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
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,
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
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).
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
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
obese, is related to higher wanting, whereas the A118G allele, seen more frequently in the BED obese is related to higher liking of food. The A118G allele might represent the hedonic component of overeating – the tendency to eat despite lack of homeostatic hunger. In a different study, seven different SNPs, all in the OPRM1 gene, were related to a preference for sweet and fatty food that was positively associated to binge eating patterns and to BMI (Davis et al. 2011).
The opioid system is one of the most crucial components regulating consumption related behavior, especially of palatable food, regardless of its caloric content (Olszewski, Alsio, Schioth & Levine, 2011). Injections of Neloxone, an opioid antagonist, were shown to decrease consumption of sweet food, but not standard food (Levine, Weldon, Grace, Cleary & Billington, 1995). Neloxone was also showed to produce opiate-like withdrawal effects in rats after long-term inlong-termittent access to sugar (Colantuoni et al., 2002). As drug-induced neural changes in the reward system are a central factor in substance dependence (Volkow et al., 2004), it has been postulated that opioids play a role in long-term dyregulation of food intake underlying the development or maintenance of obesity (Olszewski et al., 2011).
It is important to note that the relationship between sensitivity to reward and eating behavior is not necessarily linear. Low sensitivity to reward can lead to both high BMI, due to a high threshold and an attempt to compensate for it, or to low BMI due to diminished motivation to eat (Davis & Fox, 2008). In addition, individuals who overeat may develop tolerance and elevate their reward threshold, much like individuals addicted to different drugs of abuse (Wang
et al., 2004). In a study using a questionnaire to measure sensitivity to reward, an inverted
U-shape correlation was found between BMI and sensitivity to reward. Among individuals with BMI<30, a positive correlation was found, whereas among individuals with BMI>30, a negative correlation was found (Davis & Fox, 2008).
Another candidate gene related to overconsumption of food, perhaps through mediating reward signal, is the leptin receptor gene (LEP-R). Leptin plays a major role in metabolism and appetite signaling and an association was found between percent body fat, BMI and the LEP-R variant Lys109Arg (Carpenter, Ingles, Jaque, Schroder, Wong & Bernstein, 2004; Chagnon et
al., 2000; Wauters et al., 2001). Functional neuroimaging studies show that leptin has an
influence on neural activity in circuits involving food intake by changing the perception of food reward and by increasing neural response to satiety signals (Farooqi, Bullmore, Keogh, Gillard, O'Rahilly & Fletcher, 2007).
A different type of relation between overeating and addiction comes from a closer look at cannabinoid receptors, which are known to respond to cannabis intake. There are two identified kinds of cannabinoid receptors, CB1 and CB2, of which the former is mainly found in the brain, and its activation was linked to appetite (Akbas, Gasteyger, Sjodin, Astrup & Larsen, 2008). The cannabinoid system is claimed to participate in the reward effect of cannabinoids, nicotine, alcohol and opiods and in common mechanisms of drug-seeking behavior (Maldonado, Valverde & Berrendero, 2006). It was suggested that the cannabinoid system is up-regulated in obese humans (Bluher et al., 2006), and hence CB1 antagonists, already used as intervention for drug addiction (Maldonado et al., 2006) were offered as an intervention for obesity. An antagonist for CB1 was found to decrease motivation for palatable food (Higgs, Williams & Kirkham, 2003) and decrease energy intake. However, this effect appears to be short-termed. The up-regulation of the cannabinoid system found in obese individuals could stem from leptin receptor gene polymorphism, as it is known that leptin plays a role in the activation of this system (Di Marzo et
al., 2001). It could also be that an overconsumption of either food or drugs of abuse leads to the
In a recent review by Kenny (2011), another perspective on the link between overeating and addiction was suggested. The author examines the nucleus tractus solitarius (NTS), a nucleus receiving signals from both the oral cavity and gastrointestinal system, and suggests that over-consumption of palatable high-fat food may be related to decreased sensitivity of this nucleus. The NTS also projects to the limbic system, which is strongly involved in drug-related reward signals and drug dependence. Kenny (2011) concludes that the NTS regulates the satiety signal of both drug and food by influencing the activation of reward circuits. Perhaps the link between overeating and addiction is related to a deficit is the satiety signal.
