**Ethical, Stigma, and Policy Implications of Food Addiction: A Scoping Review**

### **Stephanie E. Cassin 1,2,3, Daniel Z. Buchman 4,5,6, Samantha E. Leung 2,7, Karin Kantarovich 2,7, Aceel Hawa 8, Adrian Carter 9,10 and Sanjeev Sockalingam 2,3,7,8,\***


Received: 1 February 2019; Accepted: 20 March 2019; Published: 27 March 2019

**Abstract:** The concept of food addiction has generated much controversy. In comparison to research examining the construct of food addiction and its validity, relatively little research has examined the broader implications of food addiction. The purpose of the current scoping review was to examine the potential ethical, stigma, and health policy implications of food addiction. Major themes were identified in the literature, and extensive overlap was identified between several of the themes. Ethics sub-themes related primarily to individual responsibility and included: (i) personal control, will power, and choice; and (ii) blame and weight bias. Stigma sub-themes included: (i) the impact on self-stigma and stigma from others, (ii) the differential impact of substance use disorder versus behavioral addiction on stigma, and (iii) the additive stigma of addiction plus obesity and/or eating disorder. Policy implications were broadly derived from comparisons to the tobacco industry and focused on addictive foods as opposed to food addiction. This scoping review underscored the need for increased awareness of food addiction and the role of the food industry, empirical research to identify specific hyperpalatable food substances, and policy interventions that are not simply extrapolated from tobacco.

**Keywords:** ethics; food addiction; health policy; stigma

### **1. Introduction**

The average weight of Americans increased dramatically in the 1980s, and this trend did not discriminate based on age, gender, or race [1]. Kessler notes that one remarkable change that coincided with the dramatic weight increase was the availability of "hyperpalatable" foods, specifically those engineered to combine optimal amounts of sugar, fat, and salt [2]. Some authors likened these hyperpalatable foods to addictive drugs, such as cocaine [3]. Though obesity only began garnering serious medical and public attention in recent years, the idea that obesity is a result of a food addiction was, in fact, first posited during the 1940s and 1950s [4,5]. However, this early conceptualization of food addiction resulted in much societal debate as it intensified weight stigma and contributed to ineffective policy changes around obesity and its consequences [5]. Since then, views on obesity and food addiction have been evolving, though the concept of food addiction is still highly debated today.

Food addiction is not an official diagnosis in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) [6]; however, health care professionals, researchers, patients, and the general public use the term, and a questionnaire (Yale Food Addiction Scale; YFAS) has been developed to diagnose its purported core features [7]. Many similarities have been noted between substance use disorders (e.g., alcohol, nicotine) and food addiction, including consuming more of the substance than intended or over a longer period of time, preoccupation with the substance, craving or strong urge to use the substance, and continued consumption despite knowledge of adverse effects [8].

Food addiction can have negative impacts on individuals living with obesity. Several studies have found that individuals with obesity who meet criteria for food addiction (as measured by the YFAS) demonstrate greater levels of eating disorder psychopathology, poorer general and health-related quality of life, greater depressive symptoms, and higher scores on impulsivity and self-control measures [9–11]. Together, this underscores the importance of studying the relationship between food addiction and obesity.

A food addiction model proposes that some individuals are addicted to certain foods and feel driven to engage in weight promoting eating behaviors, such as binge eating or compulsive overeating, when exposed to "addictive" food substances [7,12,13]. Foods with added fat and refined carbohydrates have been shown to be consumed in a more addictive manner [13,14] and craved more intensely [15] than less refined foods. This is thought to be, in part, a result of such hyperpalatable foods activating the mesolimbic reward-related pathway of the brain, which connects the ventral tegmental area of the midbrain to the nucleus accumbens in the ventral striatum via dopaminergic neurons [16,17]. Neuroimaging studies on individuals meeting the cut-off for food addiction according to the YFAS have been shown to have dysfunctional patterns of reward-related neural activation [12,18], and studies employing the use of genotyping have demonstrated higher multi-locus genetic profile scores in this group, which is associated with enhanced dopamine signaling [19].

Despite mounting evidence for the compulsive consumption of highly palatable foods, food addiction has continued to generate much controversy [20]. Discourses have centered around several issues, including diagnostic challenges of food addiction; arguments that food addiction is not distinct from binge eating disorder [21,22]; debates as to whether food addiction is akin to a behavioral addiction versus a substance use disorder [23]; and the notion that food (albeit not hyperpalatable foods), unlike other substances, is necessary for survival [24]. With respect to the diagnostic challenges, there is emerging evidence that food addiction is distinct from binge eating disorder [25] and may be best classified as a substance (food) use disorder as opposed to a behavioral (eating) addiction [8,26]. A recent systematic review examining the validity of food addiction concluded that the existing research supports food addiction as a unique construct [8]. Amongst the 35 articles (52 studies), the largest number of studies found evidence for brain reward dysfunction and impaired control, followed by studies on tolerance and withdrawal for foods with the greater addictive potential, specifically added sugars and fats.

In comparison to research examining the construct of food addiction and its validity, relatively little research has examined the potential ethical, stigma, and health policy implications of food addiction. Other addictions to substances, such as tobacco, cannabis, or alcohol, have seen an increase in the use of stigmatization as a policy tool in order to promote public health [27]. As a result, ethical issues have arisen surrounding public health communication and its effect on individuals and

on society as a whole [28]. Bayer has argued that the use of stigma may reduce the prevalence of behaviors linked to disease and mortality [29]. People who identify as "fat" or "obese" have long received stigmatizing "fat-shaming" messages from healthcare providers and public health officials. Stigmatization of people with obesity often has the opposite effect and is ethically indivisible given the stress and emotional and dignitary harms it causes [30]. This further emphasizes the importance of developing a nuanced understanding of the potential impact of a food addiction model on stigma, particularly given that it could have divergent effects on externalized stigma towards others and internalized stigma towards the self.

A recent systematic review of nine empirical studies examining the link between food addiction and weight stigma concluded that limited evidence suggests that food addiction explanations may reduce self-blame and stigma from others, but these benefits may be offset by the adverse impact on self-efficacy and eating behaviors [31]. However, the authors also noted that the existing empirical research is sparse and inconsistent. To our knowledge, no scoping reviews have been conducted to examine the ethical and health policy implications of food addiction, or the implications on stigma more broadly beyond weight stigma. The purpose of this scoping review was to highlight what has been published in the food addiction literature and to address these current gaps to help inform current perceptions by identifying the potential ethical, stigma, and health policy implications of food addiction.

### **2. Materials and Methods**

This review was conducted as per the Arksey and O'Malley methodological framework for scoping reviews [32]. As part of the development of our research questions and approach, a stakeholder summit was organized in collaboration with the Canadian Obesity Network (CON) involving a broad and diverse group of 18 stakeholders including local knowledge users (i.e., people with experience with obesity-related treatment and food addiction), representatives from national obesity organizations and patient advocacy groups, primary care physicians, and interprofessional research leaders nationally and internationally in food addiction and/or obesity management. Data from a pre-summit online questionnaire exploring perceptions related to the ethical and policy issues of food addiction in obesity informed summit discussions aimed at identifying key themes related to food addiction. The pre-summit online questionnaire was derived from previous studies on food addiction in obesity [33,34] and included open-ended questions regarding the potential implications of food addiction on stigma, ethics, and health policy. The following five stages were completed as part of the scoping review methodology.

### *Stage 1: Identifying the Research Questions*

Based on the analysis of themes resulting from the stakeholder summit, this scoping review was conducted to address the following question: What are the potential ethical, stigma and policy implications of food addiction in obesity?

Inclusion/exclusion criteria

We included peer- and non-peer reviewed articles, editorials, commentaries, letters, and replies to authors that met the following criteria:


We excluded book chapters, dissertations, and policy documents. Papers were also excluded if they only focused on obesity and did not relate to food addiction.

### *Stage 2: Identifying Relevant Studies*

We searched for relevant articles published up until January 26, 2017, for each question using the following databases: Medline and PsycINFO from the OvidSP platform and CINAHL from the EBSCO platform. Each of the OvidSP databases was searched individually. The searches were conducted with assistance from a research librarian from an academic health sciences center. The searches were run with the limits of human studies and English language studies only. When appropriate, controlled vocabulary terms and/or text words were used in the subject component blocks. For example, obesity/bariatric terms included one block, food addiction terms included a second block, and ethics/stigma/policy terms included a third block. Lastly, we reviewed key special issues on food addiction in prominent eating disorder and obesity periodicals to identify additional articles that may have met our inclusion criteria and were missed by our initial search. A total of 410 articles were identified from these search strategies.

### *Stage 3: Selecting Studies*

All references resulting from the literature search were reviewed and 46 duplicates were removed. Preliminary screening was conducted by titles and abstracts by two independent reviewers. Seventeen references were missing and were excluded from screening. Screened abstracts were separated into three categories: articles to include, unsure articles, and non-relevant articles to exclude. A secondary screening was then conducted by two additional independent reviewers on the articles that were deemed unsure from the first round of screening. This screening procedure resulted in 296 articles being excluded. Full text articles for the remaining 60 abstracts were then retrieved for data collection (see Figure 1 for PRISMA diagram).

### *Stage 4: Charting the Data*

Data were extracted from all included full-text articles by one reviewer into a spreadsheet that included authors, year of publication, and article type and relevant excerpts, themes, and quotes. Each domain was then separated into individual spreadsheets with the relevant articles and their respective identifiers and variables for coding and analysis.

### *Stage 5: Collating, Summarizing, and Reporting the Results*

Three independent reviewers completed this step. Each of the three main domains of ethics, stigma, and policy had two reviewers who independently reviewed the full text articles and coded the data. A thematic analysis approach was used to critically analyze the articles and generate open codes. All reviewers then came together to discuss, compare, and organize the relevant excerpts, themes, and quotes that were extracted for each of the three main domains. These iterative discussions allowed for a higher level of thematic analysis, generating broad categories and higher-level themes. Reviewers met nine times at 1- to 2-month intervals for a total of 18 h to review codes and to generate domains summarized below.

**Figure 1.** PRISMA flow diagram depicting the flow of information through the different phases of this scoping review. From: [35].

### **3. Results**

Each of the three domains of ethics, stigma, and policy implications related to food addiction are described below. All articles included from the search strategy for each of the three domains are listed in Table S1. Of the 43 studies included in the analysis, 10 were reviews, 25 were original research articles, 5 were commentaries, 2 were opinions, and 1 was a brief. Table 1 provides a summary of themes and subthemes with sample quotes extracted from articles.


