Genes or environment: is it the wrong question?

By Mark Kroese

15 November 2012


The recently published excellent debate between John Wilding and Timothy Frayling in the BMJ on whether the causes of obesity are primarily environmental brings into sharp focus the problems of framing this important public health issue in such a dichotomous manner.

Environmental and genetic factors operate together to influence risk of obesity and must be considered in the context of individuals and populations. The poll published with these papers indicated that 68% of responders agreed that the causes of obesity are primarily environmental. However both experts through their well-balanced cases clearly present evidence that for a complex disorder such as obesity both environmental and genetic factors need to be considered in attempting to address the condition. There is a clear consensus that increasing rates of obesity are a major public health priority yet there is still this unnecessary distinction between whether or not environmental factors are the primary causes. The possible consequence of persisting with such an approach is that important risk factors and opportunities for prevention will be excluded from consideration in attempts to develop programmes addressing obesity in the population.

Considerable progress has been made over the past two decades in understanding the genetic basis of obesity, although much remains unknown.There are a small number of single gene disorders that can cause severe early onset obesity and for which some treatments are beginning to be developed. Beyond these disorders with a strong genetic influence a large number of gene variants are also thought to bring about weight gain through small effects on central mechanisms in the body that drive increased energy intake. Thus, in a calorie dense environment, such as most developed countries, the distribution of weight in the population is likely to be influenced by genetic factors underlying the drive to eat. Interventions which address the latter category must surely be part of the population approach to prevention.

Importantly also, we believe that the current almost complete focus by the public health community on lifestyle and environmental factors in disease ignores the great progress that has been made in understanding the biological mechanisms underlying common disorders such as obesity. Increasingly we acknowledge that populations are heterogeneous, comprising a set of individuals with different risks for disease. This risk, which has both environmental and genetic components can allow populations to be stratified, and, potentially, allow different approaches to prevention to be applied according to risk category.

Obesity is a serious risk to population health and we will need all the tools available to try to improve the situation both at an individual and population level: it is important to consider the many different interventions that could be developed and, critically, not undermine our efforts through artificial distinctions.

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