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close this bookDelivery of Oral Doses of Vitamin A Deficiency and Nutritional Blindness: A State-of-the-art Review - Nutrition policy discussion paper No. 2 (UNSSCN, 1987, 120 p.)
View the document(introduction...)
View the documentFOREWORD
Open this folder and view contents1. INTRODUCTION
Open this folder and view contents2. EFFICACY OF ORAL VITAMIN A
Open this folder and view contents3. VITAMIN A DELIVERY SYSTEMS
Open this folder and view contents5. POPULATION COVERAGE
Open this folder and view contents6. PROGRAMME CHARACTERISTICS
Open this folder and view contents7. PROGRAMME ECONOMICS


John B. Mason
with Susan J. Eastman and Mahshid Lotfi

John Mason is Secretary, ACC/SCN. Susan Eastman and Mahshid Lotfi were consultants to the ACC/SCN.

Deficiency of vitamin A has long been identified as a serious and preventible nutritional disease. A survey first published in 1964 (Oomen et al, 1964) formed the basis for WHO's (1976) estimates of an incidence of some several hundred thousand children going blind each year due to the deficiency. More recently, awareness has broadened of the extent of the population affected by the deficiency, and of the seriousness of the effects.

The populous countries of Southern and South-East Asia still account for the most cases of vitamin A deficiency, but attention is also focusing on the many countries in Africa, the Near East, and the Americas where vitamin A deficiency is a serious public health problem. This increased awareness stems from better availability of epidemiological information from many researchers and institutions, disseminated by WHO (1976), through the efforts of the International Vitamin A Consultative Group (IVACG, 1981), and many others. Now at least 34 countries are known to have serious vitamin A deficiency problems (WHO, 1985a; ACC/SCN, 1985).

Preventing blindness has been regarded as the major reason for controlling vitamin A deficiency. As IVACG (1981, p.7) put it: “Blindness is one of the most serious disabilities from which an individual can suffer and constitutes a great social and economic burden for the community. This is especially the case in xerophthalmia in which blindness almost always occurs in early childhood with resultant life-long handicaps for those who survive.”

Basic research has now demonstrated far-reaching biological effects of the deficiency, predisposing to a range of disabilities, including effects on the intestine, respiratory tract, immune system, as well as involvement of the eyes. These mechanisms cause vitamin A deficiency, probably even in mild form, to increase the susceptibility to infection and exacerbate the effects of many diseases. For example, the severity of measles and eye damage from the disease - which is particularly serious in poor countries especially in Africa - may be worsened because of vitamin A deficiency (Oomen, 1971; Franken, 1974). The association of vitamin A deficiency with increased morbidity is well-established, and the mechanism is becoming better understood.

Damage to the eyes is the most obvious and dramatic result of vitamin A deficiency, but these signs may in fact be only the later and more readily observable effects. First, studies many years ago in man demonstrated histopathological changes, similar in nature to those observed in the eye, in epithelial tissues of the respiratory, urinary and gastrointestinal tracts (data from 1925-1938, quoted from Sommer et al, 1984); this has been widely confirmed in animal studies. Thus we would expect that internal damage, especially to the growing child, may be proceeding insidiously with inadequate vitamin A intake, before any eye signs become apparent. This is in line with clinical descriptions of vitamin A deficiency including growth retardation, defective bone formation, and other developmental abnormalities (McLaren, 1966). Xerophthalmia seems to be related to growth both in animals and in man; for example, protein supplementation of malnourished subjects with low vitamin A reserves has precipitated many cases of xerophthalmia in the past (IVACG, 1981 p.9). Second, immune function is impaired in vitamin A deficiency, and is enhanced with repletion (McLaren, 1978; Lotan, 1985); this mechanism helps explain observations of increased morbidity with mild deficiency (Sommer et al, 1984) which in turn may account for the increased mortality specifically associated with the deficiency (Sommer et al, 1986 - see below). Finally, a range of other extra-ocular effects are suspected in man, based mainly on animal results (Reddy, 1985). Of particular interest is the finding that vitamin A deficiency may cause anaemia in man, reversible by iron only when vitamin A is administered (Hodges et al, 1978; Reddy, 1985 and others).

