4
Prevention of Vitamin A Deficiency

Barbara A. Underwood, Ph.D.

National Eye Institute

Major Health Consequences

Xerophthalmia and Nutritional Blindness

Vitamin A deficiency (VAD) affects ocular tissue in two ways: by slowing the regeneration of the visual pigments following exposure to bright light and by disrupting epithelial integrity. The inability to see well in dim illumination (night blindness) is a symptom recorded in ancient Egyptian, Greek, and Assyrian medical literature and, more recently, in the writings of European physicians. Epithelial defects in ocular tissue leading to blindness were described in dogs by Magendie and in humans by Budd in the early 1800s. They observed progressive deterioration from conjunctival xerosis to corneal xerosis, ulceration, and liquefaction (keratomalacia) as a consequence of restricted diets, devoid of what we now recognize as sources of vitamin A (Wolf, 1996). Manifestations of these distinct debilitating effects were thus recognized before McCollum's discovery of an essential nutrient, coined fat-soluble vitamin A, in the early 1900s (McCollum and Davies, 1913); description of tissue changes following deprivation of this nutrient (Wolbach and Howe, 1925); elucidation of its molecular role in vision (Wald, 1968); and the recent description of its role in the regulation of genetic expression (Kastner et al., 1994; Mangelsdorf et al., 1994).

The link in humans between clinically evident symptoms and signs and a faulty diet was suggested in about 1860 and subsequently confirmed in many societies (Guggenheim, 1981; Wolf, 1996). Cure was associated with certain foods—in early times with topical application or ingestion of animal and fish liver, and in later years with ingestion of plant foods containing green and yellow pigments (Wolf, 1996). McCollum and Davies (1913), followed shortly thereafter by Osborne and Mendel (1913), described the keratomalacia-preventing, growth-limiting, fat-soluble substances isolated from efficacious foods. These substances were later designated vitamin A and carotenoids.



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--> 4 Prevention of Vitamin A Deficiency Barbara A. Underwood, Ph.D. National Eye Institute Major Health Consequences Xerophthalmia and Nutritional Blindness Vitamin A deficiency (VAD) affects ocular tissue in two ways: by slowing the regeneration of the visual pigments following exposure to bright light and by disrupting epithelial integrity. The inability to see well in dim illumination (night blindness) is a symptom recorded in ancient Egyptian, Greek, and Assyrian medical literature and, more recently, in the writings of European physicians. Epithelial defects in ocular tissue leading to blindness were described in dogs by Magendie and in humans by Budd in the early 1800s. They observed progressive deterioration from conjunctival xerosis to corneal xerosis, ulceration, and liquefaction (keratomalacia) as a consequence of restricted diets, devoid of what we now recognize as sources of vitamin A (Wolf, 1996). Manifestations of these distinct debilitating effects were thus recognized before McCollum's discovery of an essential nutrient, coined fat-soluble vitamin A, in the early 1900s (McCollum and Davies, 1913); description of tissue changes following deprivation of this nutrient (Wolbach and Howe, 1925); elucidation of its molecular role in vision (Wald, 1968); and the recent description of its role in the regulation of genetic expression (Kastner et al., 1994; Mangelsdorf et al., 1994). The link in humans between clinically evident symptoms and signs and a faulty diet was suggested in about 1860 and subsequently confirmed in many societies (Guggenheim, 1981; Wolf, 1996). Cure was associated with certain foods—in early times with topical application or ingestion of animal and fish liver, and in later years with ingestion of plant foods containing green and yellow pigments (Wolf, 1996). McCollum and Davies (1913), followed shortly thereafter by Osborne and Mendel (1913), described the keratomalacia-preventing, growth-limiting, fat-soluble substances isolated from efficacious foods. These substances were later designated vitamin A and carotenoids.

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--> Steenbock (1919) postulated, and later confirmed, that carotenoid from yellow maize could support growth and prevent ocular lesions by physiological conversion to biologically active vitamin A. Since Isler et al. (1947) discovered a cost-effective way to synthesize vitamin A, cure and prevention are also possible through commercially produced, synthetic vitamin A. Childhood Morbidity and Mortality Working at the University of Wisconsin, and later at Johns Hopkins University, McCollum pioneered the use of mice and rats in nutrition experiments. His studies of vitamin A deprived rat colonies—and those of others—were often hampered by early deaths from respiratory and diarrheal illnesses before ocular lesions occurred. These early deaths were partly attributable to loss of epithelial integrity in tissues throughout the bodies of VAD animals, and humans as well (Chytil, 1992; Hayes, 1971; Wolbach, 1937). Similar vitamin-A-deficiency-related morbidity and mortality in human populations were not clearly demonstrated, however, until the seminal community-based studies in the 1980s of Sommer and colleagues in Indonesia (summarized in Sommer and West, 1996). These studies clearly linked increased mortality risk in preschool-age children to vitamin A deficiency, a finding later confirmed among child populations in other countries in Asia and Africa where clinical eye signs occur (Beaton et al., 1993). Where eye signs are not evident, biochemical deficiency—that is, subclinical deficiency—is also believed to contribute to mortality risk. In free-living populations, however, an unequivocal tie to the incidence of infectious morbidity has not been established. Severity once infection is acquired provides the probable link to mortality (Ghana VAST Study Team, 1993; Underwood and Arthur, 1996). This finding implies a role for vitamin A in immunocompetence, a role suggested by an extensive review of interactions of nutrition and infection published in 1968 (Scrimshaw et al., 1968). That review concluded that VAD showed synergism with almost every known infectious disease. Recent basic studies have been unraveling the complex molecular mechanisms by which vitamin A influences the immune system and alters cellular integrity (Ross and Stephensen, 1996). The combined effect on cellular integrity and immunocompetence is believed to contribute to an annual loss of approximately 1.12 to about 3 million lives of children under 5 years of age that otherwise could be salvaged by normalizing vitamin A status (Gillespie and Mason, 1994; Humphrey et al., 1992). Other Health Consequences Severe vitamin A deficiency in animal models is clearly linked to other adverse health effects. These include teratogenic-developmental consequences

