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Examination of the capacity for catch-up in affluent children, with stunting secondary to disease, has the advantage that these groups are less likely to have had early developmental problems and malnourished parents. On the other hand, even with treatment, their residual disease, previous surgery, special diets and drugs may each restrict their recovery. There are many case reports of impressive catch-up (Prader, Tanner & Harnack, 1963; Prader, 1978; Tanner, 1981). For example, two hypopituitary dwarfs were treated with growth hormone and androgen when aged 23 and 24 years; they subsequently gained 22 and 21 cm (Van der Werff Ten Bosch & Bot, 1986). Another patient, who had constrictive pericarditis, corrected surgically at the age of 18, subsequently gained 32 cm (Van den Brande, 1986). The patients each had delayed bone maturity. These reports serve to illustrate that catch-up is possible even at a chronological age when growth has normally ceased; where catch-up is not observed it does not mean that it is not possible-only that we have not yet found the correct way of bringing it about.
Most children with stunting secondary to renal or intestinal disease fail to catch up to their expected adult height.
7.1. Renal disease
In patients either treated conservatively or by renal transplantation, subsequent growth has been varied and disappointing (Guest & Broyer, 1991; Ingelfinger et al., 1981; Polito et al., 1987; Van Diemen Steenvoorde et al., 1987; So et al., 1987; Fennell et al., 1986; Ellis et al., 1985; Rizzoni, Basso & Setari, 1984). In general, one third of the children have a reasonable acceleration of height, particularly if they are less than 7 years of age (Ingelfinger et al., 1981). The failure to catch-up is mainly due to treatment with steroids. Those that have other types of immuno-suppression seem to have much better compensatory growth (Knight, Roy & Sheil, 1985), although there are reports of exceptional growth when steroids are given intermittently (Steendijk, 1986).
7.2. Intestinal disease
Prader's group (Barr, Shmerling & Prader, 1972) studied compensatory growth in coeliac patients, aged 9-15 months. These patients' height and bone age were similarly retarded. Complete catch-up was observed. The children were normal in height and bone age within two years of the start of treatment. Children over 3 years of age, when diagnosed, although severely stunted, usually have heights that are in keeping with their bone ages, and so complete catch-up growth should be achievable (Exner et al., 1978); however, in other centres about half these children fail to have a significant catch-up (Fagundes-Neto, Stump & Wehba, 1981).
Older children (11 to 17 years) with Crohn's disease show a marked height 'spurt' after surgery (Lipson et al., 1990). Follow-up of groups of short children with Crohn's disease into adult life shows that most attain normal adult height (Castile, Telander & Cooney, 1980; Markokwitz et al., 1993); about one third remain stunted. Permanent growth failure was much less common in subjects with stunting due to ulcerative colitis (10%) (Markowitz et al., 1993; Kirschner, Voinchet & Bosenberg, 1978).
Unlike inflammatory bowel disease,
complete clinical reversibility, without need for continued treatment, characterises
stunted children with trichuris dysentery syndrome. Cooper et al. (1990)
gave such children anthelminthic treatment without any other change in their
circumstances. The children had an enormous height spurt. This study is important because
it shows that children living in poor conditions in countries where stunting is common
can, even in later childhood, have very substantial catch-up in height.
Compelling data to show that remarkable catch-up is possible even under conditions of extreme privation, with a high prevalence of infectious disease, are presented by Steckel (1987). Following the abolition of the slave trade from Africa by the USA in 1807, all slaves which were transported by sea had to have their names, ages, sex and heights recorded on the ship's manifest. At this time many East coast slaves were sold to the Southern states. Steckel analyzed 10,562 voyages, from 1820 to 1860, carrying 50,606 slaves. The recorded heights, presented as centiles of present day (NCHS) standards, are shown in Fig. 7. The children were tiny by modern standards, as small as the Bundi tribes of the New Guinea Highlands. Between 15 and 17 years of age they underwent a spectacular catch-up in height to above the modern 25th centile for males and 35th centile for females. Final adult height was not attained until about 25 years of age in the females. As adults these slaves, who were so stunted as children, were taller than many contemporary communities in Europe or North America. One would not have expected slaves to catch up; at adolescence exhausting work was added to their burdens of disease and diet of hominy grits. However, as workers they received regular allocations of extra food, notably pork (about 1/2 lb per day). This extra intake of meat seems to be the only substantial change in their circumstances that could account for the almost complete catch-up. Slaves in other countries (Trinidad) did not show this phenomenon.
