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*
Departments of Epidemiology, Ophthalmology and International Health, Johns Hopkins Bloomberg School of Public Health and School of Medicine, Baltimore, MD 21205 and
Office of Health, Infectious Disease and Nutrition, Bureau for Global Health, U.S. Agency for International Development, Washington, DC 20523
3To whom correspondence should be addressed. E-mail: asommer{at}jhsph.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONTHE ANNECY ACCORDSMAJOR CLARIFICATIONS AND REVISED...CONCLUSIONAPPENDIX 1APPENDIX 2LITERATURE CITED |
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KEY WORDS: • vitamin A deficiency • recommendations • assessment • control
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONTHE ANNECY ACCORDSMAJOR CLARIFICATIONS AND REVISED...CONCLUSIONAPPENDIX 1APPENDIX 2LITERATURE CITED |
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Background
The first modern series of comprehensive recommendations for the control of vitamin A deficiency (VAD) were developed at an international conference held in Jakarta, Indonesia, in 1974 (1
). These recommendations were refined and codified at the second IVACG meeting, in Port-au-Prince, Haiti, 2 y later (2
). The last comprehensive series of recommendations was issued two decades ago (3
). Since then, IVACG and other organizations have periodically issued "policy statements," "guidelines" and "recommendations" on an ad hoc basis.
After the XIX IVACG meeting in Durban, South Africa, IVACG’s Steering Committee, chaired by A. Sommer, developed a formal strategy for comprehensively reviewing issues pertinent to the control of VAD, particularly assessment tools and intervention strategies, in light of the large amount of relevant data that had become available over the past 20 y. This coincided with plans by the Food and Nutrition Board of the U.S. Institute of Medicine to issue new dietary guidelines (4
) and a decision by the World Health Organization (WHO) to convene a meeting at Yverdon-les-Bains on the appropriate use of vitamin A supplements (5
).
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THE ANNECY ACCORDS |
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TOPABSTRACTINTRODUCTIONTHE ANNECY ACCORDSMAJOR CLARIFICATIONS AND REVISED...CONCLUSIONAPPENDIX 1APPENDIX 2LITERATURE CITED |
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The IVACG Steering Committee concluded that the revised recommendations, and the rationale upon which they were based, were sufficiently important to warrant formal publication in a citable source, making the information more widely and permanently available than would a stand-alone meeting report.
The principal recommendations and conclusions, summarized below, are sufficiently concise and relevant to be of interest to policy makers and program managers. The background white papers, which are included in this supplement to the Journal of Nutrition, provide the rationale and the detailed data upon which they are based. These papers should serve the more demanding needs of scientists and technical advisors.
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MAJOR CLARIFICATIONS AND REVISED RECOMMENDATIONS |
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TOPABSTRACTINTRODUCTIONTHE ANNECY ACCORDSMAJOR CLARIFICATIONS AND REVISED...CONCLUSIONAPPENDIX 1APPENDIX 2LITERATURE CITED |
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A variety of terms have been used to characterize vitamin A status and its health effects. Three are sufficient to serve that purpose.
VAD: state of inadequate vitamin A nutriture.
It is widely accepted that VAD begins when liver stores of vitamin A fall below 20 µg/g (0.07 µmol/g). Serum retinol levels may still be within the homeostatically regulated normal range. By convention, serum retinol levels <20 µg/dL (0.70 µmol/L) are considered deficient, although in most well-nourished populations with "adequate" stores, average serum retinol levels generally exceed 30 µg/dL (1.05 µmol/L) (6
,7
).
VAD disorders (VADD): physiologic disturbances secondary to VAD.
These may be subclinical (e.g., impaired iron mobilization, disturbed cellular differentiation, depressed immune response) or clinical (increased infectious morbidity and mortality, growth retardation, anemia, xerophthalmia). VADD begins long before the onset of xerophthalmia, although the prevalence and severity of these disorders, including increased mortality, increase with the severity of deficiency (Fig. 1
) (8
,9
).