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--> (Armstrong et al., 1994), adverse reproductive performance (Takahashi et al., 1975), impaired growth (Anzano et al., 1979), and depressed iron utilization (Roodenburg et al., 1996). Except for an association with anemia (Suharno et al., 1992), similar consequences among free-living human populations are less clearly attributable to vitamin A status alone. This is because in community settings, confounding is likely from coexisting nutritional deficits and disease. Nonetheless, vitamin A deficiency is undoubtedly a contributor to adverse health effects similar to those confirmed in laboratory animals, although in human populations this vitamin may not be the most immediate causative nutrient. Magnitude And Epidemiology Of The Problem Defining Vitamin A Status Conceptually, vitamin A status can be visualized as a continuum (see Figure 4-1) from the absent or minimal tissue stores associated with symptoms and signs of deficiency to the excess tissue deposits associated with toxic symptoms and signs (Bauernfeind, 1980; Olson, 1994). Between the extremes is a relatively large zone where status cannot be easily quantified by currently available techniques (Underwood and Olson, 1993). In practice, the limited fetal stores provided from maternal circulation launches newborns, especially those with low birthweights (Chytil, 1992), into extrauterine life at the low end of the continuum of vitamin A status. That position may be rapidly augmented postnatally in infants fed vitamin A-rich colostrum and early breast milk (Chappell et al., 1985) or supplements (Humphrey et al., 1996). From birth onward, an infant's vitamin A status on the continuum may advance by small increments, be maintained, or deteriorate, depending on the balance between dietary intake relative to growth and development needs and to disease patterns that effect vitamin A economy. Breast-fed infants do not usually show clinical deficiency for at least 4 to 6 months after birth. They may be at a marginally adequate point on the continuum, however, if breast-fed by a malnourished, vitamin A-depleted mother (Underwood, 1994a). At the same time, if breast-fed, even from a malnourished mother whose breast milk vitamin A has been improved through direct maternal supplementation (200,000 IU of vitamin A given within 2 months postpartum [WHO/UNICEF/IVACG, in press]), adequate infant vitamin A status may be prolonged beyond 6 months (Stoltzfus et al., 1993). Vitamin A requirements (see Figure 4-2), therefore, are greatest during periods of rapid growth—infancy and early childhood, adolescence, and pregnancy—and when the vitamin is lost from the body through normal physiologic processes, such as lactation, or through nonphysiological losses brought about by frequent disease, such as malabsorption, diarrhea, and febrile infections (FAO/WHO, 1988).

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--> FIGURE 4-1 The logarithmic plot of vitamin A intake is depicted as a function of the biological response of man and animals in terms of deficiency, normalcy, and toxicity. The scheme at the top illustrates the response of a typical mucous epithelium, but is probably applicable to other undifferentiated blast-cell populations as well. The bottom curve indicates the clinical manifestations resulting from the altered cell function in deficiency and toxicity of vitamin A. SOURCE: Bauernfeind (1980), reproduced with permission. Recognition of factors that influence vitamin A balance provides a foundation for understanding the epidemiology of VAD (Oomen et al., 1964; Tielsch and Sommer, 1994; Underwood, 1993).

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--> FIGURE 4-2 Recommended intake of vitamin A. SOURCE: Adapted from FAO/WHO (1988). Extent of the Problem Since the debilitating—and sometimes fatal—link of VAD to health is well-established, and effective and relatively inexpensive food sources and synthetic vitamin A are available for VAD prevention and control, why does a global public health problem persist? Clearly the fault lies in the application of insufficient or ineffective knowledge to the implementation of programs to rectify uneven resource distribution among and within affected populations. WHO estimated in 1995 that at least 3 million children exhibit xerophthalmia annually—they are clinically deficient and at risk of blindness. An additional 250 million children under 5 years of age are at risk of deficient vitamin A status (based on the prevalence of serum retinol distributions below 0.70 µmol/L); they are subclinically deficient, and at risk of severe morbidities and premature death (WHO, 1995a). These estimates do not include pregnant and lactating women who are in areas of endemic childhood VAD, and are thus likely to be in poor status, but for whom epidemiological data are quite limited. A high prevalence of maternal night blindness (Katz et al., 1995) and low breast milk levels of vitamin A (Newman, 1993) are reported in such areas. A lack of sensitive, survey-applicable, nonclinical indicators specific to VAD, however, has hampered population-based evaluation of status among reproductive-age women and other age and gender groups (WHO, 1996a).

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--> Risk Factors Age Clinical and subclinical VAD are most prevalent in children 6 months through 5 years of age. This period is characterized by high requirements to support early rapid growth, the transition from breast-feeding to dependence on other dietary sources of the vitamin, and increased frequency of respiratory and gastrointestinal infections. Although growth rates decline sharply during infancy, decreasing the requirement for vitamin A per kilogram of body weight, the absolute quantity of the vitamin needed daily increases with growing total body mass (see Figure 4-2, based on FAO/WHO, 1988). If average dietary vitamin A intake from food progressively increases with body mass, body stores are likely to increase by small increments with advancing age. If diet is inadequate, and no vitamin A supplement is given, body reserves may only be maintained, or will decline if frequent disease, so prevalent among toddlers, tips the balance downward. How quickly the deficit can be restored depends on its magnitude and the repletion-rehabilitation program followed (see Figure 4-3). FIGURE 4-3 Vitamin A status.

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--> Gender There is no consistent, clear indication in humans of a gender differential in the requirement for vitamin A during childhood. Growth rates—and presumably need for vitamin A—from birth to 10 years for boys are consistently higher than those for girls (WHO, 1995b). In the context of varied cultural and community settings, however, variations in gender-specific practices for the feeding and care of children are likely to subsume a small gender differential in the requirement to account for reported gender differentials in xerophthalmia prevalence. Pregnant and lactating women, of course, require additional vitamin A to support maternal and fetal tissue growth and lactation losses that are not endured by other postadolescent adults (NAS, FNB, IOM, 1990). Quality of Diet Dietary sources of biologically active vitamin A are found preformed in some animal foods or as provitamin carotenoids from plants. There is no specific human requirement for carotenoids apart from their potential conversion to biologically active retinoid. Preformed vitamin A is highly bioavailable, whereas the bioavailability of provitamin A carotenoids varies with the kind of plant source (Rodriguez-Amaya, 1997). The bioavailability of the provitamin A carotenoids from plants is greatly influenced by the nature of the embedding matrix (i.e., fibrous, dark green leafy vegetables [DGLV] or soft-fleshed yellow/orange vegetables and fruits) and the composition of the accompanying meal. Carotenoids, once released in the gastrointestinal tract from the embedding matrix, are only absorbed when fat is concurrently available. Dietary fat is needed to stimulate intestinal and pancreatic secretions. These secretions contain lipolytic enzymes for fat digestion, and phospholipids and bile salts needed for micelles to form and solubilize both preformed vitamin A (Blumhoff et al., 1991) and carotenoids (Erdman, 1988). Only micelle-solubilized carotenoids gain entrance to enterocytes where bioconversion to retinol, or intact transfer to chylomicra, occurs; that is, they become bioavailable. Disease Occurrence Infectious diseases contribute to vitamin A depletion. Enteric infections may alter absorptive-surface area, compete for absorption-binding sites, and increase urinary loss (Alvarez et al., 1995; Solomons and Keusch, 1981). Febrile systemic infections also increase urinary loss (Stephensen et al., 1994) and metabolic utilization rates. Disease is often associated with precipitating ocular signs in the presence of latent deficiency (Curtale et al., 1995; Feacham, 1987). Infection with the measles virus is especially devastating to vitamin A metabolism,

