Adult socioeconomic, educational, social, and psychological outcomes of childhood obesity: a national birth cohort studyBMJ 2005; 330 doi: https://doi.org/10.1136/bmj.38453.422049.E0 (Published 09 June 2005) Cite this as: BMJ 2005;330:1354
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Dear Sir, It is certainly of interest that increases in birth weight are linked with increasing risks of obesity in childhood(1). However when the findings of this study (2) indicate that obesity limited to childhood has limited impact on many outcomes in later life, you cannot help but feel something is being missed? Given the adverse prognosis associated with obesity (3) in adulthood, surely it is important that the reasons for these findings become unravelled. Excuse me if what I say contains a little too much conjecture.
Several studies have found a strong link between low birth weight and an increased risk of ischaemic heart disease in later life (4). The risk of death was nearly three times as great in light babies. Several subsequent studies have confirmed the health benefits of a heavier birth weight, including reduced risks of stroke, heart disease and diabetes. From these results in can be argued that the consequences of some influences, including a high body mass index in childhood, depend on events at early critical stages of development. Simplistically this can be understood as a poorly nourished baby's body, imprinted with its prenatal experience, is born expecting to live in a state of food deprivation throughout its life. Thus its whole metabolism is geared to being small. Once born, the baby then finds itself in a time of plenty, it compensates by growing fast and certain systems are put under greater stress than previosuly expected. The evidence for the Barker hypothesis is my no means conclusive and is still a source of much discussion. The complex interactions between mother and foetus at both the level of genes and environment are clearly key in this debate and new evidence is coming to light (5,6). The thrifty phenotype hypothesis ( which suggests foetal adaptation to an adverse intra-uterine environment ) as explained above, does appear to be a good explanation of events.
However given the available evidence, it seems there may be two different groups of indiviuals who are go on to develop obesity in adulthood - one group with low birth weights and the other with high birth weights. The evidence also appears to suggest that there is a huge difference in the risk of various pathologies between the two groups. In the UK it seems that the latter group with higher birth weights may become more numerous over time, which may have some interesting consequences.
Dr B Dean
1. John J Reilly et al.Early life risk factors for obesity in childhood: cohort study. BMJ, Jun 2005; 330: 1357. 2. Russell M Viner and Tim J Cole Adult socioeconomic, educational, social, and psychological outcomes of childhood obesity: a national birth cohort study. BMJ, Jun 2005; 330: 1354. 3. M E J Lean. Prognosis in obesity. BMJ 2005:1339-1340. 4. Barker DJ, Winter PD, Osmond C, Margetts B, Simmonds SJ. Weight in infancy and death from ischaemic heart disease. Lancet. 1989 Sep 9;2(8663):577-80. 5. Kimm, Sue Y.S. Fetal origins of adult disease: the Barker hypothesis revisited-2004. Current Opinion in Endocrinology & Diabetes. 11(4):192 -196, August 2004. 6. Ong KK, Dunger DB. Birth weight, infant growth and insulin resistance. Eur J Endocrinol. 2004 Nov;151 Suppl 3:U131-9. 7. Flanagan DE et al. Reduced foetal growth and growth hormone secretion in adult life. Clin Endocrinol (Oxf). 1999 Jun;50(6):735-40. 8. Soto I N, Mericq G V. Fetal growth restriction and insulin resistance. New findings and review of the literature. Rev Med Chil. 2005 Jan;133(1):97-104. Epub 2005 Mar 10.
Competing interests: None declared
Competing interests: No competing interests