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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids 8 β-Carotene and Other Carotenoids SUMMARY Blood concentrations of carotenoids are the best biological markers for consumption of fruits and vegetables. A large body of observational epidemiological evidence suggests that higher blood concentrations of β-carotene and other carotenoids obtained from foods are associated with lower risk of several chronic diseases. This evidence, although consistent, cannot be used to establish a requirement for β-carotene or carotenoid intake because the observed effects may be due to other substances found in carotenoidrich food, or to other behavioral correlates of increased fruit and vegetable consumption. While there is evidence that β-carotene is an antioxidant in vitro, its importance to health is not known. The one clear function of certain carotenoids that is firmly linked to a health outcome is the provitamin A activity of some dietary carotenoids (α-carotene, β-carotene, and β-cryptoxanthin) and their role in the prevention of vitamin A deficiency. Establishment of a requirement for carotenoids based upon vitamin A activity must be done in concert with the evaluation of Dietary Reference In-takes (DRIs) for vitamin A, which was not included in this report, but will be addressed in a subsequent DRI report. Although no DRIs are proposed for β-carotene or other carotenoids at the present time, existing recommendations for increased consumption of carotenoid-rich fruits and vegetables are supported. Based on evidence that β-carotene supplements have not been shown to confer any benefit for the prevention of the major chronic diseases and may cause harm in certain subgroups, it is concluded that β-carotene supplements are not advisable, other than as a provitamin
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids A source and for the prevention and control of vitamin A deficiency in at-risk populations. BACKGROUND INFORMATION The most prevalent carotenoids in North American diets include the following: α-carotene, β-carotene, lycopene, lutein, zeaxanthin, and β-cryptoxanthin. The structures of these carotenoids are shown in Figure 8-1. Three of these carotenoids, namely α-carotene, β-carotene, and β-cryptoxanthin, can be converted into retinol and are thus referred to as provitamin A carotenoids. Lycopene, lutein, and zeaxanthin have no vitamin A activity and are thus referred to as nonprovitamin A carotenoids. Most naturally occurring carotenoids are in the all-trans-configuration; but under conditions of heating, for example, cis-isomers such as 13-cis-β-carotene (Figure 8-1) are formed. Functions and Actions The various biological effects of carotenoids can be classified into functions, actions, and associations. Carotenoids function in plants and in photosynthetic bacteria as accessory pigments in photosynthesis and protect against photosensitization in animals, plants, and bacteria. In humans, the only known function of carotenoids is vitamin A activity (provitamin A carotenoids only). Carotenoids also are thought to have a variety of different actions, including possible antioxidant activity, immunoenhancement, inhibition of mutagenesis and transformation, inhibition of premalignant lesions, quenching of nonphotochemical fluorescence, and activity as a pigment in primate macula (Olson, 1999). Carotenoids have also been associated with various health effects: decreased risk of macular degeneration and cataracts, decreased risk of some cancers, and decreased risk of some cardiovascular events (Olson, 1999). However, as described above, the only known function of carotenoids in humans is to act as a source of vitamin A in the diet. This function, as well as carotenoid actions and associations, is reviewed elsewhere (Krinsky, 1993; Olson, 1989) and discussed in subsequent sections. Physiology of Absorption, Metabolism, and Excretion Absorption The intestinal absorption of dietary carotenoids is facilitated by
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids FIGURE 8-1 Structure of provitamin A and nonprovitamin A carotenoids.