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--> adversely interfering with both efficiencies of utilization and conservation (Hussey and Klein, 1990; Sommer and West, 1996). Severe protein-energy malnutrition (PEM) affects many aspects of vitamin A metabolism, and even when reserve retinyl-ester stores are adequate, it can prevent transport-protein synthesis, resulting in immobilization of existing vitamin A stores (Arroyave et al., 1967; Smith et al., 1973; Smith et al., 1975). Seasonality In endemic VAD areas, fluctuations in the incidence of VAD throughout the year reflect the balance between intake and need. Times of food shortage (particularly of vitamin A-rich foods), periods of peak incidence of common childhood infectious diseases (diarrheal, respiratory, and measles infections), and periodic seasonal growth spurts affect the balance. Seasonal food availability can influence VAD prevalence in two ways. First, it directly influences access to provitamin A sources. Scarcity prevails in the hot, arid months and gluts are seen during harvest seasons—in the case of mangoes, for example (Marsh et al., 1995). Second, seasonal growth spurts in children frequently follow postharvest increases in energy and macronutrient intakes, usually from staple grains (such as rice) and tubers (light-colored yams, for example) that are not good sources of some of the micronutrients, including vitamin A, that are needed to support the growth spurt (Sinha and Bang, 1973). Cultural Factors Food habits and taboos often restrict consumption of potentially good food sources of vitamin A, such as mangoes and green leafy vegetables. Culture-specific practices in the feeding of children, adolescents, and pregnant and lactating women are common (Chen, 1972; Johns et al., 1992; Mele et al., 1991). Illness-related and pre- and postparturition proscription in the use of ''cold/hot" (yin/yang) foods pervade many traditional cultures (Mahadevan, 1961). Such influences alter shortand long-term food distribution within families that may only be detected by dietary intake surveys disaggregated by age and gender and/or in-depth focus group discussions (Kuhnlein and Pelto, 1997). Culture-specific information of this kind is pivotal to the design of food-based behavior change interventions. Clustering Epidemiological studies repeatedly report clustering of VAD, presumably because of the concurrent occurrence of several risk factors. This clustering may occur at several levels, from the national arena to neighborhoods and households

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--> (Katz et al., 1993). Identifying the level at which clustering occurs is an important consideration in the selection, design, and targeting of VAD-control strategies. Economic Costs Of VAD The cost of VAD to society includes the burden of the prolonged management and care needed for such common childhood diseases as diarrhea and measles, and when deficiency is severe, provision for lifelong care of blinded victims. To illustrate the true global societal cost, Foster and Gilbert (1996) compared the cumulative disabled years in developing countries from childhood blindness with the total from unoperated cataract, the major cause of blindness after 50-60 years of age. The estimated 1.5 million blind children have a life expectancy of 50 years, equivalent to approximately 75 million years of disability. About 16 million older adults, with a much shorter life expectancy of 5 years, account for 80 million blind years. The years of economic burden to society from these two preventable causes of blindness are thus comparable, even though there is a tenfold difference in the number of individuals affected. Moreover, these costs do not account for the premature loss of life among the VAD-blinded, as well as among the subclinically VAD-deficient child population under 5 years of age. The real tragedy is that vitamin A-related childhood blindness—accounting for at least half of the total number of blinded children—can be treated or prevented (WHO, 1992), and subclinical VAD-related deaths can be substantially reduced (Beaton et al., 1993). VAD, therefore, is costly to the individual child in lost opportunity, and it has economic and social costs for the family, community, and nation as a whole. Indicators Of VAD Identification of Groups and Populations A standardized classification system for xerophthalmia (clinically evident VAD) and universally accepted criteria for defining a public health problem were agreed upon in 1982 (WHO et al., 1982). These criteria (see Table 4-1) remain appropriate for identifying populations at high risk of vitamin A-related, blinding malnutrition—populations to the far left of the vitamin A status continuum (Figure 4-1). They are inadequate, however, for identifying populations with subclinical deficiency—tissue concentrations of vitamin A low enough to have adverse health consequences, even in the absence of xerophthalmia, WHO's current definition of VAD (WHO, 1996a).

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--> TABLE 4-1 Biological Indicators of Clinical Vitamin A Deficiency: Xerophthalmiaa in Children 6–71 Months of Age Indicator Minimum Prevalence (%) Night blindness in children 24–71 months of age (XN) > 1.0 Conjunctival xerosis/with Bitot's spot (X1B) > 0.5 Corneal xerosis/ulceration/keratomalacia (X2, X3A, X3B) > 0.01 Corneal scarsb (XS) > 0.05 NOTE: Prevalence of any one or more of the indicators indicates a public health problem. a In addition, a serum level of vitamin A (retinol) has been used with the clinical classification to provide supportive evidence of an important problem. A prevalence of > 5 percent of serum levels < 0.35 µmol/l is strong corroborative evidence of any clinical criteria met to identify an urgent public health problem. b Lack of a history of traumatic eye injury or use of topical traditional medicines increases the specificity of this VAD indicator. Unfortunately, there is no practical, single indicator of adequate specificity and sensitivity to detect subclinical deficiency under community conditions—that is, populations in the intermediate left portion of the vitamin A-status continuum (see Figure 4-1). For this reason, WHO recommends that two or more indicators be used, at least one of which is biological and below the agreed upon cutoff points provided in Table 4-2. Where it is not possible to obtain two biological indicators, WHO suggests that one such indicator should be supported by a composite of at least four of the indirect demographic and ecological risk factors given in Tables 4-3A and 4-3B. Two of the four indirect indicators should be related to nutrition and diet (Table 4-3A). Socioeconomic indicators (Table 4-3C) are also useful qualitative indicators of the characteristics of high-risk populations. The cutoff values suggested in Table 4-3 resulted from the reflections of a WHO-sponsored consultation of experts. The group pointed out the need for additional confirmation of the utility of the values and suggested prevalence cutoffs. These ecological indicators reflect a context of dietary inadequacy and social and economic deprivation that have been associated with endemic VAD through epidemiological investigations (Sommer and West, 1996). Their usefulness is in identifying high-risk areas and populations, not individuals. Biological indicators are needed to confirm that a significant public health problem exists. Monitoring Intervention Impact and Outcome Appropriate indicators in the monitoring of intervention impact will vary in accordance with the intervention objective. For example, program objectives

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--> may be to improve coverage of recipients of vitamin A supplements; to ensure that a vitamin A-fortified food meets quality-assurance standards or is selected for consumption by target groups; to cause a change in food-consumption behavior, such as the frequency of consumption of DGLV; or to increase the year-round availability of vitamin A-rich food in household or community gardens. The appropriate intervention-specific impact indicator(s) for each of these objectives will differ; in some cases process indicators will be used, in others, biological indicators are appropriate (Table 4-3). If the desired outcome of the intervention is to document a change in the vitamin A status of the recipient population, the biological indicators in Tables 4-1 and 4-2 are appropriate. Resource availability can limit the feasibility of direct biological evaluations because these indicators are usually more costly to obtain and evaluate than indirect indicator data. In such situations, outcomes derived from metabolic and/or controlled community studies lend credence to causative inferences from similar outcomes of interventions implemented in less rigorously controlled community studies. The inability to perform biological evaluations alone should not prevent initiation of, or stop, VAD control programs when and where such programs are needed. TABLE 4-2 Biological Indicators of Subclinical Vitamin A Deficiency in Children 6–71 Months of Age (percent) Indicator (cut-off) Prevalence Below Cutoffs to Define a Public Health Problem and Its Level of Importance   Mild Moderate Severe Functional       Night blindness (present at 24–71 months) >0 to <1 >1 to <5 >5 Biochemical       Serum retinol (£0.70 µmol/l) >0 to <10 >10 to <20 >20 Breast milk retinol (£1.05 µmol/l) <10 >10 to <25 >25 RDR ≤20%) <20 >20 to <30 >30 MRDR (ratio ≤ 0.06) <20 >20 to <30 >30 + S30DR (≤20%) <20 >20 to <30 >30 Histological       CIC/ICT (abnormal) <20 >20 to <40 >40

