Vitamin A

Vitamin A is a family of fat-soluble compounds that play an important role in vision, bone growth, reproduction, cell division, and cell differentiation (in which a cell becomes part of the brain, muscle, lungs, etc.). Vitamin A helps regulate the immune system, which helps prevent or fight off infections by making white blood cells that destroy harmful bacteria and viruses. Vitamin A also may help lymphocytes, a type of white blood cell, fight infections more effectively.

Vitamin A promotes healthy surface linings of the eyes and the respiratory, urinary, and intestinal tracts. When those linings break down, it becomes easier for bacteria to enter the body and cause infection. Vitamin A also helps maintain the integrity of skin and mucous membranes, which also function as a barrier to bacteria and viruses.

Retinol is one of the most active, or usable, forms of vitamin A, and is found in animal foods such as liver and whole milk and in some fortified food products. Retinol is also called preformed vitamin A. It can be converted to retinal and retinoic acid, other active forms of the vitamin A family.

Provitamin A carotenoids are darkly colored pigments found in plant foods that can be converted to vitamin A. In the United States, approximately 26% and 34% of vitamin A consumed by men and women, respectively, is provided by provitamin A carotenoids. Common carotenoids found in foods are beta-carotene, alpha-carotene, lutein, zeaxanthin, lycopene, and cryptoxanthin. Of the 563 identified carotenoids, fewer than 10% are precursors for vitamin A. Among these, beta-carotene is most efficiently converted to retinol. Alpha-carotene and beta-cryptoxanthin are also converted to vitamin A, but only half as efficiently as beta-carotene. Lycopene, lutein, and zeaxanthin are carotenoids that do not have vitamin A activity but have other health promoting properties. The Institute of Medicine (IOM) encourages consumption of carotenoid-rich fruits and vegetables for their health-promoting benefits.

Some carotenoids, in addition to serving as sources of vitamin A, have been shown to function as antioxidants in laboratory tests. However, this role has not been consistently demonstrated in humans. Antioxidants protect cells from free radicals, which are potentially damaging by-products of oxygen metabolism that may contribute to the development of some chronic diseases.

When Can Vitamin A Deficiency Occur?

Vitamin A deficiency is common in developing countries but rarely seen in the United States. Approximately 250,000 to 500,000 malnourished children in the developing world go blind each year from a deficiency of vitamin A. In the United States, vitamin A deficiency is most often associated with strict dietary restrictions and excess alcohol intake. Severe zinc deficiency, which is also associated with strict dietary limitations, often accompanies vitamin A deficiency. Zinc is required to synthesize retinol binding protein (RBP) which transports vitamin A. Therefore, a deficiency in zinc limits the body's ability to mobilize vitamin A stores from the liver and transport vitamin A to body tissues.

Night blindness is one of the first signs of vitamin A deficiency. In ancient Egypt, it was known that night blindness could be cured by eating liver, which was later found to be a rich source the vitamin. Vitamin A deficiency contributes to blindness by making the cornea very dry and damaging the retina and cornea.

Vitamin A deficiency diminishes the ability to fight infections. In countries where such deficiency is common and immunization programs are limited, millions of children die each year from complications of infectious diseases such as measles. In vitamin A-deficient individuals, cells lining the lungs lose their ability to remove disease-causing microorganisms. This may contribute to the pneumonia associated with vitamin A deficiency.

There is increased interest in subclinical forms of vitamin A deficiency, described as low storage levels of vitamin A that do not cause overt deficiency symptoms. This mild degree of vitamin A deficiency may increase children's risk of developing respiratory and diarrheal infections, decrease growth rate, slow bone development, and decrease likelihood of survival from serious illness. Children in the United States who are considered to be at increased risk for subclinical vitamin A deficiency include: toddlers and preschool age children; children living at or below the poverty level; children with inadequate health care or immunizations; children living in areas with known nutritional deficiencies; recent immigrants or refugees from developing countries with high incidence of vitamin A deficiency or measles; children with diseases of the pancreas, liver, or intestines, or with inadequate fat digestion or absorption.

