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4
Vitamin A

SUMMARY

Vitamin A is important for normal vision, gene expression, reproduction, embryonic development, growth, and immune function. There are a variety of foods rich in vitamin A and provitamin A carotenoids that are available to North Americans. Thus, current dietary patterns appear to provide sufficient vitamin A to prevent deficiency symptoms such as night blindness. The Estimated Average Requirement (EAR) is based on the assurance of adequate stores of vitamin A. The Recommended Dietary Allowance (RDA) for men and women is 900 and 700 μg retinol activity equivalents (RAE)/day, respectively. The Tolerable Upper Intake Level (UL) for adults is set at 3,000 μg/day of preformed vitamin A.

There are a number of sources of dietary vitamin A. Preformed vitamin A is abundant in some animal-derived foods, whereas provitamin A carotenoids are abundant in darkly colored fruits and vegetables, as well as oily fruits and red palm oil.

For dietary provitamin A carotenoids—β-carotene, α-carotene, and β-cryptoxanthin—RAEs have been set at 12, 24, and 24 μg, respectively. Using μg RAE, the vitamin A activity of provitamin A carotenoids is half the vitamin A activity assumed when using μg retinol equivalents (μg RE) (NRC, 1980, 1989). This change in equivalency values is based on data demonstrating that the vitamin A activity of purified β-carotene in oil is half the activity of vitamin A, and based on recent data demonstrating that the vitamin A activity of dietary β-carotene is one-sixth, rather than one-third, the vitamin



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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc 4 Vitamin A SUMMARY Vitamin A is important for normal vision, gene expression, reproduction, embryonic development, growth, and immune function. There are a variety of foods rich in vitamin A and provitamin A carotenoids that are available to North Americans. Thus, current dietary patterns appear to provide sufficient vitamin A to prevent deficiency symptoms such as night blindness. The Estimated Average Requirement (EAR) is based on the assurance of adequate stores of vitamin A. The Recommended Dietary Allowance (RDA) for men and women is 900 and 700 μg retinol activity equivalents (RAE)/day, respectively. The Tolerable Upper Intake Level (UL) for adults is set at 3,000 μg/day of preformed vitamin A. There are a number of sources of dietary vitamin A. Preformed vitamin A is abundant in some animal-derived foods, whereas provitamin A carotenoids are abundant in darkly colored fruits and vegetables, as well as oily fruits and red palm oil. For dietary provitamin A carotenoids—β-carotene, α-carotene, and β-cryptoxanthin—RAEs have been set at 12, 24, and 24 μg, respectively. Using μg RAE, the vitamin A activity of provitamin A carotenoids is half the vitamin A activity assumed when using μg retinol equivalents (μg RE) (NRC, 1980, 1989). This change in equivalency values is based on data demonstrating that the vitamin A activity of purified β-carotene in oil is half the activity of vitamin A, and based on recent data demonstrating that the vitamin A activity of dietary β-carotene is one-sixth, rather than one-third, the vitamin

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc activity of purified β-carotene in oil. This change in bioconversion means that a larger amount of provitamin A carotenoids, and therefore darkly colored, carotene-rich fruits and vegetables, is needed to meet the vitamin A requirement. It also means that in the past, vitamin A intake has been overestimated. The median intake of vitamin A ranges from 744 to 811 μg RAE/ day for men and 530 to 716 μg RAE/day for women. Using μg RAE, approximately 26 and 34 percent of vitamin A activity consumed by men and women, respectively, is provided from provitamin A carotenoids. Ripe, colored fruits and cooked, yellow tubers are more efficiently converted to vitamin A than equal amounts of dark green, leafy vegetables. Although a large body of observational epidemiological evidence suggests that higher blood concentrations of β-carotenes and other carotenoids obtained from foods are associated with a lower risk of several chronic diseases, there is currently not sufficient evidence to support a recommendation that requires a certain percentage of dietary vitamin A to come from provitamin A carotenoids in meeting the vitamin A requirement. However, the existing recommendations for increased consumption of carotenoid-rich fruits and vegetables for their health-promoting benefits are strongly supported (see Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids [IOM, 2000]). BACKGROUND INFORMATION Vitamin A is a fat-soluble vitamin that is essential for humans and other vertebrates. Vitamin A comprises a family of molecules containing a 20 carbon structure with a methyl substituted cyclohexenyl ring (beta-ionone ring) (Figure 4-1) and a tetraene side chain with a hydroxyl group (retinol), aldehyde group (retinal), carboxylic acid group (retinoic acid), or ester group (retinyl ester) at carbon-15. The term vitamin A includes provitamin A carotenoids that are dietary precursors of retinol. The term retinoids refers to retinol, its metabolites, and synthetic analogues that have a similar structure. Carotenoids are polyisoprenoids, of which more than 600 forms exist. Of the many carotenoids in nature, several have provitamin A nutritional activity, but food composition data are available for only three (α-carotene, β-carotene, and β-cryptoxanthin) (Figure 4-1). The all-trans isomer is the most common and stable form of each carotenoid; however, many cis isomers also exist. Carotenoids usually contain 40 carbon atoms, have an extensive system of conjugated double bonds, and contain one or two cyclic structures at the end