#### **Table 1.** Scoping review themes, subthemes, and representative quotes.


**Table 1.** *Cont.*

### *3.1. The Intersection of Ethics and Food Addiction*

Our search yielded 20 articles related to ethics and food addiction. We identified individual responsibility as the primary theme of this section, with the following sub-themes: (i) personal control, will power, and choice; and (ii) blame and weight bias.

### 3.1.1. Personal Control, Will Power, and Choice

We found a tension in the literature between the traditional framings of addiction that emphasized personal control over food consumption, with medicalized, neuroscientific accounts of food addiction that emphasized reduced personal control. For example, Appelhans, Whited, Schneider, and Pagoto suggested, "[d]ietary lapses or failures should be conceptualized as the result of brain systems interacting with a toxic food environment, and not as a reflection of poor personal choices or lack of willpower" [45] (p. 1135). Some scholars argue that framing food addiction within a disease model may reduce individual blame [46] as the impairment in the person's autonomy and capacity for control reflects dysfunction in the brain's reward circuitry [36,44,47]. However, some scholars are skeptical that a food addiction label or a disease model will reduce responsibility or obviate perceptions that obesity is self-inflicted [5,48]. Others worry about the potential negative influence a brain disease model of food addiction might have on people with obesity. For example, Lee and colleagues suggest that a (brain) disease model could potentially justify coercive practices on a population that is thought to have reduced autonomy and limited control over their behavior [33].

A study by Lee and colleagues found that public support for a food addiction model of obesity was associated with the view that the individual had to overcome their condition through willpower and personal choice [34]. Other studies have reported that the public considers food addiction more of a personal choice than an addiction to other substances such as alcohol [41]. Green suggests that the free autonomous behavior to consume highly palatable foods could be deterred potentially by the implementation of sin taxes (or excise taxes) on said foods [49], but others, such as Franck, Grandi, and Eisenberg, question the evidence to support this recommendation [50]. Scholars have argued that the focus on individual-level factors, such as free will and personal choice, have failed to address the public health impact of high levels of highly palatable food consumption [51,52]. Some authors have

argued that this narrow focus on individual-level factors "lets the food industry off the hook" for its contributions [53] (p. 2).

### 3.1.2. Blame and Weight Bias

Given the emphasis on personal responsibility in the literature, perspectives on who or what is to blame for food addiction are also far from stable. The literature reflects tensions between attributing blame for food addiction to the individual, the environment (including government and industry), or both, but seldom the alleged addictive properties of the food itself [5,41]. For instance, Thibodeau, Perko, and Flusberg found that participants who agreed with narratives that blamed the individual for their obesity (i.e., due to an addiction, a problem of individual behavior) were likely to support interventions that were penalizing, whereas support for narratives that blamed the environment were likely to support policy interventions that sought to protect people with obesity [37]. These tensions exist in a Western culture that values and legitimizes the over-consumption of foods and other material goods [51,54].

Weight bias is an ethically important concept in terms of its relevance to respect for persons, discrimination, and social justice, among others [38]. For example, entrenched harmful stereotypes that describe people with obesity as lazy and lacking in willpower underpins the moral view that they make poor choices with respect to food consumption and their health [38]. "Fat" people are considered "addict[ed] to inappropriate pleasures," which serves to further stigmatize and blame "fat" people [55] (p. 17).

### *3.2. Potential Implications of Food Addiction on Stigma*

Our search yielded 19 articles related to stigma and food addiction. Identified themes included the following: (i) the impact on self-stigma and stigma from others, (ii) the differential impact of substance use disorder versus behavioral addiction on stigma, and (iii) the additive stigma of addiction plus obesity and/or eating disorder. As noted below, there was extensive overlap between several of the stigma and ethics themes.

### 3.2.1. The Impact on Self-Stigma and Stigma from Others

Related to the concepts of personal control, willpower, and choice, as well as blame and weight bias described above, several authors discussed potential implications of food addiction on self-stigma (internalized stigma) and stigma from others (externalized stigma). Similar to people who use substances, people with obesity receive messages from individuals and society that their obesity is a character flaw [56]. Empirical research using hypothetical case vignettes has found some evidence to suggest that a food addiction model may have a beneficial impact on stigma towards others who are overweight. Latner, Puhl, Murakami, and O'Brien randomly assigned participants to one of four conditions in which they read about either an addiction or non-addiction explanatory model of obesity, and subsequently read a vignette about a woman that was either obese or of normal weight [46]. Regardless of the participant's weight status, a food addiction explanatory model of obesity was found to result in less stigma, less blame, and less perceived psychopathology attributed to the woman in the vignette [46]. Moreover, a food addiction model resulted in less blame towards individuals with obesity in general, leading the authors to conclude that this explanatory model of obesity could have a beneficial impact on the pervasive prejudice against individuals with obesity.

Lee et al. conducted a large survey regarding public views of food addiction [34]. They found substantial support for the concept of food addiction, particularly among individuals with obesity [34]. They were less likely to agree that obesity is caused by overeating and they reported greater support for external causes of obesity. The authors speculated that a diagnosis of food addiction may reduce some of the guilt and self-blame associated with obesity. However, a correlational study by Burmeister, Hinman, Koball, Hoffman, and Carels found that weight-loss-seeking participants with a greater severity of food addiction, as measured by the YFAS, reported greater anti-fat attitudes (e.g., dislike of

other people with excess weight), internalized weight bias (e.g., internalization of anti-fat attitudes), and body shame [39].

### 3.2.2. Differential Impact of Substance Use Disorder Versus Behavioral Addiction on Stigma

Despite evidence of shared neurobiological processes in substance use disorders and behavioral addictions, a false dichotomy permeates much of the discourse whereby substance use disorders are perceived as a neurobiological disease and behavioral addictions are perceived as a mental/psychological condition. Whether food addiction is considered a substance use disorder versus behavioral addiction may impact factors such as personal responsibility, autonomy, and blame attribution, which in turn have implications for internalized and externalized stigma. Stigma may decrease if food addiction is considered a substance use disorder because it provides an explanatory model for obesity "without invoking character flaws, such as lack of willpower" [45] (p. 1133), and shifts responsibility from the individual to the food substance and food industry. For example, Appelhans et al. state: "by emphasizing genetically-influenced neurobiological processes that confer vulnerability to overeating in a toxic food environment, the model enables dietetics practitioners to more effectively address obesity without promoting stigma" [45] (p. 1133). However, Rasmussen points out that the "neurochemical concept of obesity, as with drug addiction and eating disorders, can coexist with attribution of personal responsibility for the condition, and thus with blaming the impaired, addicted consumer rather than the supplier" (p. 217), and goes on to say that "it cannot be ruled out that attribution of addiction (as a chronic brain disease) will hurt more than it helps" [5] (p. 223).

Whereas opinions were mixed regarding whether considering food addiction as a substance use disorder would reduce internalized and externalized stigma, it was generally believed that considering food addiction as a behavioral addiction would either have little effect on stigma or actually increase stigma because it is perceived as a choice that is under personal control. DePierre, Puhl, and Luedicke conducted an empirical study to examine public perceptions of food addiction compared to nicotine and alcohol addiction. Food addiction was considered to be a disease to a greater extent than smoking and to be the product of personal choice to a greater extent than alcohol addiction, leading the authors to conclude that food addiction may be perceived as a behavioral addiction that is vulnerable to stigmatization rather than a substance addiction [41].

### 3.2.3. Additive Stigma of Addiction Plus Obesity/Eating Disorder

We found a tension in the literature regarding whether food addiction would reduce the stigma directed towards individuals with obesity or create an additional stigmatized identity. Several authors pointed out that substance-related disorders, such as nicotine, alcohol, and cocaine use disorders, are stigmatized to an even greater extent than obesity, a finding that may be due to the fact that everyone must eat food for survival, whereas a person must choose to seek out and use psychoactive substances of abuse [40,41,45]. It has also been suggested that food may be a less stigmatizing substance of abuse because it has less impact on others compared to nicotine (e.g., second-hand smoke) and alcohol (e.g., driving under the influence, impulsive behaviors) [40,41].

Several authors raised concerns that a diagnosis of food addiction could result in a double or additive stigma because the types of stigma associated with obesity and addiction differ [5,40,42,57]. For example, applying the types of stigma described by Goffman in this context, obesity could be considered a visible "abomination of the body," whereas addiction could be considered a "blemish of character" [40,58]. Foddy states: "I have said nothing about the myriad social dimensions in which we stigmatize and disadvantage addicts [sic] differently from the obese. It is hard to say exactly which group has the worse lot in this sense, since the stigma and discrimination takes different forms in each case" [36] (p. 87).

Rather than food addiction reducing stigma by providing an explanatory model for compulsive/binge eating and obesity that reduces blame and personal responsibility, several authors noted that food addiction may actually amplify the harms of stigma because obesity, eating disorders, and addictions are all stigmatized conditions, and neurobiological explanations do not necessarily modify attributions of personal responsibility. Allen et al. raised concerns about the "dietary obese being stigmatized as addicts [sic]" (p. 134) [42]. Rasmussen noted that "the stigmatizing attribution of addiction to people already stigmatized as obese may amplify the social harms that they suffer" (p. 217), "raising the risk that their combination might prove reinforcing" [5] (p. 223).

A few experimental studies have been conducted to examine the impact of food addiction on externalized stigma. Bannon, Hunter-Reel, Wilson, and Karlin randomly assigned participants to one of six conditions in which they read a vignette about a woman with obesity [59]. The independent variables were her binge eating status (present vs. absent) and the cause of her obesity (biological addiction vs. psychological vs. ambiguous). Unfortunately, the manipulation regarding the cause of her obesity was not successful, which prevented interpretation of the specific impact of food addiction on externalized stigma. However, the presence of binge eating increased externalized stigma such that participants rated individuals with obesity as less attractive and more blameworthy for their weight, and they desired greater social distance from them [59]. DePierre et al. directly examined the additive effect of food addiction on externalized stigma [40]. They found that labelling an individual as an "obese food addict" was more stigmatizing than either label on its own ("food addict" or "obese") and concluded that food addiction may increase the externalized stigma associated with obesity, but be less susceptible to stigma than other forms of addiction [40].

### *3.3. Potential Policy Implications of Food Addiction*

Our search yielded 31 articles related to policy themes for addictive foods that were extrapolated to the construct of food addiction. Policy themes related to addictive foods were generally derived from comparisons to the tobacco industry. Articles identified specific policy interventions from "Big Tobacco" that could be applied to food addiction included the following: (i) reducing access to addictive foods, (ii) food taxation, and (iii) limiting advertising for addictive foods.

