presentation of 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 dependence on contact lenses, but eating an adequate amount will support eye health.

Vitamin A also stimulates the production and activity of white blood cells, takes part in remodeling bone, helps maintain healthy endothelial cells (those lining the body’s interior surfaces), and regulates cell growth and division such as needed for reproduction.

The two main forms of vitamin A in the human diet are preformed vitamin A (retinol, retinyl esters), and provitamin A carotenoids such as alpha-carotene and beta-carotene that are converted to retinol. Preformed vitamin A comes from animal products, fortified foods, and vitamin supplements. Carotenoids are found naturally in plant foods. There are other types of carotenoids found in food that are not converted to vitamin A but have health-promoting properties; these include lycopene, lutein, and zeaxanthin.

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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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.

Daily Vitamin A Needs During Pregnancy

14–18 years	750 micrograms (mcg)	2,800 mcg
19–50 years	770 mcg	3,000 mcg

Daily Vitamin A Needs During Breastfeeding

14–18 years	1,200 mcg	2,800 mcg
19–50 years	1,300 mcg	3,000 mcg

Daily Vitamin A Needs for Children

Birth to 6 months	400 mcg	600 mcg
7–12 months	500 mcg	600 mcg
1–3 years	300 mcg	600 mcg
4–8 years	400 mcg	900 mcg
9–13 years	600 mcg	1,700 mcg
14–18 years	900 mcg	2,800 mcg

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.

Daily Vitamin A Needs for Adults Over 65

	700 mcg	3,000 mcg daily
	900 mcg	3,000 mcg daily

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 .

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

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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

StatPearls [Internet].

Vitamin a deficiency.

Christopher Hodge ; Christopher Taylor .

Affiliations

Last Update: January 2, 2023 .

Continuing Education Activity

Vitamin A is a lipid-soluble compound with several biologic actions to aid in vision and cellular differentiation. The prevalence of vitamin A deficiency is rarely seen in the first world, nutrient-rich countries; however, it can affect those with inflammatory bowel disease and post-bariatric surgery. Vitamin A deficiency can lead to ophthalmological, dermatological, and immune impairment. This activity addresses the complications of vitamin A deficiency and how to treat affected patients.

Describe the metabolism of Vitamin A in the body.
Identify common manifestations of Vitamin A deficiency.
Identify populations at risk for Vitamin A deficiency.
Introduction

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 compromise of essential physiologic processes. Natural sources of vitamin A include dark leafy greens, orange-colored vegetables, milk products, liver, and fish. [3] It is absorbed in the duodenum after hydrolyzation by pancreatic and intestinal enzymes and emulsified with dietary fats and bile acids. [4] The majority is then stored in the hepatic stellate cells. [5] Significant amounts are also stored in adipose tissue and the pancreas. [6]

The recommended dietary allowance (RDA) of vitamin A by the Institute of Medicine in healthy adults is 700 micrograms/day for women and 900 micrograms/day for men. [7] [8] For children, pregnant women, and lactating women, the RDA is 300 to 900, 770, and 1300 micrograms/day respectively. The minimum requirement to prevent symptomatic VAD in children 1 to 5 years of age is about 200 micrograms/day. Serum retinol levels are a good marker of vitamin A nutritional status. Deficiency is defined as a retinol concentration of fewer than 20 micrograms/dL. [8]

Vitamin A deficiency-associated ocular symptoms have been shown to develop at concentrations less than 10 micrograms/dL. [8] Dietary vitamin A is ingested as either carotenoid from fruits and vegetables or retinoid from animal products. Carotenoids are a provitamin A, most commonly beta-carotene, and retinoids are active forms of vitamin A, such as retinol and retinyl esters. Retinoids have been shown to have 75% to 100% absorption, whereas carotenoid absorption varies greatly depending on the food matrix and type of carotenoid. [9] [10]

A 12 to 1 ratio of beta-carotene to retinol absorption in a diet of mixed fruits and vegetables is the estimated conversion used by the Centers for Disease Control and Prevention. [7] Many populations in developing countries rarely ingest meat, dairy, or carotenoid-rich vegetables leading to difficulty obtaining sufficient quantities of vitamin A.

In resource-poor regions of the world, insufficient nutrition complicated by chronic inflammation from regular gastrointestinal (GI) infections leads to frequent micronutrient deficiencies and is the most common etiology of vitamin A deficiency worldwide. [11] Adequate vitamin A intake in children in these regions is often further complicated by a concomitant deficiency of zinc, which is required for absorption vitamin A and synthesis of retinol-binding protein (RBP), the intravascular transport protein. [12] Measles is endemic in many of these regions as well and has been shown to cause precipitous drops in serum retinol levels by greater than 30%. [13] It reduces the synthesis of RBP and results in high amounts of vitamin A excretion in the urine. Physiologic demand is also higher in measles infection due to the damage to gastrointestinal epithelial tissues. [13]

Vitamin A concentration in breastmilk varies based on maternal nutrition status. In resource-poor settings, the average breastmilk vitamin A concentration only meets the infant's minimum daily need. This does not allow the build-up of liver reserves, resulting in high levels of vitamin A deficiency shortly after weaning. [14] Conversely, VAD is extraordinarily rare in the developed world due to the abundance of foods rich in vitamin A, better sanitation, water, and healthcare. Vitamin A deficiency cases in the developed world are typically due to various primary and secondary intestinal malabsorptive pathologies.

