Commentary: Catch-up growth in humans—a comment on poverty, birthweight, and infant weight gain in Hertfordshire

Peter C Hindmarsh

London Centre for Paediatric Endocrinology and Metabolism, Institute of Child Health, University College London, London, UK

Correspondence: Professor PC Hindmarsh, Cobbold Laboratories, Middlesex Hospital, Mortimer Street, London W1T 3AA, UK. E-mail: p.hindmarsh{at}ucl.ac.uk

There is no doubting the influence of poverty on a variety of health indices particularly those associated with cardiovascular disease. Ante and immediate post-natal growth are particular stages of human growth and development that are likely to be susceptible to socio-economic factors, as each phase of growth is dependent, predominantly, on nutrient delivery.1 Marked reductions in food intake, as in the Dutch famine of 1944, do influence growth but in Western society such deprivation is unusual and the effects of more subtle reductions in nutrient intake are more difficult to discern.2 Reduced growth in utero and/or rapid post-natal weight gain have been associated with an increased likelihood of cardiovascular disease as an adult. Although considerable interest has focused on ante natal growth, the rapid accumulation of weight in the post-natal period appears to be more important.3,4 This weight gain has been loosely, and incorrectly, termed 'catch-up' growth—a process which only refers to an increase in length and not weight. Attention to this delineation of anthropometric change is important as it is not implicit that changes in weight mirror changes in length. Intrauterine growth restriction associated with smoking, for example, results in a rapid increase in post-natal weight but not length.5 This discordance implies either differences in the growth factors regulating body composition and stature or else a more lasting effect of the substance(s) in tobacco smoke on stature than on body weight.

One interesting aspect of catch-up growth is that the process is finely tuned to the target height of the individual, which is dictated in turn, by parental stature. Deviation from the trajectory by a disease process and correction of the disease abnormality often leads to a rapid phase of longitudinal growth, which comes to a natural conclusion with a normal growth rate once the original growth channel has been regained (Figure 1). Of note is the way in which the growth process gradually closes in on the predefined trajectory and that there is no overshoot as occurs in a number of other control systems.



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Figure 1 The effect of severe growth hormone (GH) deficiency on early growth and the effect of growth hormone therapy introduced at age 2.5 years. Rapid growth ensues following introduction of therapy until the growth channel expected from parental heights is reached. Thereafter normal growth follows this channel (50th centile). Closed squares illustrate bone age which is delayed and remains delayed indicating that the catch-up growth is true and not obtained at the expense of a disproportionate advance in skeletal maturity

 
In contrast weight gain shows completely different regulation. Deviations in weight, particularly those that have taken place in utero, are often associated with an increase in weight gain during the first 6–12 months of post-natal life. The trajectory that this pattern takes is not necessarily one of limitation and there does not appear to be as clearly defined a 'weight stat' as there is for length. As a result there is an opportunity for excessive weight gain, which only loosely relates to the weights of the family. A much more fluid situation appears to exist with overshoots in weight and not necessarily any return to the ideal body weight for that family in the longer term.

These observations would suggest that differing mechanisms exist to regulate these growth processes. For height, a critical factor appears to be the number of prechondrocytes that are available to undergo differentiation, cell division, and hypertrophy.6 This process appears to be regulated tightly as growth promoting therapies in short normal individuals do not lead to large gains in stature.7 With respect to weight, adipose tissue mass is largely determined in the last 8 weeks of pregnancy so any changes in the post-natal period are most likely to arise as a result of hypertrophy rather than any change in adipose cell number. Little is known of the factors that regulate these different processes, but they do appear to be modulated by a number of diverse environmental factors.

One of the factors which has been portrayed in the paper by Razzell et al.8 in this issue of the International Journal of Epidemiology is the impact of socio-economic status on post-natal growth. Despite a slight down-tracking in birthweight in the period studied between 1923–1939 there was, over the same time period, an increase in mean infant weight gain. Poverty, as measured by house rateable value, was associated with weight gain during the first year of life, but not with birthweight This appears to have taken place at a time when calorific intake per capita was rising. These observations highlight the point already made—maternal nutritional deprivation has to be quite severe to slow fetal growth whereas the post-natal period appears more susceptible to nutrient intake.4 But what might this putative nutritional 'poverty' represent? For example, protein intake in infancy stimulates early growth but not gain in fat9 highlighting again the importance of not assuming that weight or body mass index changes relate to fat as other body composition components may be involved.

What is missing from the paper is a mechanism(s) to explain these particular influences—what are the components and what is the magnitude of the effect(s). This is particularly important in the area of the fetal origin hypothesis because of concerns that the magnitude of the effect is quite small when contrasted with current and conventional risk factors.10 An understanding of the actual components is going to be important if some form of intervention strategy is to be planned for the future. The advantage, however, of identifying post-natal growth as an important factor in the whole process is that at least it is more accessible with the potential for careful interventions to be contemplated compared with the problems that face those who wish to investigate and manipulate antenatal growth.


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1 Karlberg J. On the modelling of human growth. Stat.Med 1987; 6:185–92.

2 Godfrey KM, Barker DJ, Robinson S, Osmond C. Maternal birthweight and diet in pregnancy in relation to the infant's thinness at birth. Br J Obstet Gynaecol 1997;104:663–67.[ISI][Medline]

3 Lucas A, Fewtrell MS, Cole TJ. Fetal origins of adult disease: the hypothesis revisited. BMJ 1999;319:245–49.[Free Full Text]

4 Singhal A, Lucas A. Early origins of cardiovascular disease: is there a unifying hypothesis? Lancet 2004;263:1642–45.

5 Power C, Jefferis BJ. Fetal environment and subsequent obesity: a study of maternal smoking. Int J Epidemiol 2002;31:413–19.[Abstract/Free Full Text]

6 Baron J, Klein KO, Colli MJ et al. Catch-up growth after glucocorticoid excess: a mechanism intrinsic to the growth plate. Endocrinology 1994;135:1367–71.[Abstract]

7 Hindmarsh PC, Brook CGD. Final height in short normal children treated with growth hormone. Lancet 1996;348:13–16.[CrossRef][ISI][Medline]

8 Razzell P, Spence C, Vines K. Poverty, birthweight and infant weight gain in Hertfordshire, 1923–1939. Int J Epidemiol 2004;33:1228–33.[Abstract/Free Full Text]

9 Hoppe C, Molgaard C, Thomsen BL, Juul A, Michaelsen KF. Protein intake at 9 months of age is associated with body size but not with body fat in 10 year old Danish children. Am J Clin Nutr 2004;79:494–501.[Abstract/Free Full Text]

10 Huxley R, Neil A, Collins R. Unravelling the fetal origins hypothesis: is there really an inverse association between birthweight and subsequent blood pressure? Lancet 2002;360:659–65.[CrossRef][ISI][Medline]





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