Vitamin A Deficiency
Iron Deficiency
Iodine Deficiency Disorders
Deficiencies in Vitamin C, Thiamine and Niacin
Deficiencies in the intake or absorption of vitamin A, iron, and iodine have serious consequences for health and mental and physical function. The clinical manifestations of these nutritional deficiencies - such as xerophthalmia, anaemia, and goitre - have been identified as major problems with increasing public health significance. This chapter summarizes what is known about trends in micronutrient malnutrition, focussing on these three most prevalent known deficiencies. Other micronutrient deficiencies - of vitamin C, thiamine and niacin - are also briefly referred to.
The most obvious results of vitamin A deficiency are progressive damage to the eye, eventually leading to blindness. The general term for this is “xerophthalmia”, which ranges from the mildest form, night blindness, through reversible signs in the eye, to ulceration and destruction of the cornea, thence blindness. The eye is the most observable tissue damaged by vitamin A deficiency, and progressive damage to other membranes probably occurs, unobserved, in parallel with the eye damage. Increased ill health and mortality have long been associated with vitamin A deficiency, and in recent years intervention trials have established with increasing certainty that providing vitamin A to young children in areas where the deficiency exists, has a significant effect on mortality, of around 30 percent reduction. These effects are observed in children who do not necessarily have eye signs, but may have sub-clinical deficiency. Assessment of vitamin A deficiency is most commonly feasible from clinical signs of eye damage. Dietary surveys and food balance sheet data can also be used to assess the supply of vitamin A in the diet. Vitamin A itself may be preformed in the diet from animal sources, or obtained from carotenes from vegetable sources; the unit, allowing for differential conversion to vitamin A and absorption, is retinol equivalents in mcg.
WHO reported that in 1991 nearly 14 million preschool children had eye damage due to vitamin A deficiency (WHO, 1992c). Around 10 million of these children are located in Asia. The geographical distribution by WHO regional groupings is given in Table 3.1, and mapped in Figure 3.1. Each year it is estimated mat between 250,000 to 500,000 preschool children go blind from vitamin A deficiency. About two-thirds of these children die within months of going blind.
The total number of preschool children living in areas where they are at risk of vitamin A deficiency is estimated by WHO at around 190 million, see Table 3.1. This number increases greatly if other age groups in areas known to be vitamin A deficient are included, such as school age children and women of child-bearing age.
Vitamin A deficiency, defined by eye signs, has been identified as a widespread public health problem in 37 countries worldwide (see Figure 3.1). In countries in which xerophthalmia is endemic, the dietary supply of retinol (mcg/caput/day) estimated from FAO data is often extremely low. Minimum average requirements are around 250 mcg retinol equivalents (RE)/caput/day. As examples, in Mozambique average availability is estimated as 200 mcg RE/caput/day; in Zambia, 290 mcg/caput/day; in Bangladesh, 240 mcg/caput/day. These average supplies are therefore probably below average requirement, making the existence of vitamin A deficiency inevitable in the population. Nonetheless, overall national retinol supply is not always the principal constraint. In 10 of the 37 countries, average supply was above 600 mcg RE/caput/day, and maldistribution of the available supplies is clearly involved. This is particularly the case in those countries that appear to have ample vitamin A because of red palm oil, the production and consumption of which tends to be localized, and not reach deficient areas.
Demand for vitamin A behaves differently to that for overall food intake, or calories, for a number of reasons. Firstly, vitamin A is only present in a limited number of foods especially fruits and vegetables; although these tend to be cheap, they are often subject to considerable seasonal fluctuation. Secondly, whilst appetite affects the demand for food, adequacy of vitamin A in the diet is not directly sensed. Intakes of foods rich in vitamin A thus do not respond to changes in either income or food prices in the same way as calories do. Such considerations mean that, on the one hand, vitamin A distribution does not necessarily follow income distribution or trends; on the other hand, through marketing, promotion, and consumer education, it may be possible to improve the adequacy of vitamin A dietary intake relatively cheaply.