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc FIGURE 4-1 Structure of retinol and provitamin A carotenoids. of their conjugated chain. An exception is lycopene, which has no ring structure and does not have vitamin A activity. Preformed vitamin A is found only in animal-derived food products, whereas dietary carotenoids are present primarily in oils, fruits, and vegetables. Function The 11-cis-retinaldehyde (retinal) form of vitamin A is required by the eye for the transduction of light into neural signals necessary for vision (Saari, 1994). The retinoic acid form is required to main-

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc tain normal differentiation of the cornea and conjunctival membranes, thus preventing xerophthalmia (Sommer and West, 1996), as well as for the photoreceptor rod and cone cells of the retina. Rods contain the visual pigment rhodopsin (opsin protein bound to 11-cis-retinal). The absorption of light catalyzes the photoisomerization of rhodopsin’s 11-cis-retinal to all-trans-retinal in thousands of rods, which triggers the signaling to neuronal cells associated with the brain’s visual cortex. After photoisomerization, all-trans-retinal is released, and for vision to continue, 11-cis-retinal must be regenerated. Regeneration of 11-cis-retinal requires the reduction of all-trans retinal to retinol, transport of retinol from the photoreceptor cells (rods) to the retinal pigment epithelium, and esterification of all-trans-retinol, thereby providing a local storage pool of retinyl esters. When needed, retinyl esters are hydrolyzed and isomerized to form 11-cis-retinol, which is oxidized to 11-cis-retinal and transported back to the photoreceptor cells for recombination with opsin to begin another photo cycle. Vitamin A is required for the integrity of epithelial cells throughout the body (Gudas et al., 1994). Retinoic acid, through the activation of retinoic acid (RAR) and retinoid X (RXR) receptors in the nucleus, regulates the expression of various genes that encode for structural proteins (e.g., skin keratins), enzymes (e.g., alcohol dehydrogenase), extracellular matrix proteins (e.g., laminin), and retinol binding proteins and receptors. Retinoic acid plays an important role in embryonic development. Retinoic acid, as well as RAR, RXR, cellular retinol-binding protein (CRBP), and cellular retinoic acid-binding proteins (CRABP-I and CRABP-II), is present in temporally specific patterns in the embryonic regions known to be involved in the development of structures posterior to the hindbrain (e.g., the vertebrae and spinal cord) (Morriss-Kay and Sokolova, 1996). Retinoic acid is also involved in the development of the limbs, heart, eyes, and ears (Dickman and Smith, 1996; Hofmann and Eichele, 1994; McCaffery and Drager, 1995). Retinoids are necessary for the maintenance of immune function, which depends on cell differentiation and proliferation in response to immune stimuli. Retinoic acid is important in maintaining an adequate level of circulating natural killer cells that have antiviral and anti-tumor activity (Zhao and Ross, 1995). Retinoic acid has been shown to increase phagocytic activity in murine macrophages (Katz et al., 1987) and to increase the production of interleukin 1 and other cytokines, which serve as important mediators of inflammation and stimulators of T and B lymphocyte production (Trechsel

