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YEAR SEVEN MATH EXERCISES ON LOWEST COMMON MULTIPLE, HIGHEST COMMON FACTOR, AND PRIME NUMBERS

Population numbers in millions.

A recent report from India gives an anaemia prevalence of 60%-80% for pregnant women in different regions [69]. A corresponding figure of 59% has been reported from Indonesia (see FIG.8. Anaemia among men, pregnant and non-pregnant women, and children 1-5 years old in Indonesia (data from D. Karyadi. personal communication, 1991)); D. Karyadi, personal communication, 1990). Figure 9 (see FIG. 9. Anaemia among children 0-1 and 0-4 years old in Brazil (data from Jose Dutra de Oliveira, personal communication, 1991) shows 29% of children 0-4 years old in Brazil to be anaemic and 83% of them to be iron-deficient, with even higher rates for infants (J. Dutra de Oliveira, personal communication, 1991).

Iron-deficiency anaemia affects substantial numbers of persons in the United States. If iron deficiency rather than anaemia is the criterion, one-third of premenopausal women in the United States fall into this category, with minority groups more heavily affected. NHANES 11 data for 1976-1980 [70] reveal high frequencies of impaired iron status in US preschool children and premenopausal women, particularly among those whose incomes are below the poverty level. The report documents an overall 7.2% prevalence of actual anaemia in women 15-44 years old, with the highest burden in minority and poverty groups. For example, the percentages with two or three abnormal iron-status indicators were 11.7% for white but 31.3% for black adolescents 15-19 years old [70].

Iron and behaviour

The earliest functions to be affected by iron deficiency are those of brain enzymes involved in cognition and behaviour. Performances on tests of brain function and scholastic achievement are reduced in iron deficiency, and this is usually not reversible unless the deficiency is mild. Iron supplementation has been shown to improve the cognitive performance of iron-deficient infants [71], preschool children [72], and adolescents [73] in the United States. This effect has been confirmed by studies in infants in Chile [74]. Costa Rica [75]. Guatemala [76], and Indonesia [77] and in school children in Egypt [78], India [79]. Indonesia [80, 81], and Thailand [82]. In Thailand performance on Thai language and mathematics tests was significantly related to haemoglobin status and was not reversed by supplementation that restored normal iron parameters in blood [82].

A recent article by Lozoff et al. [78], following up her earlier study in Costa Rica. reports that children who had moderately severe anaemia as infants had lower scores on tests of mental and other functioning at school entry than the rest of the children even when the data were controlled for a comprehensive set of socio-economic factors. The mechanisms by which iron deficiency impairs learning and behaviour, both reversible and non-reversible, are probably multiple and related to the stage of physical development. Nevertheless, it is now firmly established that iron deficiency can impair cognitive performance at all stages of life and that, when it occurs in infancy and childhood, its effects may not be reversible. Recent work from Israel, using an animal model, suggests that the development of neurons essential for key neurotransmitters may be inhibited, with consequences evident in later life [83-85].

Iron and infection

Next to suffer are cells of the immune system. A number of antimicrobial systems within the neutrophil are adversely affected by iron deficiency [86-89]. One is the capacity of the cell to kill ingested micro-organisms by a so-called respiratory burst [90]. This involves the iron-containing enzyme myeloperoxidase [91]. Chandra reports that iron deficiency in Indian children decreases the ability of lymphocytes to replicate when stimulated by a mitogen and lowers their capacity for respiratory bursts necessary for killing ingested organisms [92].

Figure 10 (see FIG.10. Lymphocyte proliferation, intracellular bactericidal capacity of neutrophils, and quantitative nitroblue tetrazolium test, related to serum transferrin saturation. The vertical bars indicate the means and ranges of values obtained in iron-replete controls [93]) shows the impairment with iron deficiency as indicated by transferring saturation for lymphocyte proliferation, the intracellular bactericidal capacity of neutrophils, and the ability of these cells to produce any oxidative bursts [93].