In the developed world, pancreatic, liver, and intestinal pathology are the leading causes of VAD. Similar to the frequent GI infections seen in the developing world, inflammatory bowel disease (IBD) causes chronic inflammation of the intestinal mucosa, and, when combined with decreased oral intake, it can lead to vitamin A deficiency. [15] Chronic liver disease of any type has been associated with vitamin A deficiency. The mechanism by which the deficiency develops is not entirely known: proposed mechanisms include decreased production of bile acids needed for absorption as well as altered storage patterns. [6]

Pancreatic insufficiency can result in VAD due to poor exocrine function and insufficient production of the hydrolases required for absorption. [16] Bariatric surgeries, designed to prevent fat absorption by bypassing the duodenum, consequently cause insufficient absorption of needed fat-soluble vitamins, including vitamin A. Premature neonates are at risk for vitamin A deficiency due to an immature GI tract without efficient vitamin A absorption, minimal vitamin A stores, and increased needs in a time of rapid development. [17]

Epidemiology

Worldwide, most vitamin A deficiency cases occur in children less than 5 years of age in developing countries. Global vitamin A deficiency estimates in young children are decreasing but have been approximated at 30% in children less than 5 years of age and account for about 2% of all deaths in this age group. [18] Pregnant and lactating women are also at increased risk of VAD due to increased daily requirements. A 2019 study in rural Ethiopia revealed vitamin A deficiency in 76% of lactating mothers. [19] VAD does not appear to have a gender predilection. [20] [21]

In the United States (US) general population, vitamin A deficiency is rare, estimated at 0.3% in 2013. In fact, the prevalence of vitamin A toxicity in the US is much greater than deficiency. [7] Symptomatic deficiency usually involves a malabsorptive process or a severely restrictive diet. Sixteen percent of children with IBD in the United States have vitamin A deficiency at diagnosis. A higher prevalence is found in Crohn disease than in ulcerative colitis. [15]

Patients with liver cirrhosis eligible for transplant have a 70% prevalence of vitamin A deficiency, with a positive correlation between the severity of cirrhosis and the prevalence of VAD. [22] Thirty-five percent of patients with chronic exocrine pancreatic insufficiency have VAD despite 84% of them being on pancreatic enzyme replacement therapy. [16]

Seventy percent of patients who had a biliopancreatic diversion had developed VAD at 3 years post-procedure. [23] At birth, Sixty-six percent of premature infants are vitamin A deficient and, at 36 weeks post-menstrual age, 82% had deficiency due to high requirements and low absorption. [17]

Pathophysiology

Vitamin A has a role in the regeneration of visual pigment, maintenance of mucosal membranes, and immune function. Deficiency can lead to night blindness due to poor regeneration of visual pigment in retinal rods. If the deficiency is allowed to persist, the rods will degenerate, and xerophthalmia will develop, leading to true blindness. [24] [25] [26] Intestinal and pulmonary mucosal membrane xerosis and breakdown, along with immune dysfunction, lead to frequent infections and anemia of chronic inflammation. [27] [28] [29] [30]

History and Physical

A well-performed history of a patient can raise suspicion for vitamin A deficiency. The presence of a malabsorptive process, such as IBD, chronic GI infection, cirrhosis, pancreatic insufficiency, prematurity, rubeola infection (measles), a history of living in a resource-poor country, or current pregnancy or lactation in the setting of poor nutrition should raise concern for vitamin A deficiency. The natural progression of chronic VAD most commonly presents with the gradual development of night blindness, increased frequency of GI, pulmonary, and urinary infections, and development of xeroderma and phrynoderma (follicular hyperkeratosis often found on extensor surfaces, shoulders, and buttocks). [30] [31]

As the severity of deficiency worsens, signs of xerophthalmia develop with Bitot spots (conjunctival, triangular or oval, foamy lesions) and conjunctival xerosis (appears as conjunctival wrinkling). If VAD continues to persist, its later stages present as corneal xerosis, corneal ulceration, and eventually keratomalacia as the corneal ulcers heal, corneal scarring and blindness results. In the setting of an infection, particularly measles, patients with an acute deficiency may present with corneal xerosis and ulceration without preceding night blindness or Bitot’s spots. [26] Phrynoderma (a form of follicular hyperkeratosis) may also be seen in VAD but is associated with other nutritional deficiencies as well. [31]

A clinical diagnosis of vitamin A deficiency can be made in classical exam findings and confirmatory laboratory testing. The presence of xerophthalmia is nearly pathognomonic for vitamin A deficiency. [32]

The provider can order serum retinol testing for patients with a less clear history and physical exam, with deficiency defined as less than 20 micrograms/dL. [8] However, serum retinol concentration may be normal, even if the total body stores are low, due to maintenance of circulating retinol levels by hepatic stores. The gold standard for evaluating total body vitamin A is quantifying liver retinol concentration on biopsy. [33]

Given the risks associated with liver biopsies, they are not routinely used for evaluating vitamin A levels outside of the research setting.

Treatment / Management

Treatment of vitamin A deficiency is vitamin A supplementation (VAS). A multitude of studies has concluded that VAS in vitamin A deficient populations reduce childhood morbidity and mortality. [34] VAS makes a definitive clinical difference in patients with serum retinol concentrations less than 20 micrograms/dL. Any patient with a concentration greater than 30 micrograms/dL will not benefit from supplementation and should follow the recommended dietary allowance. [35]

In regions with a high prevalence of VAD, the World Health Organization (WHO) recommends universal VAS of select populations. They recommend a one-time dose of 100,000 IU in children 6 to 11 months of age followed by doses of 200,000 IU every 4 to 6 months up to 5 years of age. [36] At-risk pregnant women should receive supplementation at lower doses due to concern for fetotoxicity; the recommended dosing is 10,000 IU daily or 25,000 IU weekly for 12 weeks. [37] The WHO no longer recommends universal supplementation for children less than 6 months of age or postpartum women. [38] [39] [40]

International guidelines do not clearly outline dosing of VAS for asymptomatic vitamin A deficiency in resource-rich regions. Instead, dosing of VAS is based on the severity of deficiency and provider discretion. The WHO recommends treating xerophthalmia with VAS of 50,000 IU for children less than 6 months of age, 100,000 IU for children 6-12 months of age, and 200,000 IU for children greater than 12 months of age daily for 2 days followed by an additional dose after 2 weeks. For any patient with a severe case of measles, the WHO recommends the aforementioned dosing once daily for 2 days, regardless of whether the patient is known to be vitamin A deficient or not. [41] Regarding specific VAS strategies, zinc-deficient patients have a poor response to VAS and should undergo concomitant zinc supplementation. [12] If the patient’s VAD is from malabsorption, providers should consider intramuscular VAS formulations.