Table 3.1 Populations at Risk of and Affected by Vitamin A Deficiency, by WHO Region, 1991
(Million pre-school children)
|
WHO region |
Vitamin A deficiency |
|
|
Total pre-school child population in countries where
xerophthalmia exists |
Estimated number with xerophthalmia |
|
|
Africa |
18 |
1.3 |
|
Americas |
2 |
0.1 |
|
Southeast Asia |
138 |
10.0 |
|
Europe |
- |
- |
|
Eastern Mediterranean |
13 |
1.0 |
|
Western Pacific |
19 |
1.4 |
|
Total |
190 |
13.8 |
Source: WHO 1992c.
The supply of vitamin A estimated from FAO’s food balance sheets indicates an improving trend for most developing countries in the last 20 years, with the notable exception of Sub-Saharan Africa. The data are shown in Figure 3.2. Countries in the Middle East and North Africa, Middle America and Caribbean, and South America, achieved levels likely to be substantially above average requirements, by the late 1980s. Vitamin A supply is increasing quite rapidly in South East Asia, to the point where it now exceeds average requirements. Vitamin A deficiency persists in this region, but the increase in supply should give potential for redistribution to begin to eliminate the deficiency. In South Asia overall supplies are particularly low, and not rising very fast. This is in line with the observation of quite extensive deficiency in this region, and the slow rate of improvement indicates particular urgency for dietary modification and promotion of consumption of higher retinol-containing diets.
The vitamin A situation in Africa requires closer examination. First, it is essential to distinguish between those countries where red palm oil is produced - in West Africa - and the other countries. This is shown in the bottom part of Figure 3.2. When this is done, it becomes clear that East and Southern Africa have very low availabilities of vitamin A, in Southern Africa probably on average below requirement, so that here vitamin A deficiency is likely to be widespread. Added to this, there are some indications that the overall supply is actually decreasing in East Africa, which would exacerbate the problem. In West Africa and the Sahel the apparently high availability does not preclude the co-existence of deficiency, as is indicated in the map in Figure 3.1. As noted above, this is related to the fact that red palm oil is not marketed all that widely in a number of these countries.
The retinol supply assessed from food balance sheets should, however, be treated only as potential supply. Effective levels of physiological intake are determined by many factors including the state of maturation of certain fruits and vegetables, effects of dietary fats on the intestinal absorption of Vitamin A, and intake of enriched foods. In 1986-88, the developing regions of the world derived more than 70 percent of vitamin A from plant sources. These include green leafy vegetables, carrots, various fruits, sweet potatoes, and palm oil. In contrast, developed countries got only 45 percent of vitamin A from food of vegetable origin. The proportion coming from animal products tends to be more in higher income countries. Countries in Middle and South America which have incomes above $2000 per capita derive about half of the total retinol supply from animals, compared to only 14 percent in Southeast Asia, a region with a per capita income of $850 on average in 1988. As countries develop, diet diversifies, mostly into consumption of more meat and fish, milk products, eggs and butter.
Growth in vitamin A availability in South Asia, South East Asia and Middle East/North Africa was explained largely by the increases in vegetable sources of the vitamin (e.g. palm oil in Malaysia), whereas the increases in China and Middle America were due primarily to increases in availability from animal sources. The elimination of Vitamin A deficiency problems has recently been adopted as one of the goals for the 1990s by the World Summit for Children (1990) and the Montreal Conference on Micronutrient Malnutrition (1991). WHO reported that programmes were in operation in 44 countries in 1991, while another 49 countries were making plans for implementing action programmes. This is markedly higher in terms of number of countries and in coverage than 1987, when only eight such countries had programmes in place.
Iron deficiency is the commonest nutritional disorder in the world and affects over one billion people, particularly reproductive-aged women and preschool children in tropical and sub-tropical zones; it also has a serious impact on school children and working males. If uncorrected it leads to anaemia of increasing severity, reduced work capacity, diminished learning ability, increased susceptibility to infection and greater risk of death associated with pregnancy and childbirth. It results from consuming diets with insufficient iron, reduced dietary iron availability, increased iron requirements to meet reproductive demands, and losses due to parasitic infections; these factors often operate concurrently.