A deficiency can occur when vitamin A is lost through chronic diarrhea and through an overall inadequate intake, as is often seen with protein-calorie malnutrition. Low blood retinol concentrations indicate depleted levels of vitamin A. This occurs with vitamin A deficiency but also can result from an inadequate intake of protein, calories, and zinc, since these nutrients are needed to make RBP. Iron deficiency can also affect vitamin A metabolism, and iron supplements provided to iron-deficient individuals may improve vitamin A nutriture as well as iron status.

Excess alcohol intake depletes vitamin A stores. Also, diets high in alcohol often do not provide recommended amounts of vitamin A. It is very important for people who consume excessive amounts of alcohol to include good sources of vitamin A in their diets. However, supplemental vitamin A may not be recommended for individuals who abuse alcohol because their livers may be more susceptible to potential toxicity from high doses of vitamin A. A medical doctor would need to evaluate this situation and determine the need for supplemental vitamin A.

What are Some Current Issues and Controversies About Vitamin A?

Vitamin A, Beta Carotene and Cancer: surveys suggest an association between diets rich in beta-carotene and vitamin A and a lower risk of many types of cancer. A higher intake of green and yellow vegetables or other food sources of beta carotene and/or vitamin A may decrease the risk of lung cancer. However, a number of studies that tested the role of beta-carotene supplements in cancer prevention did not find them to be protective. In the Alpha-Tocopherol Beta-Carotene (ATBC) Cancer Prevention Study, over 29,000 men who regularly smoked cigarettes were randomized to receive 20 mg beta-carotene alone, 50 mg alpha-tocopherol alone, supplements of both, or a placebo for 5 to 8 years. Incidence of lung cancer was 18% higher among men who took the beta-carotene supplement. Mortality was 8% greater in these men, as compared to those receiving other treatments or placebo. Similar results were seen in the Carotene and Retinol Efficacy Trial (CARET), a lung cancer chemoprevention study that provided subjects with supplements of 30 mg beta-carotene and 25,000 IU retinyl palmitate (a form of vitamin A) or a placebo. This study was stopped after researchers discovered that subjects receiving beta-carotene had a 46% higher risk of dying from lung cancer.

The IOM states that "beta-carotene supplements are not advisable for the general population," although they also state that this advice "does not pertain to the possible use of supplemental beta-carotene as a provitamin A source for the prevention of vitamin A deficiency in populations with inadequate vitamin A nutriture."

Vitamin A and Osteoporosis

Osteoporosis, a disorder characterized by porous and weak bones, is a serious public health problem for more than 10 million Americans, 80% of whom are women. Another 18 million Americans have decreased bone density which precedes the development of osteoporosis. Many factors increase the risk for developing osteoporosis, including being female, thin, inactive, at advanced age, and having a family history of osteoporosis. An inadequate dietary intake of calcium, cigarette smoking, and excessive intake of alcohol also increase the risk.

Researchers are now examining a potential new risk factor for osteoporosis: an excess intake of vitamin A. Animal, human, and laboratory research suggests an association between greater vitamin A intake and weaker bones. Worldwide, the highest incidence of osteoporosis occurs in northern Europe, a population with a high intake of vitamin A. However, decreased biosynthesis of vitamin D associated with lower levels of sun exposure in this population may also contribute to this finding.

One small study of nine healthy individuals in Sweden found that the amount of vitamin A in one serving of liver may impair the ability of vitamin D to promote calcium absorption. To further test the association between excess dietary intakes of vitamin A and increased risk for hip fractures, researchers in Sweden compared bone mineral density and retinol intake in approximately 250 women with a first hip fracture to 875 age-matched controls. They found that a dietary retinol intake greater than 1,500 mcg/day (more than twice the recommended intake for women) was associated with reduced bone mineral density and increased risk of hip fracture as compared to women who consumed less than 500 mcg/day.

