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The discussion began with an expression of concern (Waterlow) over the concept that children who become stunted at an early age might be 'programmed' so that they could never catch up. It is necessary to distinguish between what actually happens in practice, when the environment does not improve, and what is physiologically possible if it does improve. Certainly there are many situations in which catch-up does not occur. In Guatemala, for example, the distribution of length is almost normal at birth, but by 2-21/2 years there is almost no overlap with the reference distribution (Martorell). These children originally studied at INCAP are now young men and women, and their growth increment from about 3 years to adulthood is almost the same as that of the reference population, as was also found by Satyanarayana, Prasanna Krishna & Narasinga Rao (1986) in India. Thus it does seem that in these populations, once retardation of height growth is established, the deficit remains unchanged.
On the other hand, there are undoubtedly children in whom catch-up does occur, as shown in follow-up studies in South Africa (Keet et al., 1971) and Jamaica (Garrow & Pyke, 1967), and in the children in Peru who were adopted into well-off families (Graham & Adrianzen, 1972). Within any group there seems to be great individual variability. In Jamaica some children being treated for malnutrition grew phenomenally in length and others hardly at all, and there was nothing in the history or diet that differentiated them (Golden). Over the longer term, other factors may come in which are hard to measure, such as the level of social stimulation in the home (Richardson, 1976) and the extent of physical activity (Town).
Findings in different clinical conditions are also relevant. The child with renal failure who gets a transplant never catches up (Golden), whereas children with hypothyroidism or coeliac disease show complete catch-up treatment. Children with leukaemia treated by chemotherapy grow well, but not those who receive irradiation. However, even patients who have undergone radiation therapy or received renal transplants catch up when they are treated with growth hormone, provided that the delay is not too long (Lodeweyckx). Thyroid hormones are also important. Malnourished children have low levels of T4 and T3 and a low rate of conversion of T4 to T3, perhaps as a result of selenium deficiency. This should certainly be reversible. The increased growth of slave children described by Golden, when set to work and given more food, could have been triggered by increased thyroid activity.
The discussion then moved on to the question of what happens to the stunted child at puberty, although not very much is known about it. Controversy continues about the extent to which the biological clock is delayed and maturation and menarche retarded. There is some evidence of a catch-up in maturation, which would be self-defeating in terms of catch-up in final height (Martorell).
Information from cross-sectional data may be misleading. For example, current surveys of Mexican Americans in the US show growth along the 50th centile until puberty, when growth falls off This may be a cohort effect, reflecting retardation earlier in childhood, before they came to the US. Clearly longitudinal studies are essential, and the best way to analyse them is by the Preece-Baynes model. When this was applied to girls with Turner's syndrome, the pubertal growth spurt as such was normal, but the take-off point was lower, and so the end-point was lower as well (Lodeweyckx). (On the other hand, in the Indian study of Satyanarayana et al. (1989), in the boys who were most stunted at 5 years, the onset of puberty was delayed and the period of the adolescent growth spurt prolonged. Ed.).
The pubertal growth spurt involves
gain in weight as well as in height, and it has been suggested that it is the weight gain
that triggers the height gain. However, there is no evidence that intervention at the time
of puberty has any special effect on linear growth, and in any case it would not be
justifiable to delay intervention until such a late stage. The time for intervention is
early childhood, when growth is first becoming retarded.
Garrow JS & Pyke MC (1967): The long-term prognosis of severe infantile malnutrition. Lancet 1, 1-4.
Graham GG & Adrianzen TB (1972): Late 'catch-up' growth after severe infantile malnutrition. Johns Hopkins Med J. 131, 204-211.
Keet MP, Moodie AD, Wittmann W & Hansen JDL (1971): Kwashiorkor: a prospective ten-year follow-up study. S. African Med J. 45, 1427-1449.
Richardson SA (1976): The relation of severe malnutrition in infancy to the intelligence of school children with differing life histories. Pediatr. Res. 10, 57-61.
Satyanarayana K, Prasanna Krishna T & Narasinga Rao BS (1986): Effect of early childhood undernutrition and child labour on growth and adult nutritional status of rural Indian boys around Hyderabad. Hum. Nutr.: Clin. Nutr. 40C, 131-139.
Satyanarayana K, Radhaiah G, Murali Mohan R, Thimmayamma BVS, Pralhad Rao N & Narasinga Rao BS (1989): The adolescent growth spurt of height among rural Indian boys in relation to childhood nutritional background: an 18-year longitudinal study. Ann. Hum. Biol. 16(4), 289-300.
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