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Relationships among dietary quality, children's appetites, growth stunting, and efficiency of growth in poor populations

Barbara Elaine Golden and Michael Henry Nevin Golden

Abstract

In Jamica, as in other developing countries less well off, the diets of low-income children are low in energy and protein relative to recommended intakes. Dietary intake is further reduced by anorexia which accompanies infections as well as deficiencies of specific essential nutrients in the diet, such as essential amino acids, potassium, phosphorus, or zinc. Imbalanced diets also limit synthesis of lean tissue and result in growth failure. The results of food-supplementation studies in young children in the developing world have indicated little effect on weight or height gain. In spite of being offered large amounts of dietary energy, the children receive far less than intended because of the anorexia caused by infection, specific nutrient deficiencies, and imbalanced diets. Attention should be paid to nutrient balance (quality) as well as nutrient intake (quantity) in both diets and dietary supplements offered to these children.

Child feeding and growth in Jamaica

The majority of all children live in the developing world, in the tropics. Most live in poverty A major characteristic of poverty is monotony. This applies particularly to children's diets [1].

In Jamaica, poverty still prevents and tradition still forbids the feeding of a wide range of foods to small children [2]. Exclusive breast-feeding is rare. Often, within a few weeks of birth, it occurs only at night. Infants are mostly bottlefed strained, sweetened maize-meal porridge to which is added a variable, small proportion of infant formula. On analysis, the energy density of such foods is low: the children's energy intakes are low, often lower than their protein intakes relative to recommended intakes [3]. The foods are usually heavily contaminated with faecal bacteria [4]. Sweetened bush teas, a few highly toxic, are also given daily to prevent and treat fevers, colds, and diarrhoea [5]. Older children receive the same monotonous diet except that the porridge becomes thicker; solid foods, including meat, are rarely offered [2].

Appetite

Children fed such diets are not starving. Instead, at around one year of age they are still apparently satisfied with small, infrequent feedings. During their frequent infections, they are more obviously anorectic and lose weight. Often, however, they do not catch up in weight between infections [6]. In other words, their appetites seem to be inappropriately low. This relative anorexia has not been sufficiently recognized, let alone studied. Psychological problems are also common among deprived children [7].

Physical problems, particularly infections, may be present but undiagnosed. In association with undernutrition, the inflammatory response may be so diminished [6] that anorexia is the only sign of infection. Presumed small-bowel overgrowth by anaerobes, diagnosed clinically by gaseous intestinal distention, foul faeces, and anorexia, is common in undernourished children. Appetite improves with treatment with metronidazole, which strongly supports the clinical diagnosis; a height spurt occurred over six months after a five-day course of metronidazole in undernourished children [8].

We suggest that imbalanced diets also play a role in the anorexia of these children. As the diets are so limited in variety, the chance of their being imbalanced is increased. Thus, when the source of dietary protein is limited to just one main food item, vegetable in origin, an essential amino acid may be deficient for prolonged periods. For example, maize-meal protein, zein, is relatively deficient in tryptophan. In the experimental setting, imbalance of essential amino acids is a classic cause of anorexia [9]. Other essential elemental nutrients, including potassium, phosphorus, calcium, magnesium, iron, copper, and zinc, may also be relatively deficient, particularly when bioavailability from vegetable-based diets is reduced. Reduced bioavailability is due mainly to the chelating property of phytate on calcium, zinc, iron, and copper cations [10]. However, even without taking this into account, we have demonstrated previously [11], using food composition tables and recommended intakes, that it is almost impossible to receive a protein-deficient diet based on common foods that is not more deficient in zinc. Anorexia is a characteristic feature of zinc deficiency in experimental animals and humans [12; 13] and also a feature of experimental potassium [14] and phosphorus deficiencies [15; 16].

Growth

Jamaica is a relatively well-developed developing country. In the early 1980s its mean annual per capita income was US$909 [17], and its infant mortality rate was reported to be 27 per 1,000 live births. In retrospect, that was probably a gross underestimate: a more recent, more accurate estimate of perinatal mortality was 38 per 1,000 total births [18].