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids the formation of bile acid micelles. The hydrocarbon backbone of the carotenoids makes them insoluble in water, and like other non-polar lipids, they must be solubilized within micelles in the gastrointestinal tract to allow for absorption. Micellar solubilization facilitates the diffusion of lipids across the unstirred water layer. The presence of fat in the small intestine stimulates the secretion of bile acids from the gall bladder and improves the absorption of carotenoids by increasing the size and stability of micelles, thus allowing more carotenoids to be solubilized. The uptake of tene by the mucosal cell is believed to occur by passive diffusion (Hollander and Ruble, 1978). Uptake by these cells, however, is not sufficient for absorption to be completed. Once inside the mucosal cell, carotenoids or their metabolic products (e.g., vitamin A) must also be incorporated into chylomicrons and released into the lymphatics. When mucosal cells are sloughed off due to cell turnover, spilling their contents into the lumen of the gastrointestinal tract, carotenoids that have been taken up by the cells but not yet incorporated into chylomicrons are lost into the lumen (Boileau et al., 1999). Metabolism, Transport, and Excretion Carotenoids may be either absorbed intact, or in the case of those possessing vitamin A activity, cleaved to form vitamin A prior to secretion into lymph. Portal transport of carotenoids is minimal due to the lipophilic nature of their structures. Some portal transport of more polar metabolites, such as retinoic acid, can occur (Olson, 1999). Carotenoid cleavage is accomplished either by the intestinal mucosal enzyme β-carotene 15,15′-dioxygenase (EC 18.104.22.168) or by noncentral cleavage mechanisms (Boileau et al., 1999; Olson, 1999; Parker, 1996; Wang, 1994). The extent of conversion of a highly bioavailable source of dietary β-carotene to vitamin A in humans has been shown to be between 60 and 75 percent, with an additional 15 percent of the β-carotene absorbed intact (Goodman et al., 1966). However, absorption of most carotenoids from foods is considerably lower and can be as low as 2 percent (Rodriguez and Irwin, 1972). The effects of dietary and nondietary factors on the efficiency of carotenoid absorption are reviewed later. Noncentral (or excentric) cleavage of carotenoids yields a wide variety of metabolic products, some of which are further metabolized. These cleavage products include aldehyde, acid, alcohol, and epoxide derivatives (Parker, 1996; Wang, 1994). Isomerization of
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids carotenoids or their metabolic products may occur in vivo because isomers have been found upon extraction of carotenoids from human tissues (Clinton et al., 1996). Although little attention has been given to the study of carotenoid excretion pathways, epoxides and carotenoid metabolic products with less than 15 carbon chain lengths would presumably have no vitamin A activity. It is assumed that bile and urine would be excretion routes for metabolites (Olson, 1999). The carotenoids are transported in blood exclusively by lipoproteins. The carotenoid content of individual lipoprotein classes is not homogeneous. In the fasted state, the hydrocarbon carotenoids such as α-carotene, β-carotene, and lycopene are carried predominantly by low-density lipoprotein. The remaining carotenoids, including the more polar xanthophylls such as lutein and zeaxanthin, are carried by high-density lipoprotein (HDL) and, to a lesser extent, by very low-density lipoprotein (Johnson and Russell, 1992; Parker, 1996; Traber et al., 1994). It is thought that β-carotene and other hydrocarbon carotenoids reside in the hydrophobic core of the particles, whereas the more polar xanthophylls reside closer to the surface (Parker, 1996). β-Carotene is the most studied carotenoid in terms of metabolism and its potential effects on health. Lycopene, lutein, zeaxanthin, and α-carotene have received increasing attention in recent years. Much remains to be learned, however, about the relative metabolic effects of these carotenoids. Body Stores Recently, 34 carotenoids were identified in human serum and milk (Khachik et al., 1997b). Of these, 13 were geometrical isomers of their all-trans parent structures and 8 were metabolites. This finding is in contrast to the up to 50 carotenoids that have been identified in the U.S. diet and the more than 600 found in nature. The most prevalent carotenoids in human serum (Khachik et al., 1997b) are the same as those most commonly found in the diet: β-carotene, lycopene, and lutein (Nebeling et al., 1997). Cis-isomers of lycopene are commonly found in the serum and in fact have been shown to constitute more than 50 percent of the total serum lycopene (Stahl et al., 1992). In contrast, cis-isomers of β-carotene are considerably less common in serum with the trans-isomers being more common. In addition to these forms of α-carotene, β-carotene, lycopene, and zeaxanthin are also major serum carotenoids. The concentrations of various carotenoids in human serum and
