IJE Advance Access originally published online on July 19, 2006
International Journal of Epidemiology 2006 35(4):1102; doi:10.1093/ije/dyl111
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Letter to the Editor |
Author's response to comments by Pallan, Cheng and Adab, and Hawlins and Law
1 Department of Social Medicine, University of Bristol, Bristol, UK.
2 National Heart & Lung Institute, Imperial College at St Mary's, London, UK.
* Corresponding author. E-mail: d.a.lawlor{at}bristol.ac.uk
Pallen et al.1 express concern that we appear to have focussed on biological early life determinants of obesity to the exclusion of environmental factors. In contrast, Hawkins and Law suggest that we have dismissed the importance of factors acting in infancy as key to determining adult obesity.2
We fully acknowledge the comment by Pallan et al.1 that obesity is the result of a complex interaction of environmental and biological factors. While it is commonly argued that biological factors cannot explain the rapid and sustained increase in obesity worldwide, they are clearly involved in its continuation. Further, the obesogenic environment has its impact through biological pathways. For example, we discuss the fetal overnutrition hypothesis in our editorial.3 The obesogenic environment may have led to greater obesity in women of reproductive age, but the ongoing epidemic may then be fuelled by biological processes involving the transfer of glucose, amino acids, and free fatty acids to the developing fetus and fetal programming of neuroendocrine systems.3 Pallen et al. quote Ebbeling, who also commented on the fetal overnutrition hypothesis, stating that ‘the obesity epidemic could accelerate through successive generations independent of further genetic or environmental factors’.4
Despite the call by Ebbeling et al.4 for political action to detoxify the obesogenic environment, there has been no clear evidence over the last 4 years since their publication on how this can be achieved. Pallan et al.1 do not provide any clues in their letter. We do not believe that obesity prevention should be thought of as life course approaches versus continuing environmental ‘detoxification’ as they suggest, rather that complimentary approaches across the range of triggers need to be designed, evaluated, and implemented. While public health research and policy has often emphasized the more societal (upstream) determinants of disease as targets for prevention, it is important to recognize that interventions aimed at individual (downstream) determinants are often more feasible, and may, in the case of even a short duration of intervention, as we argue, be effective in the long term. These interventions are urgently required in young people already on the pathway to adult obesity and its related diseases. Upstream approaches, such as encouraging industry to market ‘healthier’ alternatives, removal of school snack food vending machines, or manipulating pricing to alter eating habits may have unpredictable and undesirable consequences for health and society and need to take account of the complex behavioural and economic relationship between government, schools, businesses, and the public.5
If effective obesity and disease prevention can be achieved by intervening with the biological mechanisms through which environmental determinants act then these interventions should be supported. Similarly if effective and feasible means for detoxifying the environment can be developed and implemented then they should be supported.
Hawkins and Law2 suggest that we may have been too hasty in our dismissal of infancy as a potentially important period for obesity prevention and cite additional systematic reviews that suggest a protective effect of breastfeeding for later obesity. We agree that these show consistent but modest associations between breastfeeding and obesity. However, the authors of these reviews have all been cautious about the ability to draw causal inferences from the available observational studies. Arenz et al. specifically noted that randomized controlled trial evidence was required to ensure that breastfeeding was causally related to lower levels of obesity and anticipated the results of the Belarus randomized trial of breastfeeding promotion.6,7 While the results of this trial with respect to obesity outcomes have not yet been published in a peer review journal they were presented at the recent Developmental Origins Conference in Toronto in Canada (November 2005) and show no association between the intervention group (in whom there was an effective increase in breastfeeding) and the control group (with very low levels of breastfeeding). It was largely on the basis of these trial findings that we concluded that the evidence for a protective effect of infant feeding on later obesity was not compelling.
Our editorial was designed to highlight our view that there is no clear evidence that individual and societal interventions currently available will be effective in the long term, and to propose alternative, if rather novel, strategies, in anticipation of provoking interest and debate in anticipation of provoking interest, debate and ultimately moving the prevention of obesity and its related health consequences forward.
References
1 Pallan MJ, Cheng KK, Adab P. Obesity prevention: life course approach versus continuing environmental ‘detoxification’. Int J Epidemiol 2006;35:1100–01.
2 Hawkins SS, Law C. Treatment and prevention of obesity—are there critical periods for intervention? Int J Epidemiol 2006;35:1101.
3 Lawlor DA, Chaturvedi N. Treatment and prevention of obesity—are there critical periods for intervention? Int J Epidemiol 2006;35:3–9.
4 Ebbeling CB, Pawlak DB, Ludwig DS. Childhood obesity: public-health crisis, common sense cure. Lancet 2002;360:473–82.[CrossRef][Web of Science][Medline]
5 Frazao E, Allshouse J. Symposium: sugar and fat: from genes to culture. J Nutr 2003;133:844S–847S.
6 Arenz S, Ruckerl R, Koletzko B, von Kries R. Breast-feeding and childhood obesity—a systematic review. Int J Obes 2004;28:1247–56.[CrossRef][Web of Science][Medline]
7 Kramer MS, Guo T, Platt RW et al. Breast feeding and infant growth: biology or bias? Pediatrics 2002;110:343–47.
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