Newsletter 02 2006.pdf - Sight and Life

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SIGHT AND LIFE 16 NEWSLETTER 2/2006 methods may be used to introduce a nutrient otherwise absent, increase nutrient density above that achievable by cross-breeding, or insert favorable agronomic traits (e.g. disease resistance or increased yield). The advantage of biofortification is that staple crops grown and consumed by the poor can be enriched with micronutrients and be available harvest after harvest without added cost. β-carotene enriched crops currently being pursued include maize, cassava and sweet potato by traditional cross-breeding and rice by transgenic technology. Golden Rice produced by Syngenta (SGR1) is the most publicized example using genetic manipulations to introduce genes to overcome the impediment to synthesis of β-carotene. Carotene enrichment of the original product was not impressive. It was about 1.6 µg/g rice, which carried limited potential for making significant contributions to vitamin A requirements in spite of heroic claims to the contrary. Announcement in 2005 of Golden Rice #2 (SGR2) changed the potential: SGR2 contains 31 µg/g β-carotene (57). This is equivalent to 1033 µg RAE in 400 g uncooked, milled rice (an adult male serving size of ~800 g cooked rice daily) and 516 µg RAE in 200 g uncooked, milled rice (an estimated serving size of 400 g cooked rice daily for a child > 3 years). These calculations assume 12:1 conversion efficiency for β-carotene to vitamin A. However, feeding tests to estimate bioequivalence have not been reported to date. Nonetheless, factoring in an approximate 20% loss during cooking, 826 µg RAE would remain for an adult and 413 µg RAE for a child. SGR2, therefore, could nearly meet the RDA across ages if the daily diet contained 800 g and 400g of cooked rice eaten by adults and children, respectively. SGR2 is an example of using transgenic technology to introduce or improve carotenoids, particularly provitamin A, in staple crops grown and/or eaten by the poor, such as cassava and maize. There remains much research to be completed before such carotenoid enriched crops are available for public consumption. Bioavailability must be determined from the biofortified crops prepared for consumption by traditional cooking procedures. Equally important is gaining acceptance by consumers skeptical of transgenically produced food crops and of more intensely colored traditional crops. Biofortification, however, is not restricted to use of transgenic technology. There is potential through traditional crossbreeding of germ plasma from varieties with higher nutrient density and other desired agronomic qualities. Perhaps the most advanced example in carotenoid-containing food plants is orange-fleshed sweet potato (OFSP) varieties. Although white sweet potato is the common staple eaten in many African countries, yelloworange varieties do exist in many countries. One particular orange variety (Resisto) has already been evaluated in a feeding trial among primary school children in South Africa and found to be acceptable and to improve vitamin A status (58). Some question whether vitamin A status can be maintained in a population using OFSP-based strategies. Jan Low recently completed a community intervention trial that found OFSP an acceptable substitute for white-fleshed sweet potato in Mozambique (59). An integrated agriculturedemand creation-market development approach was implemented to introduce OFSP into intervention areas compared with a control community not provided OFSP vines. The 24-month study provided high-dose vitamin A capsules to all children at baseline and six months, a placebo in the intervention areas at 12 months, and a high-dose capsule after specimen collection at 24 months. Hence, for 12 months, no children in either the intervention or control areas received a vitamin A capsule. The difference was that only children in the intervention areas were exposed to OFSP and an intensive campaign to promote its consumption. At the end of the 12 month period, a significant difference was seen in the percentage of children with a serum retinol level less than 0.7 µmol/l in the intervention groups, both before and after accounting for infection. Thus, vitamin A deficiency was reduced up to 24% among healthy children and 16% among those with evidence of infection. There were several other positive spin-offs from this integrated intervention, such as a substantial increase in knowledge of men and women, an increase in income for smallscale producers and an increase in daily caloric intake of the children, as well as the intake of other micronutrients in the OFSP. Biofortification of staple crops with micronutrients, including provitamin carotenoids, is still early in development. Yellow cassava, maize and banana/plantain are in the developmental stages. There is much research remaining to pair the best nutrient content with most desirable agronomic traits, bioavailability from products as consumed, consumer acceptance and economic advantages among other outstanding issues. Nonetheless, a comparison of bio-fortification with fortification and supplementation clearly shows the complementary benefits of each intervention and the potential in the long run of meeting the needs of the poor economically and safely through food, reserving high-dose supplementation for medical emergencies.