### 3.3.1. Comparisons to "Big Tobacco"

Many articles made parallels between the policy issues related to the food industry and the tobacco industry. The role of food taxation, reducing access to potentially addictive foods, litigation against the food industry, and limiting food advertising in addressing food addiction and obesity arise from this comparison to "Big Tobacco" and highlight a prominent theme amongst most articles focusing on policy issues of food addiction [38,52,53]. The association between the food industry and tobacco industry is contingent on a clear link between certain foods and their addictive potential. Authors argued that if certain foods are conceptualized as "a potentially disease-causing agent such as tobacco and alcohol then policy changes to encourage the intake of healthy food and decrease the intake of unhealthy foods are in order" [60] (p. 762). Furthermore, Schulte and colleagues argue that if the concept of food addiction is embraced by the public as it was for nicotine addiction, the shift in public perception of the substance (in this case, addictive foods) could generate enough support for change in public policies for obesity [61]. This argument has been supported by an online survey of 999 individuals from the U.S., including 52% of individuals who were overweight or obese, which showed that believing food is addictive increased support for obesity-related policies [62].

### 3.3.2. Reducing Access to Addictive Foods Through Regulation

In comparison to policies in the tobacco industry, the overall evidence for the effect of government regulations on limiting access to highly pleasurable food is still emerging and requires further exploration [63]. Current papers identified the role of government regulations on the food industry to support legislation, litigation, and regulation efforts to influence access to healthy as opposed to high fat or sugar foods [60,64]. Reports suggest that if food is deemed addictive, then governments need to establish clear policies to limit, restrict, or even ban addictive foods [52], such as limiting the number and location of fast food restaurants and soft drink vending machines in an area.

The support for policies focused on addictive food restriction for children and youth as opposed to adults. For example, in a survey of youth who were unable to lose weight using an online open-access website for obesity, participants felt that restriction of junk food and fast food outlets would be beneficial [36]. Additional articles supported early intervention efforts through increased regulation of pleasurable foods in children and youth settings such as schools, implementation of programs promoting healthy eating and food choices, and engagement of pediatricians and family physicians [65,66]. In contrast, a recent qualitative study with 23 individuals with obesity showed that individuals were skeptical about the effectiveness of restrictions on highly pleasurable foods, although they supported addictive food restrictions for children [43]. Nonetheless, reviews generally supported external control of addictive foods based on examples where cigarette smokers perceived external control as being influential or effective compared to individual motivating factors (e.g., willpower, personal choice) [67,68].

Despite this support for policy interventions focused on increased food regulation, concerns were expressed in articles around the lack of clarity around "addictive," or "good" and "bad," ingredients and foods [69]. The lack of clear evidence about foods categorized as "addictive" and the unique challenges with food being a necessary part of living (in contrast to alcohol) have complicated abstinence arguments and approaches thus far. Nonetheless, authors have used the comparison to the tobacco industry for informing food addiction policy interventions focused on restriction [56]. Empirical evidence has demonstrated that narratives where obesity was considered an addiction or a disorder led to increased public support for a protective approach to policy interventions for obesity; however, implications for obesity treatment are not fully understood [37].

Studies reiterated the importance of obesity experts being more explicit about food engineering and the need for greater public awareness of this issue beyond the traditional "obesogenic environment" discourses [44]. A greater focus on increasing public awareness about food engineering could lead to greater support for policy interventions focused on regulation and addictive food restriction. One article noted that a potential consequence of identifying and regulating specific "addictive" foods could be litigation and banning of the food industry for purposefully engineering foods to be more addictive [52].

### 3.3.3. Food Taxation

Themes related to food taxation also emerged predominantly from comparisons between the food and tobacco industries, as highlighted above [42,44]. The rationale stems from evidence for the taxation of tobacco products, which has estimated that a 10% increase in soft drink prices could result in approximately an 8–10% reduction in soft drink consumption by individuals [70,71]. Moreover, several countries, including France and Hungary, have implemented tax levies on high caloric density foods [41]. These national policy initiatives will be beneficial in evaluating the effects of these interventions longitudinally on mitigating food addiction.

Despite this early evidence, several factors complicate food taxation as a policy intervention to reduce access to caloric dense foods. In contrast to tobacco products, caloric dense foods are already cheaper than healthier food options [42]. Therefore, food taxation efforts would affect children and the poor disproportionately given the current low cost of caloric dense foods, although food taxes may potentially be used to offset costs for healthier foods in this population [42]. In addition, it is unclear what food ingredients are highly addictive and as a result, conclusive recommendations on specific ingredients warranting taxation remains a challenge [53].

### 3.3.4. Limiting Advertising for Addictive Foods

Studies have also articulated concerns about the early introduction of food advertising to young children and adolescents. Gearhardt and colleagues identified the need to limit food advertising to children to limit the potential long-term effects, such as food addiction [38]. Restriction of food marketing to youth has involved both government policies but also voluntary pledges by the food industry [38]. These initiatives have attempted to correct the default food industry messaging that has been inoculating children and youth for decades [71]. As a result, authors argue that voluntary self-regulatory efforts by the food industry are likely to be insufficient, and government protective policies are needed to counteract these trends in early childhood food marketing strategies by the food industry [38].

### 3.3.5. Limited Information on Food Addiction in Obesity Guidelines

Several papers focused on the limited discussion of food addiction within key obesity related guidelines and resources such as the World Health Organization (WHO) and Centre for Disease Control (CDC) [42]. Despite increasing public dialogue on food addiction, obesity guidelines have not included information on the controversies related to food addiction. This is complicated by the inability to differentiate specific addictive food ingredients and limited evidence for food addiction related interventions [72]. As a result, papers highlighted the need for an improved mechanistic understanding and the development and testing of new treatments for managing addictive foods.

Furthermore, there have been questions regarding the evidence for policy interventions for preventing and managing addictive foods in patients with obesity. Gostin and colleagues believe that the "lack of science" argument for food addiction policy interventions is a faulty argument given that no single intervention resulted in a substantial reduction in nicotine use and there is a need for a multi-level intervention approach [73]. Thus, further research is needed to clarify the construct of food addiction, risk factors and effectiveness of policy interventions to facilitate integration within obesity-related guidelines and resources.

### **4. Discussion**

The current scoping review examined the potential ethical, stigma, and health policy implications of food addiction, identified the major themes in the literature, and provided insights into key challenges in these areas.

### *4.1. Potential Ethical Implications of Food Addiction*

While various disease models of alcohol use disorders have circulated within the popular discourse since the early 19th century [74,75], more recently scholars have adopted the language of neuroscience to characterize addiction more generally as a chronic, relapsing brain disease [76,77]. We found that discussions in the literature lend themselves to moral debates over personal control, individual responsibility, and blame for the consequences of food consumption. Indeed, these moral framings are common in the obesity discourse [44,78]. However, the neurobiological theory of food addiction may place a disproportionate burden on the individual to treat their food addiction, which may provide less incentive for governments to scale up public health approaches, such as holding the food industry accountable for their food engineering practices as well as the social conditions that harm people who are defined as food addicted.

The focus of individual blame in the literature may be reflective of a culture of healthism, defined as the individual desire for health and well-being achieved primarily through lifestyle modification [79]. The moral assumptions underlying healthism is that individuals are responsible for making good choices as opposed to bad choices about their health. Our results suggest that healthism describes good choices as health-promoting and reflects self-control over eating while bad choices lead to food addiction or obesity. For instance, some dietary counselling recommendations include empowering the patient to take responsibility for their behaviors in the context of what they consider to be a toxic food environment [45]. Our results suggest that some authors were concerned about a culture that emphasizes healthism and individualism when the social conditions make the ability to make healthy eating choices near impossible [51]. Future research can build on the burgeoning literature in this area and provide deeper insights into the moral attitudes about food addiction held by diverse publics. It will also be important for future research to explore if the empirical findings related to moral concepts align with the concerns raised in the conceptual philosophical and bioethics literatures.

### *4.2. Potential Stigma Implications of Food Addiction*

Our review also examined the complex relationship between food addiction and stigma. Stigma is a multidimensional construct including many related concepts (e.g., labels, stereotypes, prejudice, discrimination), sources (e.g., self-stigma, public stigma, provider-based stigma [e.g., from healthcare providers], institutional stigma), characteristics (e.g., stigma of the physical body, stigma of character), and dimensions (e.g., social distance, perceptions of dangerousness) that can complicate analyses [80]. The limited empirical research conducted to date, much of which has experimentally manipulated the information provided in case vignettes, has generated mixed results regarding the impact of a food addiction model on externalized stigma. Whereas a food addiction explanation for obesity was found to reduce externalized stigma and blame towards a target in one study [45], another study found that labeling an individual as an "obese food addict" created an additive stigma that exceeded the stigma associated with either label on its own [40]. This finding is consistent with a recent qualitative study of individuals with obesity, which noted that some individuals who personally identified with the concept of food addiction felt reluctant to be described as an "addict" because they believed the label would increase self-stigma and stigma from others [43]. Interestingly, the one study identified through our scoping review that examined the association between food addiction and externalized stigma in a clinical sample found that patients with greater severity of food addiction reported greater anti-fat attitudes towards other individuals with excess weight [39]. The impact of food addiction on externalized stigma has been examined in student samples, community samples, and a clinical sample, and additional research is warranted to examine the impact of a food addiction model on externalized stigma among healthcare professionals.

In contrast to the mixed findings regarding the impact of a food addiction model on externalized stigma, the association between food addiction and internalized stigma has been fairly consistent. The aforementioned study conducted in a clinical sample found that patients with greater severity of food addiction reported greater internalized weight bias and body shame, as well as lower eating self-efficacy [39]. This finding is consistent with a recent study comparing three groups that varied with respect to food addiction (i.e., non-food-addicted, self-perceived food addicted, and food-addicted according to the YFAS) and found that internalized weight bias increased across the groups despite no differences in body mass index, whereas eating self-efficacy decreased across the groups [81]. Similarly, a recent systematic review examining the association between internalized weight bias and health-related variables reported that the published studies conducted to date have consistently found a positive association between food addiction and internalized weight bias [82]. Moreover, internalized weight bias was associated with a variety of negative mental and physical health outcomes including depression, anxiety, low self-esteem, poor body image, disordered eating, severity of obesity, reduced dietary adherence, and reduced motivation and self-efficacy to engage in health-promoting behaviors. Although much of the research conducted to date has been cross-sectional, which precludes conclusions regarding the direction of causality, if replicated in prospective research, such findings would lend support to concerns voiced by some authors that food addiction could have an adverse impact on internalized stigma and reduce the self-efficacy needed to improve eating behaviors [29]. Although the treatment implications of food addiction were beyond the scope of the current review, this important topic is recently receiving more attention in the literature [83,84] and the findings of the current review suggest that treatment approaches that reduce internalized weight bias and bolster self-efficacy would be advised.