Figure 3.1 Geographical distribution of xerophthalmia, 1987
Source: WHO (1987)
Figure 3.2. Vitamin A supply, 1961 -1989 (Retinol equivalent per caput per day) - A. South Asia
Figure 3.2. Vitamin A supply, 1961 -1989 (Retinol equivalent per caput per day) - B. Near East and North Africa
Figure 3.2. Vitamin A supply, 1961 -1989 (Retinol equivalent per caput per day) - C. South East Asia
Figure 3.2. Vitamin A supply, 1961 -1989 (Retinol equivalent per caput per day) - D. China
Figure 3.2. Vitamin A supply, 1961 -1989 (Retinol equivalent per caput per day) - E. Middle America & Caribbean
Figure 3.2. Vitamin A supply, 1961 -1989 (Retinol equivalent per caput per day) - F. South America
AFRICA SUB-REGIONS
Figure 3.2. Vitamin A supply, 1961 -1989 (Retinol equivalent per caput per day) - G. Sahelian Region
Figure 3.2. Vitamin A supply, 1961 -1989 (Retinol equivalent per caput per day) - H. West Africa
Figure 3.2. Vitamin A supply, 1961 -1989 (Retinol equivalent per caput per day) - I. East Africa
Figure 3.2. Vitamin A supply, 1961 -1989 (Retinol equivalent per caput per day) - J. Southern Africa
Source: Calculated from FAO data, see Chapter 7.Note: The band shown, for guidance in interpretation, is from 250 to 550 mcg retinol equivalents/caput/day. This is based on Tables 4.1 and 4.4 of FAO/WHO, 1988. 250 mcg approximates to the “base requirement” weighted by a typical age-sex distribution in the population. The upper bound of 550 mcg is approximately the population-weighted “safe level” of intake, usually applied to individuals and likely to be above the mean population requirements. For further discussion, see technical notes in Volume II.
Anaemia is thus a serious outcome of iron deficiency. Since there are multiple causes of anaemia, and since iron deficiency can exist without haemoglobin levels being lowered, there are potentially four different situations, or populations: those anaemic and iron deficient; those iron deficient but not (yet) anaemic; those anaemic not due to iron deficiency; and those iron replete and with normal haemoglobin. Causes of anaemia other than iron deficiency often include malaria, intestinal parasites, other nutrient deficiencies such as folate and vitamin B12, and genetically determined haemoglobinopathies such as thalassemia. It is generally held that at least half of the anaemia worldwide is directly due to dietary iron deficiency. On the other hand, there is emerging evidence that low iron stores, even in the absence of anaemia, are also related to functional disadvantages, in cognitive development, learning and behaviour. The extent of this problem has not been widely determined. However, anaemia prevalences are reasonably well established, and can generally be taken as an indicator of the extent and trends of iron deficiency. These distinctions are further discussed in the technical notes, but here we concentrate on anaemia as assessed by low haemoglobin, with cutoffs determined by WHO (bearing in mind that much of this is due to iron deficiency, although the precise amount is unknown); and the dietary supply of iron taken from FAO food balance sheet data.
Estimates of the extent of anaemia are shown in Table 3.2. These are taken from the database compiled by ACC/SCN to assess the nutritional status of women, described more extensively in Chapter 4. Results here are given by the same regions as used elsewhere in this report, and refer to anaemia in women of reproductive age (15-49 years old). The overall prevalence for women in developing countries is estimated at 42 percent, equivalent to just over 370 million women; in pregnant women (with a cut off of 11g/dl haemoglobin) the prevalence is estimated at 51 percent, and in non-pregnant women at 41 percent (cut off 12g/dl). These results are almost identical to those calculated by WHO (WHO, 1992d; with different regional groupings), which estimate 44 percent prevalence for all women in developing countries, with 56 percent prevalence for pregnant women and 43 percent for non-pregnant. While there is considerable variation in prevalence by region - from around 64 percent in South Asia to 23 percent in South America, by the SCN results - it is striking that anaemia is prevalent throughout the developing world. The geographical distribution is shown in Figure 3.3, from WHO data. Nearly half the total number of anaemic women are in South Asia.
