Who should take vitamin A? However, your doctor may recommend vitamin A or beta-carotene supplement or cream if you suffer from: Age-related macular degeneration or cataract. Research shows that people who eat more foods with beta-carotene have a lower risk of developing age-related macular degeneration or cataract.
You may need to supplement your diet if you are not eating enough of these foods. Click Here For Article Measles. Vitamin A supplements can reduce the severity and complications of measles in children. However, never give a child vitamin A supplements without a doctor's supervision. Inflammatory bowel disease IBD. Crohn's disease and ulcerative colitis can interfere with digestion and absorption of nutrients.
Your doctor may recommend taking a multivitamin containing vitamin A if you are suffering from nutrient deficiencies. Click Here For Article Acne.
A synthetic form of vitamin A called retinoids is used in prescription creams and gels for the treatment of mild to moderate acne, or in Roaccutane capsules for more severe cases of acne. Click Here For Article Other skin conditions. Retinoid ointments are available for skin conditions such as chafed skin, cracked heels, cracked nipples, eczema, and sun-damaged and pigmented skin.
How much vitamin A? How much beta-carotene? How can I increase the levels of vitamin A in my body? As the body makes vitamin A from beta-carotene, you can increase levels of vitamin A in your body, while at the same time enjoy the health benefits of the antioxidants in beta-carotene by: Eating more fruit and vegetables rich in beta-carotene.
These include vegetables such as carrot, pumpkin, sweet potato, and fruit, including mango, apricot, papaya, and peach. Leafy greens, such as spinach and kale, also contain beta-carotene, as well as broccoli. Cooking your carrots. Because carrots are high in fibre, the heat from cooking will free the carotenoids from the fibre and make them more available. Drizzling olive oil on your vegetables. As carotenoids are fat-soluble, they are absorbed in the presence of fat.
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. Additionally, based on current evidence the U. Preventive Services Task Force does not support the use of beta-carotene supplements for the prevention of any cancer. Prostate Cancer: Lycopene is a carotenoid that gives fruits and vegetables a pink or red hue, as in tomatoes and grapefruit.
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.
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. 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.
Deficiency Vitamin A deficiency is rare in Western countries but may occur. 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. Toxicity Vitamin A toxicity may be more common in the U. 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, 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 [], or some birth defects. Signs of toxicity include the following. 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. Although these intakes are lower than the RDAs for individual men and women, these intake levels are considered to be adequate for population groups. The adequacy of vitamin A intake decreases with age in children [ 4 ]. Furthermore, girls and African-American children have a higher risk of consuming less than two-thirds of the vitamin A RDA than other children [ 4 ].
Frank vitamin A deficiency is rare in the United States. However, vitamin A deficiency is common in many developing countries, often because residents have limited access to foods containing preformed vitamin A from animal-based food sources and they do not commonly consume available foods containing beta-carotene due to poverty [ 2 ]. According to the World Health Organization, million preschool-aged children and In these countries, low vitamin A intake is most strongly associated with health consequences during periods of high nutritional demand, such as during infancy, childhood, pregnancy, and lactation.
In developing countries, vitamin A deficiency typically begins during infancy, when infants do not receive adequate supplies of colostrum or breast milk [ 12 ]. Chronic diarrhea also leads to excessive loss of vitamin A in young children, and vitamin A deficiency increases the risk of diarrhea [ 5 , 13 ]. The most common symptom of vitamin A deficiency in young children and pregnant women is xerophthalmia.
One of the early signs of xerophthalmia is night blindness, or the inability to see in low light or darkness [ 2 , 14 ]. Vitamin A deficiency is one of the top causes of preventable blindness in children [ 12 ].
People with vitamin A deficiency and, often, xerophthalmia with its characteristic Bitot's spots tend to have low iron status, which can lead to anemia [ 3 , 12 ]. Vitamin A deficiency also increases the severity and mortality risk of infections particularly diarrhea and measles even before the onset of xerophthalmia [ 5 , 12 , 14 ].
In developed countries, clinical vitamin A deficiency is rare in infants and occurs only in those with malabsorption disorders [ 15 ]. However, preterm infants do not have adequate liver stores of vitamin A at birth and their plasma concentrations of retinol often remain low throughout the first year of life [ 15 , 16 ]. Preterm infants with vitamin A deficiency have an increased risk of eye, chronic lung, and gastrointestinal diseases [ 15 ]. In developed countries, the amounts of vitamin A in breast milk are sufficient to meet infants' needs for the first 6 months of life.
But in women with vitamin A deficiency, breast milk volume and vitamin A content are suboptimal and not sufficient to maintain adequate vitamin A stores in infants who are exclusively breastfed [ 17 ]. The prevalence of vitamin A deficiency in developing countries begins to increase in young children just after they stop breastfeeding [ 3 ]. The most common and readily recognized symptom of vitamin A deficiency in infants and children is xerophthalmia.
Pregnant women need extra vitamin A for fetal growth and tissue maintenance and for supporting their own metabolism [ 18 ]. The World Health Organization estimates that 9. Other effects of vitamin A deficiency in pregnant and lactating women include increased maternal and infant morbidity and mortality, increased anemia risk, and slower infant growth and development. Most people with cystic fibrosis have pancreatic insufficiency, increasing their risk of vitamin A deficiency due to difficulty absorbing fat [ 19 , 20 ].
However, improved pancreatic replacement treatments, better nutrition, and caloric supplements have helped most patients with cystic fibrosis become vitamin A sufficient [ 21 ].
Several studies have shown that oral supplementation can correct low serum beta-carotene levels in people with cystic fibrosis, but no controlled studies have examined the effects of vitamin A supplementation on clinical outcomes in patients with cystic fibrosis [ ].