More evidence for neural similarities between overeating and addiction comes from neuroimaging studies. In an fMRI study, addiction-like patterns of activation were detected in obese: both elevated activation of reward circuitries in response to food cues and reduced activation of inhibitory regions in response to food intake were detected (Gearhardt et al., 2011b). Another study used a regional cerebral blood flow to compare the response of lean and obese men to satiation. Here too, the authors discuss different activation patterns in both prefrontal inhibitory circuits and limbic appetitive-emotional circuits in obese individuals (Gautier et al., 2000). The fact that the same brain circuits are involved in overeaters' response to food and in addicts' response to drugs can imply that similar mechanisms are involved in both phenomena, yet further research is needed in order to prove this claim.
One way to account for these neural activation patterns is by considering dual processing models of addiction (Wiers & Stacy, 2006). These models discuss two systems: a slow, reflective system, creating decisions based on knowledge, and a fast, impulsive system, eliciting behaviors based on motivational orientation (Strack & Deutsch, 2004). Using drugs of abuse can lead to a change in the balance between the two systems, and create behavior which is “more stimulus
driven and outside conscious control as an addiction develops” (Wiers & Stacy, 2006, p. 293).
Considering the physical, genetic and systemic similarities of the neural structures involved in drug and food consumption, it is possible that an excessive intake of food can also disrupt the balance between the two systems. This may lead to different neuronal responses to food as suggested by the neuroimaging studies discussed above, and perhaps, as a result, to additional increase in food intake. And indeed, it has been shown that chronic intake of high fat and high sugar foods can lead to the formation of pathological pathways in the brain and to different responses to palatable food (von Deneen & Liu, 2011). Blumenthal and Gold (2010) explicitly claim that “hedonic food can act like a traditional drug of abuse, causing brain changes almost
Can overeating be considered an addiction?
Given the various lines of similarity between addiction and overeating, one might wonder whether overeaters can in fact be considered to be “food addicts”. The answer depends on how addiction is defined. If we define addiction as "a pharmacological term characterized by a
compulsion to consume that is driven by craving" (Benton, 2010, pp. 289), then many
individuals may be considered as food addicts in different situations. Looking for a more stable definition, we can use the idea of addiction as excessive appetite: ”an attachment to an appetitive
activity, so strong that a person finds it difficult to moderate the activity despite the fact that it is causing harm” (Orford, 2001, p. 18). If we adopt this definition, any overweight individual
trying to reduce food consumption can be defined as an addict. Different compulsive behaviors, such as gambling or sex addiction, also fall under this definition.
The definition of substance dependence accepted today is that of the DSM IV-TR (American Psychiatric Association, 2000), according to which a patient must show three of the following criteria within 12 months:
1. Tolerance, as defined by either of the following:
A. The need for markedly increased amounts of the substance to achieve intoxication or desired effect.
B. Markedly diminished effect with continued use of the same amount of the substance.
2. Withdrawal, as manifested by either of the following:
B. The same (or closely related) substance is taken to relieve or avoid withdrawal symptoms.
3. Taking the substance often in larger amounts or over a longer period than was intended. 4. There is a persistent desire or unsuccessful effort to cut down or control substance use. 5. Spending a great deal of time in activities necessary to obtain or use the substance or to
recover from its effects.
6. Giving up social, occupational, or recreational activities because of substance use. 7. Continuing the substance use with the knowledge that it is causing or exacerbating a
persistent or recurrent physical or psychological problem.
