Results

POPULATION

The total population of the three villages increased from 1500 in 1979 to 2700 in 1993. Annual births averaged 98 in the quinquennium 1979–83; 92 in 1984–88; and 108 in 1989–93. Overall, 1190 children aged 0–2 years are involved in our analysis.

MORTALITY

Infant mortality has not changed appreciably over the 15 year period (1979–83, 44/1000; 1984–88, 39/1000; and 1989–93, 48/1000).

DIARRHOEAL DISEASE

Table 1 shows the total number of clinic attendances for children under 2 years over the period 1979–93, together with the number and percentage of all attendances in this age group caused by diarrhoea. It is obvious that there have been large changes in both sets of figures. However, the distribution of diarrhoea over the years follows similar annual patterns (fig 1), with consistent peak levels in the rainy season (July to September) and a small peak early in the year, previously shown to be caused by rotavirus epidemics.13This seasonality is consistent with an overall reduction of diarrhoeal illness, rather than a reduction in particular epidemic pathogens.

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Figure 1

Five year averages for clinic attendance with diarrhoea in children under 2 years of age for the periods 1979–83, 1984–88, 1989–93.

Table 2 shows a very similar pattern for diarrhoea among call clinic attendees, suggesting that both the incidence of diarrhoea presenting at the clinic and the prevalence have declined. Figure 2 shows that diarrhoea is less prolonged. In 1979, 26% of children returned within 10 days still complaining of diarrhoea, whereas in 1993 the same figure was 17% of children, and most returned in the early days of the disease.

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Figure 2

Percentage of children under 2 years of age returning to clinic within 10 days of first presentation still suffering from diarrhoea, 1979–93.

WEIGHT AND LENGTH

Figure 3 shows mean weight Z scores at 1 and 2 years of age according to the year of birth, based on an annual average of 80 weights at 1 year and 55 at 2 years. There is some movement away from the villages as mothers may “transfer” after childbirth to live with their husbands in urban areas, and in the 2nd year, as children are weaned from the breast and sent to grandmothers. Despite a dramatic reduction in the incidence and prevalence of diarrhoeal disease, there was no improvement in weight gain in the study children over the first 2 years of life for the period 1979–93. Mean weight Z scores (SD) at one year were −1.8 (0.9) in 1979 and −1.8 (1.1) in 1993. At 2 years, these figures were −2.0 (0.7) in 1979 and −1.9 (0.9) in 1993. Likewise, length measurements showed no significant change over this period. Mean length Z scores at 1 year were −1.3 (1.0) in 1979 and −1.7 (1.0) in 1993. Corresponding mean length Z scores at 2 years were −2.0 (0.9) in 1979 and −2.1 (0.9) in 1993. The similarity in SD of the Z scores over the survey period rules out the possibility that the lack of change in mean Z scores is a result of some children doing better, but others doing very badly yet surviving, during the latter part of the study, whereas they might have died in the early years of study.

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Figure 3

Mean weight Z score for children at 1 year and 2 years of age, 1979–93.

Discussion

The fall in the number of children presenting to our clinics since 1979 with symptoms of diarrhoea is impressive. It could be argued that this reflects greater ability of parents to manage diarrhoea at home since the introduction of ORS,14 with its availability from the unit or from individuals within the villages altering the management of diarrhoea. However, the decline in the number of children attending with diarrhoea has been fairly steady over the years, rather than occurring in the early 1980s when the introduction of ORS might have been expected to have had an impact. Thus, we believe that the fall in cases cannot be fully explained by the use of ORS. Furthermore, we continue to see most children with diarrhoea in the first days of illness, whereas if most cases were managed at home, we would expect that only those whose home treatment had failed would attend the clinic. In this case, presentation would be later into the illness and diarrhoea more likely to be protracted. Our evidence is that not only have the numbers of presentations with diarrhoea fallen but so have the number of days children are ill with each episode of diarrhoea. Moreover, diarrhoea prevalence as suggested by call clinic data also indicates that diarrhoea is less common than in the late 1970s.

The trend towards less severe diarrhoea fits in with more widespread surveys. The overall decline in diarrhoea incidence is less well documented. As mentioned above, Bern and colleagues2 found the prevalence of diarrhoea worldwide to be about the same as 10 years before, but the overall morbidity appeared significantly less. It would be heartening to feel that the decline in diarrhoea was a reflection of greater resistance to the complications of diarrhoeal infections owing to improved nutrition. Clearly, with our children this cannot be substantiated. We have to accept that the position we adopted in the 1970s,8 that removal of diarrhoea from the population of young children would result in almost normal growth, is no longer tenable. Despite an ∼ 75% drop in diarrhoeal illness and a reduction in the number of days ill with diarrhoea, the average weights and lengths at 1 and 2 years of age in our population have not increased over the years 1979–93.