Whether food addiction is best characterized as a behavioral addiction or a substance use disorder has been a topic of debate [26]. The results of the current review suggest that characterizing food addiction as a behavioral addiction likely has an adverse impact on externalized stigma compared to characterizing it as a substance use disorder. Despite evidence that behavioral addictions and substance use disorders have many shared features, including neurobiological mechanisms and genetic contributions [85,86], behavioral addictions are still commonly perceived as being more under personal control. The general public perceives food addiction as being less of a disease and more under personal control than alcoholism [41]. Increasing public awareness regarding the engineering of hyperpalatable foods and the validity of food addiction as a diagnostic construct that shares similarities with other substance use disorders [8] may be helpful as both a public health and stigma reduction intervention.

### *4.3. Potential Policy Implications of Food Addiction*

Across reviewed articles, we found that the tobacco industry served as an example for many of the policy recommendations for managing food addiction in obesity. The challenges with these policy interventions were related to the lack of research on addictive food substances, specifically the current inability to classify foods more broadly in their addictive potential. Despite authors drawing parallels to "Big Tobacco," we identified a dearth of evidence for the effectiveness of food addiction as a driver for policy change in obesity. Therefore, many of the recommendations, such as food taxation, reducing advertising to children, and reducing access to addictive foods (especially in children and youth), were extrapolated from policy interventions observed in the tobacco industry as opposed to being specific to food addiction.

### *4.4. Limitations*

Our results are subject to the following limitations associated with scoping review. Unlike a systematic review, we are unable to grade the quality of the studies or make any specific recommendations related to level of evidence. The articles included in this scoping review included commentaries and empirical research (e.g., experimental and correlational studies). Further, although our search used multiple methods to identify potential articles, it is possible that some studies were missed. This scoping review underscored the need for future research on the effectiveness of policy interventions to mitigate the effect of addictive foods on the obesity epidemic. The inclusion of food addiction within obesity guidelines was a notable omission in the literature that was identified in our review. It is possible that the absence of food addiction in obesity guidelines reflects the need for greater research on the role of food addiction on obesity management, including questions about its benefit for healthcare professionals and patients in obesity care.

### **5. Conclusions**

This review is the first to explore the ethical, stigma, and policy issues related to food addiction using a scoping review methodology. The gaps in the evidence related to this scoping review underscore the need for additional research and increased clarity regarding the ethical and stigma related impact of a food addiction model. In addition, more rigorous studies are needed to move beyond policy interventions generated predominantly from past experiences in the tobacco industry.

**Supplementary Materials:** The following are available online at http://www.mdpi.com/2072-6643/11/4/710/s1, Table S1: Complete List of Articles from Search Strategy.

**Author Contributions:** S.E.C., D.Z.B., and S.S. contributed to the conception and design of the study. S.E.L., K.K., and A.H. conducted literature searches and provided summaries of previous research studies. All authors contributed equally to the analysis and interpretation of the data and the writing of the manuscript. All authors have approved the final manuscript.

**Funding:** This study was funded by the Canadian Institutes of Health Research (Grant No. 373261).

**Acknowledgments:** This project was funded by a Planning and Dissemination Grant from the Canadian Institutes of Health Research. We would like to thank Ashley Farrell for assisting with the scoping review methodology and literature search, as well as the individuals who participated in our food addiction retreat.

**Conflicts of Interest:** The authors declare no conflict of interest.

### **References**


© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

### *Article* **Obesity Stigma: Is the 'Food Addiction' Label Feeding the Problem?**

**Helen K. Ruddock 1,2, Michael Orwin 1,3, Emma J. Boyland 1, Elizabeth H. Evans <sup>3</sup> and Charlotte A. Hardman 1,\***


Received: 25 July 2019; Accepted: 30 August 2019; Published: 4 September 2019

**Abstract:** Obesity is often attributed to an addiction to high-calorie foods. However, the effect of "food addiction" explanations on weight-related stigma remains unclear. In two online studies, participants (*n* = 439, *n* = 523, respectively, recruited from separate samples) read a vignette about a target female who was described as 'very overweight'. Participants were randomly allocated to one of three conditions which differed in the information provided in the vignette: (1) in the "medical condition", the target had been diagnosed with food addiction by her doctor; (2) in the "self-diagnosed condition", the target believed herself to be a food addict; (3) in the control condition, there was no reference to food addiction. Participants then completed questionnaires measuring target-specific stigma (i.e., stigma towards the female described in the vignette), general stigma towards obesity (both studies), addiction-like eating behavior and causal beliefs about addiction (Study 2 only). In Study 1, participants in the medical and self-diagnosed food addiction conditions demonstrated greater target-specific stigma relative to the control condition. In Study 2, participants in the medical condition had greater target-specific stigma than the control condition but only those with low levels of addiction-like eating behavior. There was no effect of condition on general weight-based stigma in either study. These findings suggest that the food addiction label may increase stigmatizing attitudes towards a person with obesity, particularly within individuals with low levels of addiction-like eating behavior.

**Keywords:** food addiction; obesity; stigma; eating behavior; attitudes

### **1. Introduction**

According to recent statistics, more than one-third of the world's population is overweight or obesity. In the UK, these rates are even higher, with 64% of adults classed as having overweight or obesity [1]. Despite its prevalence, people with obesity frequently experience devaluation and discrimination (known as weight-related stigma) within educational, workplace, and healthcare settings [2]. Evidence also suggests that people may be more likely to face discrimination because of their weight than because of their ethnicity, gender, or sexual orientation [3]. Weight-related stigma has negative consequences for individuals' psychological and physical well-being [2,4,5] and may impede weight-loss by prompting maladaptive eating patterns and exercise avoidance [2].

Negative attitudes towards people with obesity can be exacerbated by beliefs about the *causes* of weight-gain. This is central to attribution theory, which suggests that people make judgements about the cause of a condition; in turn, these judgements determine their attitudes towards an individual [6,7]. For example, attributing obesity to factors that are within personal control (e.g., food choices) is thought to perpetuate obesity stigma [8]. Conversely, stigmatizing attitudes may be attenuated by the belief that weight-gain is caused by uncontrollable factors (e.g., genetics). In support of this,

weight-related stigma was found to be most prevalent amongst individuals who believed that obesity was within personal control and caused by a lack of willpower, inactivity, and overeating [9,10]. Similar findings have been obtained from studies in which participants' causal beliefs about obesity were experimentally manipulated. Specifically, participants who read an article that stated that obesity is caused by overeating and a lack of exercise demonstrated more stigmatizing attitudes than participants in a 'no-prime' control condition or those who read a neutral article about research into memory skills [11,12]. Conversely, participants who were led to believe that obesity is caused by physiological factors (i.e., factors that are beyond personal control) demonstrated less weight-related stigma than those in a control condition [8,13].

One increasingly prevalent etiological theory is that obesity is caused by an addiction to high-calorie foods [14]. Proponents of this idea suggest that food and drugs have similar effects on the brain and argue that the clinical symptoms of substance abuse coincide with the behaviors and experiences of people who engage in compulsive overeating [15,16]. While this idea is widely debated throughout the scientific community (e.g., [17–19]), the concept of food addiction has been readily accepted by the general public [20]. Indeed, research suggests that the majority of people believe that obesity can be caused by food addiction [21], and up to half of people believe that they are themselves addicted to food [22–24]. In light of its popularity, it is important to establish how food addiction models of obesity might affect weight-related stigma.

A small number of studies have examined the effect of the food addiction label on obesity stigma. However, results to date have been inconsistent [25,26]. In one study [27], participants' attitudes towards a person with 'food addiction' were compared with attitudes towards persons with obesity, drug addiction, and disability. The study reported similarly high levels of stigma towards the "obese" and "food addict" labels and, when combined, these labels together elicited greater stigma than either label alone. These findings align with those obtained by Lee et al. [21] who found that, while the majority (72%) of survey respondents believed that obesity could be caused by a 'food addiction', more than half held the view that people with obesity are responsible for their condition (which would be expected to perpetuate obesity stigma). However, in contrast, Latner et al. [28] found that providing a food addiction explanation for obesity appeared to *reduce* weight-stigma. In this study, participants read one of two descriptions of a woman with obesity. In one condition (i.e., the 'food addiction' condition), the woman was described as fitting "the typical profile of someone who is addicted to food". In another condition (i.e., the 'non-addiction' condition), the woman was described as "someone who makes unhealthy food choices". The study found that participants in the food addiction condition displayed lower levels of stigma towards the woman, and towards people with obesity more generally, compared with those in the non-addiction condition.

Inconsistent findings in previous studies may be explained by differences in participants' causal beliefs about food addiction. Specifically, the effect of the "food addiction" label on obesity stigma may depend on the extent to which food addiction is perceived to be a legitimate medical condition. One qualitative study found that people with overweight and obesity were reluctant to label themselves as a food addict due to concerns that this would be viewed as an 'excuse' for overeating [29]. Indeed, providing excuses for weight gain may exacerbate negative attitudes towards those with obesity [30]. In contrast, attributing obesity to a medically diagnosed 'food addiction' may legitimize the condition and help to reduce weight-related stigma by removing personal responsibility from the individual [31,32].

To test these ideas, across two studies, we examined the effect of medically-diagnosed and self-diagnosed food addiction on weight-related stigma. Using a similar technique to Latner et al. [28], participants read one of three vignettes which described a woman with obesity. In the 'medical' condition, the vignette stated that the woman had been diagnosed with food addiction by her general practitioner (GP). In the 'self-diagnosed' condition, the vignette stated that the woman believed herself to be a food addict. There was no reference to food addiction in the control condition. Subsequent attitudes towards the woman (i.e., target-specific stigma) and obesity in general (i.e., general stigma)

were then assessed. We hypothesized that weight-related stigma would be significantly lower in the medical condition, and higher in the self-diagnosed condition, relative to in the control condition. Based on previous findings [28], we predicted that the food addiction label would influence both target-specific and general weight-related stigma.

### **2. Study 1 Method**

### *2.1. Participants*

Female participants were invited to take part in a study into 'perceptions of employability among students'. Participants were recruited via social media advertisements and on internal webpages at the University of Liverpool, UK. Participants who were enrolled in the Psychology degree program at the University received course credits in exchange for taking part. A total of 440 participants completed the survey (533 participants started the study, but 93 did not complete all of the measures and so were excluded from analyses). To be eligible to take part, participants were required to be aged over 18 years old. The majority of participants were students (81%), and 90% of the sample were Caucasian. The mean age of participants was 21.2 y (SD = 7.1), and the mean self-reported body mass index (BMI) was 22.2 kg/m2 (SD = 3.4). Participants with a self-reported BMI over 30 kg/m2 (i.e., classified as having obesity) comprised 2.7% of the sample, 12.5% had a self-reported BMI between 25–29.9 kg/m2 (i.e., 'overweight'), 76.8% had a self-reported BMI between 18.5–24.9 kg/m2 (i.e., healthy weight), and 8.0% had a BMI below 18.5 kg/m2 (i.e., 'underweight'). Participants provided informed consent prior to completing the study. Ethical approval was granted by the University of Liverpool's ethics committee (approval code: IPHS-1516-SMc-259-Generic RETH000619).