Criteria 3-7 do not require physiological dependence, and since a patient can be diagnosed if presenting three criteria, physiological dependence is not necessary. The third criterion, taking in larger amounts, fits the description of overeaters eating larger portions than intended (Corsica & Pelchat, 2010). The fourth criteria, the attempt to cut back, can easily be seen by the increasing amount of people trying to lose weight. A telephone survey conducted in the US found that 57% of all women reported currently engaging in a weight loss behaviors (Neumark-Sztainer, Rock, Thornquist, Cheskin, Neuhouser & Barnett, 2000, in: Bacon et al., 2005). The fifth criterion refers to spending a great amount of time obtaining the substance, and since palatable food is easily available nowadays, not much time is needed in order to obtain it. In fact, much of the increase in obesity rates is claimed to be due to this increase in food availability (Rolls, 2007). However, some overeaters do spend excessive time pursuing activities related to food: thinking about food, planning their next intake, preparing food or sleeping after consuming a large amount (Corsica & Pelchat, 2010).
The sixth criterion, renouncing various activities due to substance use, is not necessarily relevant to overeating, since food, as opposed to some drugs of abuse, can be consumed in public. However, it may well be the case that the excess time spent consuming food comes at the expense of other, more social, activities. In addition, it is claimed that obese and especially binge eaters tend to isolate themselves and miss social activities (Ifland at al., 2009).
The seventh criterion, continued consumption despite consequences, is very relevant to overeating. A vast amount of health problems were linked to obesity, including stroke, cardiovascular disease, diabetes mellitus and increased risk of cancer (von Deneen & Liu, 2011). However, the rates of obesity continue to grow (Rolls, 2007). Due to the obvious linkage between eating habits and overweight, it can be deduced that people continue to overeat despite consequences.
Regarding the first and second criteria, the only two presenting a physiological aspect, the answer is less clear. Ifland et al. (2009) claim that individuals identifying themselves as addicted to food report a personal experience of both tolerance and withdrawal. Empirical investigations of these notions are less conclusive. Since food as a whole cannot be treated as a
substance, researchers have taken specific food ingredients as substances that can be abused.
While several animal models claim to show tolerance and withdrawal symptoms for various food substances, results from human studies are less conclusive. Some support for the development of tolerance to carbohydrates was found (Spring et al., 2008 in: Corsica & Pelchat, 2010), but no such results were found for sugar or fat (Benton, 2010).
Nonetheless, since diagnosis can be made when a patient shows three criteria, the physiological criteria are not obligatory, and it would seem that many overeaters can in fact be diagnosed as suffering from substance dependence. In fact, it was claimed that some of the DSM
IV-TR criteria for substance abuse are over inclusive with respect to overeating, meaning that they may apply to all forms of unhealthy food consumption and not just to individuals addicted to food (Delvin, 2007). A rather new diagnostic tool for food addiction, the Yale Food Addiction Scale (YFAS, Gearhardt, Corbin & Brownell, 2008), is focusing on parallels to substance dependence criteria in the DSM-IV-TR, and “preliminary data suggested that this is a valid and
reliable tool for detecting eating patterns that are similar to behaviors seen in the classic areas of addiction” (Corsica & Pelchat, 2010, p. 167).
In the suggestions for DSM-V (American Psychiatric Association, n.d.), substance dependence will be categorized together with substance abuse under substance use disorders. A substance use disorder is defined as:
A maladaptive pattern of substance-use leading to clinically significant impairment or distress, as manifested by two (or more) of the listed criteria within a 12-month period: 1. recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences or poor work performance related to substance use; substance-related absences, suspensions, or expulsions from school; neglect of children or household)
2. recurrent substance use in situations in which it is physically hazardous (e.g., driving an automobile or operating a machine when impaired by substance use)
3. continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance (e.g., arguments with spouse about consequences of intoxication, physical fights)
a. a need for markedly increased amounts of the substance to achieve intoxication or desired effect
b. markedly diminished effect with continued use of the same amount of the substance.
5. withdrawal, as manifested by either of the following:
a. the characteristic withdrawal syndrome for the substance (refer to Criteria A and B of the criteria sets for Withdrawal from the specific substances)
b. the same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms
(Note: Withdrawal is not counted for those taking medications under medical supervision such as analgesics, antidepressants, anti-anxiety medications or beta-blockers.)