In resource-rich countries, post-bariatric patients and neonates have particular dosing recommendations. Post-bariatric surgery patients are recommended to take 10,000 IU VAS daily and adjust as needed based on regular serum retinol level monitoring. Some bariatric patients have been known to need up to 100,000 IU VAS daily. [42] For premature infants, guidelines do not exist yet for VAS. Still, recent studies have shown that VAS of 10,000 IU every other day in very low birth weight neonates for 4 weeks has significant results, decreasing all-cause mortality by 56% and decreasing rates of oxygen requirement, sepsis, PDA, and length of hospital stay. [43] Supplementation of 1,500 IU daily in extremely premature infants had a significant decrease in retinopathy of prematurity (1.6% vs. 6.9%) and a nearly 50% decrease in bronchopulmonary dysplasia. [44] VAD associated with other malabsorptive processes is treated on a case-by-case basis.

Differential Diagnosis

When evaluating vitamin A deficiency, it is important not to overlook other causes of similar signs and symptoms. Night blindness is the first presenting symptom of retinitis pigmentosa and some rare retinal dystrophies. [45] [46] Additionally, cataracts and myopia are both degenerative ophthalmologic diseases that can present with night blindness. Bitot spots are also associated with niacin deficiency. [47] Pinguecula and pterygium may resemble Bitot spots.

The prognosis of vitamin A deficiency depends on the severity of the disease at treatment initiation. [26] If treated promptly, patients with subclinical VAD have a very good prognosis without long term sequelae. Treatment at any stage of severity can show improvement within a week. [48]

The early ophthalmologic signs, such as night blindness, conjunctival xerosis, and Bitot spots, will resolve completely within about 2 months of supplementation, while corneal xerosis and ulceration results in scarring that may lead to permanent vision loss despite treatment. [49] [26] At the onset of visual manifestations, patients develop an increased susceptibility to infection. In preschool children with VAD, the presence of ophthalmologic signs indicates increased overall mortality from gastrointestinal, pulmonary, and other VAD-related mucosal infections. [26]

Mortality in children with night blindness is triple the mortality found in children with subclinical VAD. Children with both Bitot’s spots and night blindness have mortality nine times that of children with subclinical VAD. Nearly two-thirds of children with keratomalacia die within months. [26]

Complications

Severe vitamin A deficiency may lead to permanent vision loss or blindness, increased susceptibility to infections, and impaired immune function, leading to high mortality. [26]

Deterrence and Patient Education

A well-balanced, nutrient-rich diet prevents vitamin A deficiency in generally healthy patients able to absorb nutrition. In resource-rich regions, the majority of the population has access to vegetables, meats, and staple foods that are fortified with vitamin A. In resource-poor countries, large scale vitamin A supplementation programs have been implemented in attempts to provide high dose vitamin A at the WHO-recommended intervals. [50]

Associated programs educate people on nutrition, breastfeeding, and VAD symptoms. These have had variable success depending on the region. [51] [52] More programs are starting to focus on the root cause of VAD by focusing on food fortification and education rather than simply supplementation. In fact, many staple foods are now fortified with important micronutrients, and genetic modifications have been made to rice, potatoes, wheat, and soybeans, among others, to increase concentrations of vitamin A. [53] [54] [55] [56] [57] These biofortified crops can be economically and agriculturally viable. [58]

Enhancing Healthcare Team Outcomes

An interprofessional team greatly contributes to the effective treatment and prevention of vitamin A deficiency. The initial care in resource-rich settings typically falls to the primary care physician, who then coordinates with dietitians and pharmacists to ensure optimal nutrition and medical treatment. Gastroenterologists, bariatric surgeons, and transplant surgeons can help treat malabsorptive patients, post-bariatric surgery patients, and liver cirrhosis patients, respectively. Ophthalmologists are vital in evaluating and treating the multitude of VAD-related eye disorders. After acute evaluation and management of vitamin A deficiency, the primary care physician resumes preventive care. [59]

In regions of the world with limited medical care, public health nurses are vital in providing high-dose VAS to the most rural areas. They are instrumental in making appropriate specialty referrals for those with more severe disease. Governments and international health organizations play huge roles in providing the funds and organization for continued supplementation, education, and fortification programs. [34] Overall, though simple to diagnose and treat, vitamin A deficiency still affects millions worldwide and continues to be a topic of international attention.

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Disclosure: Christopher Hodge declares no relevant financial relationships with ineligible companies.

Disclosure: Christopher Taylor 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.

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Vitamin A Deficiency Clinical Presentation

Author: George Ansstas, MD; Chief Editor: George T Griffing, MD more...
Sections Vitamin A Deficiency
Practice Essentials
Pathophysiology
Epidemiology
Patient Education
Physical Examination
Laboratory Studies
Imaging Studies
Medical Care
Consultations
Medication Summary
Further Inpatient and Outpatient Care
Inpatient & Outpatient Medications
Deterrence/Prevention

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 spontaneous abortion secondary to impaired embryonic development. The patient may also report increased fatigue, as a manifestation of VAD anemia.

Signs and symptoms of vitamin A deficiency include the following:

Bitot spots - Areas of abnormal squamous cell proliferation and keratinization of the conjunctiva can be seen in young children with VAD.

