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Overeating As an Addiction

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Overeating As an Addiction Overeating as an Addiction A Literature Thesis by Rony Halevy Brain & Cognitive Sciences Msc. Program Cognitive Science Center Amsterdam University of Amsterdam Supervised by: prof. dr. Reinout Wiers University of Amsterdam Co-assessor: Dr. Sanne de Wit University of Amsterdam Fabruary 2012 Introduction Over the last few decades the prevalence of obesity is increasing in many parts of the world (Farooqi & O'Rahilly, 2007) and obesity is claimed to pose a significant health threat (von Deneen & Liu, 2011). Obesity is starting to be recognized as a neurological disorder (Dagher, 2009) and a suggestion was made to include it in the DSM-V (Volkow & O'Brien, 2007). As part of the effort to reduce the rate of what is referred to as "the obesity epidemic", attempts are being made to understand the brain processes related to food intake and satiety (Rolls, 2007). A tremendous increase in the understanding of the molecular and neural mechanisms underlying these processes was made in the past two decades (Zigman & Elmquist, 2003). The role of brain reward mechanisms received a lot of attention (Davis & Fox, 2008). Various risk factors – genetic, developmental and environmental – are likely to interact among overeaters. One line of explanation is the "thrifty genotype", suggesting that the circuits involved in food consumption and storage were designed in an environment where food was scarce, and are putting some individuals at risk of overconsumption in today's western environment (Volkow & O'Brien, 2007). A separation can be made between homeostatic hunger – following a period of food deprivation, and hedonic hunger – which occurs in the absence of deprivation (Davis et al., 2009). It was claimed that some obese individuals tend to eat regardless of homeostatic hunger (Wang, Volkow, Thanos & Fowler, 2004). Perhaps this lack of connection between homeostatic hunger and feeding comes from the fact that certain foods such as carbohydrates, fats, sweet/fat combinations and processed or salty foods have an addictive potential (Corsica & Pelchat, 2010). Researchers claim that these foods can act on the brain and its reward systems much like different drugs of abuse (Gearhardt, Yokum, Orr, Stice, Corbin & Brownell, 2011b), and that repeated exposure to these foods in 2 vulnerable individuals can result in compulsive food intake and loss of control over eating (Volkow & O'Brien, 2007). The idea that eating can be viewed as an addiction is far from new (Dagher, 2009), but it is receiving a lot of attention from different disciplines nowadays. Some behavioral similarities can be seen between overeaters and drug addicts, such as loss of control and compulsive consumption (Wang et al., 2004). Direct support for the concept of food addiction comes from animal research (Avena, Long & Hoebel, 2005; Avena, Rada & Hoebel, 2008; Epstein & Shaham, 2010), genetic studies (Farooqi & O'Rahilly, 2007), neurochemistry and neuroimaging research (Wang et al., 2001; Davis et al., 2009; Davis et al., 2011; Gearhardt et al., 2011b). While a vast amount of experimental studies and numerous reviews from the last decade support the notion of addiction to food, questions are still being raised regarding the plausibility of food addiction in humans (Benton, 2010) and the usefulness of this framework with respect to treating obesity (Foddy, 2011; Blundell & Finlayson, 2011). In addition, while some scholars deduce from the possible addictiveness of food that strict food regimens should be kept in order to lose weight (Volkow & Wise, 2005; von Daneen & Liu, 2011), new approaches are trying to shift the attention from weight loss to a healthier life style, arguing that treating food as a threat and keeping a restricted diet is destructive with respect to self-esteem as well as health (Bacon, Stern, van Loan & Keim, 2005; Bacon & Aphramor, 2011). The current report will review the evidence for parallels between overeating and addiction, trying to see if indeed overeating, or specific forms of it, can be considered as addiction to food. Afterwards, a closer look will be taken at the usefulness of this framework and the threats it may possess. 3 Parallels between overeating and addiction The concept of overeating as an addiction has been addressed in the past two decades from several perspectives. A variety of animal models show some support for this line of thinking. The development of obesity in rats was coupled with deficit in reward responses, similarly to changes induced by cocaine or heroin (Johnson & Kenny, 2010). In another study, rats that were exposed to a cafeteria-style diet (i.e. high fat and/or high carbohydrate food) showed both disruptions in sensitivity to reward and insensitivity to negative consequences of self- administration (Epstein & Shaham, 2010). It was also shown that a cross-sensitization of alcohol and fat occurs in rats: consumption of both fat and alcohol leads to the production of hypothalamic orexigenic peptides, which in turn increase the consumption of these two substances (Blumenthal & Gold, 2010). Another