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). For the past 15 y, the nonocular, systemic manifestations of VAD have often been misleadingly referred to as "subclinical." There is nothing subclinical about death, severe infection and anemia. The term "subclinical" should be used only to describe physiologic or cellular disturbances that fit this precise, restricted definition.
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Extrapolations from the best available data suggest that 140 million preschool-aged children and >7 million pregnant women suffer from VAD every year; 1.2–3 million children and significant numbers of women die unnecessarily, and another 4.4 million children and 6.2 million women suffer from xerophthalmia (10
). Nearly half of all VAD and xerophthalmia occurs in South and Southeast Asia.
Population assessment
The purpose of population assessment is to determine the extent and severity of VAD in the population. Government officials ultimately must decide when, and at what level of severity, deficiency constitutes "a significant public health problem." In some countries, a single case of keratomalacia presenting to the hospital, or a small cluster of cases of XN, might be sufficient justification for immediate investigation and appropriate intervention. Other countries will desire more compelling, quantitative assessment. WHO and IVACG previously recommended population-based criteria that should elicit a public health response (3
,9
).
The Annecy and Hanoi Meetings rigorously reviewed candidate criteria with the view to increasing their validity, simplifying assessment and clarifying interpretation. Although the previous criteria remain valid, greater emphasis is placed on a new criterion (XN during pregnancy). Standards for the primary biochemical criterion, plasma retinol concentration, are revised to increase its reliability, and a simple, indirect marker is suggested that can indicate the need to conduct a formal, population-based assessment.
XN during pregnancy
XN during the latter part of pregnancy is exceedingly common in populations known to be vitamin A deficient by traditional criteria (11
). A woman’s history of having experienced XN at some point during her last pregnancy that resulted in a live birth (within the past 3 y) is likely to be even more accurate than questioning parents about XN in their preschool-aged children. In well-nourished populations, the prevalence of a positive history of XN during pregnancy consistently falls well below 3%. Among populations in which deficiency is a problem, the rate exceeds 5% and often 10%. The minimal prevalence criterion for VAD is therefore set at 5% (Table 2
). The prevalence of XN during a recent pregnancy can be ascertained as part of demographic and health surveys.
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The only biochemical parameter validated and found practical for routine survey use is serum retinol concentration. Even so, reliable results require rigorous techniques and attention to detail.
Because severely depressed serum retinol concentrations (e.g., 
0.35 µmol/L) are difficult to reproducibly and reliably detect in routine laboratory tests, the index has been raised to <0.70 µmol/L (20 µg/dL), double the concentration originally adopted in 1980 (3
). Because more children will have these higher levels, the prevalence criterion has been raised from >5% to >15% (Table 2)
(12
).
High-performance liquid chromatography (HPLC) is considered the only laboratory technique sufficiently reliable for routine use and reporting. When HPLC is not available, assessment should be limited to clinical criteria.
Appendix 2 details sample size selection and interpretation of prevalence criteria.
Under-five mortality rate (U5MR)
The clinical and biochemical criteria listed above (Table 2)
directly reflect vitamin A status. A surrogate indicator may alert countries that have not yet investigated the extent and severity of VAD among their population(s) that they need to do so. U5MR can serve this purpose. It is readily available for most countries and, when studied, populations of countries with high U5MR invariably prove to have significant VAD (13
).
Analyses of existing data suggest that any country (or more localized population) with U5MR >50 is likely to have a vitamin A problem unless proven otherwise. Countries with U5MR between 20 and 50 may have a problem, and its presence or absence needs to be documented.
Physiologic disturbances that can be objectively assessed, especially evidence of abnormal dark adaptation, have shown promise as potentially practical tools for population assessment (14
). They await additional field testing and experience.
Intervention programs
Dietary diversification. In theory, dietary strategies are the preferred solution to VAD in young children. But these have proved difficult to implement, and recent data and kinetic modeling indicate it is virtually impossible to correct widespread VAD by diet alone in developing countries where populations remain dependent on conventional plant-based foods.