### *2.2. Procedure*

The study was delivered via the online survey platform, Qualtrics (Qualtrics, Provo, UT, USA). Participants were asked to read an information sheet and, if they wished to continue with the study, were required to tick a consent box. On the first screen of the survey, a picture of a woman with obesity ("Paulina") was displayed, along with a short vignette which described her hobbies, family, and education (see online supplementary material). Paulina was also described as being 'very overweight'. Participants were randomly allocated to view one of three versions of the vignette: (1) In the 'medical' condition, the vignette stated that Paulina's "GP had recently diagnosed her as having a food addiction"; (2) in the 'self-diagnosed' condition, the vignette stated that Paulina "believes herself to be addicted to food"; (3) in the 'control' condition, there was no mention of food addiction. After reading the vignette, participants completed the measures in the following order: Modified Fat-Phobia Scale (M-FPS) (to assess target-specific stigma towards Paulina), employability questionnaire (included as part of the cover story), Anti-fat Attitudes (AFA; to assess general stigma towards people with obesity), and the Dutch Eating Behavior Questionnaire (DEBQ; to assess external, restrained, and emotional eating behavior). Participants were then asked to indicate their gender, age, ethnicity, occupation, and height and weight (which were used to calculate BMI). They then completed the item about self-perceived food addiction. After completing the study, participants read a debrief sheet which explained the true aim of the study.

### *2.3. Measures*

### 2.3.1. Target Specific Stigma: Modified Fat-Phobia Scale (M-FPS)

The 14-item Fat Phobia Scale [33] was modified such that participants were asked to indicate their beliefs about a fictional individual named Paulina (Paulina was the name of the target female featured in the vignette. See Section 2.2). This scale consists of 14 pairs of antonyms which could be used to describe individuals with obesity (e.g., 'lazy' vs. 'industrious'). Higher scores on the M-FPS (i.e., indicative of more negative attitudes) have been positively associated with beliefs that obesity is within personal control [9]. Participants were required to indicate their perceptions of Paulina by selecting one of five points between each pair of words. A mean score was calculated for each participant. Higher scores on this measure indicated more negative attitudes towards Paulina. In the current sample, the internal reliability of the M-FPS was high (Cronbach's α = 0.834).

### 2.3.2. General Stigma: Anti-fat Attitudes (AFA)

The AFA [8] consists of 13 items which assess stigmatizing attitudes toward individuals with obesity (e.g., "I dislike people who are overweight or obese"). Responses are provided on a 9-point scale ranging from 'Very strongly disagree' to 'Very strongly agree' (in Study 1, a 5-point Likert scale was used, but this was corrected to a 9-point scale in Study 2). Higher scores indicate stronger anti-fat attitudes. The scale comprises three subscales which assess dislike (i.e., obesity stigma), willpower (i.e., beliefs about weight controllability), and fear of fat (i.e., concerns about personal weight gain) (Cronbach's α = 0.796).

### 2.3.3. Dutch Eating Behavior Scale (DEBQ)

The DEBQ [34] consists of 33 items which assess eating behavior. The scale comprises three subscales assessing Restrained Eating (DEBQ-R; 10 items), Emotional Eating (DEBQ-EM; 13 items), and External Eating (DEBQ-EX; 10-items). Previous research has demonstrated the ability of the DEBQ to predict restrictive eating tendencies [35], eating in response to external food-cues [36], and stress-induced eating [37]. Responses are recorded on a 5-point Likert-type scale ranging from 'Never' to 'Very often'. Higher scores indicate greater restrained, emotional, or external eating. The DEBQ was included to ensure that participants did not differ, between conditions, with regards to their eating behavior. The internal reliability for each of the subscales was high (DEBQ-R: Cronbach's α = 0.933; DEBQ-EX: Cronbach's α = 0.869; DEBQ-EM Cronbach's α = 0.932).

### 2.3.4. Self-Perceived Food Addiction (SPFA)

To assess whether or not participants believed themselves to be a food addict, participants were presented with the statement "I believe myself to be a food addict" with response options "Yes" or "No". Similar measures have been used in previous research, and positive responses on this assessment have been associated with greater food reward, overeating [23,38], and fear of being stigmatized by others [22].

### 2.3.5. Employability Questions

For consistency with the study's cover story, seven items were included which assessed participants' beliefs about Paulina's employability (e.g., How likely would you be to employ Paulina?). Responses were recorded using Visual Analogue Scales (VAS) ranging from 0 (not at all) to 100 (extremely). Higher scores indicated more positive attitudes towards Paulina's employability. Analyses of the effect of condition on employability ratings are presented in the supplementary materials.

### *2.4. Data Analysis*

A MANOVA was conducted to check whether participants differed between conditions on age, BMI, and DEBQ subscale scores. Chi-squared tests were conducted to check for any differences between the proportion of students/non-students and Caucasian/non-Caucasian participants allocated to each condition. To examine the effect of condition on target-specific and general stigma, two ANOVAs were conducted with the condition (i.e., control, medical, self-diagnosed) as the independent variable, and M-FPS (i.e., target specific stigma) and AFA (i.e., general stigma) scores as dependent variables. Where significant main effects were identified, these were followed up by inspecting pairwise comparisons.

We conducted exploratory analyses to examine whether self-reported BMI moderated the effect of condition on mean Modified Fat Phobia Scale (M-FPS) and Anti-Fat Attitudes (AFA) scores. To do this, we conducted two hierarchical multiple linear regression to examine the relative contributions of BMI (centered) and condition to mean M-FPS scores and AFA scores. All three conditions were dummy coded with the Control condition as the reference variable. To assign dummy codes, two dummy variables were created: *D*<sup>1</sup> (Medical) and *D*<sup>2</sup> (Self-diagnosed). Participants in the medical condition were assigned '1' to *D*1, and '0' for *D*2. Participants in the self-diagnosed condition were assigned '0' to *D*<sup>1</sup> and 1 to *D*2. Participants in the control condition (i.e., the reference category) were assigned 0 to both *D*<sup>1</sup> and *D*2. (see [39] for more information about dummy coding). Dummy-coded conditions were then entered into Step 1 of each regression model, along with BMI. The interaction terms (i.e., BMI × medical vs. control/self-diagnosed vs. control) were entered into Step 2 of the model.

Additional exploratory analyses were conducted to examine whether the effect of condition on target-specific and general stigma was moderated by participants' age or DEBQ subscales. Further details and results from these analyses are provided in the supplementary materials.

### **3. Results**

### *3.1. Participant Characteristics*

The MANOVA revealed that BMI differed significantly between conditions, F(2,434) = 4.80, *p* = 0.009, ηp<sup>2</sup> = 0.022. This was due to a higher mean BMI in the medical condition relative to the self-diagnosed condition (*p* = 0.002). Participant characteristics as a function of condition are displayed in Table 1. Participants did not differ with regards to age or scores on DEBQ-subscales. Chi-squared tests (X2) revealed no difference in the proportion of students/non-students and Caucasian/non-Caucasian participants in each condition.

**Table 1.** Participant characteristics as a function of condition.


Results are means (standard deviations) unless otherwise specified (\* significant difference, *p* < 0.05).

### *3.2. E*ff*ect of Condition on Target-Specific and General Stigma*

There was a main effect of condition on mean Modified Fat Phobia Scale (M-FPS) score (i.e., target-specific stigma), F(2,437) = 9.07, *p* < 0.001, ηp2 = 0.040. Pairwise comparisons revealed that, compared to those in the control condition, M-FPS scores were higher in the medical (*p* < 0.001) and self-diagnosed (*p* = 0.001) conditions (Figure 1) (Control condition: Mean = 3.47, SD = 0.47, range = 2.29–4.71; Self-diagnosed: Mean = 3.66, SD = 0.48, range = 2.71–4.93; Medical: Mean = 3.68, SD = 0.52, range = 1.00–5.00). There was no difference in mean M-FPS scores between those in the medical and self-diagnosed conditions (*p* = 0.730). There was no effect of condition on Anti-Fat Attitudes (AFA) total scores (i.e., general stigma), F(2,437) = 0.754, *p* = 0.471, (Control condition: Mean = 1.78, SD = 0.56, range = 0.31–3.46; Self-diagnosed: Mean = 1.71, SD = 0.56, range = 0.23–3.00; Medical: Mean = 1.72, SD = 0.56, range = 0.38–3.38).

**Figure 1.** Mean Modified Fat Phobia Scale (M-FPS) scores (i.e., target specific stigma) as a function of condition. Different letters indicate significant differences. Higher scores indicate more negative attitudes towards Paulina (i.e., higher levels of target-specific stigma). Error bars denote standard error.

### *3.3. Moderating E*ff*ect of BMI*

Hierarchical linear regression analyses were conducted to examine whether BMI moderated the effect of condition on target-specific (i.e., M-FPS scores) and general (AFA scores) stigma. Results from the exploratory analysis predicting M-FPS scores are provided in Table 2. In Step 1 and Step 2 of the model, M-FPS scores were significantly predicted by both condition (medical vs. control and self-diagnosed vs. control) and BMI; higher BMI was associated with lower M-FPS scores. However, M-FPS scores were not significantly predicted by the BMI × Condition interaction terms in Step 2 of the model.

Neither BMI nor condition predicted AFA scores in Step 1 of the model (r2 = 0.005, *p* = 0.510), and the inclusion of interaction terms in Step 2 did significantly improve the fit of the model r2 = 0.015, *p*= 0.124).


**Table 2.** Regression output with mean M-FPS (i.e., target-specific stigma) as the dependent variable.

\* *p* < 0.05, \*\* *p* < 0.01. Step 1: r<sup>2</sup> = 0.051, *p* < 0.001; Step 2: r<sup>2</sup> = 0.058, *p* = 0.194

### **4. Interim Discussion**

Study 1 found that female participants who were exposed to medical and self-diagnosed food addiction vignettes exhibited more target-specific stigma towards a woman with obesity than those in the control condition. This is consistent with previous research in which the food addiction label was found to exacerbate stigmatizing attitudes towards an individual with obesity and 'food addiction' [27].