This section focuses on three diseases and disorders in which vitamin A might play a role: cancer, age-related macular degeneration AMD , and measles. Because of the role vitamin A plays 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 is unclear. Several prospective and retrospective observational studies in current and former smokers, as well as in people who have never smoked, found that higher intakes of carotenoids, fruits and vegetables, or both are associated with a lower risk of lung cancer [ 1 , 23 ]. In the Carotene and Retinol Efficacy Trial CARET , 18, current and former smokers including some males who had been occupationally exposed to asbestos took daily supplements containing 30 mg beta-carotene and 7, mcg RAE 25, IU retinyl palmitate for 4 years, on average [ 24 ].
In the beta-carotene component of the Physicians' Health Study, 22, male physicians took mg aspirin plus 50 mg beta-carotene, 50 mg beta-carotene plus aspirin placebo, mg aspirin plus beta-carotene placebo, or both placebos every other day for 12 years [ 26 ].
In all three of these studies, taking very high doses of beta-carotene, with or without 7, mcg RAE 25, IU retinyl palmitate or mg aspirin, did not prevent lung cancer.
In fact, both the CARET and ATBC studies showed a significant increase in lung cancer risk among study participants taking beta-carotene supplements or beta-carotene and retinyl palmitate supplements. The evidence on the relationship between beta-carotene and prostate cancer is mixed. However, the ATBC study found that baseline serum beta-carotene and retinol levels and supplemental beta-carotene had no effect on survival [ 28 ].
The ATBC and CARET 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. The relevance of these results to people who have never smoked or to the effects of beta-carotene or retinol from food or multivitamins which typically have modest amounts of beta-carotene is not known. More research is needed to determine the effects of vitamin A on prostate, lung, and other types of cancer.
Age-related macular degeneration AMD is a major cause of significant vision loss in older people. AMD's etiology is usually unknown, but the cumulative effect of oxidative stress is postulated to play a role. If so, 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, in particular, accumulate in the retina, the tissue in the eye that is damaged by AMD. A 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 but found that adding lutein 10 mg and zeaxanthin 2 mg or omega-3 fatty acids to the formulation did not confer any additional benefits [ 31 ].
Importantly, the study 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. Measles is a major cause of morbidity and mortality in children in developing countries. About half of all measles deaths happen in Africa, but the disease is not limited to low-income countries. Vitamin A deficiency is a known risk factor for severe measles.
The World Health Organization recommends high oral doses 60, mcg RAE [, IU] of vitamin A for two days for children over age 1 with measles who live in areas with a high prevalence of vitamin A deficiency [ 32 ]. A Cochrane review of eight randomized controlled trials of treatment with vitamin A for children with measles found that 60, mcg RAE , IU of vitamin A on each of two consecutive days reduced mortality from measles in children younger than 2 and mortality due to pneumonia in children [ 32 ].
Vitamin A also reduced the incidence of croup but not pneumonia or diarrhea, although the mean duration of fever, pneumonia, and diarrhea was shorter in children who received vitamin A supplements.
A meta-analysis of six high-quality randomized controlled trials of measles treatment also found that two doses of 30, mcg RAE , IU in infants and 60, mcg RAE , IU in older children significantly reduced measles mortality [ 33 ]. The vitamin A doses used in these studies are much higher than the UL. The effectiveness of vitamin A supplementation to treat measles in countries, such as the United States, where vitamin A intakes are usually adequate is uncertain.
The body needs vitamin A to maintain the corneas and other epithelial surfaces, so the lower serum concentrations of vitamin A associated with measles, especially in people with protein-calorie malnutrition, can lead to blindness. None of the studies evaluated in a Cochrane review evaluated blindness as a primary outcome [ 34 ]. However, a careful clinical investigation of African children with measles revealed that half of all corneal ulcers in these children, and nearly all bilateral blindness, occurred in those with vitamin A deficiency [ 35 ].
Because vitamin A is fat soluble, the body stores excess amounts, primarily in the liver, and these levels can accumulate. Although excess preformed vitamin A can have significant toxicity known as hypervitaminosis A , large amounts of beta-carotene and other provitamin A carotenoids are not associated with major adverse effects [ 36 ]. The manifestations of hypervitaminosis A depend on the size and rapidity of the excess intake.
The symptoms of hypervitaminosis A following sudden, massive intakes of vitamin A, as with Arctic explorers who ate polar bear liver, are acute [ 37 ]. Chronic intakes of excess vitamin A lead to increased intracranial pressure pseudotumor cerebri , dizziness, nausea, headaches, skin irritation, pain in joints and bones, coma, and even death [ 2 , 4 , 5 ]. Although hypervitaminosis A can be due to excessive dietary intakes, the condition is usually a result of consuming too much preformed vitamin A from supplements or therapeutic retinoids [ 3 , 5 ].
When people consume too much vitamin A, their tissue levels take a long time to fall after they discontinue their intake, and the resulting liver damage is not always reversible. Observational studies have suggested an association between high intakes of preformed vitamin A more than 1, mcg daily—only slightly higher than the RDA , reduced bone mineral density, and increased fracture risk [ 1 , 4 , 38 ].
However, the results of studies on this risk have been mixed, so the safe retinol intake level for this association is unknown. Total intakes of preformed vitamin A that exceed the UL and some synthetic retinoids used as topical therapies such as isotretinoin and etretinate can cause congenital birth defects [ ]. These birth defects can include malformations of the eye, skull, lungs, and heart [ 4 ]. Women who might be pregnant should not take high doses of vitamin A supplements [ 2 ].
Unlike preformed vitamin A, beta-carotene is not known to be teratogenic or lead to reproductive toxicity [ 1 ]. The most significant effect of long-term, excess beta-carotene is carotenodermia, a harmless condition in which the skin becomes yellow-orange [ 1 , 23 ].
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