NEWSLETTER 2/2006 17 SIGHT AND LIFE Conclusions Advances in understanding basic chemistry and functions of retinoids and carotenoids have been remarkable over the past four decades. This has paralleled progress in programs to control vitamin A deficiency through medical (supplement distribution) and market-based (food fortification) approaches. Progress has also occurred in public health programs to control immunilizable infectious diseases that drain body nutrient reserves, although there remain an estimated 1.1 billion people without safe water. Whereas little attention was given to food-based approaches until recently, the future is promising due to breakthroughs that have occurred and are on the horizon for increasing carotenoids and other micronutrient densities in staple crops eaten by the poor and in improving other agronomic characteristics that enhance yields through biofortification. For carotenoid chemists and program enthusiasts, the research opportunities are multiple to demonstrate, for example, bioavailability, cooking and preservation stability, acceptability, economic gains and biological effectiveness of these crops in contributing to control of micronutrient deficiencies, especially among the poor. References 1. Proceedings of Symposium on Vitamin A and Metabolism, Bürgenstock, Switzerland, May, 1960. Vitamins and Hormones 18: 289, 1960. (Cited by Roels OA. The fifth decade of vitamin A research. Am J Clin Nutr 22:903–7, 1969) 2. Wolf G (1978). A historical note on the mode of administration of vitamin A for the cure of night blindness. J Clin Nutr 31:290–2. 3. McCollum EV & Davis M (1913). The necessity of certain lipids in the diet during growth. J Biol Chem 15:167–75. 4. Osborne TB & Mendel LB (1913). The relation of growth to the chemical constituents of the diet. J Biol Chem 15:311–26. 5. Steenbock H (1919). White corn vs yellow corn and a probable relationship between the fat soluble vitamins and yellow plant pigments. Science 50: 352. 6. Karrer P, Morf R, & Schöp K (1931). Helv Chim Acta 14: 1431–6. 7. Wald G (1939). The porphyropsin visual system. J. General Physiology 22:775– 794. 8. Wolf G (2001). The discovery of the visual function of vitamin A. J Nutr 131:1647– 1650. 9. Dowling JE & Wald G (1960). The biological function of vitamin A acid. Proc. National Acad. Sci 56:587–608. 10. Stephenson M, Clark AB (1920). XLII. A contribution to the study of keratomalacia among rats. Biochem J 14: 502–521. 11. Roels OA (1968). The fifth decade of vitamin A research. Am J Clin Nutr 22:903–907. 12. Bessey OA, Lowry OH, Brock MJ & Lopez JA (1946). The determination of vitamin A and carotene in small quantities of blood serum. J Biol Chem 1:177–187l. 13. Neeld JB & Pearson WN (1963). Macroand micromethods for the determination of serum vitamin A using trifluoroacetic acid. J Nutr 70: 454–462. 14. Carr FH & Price EA (1926). Colour reactions attributed to vitamin A. Biochem J 20:497–501. 15. Sebrell W H, Jr (1959). Program of the Columbia University Institute of Nutrition Sciences. J Am Med Assoc 170: 1928–9. 16. Mason JB, Lotfi M, Dalmiya N, et al. (2001). The Micronutrient Report. Micronutrient Initiative, Ottawa, Ontario, Canada. 17. WHO (1995). Global Prevalence of Vitamin A Deficiency. MDIS Working Paper #2, World Health Organization, Geneva, Switzerland. 18. Micronutrient Initiative/UNICEF (2005). Vitamin/Mineral Deficiency. A Global Progress Report. 19. West KP, Jr. Katz J, Khatry SK, LeClerq SC, Pradhan EK, Shrestha SR, Connor PB, Dali SM, Parul C, Pokhrel RP, Sommer A on behalf of the NNIPS-2 Study Group (1999). Double blind, cluster randomized trial of low dose supplementation with vitamin A or β-carotene on mortality related to pregnancy in Nepal. Brit Med J 318:570–5. 