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids tissues are highly variable and likely depend on a number of factors such as food sources, efficiency of absorption, amount of fat in the diet, and so forth (Table 8-1). The serum concentration of carotenoids after a single dose peaks at 24 to 48 hours post dose (Johnson and Russell, 1992). The earliest postprandial serum appearance of carotenoids is in the chylomicron fraction. It has been proposed that the increase in carotenoids in the triglyceride-rich lipoprotein fraction (primarily chylomicrons) be used for quantitating carotenoid absorption (van Vliet et al., 1995). This would provide a more direct measure of absorption because total serum carotenoid content is not an exclusive measure of newly absorbed carotenoids. Data from the Third National Health and Nutrition Examination Survey (NHANES III) demonstrate the variability of normal serum carotenoid concentrations (Appendix Table F-4, Table F-5, Table F-6, Table F-7, through Table F-8). This variability is attributed to a variety of life-style and physiological factors. In a recent population-based study, Brady et al. (1996) reported that lower serum concentrations of α-carotene, β-carotene, β-cryptoxanthin, lutein, and zeaxanthin, but not lycopene, were generally associated with male gender, smoking, younger age, lower non-HDL cholesterol, greater ethanol consumption, and higher body mass index. The delivery of carotenoids to extrahepatic tissue is accomplished through the interaction of lipoprotein particles with receptors and the degradation of lipoproteins by extrahepatic enzymes such as lipoprotein lipase. Carotenoids are present in a number of human tissues including adipose, liver, kidney, and adrenal, but adipose tissue and liver appear to be the main storage sites (Parker, 1996). However, based on a wet tissue weight, the liver, adrenal gland, and testes contain the highest per-gram concentrations (Stahl et al., 1992). Similar to what is reported in serum, β-carotene, lutein, and lycopene are the main tissue carotenoids, although α-carotene, β-cryptoxanthin, and zeaxanthin are also present (Boileau et al., 1999). In contrast to serum profiles, 9-cis-β-carotene is consistently present in storage tissues. In both serum and tissue storage, lycopene cis-isomers constitute greater than 50 percent of the total lycopene present (Clinton et al., 1996; Stahl et al., 1992). Clinical Effects of Inadequate Intake If adequate retinol is provided in the diet, there are no known clinical effects of consuming diets low in carotenes over the short term. One study of premenopausal women consuming low-carotene
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids diets in a metabolic ward reported skin lesions (Burri et al., 1993). However, this effect was not observed after 60 days of depletion in a subsequent β-carotene depletion study by the same group of investigators (Lin et al., 1998). These studies of carotene-deficient diets were reported to increase various measures of oxidative susceptibility (Dixon et al., 1994, 1998; Lin et al., 1998), but as discussed below, this is of uncertain relevance with regard to clinical outcomes. SELECTION OF POSSIBLE INDICATORS FOR ESTIMATING THE REQUIREMENT FOR β-CAROTENE AND OTHER CAROTENOIDS Vitamin A Equivalency Vitamin A equivalency is a possible indicator for establishing requirements for provitamin A carotenoids. However, any such establishment of requirements for carotenoids based on vitamin A activity must be considered in concert with the evaluation of requirements for vitamin A. This information will be presented in a later Dietary Reference Intakes report. Markers of Antioxidant Activity The effect of increasing β-carotene intake on several markers of antioxidant activity has been investigated in a series of studies involving humans. These studies have examined