This picture corresponds to a syndrome of vitamin A deficiency, including but wider than the eye damage on which attention has hitherto been largely concentrated. Indeed, McLaren (1966, p.441) proposed that the term 'xerophthalmia', although implying only eye involvement, should be used to describe the entire syndrome. Terminology is not the key issue, except insofar as it promotes understanding. At this point we should recognize that vitamin A deficiency may be as far-reaching in its pathological effects on the individual as protein-energy malnutrition; and that prevention of the deficiency syndrome, even in its mild form, may have very important effects on child health, development and survival.

Children going blind from severe vitamin A deficiency are seriously sick and many die in the subsequent weeks. An association of severe deficiency with infant and child mortality had been established for some time (WHO, 1976, p.9; IVACG, 1981, p.8), when the deficiency was seen as at least a contributory cause of death. Of more extensive potential consequence, the possibility that mild or moderate stages of deficiency increased mortality risk was suggested from a number of studies, notably in Indonesia (Sommer et al, 1983). This was attributed to the findings that the risk of respiratory disease and diarrhoea were associated with vitamin A status, more closely here than with general nutritional status (Sommer et al, 1984). An intervention study of the effectiveness of vitamin A capsule distribution in preventing eye damage, also in Indonesia, gave crucial evidence of a direct effect of vitamin A in reducing mortality (Sommer et al, 1986). How far this may be mediated through preventing mild as well as severe deficiency awaits further study. But the demonstrated direct effect of vitamin A in reducing mortality gives added urgency to programmes for preventing vitamin A deficiency.

The Advisory Group on Nutrition of the ACC/SCN was asked to review the evidence (from the work of Sommer et al, 1986, in Indonesia) for a direct effect of vitamin A deficiency on mortality, and concluded as follows (ACC/SCN, 1986a):

(i) The approximately 30% difference in mortality in preschool children (one through five years of age) between treated and control villages was likely to be attributable to the vitamin A supplementation.

(ii) There is justification to expect that effects of this magnitude would be seen in other settings with similar conditions including at least similar severity of vitamin A deficiency with associated xerophthalmia, similar high prevalences of childhood morbidity and mortality and similar effectiveness of the xerophthalmia control programme.

(iii) It is appropriate to advise countries mounting high dose vitamin A programmes for the control of xerophthalmia that reduction of childhood mortality is a reasonable expectation and is further justification for such programmes.

Extent of the Problem

The rate of appearance (incidence) of new cases of severe vitamin A deficiency, measured as active corneal lesions (of which about 25% result in partial or total blindness) was estimated in Indonesia at around 2.7 cases per 1000 preschool children per year (Sommer, 1982). This led to an estimate of up to 500,000 new cases of active corneal lesions per year for Asia (WHO, 1985a). Applying this rate to all countries with known vitamin A deficiency gives worldwide estimates of some 700,000 new cases per year, among preschool children.

What happens to these children? It is estimated that some 60% die, and of the survivors 25% remain totally blind, and 50-60% partially blind (IVACG 1981, p.8). This amounts to some 250,000 children going blind or partially blind each year. The resulting prevalence of cases of blindness is hard to estimate, for lack of data and because of the high mortality associated with the deficiency. However, an estimate from available surveys (quoted in WHO, 1985a) of 0.2-0.4% prevalence of eye damage caused by vitamin A deficiency among pre-school children in affected countries is consistent with the incidence rate of 2.7 per 1000 per year. This would give nearly 3 million children blind from this cause, over a million of whom are in India. Vitamin A deficiency is the largest single cause of the total of 40 million people estimated worldwide to be blind (Kupfer, 1987).

Similar calculations (from basic data from the same sources) give an incidence estimate of 6-7 million new cases per year of children with mild deficiency, and some 20 to 40 million suffering from at least mild deficiency at any one time, of which nearly half are in India. This assumes around a 15% prevalence of mild/moderate deficiency, as indicated from surveys quoted by WHO (1985a) from India, Sudan and Yemen Arab Republic.

