A Happy Meal is not a healthy meal, at least according to the San Francisco Board of Supervisors. The board last week approved a preliminary ban that would strip toys from fast‐food meals in San Francisco. The ban’s backers claim the legislation gives parents a chance to convince their children to go for the healthier choice, without being tempted by a Shrek toy. If the final vote is approved this week, the ban will begin in December 2011.
The San Francisco ban, and similar proposals on both sides of the Atlantic, are predicated upon four false assumptions: the fast food sold by McDonald’s and its competitors makes kids fat; fast‐food marketing causes childhood obesity; fat children grow into unhealthy adults; fat kids incur significantly higher health care costs than skinny ones.
First, there is no evidence to support the assumption that fast‐food outlets and the food they sell make people overweight and obese. And, in fact, this assumption is contradicted by a considerable amount of research. For example, in 2004 a team of researchers, after conducting a study with 14,000 American children, found that eating junk food did not lead to obesity among children. A similar conclusion was reported in Canada the year after, when researchers concluded that eating in fast‐food restaurants was not associated with an increased risk of obesity, even in children who ate in such restaurants more than three times a week.
The claim about the association between the number of fast‐food outlets and levels of obesity is equally unfounded. A 2005 study of elementary school children in the US found no significant associations between either fast‐food prices or outlet density. Two years later, Russ Lopez, of the Boston University School of Public Health, reported similar non‐significant findings for fast‐food density.
Second, the Happy Meal ban assumes that fast‐food marketing is a cause of childhood overweightedness and obesity. Therefore, it is argued, restrictions on food marketing and advertising are necessary.
In order to establish an evidence‐based case for this claim, one would have to demonstrate that such advertising has an independent effect on children’s weight. This, in turn, would require a study design that controlled for the multiple other risk factors connected with childhood obesity (by some estimates, there are dozens such factors). However, none of the studies purporting to demonstrate that food advertising causes childhood obesity control for more than a handful of these other risk factors. These studies therefore cannot establish an evidence‐based case for the connection between food advertising and children’s weight.
Further, the causal thesis is undermined by the fact that, in the UK for example, advertising for food and drink has been falling in real terms since 1999 and is now roughly at 1982 levels, even while rates of overweightedness and obesity allegedly have been rising. Again, there is a substantial body of econometric literature that disproves the alleged connection between advertising, diets and weight.
In his research into food advertising in the UK, Peter Kyle, of the University of Lancaster, found no evidence to support the causal claim that advertising increased market size. Another researcher, Martyn Duffy, has looked at the impact of advertising on 11 food categories and found that advertising had no effect on demand. More specifically, professor Harry Henry has examined the effect of advertising on breakfast cereals and biscuits, both frequently cited as culprits in the childhood obesity epidemic. He concluded that advertising had no affect on market size.
Finally, Bob Eagle and Tim Ambler looked at the impact of advertising on chocolate consumption in five European countries in order to test the claim that a reduction in advertising would reduce consumption. They reported no significant association between the amount of advertising and the size of the chocolate market. Eagle and Ambler’s work is corroborated by evidence from the Canadian province of Quebec and from Sweden, both of which have imposed advertising bans on foods to children, with Quebec’s in operation since 1980. In both jurisdictions, however, there have not been significant reductions in childhood obesity or any marked differences in obesity rates compared with other adjacent areas.
Third, it is unclear that being a fat child carries significant health risks or increases one’s risk of becoming a fat adult. For example, a long‐running study in Aberdeen, Scotland, which looked at the health outcomes of children born in the 1950s, found that the body mass index (BMI) of children was not associated with increased risk for stroke and heart attack in later life.
In addition, the work of a group of British researchers into child health and epidemiology directly contradicts the assumption that overweight or obese children are at greater health risk and that reducing children’s weight benefits adult health. Their ‘Thousand Families Study’ followed 1,000 families in the city of Newcastle in north‐east England from 1954 in an effort to track the effects of childhood obesity on adult health. The study found that, contrary to the claim that fat children become fat adults burdened with health problems, there was little tracking from childhood overweightedness to adulthood obesity. Indeed, over 80 per cent of the obese adult participants in the study became obese as adults.
The assumption of a link between childhood and adult obesity is also contradicted by a recent US Preventive Services Task Force analysis of the efficacy of dyslipidemia screening and weight‐reduction programmes for children. It found that the evidence for effectiveness is ‘lacking, of poor quality, or conflicting’. The evidence also shows that the goal of encouraging children to eat low‐fat diets is not only unsupported by the evidence but also risks significant harm in terms of adverse effects on growth and nutrient intake. The best evidence indicates that a ‘substantial proportion of children under age 12 or 13, even with BMIs above the ninety‐fifth percentile, will not develop adult obesity’.
Revealingly, the American data has shown that fat children generally consume no more food nor are less physically active than those of ‘normal’ weight. And multiple studies have failed to find a link in children between physical activity levels, food intake and obesity. American, British, Australian, French, and Spanish studies have all found little evidence to support a relationship between energy intake in children and their weight.
Indeed, to blame either these children or their parents for being fat contradicts much of the accumulating evidence on just how small a contribution to obesity is made by the factors that anyone — parents, children or the state — can control. One recent American study found that for twins, for example, the shared environment effect for both BMI and waist circumference is only 10 per cent.
Fourth, what about the claims about how much all of these fat children are costing the health system? After all, we all know, don’t we, that fat children incur significantly higher health care costs than their slender peers?
In fact, this is not true, either. A 2008 US study examined the healthcare costs of 8,404 children in Kansas City and found that there was no relationship between a child’s BMI and his or her visits to a doctor or casualty rooms. The only extra costs associated with the obese children were down to the fact that they were 5.5 times more likely to have had extra lab screening tests ordered. It had nothing to do with the them being less healthy.
The evidence‐less Happy Meal ban should remind us that the entire idea of fat children is largely a cultural construct, not a scientific one. A hundred years ago, today’s penchant for thin children would have been considered a shocking instance of child neglect.
The idea that children weighing over a certain amount are fat or obese has no scientific foundation, as the dividing line between fat and normal is purely arbitrary, representing nothing more than a public health bureaucrat’s notion of where normal ends and fat begins.