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Access to nutritious food by poor people is being increasingly hindered by the failure of the food security system, and diminishing real income value, in most African countries undergoing Structural Adjustment Programme. Hence, nutritional disorders such as protein energy malnutrition, xerophthalmia, anaemia, low birth weight, stunting and wasting are on in the increase. Although soybean is used in quite a number of African countries as a weaning food, there are still problems such as lack of technical know-how for its processing into infant foods, cultural practices which favour the use of cereal rather than legumes for weaning infants and the long cooking time. In spite of this, the prospects for the crop as infant food is becoming brighter, and some ways of achieving this are discussed.
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PMID:Use, problems and prospects of soybean in infant weaning practices in Africa. 176 13

A total of 6636 children, aged from 6 months to 6 years and selected throughout the country using a multi-staged stratified sample design, were examined for signs of xerophthalmia. The concentrations of retinol and of beta-carotene were measured in 742 children, including those with xerophthalmia and every twentieth of the remaining children. Anthropometric measurements were made on 2909 of the children. Bitot's spots were seen in 1.0% of all children, with a higher prevalence in the pastoral (1.6%) and cropping (1.1%) agro-ecological zones than in the zones characterized by cash crops (0.4%) and 'ensete' (false banana, Ensete ventricosum) (0.0%). One case of corneal xerosis and 2 cases of corneal scar were also seen. Serum retinol levels were in the 'deficient' range (less than 0.35 mumol l-1) in 16% and 'low' (0.35-0.69 mumol l-1) in 44% of children. Serum retinol and clinical signs did not show any correlation with occupation and education of head of household, household size or anthropometric measurements. More stunting than wasting was observed, with peak prevalence of these signs of malnutrition being observed in the second year of life.
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PMID:Xerophthalmia in Ethiopia: a nationwide ophthalmological, biochemical and anthropometric survey. 178 18

Twelve to sixteen weeks following treatment of CF-1 mice with a vitamin A-deficient diet, characteristic signs of retinoid deficiency including body wasting, poor hair coat, altered gait, decreased mobility, and xerophthalmia were observed. Histological examination of tissue sections from these mice revealed dramatic changes in the urinary tract epithelium. The normal transitional epithelium was replaced by a stratified squamous epithelium that resembled hyperproliferative epidermis. Using two-dimensional gel electrophoresis, a number of new proteins were found to be synthesized in vitamin A-deficient bladder when compared to tissue from control bladders. Using antikeratin antibodies in immunoblot experiments, we found that at least some of the newly synthesized proteins were keratins. These proteins, which comprise the intermediate filaments of the cytoskeleton, are known to be specific markers of epithelial differentiation. Of particular interest was the appearance of a Mr 67,000 basic and Mr 61,000 acidic keratin pair, characteristic of terminally differentiating murine epidermal cells. Unexpectedly, several other keratins, previously associated only with hyperproliferative epidermis, were also expressed in the tissue. These results demonstrate that vitamin A deficiency in the mouse leads to the appearance of a squamous metaplasia in the urinary tract epithelium that is characterized by the expression of distinct epidermal keratins.
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PMID:Effect of retinoid deficiency on keratin expression in mouse bladder. 245 26

An average of 3481 preschool-age rural Indonesian children were re-examined every 3 months for 18 months. The mortality rate among children with mild xerophthalmia (night blindness and/or Bitot's spots) was on average 4 times the rate, and in some age groups 8 to 12 times the rate, among children without xerophthalmia. Mortality increased, almost linearly, with the severity of mild xerophthalmia (night blindness, Bitot's spots, and the two combined). These relations persisted after stratification for respiratory disease, wasting, gastroenteritis, pedal oedema, and childhood exanthems. Mild vitamin A deficiency was directly associated with at least 16% of all deaths in children aged from 1 to 6 years. These results suggest that mild xerophthalmia justifies vigorous community-wide intervention, as much to reduce childhood mortality as to prevent blindness, and that night blindness and Bitot's spots are as important as anthropometric indices in screening children to determine which of them need medical and nutritional attention.
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PMID:Increased mortality in children with mild vitamin A deficiency. 613 44