Estimates of numbers affected such as these give an idea of the extent of the problem to be prevented; but actual prevention requires reaching a much larger population. This is because, first, many more people are at risk of the deficiency than actually show signs of it, and second, because preventive measures cannot be precisely targeted only to those who would otherwise develop the disease. We need to consider the size and distribution of the population at risk, and different methods of prevention, to assess the magnitude of the task of tackling vitamin A deficiency.

A country-by-country survey conducted by WHO (1985a) was used as the basis for the ACC/SCN's formulation of a 10-year prevention plan (ACC/SCN, 1985). The geographic distribution of countries where xerophthalmia is a significant public health problem, and where sporadic cases occur, is shown in Figure 1 (DeMaeyer, 1986a).


A: Xerophthalmia a significant public health problem
B: Sporadic cases of xerophthalmia do occur

Four categories of countries were defined by WHO:

A: those where assessment has been made, with national prevention and control programmes (8 countries);

B: those where assessment has been made, or partially made, but prevention and control programme is not yet under way (13 countries);

C: those where assessment has not been made, but with high probability of problem based on indirect evidence (13 countries);

D: those where vitamin A deficiency does not appear to be a significant public health problem, but where the prevalence picture should be closely monitored (23 countries).

In 1984, 34 countries were in categories A, B, and C, of which eight had national prevention and control programmes underway (category A). Of these 34 countries, 23 have received international assistance, particularly from UNICEF and USAID (21 UNICEF, 6 USAID in 1985-6: calculated from Eastman, 1986; UNICEF, 1987; USAID, 1987).

The distribution by region of child populations in countries having vitamin A deficiency is shown in Table 1. Only those countries with established national programmes have substantial coverage of their child populations - notably Bangladesh, Haiti, India and Indonesia. For the others, coverage of the total child population is generally around 10% or less (calculated from data on capsule distribution). This demonstrates the need for greatly increased coverage, as well as where feasible more targeting: methods are introduced below and discussed in detail in this paper by Vest & Sommer. The range of need can be estimated from these figures. The total child population in the 34 countries is about 280 million - in a sense many or most of these are at risk. With a prevalence of 15% for at least mild deficiency, some 40 million are already affected. Fortunately, the most populous countries (Bangladesh, India and Indonesia) have control programmes already established, so that the immediate needs are substantially lower: excluding these three countries, the child populations in the other 31 countries amount to about 150 million, and those affected to about 22 million. Thus, to give an idea of magnitude, some 20 million children need help if the programme were perfectly targeted, or perhaps up to 100 million with less targeted delivery.

These calculations are based on preschool children, because prevalences are better known for this, the most vulnerable group; but school-age children and adults, especially pregnant and nursing mothers, are also in need. Prevention programmes must reach these people also.

In practical terms, effective prevention depends on establishing national programmes, with resources - depending on the approach chosen - for service delivery and supplies of vitamin A doses; for fortification; and/or for dietary modification. Although efforts are increasing, as of 1987 most of the 34 countries known to be affected do not yet have such programmes - a list is given in a footnote to Table 1 - and in the majority of these the coverage of preventive programmes is still very low.



Region (WHO)

Number of Countries with deficiency (WHO categories)1

Total 1-4 yr Child population in these countries

Child Pop. covered by UNICEF + AID programmes2

Number of Mild/Moderate Vitamin A Deficient Children5











S.E. Asia
(excl. India)










E. Mediterranean





Western Pacific









1 Countries by WHO category:

A - El Salvador, Haiti; Bangladesh, India, Indonesia, Nepal, Sri Lanka; Philippines.

B - Benin, Burkina Faso, Ethiopia, Malawi, Mali, Mauritania, Tanzania, Zambia; Brazil (north-east) Mexico; Oman, Sudan; Viet Nam.