This issue was also examined by researchers with the Nurses Health Study, who looked at the association between vitamin A intake and hip fractures in over 72,000 postmenopausal women. Women who consumed the most vitamin A in foods and supplements (greater than or equal to 3,000 mcg/day as retinol equivalents, which is over three times the recommended intake) had a significantly increased risk of experiencing a hip fracture as compared to those consuming the least amount (less than 1,250 mcg/day). The effect was lessened by use of estrogens. These observations raise questions about the effect of retinol because retinol intakes greater than 2,000 mcg/day were associated with an increased risk of hip fracture as compared to intakes less than 500 mcg.

A longitudinal study in more than 2,000 Swedish men compared blood levels of retinol to the incidence of fractures in men. The investigators found that the risk of fractures was greatest in men with the highest blood levels of retinol (greater than 75 mcg per deciliter [dL]). Men with blood retinol levels in the 99th percentile (greater than 103 mcg per dL) had an overall risk of fracture that exceeded the risk among men with lower levels of retinol by a factor of seven. However, high vitamin A intake does not necessarily equate to high blood levels of retinol. Age, gender, hormones, and genetics also influence these levels. Researchers did not find any association between blood levels of beta-carotene and risk of hip fracture. Researchers' findings, which are consistent with the results of animal, in vitro (laboratory), and epidemiologic studies, suggest that intakes above the UL, or approximately two times that of the RDA for vitamin A, may pose subtle risks to bone health that require further investigation.

The Centers for Disease Control and Prevention (CDC) reviewed data from NHANES III (1988-94) to determine whether there was any association between bone mineral density and fasting blood levels of retinyl esters, a form of vitamin A. No significant associations between blood levels of retinyl esters and bone mineral density in 5,800 subjects were found.

There is no evidence of an association between beta-carotene intake, especially from fruits and vegetables, and increased risk of osteoporosis. Current evidence points to a possible association with vitamin A as retinol only. If you have specific questions regarding your intake of vitamin A and risk of osteoporosis, discuss this information with your physician or other qualified healthcare practitioner to determine what's best for your personal health.

Antioxidant Nutrients

Ingestion of antioxidant vitamins and minerals from supplements has been shown to protect skin cells from free-radical damage induced by overexposure to ultraviolet light and various harmful environmental chemicals. In particular, free-radical damage from excessive UV overexposure can cause aging and wrinkling of the skin, as well as other forms of skin damage. Supplementation with specific doses of vitamin C, vitamin E, betacarotene, lycopene, selenium and zinc may boost the body's ability to intercept and neutralize free radicals, defending skin cells from many of these damaging effects.

Antioxidant supplements can greatly protect the skin from free-radical damage, which depletes the skin's antioxidant nutrient supply. A properly designed high-potency multivitamin and mineral that is fortified with optimal levels of specific antioxidant vitamins and minerals can help protect the skin from free-radical damage.

In addition to boosting the internal defenses, antioxidant vitamins and minerals can support detoxification by helping the body expel toxins that can aggravate various skin conditions (e.g., psoriasis, acne, eczema). These compounds also aid in the production of prostaglandin hormones that improve skin texture, smoothness and moisture.

Daily oral antioxidant supplementation should be viewed as a necessary component of skincare management throughout adult life. Topically applied antioxidants have been shown to be insufficient as a singular approach to protect the skin from free-radical damage, and do not influence detoxification and prostaglandin production. Only orally ingested antioxidants can provide all of these benefits.

Beyond Antioxidant Power

In addition to their role as antioxidants, several of these nutrients play additional roles in skin health. For example, zinc status is integral to achieving healthy-looking skin. This mineral is involved in sebaceous gland function, local skin hormone activation, wound healing, inflammation and tissue regeneration. Studies indicate the majority of people do not consume enough zinc, creating a marginal zinc deficiency that can result in susceptibility to unhealthy skin, acne and other problems.