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc et al., 1985). Furthermore, the growth, differentiation, and activation of B lymphocytes requires retinol (Blomhoff et al., 1992). Proposed functions of provitamin A carotenoids are described in Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids (IOM, 2000). Physiology of Absorption, Metabolism, and Excretion Absorption and Bioconversion Absorption of Vitamin A. Intestinal absorption of preformed vitamin A occurs following the processing of retinyl esters in the lumen of the small intestine. Within the water-miscible micelles formed from bile salts, solubilized retinyl esters as well as triglycerides are hydrolyzed to retinol and products of lipolysis by various hydrolases (Harrison, 1993). A small percentage of dietary retinoids is converted to retinoic acid in the intestinal cell. In addition, the intestine actively synthesizes retinoyl β-glucuronide that is hydrolyzed to retinoic acid by β-glucuronidases (Barua and Olson, 1989). The efficiency of absorption of preformed vitamin A is generally high, in the range of 70 to 90 percent (Sivakumar and Reddy, 1972). A specific retinol transport protein within the brush border of the enterocyte facilitates retinol uptake by the mucosal cells (Dew and Ong, 1994). At physiological concentrations, retinol absorption is carrier mediated and saturable, whereas at high pharmacological doses, the absorption of retinol is nonsaturable (Hollander and Muralidhara, 1977). As the amount of ingested preformed vitamin A increases, its absorbability remains high (Olson, 1972). Vitamin A absorption and intestinal retinol esterification are not markedly different in the elderly compared to young adults, although hepatic uptake of newly absorbed vitamin A in the form of retinyl ester is slower in the elderly (Borel et al., 1998). Absorption and Bioconversion of Provitamin A Carotenoids. Carotenoids are also solubilized into micelles in the intestinal lumen from which they are absorbed into duodenal mucosal cells by a passive diffusion mechanism. Percent absorption of a single dose of 45 μg to 39 mg β-carotene, measured by means of isotopic methods, has been reported to range from 9 to 22 percent (Blomstrand and Werner, 1967; Goodman et al., 1966; Novotny et al., 1995). However, the absorption efficiency decreases as the amount of dietary carotenoids increases (Brubacher and Weiser, 1985; Tang et al., 2000). The relative carotene concentration in micelles can vary in response to

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc the physical state of the carotenoid (e.g., whether it is dissolved in oil or associated with plant matrix materials). A number of factors affect the bioavailability and bioconversion of carotenoids (Castenmiller and West, 1998). Carotene bioavailability can differ with different processing methods of the same foods and among different foods containing similar levels of carotenoids (Boileau et al., 1999; Hume and Krebs, 1949; Rock et al., 1998; Torronen et al., 1996; Van den Berg and van Vliet, 1998) (also see Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids [IOM, 2000]). Absorbed β-carotene is principally converted to vitamin A by the enzyme β-carotene-15, 15′-dioxygenase within intestinal absorptive cells. The central cleavage of β-carotene by this enzyme will, in theory, result in two molecules of retinal. β-Carotene can also be cleaved eccentrically to yield β-apocarotenals that can be further degraded to retinal or retinoic acid (Krinsky et al., 1993). The predominant form of vitamin A in human lymph, whether originating from ingested vitamin A or provitamin A carotenoids, is retinyl ester (retinol esterified with long-chain fatty acids, typically palmitate and stearate) (Blomstrand and Werner, 1967; Goodman et al., 1966). Along with exogenous lipids, the newly synthesized retinyl esters and nonhydrolyzed carotenoids are transported from the intestine to the liver in chylomicrons and chylomicron remnants. Derived from dietary retinoids, retinoic acid is absorbed via the portal system bound to albumin (Blaner and Olson, 1994; Olson, 1991). Vitamin A Activity of Provitamin A Carotenoids: Rationale for Developing Retinol Activity Equivalents. The carotene:retinol equivalency ratio (μg:μg) of a low dose (less than 2 mg) of purified β-carotene in oil is approximately 2:1 (i.e., 2 μg of β-carotene in oil yields 1 μg of retinol) (Table 4-1). This ratio was derived from the relative amount of β-carotene required to correct abnormal dark adaptation in vitamin A-deficient individuals (Hume and Krebs, 1949; Sauberlich et al., 1974). The data by Sauberlich et al. (1974) were given greater consideration because (1) the actual amount (μg) of vitamin A and β-carotene consumed was cited, (2) varied amounts of vitamin A or β-carotene were consumed by each individual, and (3) a greater sample size was employed (six versus two subjects). In addition to these studies, an earlier study by Wagner (1940) estimated a carotene:retinol equivalency ratio of 4:1; however, the method employed for measuring dark adaptation was not standardized and used an imprecise outcome measure. Studies have been performed to compare the efficiency of absorption of β-carotene after feeding physiological amounts of β-carotene