C - Angola, Chad (north), Ghana (north), Kenya, Mozambique, Niger, Nigeria (north), Uganda; Bolivia; Burma; Afghanistan; Dem. Kampuchea, Lao People's Dem. Republic.

2 Calculated from capsule distribution data (1985) from Eastman (1986, Attachment 3) assuming two capsules per child per year; and from data in USAID (1987).

3 Note that coverage in Burma, Nepal and Sri Lanka were approximately 5 to 25%.

4 In India, 60 million vitamin A capsules produced domestically were distributed in 1985 (Eastman, 1986, Table 17).

5 Estimated as 15% prevalence (see text).

Possible Solutions

Vitamin A deficiency is caused by inadequate dietary intake of the vitamin itself (pre-formed retinol from animal products) or its precursors (carotenes, from plant sources), often aggravated by low absorption from the intestine. The solution is therefore to increase the dietary intake, and sometimes the absorption. Unlike most other micronutrients, reserves of vitamin A are stored in the body, and thus periodic high intakes can give adequate nutrition.

Three approaches are feasible, and have been widely put forward (e.g, WHO, 1982, 1985b, 1986; IVACG, 1984; DeMaeyer, 1986b; FAO, 1985, 1986; ACC/SCN, 1985). These correspond to short-, medium- and long-term interventions, and form the basis of the inter-agency plan endorsed by the UN (ACC/SCN, 1985, pp. 18-19).

(a) The distribution of single large oral doses of vitamin A (as capsules or oil solution) approximately every six months to vulnerable groups, usually through the health system: this is the main topic of this State-of-the-Art review.

(b) The fortification with vitamin A of a widely distributed food commodity: this is familiar in developed countries (e.g. margarine), and has been attempted at national scale, using sugar, in a few developing countries.

(c) Increasing the intake of vitamin A from the normal diet: this is clearly the long-term solution, and is the reason vitamin A deficiency has disappeared from many countries.

These interventions, particularly the first two, have been developed systematically. In principle, after identifying causes and testing remedies in the laboratory or hospital, the next step involves field trials to assess the efficacy of an intervention under controlled conditions (e.g. Solon et al, 1979). When this is established, large-scale intervention programmes can be initiated, monitored and evaluated. This process and the results for distribution of large oral doses of vitamin A is described in detail in this paper by West and Sommer. It is clearly established that such programmes are efficacious and effective, and indeed the cost-effectiveness has been assessed.

Fortification has been studied as a preventive measure, at field trial level and as national programmes, and shown to be effective in Costa Rica and Guatemala (Arroyave et al, 1979): Dr. Arroyave, in his discussion paper included here, gives some details. However, the sad fact is that the national fortification programmes in Central America have been discontinued for economic and political reasons, and other programmes have yet to progress from their successful field trial stages to national programmes. So, at the present time, there is inadequate support to establish and sustain national fortification programmes anywhere in the developing world, although a number of countries in Asia are moving in this direction.

In the long-term, increasing the regular dietary intake of vitamin A is clearly the best approach to preventing the deficiency - referred to as dietary modification (FAO, 1985). Increased intake usually occurs with economic development, vitamin A availability being closely associated with, for example, GNP (DeMaeyer, 1986a). Data from FAO Food Balance Sheets (1975-77) give an estimated average availability of vitamin A (from both retinol and carotenes) in 1975 of less than 600 mcg/caput/day (range 100 - 1700 mcg/caput/day) for many of the most seriously affected developing countries, compared with an average requirement of 250 - 575 mcg/day for children between one and twelve years of age, and 750 mcg/day for adolescents and adults. Information on trends in vitamin A supply is available for a few countries, indicating no general improvement (ACC/SCN, 1987). It seems clear that it will be many years before the deficit in vitamin A intake, particularly among the poorest population groups is made up in the absence of intervention. But several interventions are possible in principle to increase the regular intake of vitamin A from the diet itself, without waiting for economic development to solve the problem. Some examples of these are discussed by Dr. Devadas in her commentary on this paper. Options for intervention include: nutrition education; improving home production and consumption through gardens; and marketing of certain vitamin A rich commodities. These have been tested with some success in pilot programmes, but few if any are yet clearly established as effective on a large scale.