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--> Favin, M., and M. Griffiths. 1991. Social Marketing of Micronutrients in Developing Countries. The World Bank, Population and Human Resources Department. Washington, D.C. Fawzi, W. W., M. G. Herrera, W. C. Willett, P. Nestel, A. El-Amin, and D. A. Mohamed. 1995. Dietary vitamin A intake and the incidence of diarrhea and respiratory infection among Sudanese children. J. Nutr. 125:1211–1221. Feachem, R. G. 1987. Vitamin A deficiency and diarrhoea: a review of interrelationships and their implications for the control of xerophthalmia and diarrhoea. Trop. Dis. Bull. 84: R1–R16. Florentino, R. F., C. C. Tanchoco, A. C. Ramos, T. S. Mendoza, E. P. Natividad, J. B. M. Tangco, and A. Sommer. 1990. Tolerance of preschoolers to two dosage strengths of vitamin A preparation. Am. J. Clin. Nutr. 52:694–700. Florentino, R. F., R. A. Pedro, L. V. Candelaria, B. D. Ungson, R. U. Zarate, Jr., A. R. M. Ramirex, and E. M. Lanot. 1993. An Evaluation of the Impact of Home Gardening on the Consumption of Vitamin A and Iron among Preschool Children. Report No. IN-17, Vitamin A Field Support Project (VITAL), Office of Nutrition, USAID, Washington, D.C. Flores, H., M. N. A. Azevedo, F. A. C. S. Campos, M. C. Barreto-Lins, A. A. Cavalcanti, A. C. Salzano, R. M. Varela, and B. A. Underwood. 1991. Serum vitamin A distribution curve for children aged 2–6 y known to have adequate vitamin A status: a reference population. Am. J. Clin. Nutr. 54:707–711. Flores, H., N. B. Guerra, A. C. A. Cavalcanti, F. A. C. S. Campos, M. C. N. A. Azevedo, and M. B. M. Silva. 1994. Bioavailability of vitamin A in a synthetic rice premix. J. Food Sci. 59:371–377. Foster, A., and C. Gilbert. 1996. Childhood blindness. In Global Perspectives on the Control of Blindness: A Tribute to Mr. Alan Johns CMG OBE, G. Johnson and E. Cartwright, eds., pp. 45–56. London: International Center for Eye Health, Institute of Ophthalmology. Foster, A., and D. Yorston. 1992. Corneal ulceration in Tanzanian children: relationship between measles and vitamin A deficiency. Trans. R. Soc. Trop. Med. Hyg. 86:454–455. Fredrikzon, B., O. Hernell, L. Blackberg, and T. Olivecrona. 1978. Bile salt-stimulated lipase in human milk: evidence of activity in vivo and of a role in the digestion of milk retinol esters. Pediatr. Res. 12:1048–1052. Ghana VAST Study Team. 1993. Vitamin A supplementation in northern Ghana: effects on clinic attendances, hospital admissions, and child mortality. Lancet 342:7–12. Gillespie, S., and J. Mason. 1994. Controlling Vitamin A Deficiency. ACC/SCN State-of-the-Art Series, Nutrition Policy Discussion Paper No. 14. Geneva: ACC/SCN Secretariat. Graham, G. G., H. M. Creed, W. C. MacLean, C. H. Kallman, J. Rabold, and E. D. Mellitis. 1981. Determinants of growth among poor children: nutrient intake-achieved growth relationships. Am. J. Clin. Nutr. 34:539–554. Graham, R. D., and R. M. Welch. 1996. Breeding for staple food crops with high micronutrient density. Working Papers on Agricultural Strategies for Micronutrients, No. 3. Washington, D.C.: International Food Policy Research Institute. Greiner, T., and S. N. Mitra. 1996. Evaluation of the impact of a food-based approach to solving vitamin A deficiency in Bangladesh. Food Nutr. Bull. United Nations University: 183–205. Food and Nutrition Program, Boston.

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--> Guggenheim, K. Y. 1981. Nutrition and Nutritional Diseases, pp. 265–276. Lexington, Mass.: Collamore. Habte, D. 1987. Control of vitamin A deficiency through primary health care. Report for IVACG. Washington, D.C.: Nutrition Foundation. Hayes, K. C. 1971. On the pathophysiology of vitamin A deficiency. Nutr. Rev. 29:3–6. Henning, B., K. Stewart, K. Zaman, A. N. Alam, K. H. Brown, and R. E. Black. 1992. Lack of therapeutic efficacy of vitamin A for non-cholera, watery diarrhoea in Bangladeshi children. Europ. J. Clin. Nutr. 46:437–443. KHI/DOH (Helen Keller International and Department of Health), Indonesia. 1986. Monosodium Glutamate (MSG): What Impact on Health? Jakarta, Indonesia: Helen Keller International. Hofvander, Y., and B. A. Underwood. 1987. Processed supplementary foods for older infants and young children, with special reference to developing countries. Food Nutr. Bull. UNU 9:1–7. Humphrey, J. H., K. P. West, Jr., and A. Sommer. 1992. Vitamin A deficiency and attributable mortality among under-5-year-olds. Bull. WHO 70:225–232. Humphrey, J. H., G. Natadisastra, P. Muhilal, D. S. Friedman, J. M. Tielsch, K. P. West, Jr., and A. Sommer. 1994. A 210-µmol dose of vitamin A provides more prolonged impact on vitamin A status than 105 µmol among preschool children. J. Nutr. 124:1172–1178. Humphrey, J. H., T. Agoestina, L. Wu, et al. 1996. Impact of neonatal vitamin A supplementation on infant morbidity and mortality. J. Pediatr. 128:489–496. Hussey, G. D., and M. Klein. 1990. A randomized, controlled trial of vitamin A in children with severe measles. N. Engl. J. Med. 323:160–164. India, Ministry of Health and Family Welfare. 1995. Policy on Management of Vitamin A Deficiency. Government of India, pp. 7. Government of India, Ministry of Health and Family Welfare. International Nutrition Planners Forum. 1989. Report of the Fifth International Conference of the International Nutrition Planners Forum. Crucial Elements of Successful Community Nutrition Programs. Washington, D.C.: US Agency for International Development, Bureau for Science and Technology, Office of Nutrition. IOM (Institute of Medicine). Food and Nutrition Board, Subcommittee on Tenth Edition of the RDAs. 1989. Recommended Dietary Allowances, 10th ed. Washington, D.C.: National Academy Press. Isler, O., W Huber, A. Ronco, and M. Kofler. 1947. Synthese des Vitamin A. Helv. Chim. Acta 30:1911–1927. IVACG (International Vitamin A Consultative Group). 1992. Nutrition Communications in Vitamin A Programs: A Resource Book. Washington, D.C.: The Nutrition Foundation. IVACG. 1993. Toward Comprehensive Programs to Reduce Vitamin A Deficiency. Report of the XV International Vitamin A Consultative Group Meeting, 8–12 March 1993, Arusha, Tanzania. Washington, D.C.: The Nutrition Foundation. Jalal, F. 1991. Effects of deworming, dietary fat, and carotenoid rich diets on vitamin A status of preschool children infected with Ascaris lumbricoides in West Sumatra Province, Indonesia. Ph.D. Diss., Cornell University, 1991. Jalal, F., M. C. Nesheim, Z. Agus, D. Sanjur, and J. P. Habicht. 1997. Serum retinol levels in children are effected by food sources of beta-carotene, fat intake, and antihelmintic

