Current Drug Abuse Reviews - Volume 4, Issue 3, 2011

For many years researchers have noted the overlaps that exist in the brain mechanisms that promote ingestion of food and drug abuse [1, 2]. As just one example, the mesolimbic dopamine system has been implicated as being perturbed in both cases of drug dependence, as well as cases of caloric over and under consumption. Despite these known overlaps in brain mechanisms, historically, these two behaviors, feeding and drug dependence, have been studied independently. However, more recently, the idea that certain foods may have properties of addiction [3, 4] has been reinforced by empirical studies, and researchers have begun to study these behaviors simultaneously to understand whether “food addiction” might have a role in the present-day obesity crisis, as well as in certain eating disorders. The aim of this special issue is to summarize the current literature on concepts related to the intersects between food and addiction. Over the past few years a significant amount of work has been devoted to the study of “food addiction.” Preclinical studies have shown that overeating palatable foods can lead to addiction-like behaviors [3, 5]. Likewise, preclinical studies show that during some instances of aberrant eating there are concomitant changes in neurochemistry and gene expression in reward-related brain areas that are similar to the changes that can occur in response to a drug of abuse [6]. Clinical studies using patient self-report and neuroimaging support these findings, and suggest that individuals can meet criteria that suggest dependence on palatable foods [7, 8]. This raises important questions regarding the addictive nature of highly-palatable foods that are abundant in the modern food environment [9, 10]. The idea of “food addiction” has been extended and applied conceptually to disordered eating behavior. The obesity epidemic has led to many novel suggestions regarding its etiology, one of which is that some people may develop an unhealthy dependence on calorically-dense, palatable foods. Indeed, overweight individuals show altered reward responsivity and changes in the brain that are like those seen in individuals addicted to drugs, as revealed by fMRI and PET [11]. Obesity can arise when there is excessive motivation to eat and low impulse control, a situation that has been termed reinforcement pathology [12]. Theories of hypo-responsivity and hyper-responsivity to food in reward-related brain regions have been described. Further, newer data account for the possible effects of repeated overeating on brain responsivity to food and factors leading to vulnerability toward overeating [13]. Aside from obesity, the overlaps that exist between food intake and addiction have relevance to the study of eating disorders, such as anorexia nervosa and binge eating disorder. It is interesting that both over- and under-eating can perturb brain reward systems in a way that can promote the intake of drugs of abuse [14]. Anorexia nervosa, which is characterized by severe undernutrition, may result in some features of addiction. For example, patients narrow their behavioral repertoire of weight loss, restricting food intake, and excessive exercise such that these behaviors interfere with other activities in much the same way that substance abuse does [15]. Binge eating disorder has stood out as having particular relevance to “food addiction.” Binge eating, which is seen in obesity, as well as in some eating disorders, is characterized by periodic overeating. Such intermittent food consumption has been suggested to promote behaviors that are associated with dysregulation in rewardfunctioning [16]. Further, binge eating disorder shares many characteristics with addictive behaviors (e.g., diminished control and continued use despite negative consequences) [17]. While understanding the contributions that maladaptive food intake, as it relates to addiction, makes toward informing our understanding of the pathology of obesity and eating disorders, it is important to underscore that there are unique physiological and cognitive factors that contribute to each of these disorders. Nonetheless, the articles in this special issue highlight the recent research on the intersects of food reward and drug reward, and the information described posits important future considerations for treatment, policy and nutritional guidance.....

The obesity epidemic has led to the postulation that highly palatable foods may be “addictive” for some individuals. This idea is supported by the fact that there are overlaps in brain circuitry that underlie addictive behavior as well as overeating. In this paper, we discuss the utility of the concept of “food addiction” as it may relate to treating certain disordered eating behaviors. Using criteria set forth in the DSM-IV for substance-use disorders, we review data that have emerged from animal models suggesting that overeating, in the form of binge eating, fits some of the criteria for substance abuse. Further, we discuss preclinical data revealing that the addiction-like behavioral changes observed in response to overeating are concomitant with neurochemical changes that are similar to those observed in response to drugs of abuse. With this background and evidence in mind, we conclude this article with a discussion as to how “food addiction” research may translate into clinical strategies and pharmaceutical treatments useful in curtailing overeating.

Scientific interest in “food addiction” continues to grow due both to neurobiological and behavioral similarities between substance dependence and excessive food consumption. An important next step is to examine the addictive potential of highly processed foods. In this paper, we explore addiction-related changes in the modern food environment (e.g., increased potency, elevated speed of absorption), examine the historical and modern understanding of addictive substances as applied to hyperpalatable foods, and outline shared factors that increase the public health costs of both addictive drugs and certain foods.

Studies of food addiction have focused on highly palatable foods. While fast food falls squarely into that category, it has several other attributes that may increase its salience. This review examines whether the nutrients present in fast food, the characteristics of fast food consumers or the presentation and packaging of fast food may encourage substance dependence, as defined by the American Psychiatric Association. The majority of fast food meals are accompanied by a soda, which increases the sugar content 10-fold. Sugar addiction, including tolerance and withdrawal, has been demonstrated in rodents but not humans. Caffeine is a “model” substance of dependence; coffee drinks are driving the recent increase in fast food sales. Limited evidence suggests that the high fat and salt content of fast food may increase addictive potential. Fast food restaurants cluster in poorer neighborhoods and obese adults eat more fast food than those who are normal weight. Obesity is characterized by resistance to insulin, leptin and other hormonal signals that would normally control appetite and limit reward. Neuroimaging studies in obese subjects provide evidence of altered reward and tolerance. Once obese, many individuals meet criteria for psychological dependence. Stress and dieting may sensitize an individual to reward. Finally, fast food advertisements, restaurants and menus all provide environmental cues that may trigger addictive overeating. While the concept of fast food addiction remains to be proven, these findings support the role of fast food as a potentially addictive substance that is most likely to create dependence in vulnerable populations.