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc TABLE 4-1 Relative Absorption of Vitamin A and Supplemental β-Carotene Reference Study Groupa Study Design Hume and Krebs, 1949 1 adult per treatment group, England Depletion/repletion study; depletion phase ranged from 18 to 22 mo and the repletion phase ranged from 3 wk to 6 mo Sauberlich et al., 1974 2 or 4 men per treatment group, United States Depletion/repletion study; depletion phase ranged from 361 to 771 d and the repletion phase ranged from 2 to 455 d a Treatment group received supplemental vitamin A or β-carotene. b Based on the assumption that 1 IU is equivalent to 0.3 μg of vitamin A (WHO, 1950). c One IU is equivalent to 0.6 μg of β-carotene (Hume and Krebs, 1949). in oil, in individual foods, and as part of a mixed vegetable and fruit diet. Many of the earlier studies analyzed the fecal content of β-carotene after the consumption of a supplement, fruit, or vegetable. Data from these studies were not considered because the portion of unabsorbed β-carotene that is degraded by the intestinal microflora is not known. The efficiency of absorption of β-carotene in food is lower than the absorption of β-carotene in oil by a representative factor of a. Assuming that after absorption of β-carotene, whether from oil or food, the metabolism of the molecule is similar and that the retinol equivalency ratio of β-carotene in oil is 2:1, the vitamin A activity of β-carotene from food can be derived by multiplying a by 2:1. Until recently it was thought that 3 μg of dietary β-carotene was equivalent to 1 μg of purified β-carotene in oil (NRC, 1989) due to a relative absorption efficiency of about 33 percent of β-carotene from food sources. Only one study has compared the relative absorption of β-carotene in oil versus its absorption in a principally mixed vegetable diet in healthy and nutritionally adequate individuals (Van het Hof et al., 1999). This study concluded that the relative absorption of β-carotene from the mixed vegetable diet compared to β-carotene in oil is only 14 percent, as assessed by the increase in plasma β-carotene concentration after dietary interven-

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Diet/Dose Results Low (< 21 μg/d) vitamin A diet plus a single dose of supplemental vitamin A or β-carotene were provided to subjects after depletion period Abnormal dark adaptation was reversed with 1,300 IU (390 μg)b of vitamin A and 2,500 IU (1,500 μg)c of β-carotene; thus the retinol equivalency ratio is assumed to be 3.8:1 Low vitamin A diet (< 23 μg) plus varying doses of supplemental vitamin A (37.5–25,000 μg/d) or β-carotene (150–2,400 μg/d) were provided after the depletion period 600 μg/d retinol corrected dark adaptation; 1,200 μg/d β-carotene corrected dark adaptation; therefore the retinol equivalency ratio was concluded to be 2:1 tion. Based on this finding, approximately 7 μg of dietary β-carotene is equivalent to 1 μg of β-carotene in oil. This absorption efficiency value of 14 percent is supported by the relative ranges in β-carotene absorption reported by others using similar methods for mixed green leafy vegetables (4 percent) (de Pee et al., 1995), carrots (18 to 26 percent) (Micozzi et al., 1992; Torronen et al., 1996), broccoli (11 to 12 percent) (Micozzi et al., 1992), and spinach (5 percent) (Castenmiller et al., 1999) (Table 4-2). Only one study has been published to assess the relative bioconversion of β-carotene from fruits versus vegetables by measuring the rise in serum retinol concentration after the provision of a diet high in vegetables, fruits, or retinol (de Pee et al., 1998). This study used methods similar to those employed by other researchers (Castenmiller et al. [1999], de Pee et al. [1995], Micozzi et al. [1992], Torronen et al. [1996], and Van het Hof et al. [1999]), and indicated that the vitamin A activity was approximately half the activity for dark, green leafy vegetables compared to equal amounts of β-carotene from orange fruits and some yellow tubers, such as pumpkin squash (de Pee et al., 1998) (Table 4-2). Because of the low content of fruits contained in the principally mixed vegetable diet of Van het Hof et al. (1999) and the low proportion of dietary β-carotene that is consumed from fruits compared to vegetables in

