Head To Head

Are the causes of obesity primarily environmental? Yes

BMJ 2012; 345 doi: http://dx.doi.org/10.1136/bmj.e5843 (Published 11 September 2012) Cite this as: BMJ 2012;345:e5843
  1. John Wilding, professor of medicine
  1. 1Department of Obesity and Endocrinology, University of Liverpool Clinical Sciences Centre, University Hospital Aintree, Liverpool L9 7AL, UK
  1. j.p.h.wilding{at}liv.ac.uk

John Wilding believes that changes in our environment are responsible for increasing obesity, but Timothy Frayling (doi:10.1136/bmj.e5844) thinks that it is genetic factors that determine who gets fat

The ongoing epidemic of obesity and its associated complications such as diabetes, increased cancer risk, and cardiovascular disease is creating an unprecedented challenge for healthcare systems around the world and threatens to slow or even reverse the gains in life expectancy that have been achieved over the past 50 years.1 To tackle this growing problem it is essential to consider the fundamental causes of obesity and apply this knowledge to develop effective strategies to prevent and treat the condition and its consequences.

There is no question that regulation of body weight and fat content is under powerful biological control, and that much of this biology is rooted in genetics; identical twins are only rarely discordant for adiposity, and about 40-70% of body fatness is inherited.2 Given the importance of this genetic component, it may seem counterintuitive to suggest that the main causes lie in our environment. However, known single gene defects, such as leptin deficiency, are rare causes of obesity,3 and the only common gene polymorphism with well characterised effects on body weight, FTO, has a relatively small effect size (about 3 kg greater weight for those who are homozygous for the variant associated with obesity, and about 1.5 kg for heterozygotes).4

For someone to become obese, overall energy balance (the difference between energy consumed in the form of food and that expended in normal biological processes and physical activity) must be positive over time. Of course, this is more likely to occur in those genetically predisposed to gaining weight, especially if the environment is more conducive to increased consumption and decreased activity. The increase in the prevalence of obesity has mainly occurred over the past 30 years and has been seen in most parts of the world. Such rapid change cannot be due to genetic (or even epigenetic) changes. In contrast, the evidence that the environment has changed is overwhelming. The environmental changes are complex and include substantial shifts in the production and availability of food, occurring simultaneously with alterations in the physical environment that encourage sedentary behaviour.

Environmental contributions

The relative cost of food has fallen in recent years, partly as a result of the industrialisation of food production. But the overall trend hides important differences—the cost of energy dense foods high in fat, sugar, and salt has fallen most, whereas that of healthier options has increased in relative terms. This may partly explain why obesity is more common in those on lower incomes.5 6 The food industry, now an unhealthy alliance of producers and marketeers, has successfully promoted energy dense foods, many of which provide positive reinforcement that increases consumption,7 effectively producing a “cafeteria diet” for the whole human population—a well proved way of causing obesity in experimental animals.8

At the same time as the food environment has provided fertile ground for the development of obesity, physical activity has declined and time spent being sedentary has increased. This can be attributed to changes in transport, especially increased use of the car, and in time spent being inactive during work and leisure time, partly as a result of developments in technology (television, computers, computer games, etc). The built environment does not always encourage outdoor activities, and safety fears may underlie the reductions in walking and cycling that have been seen in recent years.

Social norms may also have changed over the last few decades, so that obesity is not as readily recognised as it would have been in the past. Eating and activity patterns have also changed in ways that may promote the development of obesity.


It will be important to identify genetic causes for rare cases that may be treated, and both pharmacological and surgical options may be necessary for some people (and could be targeted on the basis of genetic or other biomarkers that predict response). However, changes to the food and physical environment are going to be essential if we are to have a meaningful impact on the obesity epidemic. Success will almost certainly require a comprehensive and radical approach across systems, backed by strong legislation influencing food production and marketing, and ensuring the built environment and transport systems are designed to encourage active living. Comprehensive community based public health interventions are beginning to show some encouraging results in reducing childhood obesity9; such an approach is being tested across Europe in the Ensemble Prévenons l’Obésité Des Enfants (EPODE) project, which engages whole communities, including local government and businesses, to try to reduce the prevalence of obesity in children.10 It has been questioned whether initiatives such as the so called “responsibility deal” in England, in which companies pledge to reduce the energy content of their products and promote lower calorie options, are likely to be effective,11 12 and if this approach fails, stronger legislative approaches may be required.

In summary, obesity is a complex disorder with both genetic and environmental causes. The predominant driver is environmental, and changes to the environment will be essential if we are to tackle the current epidemic.


Cite this as: BMJ 2012;345:e5843


  • Competing interests: The author has completed the ICMJE unified disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declares no support from any organisation for the submitted work; no financial relationships with any organisation that might have an interest in the submitted work in the previous three years; JW is a trustee of the Association for the Study of Obesity, which has received charitable income donated unconditionally by food industry, pharmaceutical, and medical devices companies.

  • Provenance and peer review: Commissioned; not externally peer reviewed,