OCR for page 103
--> drug treatment. Division of Nutritional Sciences, Cornell University, Ithaca, New York. Jayarajahn, P., V. Reddy, and M. Mohanram. 1980. Effect of dietary fat on absorption of β-carotene from green leafy vegetables in children. Indian J. Med. Res. 71:53–56. Johns, T., S. L. Booth, and H. V. Kuhnlein. 1992. Factors influencing vitamin A intake and programmes to improve vitamin A status. Food Nutr. Bull. 14:20–33. Karim, R., M. Shahjahan, S. Begum, and I. Kabir. 1996. Integration of vitamin A supplementation with EPI program in Bangladesh: an approach to increase coverage of vitamin A administration . In Virtual Elimination of Vitamin A Deficiency: Obstacles and Solutions for the Year 2000, Report of the XVII IVACG meeting, Guatemala City, Guatemala, 1996. ILSI, Human Nutrition Institute, Washington, D.C. Kastner, P., P. Chambon, and M. Leid. 1994. Role of nuclear retinoic acid receptors in the regulation of gene expression. In Vitamin A in Health and Disease, R. Blomhoff, ed., pp. 189–238. New York: Marcel Dekker. Katz, J., S. L. Zeger, K. P. West, J. M. Tielsch, and A. Sommer. 1993. Clustering of xerophthalmia within households and villages. Intl. J. Epidemiol. 22:709–715. Katz, J., S. K. Khatry, K. P. West, J. H. Humphrey, S. C. Leclerq, E. K. Pradhan, R. P. Pohkrel, and A. Sommer. 1995. Night blindness is prevalent during pregnancy and lactation in rural Nepal. J. Nutr. 125:2122–2127. Kavishe, F. P. 1992. Development of Vitamin A Control Programs: An Example from Tanzania. Publication NU 3:21–26, International Child Health Unit, University Hospital, Uppsala, Sweden. Kavishe, F. P. 1993. Nutrition-Relevant Actions in Tanzania. UN ACC/SCN Case Study, XV Congress of the International Unity of Nutritional Sciences, Sept. 26–Oct. 1, 1993, Adelaide, Australia. Keusch, G. T., and N. S. Scrimshaw. 1986. Selective primary health care: strategies for control of disease in the developing world. XXIII. Control of infection to reduce the prevalence of infantile and childhood malnutrition. Rev. Infectious Dis. 8:273–287. Kuhnlein, H. V., and G. H. Pelto, eds. 1997. Culture, Environment and Food to Prevent Vitamin A Deficiency. Boston: International Nutrition Foundation for Developing Countries. Kuhnlein, H. V., G. H. Pelto, L. S. Blum, P. J. Pelto, and members of IUNS Committee II-6 (1992–1994). 1996. Focused ethnography for community assessment of natural food sources of vitamin A. Report of XVII International Vitamin A Consultative Group Meeting: Virtual Elimination of Vitamin A Deficiency: Obstacles and Solutions for the Year 2000, Guatemala City, Guatemala, 18–22 March 1996. Layrisse, M., J. F. Chaves, H. Mendez-Castellano, V. Bosch, E. Tropper, B. Bastardo, and E. Gonzalez. 1996. Early response to the effect of iron fortification in the Venezuelan population. Am J. Clin. Nutr. 64:903–907. Linehan, M. 1994. Assessment of Food Preservation for Vitamin A Nutrition. VITAL, USAID Vitamin A Field Support Project. Office of Nutrition, USAID, Washington, D.C. Linehan, M., K. Paddack, and M. Mansour. 1993. Solar Drying for Vitamin A. VITAL, USAID Vitamin A Field Support Project, Washington, D.C. Lotfi, M., M. G. V. Mannar, R. J. H. M. Merx, and P. Naber-van den Heuvel. 1996. Micronutrient fortification of foods. Current practices, research, and opportunities. Micronutrient Initiative, Ottawa, and International Agricultural Centre, Wageningen, The Netherlands.

OCR for page 103
--> Mahadevan, I. 1961. Belief systems in food of the Telugu-speaking people of the Telengana region. Indian J. Social Work 21:387–396. Mahalanabis, D. 1991. Breast feeding and vitamin A deficiency among children attending a diarrhoea treatment center in Bangladesh: a case-control study. Brit. Med. J. 303:493–496. Mahalanabis, D., T. W. Simpson, M. L. Chakraborty, C. Ganguli, A. K. Bhattacharjee, and K. L. Mukherjee. 1979. Malabsorption of water miscible vitamin A in children with giardiasis and ascariasis. Am. J. Clin. Nutr. 32:313–318. Mangelsdorf, D. J., K. Umesono, and R. M. Evans. 1994. The retinoid receptors. In The Retinoids, 2nd ed., M. B. Sporn, A. B. Roberts, and D. S. Goodman, eds., pp. 319–350. New York: Raven. Mariath, J. G. R., M. C. C. Lima, and L. M. P. Santos. 1989. Vitamin A activity of buriti (Mauritia vinifera Mart) and its effectiveness in the treatment and prevention of xerophthalmia. Am. J. Clin. Nutr. 49:849–853. Marinho, H. A., R. Shrimpton, R. Giugliano, and R. C. Burini. 1991. Influence of enteral parasites on the blood vitamin A levels in preschool children orally supplemented with retinol and/or zinc. Eur. J. Clin. Nutr. 45:539–544. Marsh, R. R., A. Talukder, S. K. Baker, and M. W. Bloem. 1995. Improving food security through home gardening: A case study from Bangladesh. In Technology for Rural Homes: Research and Extension Experiences. Reading, U.K.: University of Reading. Mata, L. 1992. Diarrheal disease as a cause of malnutrition. Am. J. Trop. Med. Hyg. 47(1) (Suppl):16–27. McCollum, E. V., and M. Davies. 1913. The necessity of certain lipids during growth. J. Biol. Chem. 15:167–175. Mele, L., K. P. West, Jr., Pandji A Kusdiano, H. Nendrawati, R. L. Tilden, I. Tarwotjo, and Aceh Study Group. 1991. Nutritional and household risk factors for xerophthalmia in Aceh, Indonesia: A Case-Control Study. Am. J. Clin. Nutr. 53:1460–1465. MI/Keystone Center/PAMM, et al. 1996. Sharing Risk and Reward. Public–Private Collaboration to Eliminate Micronutrient Malnutrition. Report of the Forum on Food Fortification, 6–8 December, 1995, Ottawa, Canada. Motarjemi, Y., F. Kaferstein, G. Moy, and F. Quevedo. 1993. Contaminated weaning food: a major risk factor for diarrhoea and associated malnutrition. Bull. WHO 71:79–92. Muhilal, P., A. Murdiana, I. Azis, S. Saidin, A. B. Jahari, and D. Karyadi. 1988a. Vitamin A-fortified monosodium glutamate and vitamin A status: a controlled field trial. Am. J. Clin. Nutr. 48:1265–1270. Muhilal, P., D. Permeisah, Y. R. Kdjradinata, Muherdivantiningsih, D. Karyadi. 1988b. Vitamin A-fortified monosodium glutamate and health, growth, and survival of children: a controlled field trial. Am. J. Clin. Nutr. 48:1271–1276. Muhilal, P., I. Tarwotjo, B. Kodyat, S. Herman, D. Permaesih, D. Karyadi, S. Wilbur, and J. M. Tielsch. 1994. Changing prevalence of xerophthalmia in Indonesia, 1977–1992. Euro. J. Clin. Nutr. 48:708–714. Nathan, R. 1995. Food Fortification. Legislation and Regulations Manual, 2nd ed. Program Against Micronutrient Malnutrition (PAMM), Rollins School of Public Health, Emory University, Atlanta, Georgia.