Nutrition education in this context aims to increase the intake of dark green leafy vegetables and other carotene and vitamin A rich foods. Where necessary, increasing fat consumption may also be promoted. Devadas describes in her commentary one study where dietary practices were modified, and signs of vitamin A deficiency reduced. In general, nutrition education has a mixed record (see Hornik, 1985), but, for example, the recently successful social marketing approach in Indonesia apparently improved vitamin A status among other benefits. Messages aimed at increasing vitamin A intake should be part of nutrition education programmes, even if such programmes may usually have broader objectives.

Promotion of local production of carotene-rich foods for home consumption, by home and school gardens, has obvious potential for preventing vitamin A deficiency. Households with even small gardens in Bangladesh, for example, had less vitamin A deficiency than those with no gardens (Cohen et al, 1985). The Asian Vegetable Research and Development Centre (AVRDC), supported by USAID, has long experience in this. Again, the position seems to be that small-scale trials are efficacious, but expansion for wide impact is yet to come.

Certain carotene-rich commodities, of which red palm oil is an important example, are culturally well-accepted in the diet, indeed potentially in high demand in certain countries where vitamin A deficiency occurs. The prospect of preventing vitamin A deficiency by more effective marketing of red palm oil has been put forward in Tanzania, for instance (Kavishe, 1985). In such cases, the economic and social constraints to wider consumption must first be understood. Here interventions on supply, pricing and market distribution could bring long-term improvement in vitamin A status.

Choice of Interventions

The decision on the part of agencies and governments to commit resources to controlling vitamin A deficiency depends on an appreciation of the priority of the problem - severity, extent, trends, and consequences; and knowledge of possible solutions - in terms of feasibility, costs (financial, organizational), effectiveness, sustainability, benefits, and the like. Present knowledge relating to the priority for controlling vitamin A deficiency was introduced above, and the West and Sommer paper gives many more details. Possible solutions are widely agreed as mass distribution, fortification, and/or dietary modifications. West and Sommer focus on mass distribution below. What guidance is available on the choice of control method, and specifically where does mass distribution fit?

Recommendations from international bodies, and decisions taken by governments and agencies, are consistent in the view that a combination of interventions is usually appropriate. Mass distribution is considered an essential first component of a control programme, certainly where severe deficiency exists, because of the immediate risks to sight, health and life and the possible rapid effectiveness of the distribution programme, moreover at moderate initial cost. The case for fortification, made by Dr. Arroyave in his commentary, requires initial research on suitable methods, and although widely applicable, it may not invariably reach those most at risk. Nonetheless, fortification programmes once established hold promise of sustained control over periods of years. Both mass distribution and fortification need to be underpinned by the increasing dietary intake of vitamin A, as discussed above; but this approach will take the longest time to establish. Thus in most cases, the first intervention to be established should be distribution of oral doses of vitamin A as capsules or oil solution.

A decision to tackle vitamin A deficiency will thus usually need to consider the details of mass distribution methods laid out in this paper. In principle there are three major systems for vitamin A capsule delivery, defined by West and Sommer (Section 3) as: medical, targeted and universal. “Medical” delivery means treating with vitamin A children with xerophthalmia or those at risk because of sickness; “targeted” delivery refers to a periodic preventive dosing directed to designated groups, generally within the health outreach programme; and “universal” delivery refers to a wider distribution aiming to cover all children (and other select groups) on a regular basis. These systems overlap. Vest and Sommer compare combined medical and targeted approaches with universal delivery. To maximize the impact of the vitamin A dose delivery, they also note the possibility of selecting target groups based on age (in Indonesia, 89% of corneal disease were found in children between one- and three-years-old), neighbourhood (in Indonesia, a “clustering” of xerophthalmic children was found in neighbouring houses) or region (in Bangladesh, a six-fold difference in mild xerophthalmia prevalence rates was reported between regions). Policy makers must determine the most efficient and effective approach for their country, based on the extent to which xerophthalmia is a problem, the degree to which an infrastructure exists for intervention, as well as resources available for programme implementation. One purpose of the Vest and Sommer paper is to provide information to guide this choice.