One other group of subjects has replicated this observation: boys admitted to the military school of the Habsburgs in the 19th century (Komlos, 1986). The students were children of ordinary soldiers who were markedly stunted, by modern standards, when they were admitted to the school. The nutritional conditions in the school are not reported but almost certainly exceeded those in their homes. The nutritional improvement was particularly great in those admitted just after the Napoleonic wars.
Both these data sets clearly show
that with an improved diet even adolescents can have an almost complete catch-up in height
without any change in hygiene, exposure to disease or purposeful intervention.
It is clear that many children do not catch up because we do not know what component of the diet is critical. There is evidence that some component of animal protein is particularly important (Allen et al., 1992). Certainly, it was milk that led to the dramatic catch-up growth of Bundi children (Lampl, Johnston & Malcolm, 1978), American teenagers (Dreizen et al., 1950; 1954; Spies et al., 1959) and Scottish school children (Orr, 1928): successful interventions that have rarely been emulated in the Third World. I have argued before that the major cause of stunting is a deficiency of one, or more, of the type 2 nutrients (Golden, 1988). However, the requirements for longitudinal growth and for ponderal growth seem to be quite different. This is best illustrated by examination of seasonal changes in height and weight gain. Brown, Black & Becker (1982) demonstrate that rural children in Bangladesh start to gain weight in September and continue to do so until about April of the following year. In contrast, they gain height from April until September. During the period of height gain their weight-for-age decreases. Assuming that the driving force is nutritional, what could be the reason for the difference?
In general, the type 2 nutrients are required by lean body mass to the same, or a greater, extent than skeletal tissue. The exception is sulphur and, perhaps, phosphorus. Cartilage, the tissue which expands in growth, is composed of a network of collagen fibrils with glycosaminoglycan (GAG) packaging. The essential amino acid content of collagen is much less than in most lean tissues, so their deficiency is unlikely to cause the differential. In contrast, the GAGs are composed of an amino acid stalk with numerous long sulphated carbohydrate side chains; each hexose unit contains a sulphate moiety as the only dietary essential component. This is why sulphur is required in much larger amounts to form cartilaginous tissue than soft tissue.
Could a diet limiting in sulphur cause a specific defect in longitudinal, as opposed to ponderal, growth? Most diets in the Third World are very low in sulphur, and urinary sulphate excretion is low in the normal population and in malnourished children (Ittyerah, 1969; Simmons, 1971). When sulphur amino acids are ingested, the requirements for methionine, cystine and glutathione will be met first; next taurine, sulphate for the cerebral sulpho-lipids, hepatic detoxification and thiosulphate formation (where cyanogenic glycosides are consumed - cassava). The sulphate destined for cartilage will then compete with that used for the production of mucus and the components of interstitial ground substance. Skeletal tissue is at the end of the pathway; it takes the residue; if there is no residue, there will be no growth in height.
There is very limited data to
support or refute the hypothesis that sulphur is specifically important in skeletal
growth. However, a sulphur drain, caused by tremendous mucus production, would
satisfactorily explain why diseases of the large intestine seem to be disproportionately
associated with severe stunting. Further, trichuriasis, a worm infestation which
causes very little inflammation but marked loss of mucus (Cooper & Bundy, 1988), is
associated with very marked stunting.
Although malnourished children are stunted, their bone maturity is usually retarded to a comparable degree. This is seen in impoverished societies as well as in diseases such as coeliac disease, inflammatory bowel disease and hormonal deficiency. When these children are followed to adulthood they normally have some degree of spontaneous catch-up.
With a change in environment, through adoption, emigration or with treatment of the disease there is usually definite catch-up growth, although it is often not to the NCHS standards. If puberty is delayed and/or growth continues into the early or mid twenties, then an acceptable final adult height is achieved. However, there may be a limitation imposed on an individual's maximum height by genetic imprinting in very early development. This may be the case where full catch-up appears to have taken place but is followed by an advanced puberty and early cessation of growth (Proos, Hofvander & Tuvemo, 1991a).
The data from US slaves and cases of hormonal replacement, where treatment was initiated after age 18, each show that, if the circumstances of children in the Third World change, almost complete reversal of stunting is possible. The children can reach their own height potentials. Total reversal to affluent societal norms would probably require cross-generational catch-up. The most obvious reason why catch-up is not seen regularly is that an appropriate diet is not available over a sufficient period of time. We do not know the optimum ingredients for such a diet. Sulphur has been neglected as an essential nutrient; its economy should be examined in relation to skeletal growth in stunted populations.
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