These new estimates now also cover China, updating the figures in the First Report on the World Nutrition Situation (ACC/SCN, 1987). The current figures confirm that levels of anaemia worldwide are very high, but indicate little global change (excluding China) since the previous assessment. This may partly be because of scarcity of data. In the two regions where survey results extend across the last 15 years, Sub-Saharan Africa and South Asia, there are some indications that the prevalence of anaemia is, if anything, increasing, as discussed in Chapter 4 (see Figure 4.8). Relating trends in anaemia to estimates of iron availability does give a consistent picture, as will be indicated in Table 3.3.
Table 3.2 Prevalence of Anaemia in Women (15-49 years old) by Region, in 1980s
|
|
Pregnanta |
Non-pregnantb |
All |
|||
|
Percent |
Millionc |
Percent |
Millionc |
Percent |
Millionc |
|
|
Sub-Saharan Africa |
50 |
6 |
40 |
35 |
42 |
41 |
|
Near East/North Africa |
44 |
2 |
31 |
13 |
33 |
15 |
|
South Asia |
64 |
19 |
64 |
139 |
64 |
158 |
|
South East Asia |
56 |
8 |
47 |
49 |
48 |
57 |
|
China |
34 |
11 |
26 |
64 |
26 |
75 |
|
Middle America/Caribbean |
34 |
1 |
27 |
8 |
28 |
9 |
|
South America |
31 |
3 |
21 |
12 |
23 |
15 |
|
Total (all regions above) |
51 |
50 |
41 |
320 |
42 |
370 |
a. Proportion and numbers with haemoglobin below 11 g/dl.b. Proportion and numbers with haemoglobin below 12 g/dl.
c. Numbers are based on population estimates for 1985 (UN. 1991) in developing countries.
Figure 3.3 Prevalence of anaemia in pregnant women (1988)
Source: WHO, 1992d
Figure 3.4. Dietary iron supply, 1961-1989 (Mg. per caput per day) - A. Sub-Saharan Africa
Figure 3.4. Dietary iron supply, 1961-1989 (Mg. per caput per day) - B. Near East and North Africa
Figure 3.4. Dietary iron supply, 1961-1989 (Mg. per caput per day) - C. South Asia
Figure 3.4. Dietary iron supply, 1961-1989 (Mg. per caput per day) - D. South East Asia
Figure 3.4. Dietary iron supply, 1961-1989 (Mg. per caput per day) - E. China
Figure 3.4. Dietary iron supply, 1961-1989 (Mg. per caput per day) - F. Middle America and Caribbean
Figure 3.4. Dietary iron supply, 1961-1989 (Mg. per caput per day) - G. South America
Source: Calculated from FAO data, see Chapter 7.Note: The band is the range of iron intake needed to prevent anaemia in women of reproductive age on low and intermediate bioavailability diets (5% bioavailability. 17 mg. per day; 10% bioavailability, 8 mg. per day). This is taken from FAO/WHO (1988), Table 5.6. The estimated dietary requirements for iron in mg. per day, taking the lowest values, which are the median requirements to prevent anaemia, by age and physiological group areas follows:
|
Median requirements to prevent anaemia (Mg. iron per
day) |
||||||||||
|
|
Infants |
Children |
Boys |
Girls |
Men |
Women |
||||
|
Age group (years) |
(0-1) |
(1-2) |
(2-6) |
(6-12) |
(12-16) |
(12-16) |
(16+) |
Menstruating |
Post- menopausal |
Lactating |
|
Low bioavailability |
11.0 |
6.5 |
7.5 |
12.5 |
19.0 |
22.0 |
12.0 |
17.0 |
10.0 |
16.0 |
|
Intermediate bioavailability |
5.5 |
3.5 |
3.5 |
6.0 |
9.5 |
11.0 |
6.0 |
8.0 |
6.5 |
7.0 |
Dietary iron sources are distinguished between vegetable and animal in the supply data shown in Figure 3.4. Moreover, these are not added together in the figures, since with the large variations in bioavailability this might be misleading. It can be seen that in developing countries the predominant source of dietary iron is from vegetable sources, and the diets are likely to be usually of low bioavailability. In Figure 3.4 an indication of rough levels of adequacy is given, for guidance; but with the added uncertainty of distributional effects, relative levels between regions and trends are more informative.