One possibility is that 'food addiction' stigma may be particularly high amongst those who perceive addiction to be within personal control [7]. This is supported by previous research in which perceiving addiction as a disease, rather than due to personal choice, was associated with reduced stigma towards people with addictive disorders [40,41]. Similarly, biogenetic explanations have been found to reduce stigma towards obesity, problematic eating, and substance abuse, relative to behavior-based explanations [10,31,42]. In Study 2, we examined whether the effect of food addiction condition on stigma would be moderated by the extent that addiction is viewed as a 'disease' relative to personal choice.

We also examined whether stigmatizing attitudes towards the target with food-addiction would be moderated by individuals' scores on a measure of addiction-like eating. Previous research has found that individuals with personal experience of addiction have less negative attitudes towards others with addiction [43]. Furthermore, social identity theory suggests that individuals view other 'in-group' members more favorably than out-group members [44]. Therefore, we predicted that the effect of condition on target-specific stigma would be attenuated in participants with greater levels of addiction-like eating behavior.

Finally, we examined whether the effect of condition on target-specific and general stigma would differ between males and females. Previous research has found that females demonstrate less obesity-related stigma and stigma towards the 'food addiction' label than males [27]. We, therefore, hypothesized that the exacerbating effect of the food addiction label on stigma would be most pronounced in males.

To summarize, Study 2 examined the following hypotheses: (1) The effect of condition on target-specific and general stigma would be attenuated in those with greater support for the disease model of addiction. (2) The effect of condition on stigma would be attenuated in those who score highly on a measure of addiction-like eating, relative to those who score lower on addiction-like eating. (3) The effect of condition on stigma would be attenuated in females, relative to males.

### **5. Study 2 Method**

### *5.1. Participants*

Male and female participants, aged over 18 years, were invited to take part in a study into 'employability perceptions'. A total of 523 (190 males; 314 females; 19 did not disclose their gender) participants completed the study. Six hundred and ten participants started the online survey, but 87 either did not complete it or were aged under 18 years old and were excluded from analyses. Participants were recruited from the University of Liverpool (*n* = 333) and Newcastle University (*n* = 190) in the UK. The mean age of participants was 27.1 (SD = 11.3) years, and the mean self-reported BMI was 23.6 kg/m2 (SD = 4.1). Participants with self-reported BMI over 30 kg/m<sup>2</sup> (i.e., classified as having obesity) comprised 7.1% of the sample, 21.6% had a self-reported BMI between 25–29.9 kg/m2 (i.e., 'overweight'), 64.4% had a self-reported BMI between 18.5–24.9 kg/m<sup>2</sup> (i.e., healthy weight), and 5.5% had a self-reported BMI below 18.5 kg/m<sup>2</sup> (i.e., 'underweight'). Just over half of the sample were university students (*n* = 275, 52.4%) and the majority were Caucasian (*n* = 465, 88.9%). Ethical approval was granted by the relevant ethics committee at each of the two sites (University of Liverpool approval code: IPHS-1516-SMc-259-Generic RETH000619; Newcastle University approval code 1485/4293).

### *5.2. Materials and Procedure*

Study 2 used the same materials and procedure as Study 1 but with the following additional measures:

### 5.2.1. Addiction Belief Scale (ABS)

The ABS [39] was used to measure beliefs about addiction. Nine items assessed the belief that addiction is a disease (disease subscale, Cronbach's α = 0.590), and nine items assessed the belief that addiction is within personal control (free will subscale, Cronbach's α = 0.546). Items were rated on a 5-point Likert scale ranging from 'strongly disagree' to 'strongly agree'. Higher scores indicate greater support for the belief that addiction is akin to a disease (disease subscale), and a matter of personal choice (free will subscale).

### 5.2.2. Addiction-Like Eating Behaviour Scale (AEBS)

The AEBS [45] consists of 15 items which assess the presence of behaviors that are commonly associated with addiction-like eating (e.g., 'I continue to eat despite feeling full'). Responses are provided on 5-point Likert Scales ranging from 'Strongly disagree' to 'Strongly agree', and from 'Never' to 'Always'. The scale comprises two subscales: appetitive drive (9 items, Cronbach's α = 0.890) and low dietary control (6 items, Cronbach's α = 0.806). Higher scores indicate greater addiction-like eating behavior. Previous research suggests that this measure correlates positively with other measures of disinhibited eating (i.e., the Binge Eating Scale, [46]) and explains greater variance in BMI over and above other measures of 'food addiction' such as the Yale Food Addiction Scale [47].

### 5.2.3. Data Analysis

A MANOVA was conducted to check whether participants differed, between conditions, with regards to age, BMI, DEBQ subscales scores, and scores on the Addiction-like Eating Behaviour Scale (AEBS) and Addiction Belief Scale (ABS). Chi-squared tests were conducted to check for any differences between the proportion of students/non-students, Caucasian/non-Caucasian, and males/females allocated to each condition. As in Study 1, two univariate ANOVAs were conducted to examine the effect of condition on Anti-fat Attitudes (AFA; general stigma) and Modified-Fat Phobia Scale (M-FPS) scores (target-specific stigma). Gender was also included in the model as a between-subjects variable.

Hierarchical multiple linear regression analyses were conducted to examine whether any effects of condition on target-specific and general stigma were moderated by support for the 'disease' model of addiction (i.e., ABS-disease scores), and addiction-like eating behavior (i.e., AEBS scores). All three conditions were dummy coded with the Control condition as the reference variable. To assign dummy codes, two dummy variables were created: *D*<sup>1</sup> (Medical) and *D*<sup>2</sup> (Self-diagnosed). Participants in the medical condition were assigned '1' to *D*1, and '0' for *D*2. Participants in the self-diagnosed condition were assigned '0' to *D*<sup>1</sup> and 1 to *D*2. Participants in the control condition (i.e., the reference category) were assigned 0 to both *D*<sup>1</sup> and *D*2. (see [48] for more information about dummy coding). Dummy-coded conditions were then entered into Step 1 of each regression model, along with Addiction Belief Scale (disease subscale) or AEBS scores. The interaction terms (i.e., AEBS/Addiction Belief Scale (disease subscale) × medical vs. control/self-diagnosed vs. control) were entered into Step 2 of the model. Separate regression analyses were conducted to examine the ability of each interaction term to predict AFA scores (i.e., general stigma) and M-FPS scores (i.e., target-specific stigma). Addiction Belief Scale (disease subscale) and AEBS scores were centered prior to analyses.

### **6. Results**

### *6.1. Participant Characteristics*

Participants did not differ between conditions on any of the assessed characteristics (Table 3).


**Table 3.** Participant characteristics as a function of condition (Study 2).

Abbreviations: AEBS, Addiction-like Eating Behavior Scale; ABS, Addiction Beliefs Scale; DEBQ, Dutch Eating Behaviour Scale.

### *6.2. E*ff*ect of Condition and Gender on Target Specific Stigma*

In contrast to Study 1, there was no main effect of condition on target-specific stigma, F(2,517) = 0.69, *p* = 0.501, (Control condition: Mean = 3.56, SD = 0.48, range = 2.43–5.00; Self-diagnosed: Mean = 3.63, SD = 0.47, range = 2.36–4.64; Medical: Mean = 3.63, SD = 0.47, range = 2.57–4.93). Contrary to hypothesis 3, there was no gender × condition interaction for target-specific stigma, F(2,517) = 1.18, *p* = 0.309. However, there was a main effect of gender, F(1,517) = 5.13, *p* = 0.024, ηp<sup>2</sup> = 0.010, such that males had significantly higher scores on the Modified Fat Phobia Scale (M-FPS) than females i.e., they showed higher levels of target-specific stigma (Males: M = 3.67, SE = 0.034; Females: M = 3.57, SE = 0.026).

### *6.3. E*ff*ect of Condition and Gender on General Stigma*

As in Study 1, there was no effect of condition on Anti-fat Attitudes (AFA) scores (i.e., general stigma), F(2,517) = 1.18, *p* = 0.308, (Control: Mean = 4.34, SD = 1.00, range = 2.15–7.31; Self-diagnosed: Mean = 4.17, SD = 1.00, range = 1.54–7.15; Medical: Mean = 4.29, SD = 1.09, range = 1.31–7.85). Contrary to hypothesis 3, there was no gender × condition interaction, F(2,517) = 0.02, *p* = 0.978. There was also no main effect of gender on AFA scores, F(1,517) = 0.02, *p* = 0.978. For further analyses of gender differences on the AFA subscales, please see the supplementary materials (Figure S1).

### *6.4. E*ff*ect of Disease Beliefs on Stigma*

Scores on the disease subscale of the Addiction Belief Scale (ABS) significantly predicted mean Modified-Fat Phobia Scale (M-FPS) scores in Step 1 and Step 2 of the model such that higher scores on the scale (i.e., greater belief that addiction is akin to a disease) were associated with greater target specific stigma (i.e., higher M-FPS scores) (Table 4). However, M-FPS scores were not significantly predicted by condition, and there was no condition × ABS-disease interaction, contrary to our hypothesis. Step 1: r = 0.204, r<sup>2</sup> = 0.042, *p* < 0.001; Step 2: r = 0.204, r<sup>2</sup> = 0.042, *p* = 0.972.


**Table 4.** Regression output for Addiction Belief Scale (ABS)-disease with M-FPS (target-specific stigma) as the dependent variable.

\*\* *p* < 0.01. The control condition was used as the reference category against which medical and self-diagnosed conditions were compared. Abbreviations: ABS, Addiction Belief Scale. Step 1: r2 = 0.042, *p* < 0.001; Step 2: r2 = 0.042, *p* = 0.972).

Similarly, scores on the disease subscale of the ABS significantly predicted Anti Fat Attitude (AFA) scores (i.e., general stigma) in Step 1 and Step 2 of the model such that higher scores on the ABS-disease subscale predicted higher AFA scores (Table 5). Contrary to hypothesis 1, AFA scores were not significantly predicted by condition, and there was no interaction between condition and disease scores on AFA.


**Table 5.** Regression output for ABS-disease with Anti Fat Attitude (AFA; general stigma) as the dependent variable.

\*\* *p* < 0.01. The control condition was used as the reference category against which medical and self-diagnosed conditions were compared. Step 1: r = 0.198, r<sup>2</sup> = 0.039, *p* < 0.001; Step 2: r = 0.201, r<sup>2</sup> = 0.040, *p* = 0.707.

### *6.5. Addiction-Like Eating Behavior*

Addiction-like Eating Behavior Scale (AEBS) scores and condition did not predict Modified Fat Phobia Scale (M-FPS) (target-specific stigma) scores in Step 1 of the model. However, the inclusion of the interaction terms in Step 2 significantly improved the fit of the model. Regression coefficients revealed a significant interaction between AEBS scores and medical (vs. control) condition on M-FPS scores (Table 6).