Blindness due to retinal injury - Vitamin A has a major role in phototransduction. The cone cells are responsible for the absorption of light and for color vision in bright light. The rod cells detect motion and are responsible for night vision. In the rod cells of the retina, all-trans-retinol is converted into 11- cis -retinol, which then combines with a membrane-bound protein called opsin to yield rhodopsin. [ 21 ] A similar type of reaction occurs in the cone cells of the retina to produce iodopsin. The visual pigments absorb light at different wavelengths, according to the type of cone cell they occupy. VAD leads to a lack of visual pigments; this reduces the absorption of various wavelengths of light, resulting in blindness.

Poor adaptation to darkness (nyctalopia)

Dry skin (see Dermatologic Manifestations of Vitamin A Deficiency for more detail)

Broken fingernails

Keratomalacia

Xerophthalmia

Corneal perforation

Follicular hyperkeratosis (phrynoderma) secondary to blockage of hair follicles with plugs of keratin.

Other signs of VAD include excessive deposition of periosteal bone secondary to reduced osteoclastic activity, anemia, keratinization of mucous membranes, and impairment of the humoral and cell-mediated immune system.

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Gorstein JL, Dary O, Pongtorn, et al. Feasibility of using retinol-binding protein from capillary blood specimens to estimate serum retinol concentrations and the prevalence of vitamin A deficiency in low-resource settings. Public Health Nutr . 2008 May. 11(5):513-20. [QxMD MEDLINE Link] .

Russell RM. The vitamin A spectrum: from deficiency to toxicity. Am J Clin Nutr . 2000 Apr. 71(4):878-84. [QxMD MEDLINE Link] . [Full Text] .

Mayo-Wilson E, Imdad A, Herzer K, Yakoob MY, Bhutta ZA. Vitamin A supplements for preventing mortality, illness, and blindness in children aged under 5: systematic review and meta-analysis. BMJ . 2011 Aug 25. 343:d5094. [QxMD MEDLINE Link] . [Full Text] .

Dietary Guidelines for Americans, 2005. Department of Health and Human Services, Department of Agriculture . Jan 2005. Available at http://www.health.gov/dietaryguidelines/dga2005/document/default.htm .

Dietary Supplement Fact Sheet: Vitamin A and Carotenoids. National Institutes of Health, Office of Dietary Supplements . Apr 23 2006. Available at http://ods.od.nih.gov/factsheets/vitamina.asp .

Fletcher RH, Fairfield KM. Vitamin supplementation in disease prevention II. UpToDate . 2002.

Contributor Information and Disclosures

George Ansstas, MD Assistant Professor of Medicine, Division of Medical Oncology, Washington University School of Medicine George Ansstas, MD is a member of the following medical societies: American Medical Association Disclosure: Nothing to disclose.

N Gopalswamy, MD Chairman, Professor of Internal Medicine, Department of Gastroenterology, Wright State University, Boonshoft School of Medicine, Veterans Affairs Medical Center Disclosure: Nothing to disclose.

Jigna Thakore, MD Fellow, Department of Gastroenterology, Dayton Veterans Administration Medical Center Jigna Thakore, MD is a member of the following medical societies: American College of Gastroenterology , American Society for Gastrointestinal Endoscopy Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. for: Medscape.

Romesh Khardori, MD, PhD, FACP (Retired) Professor, Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Eastern Virginia Medical School Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists , American College of Physicians , American Diabetes Association , Endocrine Society Disclosure: Nothing to disclose.

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine George T Griffing, MD is a member of the following medical societies: American Association for Physician Leadership , American Association for the Advancement of Science , American College of Medical Practice Executives , American College of Physicians , American Diabetes Association , American Federation for Medical Research , American Heart Association , Central Society for Clinical and Translational Research , Endocrine Society , International Society for Clinical Densitometry , Southern Society for Clinical Investigation Disclosure: Nothing to disclose.

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Vitamin A. Retin oids Precursors of vitamin A 1 - Retin o l It is found in animal tissues as a retinyl ester with long-chain fatty acids. 2 - Retin a l The aldhyde derived from the oxidation of retinol. Retinol and retinal can be interconverted . 3 - Retin oic acid

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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. It can not be reduced in the body, and therefore, can not give rise to either retinal or retinol 4-b-carotene Plantfoods contain b-carotene, which can be cleaved in the intestine to two moleculesofretinal In humans, the conversion is insufficient, and vitamin A activity of b-carotene is only about one sixth(1/6) of that of retinol

Retinol (Animal Source) Retinalb-carotene (Plant Source) Retinoic Acid RETINOIDS PRECURSOR OF VITAMIN A

Absorption & Transport of vitamin A Transport to the Liver I- Retinol is derived from (DIET SOURCES) 1-DIET Retinyl esters (animal source) which are hydrolyzed in the intestinal mucosa, releasing retinoland free fatty acids 2- DIET b-carotenes(plant source) which is cleaved 2 retinalretinol II- Retinol is esterified with fatty acids to give retinylesters III-Retinyl esters are collected by the chylomicronsinto the lymphatic system. IV- Retinyl esters contained in the chylomicrons are taken up and stored by the liver

Release from the Liver • When needed, retinol is released from the liver and transported to extra hepatic tissue by plasmaretinol binding protein(RBP) • Theretinol - RBP complex attaches to specific receptors on the surface of the cells of peripheral tissues permitting retinol to enter

Mechanism of Action of vitamin A • Retinolis oxidized to retinoic acidinside cells. • Retinoic acidbinds with high-affinity to specific receptor proteins present in the nucleus of target tissue, such as epithelial cell. • The activated retinoic acid - receptor complexinteracts with nuclear chromatin (genes) to stimulate retinoid-specific mRNAsynthesis, resulting in the production of specific proteins that mediate several physiological functions. e.g. retinoids control the expression of keratin gene in most epithelial tissues.