antioxidant marker activity in apparently healthy men and women as well as in subjects who were physiologically challenged (i.e., smokers and patients with coronary disease or cystic fibrosis). Studies of the effect of β-carotene intake on measures of antioxidant activity are summarized in Table 8-2. The dietary source of β-carotene ranged from modification of diets with normally consumed foods to giving supplements that provided as much as 120 mg/day of a highly bioavailable preparation. In general, subjects in most studies consumed β-carotene in amounts that would be difficult to achieve from foods alone and, as a result, relate to the pharmacological range of intakes. The findings reported in Table 8-2 indicate that β-carotene supplementation did not alter, or inconsistently alter, markers of antioxidant activity, which were somewhat dependent on β-carotene intake. In studies in which subjects were fed less than 25 mg/day of β-carotene, either from foods or as a supplement, changes in the markers for antioxidant activity were minimal. Exceptions noted
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids TABLE 8-1 Concentrations of Selected Carotenoids in Human Serum and Tissues Carotenoid Serum (µmol/L) Liver (µmol/g) α-Carotene 0.02–0.47 0.075–10.8 (1.0–25.3 µg/dL) (0.04–5.8 µg/g) β-Carotene 0.04–2.26 0.39–19.4 (2.2–122.7 µg/dL) (0.21–6.3 µg/g) β-Cryptoxanthin 0.03–0.70 0.037–20.0 (1.4–38.2 µg/dL) (0.05–11.0 µg/g) Lutein 0.10–1.23 0.10–3.0 (5.8–69.8 µg/dL) (0.06–6.9 µg/g) Lycopene 0.05–1.05 0.20–17.2 (2.7–54.6 µg/dL) (0.11–11.1 µg/g) SOURCE: Data from Schmitz et al. (1991) and Kaplan et al. (1990) for tissues and Iowa State University Department of Statistics (1999) for serum. were decreased deoxyribonucleic acid strand breaks observed when 22 mg/day of β-carotene was administered as carrot juice (Pool-Zobel et al., 1997) and lowered copper-induced oxidation of low-density lipoprotein when 12 or 24 mg/day of β-carotene was given along with vitamins C and E (Mosca et al., 1997). As shown in Table 8-2, feeding β-carotene in amounts greater than 25 mg/day generally resulted in inconsistent responses of the biological markers monitored. Administration of β-carotene to subjects with increased oxidative stress (e.g., smoking, cystic fibrosis) was associated with more consistent evidence of decreased lipid peroxidation compared to studies in which subjects without known additional oxidative stress were given β-carotene. In studies that involved depletion followed by repletion of body stores of β-carotene, as indicated by plasma concentrations, the biological markers that were negatively altered as a result of depleted body stores of β-carotene were restored to baseline values as a consequence of repletion (Table 8-2). In summary, results from some studies show improvement of measures of antioxidant activity due to intake of relatively high levels of β-carotene, while studies that investigated low to modest levels of β-carotene show no or inconsistent changes in the same activities.
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids Kidney(µmol/g) Lung(µmol/g) 0.037–1.5 0.1–1.0 (0.02–0.80 µg/g) (0.05–0.54 µg/g) 0.093–2.8 0.1–1.6 (0.05–1.5 µg/g) (0.05–0.86 µg/g) 0.019–3.9 0.1–2.5 (0.05–2.2 µg/g) (0.05–1.4 µg/g) 0.037–2.1 0.1–2.3 (0.05–5.9 µg/g) (0.05–1.3 µg/g) 0.093–2.4 0.1–1.0 (0.05–1.3 µg/g) (0.05–2.3 µg/g) Some benefit of feeding increased amounts of β-carotene was observed for several markers of antioxidant activity when body stores were relatively low or when an oxidant-type stress was present. These observations suggest that the lack of effect in some studies may be due to study populations whose baseline β-carotene status was already adequate. Nevertheless, current data do not provide convincing evidence that substantially increasing β-carotene intake above current dietary intakes has a significant effect on measures of antioxidant status. Also, none of these markers has been validated to be predictive of any known health outcomes. Therefore, these data are inadequate for the estimation of a requirement for β-carotene. Gap Junctional Communication Appropriate communication among cells is essential for the coordination of biochemical functions in complex, multicellular organisms. One theory suggests that failure of signaling is one cause of cell overgrowth and eventually cancer. Two research groups have demonstrated that carotenoids stimulate gap junction communication between cells in vitro (Sies and Stahl, 1997; Zhang et al., 1991).