OCR for page 103
--> NAS (National Academy Sciences). 1975. Underexploited Tropical Plants with Promising Economic Value. Washington, D.C.: National Academy Press. NAS, FNB, IOM. (NAS, Food and Nutrition Board, Institute of Medicine). 1990. Nutrition During Pregnancy, Part II, Nutrient Supplements. Washington, D.C.: National Academy Press. Nestel, P. 1993. Food fortification in developing countries. VITAL/USAID, Washington, D.C. Newman, V. 1993. Vitamin A and Breastfeeding: A Comparison of Data from Developed and Developing Countries. San Diego, CA: Wellstart International. NRC (National Research Council). 1989. Lost Crops of the Incas: Little-Known Plants of the Andes with Promise for Worldwide Cultivation. Washington, D.C.: National Academy Press. Olson, J. A. 1994. Vitamins: the tortuous path from needs to fantasies. J. Nutr. 124: 1771S–1776S. Oomen, H. A. P. C., D. S. McLaren, and H. Escapini. 1964. Epidemiology and public health aspects of hypovitaminosis A. Trop. Geograph. Med. 16:271–315. Osborne, T. B., and L. B. Mendel. 1913. The relation of growth to the chemical constituents of the diet. J. Biol. Chem. 15:311–326. Parlato, M., and P. Gottert. 1996. Promoting vitamin A in rural Niger: strategies for adverse conditions. In Strategies for Promoting Vitamin A Production, Consumption, and Supplementation: Four Case Studies, R. E. Seidel, ed. Washington, D.C.: The Academy for Educational Development. Parlato, M., C. Green, and C. Fishman. 1992. Communication to Improve Nutrition Behavior: The Challenge of Motivating the Audience to Act. Paper prepared for International Conference on Nutrition, Rome, 1992. Philippines, National Nutrition Council. 1995. Vitamin A rich foods, recipes and their promotion in the Philippines. In Empowering Vitamin A Foods: A Food-Based Process for Asia and the Pacific Region, E. Wasantwisut and G. Attig, eds., pp. 91–116. Salaya, Thailand: Institute of Nutrition, Mahidol University. Phillips, M., T. Sanghvi, R. Suárez, J. McKigney, V. Vargas, and C. Wickham. 1994. The Costs and Effectiveness of Three Vitamin A Interventions in Guatemala, Final Report. Working Paper No. 2, Nutrition Cost-Effectiveness Studies, USAID, Washington, D.C. Pollard, R., and M. Favin. 1996. Social Marketing of Vitamin A in Three Asian Countries. The Manoff Group, Washington, D.C. Rahman, M. M., D. Mahalanabis, M. A. Islam, and E. Biswas. 1992. Can infants and young children eat enough green leafy vegetables from a single traditional meal to meet their daily vitamin A requirements? Europ. J. Clin. Nutr. 47:68–72. Rahman, M. M., D. Mahalanabis, J. O. Alvarez, M. A. Wahed, M. A. Islam, D. Habte, and M. A. Khaled. 1996. Acute respiratory infections prevent improvement of vitamin A status in young infants supplemented with vitamin A. J. Nutr. 126:628–633. Rahmathullah, L., B. A. Underwood, R. D. Thulasiraj, R. C. Milton, K. Ramaswamy, R. Rahmathullah, and G. Babu. 1990. Reduced mortality among children in southern India receiving a small weekly dose of vitamin A. N. Engl. J. Med. 323:929–935. Rahmathullah, L., B. A. Underwood, R. D. Thulasiraj, and R. C. Milton. 1991. Diarrhea, respiratory infections, and growth are not affected by a weekly low-dose vitamin A

OCR for page 103
--> supplement: a masked controlled field trial in children in southern India. Am. J. Clin. Nutr. 54:568–577. Reddy, V., and K. Vijayaraghavan. 1995. Carotene-Rich Foods for Combating Vitamin A Deficiency. National Institute of Nutrition, Hyderabad, India. Reddy, V., N. Raghuramullu, Arunjyoti, M. Shivaprakash, and B. Underwood. 1986. Absorption of vitamin A by children with diarrhoea during treatment with oral rehydration salt solution. Bull. WHO 64:721–724. Reddy, V., B. Underwood, S. de Pee, C. E. West, P. Muhilal, D. Karyadi, and J. G. A. J. Hautvast. 1995. Vitamin A status and dark green leafy vegetables. Lancet 346:1634–1636. Reis, T. K., R. E. Seidel, S. Sudaryono, and A. Palmer. 1996. The use of integrated media for promotion of vitamin A capsule consumption in central Java, Indonesia. In Strategies for Promoting Vitamin A Production, Consumption, and Supplementation: Four Case Studies, R. E. Seidel, ed. Washington, D.C.: The Academy for Educational Development. Rodriguez-Amaya, D. B. 1997. Carotenoids and Food Preparation: The Retention of ProVitamin A Carotenoids in Prepared, Processed, and Shared Foods. John Snow Inc./OMNI, Washington, D.C. Roodenburg, A. J. C., C. E. West, and A. C. Beynen. 1996. Iron status in female rats with different stable plasma retinol concentrations. Nutr. Res. 16:1199–1209. Rosales, F. J., and C. L. Kjolhede. 1993. Multiple high dose vitamin A supplementation. A report on five cases. Trop. Geogr. Med. 45:41–43. Ross, A. C., and C. B. Stephensen. 1996. Vitamin A and retinoids in antiviral responses. FASEB J. 10:979–985. Rukmini, C. 1994. Red palm oil to combat vitamin A deficiency in developing countries. Food Nutr. Bull. UNU 15:126–129. Scrimshaw, N. S., C. E. Taylor, and J. E. Gordon. 1968. Interactions of Nutrition and Infection. Geneva: World Health Organization. Seidel, R. E., ed. 1996. Strategies for Promoting Vitamin A Production, Consumption and Supplementation: Four Case Studies. Washington, D.C.: The Academy for Educational Development. Shaw, W. D., and C. P. Green. 1996. Vitamin A promotion in Indonesia: scaling up and targeting special needs. In Strategies for Promoting Vitamin A Production, Consumption and Supplementation: Four Case Studies, R. E. Seidel, ed. Washington, D.C.: The Academy for Educational Development. Sinha, D. P., and F. B. Bang. 1973. Seasonal variation in signs of vitamin-A deficiency in rural West Bengal children. Lancet ii: 228–231. Smitasiri, S. 1994. Nutri-Action Analysis. Going Beyond Good People and Adequate Resources. Salaya, Thailand: Institute of Nutrition, Mahidol University. Smitasiri, S., G. A. Attig, and S. Dhanamitta. 1992. Participatory action for nutrition education: social marketing vitamin A-rich foods in Thailand. Ecol. Food Nutr. 28:199–210. Smith, R. S., D. S. Goodman, M. S. Zaklama, M. K. Gabr, S. El Maraghy, and V. N. Patwardhan. 1973. Serum vitamin A, retinol-binding protein, and prealbumin concentrations in protein-calorie malnutrition. 1. A functional defect in hepatic retinol release. Am. J. Clin. Nutr. 28:973–981. Smith, R. F., R. Suskind, O. Thanangkul, C. Leitzmann, D. S. Goodman, and R. E. Olson. 1975. Plasma vitamin A, retinol-binding protein and prealbumin concentrations