line of work in animal models specifically investigated sugar as a substance of abuse. Rats that were exposed to sugar for 28 days and then had sugar withheld for 14 days consumed more sugar after the abstinence than rats that had a shorter initial exposure (Avena, Long & Hoebel, 2005). It seems that the abstinence increased the consumption of the substance only if it occurred after sufficient exposure. The authors compare this to a deprivation effect shown with drugs of abuse, and suggest that a sensitization of the dopamine system leads to pathological motivation for the stimulus. Rats exposed to sugar and then deprived from it also show cross-sensitization with amphetamines (Avena & Hoebel, 2003 in: Avena, Long & Hoebel, 2005). Several other markers of addiction, such as binging, withdrawal, craving and gateway effect were also claimed to be seen in rats after excessive sugar intake (Avena, Rade & Hoebel, 2008). 4 However, the notion of sugar addiction, and especially the relevance of animal models to humans, is still controversial. It has been claimed that the predictions that follow the notion of sugar addiction in humans are not supported by the data (Benton, 2010). Nevertheless, animal models are helpful in pointing similarities between addiction and overeating, which can be further investigated in human subjects. One possible target when seeking such similarities is the dopaminergic system. Dopamine release in the nucleus accumbens has been linked to unconditioned reward signals, and the dopaminergic system is claimed to be crucial for motivation and goal-directed behavior (Wise, 2004). Dopamine projections from the ventral-tegmental area and the substantia nigra to the nucleus accumbens and striatum, circuitries normally involved in pleasure, motivation and learning, are affected by various drugs. Addictive drugs are claimed to alter these circuitries, causing hyper-sensitization (Volkow, Fowler & Wang, 2004). These changes can lead to pathological “wanting” of drugs, but the increase in drug “wanting” is not necessarily linked to an increase in drug “liking” (Robinson & Berridge, 2003). The repeated stimulation of dopamine reward pathways by food or drugs is said to trigger adaptations in other brain circuitries, leading to an increase in compulsive behaviors affecting both drug and food consumption (Volkow & Li, 2004). Of special interest are dopamine D2 receptors. A low availability of D2 in the striatum was reported in individuals addicted to various types of drugs, including cocaine (Volkow et al., 1993), alcohol (Hietala et al., 1994) and opiates (Wang et al., 1997). Interestingly, a low availability of D2 receptor in the striatum was also linked to excessive weight. Wang et al. (2001) used a PET scan to show that striatal D2 receptor availability was significantly lower in obese individuals. In addition, within the obese group, a correlation was found between the receptors’ availability and Body Mass Index (BMI). The authors suggest that the dopamine 5 deficiency is a risk factor for obesity (among other disorders). The deficiency may lead to pathological eating as a mean of compensation. This claim is supported by the fact that knockout of striatal D2 receptors accelerated the development of addiction-like reward deficits, as well as the onset of compulsive food seeking in rats (Johnson & Kenny, 2010). However, it is also possible that the low availability is a consequence of overeating. Some animal models support the second notion, by reporting a decrease of D2 receptors in the striatum of rats that were fed daily with glucose (Colantuoni et al., 2001). Another model linking dopamine to eating behavior suggested a somewhat different perspective (Davis et al., 2009). The authors used a group of obese individuals diagnosed as suffering from Binge Eating Disorder (BED) and another group of obese non-BED individuals. Examining three different polymorphisms related to D2 receptors and one polymorphism related to the Mu opioid-receptor (OPRM1), the authors found significant differences between the groups. The BED group showed higher frequency of the A118G allele (G-allele) of the OPRM1 (an allele linked to increased responsiveness to opiates). This allele, previously linked to alcohol addiction (Filbey, Ray, Smolen, Claus, Audette & Hutchison, 2008), was underrepresented in the obese without BED. Wiers, Rinck, Dictus & van den Wildenberg (2009) found that the G-allele of the OPRM1 is related to a strong approach bias to both alcohol cues and other appetitive stimuli, in a group of heavy drinkers. By contrast, the Taq1A1 allele for the D2 receptor, which was also linked to an increased risk of addiction, was more frequent in obese without BED. This allele is related to lower dopaminergic reactivity in the mesolimbic system. Davis et al. (2009) used a framework of “liking” and “wanting”, suggested by Robinson and Berridge (2003) to account for these findings. The authors suggested that the Taq1A1 allele, seen more frequently in the non-BED 6 obese, is related to higher wanting, whereas the A118G allele, seen more frequently in the BED obese is related to higher liking of food.
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