel P, et al. Br J Nutr 2017. Interaction between divalent mineral ions and carotenoid bioavailability.

19. Office of Dietary Supplements, NIH. Dietary Supplement Label Database. 2021.

20. Opinion on Vitamin A, European Commission SCCS 2016.

21. Kikuchi K, et al. J Dermatolog Treat 2009.

22. Babamiri K, et al. Aesthet Surg J 2010.

23. Differin Prescribing Information, Last Updated 2/2012.

24. Vestergaard P, et al. Arch Dermatol 2010.

25. Hulzen K, et al. Am J Ophthalmol Case Rep 2022.

26. Lima VC, et al. Int Ophthalmol 2014.

27. Kawase Y, et al. Pediatr Int 2022.

28. Vetrugno M, et al. Vitamin A plus vitamin E for PRK recovery. Br J Ophthalmol 2001.

29. Cumming RG, et al. Ophthalmology 2000.

30. Fleckenstein M, et al. Age-related macular degeneration. Nat Rev Dis Primers 2021;7:31. PubMed

31. Age-Related Eye Disease Study Research Group. AREDS Report No. 8. Arch Ophthalmol 2001;119:1417-36. PubMed

32. Age-Related Eye Disease Study 2 Research Group. AREDS2 randomized clinical trial. JAMA 2013;309:2005-15. PubMed

33. Chew EY, et al. AREDS2 Report #28. JAMA Ophthalmol 2022. PubMed

34. Agron E, et al. Dietary nutrient intake and progression to late AMD. Ophthalmology 2021;128:425-42. PubMed

35. Rowles JL 3rd, et al. Lycopene and reduced prostate cancer risk. Prostate Cancer Prostatic Dis 2017;20:361-77. PubMed

36. Chen F, et al. Carotenoid intake and risk of non-Hodgkin lymphoma. Ann Hematol 2017;96:957-65. PubMed

37. Chen J, et al. Antioxidant intake and pancreatic cancer risk. Int J Food Sci Nutr 2016;67:744-53. PubMed

38. Leoncini E, et al. Carotenoid intake and head and neck cancer. Cancer Epidemiol Biomarkers Prev 2015;24:1003-11. PubMed

39. Li H, et al. Plasma retinol levels and all-cause mortality in hypertensive patients. J Clin Hypertens 2020;22:906-13. PubMed

40. Li X, Xu J. Lycopene intake and ovarian cancer risk in postmenopausal women. Sci Rep 2014;4:4885. PubMed

41. Wang Q, He C. Dietary vitamin A intake and ovarian cancer risk. Biosci Rep 2020;40. PubMed

42. Lv W, et al. Dietary vitamin A intake and glioma risk. Nutrients 2015;7:8897-904. PubMed

43. Tang JE, et al. Vitamin A and bladder cancer risk. World J Surg Oncol 2014;12:130. PubMed

44. Leelakanok N, et al. Vitamin A intake, serum vitamin A, and liver cancer risk. Nutr Health 2018;24:121-31. PubMed

45. Psaltopoulou T, et al. Micronutrient intake and hematological malignancies. Nutr Cancer 2018;70:821-39. PubMed

46. Wang X, et al. Lycopene and colorectal cancer risk. Nutr Cancer 2016;68:1083-96. PubMed

47. Aune D, et al. Antioxidants and cardiovascular disease, cancer, and all-cause mortality. Am J Clin Nutr 2018;108:1069-91. PubMed

48. Asgari MM, et al. J Invest Dermatol 2012.

49. Kim J, et al. JAMA Dermatol 2019.

50. Zhang S, et al. J Natl Cancer Inst 1999.

51. Omenn GS, et al. Beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med 1996;334:1150-5. PubMed

52. Goodman GE, et al. CARET: lung cancer and cardiovascular mortality after stopping supplements. J Natl Cancer Inst 2004;96:1743-50. PubMed

53. Neuhouser ML, et al. Supplement use and prostate cancer risk in CARET. Cancer Epidemiol Biomarkers Prev 2009;18:2202-6. PubMed

54. Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study Group. Vitamin E and beta carotene on lung cancer in male smokers. N Engl J Med 1994;330:1029-35. PubMed

55. Virtamo J, et al. α-Tocopherol and β-carotene supplementation: 18-year post-intervention follow-up of ATBC. Int J Cancer 2014;135:178-85. PubMed

56. Cortes-Jofre M, et al. Drugs for preventing lung cancer in healthy people. Cochrane Database Syst Rev 2020;3:CD002141. PubMed

57. Hennekens CH, et al. Long-term beta carotene supplementation and malignant neoplasms. N Engl J Med 1996;334:1145-9. PubMed

58. Lin J, et al. Vitamins C, E and beta carotene and cancer risk. J Natl Cancer Inst 2009;101:14-23. PubMed

59. Kamangar F, et al. Lung cancer chemoprevention in Linxian, China. Cancer Epidemiol Biomarkers Prev 2006;15:1562-4. PubMed

