Ten Putative Contributors to the Obesity Epidemic
1 Department of Infections and Obesity, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana
2 Section on Statistical Genetics, Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL
3 Comprehensive Weight Control Program Weill Medical College of Cornell University, NY
4 Wisconsin Primate Research Center, University of Wisconsin-Madison, WI
5 Department of Medicine, University of Wisconsin Medical School, WI
6 Clinical Nutrition Research Center, University of Alabama at Birmingham, Birmingham, Al
7 Department of Psychiatry, University of Wisconsin-Madison, WI
8 Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, Al
9 Formerly M. M. Hagan; Dept. of Psychology, Behavioral Neuroscience Division, University of Alabama at Birmingham, Birmingham, AL
10 Department of Kinesiology, Michigan State University, East Lansing, MI
11 Division of Rheumatology, Johns Hopkins University, Baltimore, MD
12 The Liggins Institute, The University of Auckland, Auckland, New Zealand
13 Neuroscience Training Program, University of Wisconsin-Madison, WI
14 Population Science, Penninton Biomedical Research Center, Louisiana State University, Baton Rouge, LA
15 Paediatric Unit, Verona University Medical School, Verona, Italy
16 Institute of Environmental Health Sciences, Wayne State University, Detroit, MI
17 Department of Epidemiology and Clinical Investigation of Sciences, University of Louisville Health Sciences Center, KY
18 U.S.D.A. Children’s Nutrition Research Center, Departments of Pediatrics and Molecular and Human Genetics, Baylor College of Medicine, Houston, TX
Overall Summary & Conclusions
Overall it is clear that multiple plausible causes of obesity exist outside of the big two and that as of yet these alternatives have had little if any influence on mainstream discussions of clinical and public health approaches to obesity. This is unfortunate because some of these putative causes could lead directly to practical intervention and prevention approaches. An obvious example building on the idea of sleep debt would be to try to get people to sleep more and then to see if doing so produced more weight loss or less weight gain. According to the ClinicalTrials.gov website, at least one such study is underway in adults (ClinicalTrials.gov Identifier: NCT00261898) and another in infants (ClinicalTrials.gov Identifier: NCT00125580). Perhaps instead of additional large scale studies investigating increasing PE in schools as an obesity reduction strategy, when such programs have often been shown to be ineffective, we should be promoting napping in children during school hours and then assessing the results. It is certainly possible that such a program would work no better then PE, but given the available data it seems worth trying.
How well supported are the putative causes we have reviewed? illustrates the increasing prevalence of some of these putative contributing factors over time, and Table 4 provides an overall summary, permitting one to obtain a sense of a reasonable ranking of each factor in terms of the strength of the evidence that there is a nonzero effect. In some cases, e.g. drug-induced weight gain, data are clear and consistent in every area of evidence including relatively long-term randomized controlled trials in humans that this is indeed an influence. It would obviously be useful to rank the factors in terms of the magnitude of their effects, but at present, we have insufficient information to do so. In other such cases as, for example, increased fecundity among certain segments of the BMI distribution, the evidence is too inchoate to support firm conclusions.
Figure 11 Prevalence of putative contributors against the increasing prevalence of obesity. a) prevalence of obesity (CDC), b) mean age of mothers at first birth (NCHS, 2003), c) percentage of homes using air conditioning (Energy Information Administration), d) (more ...)
For all of these putative causes, we believe further research is warranted. For some such as sleep debt, research is warranted to determine whether the factor is indeed contributing to obesity levels. For some such as obesity-promoting drugs, research investigating mechanisms that may lead to an understanding of how to modulate the effects or design alternatives that will not have such deleterious effects is warranted. For some, such as sleep debt or ambient temperature effects, studies involving manipulation of these factors in human randomized controlled trials to evaluate effects (if any) on weight seem warranted, and indeed some such studies are underway (the sleep studies were mentioned above; for ambient temperature, see ClinicalTrials.gov Identifier: NCT00521729).
Finally, we believe that the factors we identify above do not exhaust the list of plausible contributors. Rather they serve as a clarion call for scientists to remain skeptical of simplistic conclusions about complex phenomena which public health advocates in the obesity field in particular seem prone to accept as complete and adequate explanations. In this unusually public discussion it is imperative that scientists remain open to alternative ideas, insist that claims about the causes of the obesity epidemic be grounded in the best available data, and recognize that any one explanatory theory must be viewed in the context of the constellation of plausible, interrelated, and in many cases still unproven hypotheses.