IJE Advance Access originally published online on February 28, 2005
International Journal of Epidemiology 2005 34(2):481-482; doi:10.1093/ije/dyi017
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Published by Oxford University Press on behalf of the International Epidemiological Association
Letters to the Editor |
Adult chronic disease and childhood obesity: a life course approach in developing countries?
Department of Pharmacology and Pharmacotherapeutics, Trinity Centre for Health Sciences, St James's Hospital, Dublin 8, Ireland. E-mail: kabirzin{at}yahoo.com
The developing world is undergoing nutritional transition, along with anthropometrical transition. Many developing countries have been advocating blanket childhood food supplementation programmes for decades. As a public-health doctor, I am concerned about such health promotional activities where short-term benefits may outweigh any long-term harm. A recent study in India also showed that childhood obesity, together with low birth weight, is associated with Type 2 Diabetes in early adulthood among an urban slum community.1
Low birth weight and undernutrition are still considered the two main causes of childhood mortality and morbidity in developing countries. Consequently, an apparent association between low birth weight and childhood obesity seems to be counter-intuitive for the lay public. For reproductive epidemiologists, birth weight (a surrogate measure for intrauterine environment) has been a paradox, because birth weight is argued not to be on the ‘causal’ pathway to population-health outcomes.2 This is in contrast to Barker's hypothesis of foetal origin of adult chronic disease that is currently receiving greater attention among investigators.3
The recent study1 in India is a snapshot of the urban elite. Despite the advantage of a longitudinal birth cohort,1 the investigators have not adequately addressed the two potential environmental risk factors for excess weight gain across the life course: altered nutrition and physical inactivity levels. Delhi is experiencing a plethora of fast food outlets, with disposable income in the hands of many. There is also the onslaught of increased mechanization leading to a relatively sedentary lifestyle. Such changing lifestyles compounded with a rapid urbanization may result in the emergence of another paradox—‘affluence’. The authors proposed a ‘growth trajectory’ phenomenon,1 but reverse causality bias cannot be ruled out, particularly when body mass index has been used as a proxy measure for adiposity.
Historical birth cohorts are rich national resources for providing powerful evidence across the life course as regards exposure timing, biological pathways, and potential mechanisms such as ‘inter-generational effects’, ‘intra-uterine programming’, ‘adiposity rebound’ phenomenon, or ‘thrifty phenotype’.3,4 While such epidemiological paradigms are fashionable, the narrow framework of Barker's hypothesis3 has also been extended to post-natal growth and developmental trajectories.4 However, it is difficult to disentangle the real culprit of nature from nurture: junk food, an elusive ‘fat gene’, gene-environment interactions, or the heterogeneity of biological pathways linking early life exposures to later outcomes.
To date, limited life course epidemiological evidence exists in developing countries. Such evidence reported in the developed world cannot be generalized. Therefore, historical birth cohorts and expertise are both necessary for the resource-poor countries where cost-effective public-health policies drawn on the conventional ‘black box’ (risk factor) epidemiology are also firmly established. So, how realistic can long-term untested policies based on interdisciplinary life course epidemiological approaches4 or utilizing sophisticated ‘Mendelian randomisation’ techniques5 be in situations where ‘joined-up thinking’ is not even the norm! Should our policy makers and public-health leaders replace ‘prevarication with imagination’6 as to empower our future generations with the ultimate health prevention models that are built on life course approaches, and integrated into a macro-environment?
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1 Bhargava SK, Sachdev HS, Fall CH et al. Relation of serial changes in childhood body-mass index to impaired glucose tolerance in young adulthood. N Engl J Med 2004; 350:865–75.
2 Wilcox AJ. On the paradoxes of birth weight. Int J Epidemiol 2003; 32:632–33.
3 Barker DJP. Mothers, babies and health in later life. Edinburgh: Churchill Livingstone, 1998.
4 Ben-Shlomo Y, Kuh D. A life course approach to chronic disease epidemiology: conceptual models, empirical challenges and interdisciplinary perspectives. Int J Epidemiol 2002; 31:285–93.
5 Davey Smith G, Ebrahim S. Mendelian randomization: prospects, potentials, and limitations. Int J Epidemiol 2004; 33:30–42.
6 Editorial. The catastrophic failures of public health. Lancet 2004; 363:745.[CrossRef][Web of Science][Medline]
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