|Causes and Mechanisms of Linear Growth Retardation (International Dietary Energy Consultative Group - IDECG, 1993, 216 pages)|
|Linear growth retardation in relation to the three phases of growth|
There is still room for discussion about the natural history of stunting. In the Pakistan study there was some fall-off in linear growth even during the 'infancy' phase. This may be related, at least in part, to size at birth (see discussion of paper by Falkner). Deaths during the first month were related to length at birth. The general opinion was that, in this early phase, the problem was not one of nutritional deficiency. In Pakistan, during the first 6 months, only 15% of children had a seriously low weight-for-length (below -2 SD). Therefore it does not seem likely that the deficit in linear growth was a consequence of failure to gain weight. Similarly, in Chile young children get all the food they need and become overweight for length, but still lag behind in linear growth (Uauy).
It seems probable that infections have something to do with early growth retardation. Breast-fed children without diarrhoea gained 1.5 cm more than those who were not breast-fed and did have diarrhoea. Even in the absence of diarrhoea there was a small difference (about 0.5 cm) between children who were or were not breast-fed. Moreover, it must be remembered that there are other benefits from breast-feeding, in addition to the prevention of infection; it provides a special type of emotional bonding, which is very important for the child's growth (see paper by Skuse). Breast-feeding, however, did not give total protection against stunting because these children also received water, and water carries pathogens.
In any case, the main problem is the growth retardation that becomes much more serious after 6 months. In the Pakistan sample, only 3% had a deficit in linear growth between birth and 6 months, compared with 31% between 6 and 20 months. This is the time when weaning foods are being introduced and infections become more frequent. According to one opinion, this could be an adequate explanation of the falling off in growth and there is nothing more to be said (Neumann). Others, however, preferred to dig more deeply. The hypothesis proposed is that there is a lag in the onset of the childhood phase of growth, but what causes this lag? Karlberg's data showed that the children who faltered in the first 6 months were not necessarily those whose growth was most retarded later on. Growth in these two phases appeared to be independent. The correlation between growth velocity at 1 month and at 1 year was only about 0.6. Thus, though short-term changes may be useful for exploring mechanisms, they cannot provide projections.
There followed a discussion of hormonal responses, which may well be mediated by nutritional factors such as amino acids or minerals (see paper by Allen). No measurements of growth hormone were made in the Pakistan study' because it was not considered ethical to take the large number of blood samples needed to give a profile of GH secretion over 24 hours; in the future it may be possible to overcome this difficulty by urine assays - a possibility that is being explored at INCAP (Torun). It is well established that early in severe PEM, GH levels are increased. The hypothesis is that GH fails to stimulate growth in the childhood phase because of a defect in the receptors. One way of investigating this would be to see if there is any change in the amounts of receptor mRNA, but this has not yet been done (Nilsson). Another possibility is that there is no change in receptors, but a reduced production of IGF-1, so that the defect would be at the post-growth hormone receptor level. On either hypothesis, the defect would only appear when growth hormone enters the picture, at about 6 months. One example is coeliac disease; infants with this condition grow perfectly normally from birth to 6 months, but then they do not start the second phase of growth until they have been treated. If they are treated properly, growth resumes after 1-1½ months (Karlberg). But the question remains: what is holding up entry into the second phase? Even if we accept that the lag results from chronic malnutrition and/or infection, what is the mechanism? This remains a question for the future.