The U.S. Institute of Medicine recently concluded that the bioavailability of provitamin A ß-carotene from plant sources is only half that previously assumed (4
). Studies in developing countries estimate that it takes 21 µg of ß-carotene from a typical mixed plant diet of vegetables and fruits and 27 µg of ß-carotene from green leafy vegetables to yield 1 µg of retinol equivalent. At these rates, it is impossible for young children to consume sufficient quantities of vegetables and seasonal fruits to overcome the inefficiencies of ß-carotene conversion. Most developing areas of the world neither produce nor consume adequate ß-carotene plant foods to achieve normal vitamin A status (15
,16
). As shown in calculated models, supplementing both mother and child is necessary to achieve near-normal vitamin A stores by 2 y of age (16
).
This is an important conclusion with immense programmatic implications. It does not mean one should not strive to maximize ß-carotene consumption by these children and their mothers. Women can eat larger quantities than can young children. Improved maternal vitamin A status will increase vitamin A concentration in breast milk, the single most important source of vitamin A for young children. Maximizing dietary vitamin A intake by children will reduce the amount that needs to be supplemented, but dietary modification is not a strategy that can normalize vitamin A status on its own.
Supplementation and fortification.
Wealthy, well nourished populations have achieved vitamin A sufficiency to a significant extent through diets that contain animal (and dairy) products rich in preformed vitamin A, usually augmented by fortification of commonly consumed dietary items and consumption of multivitamin supplements (15
,17
).
Periodic supplementation is the most widely implemented intervention for controlling VAD in the developing world. A recent WHO-sponsored multicountry study (18
) indicated that the currently recommended supplementation schedule for postpartum women and young infants is inadequate to sustain adequate (or even improved) vitamin A status among children beyond 6 mo of age. Clinical trials and kinetic modeling (16
,19
,20
) indicate that supplements in larger doses should increase vitamin A status of infants and young children at minimal risk. IVACG therefore endorses the recommendation (5
,21
) that the dosing schedule be revised as shown in Table 3
. New mothers should receive 400,000 international units (IU), split between two doses given at least 1 d apart, within 6 wk of delivery; their infants should receive 50,000 IU at 6, 10 and 14 wk (which can conveniently be given at Expanded Program on Immunization contacts). These doses are entirely safe and may reduce VADD during the first 9 mo of life, but they represent a small amount of the total vitamin A a child needs.
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). The most common problem is inadequate provision of vitamin A; rarely, if ever, is too frequent dosing a problem.
Fortification of a dietary item commonly consumed by the target group can significantly reduce the prevalence and severity of VAD. However, political, regulatory and trade barriers can prove formidable and require thoughtful attention (22
).
Genetically modified crops provide a new approach to increasing ß-carotene content and/or bioavailability of vitamin A and provitamin A carotenoids from plant foods. Early attempts to date have provided "proof of concept," but the issue requires a great deal more study and evaluation before this promising technology becomes a viable, additional intervention strategy (23
).
Whatever vitamin A intervention programs are selected, they require rigorous and repeated evaluation to ensure they are achieving their goal (24
).
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CONCLUSION |
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TOPABSTRACTINTRODUCTIONTHE ANNECY ACCORDSMAJOR CLARIFICATIONS AND REVISED...CONCLUSIONAPPENDIX 1APPENDIX 2LITERATURE CITED |
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). This XX IVACG meeting used the best available science to rationalize and simplify existing recommendations for identifying populations with VAD and dealing effectively with the problem. It is hoped that these recommendations will prove even more practical and helpful than those they replace and make for more effective and efficient control programs.
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APPENDIX 1 |
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TOPABSTRACTINTRODUCTIONTHE ANNECY ACCORDSMAJOR CLARIFICATIONS AND REVISED...CONCLUSIONAPPENDIX 1APPENDIX 2LITERATURE CITED |
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Participants in Annecy workshop, Les Pensieres, Fondation Marcel Mérieux, October 30 to November 2, 2000
Participants at concluding session only (November 2, 2000)
Additional participants at Annecy follow-up session (February 11, 2001, Hanoi)
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APPENDIX 2 |
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TOPABSTRACTINTRODUCTIONTHE ANNECY ACCORDSMAJOR CLARIFICATIONS AND REVISED...CONCLUSIONAPPENDIX 1APPENDIX 2LITERATURE CITED |
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Prevalence surveys are a proven approach to assessing the vitamin A status of a defined population. The population of interest may be a group of villages, a region, a province or an entire nation. Given geographic variations in dietary practices, weather patterns and infectious diseases, vitamin A status may vary considerably within a single political entity.