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc TABLE 4-2 Relative Absorption of Supplemental and Dietary β-Carotene Reference Subjects Study Design Micozzi et al., 1992 30 men, 20–45 y, United States Diet/supplementation intervention, 6 wk de Pee et al., 1995 173 children, 7–11 y, Indonesia Diet intervention, 9 wk Torronen et al., 1996 42 women, 20–53 y, Finland Diet/supplementation intervention, 6 wk de Pee et al., 1998 188 anemic school children, 7–11 y, Indonesia Diet intervention, 9 wk Castenmiller et al., 1999 72 men and women, 18–58 y, Netherlands Diet/supplementation intervention, 3 wk Van het Hof et al., 1999 55 men and women, 18–45 y, Netherlands Diet/supplementation intervention, 1 mo the United States (16 percent from the 14 major dietary contributors of β-carotene which provide a total of 70 percent of dietary β-carotene) (Chug-Ahuja et al., 1993), it is estimated that 6 μg, rather than 7 μg, of β-carotene from a mixed diet is nutritionally equivalent to 1 μg of β-carotene in oil. Therefore, the retinol activity equivalency (μg RAE) ratio for β-carotene from food is estimated to be 12:1 (6 × 2:1) (Figure 4-2). Unfortunately, studies using a positive control group (preformed vitamin A) at a level equivalent to β-carotene from a mixed vegetable and fruit diet using levels similar to the RAE have not been conducted in healthy and nutritionally adequate individuals. An RAE of 12 μg for dietary β-carotene is supported by Parker et al. (1999) who reported that 8 percent of ingested β-carotene from carrots was absorbed and converted to retinyl esters

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Diet/Dose of β-Carotene Results Supplement, 30 mg/d Carrots, 30 mg/d Broccoli, 6 mg/d Increase of plasma β-carotene from carrots compared to supplemental β-carotene in gelatin beadlets was 18% Increase of plasma β-carotene from broccoli compared to supplemental β-carotene in gelatin beadlets was 12% Vegetable diet, 3.5 mg/d Fruit diet, 2.3 mg/d Increase of serum β-carotene from fruit diet was 5–6 times higher than from vegetable diet Low carotenoid diet + Raw carrots, 12 mg/d + Supplement, 12 mg/d Increase of serum β-carotene from raw carrots was 26% compared to that from supplemental β-carotene in a gelatin beadlet Fruit/squash diet, 509 μg/d Dark green leafy vegetables + carrots, 684 μg/d Low vitamin A/β-carotene diet, 44 μg/d Increase of serum β-carotene from fruit/squash diet was 3.5-fold greater than that for the dark green leafy vegetables + carrots diet Control diet, 0.5 mg/d Supplement diet, 9.8 mg/d Spinach diet, 10.4 mg/d Increase of serum β-carotene from spinach was 5% compared to that from supplemental β-carotene in oil Supplement, 7.2 mg/day High vegetable diet, 5.1 mg/d Increase of plasma β-carotene from high vegetable diet compared to supplemental β-carotene in oil was 14% contained in chylomicrons, resulting in a carotene:retinol equivalency ratio of 13:1. One RAE for dietary provitamin A carotenoids other than β-carotene is set at 24 μg on the basis of the observation that the vitamin A activity of β-cryptoxanthin and α-carotene is approximately half of that for β-carotene (Bauernfeind, 1972; Deuel et al., 1949). Therefore, the amount of vitamin A activity of provitamin A carotenoids in μg RAE is half the amount obtained if using μg RE (Table 4-3). Example: A diet contains 500 μg retinol, 1,800 μg β-carotene and 2,400 μg α-carotene. 500 + (1,800 ÷ 12) + (2,400 ÷ 24) = 750 μg RAE.

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc FIGURE 4-2 Absorption and bioconversion of ingested provitamin A carotenoids to retinol based on new equivalency factors (retinol activity equivalency ratio). TABLE 4-3 Comparison of the 1989 National Research Council and 2001 Institute of Medicine Interconversion of Vitamin A and Carotenoid Units NRC, 1989 IOM, 2001 1 retinol equivalent (μg RE) 1 retinol activity equivalent (μg RAE) =1 μg of all-trans-retinol = 1 μg of all-trans-retinol =2 μg of supplemental all-trans-β-carotene =2 μg of supplemental all-trans-β-carotene =6 μg of dietary all-trans-β-carotene = 12 μg of dietary all-trans-β-carotene = 12 μg of other dietary provitamin A carotenoids = 24 μg of other dietary provitamin A carotenoids NOTE: 1 μg retinol = 3.33 IU vitamin A activity from retinol (WHO, 1966); 10 IU β-carotene = 3.33 IU retinol (WHO, 1966); 10 IU is based on 3.33 IU vitamin A activity × 3 (the relative vitamin activity of β-carotene in supplements versus in diets). Thus, when converting from IU β-carotene from fruits or vegetables to μg RAE, IU is divided by 20 (2 × 10).