OCR for page 103
--> in protein-calorie malnutrition. III. Response to varying dietary treatments. Am. J. Clin. Nutr. 28:732–738. Soekirman and F. Jalal. 1994a. Priorities in dealing with micronutrient problems in Indonesia. Proceedings of Ending Hidden Hunger (A policy conference on micronutrient malnutrition), Montreal, Quebec, October 10–12, 1991, p. 88. Soekirman and F. Jalal. 1994b. Eradicating xerophthalmia: Indonesian experience. Presentation XVI IVACG meeting, 24–28 October, Chaing Rai, Thailand, 1994. Soekirman and F. Jalal. 1996. Outline of school feeding program in poor villages in Indonesia, National Development Planning Agency (Bappenas), IOM committee meeting, 4–6 December 1996. Soekirman, Tarwotjo I., I. Jus'at, G. Sumodiningrat, and F. Jalal. 1992. Economic growth, equity and nutritional improvement in Indonesia. UN ACC/SCN country case study for XV Congress of the International Union of Nutritional Sciences, September 26–October 1, 1993 , Adelaide, Australia. Solomons, N. W., and J. Bulux. 1993. Plant sources of provitamin A and human nutriture. Nutr. Rev. 51:199–204. Solomons, N. W., and G. T. Keusch. 1981. Nutritional implications of parasitic infections. Nutr. Rev. 39:149–161. Solon, F., T. L. Fernandez, M. C. Latham, and B. M. Popkin. 1979. An evaluation of strategies to control vitamin A deficiency in the Philippines. Am. J. Clin. Nutr. 32:1443–1453. Solon F. S., M. S. Solon, H. Mehansho, et al. 1996. Evaluation of the effect of vitamin A-fortified margarine on the vitamin A status of preschool Filipino children. Europ. J. Clin. Nutr. 50:720–723. Sommer, A., and K. P. West, Jr. 1996. Infectious morbidity. In Vitamin A Deficiency, Health, Survival, and Vision, pp. 19–98. New York: Oxford University Press. Sommer, A., I. Tarwotjo, E. Djunaedi, K. P. West, A. A. Loeden, R. Tilden, L. Mele, and the Aceh Study Group. 1986. Impact of vitamin A supplementation on childhood mortality. A randomized controlled community trial. Lancet i:1169–1173. Stansfield, S. K., M. Pierre-Louis, G. Lerebours, and A. Augustin. 1993. Vitamin A supplementation and increased prevalence of childhood diarrhoea and acute respiratory infections. Lancet 341:578–582. Steenbock, H.1919. White corn vs. yellow corn and a probable relation between the fat-soluble vitamin and yellow plant pigments. Science 50:352–353. Stephensen, C. B., J. O. Alvarez, J. Kohatsu, R. Hardmeier, J. I. Kennedy, Jr., and R. R. Gammon, Jr. 1994. Vitamin A is excreted in the urine during acute infection. Am. J. Clin. Nutr. 60:388–392. Stoltzfus, R. J., M. Hakimi, K. W. Miller, K. M. Rasmussen, S. Dawiesah, J-P Habicht, and M. J. Dibley. 1993. High dose vitamin A supplementation of breast-feeding Indonesian mothers: effects on the vitamin A status of mother and infant. J. Nutr. 123:666–675. Suharno, D., C. E. West, Muhjilal, M. H. G. M. Logman, F. G. de Waart, D. Karyadi, and J. G. A. J. Hautvast. 1992. Cross-sectional study on the iron and vitamin A status of pregnant women in West Java, Indonesia. Am. J. Clin. Nutr. 56:988–993. Takahashi, Y. I., J. E. Smith, M. Winick, and D. S. Goodman. 1975. Vitamin A deficiency and fetal growth and development in the rat. J. Nutr. 105:1299–1310. Tanumihardjo, S. A., D. Permaesih, Muherdiyantiningsih, E. Rustan, K. Rusmil, A. C. Fatah, S. Wilbur, P. Muhilal, D. Karyadi, and J. A. Olson. 1996. Vitamin A status

OCR for page 103
--> of Indonesian children infected with Ascaris lumbricoides after dosing with vitamin A supplements and albendazole. J. Nutr. 126:451–457. Tielsch, J. M., and A. I. Sommer. 1994. The epidemiology of Vitamin A deficiency and xerophthalmia. Annual Review of Nutrition 4:183–205. Tilden, R. L., F. Curtale, R. P. Pokhrel, P. Muhilal, C. R. Pant, S. Pak, J. Gorstein, G. P. Pokhrel, Atmarita, J. Lepkowski, R. N. Grosse, and the Vitamin A Child Survival Project Team. 1993. Cost, Coverage, and Changes of Several Measures of Health Status Associated with Alternative Approaches to the Control of Vitamin A Deficiency in Nepal. Paper presented at the XV IVACG meeting, March 1993, Katmandu. Tilden, R. L., B. Kodyat, and P. Muhilal. 1996. Lessons Learned in the Development of the MSG Vitamin A Fortification Project. Report of the XVII IVACG meeting, 18–22 March 1996, Guatemala City, Guatemala. Trowbridge, F. L., S. S. Harris, J. Cook, J. T. Dunn, R. F. Florentino, B. A. Kodyat, M. G. V. Mannar, V. Reddy, K. Tontisirin, B. A. Underwood, and R. Yip. 1993. Coordinated strategies for controlling micronutrient malnutrition: A technical workshop. J. Nutr. 123:775–787. Underwood, B. A. 1990a. Methods for assessment of vitamin A status. J. Nutr. 120:1459–1463. Underwood, B. A. 1990b. Vitamin A prophylaxis programs in developing countries: past experiences and future prospects . Nutr. Rev. 48:265–274. Underwood, B. A. 1993. The epidemiology of vitamin A deficiency and depletion (hypovitaminosis A) as a public health problem. In Retinoids. Progress in Research and Clinical Applications, M. A. Livrea and L. Packer, eds., pp. 171–184. New York: Marcel Dekker. Underwood, B. A. 1994a. The role of vitamin A in child growth, development and survival. In Nutrient Regulation during Pregnancy, Lactation and Infant Growth, L. Allen, J. King, and B. Lonnerdahl, eds., pp. 201–208. New York: Plenum. Underwood, B. A. 1994b. Was the "anti-infective" vitamin misnamed? Nutr. Rev. 52:140–143. Underwood, B. A., and P. Arthur. 1996. The contribution of vitamin A to public health. FASEB J. 10:1040–1048. Underwood, B. A., and J. A. Olson, eds. 1993. A Brief Guide to Current Methods of Assessing Vitamin A Status. International Vitamin A Consultative Group (IVACG), The Nutrition Foundation, Washington, D.C. UNICEF (United Nations Children's Fund). 1990. First Call for Children. New York. UNICEF-Manila and Helen Keller International, Philippines. 1996. Sangkap Pinoy. The Philippine Experience in Massive Micronutrient Iintervention. Manila: UNICEF. University of Michigan, Department of Population Planning and International Health, School of Public Health. 1993. The Influence of Alternative Vitamin A Deficiency Control Strategies on Xerophthalmia Risk and Nutritional Status among Nepalese Children, 1988–1992. Final Report Vitamin A Child Survival Project. Ann Arbor, Michigan. United Nations University Food and Nutrition Bulletin. 1985. Vol. 27:1–76. Boston, Mass. van der Haar, F. 1992. Report of a Consultancy Mission to NOVIB-Sponsored Home Gardening Projects in Bangladesh. International Agricultural Centre, Wageningen, The Netherlands.