In late 1988 in Ethiopia, a physician and a nutritionist examined 240 registered children in the village of Melkaye (Farmers' Association No. 34) in Darolobo District of Habro Province for vitamin A deficiency. These children had been dependent on food aid because of consistent drought and crop failures since, at least, 1982. The food aid, which was the main food source, included food deficient in vitamin A and beta-carotene: wheat flour, vegetable oil, butter-oil, and beans. 53.2% of the boys and 43.1% of the girls had at least 1 sign of vitamin A deficiency, especially night blindness, an early manifestation of vitamin A deficiency. 28.8% of all children had night blindness without signs of xerophthalmia compared with the WHO cut-off point of 1%. (The cut-off point is used to determine the public health significance of vitamin A deficiency.) 6.7% had Bitot's spots compared with a cut-off point of 0.5%. 7.1% had corneal xerosis/ulceration compared with a cut-off point of .01%. 5.8% had corneal scars compared with a cut-off point of .05%. 30.2% had a serum retinol level less than .35 mcmol/l compared with a cut-off point of 5%. 17 of 70 children (24.3%) who had died in the last 2 years had ruptured or damaged eye(s). The median levels of serum retinol-binding protein, iron, transferrin saturation, and ferritin were lower than normal levels. On the other hand, parameters of iodine status, total triiodothyronine, and total thyroxine and thyrotropin were all normal. 78.8% and 82.4% of the children experienced high levels of IgG and IgM, respectively. 42.4% had high C-reactive protein levels. Wasting was more common than stunting (33% vs. 10%). 8% suffered from both stunting and wasting. The severity of xerophthalmia was perhaps the most severe ever recorded and prompted health workers to distribute vitamin A capsules to all children in Melkaye and nearby villages.
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PMID:Severe vitamin A deficiency in a rural village in the Hararge region of Ethiopia. 843 88

In 1989, in the Republic of Kiribati, two teams consisting of an ophthalmologist, a nurse, two field officers, and two village welfare group members conducted a population-based cross-sectional xerophthalmia survey among 4619 children aged 6-72 months living in the northern atolls of South Tarawa, Abaiang, and Butaritari and the southern atolls of Tabiteuea North, Nonouti, and Abemama. The study aimed to identify risk factors for xerophthalmia in Kiribati. Kiribati has among the highest xerophthalmia rates in the world. 666 children had xerophthalmia, while 816 children did not. The multivariable logistic regression (controlling for age and sex) revealed that significant independent risk factors for xerophthalmia were diarrhea (odds ratio [OR] = 1.45) and wasting (OR = 3.07 for mild wasting; OR = 3.55 for moderate wasting; OR = 3.82 for severe wasting). Factors associated with a protective effect against xerophthalmia included breast feeding (OR = 0.3), consumption of foods rich in vitamin A (OR = 0.93), and presence of a garden project of the Foundation for the Peoples of the South Pacific in the village (OR = 0.7). When the researchers controlled for age, sex, breast feeding status, diarrhea, protein-energy malnutrition, frequency of consumption of foods rich in vitamin A, and the presence of a village garden project, the association between measles and corneal xerophthalmia persisted (OR = 7.73). These findings suggest that greater availability and consumption of foods rich in vitamin A reduces the risk of xerophthalmia among preschool children.
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PMID:Risk factors for xerophthalmia in the Republic of Kiribati. 893 24

Inconsistencies have been observed in the impact of vitamin A (VA) supplementation on early child growth. To help clarify this issue, a cohort of 3377 rural Nepalese, nonxerophthalmic children 12-60 mo of age were randomized by ward to receive vitamin A [60,000 microg retinol equivalents (RE)] or placebo-control (300 RE) supplementation once every 4 mo and followed for 16 mo. VA had no impact on annual weight gain or linear growth. However, arm circumference (AC) and muscle area (MA) growth improved in VA recipients, by 0.13 cm and 25 mm2, respectively, over controls. Growth of children with xerophthalmia, who were treated with >/= 120, 000 RE at base line, was also compared to that of nonxerophthalmic children, stratified by initial wasting status, and adjusted for sex, baseline age and measurement status. Among initially nonwasted children (AC >/= 13.5 cm), VA-treated xerophthalmic children (n = 86) gained 0.7 cm more in linear growth than nonxerophthalmic children. Among initially wasted children (AC < 13.5 cm), VA-treated children (n = 34) gained additional weight (672 g), height (approximately 1 cm), muscle (76 mm2) and fat (79 mm2) areas, and subscapular skinfold (1.3 mm) compared to changes observed in nonxerophthalmic children. Relative increments in soft tissue growth occurred within 4 mo of VA treatment, while the effect on linear growth was gradual. Moderate-to-severe VA deficiency, marked by xerophthalmia, is likely to impair normal physical growth, but milder stages of deficiency may not have this effect in rural South Asia.
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PMID:Effects of vitamin A on growth of vitamin A-deficient children: field studies in Nepal. 931 51