Figure 3.5 Iron density in the diet, 1970-1989 (Mg iron per 1,000 calories)
Source: Calculated from FAO (1990a).
The iron intake patterns in the various regions of the developing world (in Figure 3.4) show the dominance of non-haem iron (plant/vegetable). In China for example, out of the 11.7 mg iron consumed per day, around 10.3 mg comes from plant sources, mainly rice, wheat and vegetables. In most developing countries, the diet typically contains cereal, roots and/or tubers and only small quantities of meat, fish or ascorbic acid-rich foods. Thus, cereals and roots/tubers account for a large proportion of iron in the diet - ranging from 25 percent for those primarily dependent on roots and tubers to around 40 percent for rice, and 60 percent for those consuming millet and sorghum. The rest of the vegetable sources of iron comes from pulses, and green leafy vegetables. In Sub-Saharan Africa, and South Asia, iron supplies from animal sources are extremely low - typically accounting for about 1 mg or less per caput compared with a total of around 13-15 mg from plant sources. Such a combination of foods in the diet is conducive to very low absorption of iron.
The overall iron supply is particularly limiting in Sub-Saharan Africa, South Asia, and South East Asia. In these three regions animal sources are low, the average diet is likely to be of low bioavailability, and for many people the supply probably does not reach even the minimum average requirement. This is in line with these regions having the highest estimated prevalence of anaemia, as shown in Table 3.2. Results from China are inconsistent, and few anaemia estimates are available. In the other regions, the iron supply, particularly taking into account the higher level of animal iron sources, may on average be just adequate; this gives a potential for improvement with redistribution.
More important, perhaps, is the observation that the overall per caput supply of iron appears to be static or perhaps decreasing in all regions except Near East and North Africa. In South Asia this is at least partly due to a major decrease in the production and availability of pulses (lentils, beans, etc.), which have been squeezed out in many areas by the green revolution emphasis on cereal crops. In Sub-Saharan Africa, the decrease may be partly related to a shift away from millets and sorghums; in South East Asia these plus other factors may apply. Thus, the diet quality in terms of iron seems to be deteriorating, and this can be assessed by the iron concentration in me diet, expressed mg iron/1,000 calories. The trends in this indicator are shown in Figure 3.5. These results demonstrate the deterioration (or lack of improvement) in the diet quality in terms of iron over the last two decades in all regions except Near East/North Africa.
Table 3.3 Regional Trends in Iron Availability and Anaemia (1970-1990)
|
Region |
Trends in Dietary Iron Supply |
Trends in Anaemia (non-pregnant Women) |
|
Sub-Saharan Africa |
Down slightly, especially from animal sources |
Up, see Fig. 4.6 |
|
Near East/North Africa |
Up, from both animal and vegetable sources |
Probably down (est. 36% 1975/80, 28% 1985/90) |
|
South Asia |
Down, due to reduced pulse production (?) |
High and increasing, see Fig. 4.6 |
|
South East Asia |
Down slightly, especially vegetable sources from
1980 |
Probably up (est. 40% 1970-80, 57% 1980-90) |
|
Middle America/Caribbean |
Down vegetable sources, but animal sources up |
Probably up (est. 20% 1970-80, 30% 1980-90) |
|
South America |
Down, but animal sources relatively high |
Probably down (est. 24% 1970-80, 20% 1980-90) |
Average iron consumption based on national figures generally hide the distribution across various locations and socioeconomic groups. Recent research on micronutrients indicate that iron consumption behaves differently from other nutrients. It is more income elastic (perhaps the most of major nutrients), owing to the fact that as income increases consumers will purchase more meat and fish. In the Philippines for example, the highest income quintile consumed three to four times more meat and pulses than households in the lowest income quintile. This means that iron consumption overall is likely to be inadequate for poorer households.