Physiological Functions of Vitamin A • Vision • Growth • Reproduction • Epithelial cell maintenance

Functions of Vitamin A 1-Vision • Vitamin A is a component of the visual pigments of rodand cone cells. • Rhodopsin, the visual pigment of the rod cells in the retina, (for vision in dim light) consists of 11-cis retinal specially bound to the protein opsin. • When rhodopsin is exposed to light, a series of photochemical isomerization occurs, which results in release of all trans retinal and opsin (with bleaching of the visual pigment). • This process triggers a nerve impulse that is transmitted by the optic nerve to the brain. • Regeneration of rhodopsin requires isomerization of all trans retinal back to 11-cis retinal, which spontaneously combines with opsin to form rhodopsin.

2- Growth • Vitamin A is essential for normal growth of cells (by synthesis of important proteins) • bone growth is slow in vitamin A deficiency. • Animals deprived of vitamin A suffers keratinzation of taste buds leading to losing of their appetites.

3-Reproduction • Retinol & retinalare essential for normal reproduction 1- supporting spermatogenesis in males 2- preventing fetal resorption in females • Retinoic acid is inactivein maintaining reproduction & the visual cycle, BUT promotes growth. Thus, retinoic acids given only since birth to animals, leads to blindness & sterility. 4-Epithelial cells maintenance • Vitamin A is essential for normal differentiation of epithelial tissues and mucus secretion.

Diet Sources of Vitamin A • Sources of retinol(retinyl esters) : animal source Liver, kidney, cream, butter & egg yolk • Sources of carotenes(precursors of vitamin A) : plant source Yellow & dark green vegetables & fruits Requirement for Vitamin A • OneRE(retinol equivalents) = 1mg of retinol 12mg of b-carotene 24mg of other carotenoids • RDA for adults 900 RE for males 700RE for females

Clinical indications of vitamin A 1-Dietary deficiency Vitamin A, administered asretinolor retinyl esters, is used to treat patients deficient in the vitamin (not retinoic acid) Night blindness One of the earliest signs of vitamin A deficiency Difficulty in seeing in dim light. Prolonged deficiency leads to irreversible loss of visual cell. (affection of rods of retina) Xerophthalmia Severe deficiency of vitamin A Pathological dryness of the epithelium conjunctiva & cornea. It may end in corneal ulcerations and blindness.

2-Acne & Psoriasis Dermatologicproblemsofacne andpsoriasis are effectively treated with retinoic acidor its derivatives. • Mild cases of acneis treated by topical application of tretinoin (All- trans retinoic acid) which is too toxic for systemic administration. • Severe recalcitrant cystic acneunresponsive to conventional therapies, isotretinoin(13-cis retinoic acid) is administered orally

3-Prevention of chronic diseases • Populations consuming diets high in b-carotene show decreased incidence of heart diseases & lung & skin cancer • Consumption of foods rich in b-carotene is associated with reduced risk of cataracts and macular degeneration

Toxicity of Retinoids I. Vitamin A excess(hypervitaminosis A syndrome) Amounts exceeding 7.5 mg/day of retinol 1-Excessive intake of vitamin A may cause the followings: • dry skin & pruiritis are early signs • liver enlarged, cirrhotic • increased intracranial pressure (mimic symptoms of brain tumours e.g. headache etc…) 2-Pregnant females should not ingest excessive amounts of vitamin A because of its potential for causing congenital malformations in developing fetus.

II. Isotretinoin drug(13-cis retinoic acid) 1-Teratogenic • So, absolutely contraindicated in women with childbearing potential. • Pregnancy should be excluded before initiation of treatment & adequate contraceptive (birth control) must be used 2-Risk of coronary heart diseases Prolonged treatment with 13-cis retinoic acid leads to hyperlipidemia & increase in LDL/HDL ratio with increased risk of coronary heart diseases.

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Vitamin A: Structure, Properties, Functions, and Deficiency

Are you looking for the details of vitamin A Structure, functions, properties, and Deficiencies?

Vitamins are organic compounds occurring in small quantities in different natural foods and are necessary for the growth and maintenance of good health in human beings and in experimental animals. Basically, vitamins can be divided into two types based on solubility. Vitamins are vital amines.

They are

Fat-soluble (vitamin A, D, E, and K)
Water-soluble (B-Complex vitamins and vitamin C)

In this article, we are adding the details of vitamin A.

Table of Contents

Historical aspects of Vitamin A

Vitamin A was first isolated by McCollum, Davis Simmonds, and Kennedy in 1913.
Richard Kuhn identified carotene and received the Nobel Prize in 1937.
Vitamin A’s structure was elucidated by Paul Karrer in 1931.

Common names for Vitamin A

Anti-xerophthalmic factor
Bright eyes Vitamin

Other Names

3-Dehydroretinol,
3-Déhydrorétinol,
Acétate de Rétinol,
Antixerophthalmic Vitamin,
Axerophtholum,
Dehydroretinol,
Déhydrorétinol,
Fat-Soluble Vitamin,
Oleovitamin A,
Palmitate de Rétinol,
Retinoid, Retinoids,
Rétinoïdes, Retinol,
Retinol Acetate,
Retinol Palmitate,
Retinyl Acetate,
Rétinyl Acétate,
Retinyl Palmitate,
Vitaminum A
Rétinyl Palmitate,
Vitamin A Acetate,
Vitamin A Palmitate,
Vitamin A1,
Vitamin A2,
Vitamina A,
Vitamine A,
Vitamine A1,
Vitamine A2,
Vitamine Liposoluble,

Sources of Vitamin A

Rich sources of vitamin A foods are “cod liver oil” and “shark liver oil”.
Fish liver oil, butter, milk, eggs, and kidneys.
Pigmented vegetables and fruits
Carotene is the provitamin of vitamin A and is widely found in carrots and yellow vegetables.

Structure of Vitamin A

It contains a beta-iodine ring and a side chain. The side chain consists of two isoprene units, four double bonds, and one alcoholic group.