Selenium also is vital for healthy skin, playing a key role in antioxidant protection and the prevention and management of various skin conditions. Selenium and zinc supplementation boosts the skin's antioxidant defenses and helps reduce freeradical damage and mutations to the DNA of skin cells. A high-potency multi- and mineral formula should contain 10-20 mg of zinc and 75-200 mcg of selenium to further boost antioxidant function within skin cells and enhance skin's vitality and appearance.

The fat-soluble vitamins A and D also are important in the normal growth and development of skin cells. Skin cells have vitamin D receptors, and adequate vitamin D stimulation from within the body is required for those cells to develop normally. Vitamin A, meanwhile, is involved in the growth and repair of skin cells; in fact, vitamin A deficiency is known to cause thickened dry skin that is prone to infection. However, too much vitamin A also can damage skin and internal organs. Ideally, optimal dosages will be incorporated in a high-potency vitamin and mineral multiple to provide a full cohort of complementary nutrients.

Complementary Anti-Aging Benefits

While beneficial for limiting skin problems associated with aging, daily supplementation with a high-potency multiple vitamin and mineral can help address other body areas prone to aging and environmental damage. For instance, a good multi-vitamin can provide the body with the right blend and doses of nutrients needed to enhance nail hardness and the sheen and quality of hair. Also, supplements with 500 mg of elemental calcium and 400 IU of vitamin D - along with other bone support nutrients such as magnesium, copper and vitamin C - can help guard against osteoporosis.

The daily ingestion of a high-potency multiple vitamin and mineral supplement is an important aspect of skincare and health promotion. A comprehensive formula will supply optimal levels of the vitamins and minerals required for radiant, healthy-looking skin, lustrous hair and smooth, hard nails while supporting the body's total well-being and vitality.

1. Underwood BA, Arthur P. The Contribution of Vitamin A to Public Health. FASEB J. 1996 Jul;10(9):1040-8.

Vitamin A deficiency among children in developing countries remains the leading cause of preventable severe visual impairment and blindness, and is a significant contributor to severe infections and death, particularly from diarrhea and measles. Vitamin A deficiency is also likely to increase vulnerability to other illnesses in both women and children, such as iron-deficiency anemia, and may be an important factor contributing to poor maternal performance during pregnancy and lactation and to growth deficits in children. Benefits to public health can be expected by improving the vitamin A status of deficient populations through an appropriate mix of acceptable, affordable, and available programs including promotion of breast-feeding, control of infections, dietary diversification, food fortification, and supplementation. Benefits include not only improved health and welfare for individuals and their families, but also improved chances of survival for an estimated 254 million children.

2. Mao CT, Li TY, Liu YX, Qu P. Effects of Marginal Vitamin A Deficiency and Intervention on Learning and Memory in Young Rats. Zhonghua Er Ke Za Zhi. 2005 Jul;43 (7):526-30.

Objective: Previous studies have demonstrated that vitamin A and its active derivatives function as essential competence factors for long-term synaptic plasticity within the adult brain. But little is known if marginal vitamin A deficiency (MVAD) beginning from embryonic period affects the brain development and the ability of learning and memory in young rats. The aim of this study was to identify the effects of MVAD and vitamin A intervention (VAI) on learning, memory and the hippocampal CA1 long-term potentiation (LTP) in young rats.

Methods: Rats were divided into control, MVAD and VAI groups in this study. In control group (10 young rats) the dams and pups were fed with normal diet (VA 6500 IU/kg). In MVAD group (19 young rats) the dams and pups were fed with MVAD diet (VA 400 IU/kg). In VAI group (9 young rats) the dams were fed with MVAD diet and the pups were fed with normal diet from postnatal week 4. All the young rats were killed at the age of 7 weeks. During the last week of the experiment, the shuttle box active avoidance reaction tests were carried out. At week 7, the hippocampal CA1 LTP was detected by electrophysiological technique and relative intensity of fluorescence in cells in hippocampal slices was measured by confocal laser scanning microscopy labeled by fluo-3.

