Gene–environment interactions related to body mass: School policies and social context as environmental moderators
| Author | Kathleen Mullan Harris,Benjamin W Domingue,Brett C Haberstick,Matthew B McQueen,Michael E Roettger,Jason D Boardman |
| DOI | 10.1177/0951629812437751 |
| Date | 01 July 2012 |
| Published date | 01 July 2012 |
| Subject Matter | Articles |
Article
Gene–environment
interactions related to body
mass: School policies and
social context as
environmental moderators
Journal of Theoretical Politics
24(3) 370–388
©The Author(s) 2012
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DOI:10.1177/0951629812437751
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Jason D Boardman
Institute of Behavioral Science and Department of Sociology, University of Colorado at Boulder, USA
Michael E Roettger
Institute of Behavioral Science, University of Colorado at Boulder, USA
Benjamin W Domingue
Institute of Behavioral Science and School of Education, University of Colorado at Boulder, USA
Matthew B McQueen and Brett C Haberstick
Institute for Behavioral Genetics, University of Colorado at Boulder, USA
Kathleen Mullan Harris
Department of Sociology, University of North Carolina, USA
Abstract
This paper highlights the role of institutional resources and policies, whose origins lie in political
processes, in shaping the genetic etiology of body mass among a national sample of adolescents.
Using data from Waves I and II of the National Longitudinal Study of Adolescent Health, we
decompose the variance of body mass into environmental and genetic components. We then
examine the extent to which the genetic influences on body mass are different across the 134
schools in the study. Taking advantage of school differences in both health-related policies and
social norms regarding body size, we examine how institutional resources and policies alter the
relative impact of genetic influences on body mass. For the entire sample, we estimate a heritabil-
ity of .82, with the remaining .18 due to unique environmental factors. However, we also show
Corresponding author:
Jason D Boardman, University of Colorado, Institute of Behavioral Sciences, 1440 15th Street, Boulder, CO
80309-0483, USA
Email: boardman@colorado.edu
Boardman, Roettger, Domingue et al. 371
variation about this estimate and provide evidence suggesting that social norms and institutional
policies often mask genetic vulnerabilities to increased weight. Empirically, we demonstrate that
more restrictive school policies and policies designed to curb weight gain are also associated with
decreases in the proportion of variance in body mass that is due to additive genetic influences.
Keywords
BMI; gene–environment interactions; obesity; policies; schools
1. Introduction
According to recent estimates, more than one in three adolescents are overweight or at
risk of being overweight (Ogden et al., 2006), and prevalence rates of obesity are 10
times higher in the United States than in other developed nations (Lissau et al., 2004).
Given the links of obesity to chronic health problems such as type-2 diabetes and hyper-
tension, understanding the social, behavioral, and biological mechanisms responsible
for differences in the risk of obesity is a critical public health issue. ‘Obesity politics’
(Kersch, 2009) has taken center stage in policy debates regarding the most effective
means to improve the health of the public but the bulk of policy research on obesity
has focused on individuals and their corresponding behavioral risk factors such as diet
and exercise. Recent research, however, has begun to examine characteristics of the built,
social, and institutional environment that may facilitate or hinder proper energy balance
behaviors (Brescoll et al., 2008; Gordon-Larsen et al., 2006). By contributing to the
knowledge and understanding of political and institutional processes at play, political
science has the potential to be centrally located in debates regarding the causes and con-
sequences of obesity and can help to develop weight-management initiatives that begin
with institutions such as schools and work places.
The heritability (the proportion of variance that is due to genetic factors) of body
mass index has ranged from as low as .3 to as high as .9 (Cornes et al., 2007; Franz et al.,
2007; Haberstick et al., 2010; Haworth et. al., 2008; Maes et al., 1997; Ordonana et al.,
2007; Schousboe et al., 2003; Silventoinen et al., 2007; Wardle et al., 2008). Despite this
large range, to date no research has examined the effectiveness of institutional norms and
policies as a function of genetic vulnerability to weight gain. That is, some policies may
be effective at reducing the intake of fatty or high-caloric food and increasing the preva-
lence of regular exercise for the overall population, but these policies may be relatively
ineffective for those who are more likelyto gain weight because of very small differences
across their genome. As such, the interplay of genetics and environment (GxE) paradigm
is critical for generating effective policies aimed at reducing the prevalence of obesity by
identifying and creating environmental sources which also reduce the genetic influences
on weight gain and energy balance behaviors (Faith and Kral, 2006).
This is particularly relevant to current state of the ‘obesity epidemic’ (Mokdad
et al. 2000) and the related ‘obesity politics’ (Kersch, 2009). Health policy makers have
been engaged in heated debates about the implementation of punitive sanctions for those
who are obese. For example, Arizona has proposed introducing a US$50 fee for engag-
ing in unhealthy behaviors and they single out obese individuals (Williams, 2011). This
emphasis on choices frames the increased prevalence of obesity as an individual-level
phenomenon and the corresponding policies are aimed at influencing an individual’s
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