Within households, a number of studies show highly disproportionate distribution of iron relative to individual requirements. In the Philippines, adequacy ratios for mothers in three provinces was estimated at 0.65 compared to 1.05 percent for fathers, 0.77 for adolescent girls compared to 0.91 for adolescent boys. While a substantial part of iron adequacy reflects the higher dietary requirements for pregnant mothers and adolescent girls, it is evident that given similar intakes, these sub-groups are likely to suffer most from low availability of iron in the diet due to their different physiological needs. An NNMB 1979 study in India showed that average iron intakes of children 1 to 4 years was 10.2 mg per day, compared to 34.5 mg for adult men, although children have more than half the requirements of adults.
There are in principle two strategies used in controlling iron deficiency - (a) through dietary improvement and (b) by food supplementation and fortification. In clinical practice, those suspected of being anaemic are treated with medicinal iron supplements. In a public health setting, however, it is impossible to test each patient and therefore the approach is to give supplements to entire high-risk groups - mainly pregnant women. There are well defined delivery mechanisms which have been tried for supplementation (ACC/SCN, 199 la). A number of these programmes are now in operation in developing countries. However, many programmes limit effectiveness and sustainability partly because of the need for frequent administration (e.g. daily) in contrast to vitamin A and iodine. WHO reported that in 1991, a total of 102 countries have been preparing plans for the implementation of anaemia control programmes, and 11 countries have so far set up comprehensive control programmes within the health ministries. Another 65 countries have reported to establish monitoring and evaluation systems.
The longer term solution to the problem of iron deficiency is dietary modification. This includes increasing the uptake of haem iron from animal products and vitamin C which enhances absorption in iron, and increasing household level availability of iron rich fruits and vegetables. The latter will mainly be in the realm of policies to encourage the availability of iron rich foods.
The indication here that dietary iron supplies maybe decreasing in many places has important implications for food policy. While the substantial reduction in production of pulses has been of concern for some time, the effect on iron status is only now being indicated on a wide scale. Reduced iron availability in other areas need further study. However, steps will be needed to reverse the trend.
Iodine deficiency exists in most regions of the world, resulting from a low intake of iodine in the diet. The consequences of iodine deficiency include goitre, reduced mental function, increased rates of still births and abortions, and infant deaths. Severe mental and neurological impairment known as cretinism occurs in babies with severely iodine deficient mothers. Deficiencies in iodine later in infancy and childhood cause mental retardation, delayed motor development, growth failure and stunting, neuromuscular disorders and speech and hearing defects. Mild deficiency can cause lethargy, and this is reversible when iodine status improves, as is goitre.
The commonest measure of iodine deficiency is from observation of goitre, enlargement of the thyroid gland, usually obtained by specific surveys in iodine deficient regions. Since goitre tends to be localized in such regions, most data are not nationally representative, and thus prevalence estimates are somewhat tentative; trends have not yet been assessed.
WHO estimates that in 1990 around 1,000 million people lived in iodine deficient environments around the world (see Table 3.4). These tend to be regions where the iodine, normally supplied from soil and water, has been leached from the topsoil by rain, flooding, glaciation, and snow. These regions tend therefore to be mountainous and remote, as well as flood plains. In Figure 3.6 areas in which iodine deficiency control measures have been implemented are shown; since these tend to be quite effective, it can be taken that in most of these regions the extent of iodine deficiency is likely to be improving.
The extent of goitre has been estimated (by WHO and ICCIDD) as more than 200 million people, added to which should be around 6 million with overt cretinism. These figures are shown by WHO region in Table 3.4. Around half of these are in South East Asia, including India. It is further estimated (WHO, 1992c) that some 20 million people worldwide are mentally defective as a result of the deficiency.