Chemical names

Retinol (A1)	C H O
3-dehydroretinol (A2)	C H O

Chemical Properties

It is a colorless, oily substance. It forms a transient blue color with saturated “antimony trichloride” (AnCl3). ( It is an important principle in the “Cataract” method used to determine vitamin A.
Vitamin A absorbs UV light. It shows maximum absorption at 325 nm.
It is quite stable without air and light. Furthermore, it creates esters with higher fatty acids.
Additionally, it is soluble in fat solvents and fats . but insoluble in water.

Biochemical Functions

1. visual cycle.

Rhodopsin plays a pivotal role in vision. It is a membrane protein found in the photoreceptor cells of the retina. The proteins are oriented in such a way that their N-terminal ends face the intradermal space of the receptor matrix.

Rhodopsin is made up of the protein Opsin and 11-cis-retinal, attached through a Schiff baser to a lysine residue of the protein. The 11-cis-retinal is photosensitive.

When light falls on the retina, the 11-cis-retinal isomerases turn into all-trans-retinal. This creates a series of unstable molecules, and the Schiff base linkage is finally broken. Then all-trans-retinal is released from the protein. Opsin remains in the retina. But trans-retinal enters the blood circulation.

The main role of vitamin A is vision. The retina contains two types of light receptors, i.e., “rods” and “cones”.

Rods function in dim light but do not recognize color.
Cones function in bright light and are responsible for color vision. Rods contain the proteins “opsin” and “ 11-cis retinol ”, which is a prosthetic group.

11-cis retinol is synthesized from trans retinol . All trans-retinol is converted into 11-cis-trans retinal by several steps. Rods absorb light within picoseconds. It undergoes several changes, i.e., 11-cis retinol is converted to trans retinol.

Thus, trans retinol is dissociated from Opsin and transported to the liver. Where it is converted to 11-cis retinal. It is ready for another visual cycle.

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. This may account for the requirement for vitamin A for normal reproduction.
Vitamin A is required for “sulfation” of the mucopolysaccharides in the matrix of bone .

Deficiency Disorders

Here are the vitamin deficiency symptoms:

Night Blindness: In the early stage of vitamin A deficiency, individuals cannot see well in dim light. This condition is called “ Night Blindness ” (or) “ Nyctalopia ”. This is due to an inadequate amount of vitamin A required for the regeneration of “Rhodopsin.”
Xerophthalmia: In this condition, lachrymal glands get keratinized and stop secreting. Thus, the eyes become dry. This is due to a deficiency of vitamin A.
If xerosis of the conjunctiva and cornea is severe, it leads to a condition called “keratomalacia”. Symptoms are “metaplasia” and “degeneration of the corneal epithelium.”

Overdose of Vitamin A

The side effects of too much vitamin A cause serious problems in pregnant women. They are fatigue, brittle bones, joint pain, vomiting, and severe gastrointestinal distress.

If pregnant women take an excessive amount of vitamin A, it leads to a serious problem for the unborn child, including birth defects. The recommended RDA values are given below.

What are the benefits of vitamin A?

Here are a few of the benefits of vitamin A. They are

It protects your eyes from age-related issues with vision and night blindness.
It protects against some types of cancer.
It gives good strength to the immune system.
It gives good support for your bone health.
It promoted healthy growth and reproduction.

Frequently Asked Questions (FAQs) on Vitamin A

Which foods are high in vitamin a.

The best sources of vitamin A are Cod liver oil, Eggs, Fortified breakfast cereals, fortified skim milk, orange, Yellow vegetables, fruits, Other sources of beta-carotene such as broccoli, spinach, the darkest green, and leafy vegetables.

What does vitamin A do in the human body?

Vitamin A is insoluble in water and soluble in Fats (So it is called “Fat-soluble vitamin”). It is essential for normal vision, immune system development, and reproduction. It also helps sensitive organ developments like Lungs, Kidneys, and other organs.

How do we get vitamin A?

To get a good amount of vitamin A, we have to take the good sources of beta-carotene in our diet. It will convert into vitamin A in our body. The good sources are Yellow, red, and green leafy vegetables – spinach, sweet potatoes, carrots, and red pepper. Yellow fruits like papaya, apricots, and mango are other good sources of vitamin A-rich foods.

What is the recommended dose of vitamin A?

According to RDA (Recommended Dietary Allowance) Values, here are the vitamin dosage per day 1. For men – 900 mcg per day, 2. For Women – 700 mcg per day, 3. For Pregnant Women – 700 mcg per day, 4. For breast-feeding women – 1300 mcg daily

Focus Points

What is the storage form of vitamin A? It is a retinyl palmitate . Its overdose causes injury to lysosomes.
Retinal is a visual pigment.
Which is the carrier for oligosaccharides in glycoprotein synthesis? Retinoic acid

Vitamin A is a vital nutrient that is essential for human health. It helps the body to form cell membranes and performs numerous other functions, including aiding in the absorption of other nutrients. In this blog post, we provide a detailed overview of the vitamin A structure and properties, as well as explain how it is helpful for students.

By reading this blog, you will be able to better understand why it is important to include this nutrient in your diet and why students should be especially diligent in ensuring they are getting enough of it. Do you have any questions about vitamin A? Let us know in the comments below!

VITAMINS : The Micro-Nutrients in Our Body

Fat soluble Vitamins: An In-Depth Look

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Correction: Novel protective circulating miRNA are associated with preserved vitamin D levels in patients with mild COVID-19 presentation at hospital admission not progressing into severe disease

Affiliations.