There is also extensive evidence from India [90, 94-96] for a direct relationship between iron status and the concentration of cells responsible for cell-mediated immunity. The skin-test response to common antigens, indicating the development of immunity, has been found to be reduced in studies in iron-deficient children in India [9O, 94]. Additional evidence for the effects of iron deficiency on immunity has been reviewed by Keusch [97].

Iron deficiency in Alaskan native children has been reported to be associated with increased diarrhoeal and respiratory disease [98], and meningitis was observed to be fatal only in anaemic children [99]. A study by Basta et al. in Indonesia [100] found that the greater morbidity from infection among anaemic rubber tappers decreased after iron supplementation. In field studies in both Egypt [101] and Indonesia [102] a decrease in diarrhoeal and respiratory infections was observed in the groups receiving iron supplementation.

Iron deficiency, work performance, and productivity

Figure 11 (see FIG.11. Correlation of haemoglobin status with Harvard step-test performance as a measure of physical fitness in Guatemalan agricultural labourers [103}) shows a linear correspondence between haemoglobin status and the Harvard step test (HST) in adult plantation workers in Guatemala [103]. When the individuals with low haemoglobin received an iron supplement, their performance improved markedly. In Indonesia Basta et al. [100] found similar differences in HST scores between anaemic and non-anaemic road-construction workers and rubber tappers. The anaemic workers had markedly improved performances when they were given iron for 60 days.

The results among male tea pickers in Sri Lanka were similar [104-106]. In both Sri Lanka and Kenya [107, 108] treadmill performance was shown to be proportional to plasma haemoglobin. Spurr et al. [109] found linear correlations between haemoglobin status, aerobic power, and other measures of physical capacity in Colombian sugar cane workers. Low plasma haemoglobin was also associated with poor running performance in Gambian children [110].

The question remains whether these observed differences in physical capacity affect productivity. Basta et al. [100] subsequently showed a strong correlation between haemoglobin status, HST performance, and the take-home pay of Indonesian rubber-plantation workers. Tappers given iron supplementation for 60 days increased their take-home pay by more than 30%. Even among the weeders who were not paid on an incentive basis, less area was weeded by those who were anaemic, and their output also increased with supplementation.

In a subsequent study in Indonesia [102, 111], the quantity of tea leaves collected per hour was significantly less for anaemic women; work output increased by 24% after four months of iron supplementation. Similar results were obtained in a larger follow-up study sponsored by the United Nations University on four other tea plantations in the same area. The daily productivity of the anaemic male tea pickers in Sri Lanka increased more than 20% after iron supplementation for one month [104, 1()5]. An increase in agricultural productivity of Indian women given iron supplementation has been reported [112]. Productivity also increased after iron supplementation of anaemic male agricultural workers in Colombia [109] and industrial workers in East Africa [108].

The impact of iron deficiency on mothers

There are additional adverse consequences of iron deficiency in childbearing women. Maternal mortality, prenatal and perinatal infant loss, and prematurity are significantly increased [113, 114]. Favourable pregnancy outcomes are 30%-45% less frequent in anaemic mothers than in normal mothers, and their infants have less than one-half of normal iron reserves. Such infants are at greater risk of morbidity and mortality during infancy [115]. Undernutrition during pregnancy leads to low-birth-weight infants who exhaust their iron stores at an earlier age. They then require more iron than supplied by breast milk at an earlier age than infants of normal birth weight [116, 117]

The impact of iron deficiency on child growth

Iron-deficient children given supplementary iron showed improved growth in Indonesia [118], Kenya [119], and Bangladesh [120]. This was also evident in studies in the United Kingdom [121] and the United States [122]. Whether or not an effect of iron supplementation is observed apparently depends on local factors, including infections, age at depletion, and possibly other dietary factors [72].

Iron deficiency and temperature regulation

On the basis of studies in experimental animals showing that iron-deficient anaemic animals readily become hypothermic and have depressed thyroid function, human studies were conducted first in Venezuela [123-126]. Martinez-Torres et al. (126] observed that iron-deficient anaemic subjects submerged in relatively warm water (28 C) for one hour were unable to maintain normal body temperature. This has since been confirmed by additional studies in the United States [127].