Results: (1) The times to reach the learning standard in both VAI group (28.8 +/- 4.1) and MVAD group (45.6 +/- 12.1) were more than control group (17.1 +/- 4.4) (P < 0.01), and that of MVAD group was more than VAI group (P < 0.05) in active avoidance reaction tests. (2) The changes of field excitatory postsynaptic potentials (fEPSP) slope for MVAD group (22.9% +/- 9.4%) and VAI group (29.5% +/- 13.7%) were less than that of control group (57.5% +/- 27.3%), respectively (P < 0.01). No significant difference was found between VAI and MVAD groups (P > 0.05). (3) No significant differences of relative intensity of fluorescence in cells were found among the three groups before the tetanus stimulation. However, the significantly low relative intensity of fluorescence in cells was seen in MVAD (65.1 +/- 17.0) and VAI (85.8 +/- 17.1) groups compared with control group (113.6 +/- 20.5) after the tetanus stimulation (P < 0.01), and that of VAI group was higher than that of MVAD group (P < 0.05).

Conclusion: MVAD beginning from embryonic period impairs learning, memory and LTP in young rats. But the losses might not be reversible if the vitamin A supplementation is late especially missing the critical period of hippocampus development. According to the experimental data, it is speculated that vitamin A may modulate the influx of calcium ion to influence the LTP and lead to the change of learning and memory.

3. Kelleher SL, Lonnerdal B. Low Vitamin A Intake Affects Milk Iron Level and Iron Transporters in Rat Mammary Gland and Liver. J Nutr. 2005 Jan;135(1):27-32.

Marginal vitamin A deficiency is common and can result in a secondary iron (Fe) deficiency. A positive correlation between maternal Fe status and milk Fe was observed in lactating women supplemented with both vitamin A and Fe but not with Fe alone, suggesting effects of vitamin A on mammary gland Fe transport. We hypothesized that low vitamin A intake during lactation elicits differential effects on mammary gland and liver Fe transport and storage proteins, thus affecting milk Fe concentration but not maternal Fe status. We fed rats a control (CON, 4 RE/g) or a marginal vitamin A diet (AD, 0.4 RE/g) through midlactation. Effects on plasma, milk, liver and mammary gland Fe and vitamin A concentrations, and divalent metal transporter-1 (DMT1), ferroportin (FPN), ferritin (Ft), and transferrin receptor (TfR) expression were determined. Dams fed AD were not vitamin A or Fe deficient. Milk and liver vitamin A and Fe and mammary gland Fe concentrations were lower in rats fed AD compared with rats fed CON. Liver TfR expression was higher, whereas mammary gland TfR expression was lower in rats fed AD compared with rats fed CON. Liver Ft was unaffected, whereas mammary gland Ft was lower in rats fed AD compared with rats fed CON. Liver and mammary gland DMT1 and FPN protein levels were lower in rats fed AD compared with rats fed CON. Our results indicate that the mammary gland and liver respond differently to marginal vitamin A intake during lactation and that milk Fe is significantly decreased due to effects on mammary gland Fe transporters, putting the nursing offspring at risk for Fe deficiency.

4. Albright CD, Salganik RI, Van Dyke T. Dietary Depletion of Vitamin E and Vitamin A Inhibits Mammary Tumor Growth and Metastasis in Transgenic Mice. J Nutr. 2004 May;134(5):1139-44.