60. USPSTF. Vitamin, mineral, and multivitamin supplementation to prevent cardiovascular disease and cancer. JAMA 2022. DOI

61. Satia JA, et al. Long-term retinol supplementation and lung cancer risk. Am J Epidemiol 2009 (VITAL study).

62. Minta AA, et al. Progress toward measles elimination — worldwide, 2000–2023. MMWR 2024;73:1036-42. PubMed

63. World Health Organization. Measles. 2024.

64. American Academy of Pediatrics. Red Book 2024–2027; CDC Yellow Book 2024.

65. Imdad A, et al. Vitamin A supplementation for preventing morbidity and mortality in children. Cochrane Database Syst Rev 2022;3:CD008524. PubMed

66. Guo M, et al. Brain Res Bull 2017.

67. Hyman SL, et al. Pediatrics 2012.

68. Milani M, et al. Cosmetics 2023.

69. Cook MK, et al. J Drugs Dermatol 2022.

70. Anderson IF. Br Med J 1963.

71. Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academy Press; 2000.

72. Rana M, et al. Fat-soluble vitamin deficiency in children with cystic fibrosis. J Clin Pathol 2014;67:605-8. PubMed

73. Woestenenk JW, et al. Vitamin A intake and serum retinol levels in children with cystic fibrosis. Clin Nutr 2016;35:654-9. PubMed

74. Goyal A, et al. Cancer Epidemiol Biomarkers Prev 2013.

75. Bromley D. Am Fam Physician 2000.

76. Turner JJO, et al. Clin Med (Lond) 2017.

77. Borgan SM, et al. Cleve Clin J Med 2022.

78. Vyas AK, et al. Case Rep Endocrinol 2011.

79. Alchalabi B, et al. Cureus 2025.

80. Ford ES. Nutr Res 2015.

81. Shmunes E. Arch Dermatol 1979.

82. Said MA, et al. J Adv Res 2021.

83. Melhus H, et al. Ann Intern Med 1998.

84. Bjelakovic G, et al. Antioxidant supplements for prevention of mortality. Cochrane Database Syst Rev 2012. PubMed

85. EFSA Panel. EFSA J 2024.

86. NHS. Vitamins, supplements and nutrition in pregnancy. Updated 9/1/2023.

87. Browne H, et al. Obstet Gynaecol 2014.

88. N Engl J Med 2004 (ATBC outcomes — stroke and cardiovascular mortality in smokers).

89. Ulbricht C, et al. An evidence-based systematic review of vitamin A. J Diet Suppl 2012;9:299-416. PubMed

90. Zhi J, et al. Orlistat and beta-carotene pharmacokinetics. J Clin Pharmacol 1996;36:152-9. PubMed

91. Ulbricht C, et al. J Diet Suppl 2012;9:299-416. PubMed

92. Genentech USA, Inc. Xenical Package Insert. 2017.

93. GlaxoSmithKline. Alli Package Insert. 2017.

94. Berner LA, et al. Fortified foods are major contributors to nutrient intakes in US children and adolescents. J Acad Nutr Diet 2014;114:1009-22. PubMed

95. Schwartz E, et al. Vitamin A supplementation for prevention of bronchopulmonary dysplasia. Nutr Clin Pract 2017;32:346-53. PubMed

96. Darlow BA, Graham PJ. Vitamin A for very low birthweight infants. Cochrane Database Syst Rev 2007:CD000501. PubMed

97. Sun H, et al. Early vitamin A supplementation for retinopathy of prematurity. Retina 2020;40:1176-84. PubMed

98. World Health Organization. Guideline: Vitamin A Supplementation in Infants and Children 6-59 Months. 2011.

99. World Health Organization. Global Prevalence of Vitamin A Deficiency in Populations at Risk 1995–2005. Geneva: WHO; 2009.

100. Oliveira JM, et al. Vitamin A supplementation for postpartum women. Cochrane Database Syst Rev 2016;3:CD005944. PubMed

101. Weisshof R, et al. Curr Opin Clin Nutr Metab Care 2015.

102. Santucci NR, et al. Vitamin and zinc status in patients with IBD. J Pediatr Gastroenterol Nutr 2014;59:455-7. PubMed

103. Fabisiak N, et al. Fat-soluble vitamin deficiencies and IBD. J Clin Gastroenterol 2017;51:878-89. PubMed

104. Rempel J, et al. Micronutrient deficiencies in children with IBD. Nutrients 2021;13:236. PubMed

105. Tokgöz Y, et al. Fat soluble vitamin levels in children with celiac disease. BMC Pediatr 2018;18:130. PubMed

106. Wierdsma NJ, et al. Vitamin and mineral deficiencies in newly diagnosed celiac disease. Nutrients 2013;5:3975-92. PubMed

107. McGrogan L, et al. Micronutrient deficiencies in children with coeliac disease. Clin Nutr 2021;40:2784-90. PubMed

108. Shepherd SJ, Gibson PR. Nutritional inadequacies of the gluten-free diet in coeliac disease. J Hum Nutr Diet 2013;26:349-58. PubMed