Growth failure, estimated usually as an increasing deficit in weight (and height) for age, tends to occur from about four months of age among the poor. A recent islandwide survey [19] showed that 17% of all children under five years old weighed below 80% of the NCHS standard for age. In much of the developing world this proportion is far higher. Most of the weight deficit is associated with height deficit: stunting often occurs without wasting, but only very shortterm wasting occurs without stunting.

The heights of low-income Jamaican teenage boys were compared with those of middle-income Jamaican boys of similar African origin and with the NCHS standards [20]. The heights of the two latter groups remained similar from 11 to 17 years but significantly greater, by about 9 cm, than those of the low-income boys. Thus, the low-income boys appeared to be stunted due to earlier, chronic, environmental stress: they did not catch up during their teens. This probably explains why the reported world prevalence of stunting (30%) is so high.

Unfortunately, evidence of impaired mental and physical development in stunted individuals [21; 22] implies that stunting may not be the only long-term effect of undernutrition in childhood. Thus, the problem of early growth failure, so common in the developing world, must be tackled urgently and successfully.

Prevention of growth failure

Among the many features of poverty associated with growth failure are low energy and protein intakes in early childhood. Thus, many attempts have been made to prevent growth failure by supplementing food intakes [23].

An examination of the results of many studies of the effects of providing food supplements - usually skimmed milk, various combinations of wheat and soya, or local foods - for young children in the developing world [24] concluded that the supplementation made little difference to weight or height gain. In many of the studies, the differences did not even reach statistical significance, let alone biological relevance, in spite of the offering of large amounts of energy. Clearly, the children were receiving far less than the intended extra energy. Supplements were shared and were substituted. It was recognized that this was probably, in part, due to anorexia "consequent to recurrent infection" in the index child. As indicated above, however, anorexia could also have occurred because of an imbalanced diet, a past or present diet chronically deficient of an essential nutrient such as potassium, phosphorus, zinc, or an essential amino acid.

Efficiency of growth

Normal growth requires a relatively large component of lean-tissue as well as adipose-tissue synthesis. The dietary requirements of these two differ. Lean-tissue synthesis requires, in particular, an optimal balance of amino acids and essential elements such as potassium, magnesium, calcium, phosphorus, and zinc. Adiposetissue synthesis requires, in particular, energy for storage as fat. If any one of the essential amino acids or elements is deficient relative to energy intake, as occurs on an imbalanced diet, the deficient nutrient would be expected to limit leantissue synthesis in particular. As a result, surplus energy and nutrients consumed - that is, other than the deficient nutrient - should become redundant and have to be either stored (e.g., energy in fat; iron in ferritin) or excreted. Hence, the energy cost of tissue deposition (ECTD) and the excretion rates of surplus nutrients should both be higher with an imbalanced than with a balanced diet.

Considerable evidence supports this hypothesis. When two healthy adults were fed a milk diet particularly depleted of potassium, they both developed negative phosphorus and nitrogen balances [25]. After nitrogen, phosphorus, potassium, sodium, chlorine, and calcium balances were measured in underweight adult patients receiving only parenteral nutrition, the supply of one of these essential elements was withdrawn, first nitrogen and then, in later experi meets, phosphorus, potassium, and sodium [26]. Removal of each element in turn resulted in a dramatic and statistically significant decrease in rate of weight gain and the balance of all the elements. Except for a lack of effect of the removal of potassium on the sodium balance, most of the balances became negative. The energy supplied, which was not altered, was incorporated in energy-rich adipose tissue. Since this accounted for most of the small weight gain, the ECTD increased considerably.

TABLE 1. Effect of zinc supplementation on children receiving a high-energy soy-based formula during recovery from severe wasting

Source: Ref. 31.
Values are means (SEM).
a. Energy cost of tissue deposition.

