A modern epidemic

Why a condition that spread across the world in two generations is still argued about as a personal failing

A The condition now described as a global epidemic of obesity was, within living memory, a rarity outside the wealthiest classes of the wealthiest countries. Its spread has been rapid, geographically comprehensive and remarkably consistent in its sequence: prevalence rises first among the affluent of a developing economy, then falls among them and rises steeply among the poor, until it settles into the pattern familiar in rich countries, where the condition is concentrated at the bottom of the income distribution. Any explanation that cannot account for that inversion is incomplete, and a good many of the explanations offered in public cannot.

B The oldest explanation, and still the most widely held outside the research literature, treats the problem as a failure of individual restraint. Its appeal is that it is not entirely wrong: consumption exceeds expenditure, and consumption is something people do. Its weakness is that it explains a change in populations by an appeal to something that has not changed. There is no plausible account of why the inhabitants of dozens of unrelated societies should have simultaneously become less disciplined within two generations, and the explanation collapses precisely where an explanation is most needed. It also has a curious history: the same reasoning was applied to tuberculosis, to infant mortality and to alcoholism in their day, in each case attributing to the character of the poor a pattern that was subsequently traced to their circumstances.

C The alternative locates the change outside the individual, in what researchers call the food environment. Over the same period, the cost of energy-dense manufactured food fell steeply relative to income, portions grew, such food became purchasable within a few minutes of nearly anywhere at nearly any hour, and its formulation was refined by an industry with strong commercial reasons to make it difficult to stop eating. Physical activity, meanwhile, was engineered out of employment and transport. On this account the population did not lose its willpower; the environment in which that willpower operates was rebuilt around it. The reconstruction was neither conspiratorial nor accidental. Each individual change — a larger portion, a longer opening hour, a cheaper sweetener, a shorter walk from the car park — was a rational commercial decision, and their combined effect on a population was nobody's responsibility in particular.

D Evidence from unwilling participants supports the environmental reading. Populations that migrate from countries with low prevalence to countries with high prevalence acquire the prevalence of the destination within a generation, which their genes cannot explain. Companion animals living in households have grown heavier over the same decades, and laboratory colonies fed unchanged diets under unchanged protocols appear to have done so as well. None of these groups can be accused of a decline in personal responsibility, and the fact that the trend appears among them at all points away from any explanation resting on individual choice. The animal evidence is the weakest of the three and the most frequently quoted, which is unfortunate, since the migration data are far harder to dismiss and require no assumptions about what a household feeds its dog.

E Biology then locks the change in place. The body defends a weight it has reached with a persistence it does not apply to preventing the gain: after deliberate weight loss, appetite hormones shift towards hunger, resting energy expenditure falls below what the smaller body should require, and both changes persist for years. This is why the great majority of deliberate weight loss is regained, and why the medical advice offered for decades — eat less, move more — has a record of failure that would have discredited any pharmaceutical intervention with comparable results. The defence usually offered — that the advice works when it is followed — is not a defence at all, since an instruction that the body is organised to resist is one that most people will predictably fail to follow.

F That record is the context for the recent arrival of drugs which mimic a gut hormone regulating appetite, and which produce, for the first time, losses of a magnitude previously achieved only by surgery. Their appearance has sharpened rather than settled the argument. To some the class represents overdue recognition that a physiological problem warrants a physiological treatment, and an end to the moralising that has accompanied the condition throughout its history. To others it represents the medicalisation of a commercial failure: a costly permanent prescription, taken indefinitely because the effect reverses when it stops, sold to individuals in order to compensate for an environment that nobody is willing to regulate. Both readings accept the same pharmacology and disagree about what the pharmacology is for.

G The two positions are not, on inspection, incompatible, and treating them as rivals has been the least productive feature of the debate. A drug that helps an individual and a policy that changes a population are answers to different questions, and the evidence on the policy side is genuinely thin: taxes on sweetened drinks reduce their purchase, but the effect on the condition itself is small, and interventions on labelling, advertising and school food have produced results that are real, modest and easily overstated. What is not thin is the evidence that treating the condition as a defect of character has failed for fifty years, and that the burden of that failure has fallen hardest on the people with least capacity to escape the environment producing it.