6. the substance is often taken in larger amounts or over a longer period than was intended
7. there is a persistent desire or unsuccessful efforts to cut down or control substance use
8. a great deal of time is spent in activities necessary to obtain the substance, use the substance, or recover from its effects
9. important social, occupational, or recreational activities are given up or reduced because of substance use
10. the substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance
11. Craving or a strong desire or urge to use a specific substance.
Four new criteria are added to the seven listed in the DSM-IV-TR. While the first and second criteria are not very applicable with respect to food as a substance of abuse, the third criterion (continuing consumption despite social or interpersonal problems) might be relevant in today's western society. As rates of obesity continue to rise, western society is claimed to devalue overweight individuals, and especially overweight women (Bacon et al., 2005). If that is the case, social and interpersonal problems derived from overeating are quite plausible.
The eleventh criteria, craving, is directly relevant to overeating. Craving is claimed to take a leading role in overeating and especially in binge eating, and carbohydrate craving was verified and demonstrated in a highly controlled experimental environment (Corsica & Pelchat, 2010). Food craving also leads to patterns of fMRI signals in the hippocampus, insula and caudate, areas that are involved in drug craving (Pelchat, 2009). It is important to note that the relevance of food craving to obesity has been questioned. It was claimed that craving decreases with dieting, and that cravings for food, as opposed to drug cravings, "do not occur regularly
enough to explain habitual food intake" (Benton, 2010, p. 293). Nonetheless, the existence of
food craving is not a matter of debate.
To conclude, even if we assume the additional first two criteria are not applicable to food addiction, the seven criteria taken from the DSM-IV-TR, together with the third and the eleventh new criteria, makes the diagnosis of overeating as substance disorder possible according to the
The usefulness of the “Overeating as an Addiction” framework
As we have seen, the concept of overeating as an addiction has received heightened attention in the last few decades. Furthermore, according to the DSM-IV-TR and DSM-V, overeaters might meet criteria for substance dependence and substance disorder respectively. Given these facts, the question arises as to the benefit of this approach. If we consider overeating as an addiction, how does this change the way we conceive or treat overeating? As previously discussed, obesity is not always linked to addiction to food. “Food addiction is neither necessary nor sufficient for
obesity” (Epstein & Shaham, 2010, p. 530). Therefore, it might be useful to screen obese
individuals seeking help for food addiction (Corsica & Pelchat, 2010).
It was suggested that if food is addictive, improving eating habits and maintaining a highly controlled eating environment and strict food regimen should help people control their weight (von Deneen & Liu, 2011). Some of the behavioral interventions for addiction, such as cognitive behavioral therapy and 12-step-programs, are claimed to be promising for treatment of obesity stemming from food addiction (Volkow & Wise, 2005). However, experimental studies describing such intervention methods are hard to find. A study using an intervention based on the 12-steps philosophy showed promising results with female adolescents suffering from eating disorders (Trotzky, 2002), but a more recent study using a similar intervention was less conclusive (McAleavey, 2010). One reason for the difficulty of adopting addiction interventions could be the fact that refraining from food, as oppose to other substances of abuse, is neither possible nor desired. Perhaps refraining from specific types of food can help individuals at risk of food addiction to avoid compulsive eating patterns (Volkow & Wise, 2005).
In addition to behavioral interventions, since dopamine deficiency was detected in overeaters, “strategies aimed at improving DA function might be beneficial in the treatment and
prevention of obesity” (Wang et al., 2004, p. 50). Three pharmacological treatments for obesity,
derived from addiction models, are currently at clinical trials: 1) Contrive 2) Nixa & 3) Lorca Erin, yet all three have significant side effects (Blumenthal & Gold, 2010). In addition, pharmacogenetic research is showing promising results in treating various diseases, and may be relevant to this line of research. Since the same set of symptoms may be caused by different genes, leading to different effectiveness of treatment (Kalow, 2006), perhaps it will be beneficial to pretest subjects for genes that are related to obesity or to addiction before starting obesity interventions. According to Farooqi and O’Rahilly (2007), “heritable factors are likely to be
responsible for 45-75% of the inter-individual variation in body mass index” (Farooqi &
O'Rahilly, 2007, p. 37). The authors suggest that screening for specific genes might enable classification of obese subjects into subgroups, which may help in finding more suitable interventions for each patient.