**Table 6.** Regression output for Addiction-like Eating Behavior Scale (AEBS) scores with M-FPS (target-specific stigma) as the dependent variable.

\* *p* < 0.05. The control condition was used as the reference category against which medical and self-diagnosed conditions were compared. Abbreviations: AEBS, Addiction-like Eating Behavior Scale. Step 1: r2 = 0.009, *p* = 0.214; Step 2: r<sup>2</sup> = 0.023, *p* = 0.020.

To further examine the interaction between AEBS scores and condition on M-FPS scores, we used the Johnson–Neyman technique [49] to identify the levels of addiction-like eating (i.e., AEBS scores) at which condition elicited a significant difference on M-FPS scores [50]. Using PROCESS (Version 3.1., [51]), the Medical (dummy-coded) condition was entered as the predictor variable, AEBS scores were entered as the moderator variable, and Self-diagnosed condition (dummy-coded) and the Self-diagnosed × AEBS interaction term were entered as covariates. Mean-FPS scores were entered as the dependent variable. This analysis showed that the Medical condition resulted in significantly greater M-FPS scores, relative to the Self-diagnosed and Control conditions (ps < 0.05), but only for those with low AEBS scores (centered AEBS score ≤ –2.81) (Figure 2). Findings are, therefore, consistent with our hypothesis that the effect of condition on stigma would be attenuated in those with higher levels of addiction-like eating behavior.

**Figure 2.** The effect of condition on M-FPS scores at different levels of addiction-like eating behavior (assessed using the AEBS). The shaded area represents the region of significance identified using the Johnson-Neyman technique.

The condition × AEBS scores model predicting (general stigma) AFA scores was not significant (Step 1: r = 0.069, r<sup>2</sup> = 0.005, *p* = 0.484; Step 2: r = 0.084, r2 = 0.007, *p* = 0.540).

### **7. Discussion**

Across two studies, we examined the effect of the food addiction label on stigmatizing attitudes towards an individual with obesity (i.e., target specific), and towards people with obesity more generally (i.e., general stigma). In Study 1, participants in both the medical and self-diagnosed food addiction conditions demonstrated greater target-specific stigma relative to the control condition. There was no effect of condition on general stigmatizing attitudes towards people with obesity. However, findings from Study 1 were not replicated in Study 2, in which we included both male and female participants. That is, we found no overall differences between the food addiction conditions and the control condition on target-specific stigma. The effect of condition on target-specific or general stigma was also not moderated by addiction disease beliefs (i.e., the extent to which addiction is perceived as a disease) or gender, in Study 2. However, there was a significant condition by addiction-like eating behavior interaction on target-specific stigma; participants who scored low on a measure of addiction-like eating demonstrated greater target-specific stigma in the Medical condition relative to Control and Self-diagnosed conditions. In contrast, target-specific stigma did not differ as a function of condition for those with high levels of addiction-like eating.

Findings from Study 1 are consistent with previous findings in which the food addiction label added to the stigma of obesity [27]. Higher levels of stigma towards the 'self-perceived' food-addicted target in the current study may reflect perceptions of food addiction as an 'excuse' for overeating. This is supported by qualitative evidence that individuals with overweight or obesity may be reluctant to label themselves as food addicts due to concerns that this would be perceived as an 'excuse' for their weight [29].

We predicted that the medical condition might legitimize the concept of food addiction and thereby reduce weight-related stigma (i.e., by removing personal responsibility from the individual). However, contrary to our hypothesis, in Study 1, we found that target-specific stigma was also higher in the medical condition compared to the control condition and did not differ from levels observed in the self-diagnosed condition. This finding is inconsistent with predictions from attribution theory [7] in which undesirable behaviors that are perceived as beyond personal control are thought to elicit less stigma than those that are perceived as controllable. One possibility is that food addiction explanations increase stigma by inadvertently emphasizing the behavioral aspect of obesity. That is, food addiction may imply a loss of control over eating, and previous studies have found that this may increase stigmatizing attitudes towards obesity [52]. Another possible explanation is that food addiction, unlike other biological causes of obesity, is believed to be within personal control and that medicalizing the term does not remove perceptions of personal responsibility. Indeed, Lee et al. [21] reported that almost three-quarters of people supported food addiction as a cause of obesity, and yet obesity was still viewed as a condition that individuals need to take responsibility for. Therefore, it may be the case that stigmatizing attitudes towards 'food addicted' individuals are dependent upon the extent that addiction is perceived as being outside of personal control and/or akin to a disease. In relation to this, Study 2 examined whether the effect of food addiction condition on stigma would be attenuated in those with greater support for the disease model of addiction (results discussed below).

Study 1 therefore suggests that the food addiction label exacerbated stigmatizing attitudes towards a woman with obesity, regardless of whether the food addiction was medically diagnosed or self-diagnosed. Notably, findings from Study 1 are inconsistent with those obtained in a previous study in which a 'food addiction' explanation for obesity elicited *lower* levels of target-specific and general stigma than a control explanation [28]. This inconsistency may be attributable to the control conditions used in ours and Latner et al.'s [28] study; in the current study, participants in the control condition were not provided with any explanation for the target's weight status. In contrast, participants in Latner et al.'s [28] study read that obesity is caused by repeatedly choosing to consume high-calorie foods. By emphasizing the role of personal choice, it is possible that the control condition used by Latner et al. [28] may have elicited greater stigma than a 'food addiction' explanation for obesity.

In Study 2, we found that greater support for the disease model of addiction was associated with greater target-specific and general stigma towards obesity. This finding was unexpected and is contrary to predictions derived from attribution theory. One possibility is that the perception of addiction as a 'disease' encourages the view that addicts are abnormal and perpetuates an 'us-them' distinction [53]. Holding disease views of addiction also suggests that the person's condition is irrevocable and permanent [54]. Another possibility is that causal beliefs about food addiction do not coincide with perceptions of other addictions. That is, individuals who support the 'disease' model for substance-based addictions may not necessarily attribute food addiction to a disease. Previous research supports this, indicating that addictions vary in the extent to which they are attributed to disease or personal choice. In particular, de Pierre et al. [40] found that food addiction was perceived as less of a disease and more within personal control compared with other addictions such as alcoholism. The measure of addiction beliefs (i.e., the ABS) used in the current study referred to addiction in general, and thus may not have reflected participants' beliefs about food addiction per se.

However, the moderating effect of addiction-like eating on target-specific stigma, observed in Study 2, suggest that medically diagnosed food addiction could exacerbate weight-related stigma but only for people with low levels of addiction-like eating tendencies. A possible explanation for this finding is that individuals with personal experience of problematic eating (i.e., high AEBS scores) may have identified more with the target in the vignette and thereby displayed less negative attitudes towards her food addiction (e.g., see [43,44]) as opposed to participants with low AEBS scores.

In Study 2, male participants demonstrated significantly higher target-specific stigma, relative to female participants. Males and females did not differ on a measure of general weight-related stigma. However, the lack of interaction between gender and condition is inconsistent with previous research [27] in which stigmatizing attitudes towards a 'food addicted' target were lower in females, relative to males. This null result may be explained by the fact that, in the current study, males had a significantly higher mean BMI than females (see Table S1). A previous study found that people with higher BMI hold less stigmatizing attitudes towards the 'food addict' label, relative to those with lower BMI [27]. Consistent with this, in Study 1, we found that higher BMI was associated with lower target-specific weight stigma. It is therefore possible that, in the current study, any moderating effect of gender on stigma may have been masked by the higher BMI of male, relative to female, participants. Future research should examine the moderating effect of gender on stigmatizing attitudes towards a food-addicted target in samples of males and females matched for BMI.

The inconsistent findings obtained across Studies 1 and 2 could not be attributable to the inclusion of males in Study 2 as the effect of condition on target-specific stigma was not moderated by gender. The sample tested in Study 2 comprised a larger proportion of older, non-students than the sample tested in Study 1. However, exploratory analyses revealed that the effect of condition on stigma was not moderated by student status or age (see online supplementary material). Differences between Studies 1 and 2 are, therefore, likely due to another (unknown) variable. Moreover, these findings suggest that the effects of the food addiction label on weight-related stigma may not be generalizable across populations.

There are several limitations to the current study that require consideration. Firstly, we note that the Addiction Belief Scale, used in Study 2, examined beliefs about the causes of addiction in general, and thus may not have captured individual differences in beliefs about the causes of food addiction. Future research could use an adapted version of the ABS (such as that used by de Pierre et al. [40]) to test whether food addiction stigma is attenuated in individuals who have greater support for a disease model of food addiction. Secondly, we did not examine whether participants believed the food addiction explanation for obesity, nor did we check whether participants had guessed the study aims. It is, therefore, possible that the effect of the food addiction label on stigma, observed in Study 1, could be due to demand characteristics that were not present in Study 2. Thirdly, the use of a female target in the current study precludes the generalizability of our findings to males. Previous research suggests that females are more likely than males to be stigmatized due to their weight [55], and so

attitudes towards the food addiction label may similarly differ as a function of the target's gender. Finally, it is important to consider that the findings may have been affected by the order in which the questionnaires were presented. In particular, the significant effect of condition on target-specific stigma (M-FPS) (in Study 1), and lack of effect of general stigma (AFA), may be due to the fact that participants completed the M-FPS immediately after reading the vignette, while general stigma (i.e., AFA scores) were assessed later in the study.

Future research should aim to clarify the effect of the food addiction label on weight-related stigma. This may be achieved by considering possible moderating effects of pre-existing beliefs about food addiction (e.g., the extent that it is a legitimate condition, whether it is controllable, etc.). There has been much debate in the scientific literature about whether addiction-like eating should be considered a substance-based 'food addiction' or a behavioral 'eating addiction' (e.g., [11]). Therefore, it will also be important to compare attitudes elicited by a 'food addiction' label, with attitudes towards an 'eating addiction' label. It would also be interesting to compare the effect on the stigma of medically-diagnosed food addiction, with other medical causes of weight gain (e.g., hypothyroidism). Doing so would provide insight into whether the potential exacerbating effect of medicalization on stigma is specific to the food addiction label or whether it extends to the medical model per se. It is also possible that emphasizing the non-behavioral aspect of food addiction (e.g., brain differences to food) may reduce any deleterious effect of a medical diagnosis on stigma. More broadly, the clinical implications of food addiction labels on weight-related stigma must now be considered. In particular, it is important to consider whether the food addiction label may affect people's approaches to treatment (e.g., seeking pharmacological solutions rather than psychotherapy). It is also possible that, by perpetuating weight-related stigma, the food addiction label could be detrimental to psychological well-being and undermine people's attempts to lose weight.