Ideally, surveys will be targeted to areas at highest risk, with sufficient numbers of participants to detect significant deficiency in localized populations. A cluster of significant deficiency needs to be identified and acted upon, even if other defined groups are better nourished and pooled prevalence rates for the country as a whole do not exceed the recommended prevalence criteria for a significant problem.
Sample size requirements The number of individuals who need to be surveyed (e.g., sample size) for each defined population of interest depends on the certainty with which one wishes to be able to detect deficiency (if it exists), the prevalence rate established as the criterion and the actual rate in that population (e.g., the rate you would find if you examined every eligible person, instead of a sample of the population).
Table 4
provides an estimate of the number of individuals who need to be examined to have an 80% likelihood of exceeding the recommended prevalence criterion if the actual rate among all eligible participants is "somewhat" or "considerably" greater. For a 90% probability of detecting rates that exceed the prevalence criterion, the number of participants needed (sample size) is larger.
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). Government officials and others considering conducting population assessment surveys will decide which criterion is most useful, which is most practical, and the number and size of the population units for which they would like to estimate vitamin A status (e.g., for each village, district or province, or for the country as a whole). A survey of the required sample size needs to be conducted for each defined population of interest. For example, if information is desired for each of a country’s 12 districts, then an adequate sample size is needed for each of the 12 districts (e.g., 418 children ages 2–5 y from each of the 12 districts if childhood XN is chosen as the prevalence criterion).
Although any appropriate sample size might be selected, for the purposes of simplicity and practicality, the following guidelines are suggested (Table 5
).
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2. For the serum retinol criterion, at least 60 children should be studied. The prevalence of serum retinol <0.7 µmol/L in affected childhood populations generally exceeds 25%.
3. For XN during a recent pregnancy, 130 women who delivered a live birth within the past 3 y should be included, because the rates in most countries studied usually exceed 7.0%.
As with any sample survey, every effort must be made to ensure that the sample selected is representative of the entire defined population it is meant to reflect.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Supported by U.S. Agency for International Development Cooperative Agreement HRN-A-00-97-00015-00, Sight and Life Research Institute and the Bill and Melinda Gates Foundation.
4 Abbreviations used: HPLC, high-performance liquid chromatography; IU, international unit; IVACG, International Vitamin A Consultative Group; U5MR, under-five mortality rate; UNICEF, United Nations Children’s Fund; USAID, U.S. Agency for International Development; VAD, vitamin A deficiency; VADD, VAD disorders; WHO, World Health Organization; X1B, Bitot’s spots; XN, night blindness.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONTHE ANNECY ACCORDSMAJOR CLARIFICATIONS AND REVISED...CONCLUSIONAPPENDIX 1APPENDIX 2LITERATURE CITED |
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1. WHO/USAID (1976) Vitamin A deficiency and xerophthalmia: report of a joint WHO/USAID meeting. WHO Technical Report Series 590 1976 World Health Organization Geneva, Switzerland. .
2. International Vitamin A Consultative Group (1976) Guidelines for the eradication of vitamin A deficiency and xerophthalmia: a report of the International Vitamin A Consultative Group (IVACG) 1976 The Nutrition Foundation Washington, DC. .
3. WHO/UNICEF/USAID/Helen Keller International/IVACG (1982) Control of vitamin A deficiency and xerophthalmia: report of a joint WHO/UNICEF/USAID/Helen Keller International/IVACG meeting. WHO Technical Report Series 672 1982 World Health Organization Geneva, Switzerland. .
4. Food and Nutrition Board, Institute of Medicine (2001) Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc: Panel on Micronutrients, Subcommittees on Upper Reference Levels of Nutrients and of Interpretation and Use of Dietary Reference Intakes and the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes 2001 National Academy Press Washington, DC. .