Resources Needed for Distribution of High Doses of Vitamin A

The major resources required are more the means to deliver doses than the cost of the capsules themselves. Cost estimates are available based on existing studies, as discussed below by Vest and Sommer. For example, although one standard dose vitamin A capsule costs less than $0.02, the cost to actually deliver the vitamin in the field is estimated at around $0.4 per recipient per year. The principle of marginality may be applied, so that costs normally occurring without vitamin A distribution should not be attributed to the vitamin A programme, and additional costs may be less than this figure. Thus integration is critical in determining cost-effectiveness. For example, essential drug programmes include delivery of standard medical packages to the field clinics. In designating vitamin A as an essential drug in the country's health system, an efficient mechanism of distribution may exist, and the marginal cost of distributing vitamin A may be reduced. A comparable estimate for fortification would be around $0.5 per child recipient per year (Arroyave et al, 1979).

The major supplier of the standard dose vitamin A capsule is UNICEF, except in India where doses are manufactured locally. UNICEF's vitamin A procurement increased between 1981 and 1985 from 3 to 80 million capsules annually, with a 1985 expenditure of $1.2 million. However, only around 20% of estimated global requirements are being met (Eastman, 1986).

Vest and Sommer discuss cost-benefit calculations for vitamin A distribution (See Section 7). In preventing nutritional blindness in children, not only are the well-being and livelihood of the child affected, but also the status of the surrounding support system. Additionally, with the data emerging from Indonesia on child survival, preventing vitamin A deficiency can clearly impact on child morbidity and mortality. With the lifetime disability arising from nutritional blindness, compounded by the morbidity and mortality influences which now seem evident from vitamin A deficiency, the authors are clear that economic benefits are far in excess of programme costs.

Both managerial and technical issues are discussed in this paper and the commentaries. The managerial issues of programme implementation are crucial. These are not unique to vitamin A. The vitamin A dose itself is considered generally safe, with due attention to preventing too-frequent dosing; distribution does not require a cold chain; and the programme is normally well accepted by a community. Operational difficulties range from logistics and supplies to supervision and worker incentives, from training and use of all levels of health workers to community participation and education. Many vitamin A programmes begin semiautonomously, as part of a health system yet retaining a separate budget and specific mandate, expecting that once institutionalized within a medical/health training curriculum, incorporated into existing job descriptions, and part of routine supply packages, the programme will be sustained over time. Experience with sustainability is limited, and is a question of continuing concern.

Prevention and Control of Vitamin A Deficiency

Vitamin A deficiency can be prevented by well-proven interventions. The mass distribution of high doses periodically, as described by Vest and Sommer, would almost always form an early and crucial part of any control programme. Activities in this area are underway, but must be greatly accelerated otherwise preventible blindness and child deaths from vitamin A deficiency will continue far into the future. The United Nations system has put forward a ten-year plan (ACC/SCN, 1985), launched at WHO in Geneva in October (ACC/SCN, 1986b). The objective of this inter-agency programme is to reduce the worldwide prevalence and severity of vitamin A deficiency, xerophthalmia and nutritional blindness to the point where they are no longer significant public health problems. What needs to be done to start this process?

Countries with vitamin A deficiency in their populations need to establish or build up national prevention and control programmes. A number of government sectors may be involved, particularly agriculture, education, health and social services. Programme development requires assessment of the problem and of potential interventions; decisions on policy and resource commitments; and, in many cases, access to external assistance - financial, supplies, and/or technical. National capabilities may need to be strengthened in these areas.