We showed previously that dietary antioxidant depletion enhances tumor reactive oxygen species (ROS) and apoptosis, resulting in a reduction in brain tumor size in the TgT(121) transgenic mouse model, a nonmetastatic tumor model. Here, in a transgenic mouse model of mammary tumorigenesis with defined rates of tumor growth and lung-targeted metastasis, we determined the ability of dietary antioxidant depletion to inhibit tumor growth and metastasis. Compared with control mice fed a standard diet, antioxidant-depleted mice exhibited tumor-targeted generation of ROS manifested by increased levels of oxidatively modified DNA/RNA (8- hydroxy-2'-deoxyguanine, 8-hydroxyguanine) and lipid peroxidation (4-hydroxy-2-nonenal) in primary and metastatic tumor foci. In addition to increased tumor-targeted ROS, the number of apoptotic cells was increased approximately 500% (P < 0.01) and terminal dUTP nucleotide DNA end-labeling-positive cells 200% (P < 0.01) in mice fed the antioxidant-depleted diet, whereas the percentage of tumor cells undergoing mitosis was >50% lower than in controls (P < 0.01). The proportional distribution of small (<1.5 cm) and large (> or = 1.5 cm) primary mammary tumors differed. The mice fed the antioxidant-depleted diet had more small primary tumors (P <0.05) and fewer large primary tumors (P < 0.05). Importantly, they also had fewer lung metastatic tumor foci compared with mice fed the control diet (4.5 +/- 1.3 vs. 15.8 +/- 8.5 foci/lung, P < 0.01). These findings may be important in understanding the role of dietary antioxidant vitamins in tumor growth and metastasis.

5. Matthews KA, Rhoten WB, Driscoll HK, Chertow BS. Vitamin A Deficiency Impairs Fetal Islet Development and Causes Subsequent Glucose Intolerance in Adult Rats. J Nutr. 2004 Aug;134(8):1958-63.

To determine the role of vitamin A in fetal islet development, beta- and alpha-cell mass, apoptosis, and alpha- and beta-cell replication were measured in rats using a model of marginal vitamin A deficiency. Female rats before and during pregnancy and their offspring postweaning were fed a diet containing retinol as retinyl palmitate at a low marginal (LM, 0.25 mg/kg diet) or a sufficient (SUFF, 4.0 mg/kg diet) level. Fetal islet size, replication, apoptosis, and offspring glucose tolerance were examined. Both beta-cell area and number per islet were reduced approximately 50% in fetuses from dams fed an LM vitamin A diet compared with those from dams fed the SUFF vitamin A diet. The alpha-cell area and number per fetal islet were not affected by vitamin A deficiency. Apoptosis was not increased. The percentage of newly replicated beta-cells in the LM fetal pancreas was 42% less than that of SUFF offspring, but alpha-cell replication was not affected. To determine whether this decrease in beta-cell area affected adult glucose tolerance and insulin secretion, 65-d-old offspring were subject to glucose tolerance tests. LM rats had a 55% lower plasma insulin level and a 76% higher serum glucose than SUFF rats. The same pattern could be seen in 35-d-old rats. These findings show that vitamin A deficiency decreases beta-cell mass and this reduction can be attributed to a reduced rate of fetal beta-cell replication in LM offspring. This may contribute to impaired glucose tolerance later in adult life.

6. James Meschino. Slow Aging And Enhance The Complexion. Vitamins And Minerals.

The skin is the largest organ in the human body. Each day many thousands of skin cells are shed from the outermost layer and continually replaced by rapidly dividing cells from the skin layers underneath. Due to their short lifespan and rapid growth rate, developing skin cells require a steady supply of specific nutrients, fed to them from the bloodstream, to remain and look healthy from one generation of cells to the next.

It is a simple fact that radiant, more youthful skin demands proper external care plus adequate vitamin and mineral intake to provide nourishment to developing skin cells. Optimal consumption of nutrients is an essential, but often overlooked, step in enhancing the texture and beauty of the skin. In the past few years, studies have revealed the optimal doses of various compounds required to help the body manufacture the smoothest, softest and most radiant skin, as well as minimize the formation of wrinkles and slow other characteristics of skin aging.

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