There is no “obesity epidemic”

In the issue of Nature to be published tomorrow is a very interesting article which discusses the causes and control of excess body weight.

Contrary to the simplistic arguments presented by militant carrot nibblers on the one hand, and those who claim that obesity has little or nothing to do with overeating, Rockefeller University geneticist Jeffrey Friedman explains that the causes of the condition are a combination of free access to calorie-rich foods, and a biological feedback mechanism that resists weight change.

We often hear talk of an “obesity epidemic”, but this is an abuse of a term which properly describes a disease that spreads from person to person, and which has a rapidly increasing incidence. Neither of these apply to obesity.

“Variation in body weight is a continuous trait, whereas obesity is a dichotomous trait.”

What this means is that a small change in average weight within a population will lead to a large increase in the number of people who exceed what may be an arbitrarily-defined threshold.

In the United States, there was in the 1980s a 33% increase in the incidence of obesity, defined as a body-mass index of over 30. That dramatic rise was the result of only a 3–5 kilogramme average weight gain, yet an individual’s body weight may vary by a few kilogrammes over the course of a week, depending on such things as fluid intake and bowel movements. It makes no sense to define a person with an average BMI of 29.8 as obese if, for example, they happen to be particularly thirsty or constipated during the week in which their weight is recorded for a study of body fat levels in bourgeois societies.

We talk of a public health problem arising from obesity, but, given our ready access to cheap, energy-rich food, why are so few people obese, relatively speaking?

The answer to that question lies in an energy balance controlled by an unconscious biological system driven by evolutionary pressure. Hunter-gatherers would not survive long on low fat yoghurt, but too much fat intake increases the risk of predation and disease. Genetics plays a large part in defining the levels of leanness and obesity beneficial to particular populations, and this, says Friedman, might explain why populations that have been historically undernourished often become the most obese when provided with unlimited calories.

A motivated dieter will lose weight by eating less and moving around more, but their body will attempt to maintain the original weight by inducing feelings of hunger that drive them to eat more. Friedman doesn’t discuss this, but there is a limit to this biological impetus: a limit which human willpower can overcome given the right circumstances.

In my own case, I burn more than 2,000 calories per day while cycling or running. I certainly eat more than my basal metabolic rate of 1,900 calories, but I would find it difficult to consume more than 4,000 calories a day without switching to the kind of fatty foods that make me feel sick. I’m therefore losing body fat at a considerable rate, and, while I eat a fair amount of carbohydrate-rich food, the biological mechanism to which Friedman refers cannot keep up. This could soon present me with a problem, and it shows how central lifestyle is to weight control.

For reference, I should point out that 4,000 calories corresponds to around half a kilogramme of body fat. This, however, doesn’t take into account muscle building in those who engage in sporting activities. Muscle tissue is much more dense than body fat, and this is one of the reasons why BMI is a poor indicator of healthy weight in athletes.

There is as Friedman says considerable evidence for a biological basis to obesity, but no scientific study can wholly attribute obesity to genetic factors:

“Because no one becomes obese if they are starved, the environment – primarily, free access to calories – is probably a permissive factor that sets the stage for the genetically predisposed to become obese.”

Metabolic rates vary from person to person, but they do not depend on lean body mass. Friedman points out that when obese people lose weight, they use less energy than skinny individuals of the same body mass who have not been obese. To maintain their reduced weight, the formerly obese must consume fewer calories than their always slim counterparts. This can to some degree explain the rate of recidivism after dieting, and it illustrates the importance of lifestyle in maintaining a healthy weight.

Lest Friedman be accused of playing down the role of lifestyle, he is most clear in his advice to those concerned about their weight:

“Eat a healthy diet, begin a programme of physical activity, and try to lose as much weight as is required to improve your health, without feeling compelled to ‘normalize’ your weight.”

That last bit is very important, as it highlights the importance of individual circumstances.

We might expect that evolution will select against obesity where there is no risk of starvation, and there is evidence for this in the case of the Pacific island of Nauru, where the incidence of diabetes rose and then fell in response to the introduction of high-calorie diets. In the United States, obesity may be reaching a plateau, and Friedman anticipates that average body weight in that country will stabilise over the coming decades.

These are long-term trends, and in acknowledging them we should not lose sight of the negative impact of excess weight on individuals in the here and now. Anti-obesity public health strategies are essential, says Friedman, and their focus should be on stably maintaining moderate weight loss. We must also de-stigmatise obesity, he says, and reduce the pressure on overweight individuals to achieve some arbitrary ideal.

Read the whole thing, and inwardly digest.