There are three aspects of possible external assistance in this. In the first place, national prevention and control programmes require planning, as a prerequisite for funding and organizational commitments. Governments should be able to call on the UN agencies, and donor governments, to help where necessary: often through assistance to national institutions. Second, many countries will wish to request external assistance for implementing prevention programmes, which in turn requires drawing up suitable proposals for donor agencies and governments: here again, help either in developing the proposals themselves, or in building the capability to do this may be warranted. Third, national capacity for implementing prevention programmes - for organization, monitoring, and administration - may be inadequate and external assistance may be appropriate to develop this capacity. Assistance in these and other areas is proposed in the UN ten-year programme, to support a sustained effort.

The costs of a global ten-year programme to control vitamin A deficiency can only be approximated at this stage. Early steps in the programme would involve better assessment of the extent and distribution of the problem, and methods of delivery of vitamin A. Results of these assessments will determine expected costs. Here, we should distinguish costs of supplies - primarily for vitamin A capsules - and for programme development and delivery. Cost of supplies is a relatively small proportion of the overall need. Vitamin A is cheap, about two US cents per capsule, and only two per person per year are required for effective prevention. Delivery costs depend on targeting, degree of reliance on existing services, etc., and are hard to estimate (especially as additional or marginal costs). However, some preliminary estimates can be made, from UN agency contributions to the ACC/SCN ten-year proposal, and from estimates of populations at risk discussed above (see Table 1).

First, the estimated pre-school population in the 34 affected countries is about 280 million. Total coverage of pre-schoolers would thus require about 500 million capsules per year. UNICEF (1987) estimates that current (1985) capsule procurement is 21% of need; this procurement is estimated at 148 million (Eastman, 1986, Table 17), i.e. total requirement is about 700 million capsules, including older children and mothers. On the other hand, the numbers of cases of mild/moderate vitamin A deficiency may be around 40 million children, so with exact targeting 80 million capsules per year would be needed for this group. This data at least gives bounds to the estimate, say between 100 and 700 million capsules per year, i.e. $2 to $14 million per year, for supplies. Second, WHO's (1985a) proposal is costed at $25 million over 5 years, which includes planning, support to delivery systems, etc. FAO (1985) has estimated that $7.5 million over 5 years is required to develop programmes for dietary modification in 21 countries (those in WHO categories A and B). In addition, USAID's prevention programme in 6 countries is budgeted at approximately $3 million (excluding research, USAID, 1987).

Such estimates do not generally include the costs of the delivery system, for capsules; Vest and Sommer below quote estimates of around $0.2 per capsule dose taken, about ten times the cost of the capsule itself. These figures attempt to estimate the marginal or additional cost of delivering vitamin A doses, for example through the health system. However, the additional costs will vary greatly and can presumably be substantially reduced by effective use of - or integration with - the existing services. For example, distribution as part of essential drugs programmes, and with immunization campaigns, is being explored.

The inter-agency meeting for launching the ten year coordinated programme for prevention of vitamin A deficiency was attended by representatives of many agencies and governments. The proposed programme was firmly supported, coordination of roles and sharing of experience were agreed, and the intention of finally reducing the human toll from vitamin A deficiency whole-heartedly endorsed. The technology and the coordinating mechanisms at international level are in place. The reality has now to be brought about.

This State-of-the-Art paper, by two of the leading researchers in the vitamin A field, Drs. Keith West and Alfred Sommer, is intended as a contribution to the worldwide, inter-organizational efforts. It can provide authoritative guidance and practical details based on their own and others' work. The commentaries, from experienced contributors to the vitamin A field, expand on their views, give alternatives, and introduce the two other strategies of fortification and dietary modification.

Finally, we can echo the conclusion of the meeting (ACC/SCN, 1986b) that launched the ten-year programme - when the reality of scarce resources was addressed. “It would be a terrible irony, at a time when all of the major ingredients for success are at hand - scientific knowledge, inexpensive and effective technology, and accumulated practical experience - if the world development community were prevented from taking action for want of a modest increase in resources. It is indeed possible to envision a time when vitamin A deficiency will rank among the nutritional scourges of the past. Participants in the meeting were unanimous in the view that this historic opportunity must not be missed”.


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