TABLE 2. Tentative classification of essential nutrients

Jamaican children recovering rapidly from severe malnutrition become fat: muscle synthesis lags behind adiposetissue synthesis [27]. Histologically, muscle fibre size in recovered Jamaican children nearly 14 months old was only 60% of that of normal 6-monthold children [28]. The results were the same in a study in Peru [29]. In both Jamaica and Peru the children's ECTD during recovery was high.

We have observed that those fed a high-energy soy-based formula with low zinc availability had an even higher ECTD than those fed a high-energy cow's-milk-based formula [30]. We hypothesised that this was because dietary zinc deficiency was limiting the synthesis of zinc-rich muscle in the children fed the soy-based formula, and that this formula was imbalanced at least with respect to zinc relative to energy. Subsequent zinc supplementation of the same formula resulted in increased rates of weight gain and decreased ECTD. Both changes correlated with the observed increase in plasma zinc (table 1) [31]. This evidence in favour of the hypothesis was subsequently supported by more direct studies of the effect of zinc supplementation on the composition of tissue synthesized during recovery from severe wasting [32].

Thus the efficiency of growth (albeit not "normal" growth), which is closely related to the capacity to synthesize protoplasm, has been demonstrated to be related to the dietary balance of nutrients essential to the synthesis of protoplasm in humans. This, of course, has already been put to use in the meat industry [33]: in Jamaica and elsewhere in the developing world, animals and poultry reared for their meat are fed cereal supplemented with essential minerals and vitamins. Children are fed the same cereal without supplements.

Type-I and type-II nutrients

Many essential nutrients, especially trace elements and vitamins, are not required primarily for synthesis of protoplasm. They have no obvious, direct effect on growth but are required for more specific tasks, such as the synthesis of thyroid hormones (iodine), haemoglobin (iron, cobalamine), and antioxidants (selenium, vitamins A, C, and E). Nutrients essential for specific functions other than growth have been called type-I nutrients, and those essential for growth type-II nutrients (table 2).

Diagnosis of deficiency of individual type-l nutrients is relatively simple in that they result in specific abnormalities of function, both clinical and biochemical. In contrast, deficiencies of type-ll nutrients are difficult to diagnose as a whole, let alone as individual deficiencies, because they all result in growth failure, but so do a variety of other, nondietary abnormalities, such as infections and inherited structural and metabolic abnormalities. Most of these are also associated with anorexia. When growth failure occurs for any reason, requirements for all the essential nutrients and energy are reduced [26]. Thus, if several type-ll nutrient deficiencies are present, growth will be limited only by the nutrient that is most deficient: the other deficiencies will be undetectable. If the most deficient nutrient is then given, growth failure will quickly recur because of the next most deficient nutrient, and so on.

In a similar way, a diet relatively short of a type-11 nutrient will not result in growth failure if growth has already failed for a non-dietary cause. When a type-lI nutrient deficiency causes growth failure, tissue concentrations of that nutrient and enzyme activities dependent on it tend not to be altered to anywhere near the extent expected. For example, zinc is required for muscle synthesis, but zinc-deficient rats show reduced muscle synthesis but no obvious change in muscle composition, including zinc concentration [35; 36].

Summary and conclusions

Many reasons exist for growth failure in poor children in the developing world. The usual diet supplies lower than recommended intakes of energy and protein. Anorexia further reduces food intake. It accompanies infections, including small bowel overgrowth. It may result from monotonous, imbalanced diets, as well as from diets deficient in particular essential nutrients such as amino acids, potassium, phosphorus, or zinc (type-II nutrients). Experimental evidence shows that such imbalanced diets also limit synthesis of protoplasm, in particular, lean tissue. This is associated with reduced growth efficiency.

In conclusion, growth failure in children living in poverty in the developing world may be due in part to a monotonous, imbalanced diet deficient in a type-II nutrient. If such is the case, there is no point in offering more of that diet or a supplement that does not supply an excess of the deficient nutrient. Thus, attention should be paid to nutrient balance (quality) as well as to nutrient intake (quantity) in both diets and supplements offered to these children.

Acknowledgement

Both authors are fully supported by the Wellcome Trust.

References

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