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It was accepted that impairment of linear growth is multifactorial. The important causal factors are threefold: nutrition, infection and the mother-infant interaction, which depends in part on the socio-economic/educational level of the family.
As far as concerns nutrition, the Panel agreed that although inadequate quantity of food cannot be excluded altogether, most stunted children are of normal weight for length or height. The emphasis was therefore on the quality of their diet. Several studies have suggested an effect of animal food on linear growth; the limiting factor could be amino acids, for example the sulphur-containing amino acids; micronutrients such as zinc; total fat, or specific components of fat. There is also the possibility of toxic factors in the nutrient supply.
Infections contribute through injury to the gastro-intestinal mucosa, leading to malabsorption, particularly of micronutrients, and to increased permeability to antigens and bacteria. The systemic effects of infections, mediated by cytokines, result in extra losses of nutrients.
Maternal nutrition and stores at birth are also important for the later development of the infant. The interaction between the mother and child is a very special one; even within the same family one child could have the right interaction and another not.
The epidemiological evidence suggests that falling off in linear growth usually begins within 4-6 months of birth. It is reasonable to suppose that up to this time the development of stunting is prevented by breast-feeding, not only through the nutrients, particularly micronutrients, that it supplies, but also the protective immunoglobulins and possibly growth factors. However, the work of Whitehead's group in Cambridge (UK) has shown that even in exclusively breast-fed children in a healthy environment linear growth begins to fall below the NCHS reference at about 4 months (Whitehead & Paul, 1985). It may be argued that this does indeed represent a temporary failure to achieve the full genetic potential for growth, since later these children catch up. It is therefore necessary to be cautious about stating that exclusive breast-feeding protects against stunting. In any case, exclusive breast-feeding up to 6 months is quite unusual, even in Third World populations. A further factor is appetite, which in weaning diets may be constrained by the bulk of the food or by too infrequent feeding. The high carbohydrate content of the diet perhaps has a satiating effect. Micronutrients may stimulate appetite, and infections have an important effect in reducing it. Here also the interaction with the mother plays a key role.
The above is a brief summary of the
general conditions that underlie the development of stunting. The Panel then went on to
consider mechanisms. At about the age when stunting begins the second growth spurt
described by Karlberg (see above) and attributed to growth hormone (GH) should be setting
in. Before that, growth hormone is present in very high amounts, but the receptors seem to
be inactive or in some species even absent (Lodeweyckx). The bone growth plate is formed
after birth (Nilsson) as a result of the formation of the bone epiphysis, and it is known
from rat experiments that GH can act on the formation of the epiphysis if the GH receptor
is present. Perhaps the retardation of growth is due to the fact that the GH receptor is
not expressed. This possibility might be studied, at least in muscle and fat tissue, by
biopsies taken in the course of elective surgery, for example for repair of hernias. To
relate the extent of expression of GH receptors to growth it is also necessary to have an
instantaneous measure of growth velocity. It was suggested that it might be possible to
measure the thickness of the growth plate by ultrasound. (NB: the question of biochemical
markers which might provide a measure of growth velocity is discussed in Robins' paper).
Whitehead RG & Paul AA (1985): Human lactation, infant feeding, and growth: secular trends. In Nutritional needs and assessment of normal growth, eds M Gracey & F Falkner, pp. 85-122. New York: Raven Press.
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