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids TABLE 8-2 β-Carotene Intake and Measures of Antioxidant Activity in Selected Studies Reference, Country Subjects β-Carotene Dose Richards et al., 1990 South Africa 40 smokers, average age 33 y; received placebo and 20 received treatment 40 mg/d, Roche prep Mobarhan et al., 1990; Gottlieb et al., 1993 United States 15 healthy men, aged 19–30 y; randomly assigned repletion levels Carotene-free diet (depletion); Repletion: 15 mg/d or 120 mg/d, Roche prep Van Poppel et al., 1992a, 1992b, 1995 Holland 143 male smokers, average age 39 y; randomly assigned to placebo or treatment 40 mg/d first 2 wk 20 mg/d next 12 wk Allard et al., 1994 Canada 38 male nonsmokers, 25 male smokers, aged 20–75 y; randomly assigned to placebo or treatment 20 mg/d, Roche prep Calzada et al., 1995 United States 12 healthy men and 7 women, aged 21–50 y; randomly assigned to placebo or treatment 15 mg/d, Roche prep Gaziano et al., 1995 United States 4 healthy men and 12 women, aged 25–47 y; randomly assigned to either synthetic (BASF) or natural (Henkel) β-carotene 100 mg/d load dose; natural treatment, 66 or 100 mg/2d; synthetic treatment, 50 mg/2 d Winklhofer-Roob et al., 1995 Switzerland CFm patients, 32 boys and girls; average age 10.8 y 0.5 mg/kg BWn/d, 3M Medica, Ltd. Clevidence et al., 1997 United States 5 healthy men and 7 women, aged 27–61 y 18 mg/d additional as foods; kale, tomato juice, sweet potato
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids Duration Plasma β-Carotene (µmol/L) Findings 6 wk Baseline—0.50 (27 µg/dL) Trta—2.06 (111 µg/dL) No change in leukocyte sister chromatid exchange 2 wk 4 wk Baseline—0.24 (13 µg/dL) Depletion—0.09 (5 µg/dL) 15 mg/d—3.32 (178 µg/dL) 120 mg/d—8.74 (469 µg/dL) ↓ Breath pentane on 120 mg/d only; ↓ Serum lipid peroxide levels, both repletion levels 2 wk 12 wk Baseline—0.33 (18 µg/dL) Trt at 14 wk—4.36 (234 µg/dL) ↓ Sputum nuclei No change in lymphocyte sister chromatid exchange or urinary 8-oxodG b 4 wk Placebo/NSc—0.38 (20 µg/dL) Placebo/Sd—0.27 (14 µg/dL) Trt/NS—3.50 (188 µg/dL) Trt/S—3.38 (181 µg/dL) ↓ Breath pentane in smokers No change in breath pentane in nonsmokers No change in breath ethane, RBCe, MDAf or plasma SeGSHPxg in either group 14 d 56 d Baseline—0.87 (47 µg/dL) Trt—3.07 (165 µg/dL) No change in plasma Trolox equivalent antioxidant activity 6 d load; followed by 21 d treatment Baseline—0.25 (13 µg/dL) Both Trts—1.39 (75 µg/dL) ↑ Cu2+-induced LDLk oxidation No change in AAPHl -induced LDL oxidation 3 m Baseline—0.09 (5 µg/dL) Trt—1.07 (57 µg/dL) ↓ Plasma MDA and Cu2+-induced LDL oxidation 3 wk Baseline—0.29 (15 µg/dL) Trt—0.76 (40.2 µg/dL) No change in plasma ORACo, plasma hydroperoxides, LDL TBARS, or 8-oxodG
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids observational studies, in animal models, and in human intervention trials, if justified. Studies should consider not only the other carotenoids, but also the cis-versus trans-configuration of the carotenoid. Since the data from the human intervention trials of β-carotene are contradictory, additional data are needed from intervention trials involving β-carotene, several of which are ongoing. An examination is needed of health effects in populations with varying baseline risk profiles and, in particular, of studies evaluating interventions in populations with poor baseline nutritional status. Post-trial follow-up of completed β-carotene trials is also needed. Studies aimed at the identification of correlates of higher β-carotene intake and plasma concentrations, which might help to explain the lower risks of cancer associated with carotene-rich diets, are needed. Additional research is needed that targets putative mechanisms to explain a possible increase in lung cancer risk in heavy smokers taking high-dose β-carotene supplements (animal studies, biochemical studies, and molecular studies). In particular, confirmation and extension of findings such as those of recent reports regarding lung metaplasia (Wang et al., 1999) and carotenoid oxidation products (Salgo et al., 1999), and their relevance to cancer development in humans, are needed. Surveys are needed that routinely assess and report dietary intakes of individual food carotenoids from large, representative population samples. Intakes from both foods and dietary supplements must be considered. Efforts should be directed toward evaluating equivalency and demonstrating efficacy of carotenoids in foods to meet vitamin A needs in vitamin A-deficient populations, in order to develop sustainable strategies to eradicate this worldwide public health problem. REFERENCES Albanes D, Heinonen OP, Taylor PR, Virtamo J, Edwards BK, Rautalahti M, Hartman AM, Palmgren J, Freedman LS, Haapakoski J, Barrett MJ, Pietinen P, Malila N, Tala E, Liippo K, Salomaa ER, Tangrea JA, Teppo L, Askin FB, Taskinen E, Erozan Y, Greenwald P, Huttunen JK. 1996. α-Tocopherol and β-carotene supplements and lung cancer incidence in the Alpha-Tocopherol Beta-Carotene Prevention Study: Effects of base-line characteristics and study compliance. J Natl Cancer Inst 88:1560–1570. Albanes D, Virtamo J, Taylor PR, Rautalahti M, Pietinen P, Heinonen OP. 1997. Effects of supplemental beta-carotene, cigarette smoking, and alcohol co sumption on serum carotenoids in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Clin Nutr 66:366–372.
