Causal Beliefs about Obesity and Associated Health Behaviors : Results from a Population-Based Survey

Background: Several genetic variants are associated with obesity risk. Promoting the notion of genes as a cause for obesity may increase genetically deterministic beliefs and decrease motivation to engage in healthy lifestyle behaviors. Little is known about whether causal beliefs about obesity are associated with lifestyle behaviors. Study objectives were as follows: 1) to document the prevalence of various causal beliefs about obesity (i.e., genes versus lifestyle behaviors), and 2) to determine the association between obesity causal beliefs and self-reported dietary and physical activity behaviors. Methods: The study data were drawn from the 2007 Health Information National Trends Survey (HINTS). A total of 3,534 individuals were included in the present study. Results: Overall, 72% of respondents endorsed the belief that lifestyle behaviors have ‘a lot’ to do with causing obesity, whereas 19% indicated that inheritance has ‘a lot’ to do with causing obesity. Multinomial logistic regression analyses indicated that the belief that obesity is inherited was associated with lower reported levels of physical activity (OR = 0.87, 95% CI: 0.77-0.99) and fruit and vegetable consumption (OR = 0.87, 95% CI: 0.76-0.99). In contrast, the belief that obesity is caused by lifestyle behaviors was associated with greater reported levels of physical activity (OR = 1.29, 95% CI: 1.03-1.62), but was not associated with fruit and vegetable intake (OR = 1.07, 95% CI: 0.90-1.28). Conclusions: Causal beliefs about obesity are associated with some lifestyle behaviors. Additional research is needed to determine whether promoting awareness of the genetic determinants of obesity will decrease the extent to which individuals will engage in the lifestyle behaviors essential to healthy weight management. Introduction The causes of obesity are multifactorial [1]. Recent evidence has begun to shed light on the genetic contributions to obesity [2]. In the 2005 update of the human obesity gene map, 127 candidate genes for obesity were reported, 22 of which were replicated with multiple populations [3]. The majority of rare monogenic or single-gene disorders related to obesity appear to function via the regulation of appetite and impairment of satiety rather than the regulation of metabolism [2,4,5]. Common obesity, however, is mostly polygenic and due to the contribution of multiple genes and genetic variants. Advances in obesity genetics, as well as the genetics of common diseases, has led to a proliferation of direct-toconsumer marketing of genetic tests that enable the identification of one’s genetic risk for these conditions. It has been argued that such testing is premature, given the state of the science, and concerns have been raised about the clinical utility of this type of risk information [6-8]. Currently, it is unknown whether providing individuals with information about the genetic determinants of obesity will motivate or discourage weight management behaviors. Researchers have postulated that the provision of genetic information will influence both the cognitive representations or beliefs that people hold about the causes of a disease, as well as their beliefs about the solutions to reducing risk for disease [9,10]. Consequently, genetic risk information for obesity could have negative * Correspondence: clwang@bu.edu Boston University School of Public Health, Boston MA, USA Wang and Coups International Journal of Behavioral Nutrition and Physical Activity 2010, 7:19 http://www.ijbnpa. org/content/7/1/19 © 2010 Wang and Coups; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. implications if providing feedback increased people’s beliefs about the role of genetics in obesity, but decreased their beliefs about the efficacy and importance of lifestyle behaviors to manage obesity risk. Underlying this notion is the possibility that communicating the genetic risks of obesity might inadvertently serve to reinforce genetically deterministic thinking, which may reduce individuals’ engagement in lifestyle behaviors important in maintaining a healthy weight. As a first step to understanding the possible implications of communicating obesity-related genetic information, this study was undertaken with two main objectives. First, we set out to document the prevalence and correlates of causal beliefs about obesity (i.e., genes versus lifestyle behaviors) in a population-based sample in the United States. Second, we sought to determine the association between obesity causal beliefs and selfreported dietary and physical activity behaviors. The results of this study can shed light on whether obesity causal beliefs might function as a potential mechanism by which the provision of information about the genetic determinants of obesity influences behaviors important in healthy weight management. Methods and Procedures Procedure The study data were drawn from the 2007 Health Information National Trends Survey (HINTS), a national probability survey of health information among U.S. adults conducted by the National Cancer Institute. Participants in the 2007 HINTS were recruited via random digit dialing or a mailing sent to a random sample of U.S. addresses. Participants completed a one-time telephone or paper and pencil survey. Some survey questions differed between the two modes of administration. For the purposes of the current study, we only used data from the mailed paper and pencil survey, as it utilized a two-item cups measure of fruit and vegetable intake that may have greater validity than the two-item servings measure used in the telephone survey (Amy Yaroch, PhD, personal communication, March 2009). The household response rate to the mailed survey was 44.0% and the within-household response rate was 77.4%. The 2007 HINTS utilized a cross-sectional, complex sample survey design, data weighting, and jackknife variance estimation. Further information about the HINTS is available elsewhere [11]. Participants A total of 7,674 individuals were recruited to the 2007 HINTS, 3,582 of whom completed the survey via mail. We excluded 48 individuals who were missing data for both of the obesity causal belief items, leaving an available sample size of N = 3,534. Measures