This review is aimed at understanding some of the common neurochemical, behavioral and physiological determinants of drug and food overconsumption. Much current work has been devoted to determining the similarities between the brain circuits controlling excessive use of addictive drugs and the overconsumption of palatable foods. The brain systems involved likely include peptides of both mesolimbic and hypothalamic origin. Evidence gathered from expression and injection studies suggests that the consumption of drugs, such as ethanol and nicotine, and also of palatable foods rich in fat is stimulated by different orexigenic peptides, such as enkephalin, galanin, orexin, and melaninconcentrating hormone, acting within the hypothalamus or various limbic structures, while another peptide, neuropeptide Y, is closely related to carbohydrate consumption and shows an inverse relationship with ethanol and nicotine consumption. Moreover, studies in animal models suggest that a propensity to overconsume these reinforcing substances may result from preexisting disturbances in these same peptide systems. These neurochemical disturbances, in turn, may also be closely linked to specific behaviors associated with excessive consummatory behavior, such as hyperactivity or novelty-seeking, palatable food preference, and also fluctuations in circulating lipid levels. Clear understanding of the relationship between these various determinants of consummatory behavior will allow researchers to effectively predict and examine at early stages of exposure animals that are prone to drug and food overconsumption. This work may ultimately aid in the identification of inherent traits that increase the risk for drug abuse and palatable food overconsumption.

The idea that foods rich in fat and sugar may be addictive has generated much interest, as well as controversy, among both scientific and lay communities. Recent research indicates that fatty and sugary food in-and-of itself is not addictive. Rather, the food and the context in which it is consumed interact to produce an addiction-like state. One of the contexts that appears to be important is the intermittent opportunity to consume foods rich in fat and sugar in environments where food is plentiful. Animal research indicates that, under these conditions, intake of the fatty sugary food escalates across time and binge-type behavior develops. However, the mechanisms that account for the powerful effect of intermittency on ingestive behavior have only begun to be elucidated. In this review, it is proposed that intermittency stimulates appetitive behavior that is associated with uncertainty regarding what, when, and how much of the highly palatable food to consume. Uncertainty may stimulate consumption of optional fatty and sugary treats due to differential firing of midbrain dopamine neurons, activation of the stress axis, and involvement of orexin signaling. In short, uncertainty may produce an aversive state that bingeing on palatable food can alleviate, however temporarily. “Food addiction” may not be “addiction” to food at all; it may be a response to uncertainty within environments of food abundance.

Advances in neuroimaging techniques have provided insight into the role of the brain in the regulation of food intake and weight. Growing evidence demonstrate that energy dense, palatable foods elicit similar responses in rewardrelated brain regions that mimic those of addictive substances. Currently, various models of obesity's relation to reward from food have been theorized. There is evidence to support a theory of hypo-responsivity of reward regions to food, where individuals consume excess amounts to overcome this reward deficit. There is also data to support a theory of hyper-responsivity of reward regions, where individuals who experience greater reward from food intake are at risk for overeating. However, these seemingly discordant theories are static in nature and do not account for the possible effects of repeated overeating on brain responsivity to food and initial vulnerability factors. Here we review data that support these theories and propose a dynamic vulnerability model of obesity that appears to offer a parsimonious theory that accommodates extant findings.

Obesity is, in part, a result of positive energy balance or energy intake exceeding physiological needs. Excess energy intake is determined by a series of food choices over time. These choices involve both motivational and executive function processes. Problems arise when there is excessive motivation to eat and low impulse control, a situation we have termed reinforcement pathology. Motivational and executive function processes have also been implicated in the development of drug dependence and addiction. In this review we discuss the application of reinforcement pathology to obesity, and implications of this approach for obesity treatment.

Anorexia nervosa is a severe psychiatric disorder characterized by unrelenting self-starvation and lifethreatening weight loss. The relentlessness with which individuals with anorexia nervosa pursue starvation and in some cases exercise despite the negative physical, emotional, and social consequences parallels features of addictive disorders. From a clinical perspective, individuals with anorexia nervosa behave similarly to individuals with substance abuse by narrowing their behavioral repertoire so that weight loss, restricting food intake, and excessive exercise interfere with other activities in much the same way that substance abuse does. However, fundamental differences exist between anorexia nervosa and substance abuse that suggest anorexia nervosa is not an addiction in and of itself.

Binge eating disorder (BED) shares many characteristics with addictive behaviors (e.g., diminished control, continued use despite negative consequences), and a body of scientific literature is building to support addiction conceptualizations of problematic eating. Despite similarities, BED and “food addiction” may represent unique yet overlapping conditions. Although the exploration of food addiction is relatively new, understanding the relationship between food addiction and BED may be informative in understanding the mechanisms underlying the development and maintenance of problematic eating. In the following paper, we 1) examine the theoretical similarities and differences between BED and addiction, 2) review recent empirical evidence that speak to the relationship between BED and food addiction and 3) discuss the implications of associations between BED and food addiction with respect to clinical interventions.