20. Furr HC (2004). Analysis of retinoids and carotenoids: problems resolved and unsolved. J Nutr 134:281S–285S. 21. Congdon N, Sommer A, Severns M. et al. (1995). Pupillary and visual thresholds in young children as an indicator of population vitamin A status. Am J Clin Nutr 61:1076–82. 22. Craft NE (2001). Innovative approaches to vitamin A assessment. J Nutr 131:1626S– 1630S. 23. Haskell MJ, Mazumder RN, Peerson JM, Jones AD, Wahed MA, Mahalanabis D & Brown KH (1999). Use of the deuteratedretinol-dilution technique to assess totalbody vitamin A stores of adult volunteers consuming different amounts of vitamin A. Am J Clin Nutr 70:874–80. 24. Tang G, Qin J, Dolnikowski G, Russell R, & Grusak MA (2005). Spinach or carrots can supply significant amounts of vitamin A as assessed by feeding with intrinsically deuterated vegetables. Am J Clin Nutr 82:821–8. 25. Olson JA & Hayaishi O (1965). The enzymatic cleavage of β-carotene into vitamin A by soluble enzymes of rat liver and intestine. Proc Natl Acad Sci, US 54:1364. 26. Goodman DS & Huang HS (1965). Biosynthesis of vitamin A with rat intestinal enzymes. Science 149: 879. 27. Goodman DS & Blaner WS (1984). Biosynthesis, absorption and hepatic metabolism of retinol. In: The Retinoids, Vol 2. Eds: Sporn MB, Roberts AB & Goodman DS, pp. 2–39. New York: Academic Press, Inc., 28. Goodman DS, (1984). Plasma retinolbinding protein. In: The Retinoids, Vol. 2. Eds: Sporn MB, Roberts AB & Goodman DS. pp. 42–88. New York: Academic Press, Inc. 29. Loerch J, Underwood B & Lewis K (1979). Response of plasma levels of vitamin A to a dose of vitamin A as an indicator of hepatic vitamin A reserves in rats. J Nutr 109:778–86. 30. Tanumihardjo SA, Furr HC, Erdman JW, Jr & Olson JA (1990) Use of the modified relative dose response (MRDR) assay in rats and its application to humans for the measurement of vitamin A status. Eur J Clin Nutr 44:219–24. 31. Oomen HAPC, McLaren DS, Escapini H (1964). Epidemiology and public health aspects of hypovitaminosis A. A global survey on xerophthalmia. Trop Geograph Med 16:271–315. 32. McCormick AM, Napoli JL & DeLuca HF (1978). High-pressure liquid chromatographic resolution of vitamin A compounds. Anal Biochem 86:25–33. 33. Roberts AB, Nichols MD, Frolik CA, Newton DL & Sporn MB (1978). Assay of retinoids in biological samples by reversephase high-pressure liquid chromatography. Cancer Res 38:3327–32. 34. Report of a Joint WHO/USAID meeting (1976). Vitamin A deficiency and xerophthalmia. Tech Rept Ser 590. World Health Org., Geneva. 35. Underwood B (2004). Vitamin A deficiency disorders: International efforts to control a preventable “pox”. J Nutr 134: 231S–236S. 36. McLaren DS (1987). A decade of achievement: The International Vitamin A Consultative Group (IVACG) 1975–1985. International Life Science Institute-Nutrition Foundation, Washington, D.C. 37. WHO/UNICEF/USAID/Helen Keller International/IVACG (1982). Control of vitamin A deficiency and xerophthalmia. Tech Rept Ser 672, World Health Organization, Geneva. 38. Chambon P (1996). A decade of molecular biology of retinoic acid receptors. FASEB J 10:940–54. 39. Sommer A (1982). Nutritional Blindness. New York: Oxford University Press, Inc. 40. Sommer A, Tarwotjo L, Djunadi E, West KP, Loeden AA, Tilden R, Mele L & Aced study group (1986). Impact of vitamin A supplementation on childhood mortality. A randomized controlled community trial. Lancet 327:1169–73. 41. Sommer A & West KP, Jr (1996). Vitamin A Deficiency Health, Survival, and Vision. New York: Oxford University Press, Inc., pp 438. 42. West KP, Jr, Pokhrel RP, Katz J, LeClercq SC, Khatry SK, Shrestha SR, Pradhan EK, Tielsch JM, Pandey MR, Sommer A (1991). Efficacy of vitamin A in reducing preschool child mortality in Nepal. Lancet 338:67–71. 43. Ghana Vast Study Team (1993). Vitamin
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