The prevalence of weight problems in the U.S. has become alarmingly high, with over 30% of the adult population overweight and another 30% obese (Flegal, Carroll, Ogden, & Curtin, 2010). The current environment, with its abundance of highly palatable, high caloric density foods, is known to play a major role in promoting obesity (Hill & Peters, 1998). But not all individuals exposed to this obesogenic environment become overweight or obese. Thus, understanding the factors that predispose people to unhealthy eating – including overeating in response to external food cues or negative emotional states, and choosing “junk foods” in favor of healthier food options – is a critical challenge in behavioral and neuroscience research on obesity and in promoting population health.
Decades of research show that eating behaviors in humans are regulated by a complex interplay of metabolic and cognitive control processes in the brain (Berthoud, 2007). Metabolic control processes initiate food intake in response to low-energy states via hunger signaling, and terminate food intake when energy needs have been satisfied via satiety signals. Since eating behaviors are to a large degree shaped by experience, the cognitive processes involved in regulating food intake include reward-based learning (Petrovich et al., 2005, Petrovich et al., 2007 and Petrovich et al., 2002) as well as top–down control over such learned responses in the service of more abstract goals such as to maintain a healthy weight (Hare et al., 2009 and Hare et al., 2011). While metabolic control processes are a strong defense against body weight loss in an environment where food is scarce, which is the environment in which the human brain evolved, they are insufficient to guard against body weight gain when food is abundant (Hill & Peters, 1998). Thus, in obesogenic environments, cognitive factors may override metabolic regulation and become a critical determinant of eating behavior and the risk of obesity (Berthoud, 2007). Consistent with this view, human neuroimaging studies suggest that unhealthy eating habits may share neurobiological bases with substance addiction, including hyper-reactivity to rewarding stimuli as well as impaired cognitive control (Mathes et al., 2009 and Volkow et al., 2011).
The current study examined the role of impulsivity and inhibitory control in eating behavior. Although impulsivity is known to be a multi-faceted construct (Whiteside & Lynam, 2001), it is typically defined as a general tendency towards quick, unplanned reactions to internal or external stimuli without a consideration of the consequences of these actions to self or others. It is thought to encompass a broad set of behaviors including rapid decision-making, inattention, lack of perseverance, acting without thinking, lack of planning, sensation seeking, and risk-taking (Moeller, Barratt, Dougherty, Schmitz, & Swann, 2001). Furthermore, heightened impulsivity is thought to arise, at least in part, from impairments in inhibitory control (Logan, Schachar, & Tannock, 1997), defined as the ability to stop or suppress responses that are no longer required, inappropriate, or in conflict with current goals (Verbruggen & Logan, 2009).
Impulsivity and inhibitory control have long been postulated to play a key role in the ability to maintain a healthy diet and a healthy weight (Wardle, 1988). Growing evidence suggests that heightened impulsivity and reduced inhibitory control are associated with overeating (Guerrieri et al., 2007), including overeating in response to negative emotional states (Bekker et al., 2004 and Racine et al., 2009), as well as with a higher risk of eating disorders characterized by binge eating (for reviews, see (Fischer et al., 2008 and Waxman, 2009)). Individuals who are more impulsive and have worse inhibitory control are more likely to be overweight or obese (Guerrieri et al., 2008, Nederkoorn et al., 2006, Nederkoorn et al., 2009 and Nederkoorn et al., 2007), and inhibitory control efficiency is inversely correlated with body mass index (BMI) (Batterink et al., 2010 and Cohen et al., 2011). The emerging consensus is that heightened impulsivity and the associated inhibitory control deficits may lead to elevated BMI by undermining the person’s ability to resist the temptations of tasty but unhealthy foods (Appelhans, 2009 and Nederkoorn et al., 2006), a trait also referred to as disinhibition in eating (Bryant, King, & Blundell, 2008). However, the impact of individual differences in impulsivity and inhibitory control on specific aspects of eating behavior is still incompletely understood, and may be critical for estimating risk and selecting optimal treatment for individuals at risk for obesity.
Consequently, the goal of the current study was to investigate the role of impulsivity and inhibitory control in key aspects of eating behavior, including both stable eating characteristics as assessed with self-report, and food-related decisions as assessed with a laboratory task. To accomplish this, we used a series of established measures in a sample of participants with an extended weight range, and conducted structural equation modeling analyses to test the relationships between impulsivity, inhibitory control, unhealthy eating, and BMI. We hypothesized that both heightened impulsivity (Hypothesis 1) and deficient inhibitory control (Hypothesis 2) should be associated with higher measures of unhealthy eating, and that unhealthy eating would in turn be associated with elevated BMI (Hypothesis 3).
