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Editorials

Adult obesity and growth in childhood

BMJ 2001; 323 doi: https://doi.org/10.1136/bmj.323.7325.1320 (Published 08 December 2001) Cite this as: BMJ 2001;323:1320

Children who grow rapidly during childhood are more likely to be obese as adults

  1. Catherine Law, senior lecturer (claw{at}mrc.soton.ac.uk)
  1. MRC Environmental Epidemiology Unit, Southampton SO51 0QJ

    Over half of all adults in the United States and the United Kingdom are overweight, and developing countries are increasingly facing the public health problems of overnutrition as well as undernutrition.1 In the past 20 years or so, the prevalence of obesity and overweight in both adults and children has increased dramatically.2 These time and geographical trends argue against a primarily genetic cause of obesity, and both behavioural and pharmaceutical interventions in obesity have limited effectiveness.3 Prevention through environmental, social, or behavioural interventions is a logical focus for tackling this epidemic.

    The possibility of preventing adult obesity by taking action in infancy and childhood is attractive. Several studies have shown a weak relation between being heavy at birth and becoming overweight in later life. Others have found that faster growth in childhood predicts obesity in adulthood.4 In this week's issue (p 1331) Parsons et al replicate these findings in a large British birth cohort study followed to age 33.5 Unlike earlier studies, this study has data to take account of confounding factors that may be associated with both birth weight and with later fatness and to examine whether the relation between birth weight and obesity is modified by childhood growth. These potentially complex interrelationships may hold the key to effective preventive strategies.

    Parsons et al find that the positive relation between birth weight and later body mass index is largely accounted for by maternal weight—heavier mothers have heavier babies who tend to become heavier adults. A father's weight, however, does not influence the risk of adult obesity in his children. Though the poorer quality of measurements of fathers' variables may explain this discrepancy, the greater influence of maternal nutrition seems more likely. Whether this acts biologically or behaviourally, prenatally or postnatally, cannot be determined by this study. It suggests that interventions to prevent obesity in women of childbearing age give long term benefit to their children, and the women themselves; such interventions merit evaluation.

    Because rapid linear growth is often accompanied by accelerated weight gain, it may not be surprising that children who grow rapidly during childhood are more likely to be obese as adults. Many of these children would also have been heavy at birth. Parsons et al found, however, that those who were most vulnerable to developing obesity in association with rapid childhood growth were men who had been light at birth or who had thin or light mothers. This is an important finding as this pattern of growth is becoming common in developing countries that are experiencing a nutritional transition to Western lifestyles. In such countries, women tend to be small, following an impoverished childhood, and intergenerational effects lead to the persistence of high prevalences of low birth weight.6 Changing economic circumstances and population lifestyles, however, make rapid postnatal weight gain likely, perhaps particularly in boys, who may receive preferential treatment in the sharing of food.7 In developed countries, individuals who may be at increased risk because of their pattern of growth are those born prematurely or after intrauterine growth restriction. They have low birth weight and then grow up in a society with low levels of activity and high levels of dietary fat and sugar.8

    During critical periods of their lives individuals are particularly vulnerable to external influences. Programming occurs when an adverse influence acting during a critical period permanently alters the structure or function of a developing or plastic organism.9 The role of intrauterine life as a critical period for the aetiology of adult disease, particularly in the development of cardiovascular disease and its risk factors, has been debated vigorously. 10 11 The observations of Parsons et al suggest that early childhood is one critical period for the development of obesity. Intrauterine life is a further critical period in defining a group of individuals (boys who are light at birth) who are more vulnerable to the effects of rapid growth in childhood.

    The critical period for intervention and the potential of programming to prevent disease has received less attention in research and debate. Experience in clinical intrauterine growth restriction and in the management of high risk pregnancies has shown that fetal growth is difficult to influence. Childhood growth may be more amenable to environmental interventions, but there is limited information on the prevention of obesity in children.12 Instead of concentrating research efforts on developing drug treatments for established adult obesity, perhaps we should use what we know already to design and evaluate social, behavioural, or policy interventions aimed at children.13 Association does not equal causation, but systematic reviews of observational studies such as Parsons et al's may guide us to the groups of individuals who are most at risk of adult obesity and the critical periods for intervention.

    Footnotes

    • CL gave an invited talk at the European Obesity Congress 2001, for which she was paid expenses.

    References

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    View Abstract