Table 3.4 Estimated Prevalence of Iodine Deficiency Disorders in Developing Countries, by Region, and Numbers of Persons at Risk
(in millions)
|
|
At Risk |
With Goitre |
Overt Cretinism |
|
Africa |
227 |
39 |
0.5 |
|
Latin America |
60 |
30 |
0.3 |
|
South East Asia |
280 |
100 |
4.0 |
|
Asia (other countries including China) |
400 |
30 |
0.9 |
|
Eastern Mediterranean |
33 |
12 |
- |
|
Total |
1,000 |
211 |
5.7 |
Source: WHO 1990c.
Growing international awareness of the problem has led to increased programme and surveillance activities. The problem is largely preventable, and cost-effective methods of eliminating the problem are well known. WHO/UNICEF has declared the goal of eliminating IDD by year 2000, and activities now on-going in collaboration with ICCIDD (International Council for the Control of Iodine Deficiency Disorders).
Control of IDD is mainly through fortification of salt with iodine (salt iodination), and/or periodic distribution of iodized oil, either administered orally or by injection (every three to six months orally, up to two year interval by injection). The coverage of control programmes is shown in Figure 3.6. Further extension of iodine deficiency control is likely, and preparations are under way in many countries. For example, in the African region, 36 countries have data on the magnitude of problems of which 14 carried out surveys since 1987. National control programmes are now operational in Algeria, Congo, Ethiopia, Kenya, Malawi, Mali, Tanzania, and Zaire. National programmes are being drawn up and ready to be implemented in 10 more countries.
In Asia, where the largest global concentration of population affected by IDD is located, intensification of salt fortification and iodized oil distribution, training and education have produced improvements in Indonesia, Bhutan, Nepal and Thailand. As of 1990, about 10 million injections of iodized oil were administered in Indonesia, successfully preventing cretinism. National programmes are in place in Bangladesh, India, Myanmar, Nepal, and new initiatives started in Korea and Sri Lanka.
The problem of IDD in South America is highest in the Andean region, mostly in rural areas where iodized salt is not available. In Ecuador, a national programme which includes the distribution of iodized salt through a single private company has been successful. Some assessments of the problem have been done in Costa Rica, El Salvador, Guatemala, Honduras, Nicaragua, and Panama. Targeted programmes in Bolivia and Peru have been intensified.
Figure 3.6 Iodine deficiency disorders: Areas affected and control programmes, 1991
Source: Map drawn with data from Table 4 in WHO, 1990c
The ICCIDD has summarized the increases in programmes to control IDD. As of 1991, 22 countries were implementing control programmes and another 40 countries were planning to implement action plans. Five years earlier only around six developing countries had IDD programmes in place. Intensified and accurate assessments of the problem, public awareness followed by monitoring and evaluation are essential for reaching the objective of complete elimination of the problem by the end of the century.
In recent years, outbreaks of micronutrient deficiency diseases among populations in refugee camps have occurred. Scurvy (vitamin C deficiency) has been reported among refugees and displaced persons especially in Somalia and Ethiopia. Pellagra (niacin deficiency) has affected Mozambican refugees in Malawi when groundnut supplies were interrupted. Beri-beri (thiamine deficiency) was reported among Cambodian refugees in Thailand. In principle, these diseases are preventable and methods of diagnosis and treatment are well known.
Deficiencies in vitamin C, niacin and thiamine generally occur in long-stay refugee camp populations when there is total or near-total dependence on rations provided, or when rations are of very limited variety and when trading of fresh foods is for various reasons not possible. Pellagra occurs in maize eating populations. When maize is not complemented with either legumes or fish in the diet, the risk of pellagra increases. Beri-beri on the other hand occurs among rice eating populations - when these diet are undiversified and based on milled (polished) rice. Including other foods such as whole cereals, legumes, and fresh vegetables in the diet reduces the risk of beri-beri. These micronutrient deficiency problems had previously been virtually eliminated, and their re-appearance in refugee camps is an indication of food management constraints in the camps.
