Abstract
The global obesity epidemic continues its relentless advance, currently affecting >2 billion people. This paper explores alternative ways to assess the potential disease impact of the epidemic, which is currently based almost exclusively on body mass index (BMI) data. It also argues in favor of concerted efforts to modify the built ecosystem that is driving the obesity epidemic. Most of the epidemiologic data on obesity are based on BMI (in kg/m2) and use the ranges of 18.5-24.9 for normality, 25-29.9 for overweight, and ≥30 for obesity. But the gap between the median of the "normal" BMI distribution (∼22) and the current population BMI of, for example, the United States (27.7) has become so wide that it is unlikely that we will be able to close that gap in the near future. Furthermore, the correlation between BMI and disease risk is not linear. Over 60% of the global disease burden of obesity affects individuals with a BMI ≥30, who comprise only ∼10% of the global population of overweight/obese persons. Furthermore, BMI accounts for only ∼17% of the risk of insulin resistance and subsequent type 2 diabetes in the BMI ≥25 population. Epigenetics, specifically DNA methylation, appears to play a far more important role than BMI in determining the risk of obesity's comorbidities, such as diabetes. Similarly, socioeconomic status carries a higher risk than BMI level for the development of obesity-related noncommunicable diseases. Finally, the built environment that sustains our species' lifestyle is a major driver of the obesity epidemic. Modifying that ecosystem will require no less than a social movement, one able to promote and sustain the necessary coordinated action of virtually all sectors of society.