Two approaches to improve vitamin A nutriture are compared: nutrition education and mega-dose capsule distribution. The impact of these programmes on vitamin A deficiency (VAD), wasting malnutrition, and excessive childhood mortality are compared for approximately 40,000 children who were assigned to either intervention cohorts or a control group from 75 sites within seven districts in two ecological settings (Terai, or lowland, and hills) of Nepal. Twenty-four months after the implementation of the project, the reduction of risk of xerophthalmia was greater among children of mothers who were able to identify vitamin A-rich foods [relative risk (RR) = 0.25; 95% CI = 0.10-0.62] than among children who received mega-dose capsules (RR = 0.59; 95% CI = 0.41-0.84). The risk of mortality at two years was reduced for both the nutrition education cohort (RR = 0.64; 95% CI = 0.48-0.86) and capsule distribution cohort (RR = 0.57; 95% CI = 0.42-0.77). The nutrition education program, however, was more expensive to deliver than the capsule distribution programme. High rates of participation in the supplementation programme were achieved within a short period. The nutrition education message spread rapidly throughout the study population, although practice was slower to change. Where maternal literacy was low and channels of communication were limited, the capsule programme appeared to be more cost-effective. However, economies of scale for nationwide programmes exist for nutrition education programmes that do not exist for capsule distribution programmes. A comprehensive national programme requires both dietary supplementation and nutrition education.
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PMID:Nutrition education and mega-dose vitamin A supplementation in Nepal. 1077 3

Vitamin A deficiency is a major controllable nutritional problem in developing countries. It is estimated that 30-40,000 children in India, may lose their eye-sight because of vitamin A deficiency. The drying of conjunctiva and cornea may lead to ulceration, which causes permanent scarring or irreversible damage and blindness. Xerophthalmia occurs when the body stores of vitamin A are exhausted owing to low dietary intake of vitamin A rich foods or interference in absorption of retinol in the body. Symptoms of xerophthalmia are night blindness; Bitot's spots; and corneal xerosis/ulceration. If the xerosis is not treated, it can progress within hours to an ulcer in the cornea. If not treated, a corneal ulcer can lead to wasting of the cornea or keratomalacia which can lead to a corneal scar. The National Prophylaxis Program against Blindness due to Vitamin A Deficiency was started in 1970 in 7 states. The Program today covers 30 million children under 5 years of age and utilizes the short-term strategy of administering a megadose of vitamin A solution periodically to children under 5 years of ages; and the long term promotion of dietary intake of vitamin A. The program is not extended to cover children 6-11 months and is proposed for 6-months to 3-year old children. The ultimate solution for the prevention of vitamin A deficiency lies in educating people to eat food rich in vitamin A. Breast feeding will protect children from vitamin A deficiency during the first 6 months. From the age of 4-6 months, it is crucial to introduce semisolid foods containing vitamin A such as dark green and yellow leafy vegetables and fruits, and to ensure adequate intake of vitamin A by preschool children, and pregnant and lactating women. The implementation of the national program can be achieved only by training the health delivery team and the functionaries of the Integrated Child Development Services Program and by a high level of community awareness.
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PMID:Vitamin A deficiency in India. 1228 94

A child responds to a deficiency of an essential nutrient either by continuing to grow and consuming body stores with eventual reduction in the bodily functions (Type I) or by reducing growth and avidly conserving the nutrient to maintain the concentration of the nutrient in the tissues (Type II). Examples of Type I nutrient deficiency are anemia (iron deficiency), beri-beri (thiamin deficiency), pellagra (niacin or nicotinic acid deficiency), scurvy (vitamin C or ascorbic acid deficiency), xerophthalmia (vitamin A or retinol deficiency) and iodine deficiency disorders. Diagnosis is relatively simple via clinical symptoms and measurement of the concentration of the nutrient itself. There are no characteristic symptoms to distinguish which Type II nutrient deficiency an individual has; all deficiencies result in the poor growth, stunting, and wasting generally ascribed to protein-energy malnutrition. In Type II, growth stops, the body starts to conserve the nutrient, and its excretion falls to very low levels. In severe deficiency the body may start to break down its own tissues and the reduction of appetite accompanies this condition. An animal can die from zinc deficiency even though it is has a normal concentration of zinc in its tissues, but it can respond rapidly to small amount of dietary zinc. The mechanisms by which the body stops growing in response to nutritional lack are similar to the hormonal picture seen in endocrine disease (reduction of the production of the hormonal mediators of growth, down-regulation of receptors, and reduction of protein synthesis). Growth failure is the clinical sign characteristic of a diet deficient in protein, zinc, magnesium, phosphorus, and potassium. Wasting may be also ascribed to toxins, infection, worms, or persistent diarrhea. Anorexia is another common response in nutrient deficiency. Only a supplementation diet with a balance of nutrients will promote rapid recovery.
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PMID:Specific deficiencies versus growth failure: type I and type II nutrients. 1234 13


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