OCR for page 103
--> van Dillen, J., A. de Francisco, and W. C. G. Overweg-Plandsoen. 1996. Long-term effect of vitamin A with vaccines. Lancet 347:1705. van Vliet, T., F. V. van Schaik, H. van den Berg, and W. H. P. Schreurs. 1993. Effect of vitamin A and beta-carotene intake on dioxygenase activity in rat intestine. Ann. N.Y. Acad. Sci. 691:220–222. Venkataswamy, G., K. A. Krishnamurthy, P. Centra, S. A. Kabir, and A. Pirie. 1976. A nutrition rehabilitation centre for children with xerophthalmia . Lancet I:1120–1122. Villard, L., and C. J. Bates. 1986. Carotene dioxygenase (EC 1.13.11.21) activity in rat intestine: effect of vitamin A deficiency and of pregnancy. Brit. J. Nutr. 56:115–122. Wald, G. 1968. Molecular basis of visual excitation. Science 162:230–239. Wasantwisut, E., P. Sungpuag, V. Chavasit, U. Chittchang, S. Jittinandana, and T. Viriyapanich. 1995. Identifying and recommending vitamin A rich foods in Northeast Thailand. In Empowering Vitamin A Foods: A Food-Based Process for Asia and the Pacific Region, E. Wasantwisut and G. Attig, eds., pp. 69–89. Salaya, Thailand: Institute of Nutrition, Mahidol University. West, K. P., Jr., and A. Sommer. 1987. Delivery of Oral Doses of Vitamin A to Prevent Vitamin A Deficiency and Nutritional Blindness: A State-of-the-Art Review. ACC/SCN State-of-the-Art Series, Nutrition Policy Discussion Paper No. 2, Administrative Committee on Coordination–Subcommittee on Nutrition of the United Nations, Geneva. West, K. P., S. K. Khatry, S. C. LeClerq, R. Adhikari, L. See, J. Katz, S. R. Shrestha, E. K. Pradhan, R. P. Pokhrel, and A. Sommer. 1992. Tolerance of young infants to a single, large dose of vitamin A: a randomized community trial in Nepal. Bull. WHO 70:733–739. Wolbach, S. B., and P. R. Howe. 1925. Tissue changes following deprivation of fat-soluble A vitamin. J. Exp. Med. 42:753–780. WHO (World Health Organization). 1992. Prevention of Childhood Blindness. Geneva. WHO 1994. Using immunization contacts as the gateway to eliminating vitamin A deficiency: a policy document. WHO/EPI/GEN/94.9. Geneva. WHO. 1995a. Global prevalence of vitamin A deficiency. MDIS Working Paper #2. Geneva. WHO. 1995b. Physical Status: The Use and Interpretation of Anthropometry. Report of a WHO Expert Committee, WHO Technical Report Series 854. Geneva. WHO, Vitamin A and Pneumonia Working Group. 1995c. Potential interventions for the prevention of childhood pneumonia in developing countries: a meta-analysis of data from field trials to assess the impact of vitamin A supplementation on pneumonia morbidity and mortality. Bull. WHO 73:609–619. WHO. 1996a. Indicators for Assessing Vitamin A Deficiency and Their Application in Monitoring and Evaluating Intervention Programmes. Document WHO/NUT/96.10, World Health Organization, Geneva. WHO. 1996b. Safe Vitamin A-Dosage During Pregnancy and the First Six Months Postpartum. Report of a consultation 19–21 June 1996, World Health Organization, Geneva. WHO. 1996c. Indicators for Assessing Vitamin A Deficiency and Their Application in Monitoring and Evaluating Intervention Programs, WHO/NUT/96.10, World Health Organization, Geneva.

OCR for page 103
--> WHO/IVACG (International Vitamin Consultative Group). 1992. Using Immunization Contacts to Combat Vitamin A Deficiency. Report of a consultation, WHO Geneva, 30 June–1 July 1992. Nutrition Unit, World Health Organization, Geneva. WHO/UNICEF/ICCIDD. 1994. Indicators for Assessing Iodine Deficiency Disorders and Their Control Through Salt Iodization, WHO/NUT/94.6 Geneva: WHO. WHO/UNICEF/World Bank/Canadian International Development Agency/USAID/FAO/UNDP. 1991. Ending Hidden Hunger: A Policy Conference on Micronutrient Malnutrition. Montréal, Québec. Canada. October 10–12, 1991. Task Force for Child Survival and Development, Atlanta, Georgia. WHO/UNICEF/IVACG. In press. Vitamin A Supplements: A Guide to Their Use in the Treatment and Prevention of Vitamin A Deficiency and Xerophthalmia. World Health Organization: Geneva. WHO/UNICEF/UNU. 1997. Indicators for Assessing, and Strategies for Preventing, Iron Deficiency (WHO/NUT/96.12) Geneva: WHO. WHO/UNICEF/USAID/Helen Keller International/IVACG. 1982. Report of a Joint Meeting, Control of Vitamin A Deficiency and Xerophthalmia. Technical Report Series 672, World Health Organization, Geneva. Wolbach, S. B. 1937. The pathologic changes resulting from vitamin deficiency. J. Am. Med. Assoc. 108:7–13. Wolbach, S. B., and P. R. Howe. 1925. Tissue changes following deprivation of fatsoluble A vitamin. J. Expt. Med. 42:753–780. Wolf, G. 1996. A history of vitamin A and retinoids. FASEB J 10:1102–1107. World Bank 1993. World Development Report 1993: Investing in Health. Washington, D.C.: Oxford University Press for the World Bank. Yusuf, H. K. M., and M. N. Islam. 1994. Improvement of night blindness situation in children through simple nutrition education intervention with the parents. Ecol. Food Nutr. 31:247–256. Zeitlin, M. F., R. Megawangi, E. M. Kramer, and H. C. Armstrong. 1992. Mothers and children's intakes of vitamin A in rural Bangladesh. Am. J. Clin. Nutr. 56:136–147.

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