Prevention intervention is another approach that might be beneficial for food addiction. Some of the decrease in smoking rates in the US over the past 30 years is claimed to be due to educational campaigns, deliberate price increase and the restriction of smoking in public spaces. A similar campaign, promoting healthy eating habits and exercise, could help decrease obesity rates (Volkow & Wise, 2005). When such prevention interventions are considered, it is important to pay attention to the engineering and marketing of food, which may interact with personal risk factors. Nowadays, ingredients of potentially addictive foods, such as sugar and corn, are extremely cheap due to government subsidies in many countries. Based on the experience with alcohol and tobacco, increasing taxation on hyper-palatable food while making healthy food more available can lead to real change (Gearhardt, Grilo, DiLeone, Brownell & Potenza, 2011a).
Criticism and dangers
As evidence for the similarity between overeating and various substance disorders continues to accumulate, and some interventions used for treating addiction may help treat overeating, concerns have been raised regarding the amount of attention this concept receives and the risks it may hold. It was suggested that the notion of food addiction is only relevant to binge eating, while binge eating is not strongly related to obesity (Epstein & Shaham, 2010). The prevalence of obesity among binge eaters in the US is 42%, only slightly higher than the prevalence in the general population (Wonerlich, Gordon, Mitchell, Crosby & Engel, 2009, in: Epstein & Shaham, 2010). As opposed to binge eating, “the route to obesity is generally a rather modest daily
excess of energy intake over energy expenditure” (Rogers, 2011, p. 1213). If that is the case,
perhaps a notion of “food addiction” is not very applicable to human obesity.
Moreover, it has been recently claimed that the concept of food addiction adds confusion to the already confusing field of food overconsumption. Blundell and Finlayson (2011) claim that the excess consumption of food is part of a general trend in our society, which is strongly linked to our economy. Over-consumption is needed in order to keep the economic growth, and hence it is encouraged by governments. Given this, together with our powerful reward system, the authors claim it is surprising that the level of obesity is not higher. They claim the term food
addiction is not necessary to account for massive intake of food.
In addition to general considerations regarding the usefulness of the concept, it was also suggested that that a concept of food addiction can be used by overeaters as an excuse for unhealthy eating (Epstein & Shaham, 2010). It was shown already in the 1980s that the ability to quit smoking is related to the expectancy of success (Eiser & van der Pligt, 1986a) and that smokers who perceived themselves as hooked, a feeling of inability to give up smoking, had a
lower chance of quitting (Eiser & van der Pligt, 1986b). In addition, treating alcoholism as a disease was claimed to lead to a transfer of responsibility to medical professionals (Eiser & van der Pligt, 1986a). Perhaps the same could be said about overeating: if people see their bad eating habits as an addiction, they might have a harder time mending them.
With respect to food, a more general claim was made about public attention to weight loss. It was suggested that risks of obesity are overestimated, and that the association between obesity and health risks are mainly due to the relations of both to poor nutrition and sedentary lifestyle (Bacon et al., 2005). Overweight per se may not hold the threat it is said to have. According to current guidelines, obese individuals are encouraged to lose weight by dieting and exercise, but the effect of these changes is usually short-term, so no real improvement in morbidity is achieved. In addition, it was suggested that these changes may lead to weight cycling, food preoccupation, reduced self-esteem and distraction from other health goals (Bacon & Aphramor, 2011).
A new movement, called Health at Every Size (HAES) is trying to promote a shift in focus. The new focus is on homeostatic regulation and eating intuitively, and decreased eating restraints. It is claimed that food restraints lead to low self-esteem and are rarely kept for long periods and hence that the focus should shift toward a more flexible pattern of self-care. Participants in interventions based on this approach are guided to end restrictive eating behaviors and be more tuned to internal rather than external eating cues. A randomized clinical trial comparing intervention based on HAES to a diet program, showed significantly better outcomes for the HAES method with respect to blood pressure, blood lipids, eating behavior, self-esteem, depression and even BMI. Moreover, subjects in the HAES group were better at maintaining these outcomes (Bacon et al., 2005).