Vitamin A

Vitamin A is converted directly to the visual pigment of the eye which is essential for night vision. An early sign of vitamin A deficiency is night blindness. The epithelium of the conjunctiva and cornea is also particularly susceptible to lesions due to vitamin A deficiency. The eye becomes dry, and foamy areas may appear on the conjunctiva. As the deficiency progresses, the cornea becomes eroded, the iris prolapses, the lens is extruded, and a corneal scar develops, resulting in blindness.

WHO estimates that about 40 million children in the world suffer from vitamin A deficiency, although this varies greatly between regions and countries [68]. About 350,000 infants and young children become blind annually because of vitamin A deficiency, and 70% of these die within one year, mainly because of susceptibility to infections. Vitamin A deficiency is recognized as a public health problem in 37 countries. Subclinical deficiency undoubtedly affects many more. Most children who go blind from vitamin A deficiency die within a year, but about 250,000 who go blind each year survive to burden their societies.

Four recent studies, summarized in figure 12 (see FIG. 12. Reduction in the mortality of children 0-5 years old with vitamin A supplementation for 12 months in Aceh [130], and West Java [131], Indonesia; Madurai, India [132]; and Sarlahi, Nepal [129]), have reported dramatic decreases in the mortality of children 0-5 years old given supplementary vitamin A for 12 months [128]. The decreases ranged from 30% in Sarlahi, Nepal [129], and 34% in Aceh, Indonesia [130], to 45% in Java [131] and 54% in Madurai, India [132]. Significant effects were not reported from studies in Hyderabad, India [133], and the Sudan [134]. The children in the Sudan study were so malnourished that other nutrients may have been limiting. There is extensive evidence from experimental animals that vitamin A deficiency can adversely effect immunocompetence and other resistance to infections [135]. However, the reason for the effect of vitamin A supplementation on mortality with little or no detectable effect on morbidity is not yet known.

A study in Tanzania [136] and two in South Africa [137, 138] have shown a sharp reduction in measles mortality and other complications in children given vitamin A when the disease is diagnosed. As a consequence, WHO recommends administration of vitamin A with the onset of measles wherever the case fatality rate exceeds 1% [139]. Reduction in morbidity from infectious disease with improved vitamin A status has also been shown in studies in Indonesia [140], India [141], and Thailand [142], but this seems situation-dependent [128].

Iodine

Until recently, iodine deficiency was identified only with a compensatory swelling of the thyroid gland known as endemic goitre and with cretinism, a manifestation in the child of severe iodine deficiency during gestation. The typical cretin has profound mental deficiency, a characteristic appearance, a shuffling gait, shortened stature, and spastic dysplasia. The subject is usually deaf and mute, and usually dies unless given good care. It is now recognized that, even when cases of cretinism are few in number, they indicate a much larger number of persons who do not have the classic signs of cretinism but whose linear growth, intellectual capacity, and other neurological functions such as coordination are compromised to varying degrees because of iodine deficiency in their mothers [143-147]. In addition. iodine deficiency causes an increased rate of stillbirths and abortions and may have other adverse effects. Endemic goitre rates in schoolchildren are the most convenient indicator of iodine deficiency in a population. WHO recommends that a goiter prevalence above 10% in a population should be taken to indicate a public health problem requiring preventive measures.

About one billion people of all ages are considered to be at risk from iodine deficiency, although cases of endemic goitre are estimated at 200-300 million. About 20 million of these are believed to experience some degree of mental retardation or other neurological change, and about six million show signs of cretinism. Iodine deficiency disorders are significant in at least 90 countries [148, 149].

Endemic goitre is global in distribution wherever populations depend on local food supplies grown on iodine-poor soil. Such soils are found in regions that have been glaciated, in mountainous areas, and where heavy rainfall leaches micronutrients. Except where iodated salt has been introduced, goitre is still prevalent along the Andes, across central Africa, in the Asian subcontinent, and along the entire length of the Himalayan chain, with large pockets of severe disease in Burma, Viet Nam, Indonesia, and New Guinea [146, 150].