5. De Benoist, B., Martines, J. & Goodman, T. (2001) Food and Nutrition Bulletin: Special Issue on Vitamin A Supplementation and the Control of Vitamin A Deficiency. Vol. 22, No. 3 2001 The United Nations University Press New York, NY. .
6. Ballew, C., Bowman, B. A., Sowell, A. L. & Gillespie, C. (2001) Serum retinol distributions in residents of the United States: Third National Health and Nutrition Examination Survey, 1988–1994. Am. J. Clin. Nutr. 73:586-593.
7. Olmedilla, B., Granado, F., Southon, S., Wright, A. J., Blanco, I., Gil-Martinez, E., van den Berg, H., Corridan, B., Roussel, A., Chopra, M. & Thurnham, D. I. (2001) Serum concentrations of carotenoids and vitamins A, E, and C in control subjects from five European countries. Br. J. Nutr. 85:227-238.[Medline]
8. Sommer, A. (1997) Clinical research and the human condition: moving from observation to practice. Nat. Med. 10:1061-1063.
9. Sommer, A. & West, K. (1996) Vitamin A Deficiency: Health Survival and Vision 1996 Oxford University Press New York, NY. .
10. West, K. P. (2002) Extent of vitamin A deficiency among preschool children and women of reproductive age. J. Nutr. 132:2857S-2866S.
11. Christian, P. (2002) Recommendations for indicators: night blindness during pregnancy—a simple tool to assess vitamin A deficiency in a population. J. Nutr. 132:2884S-2888S.
12. dePee, S. & Dary, O. (2002) Biochemical indicators of vitamin A deficiency: serum retinol and serum retinol binding protein. J. Nutr. 132:2895S-2901S.
13. Schultink, W. (2002) Use of under-five mortality rate as an indicator for vitamin A deficiency in a population. J. Nutr. 132:2881S-2883S.
14. Congdon, N. & West, K. P. (2002) Physiologic indicators of vitamin A status. J. Nutr. 132:2889S-2894S.
15. West, C. E., Eilander, A. & van Lieshout, M. (2002) Consequences of revised estimates of carotenoid bioefficacy for dietary control of vitamin A deficiency in developing countries. J. Nutr. 132:2920S-2926S.
16. Miller, M., Humphrey, J., Johnson, E., Marinda, E., Brookmeyer, J. & Katz, J. (2002) Why do children become vitamin A deficient?. J. Nutr. 132:2867S-2880S.
17. Berner, L. A., Clydesdale, F. M. & Douglas, J. S. (2001) Fortification contributed greatly to vitamin and mineral intakes in the United States, 1989–1991. J. Nutr. 131:2177-2183.
18. WHO/CHD Immunisation-Linked Vitamin A Supplementation Study Group (1998) Randomised trial to assess benefits and safety of vitamin A supplementation linked to immunisation in early infancy. Lancet 352:1257-1263.[Medline]
19. Ross, D. A. (2002) Recommendations for supplementation. J. Nutr. 132:2902S-2906S.
20. Allen, L. H. & Haskel, M. (2002) Estimating the potential for vitamin A toxicity in women and young children. J. Nutr. 132:2907S-2919S.
21. World Health Organization (2000) Report of an Informal Consultation on Vitamin A Supplementation, Yverdon-les-Bains, Switzerland 2000 World Health Organization Geneva, Switzerland. .
22. Dary, O. & Mora, J. O. (2002) Food fortification to reduce vitamin A deficiency: IVACG recommendations. J. Nutr. 132:2927S-2933S.
23. Toenniessen, G. H. (2002) Crop genetic improvement for enhanced human nutrition. J. Nutr. 132:2943S-2946S.
24. Wasantwisut, E. (2002) Recommendations for monitoring and evaluation of vitamin A programs: outcome indicators. J. Nutr. 132:2940S-2942S.
25. Reddy, V. (2002) History of the International Vitamin A Consultative Group (IVACG), 1975–2000. J. Nutr. 132:2852S-2856S.
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