| Home | Help | Search/Archive | Feedback | Table of Contents |
|
|
||||||||
Children who grow rapidly during childhood are more likely to be obese as adults
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 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. MRC Environmental Epidemiology Unit, Southampton SO51 0QJ (claw@mrc.soton.ac.uk)
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.
Footnotes
CL gave an invited talk at the European Obesity Congress 2001, for which she was paid expenses.
| 1. | World Health Organization. Obesity: preventing and managing the global epidemic. Geneva: World Health Organization, 1998. |
| 2. | James WPT. The epidemiology of obesity. In: Chadwick DJ, Cardew G, eds. The origins and consequences of obesity. Chichester: Wiley, 1996:1-16. |
| 3. | NHS Centre for Reviews and Dissemination. Systematic review of interventions in the treatment and prevention of obesity. York: NHS Centre for Reviews and Dissemination, 1997:1-147. (Report No 10.) |
| 4. | Parsons TJ, Power C, Logan S, Summerbell CD. Childhood
predictors of adult obesity: a systematic review. Int J Obesity
1999; 23: S1-107 |
| 5. | Parsons TJ, Power C, Manor O. Fetal and early life growth
and body mass index from birth to early adulthood in 1958 British
cohort: longitudinal study. BMJ 2001; 323: 1331-1335 |
| 6. | United Nations Children's Fund. The state of the world's children 2001. New York and Geneva: Unicef, 2001. |
| 7. | Ramalingaswami V, Jonsson U, Rohde J. The Asian enigma. In: The progress of nations. New York: Unicef, 1996:11-17. www.unicef.org/pon96/nuenigma.htm (accessed 5 Oct 2001). |
| 8. | Childhood obesity: an emerging public-health problem.
Lancet 2001; 357: 1989 |
| 9. | Barker DJP. Mothers, babies and health in later life. Edinburgh: Churchill Livingstone, 1998. |
| 10. | Robinson R. The fetal origins of adult disease. BMJ
2001; 322: 375-376 |
| 11. | Dietz WH. Critical periods in childhood for the development
of obesity. Am J Clin Nutr 1994; 59: 955-959 |
| 12. | Campbell K, Waters E, O'Meara S, Summerbell C. Interventions for preventing obesity in children. Cochrane Library 2001;(3):CD001871. |
| 13. | Després JP. Drug treatment for obesity. BMJ 2001;
322: 1379-1380 |
|
|
||||||||
Read all Rapid Response responses
| Home | Help | Search/Archive | Feedback | Table of Contents |