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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc Figueira F, Mendonca S, Rocha J, Azevedo M, Bunce GE, Reynolds JW. 1969. Absorption of vitamin A by infants receiving fat-free or fat-containing dried skim milk formulas. Am J Clin Nutr 22:588–593. Filteau SM, Morris SS, Raynes JG, Arthur P, Ross DA, Kirkwood BR, Tomkins AM, Gyapong JO. 1995. Vitamin A supplementation, morbidity, and serum acute-phase proteins in young Ghanaian children. Am J Clin Nutr 62:434–438. Flores H. 1993. Frequency distributions of serum vitamin A levels in cross-sectional surveys and in surveys before and after vitamin A supplementation. In: A Brief Guide to Current Methods of Assessing Vitamin A Status. A report of the International Vitamin A Consultative Group (IVACG). Washington, DC: The Nutrition Foundation. Pp. 9–11. Flores H, de Araujo RC. 1984. Liver levels of retinol in unselected necropsy specimens: A prevalence survey of vitamin A deficiency in Recife, Brazil. Am J Clin Nutr 40:146–152. Freudenheim JL, Johnson NE, Smith EL. 1986. Relationships between usual nutrient intake and bone-mineral content of women 35–65 years of age: Longitudinal and cross-sectional analysis. Am J Clin Nutr 44:863–876. Friedman A, Sklan D. 1989. Impaired T lymphocyte immune response in vitamin A depleted rats and chicks. Br J Nutr 62:439–449. Furr HC, Amedee-Manesme O, Clifford AJ, Bergen HR, Jones AD, Anderson LD, Olson JA. 1989. Vitamin A concentrations in liver determined by isotope dilution assay with tetradeuterated vitamin A and by biopsy in generally healthy adult humans. Am J Clin Nutr 49:713–716. Geelen JA. 1979. Hypervitaminosis A induced teratogenesis. CRC Crit Rev Toxicol 6:351–375. Geubel AP, De Galocsy C, Alves N, Rahier J, Dive C. 1991. Liver damage caused by therapeutic vitamin A administration: Estimate of dose-related toxicity in 41 cases. Gastroenterology 100:1701–1709. Ghana VAST Study Team. 1993. Vitamin A supplementation in northern Ghana: Effects on clinic attendances, hospital admissions, and child mortality. Lancet 342:7–12. Glasziou PP, Mackerras DE. 1993. Vitamin A supplementation and infectious disease: A meta-analysis. Br Med J 306:366–370. Golner BB, Reinhold RB, Jacob RA, Sadowski JA, Russell RM. 1987. The short and long term effect of gastric partitioning surgery on serum protein levels. J Am Coll Nutr 6:279–285. Goodman DS, Blaner WS. 1984. Biosynthesis, absorption, and hepatic metabolism of retinol. In: Sporn MB, Roberts AB, Goodman DS, eds. The Retinoids, Vol. 2. Orlando: Academic Press. Pp. 1–39. Goodman DS, Huang HS, Shiratori T. 1965. Tissue distribution and metabolism of newly absorbed vitamin A in the rat. J Lipid Res 6:390–396. Goodman DS, Blomstrand R, Werner B, Huang HS, Shiratori T. 1966. The intestinal absorption and metabolism of vitamin A and β-carotene in man. J Clin Invest 45:1615–1623. Gudas LJ, Sporn MB, Roberts AB. 1994. Cellular biology and biochemistry of the retinoids. In: Sporn MB, Roberts AB, Goodman DS, eds. The Retinoids: Biology, Chemistry, and Medicine, 2nd ed. New York: Raven Press. Pp. 443–520. Hallfrisch J, Muller DC, Singh VN. 1994. Vitamin A and E intakes and plasma concentrations of retinol, beta-carotene, and alpha-tocopherol in men and women of the Baltimore Longitudinal Study of Aging. Am J Clin Nutr 60:176–182.

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