The change in the number of children presenting with diarrhoea is dramatic. Why has this occurred? Poor quality water sources and inadequate sanitation are often considered as contributing to the prevalence of diarrhoea.15 16 Have changes in these accounted for the changes in the incidence of diarrhoea in our villages over the 15 years of study? In the early days of the Dunn Nutrition Group in Keneba, most water was obtained from hand drawn wells on the compounds.17 There were fewer latrines and specific areas of the bush were often used for sanitary purposes. Now one village has four taps delivering water from a borehole and all villages have covered hand pumped wells. Open wells on the compounds have largely run dry owing to a falling water table and lack of use because of other water sources. Most villagers have shallow pit latrines on their compounds. These changes have all been present for the past 10 years and do not adequately explain the progressive fall in diarrhoea. A study here in 1990, involving a health promotion programme which stressed the importance of hand washing, showed decreased skin and eye infections and reduced rates of diarrhoea but no decrease in respiratory tract infections in the children of families receiving the hand washing advice.18 However, this project cannot account for the decline in diarrhoeal incidence and prevalence before 1990. After 1990, the decline seems to continue a steady downward, rather than sudden stepwise, trend. Studies elsewhere have suggested that it is only with substantial changes in sanitation and water sources (flush toilets as well as tapped water supply) that falls in diarrhoea prevalence are associated with water/hygiene developments.19 20

We are disappointed by the lack of association between reduction in diarrhoea cases and nutritional status of the children. However, our findings are not unique in this respect.10 11 A recent retrospective study of Aboriginal children in north west Australia21 from 1969 to 1993 demonstrated that declines in the incidence of low birth weight, mortality, and infectious disease were not accompanied by improvements in the growth patterns of children 0–60 months old. Reductions in the incidence and prevalence of diarrhoea are undoubtedly important for child health and morbidity; but it is clear that policies to reduce diarrhoea cannot alone be expected to achieve the hoped for improvements in growth and in rates of malnutrition in young children.

It could be interpreted that our study shows the importance of inadequate dietary intake, as opposed to infection, in leading to growth faltering and failure of catch up growth in poor village children. Yet we have shown previously that communal macronutrient supplementation of village weanlings does not improve overall growth.22 Catch up growth has been induced in our young child population after diarrhoea by ensuring energy intakes 50% in excess of recommendations and protein intakes 100% more than recommended.23 But such intakes only achieved rapid catch up growth during the period of supplementation and even then the rates of growth fell far below the catch up expected in recovery from acute severe protein energy malnutrition: kwashiorkor and marasmus.24 That catch up growth can be induced with these very high intakes is not in itself evidence that poor growth is caused by intakes below recommended levels. Energy and protein supplementation can induce improved growth in conditions such as cystic fibrosis25 and in high output congenital heart disease.26 This does not indicate that affected children are necessarily having intakes less than recommended, but that extra food can overcome some of the consequences of illness.

We are still left with the question: why do young children in so many underdeveloped rural communities grow so poorly? In Keneba we have studied the effects of providing macronutrient supplementation22 23 and micronutrient supplementation27 28; we have succeeded in reducing the prevalence of severe illness and mortality in young children29; we have carried out vigorous programmes of nutrition education¹⁸; and currently we are in the process of investigating the role of enteropathy in young Gambian children.30 31 Yet we continue to see patterns of growth that define half the village children as moderately malnourished (< 80% expected weight for age) by the end of their 1st year, despite above average rates of growth in the first 4 months of life.

It is sometimes suggested to us that the “growth faltering” we are studying is “normal growth” for these children. This is not likely, given that they show such good growth in the first 4 months. The shape of the growth curve is not equivalent to any known normal childhood growth pattern. Moreover, within our population there are some children who do pursue expected patterns of growth. We must accept that the average growth pattern of Keneba children is abnormal and pathological.

Again, it could be argued that if these children grow poorly because of malnutrition this might be a natural way of using the limited amounts of food available to best advantage. However, small is not beautiful in terms of childhood nutrition. There is good evidence that even mildly malnourished children are more at risk of death from infection32; low physical fitness as older children and adults33; neurodevelopmental impairment34 35; and a greater propensity to conditions such as hypertension36 and diabetes37 in later life. We might be unable to explain nutritional stunting in disadvantaged populations, but we believe that it is a problem that we must continue to explore for the benefit of present and future generations.