1 Institute of Endocrine and Metabolic Sciences, San Raffaele Vita Salute University and IRCCS San Raffaele Hospital, Milan, Italy.
2 Galileo Research Srl, Pisa, Italy.
3 Institute of Endocrine and Metabolic Sciences, San Raffaele Vita Salute University and IRCCS San Raffaele Hospital, Milan, Italy. [email protected].
PMID: 38937301
DOI: 10.1007/s12020-024-03939-5

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Novel protective circulating miRNA are associated with preserved vitamin D levels in patients with mild COVID-19 presentation at hospital admission not progressing into severe disease. di Filippo L, Terenzi U, Di Ienno G, Trasciatti S, Bonaretti S, Giustina A. di Filippo L, et al. Endocrine. 2024 Jun 10. doi: 10.1007/s12020-024-03900-6. Online ahead of print. Endocrine. 2024. PMID: 38856841

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Sjogren’s syndrome is a known cause of renal tubular acidosis (RTA). However, osteomalacia associated with Sjogren’s syndrome is rare and seldom reported in literature. We report a case of pseudofractures of both femora due to osteomalacia as a result of RTA secondary to Sjogren’s syndrome, which was initially misdiagnosed as a stress fracture. A man in his 30s presented with hip pain and was initially misdiagnosed to have stress fractures because of the ‘through and through’ extension of the ‘fracture’ lines at the neck of both femora. The patient had a normal serum biochemistry profile except for elevated alkaline phosphatase levels. On further evaluation, he was found to have distal RTA secondary to Sjogren’s syndrome. The patient responded to sodium bicarbonate therapy with clinical, biochemical and radiological improvement. A high index of suspicion for RTA should be kept in a patient with osteomalacia with a normal calcium profile and vitamin D level.

Calcium and bone
Sjogren's syndrome

https://doi.org/10.1136/bcr-2023-256661

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Contributors The following authors were responsible for drafting of the text, sourcing and editing of clinical images, investigation results, drawing original diagrams and algorithms, and critical revision for important intellectual content: SM, DA, SB and AS. The following authors gave final approval of the manuscript: SM, DA, SB and AS.

Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

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Association between osteocalcin and residual β-cell function in children and adolescents newly diagnosed with type 1 diabetes: a pivotal study

Original Article
Published: 04 July 2024

Cite this article

M. Valenzise 1 na1 ,
B. Bombaci ORCID: orcid.org/0000-0002-7081-5884 1 ,
F. Lombardo 1 ,
S. Passanisi ORCID: orcid.org/0000-0002-4369-7798 1 ,
C. Lombardo 2 ,
C. Lugarà 1 ,
F. D’Amico 1 ,
L. Grasso 3 ,
M. Aguennouz 3 na2 ,
A. Catalano 3 na2 &
G. Salzano ORCID: orcid.org/0000-0003-2180-4510 1

This pivotal study aimed to evaluate circulating levels of bone remodeling markers in children and adolescents at the onset of type 1 diabetes (T1D). Additionally, we assessed their correlation with glucose control, residual β-cell function, and the severity of presentation.

In this single-center cross-sectional study, we recruited children and adolescents newly diagnosed with T1D at our tertiary-care Diabetes Centre. Anamnestic, anthropometric, clinical, and biochemical data at T1D diagnosis were collected. Basal and stimulated C-peptide levels were assessed, along with the following bone remodeling biomarkers: osteocalcin (OC), alkaline phosphatase (ALP), parathormone (PTH), 25-OH Vitamin D (25OH-D), and the C-terminal cross-linked telopeptide of type 1 collagen (CTX).

We enrolled 29 individuals newly diagnosed with T1D, with a slight male prevalence (51.7%). The mean age was 8.4 ± 3.7 years. A positive correlation between OC and stimulated C-peptide (R = 0.538; p = 0.026) and between PTH and serum HCO3- (R = 0.544; p = 0.025) was found. No other correlations between bone remodeling biomarkers and clinical variables were detected.

Our data showed a positive correlation between OC levels and residual β-cell function in children and adolescents at T1D presentation. Further longitudinal studies evaluating OC levels in pediatric subjects with T1D are needed to better understand the complex interaction between bone and glucose metabolisms.

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Data availability

The datasets generated during and/or analysed during the current study are available from the corresponding author on reasonable request.

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Mariella Valenzise and Bruno Bombaci have contributed equally to this work.

Antonino Catalano and Giuseppina Salzano co-last authors.

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Department of Human Pathology in Adult and Developmental Age “Gaetano Barresi”, University of Messina, Messina, Italy

M. Valenzise, B. Bombaci, F. Lombardo, S. Passanisi, C. Lugarà, F. D’Amico & G. Salzano

Department of Biomedical Sciences and Morphological and Functional Imaging, University of Messina, Messina, Italy

C. Lombardo

Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy

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Conceptualization: Mariella Valenzise, Antonino Catalano; Methodology: Mhammed Aguennouz, Antonino Catalano; Formal analysis and investigation: Cristina Lombardo, Cecilia Lugarà, Federica D’Amico, Loredana Grasso; Writing—original draft preparation: Stefano Passanisi; Writing—review and editing: Giuseppina Salzano, Fortunato Lombardo.

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Valenzise, M., Bombaci, B., Lombardo, F. et al. Association between osteocalcin and residual β-cell function in children and adolescents newly diagnosed with type 1 diabetes: a pivotal study. J Endocrinol Invest (2024). https://doi.org/10.1007/s40618-024-02414-2

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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 ].

Table 1: Recommended Dietary Allowances (RDAs) for Vitamin A [ ]
Age	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

*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.

Table 2: Vitamin A Content of Selected Foods [ ]
Food	microgram (mcg) RAE per serving	Percent DV*
Beef liver, pan fried, 3 ounces	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 ounces	219	24
Ice cream, French vanilla, soft serve, ⅔ cup	185	21
Milk, skim, with added vitamin A and vitamin D, 1 cup	149	17
Cantaloupe, raw, ½ cup	135	15
Cheese, ricotta, part skim, ½ cup	133	15
Peppers, sweet, red, raw, ½ cup	117	13
Mangos, raw, 1 whole	112	12
Breakfast cereals, fortified with 10% of the DV for vitamin A, 1 serving	90	10
Egg, hard boiled, 1 large	75	8
Black-eyed peas (cowpeas), boiled, 1 cup	66	7
Apricots, dried, sulfured, 5 apricots	63	7
Broccoli, boiled, ½ cup	60	7
Salmon, sockeye, cooked, 3 ounces	59	7
Tomato juice, canned, ¾ cup	42	5
Yogurt, plain, low fat, 1 cup	32	4
Tuna, light, canned in oil, drained, 3 ounces	20	2
Baked beans, canned, plain or vegetarian, 1 cup	13	1
Summer squash, all varieties, boiled, ½ cup	10	1
Chicken, breast meat and skin, roasted, ½ breast	5	1
Pistachio nuts, dry roasted, 1 ounce	4	0

*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.