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids Allard JP, Royall D, Kurian R, Muggli R, Jeejeebhoy KN. 1994. Effects of beta carotene supplementation on lipid peroxidation in humans. Am J Clin Nutr 59:884–890. ATBC (Alpha-Tocopherol, Beta Carotene) Cancer Prevention Study Group . 1994. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med 330:1029–1035. Baker DL, Krol ES, Jacobsen N, Liebler DC. 1999. Reactions of beta-carotene with cigarette smoke oxidants. Identification of carotenoid oxidation products and evaluation of the prooxidant/antioxidant effect. Chem Res Toxicol 12:535–543. Batieha AM, Armenian HK, Norkus EP, Morris JS, Spate VE, Comstock GW. 1993. Serum micronutrients and the subsequent risk of cervical cancer in a popul tion-based nested case-control study. Cancer Epidemiol Biomarkers Prev 2:335–339. Bendich A. 1988. The safety of beta-carotene. Nutr Cancer 11:207–214. Block G, Patterson B, Subar A. 1992. Fruit, vegetables, and cancer prevention: A review of the epidemiological evidence. Nutr Cancer 18:1–29. Blot WJ, Li J-Y, Taylor PR, Guo W, Dawsey S, Wang G-Q, Yang CS, Zheng S-F, Gail M, Li G-Y, Yu Y, Liu B-Q, Tangrea J, Sun Y-H, Liu F, Fraumeni JF Jr, Zhang Y-H, Li B. 1993. Nutrition intervention trials in Linxian, China: Supplement tion with specific vitamin/mineral combinations, cancer incidence, and disease-specific mortality in the general population. J Natl Cancer Inst 85:1483–1492. Blot WJ, Li J-Y, Taylor PR, Li B. 1994. Lung cancer and vitamin supplementation. N Engl J Med 331:614. Boileau TW, Moore AC, Erdman JW Jr. 1999. Carotenoids and vitamin A. In: Papas AM, ed. Antioxidant Status, Diet, Nutrition, and Health. Boca Raton, FL: CRC Press. Pp. 133–158. Bone RA, Landrum JT, Tarsis SL. 1985. Preliminary identification of the human macular pigment. Vision Res 25:1531–1535. Bone RA, Landrum JT, Hime GW, Cains A, Zamor J. 1993. Stereochemistry of the human macular carotenoids. Invest Ophthalmol Vis Sci 34:2033–2040. Bonithon-Kopp C, Coudray C, Berr C, Touboul P-J, Feve JM, Favier A, Ducimetiere P. 1997. Combined effects of lipid peroxidation and antioxidant status on carotid atherosclerosis in a population aged 59–71 y: The EVA Study . Am J Clin Nutr 65:121–127. Brady WE, Mares-Perlman JA, Bowen P, Stacewicz-Sapuntzakis M. 1996. Human serum carotenoid concentrations are related to physiologic and lifestyle factors. J Nutr 126:129–137. Brown L, Rimm EB, Seddon JM, Giovannucci EL, Chasan-Taber L, Spiegelman D, Willett WC, Hankinson SE. 1999. A prospective study of carotenoid intake and risk of cataract extraction in US men. Am J Clin Nutr 70:517–524. Burri BJ, Dixon ZR, Fong AK, Kretsch MJ, Clifford AJ, Erdman JW Jr. 1993. Possible association of skin lesions with a low-carotene diet in premenopausal women. Ann NY Acad Sci 691:279–280. Butte NF, Calloway DH. 1981. Evaluation of lactational performance of Navajo women. Am J Clin Nutr 34:2210–2215. Calzada C, Bizzotto M, Paganga G, Miller NJ, Bruckdorfer KR, Diplock AT, Rice-Evans CA. 1995. Levels of antioxidant nutrients in plasma and low density lipoproteins: A human volunteer supplementation study. Free Radic Res 23:489–503.
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