Given these findings it seems that weight loss is not a good target for public health interventions (Bacon & Aphramor, 2011). If that is the case, the concept of overeating as an addiction could have negative consequences. One possible threat is the fact that reviewing this concept, some scholars conclude that if food is addictive, the solution is a highly controlled diet (von Daneen & Liu, 2011), avoidance of specific food ingredients or detoxification of unhealthy foods (Volkow & Wise, 2005). As mentioned above, restraining eating habits may have negative outcomes with respect to health improvement and weight loss. In addition, the idea of intuitive eating, based on internal cues, assumes that these cues represent healthy choices. The concept of overeating as an addiction implies changes in neural circuits, leading to pathological internal cues which one should try to ignore. The question of whether or not the intuitions of an overeater regarding food intake should be trusted remains open.
However, the two frameworks do not necessarily contradict each other. It was claimed that, at least with respect to sugar, it is not the food itself that leads to addiction, but rather the pattern of consumption: excessive intake followed by abstinence (Avena et al., 2005). If that is the case, perhaps it is the cycles of dieting and losing control over food intake, which characterize many of the attempts to lose weight (Bacon & Aphramor, 2011), that lead to addiction to food as described above. If some obese individuals are indeed addicted to food, an attempt to adopt an intuitive eating approach, together with policy changes as suggested above, can help diminish addiction symptoms and regain control over eating, assuming that neurological changes are reversible.
Conclusions
Evidences showing parallels between addiction and overeating were accumulated in the previous decade, and numerous reviews looking at the accumulated data support the framework of treating overeating as an addiction. Some scholars still claim that the concept is somewhat provocative (Rogers, 2011), and receives more attention than it should. However, behavioral, genetic and neural similarities between overeating and addiction are now acknowledged, and drug addiction may help us understand obesity (Volkow & Wise, 2005).
While not applicable to all obese people, this new framework may give rise to ideas for means of intervention in treating obesity. The dangers of overeating might be exaggerated (Bacon & Aphramor, 2011), but there is no doubt that many people eat more than they should, or at least not as healthy as they should. Some behavioral interventions that were useful in treating addiction might be promising in treating overeating (Volkow & Wise, 2005). Policy changes, inspired by procedures done with respect to alcohol and tobacco, could be helpful in diminishing the consumption of certain types of food. In addition, pharmacogenetics is bringing hope of personalized medicine (Kalow, 2006), and a closer examination of genes that have already been linked to addictions may be helpful in treating different patterns of pathological eating.
However, not all attempts to use methods based on addiction treatment are successful, perhaps due to fundamental differences between food and other possible drugs of abuse. A careful approach is needed when trying to "translate" addiction interventions to obesity treatment, since interventions that are not suitable can be unhelpful or even harm patients. Viewing food as an enemy, a threat to be avoided, might be destructive. Food is not only essential for our survival, it also takes a major part in all human cultures, and it is one of the most
not to demonize food or to encourage strict eating regimens that are doomed to be broken. Balanced eating patterns should be promoted by encouraging healthier food choices, not necessarily by focusing on weight loss.
To conclude, while including overeating as a mental disorder in the DSM-V holds some benefits and may encourage the development of therapeutic interventions (Volkow & O’Brien, 2007), using criteria of substance disorders as they are seems inadequate. While obvious similarities are found between addiction and overeating, there are also some fundamental differences between the two. It seems, therefore, that simply adding food as another substance of abuse might hold certain threats that can not be overlooked, and that the DSM-V should include separate diagnosis criteria for overeating. A careful consideration should be taken when formulating criteria for the diagnosis of overeating, and guidelines are needed in order to assure the diagnosis is used correctly. The criteria for substance disorders, as well as existing overeating diagnostic tools and criteria for other eating disorders may be used as inspiration.
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