Table 3: Tolerable Upper Intake Levels (ULs) for Preformed Vitamin A [ ]*
Age	Male	Female	Pregnancy	Lactation
Birth to 12 months	600 mcg	600 mcg
1–3 years	600 mcg	600 mcg
4–8 years	900 mcg	900 mcg
9–13 years	1,700 mcg	1,700 mcg
14–18 years	2,800 mcg	2,800 mcg	2,800 mcg	2,800 mcg
19+ years	3,000 mcg	3,000 mcg	3,000 mcg	3,000 mcg

*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.
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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: Benefits, Sources, and Side Effects
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Vitamin A
Some key points: - Vitamin A is a fat-soluble vitamin that is essential for vision, growth, reproduction, and epithelial cell maintenance. It cannot be made by the body and must come from diet. - Major sources include liver, dairy, eggs, carrots and other orange vegetables. Beta-carotene from plants is a provitamin A that the body can convert ...
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 ...
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
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 dependence on contact lenses, but eating an adequate amount will support eye health.
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: 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
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: Health benefits and risks
Vitamin A is a vital nutrient for healthy vision, skeletal tissue, hair, and skin. Food sources include liver, carrots, and green, leafy vegetables. Learn more.
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 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 Deficiency: Practice Essentials, Background ...
The word vitamin was originally derived from Funk's term "vital amine." In 1912, he was referring to Christian Eijkman's discovery of an amine extracted from rice polishings that could prevent beriberi.Funk's recognition of the antiberiberi factor as vital for life was indeed accurate. Researchers have since found that vitamins are essential organic compounds that the human body cannot synthesize.
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 ...
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 ...
Vitamin A
Dec 31, 2008 •. 36 likes • 33,885 views. G. guestb2d17a. This presentation is ment to train Paramedicals & persons seeking health information. It is enjoyable to learn What & How about Vitamin A & its Role in Human Body. it educate general people in very palatable forms. Read more. 1 of 31. Vitamin A - Download as a PDF or view online for free.
Vitamin A chemistry, functions and deficiency
1) Vitamin A plays an essential role in vision, immune function, cell growth and differentiation. It exists in two forms - retinoids found in animal foods and carotenoids which are plant-derived provitamin A compounds. 2) Dietary vitamin A is absorbed in the intestine and transported to the liver where it is stored.
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: 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.
Production of Vitamin A by Suman Rai Dept of Microbiology ...
Vitamin-A.pptx - Free download as Powerpoint Presentation (.ppt / .pptx), PDF File (.pdf), Text File (.txt) or view presentation slides online. The document summarizes the production of vitamin A, its forms, and the microbial fermentation process for producing beta-carotene. Blakeslea trispora fungus is used in submerged fermentation to produce beta-carotene.
VITAMIN A
Vitamin A is a fat-soluble vitamin that exists in multiple forms including retinol, retinal, and retinoic acid. It plays an essential role in vision, cell growth and differentiation. Vitamin A is absorbed in the small intestine and transported to the liver where it is stored. A deficiency can impair vision and cause dry eyes and corneal ...
Correction: Novel protective circulating miRNA are associated ...
Novel protective circulating miRNA are associated with preserved vitamin D levels in patients with mild COVID-19 presentation at hospital admission not progressing into severe disease. di Filippo L, Terenzi U, Di Ienno G, Trasciatti S, Bonaretti S, Giustina A. di Filippo L, et al. Endocrine. 2024 Jun 10. doi: 10.1007/s12020-024-03900-6.
Unusual presentation of Sjogren's syndrome
On further evaluation, he was found to have distal RTA secondary to Sjogren's syndrome. The patient responded to sodium bicarbonate therapy with clinical, biochemical and radiological improvement. A high index of suspicion for RTA should be kept in a patient with osteomalacia with a normal calcium profile and vitamin D level.
Vitamin A and its deficiency
The term Xerophthalmia comprises of all the ocular manifestations of Vit.A def. Impaired vision in dim light and in the dark, due to impaired function of specific vision cells (namely, the rods) in the retina. *Xerosis-dryness *Conjunctiva-lines the eyelids and surface of the eyes. Opaque-not able to be seen through; not transparent.
Association between osteocalcin and residual β-cell ...
Purpose This pivotal study aimed to evaluate circulating levels of bone remodeling markers in children and adolescents at the onset of type 1 diabetes (T1D). Additionally, we assessed their correlation with glucose control, residual β-cell function, and the severity of presentation. Methods In this single-center cross-sectional study, we recruited children and adolescents newly diagnosed with ...
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 []. ...

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Vitamin A Deficiency

Vitamin A Supplementation

Vitamin A deficiency

VEGGIES AND VITAMIN A

Fat Soluble Vitamins Vitamin A Vitamin E Vitamin D Vitamin K

Vitamin D A Superhero ?

Vitamin A: Structure, Properties, Functions, and Deficiency

Historical aspects of Vitamin A

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Structure of Vitamin A

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2. Other Biochemical Functions

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Overdose of Vitamin A

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Correction: Novel protective circulating miRNA are associated with preserved vitamin D levels in patients with mild COVID-19 presentation at hospital admission not progressing into severe disease

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Association between osteocalcin and residual β-cell function in children and adolescents newly diagnosed with type 1 diabetes: a pivotal study

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