Demographic significance of child mortality due to hunger

One of the most logical but pernicious misconceptions is that high mortality rates restrain population growth rates in countries with high fertility rates, and that lowering death rates will increase that growth. On the basis of this false premise, some have suggested that resources devoted to improving child survival should be diverted to family planning. There is no doubt that a spectrum of family planning methods should be made available to all populations. Nor is there any question that high birth rates are still a major problem for most developing countries. Bangladesh, Egypt, Kenya, India, Pakistan, and the Philippines are notorious examples. However, it is also a reality that promoting family planning without improving nutrition, health, education, and social equity has consistently failed.

India has spent more per capita on family planning than any other country and achieved essentially nothing. Egypt has had lavish assistance in family planning from the World Bank and US AID with meagre results. By contrast, Chile Cuba, Korea, Taiwan, Thailand, and other countries that have reduced their infant and preschool mortality have achieved relatively high receptor rates for family planning. Within India, the state with the lowest infant mortality and highest literacy has the lowest fertility rates, despite the fact that it is also relatively poor among the states in per capita income.

I had an opportunity to compare infant mortality and the acceptance of family planning in the provinces with the highest and lowest infant mortality rates in Indonesia in 1990. Where mortality was lowest, Yogyakarta, most families had adopted an effective contraception method. Their goal was no more than two or three children, and we rarely saw preschool children who were closely spaced. In the districts with the highest infant mortality, few families had accepted family planning. Many wanted as many children as "God would give them," and crowds of children were in evidence. This could be dismissed as anecdotal were it not repeated in many other developing countries [151-154].

Figure 13 (see FIG. 13. Rate of annual population increase versus infant mortality in 73 countries (data from PC Globe, 1990) shows that, over a broad range of countries, those with high infant mortality also tend to have high rates of population increase, while those with low infant mortality are the ones with low fertility. The UNICEF report The State of the World's Children, 1991 [155] provides other evidence that reducing infant deaths does not necessarily lead to higher birth rates. It describes the relationship between the mortality rates of children 0-5 years old and total fertility rates in 1960, 1980, and 1988 for 18 developing countries. As illustrated in figure 14 (see FIG. 14. Average drop in countries' crude birth rate, 1960-1988, versus infant mortality in 1960 [156]), the lower the infant mortality rate of a country, the greater the decline in the birth rate between 1980 and 1988 [156]. The data indicate that, although there is a lag between initial steep falls in mortality and a fall in fertility rates, as time passes and mortality rates fall further, fertility rates drop sharply. The message is that reducing the malnutrition that is the major factor in high infant mortality rates is an essential prerequisite to successful family planning.

Overcoming hunger

It is time to turn from the consequences of hunger to the cost of not overcoming it, and to an examination of what will be required to abolish hunger as a public health problem in the world. I will now review what can and must be done to prevent the hidden hungers described, beginning with the easiest, iodine deficiency, followed by avitaminosis A, iron deficiency, and, most difficult of all, deficiencies of energy and protein.

Iodine

Iodine deficiency disorders are the easiest of the hidden hungers to prevent. Table 8 shows the prompt drop of endemic goitre following the addition of iodine to salt for human consumption in the state of Caldas, Colombia [157], and on a national scale in Guatemala [158]. Legislation requiring the ionization of all salt for human consumption need not require either government subsidy or an increase in retail price. At the time it was introduced in Guatemala the cost of ionization was only about five US cents per hundred pounds. It does require legislation and cooperation on the part of the producers. Where there are several large producers and a few localized groups of small producers, as in the countries of Latin America, each large producer can be required to have separate ionization equipment, and the small producers can bring their salt to a common centre for the addition of potassium iodate.

TABLE 8. Effect of iodized salt on the prevalence of endemic goitre in two Latin American countries

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