### **8. Conclusions**

The results indicate that the food addiction label may exacerbate stigmatizing attitudes towards an individual with obesity. Furthermore, there is preliminary evidence that this effect may be most pronounced in people with pre-existing low levels of addiction-like eating behavior. Further research is needed to determine the longer-term effects of the food addiction label on weight stigma and clinical implications.

**Supplementary Materials:** The following are available online at http://www.mdpi.com/2072-6643/11/9/2100/s1, Figure S1: Scores on AFA-Willpower subscale as a function of condition and gender. Table S1: Participant characteristics as a function of gender.

**Author Contributions:** Conceptualization, E.J.B. and C.A.H.; Data curation, H.K.R. and M.O.; Formal analysis, H.K.R. and M.O.; Methodology, M.O., E.J.B. and C.A.H.; Supervision, E.H.E. and C.A.H.; Writing—original draft, H.K.R. and C.A.H.; Writing—review & editing, M.O., E.J.B., E.H.E. and C.A.H.

**Funding:** The work reported in this manuscript received no external funding.

**Acknowledgments:** The authors thank Kerry Boult, Richard Ensell, Helena Leech, and Belen Valle-Metaxas for assistance with data collection.

**Conflicts of Interest:** C.A.H. receives research funding from the American Beverage Association and speaker fees from the International Sweeteners Association for work outside of the submitted manuscript.

### **References**


© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

### *Article*

## **The E**ff**ect of a Food Addiction Explanation Model for Weight Control and Obesity on Weight Stigma**

**Kerry S. O'Brien 1,\*, Rebecca M. Puhl 2, Janet D. Latner 3, Dermot Lynott 4, Jessica D. Reid 1, Zarina Vakhitova 1, John A. Hunter 5, Damian Scarf 5, Ruth Jeanes 6, Ayoub Bouguettaya <sup>1</sup> and Adrian Carter <sup>7</sup>**


Received: 27 September 2019; Accepted: 7 January 2020; Published: 22 January 2020

**Abstract:** There is increasing scientific and public support for the notion that some foods may be addictive, and that poor weight control and obesity may, for some people, stem from having a food addiction. However, it remains unclear how a food addiction model (FAM) explanation for obesity and weight control will affect weight stigma. In two experiments (*N* = 530 and *N* = 690), we tested the effect of a food addiction explanation for obesity and weight control on weight stigma. In Experiment 1, participants who received a FAM explanation for weight control and obesity reported lower weight stigma scores (e.g., less dislike of 'fat people', and lower personal willpower blame) than those receiving an explanation emphasizing diet and exercise (*F*(4,525) = 7.675, *p* = 0.006; and *F*(4,525) = 5.393, *p* = 0.021, respectively). In Experiment 2, there was a significant group difference for the dislike of 'fat people' stigma measure (*F*(5,684) = 5.157, *p* = 0.006), but not for personal willpower weight stigma (*F*(5,684) = 0.217, *p* = 0.81). Participants receiving the diet and exercise explanation had greater dislike of 'fat people' than those in the FAM explanation and control group (*p* values < 0.05), with no difference between the FAM and control groups (*p* > 0.05). The FAM explanation for weight control and obesity did not increase weight stigma and resulted in lower stigma than the diet and exercise explanation that attributes obesity to personal control. The results highlight the importance of health messaging about the causes of obesity and the need for communications that do not exacerbate weight stigma.

**Keywords:** stigma; obesity; food addiction; weight bias; weight stigma; obesity prejudice reduction

### **1. Introduction**

Research on the extent, nature, and impact of weight stigma (also termed weight bias, obesity stigma) suggests that weight stigma has increased over time in adults [1] and children [2] and is

associated with a host of negative social and health outcomes [3]. For example, research shows that women perceived to be overweight or obese encounter discrimination in education, health, and employment settings [4–6]. Similarly, experiences of weight stigma are associated with poorer psychological and physical outcomes arising from stigma-related stress, including increased depression and anxiety [7], emotional and stress-related eating [8], and avoidance of health care settings [9]. As such, there is a need for research that seeks to understand factors that contribute to and reinforce weight stigma.

Attribution theories, and specifically, the attribution-value model [10] suggests that antipathy toward a specific group or target is maintained by beliefs about the controllability of specific group behaviours. In the case of overweight and obesity, studies show that weight stigma is increased by attributions about controllability of weight and obesity [11,12]. That is, because people are exposed to public health and media messages that weight is under personal control, people conclude that obesity must be due to an individual's personal failures, which in turn leads to greater weight stigma [13,14]. Dominant public health messages on the cause of overweight and obesity remain focused, if simplistically, on individual control of diet and physical activity [15]. This individualistic public health narrative is increasingly criticised [16], as it ignores research on the myriad of uncontrollable factors contributing to weight control and obesity, such as neurophysiology, environment, and the interplay with genetics/epigenetics. Experimental evidence suggests that changing people's attributions about the causes of obesity away from individual blame, and to more biologically and environmentally pre-determined factors, can help to reduce weight stigma [11]. Accordingly, correcting public misattributions about weight has the potential not only to improve knowledge about the complex causes of obesity, but also the potential to reduce weight stigma and discrimination [17].

Recent research posits that some people may have a neurobiological addiction to certain foods, particularly ultra-processed hyper-palatable foods. This addiction may, in part, contribute to people's food choices and consumption behaviour, and in turn obesity rates [18,19]. Termed *food addiction*, neuropsychological and behavioural research on the addictive properties of food identifies considerable overlap in the food and drug reward and addiction-related centres and pathways of the brain; as a result, food can be as rewarding and addictive as other addictive substances such as drugs, which share overlapping brain reward pathways [20,21]. Large-scale studies suggest that a significant proportion (15%) of the general population [22], and a greater proportion of those with obesity (up to 30%) meet criteria for a diagnosis of food addiction [23]. Furthermore, between 28% and 52% of the general population perceive themselves to be addicted to food [24].

The food addiction model (FAM) for weight control and obesity raises questions about whether a FAM explanation could be helpful or harmful in efforts to reduce weight stigma. While it could be argued that a FAM explanation might increase weight stigma as a result of labelling individuals with obesity as having an addiction, it is possible that a FAM explanation could instead reduce stigma towards people perceived to have obesity by reducing attributions of individual controllability of weight [25]. Research examining these questions is scarce [26]. Some research suggests that the addition of the addiction label to obesity is associated with increased vulnerability to stigmatization [27], and experimental work suggests that the FAM explanation may increase stigma associated with obesity [28]. In contrast, experimental research by Latner and colleagues [25] found that a FAM explanation for weight control and obesity resulted in less stigma and less blame for targets at both lower and higher body weights. These mixed findings indicate the need for additional research to establish whether a FAM explanation increases or decreases weight stigma relative to current public health messaging that suggests diet and exercise as the primary drivers of weight and obesity [29,30].

The present study aimed to examine whether a food addiction explanation for weight control would exacerbate or ameliorate weight stigma relative to the dominant public health messaging emphasizing personal control of diet and exercise. We conducted two experiments to assess the impact of a food addiction explanation for obesity on expressions of weight stigma. In line with previous research with the attribution value model [10] for weight stigma, we predicted that the FAM explanation would result in less weight stigma towards people perceived to be obese or "fat".

### **2. Methods (Experiment 1 and 2)**

### *2.1. Participants*

Table 1 details the demographic characteristics of participants in Experiment 1 and 2. For Experiment 1, a sample of *N* = 652 university (college) students was invited to participate in the experiment in return for course credit. Most students (86%; *N* = 561) agreed to participate, with *N* = 530 (94%) of those agreeing to participate providing data on the outcome variables. For Experiment 2, university (college) students (*N* = 717) were invited to participate in the experiment in return for course credit. Most (96%; *N* = 696) agreed to participate, with *N* = 690 providing data on the outcome variables.


**Table 1.** Participant characteristics for Experiment 1 and Experiment 2.

A priori sample size calculations indicated a required minimum sample of *N* = 142 for Experiment 1 and *N* = 216 for Experiment 2 (72 per group) to detect a small to moderate effect size (*d* = 0.30) between experimental groups with desired power at 0.80 and α set at 0.05 (two-sided). The present sample sizes were sufficient for experimental designs and planned analyses.

### *2.2. Design (Experiments 1 and 2)*

Experiment 1 used a between-subjects experimental design to test the effect of a food addiction explanation (*N* = 263) for weight control and obesity vs. the diet and exercise explanation (*N* = 267) on weight stigma (prejudice towards "fat" people). The host university's Qualtrics research platform randomisation function with a 1:1 ratio was used for randomisation to conditions. Participants received either a simulated news article from The Guardian on the food addiction explanation for weight control and obesity (food addiction condition) or an identically formatted news article positing the dominant public health message that weight control and obesity are due to poor dieting and/or exercise behaviour. Single-item post-manipulation measures were taken for all variables.

Experiment 2 (*N* = 690) was identical to Experiment 1, but introduced a control group that received no newspaper article. The randomisation ratio was set at 2:1:1 with the control condition (*N* = 346) having two participants for every one participant allocated to the food addiction (*N* = 167) and diet and exercise conditions (*N* = 175).

### *2.3. Manipulation (Food Addiction vs. Diet and Exercise News Articles, vs. Control*/*No News Article)*

Two newspaper articles were constructed for the experiments. The two articles appeared authentic and were structurally identical, using The Guardian newspaper format, with identical author, date/time of publication, word length, and text/photo placement. Both articles contained identical text reporting on research from The Lancet suggesting that mortality from obesity-related diseases was high and, for the first time, greater than mortality from starvation. However, the articles differed considerably in the text regarding explanations for weight control and obesity.

The *food addiction* article described the concept of food addiction and explained how foods can be addictive through the involvement of the pleasure/reward centres of the brain, and the release of dopamine when eating some foods, which in turn leads to cravings and a vicious cycle of addiction. The article named the originator of the term food addiction, and stated that approximately 20% of the population may have a food addiction, particularly to highly processed or convenience foods. The article also suggested that food addiction was a key factor in weight control and overweight and obesity.

The *diet and exercise* news article made no reference to food addictions or cravings, but instead focused on people's lack of physical exercise, sedentary lifestyles, and overconsumption of unhealthy foods. The article stated that these personal behaviours were the cause of obesity. The article cited research from experts stating that more self-control was needed when choosing what foods to eat, and it concluded by stating that diet and exercise programs are our best chance at reducing the obesity epidemic and that people need to get moving more.

### *2.4. Measures*

Along with demographic characteristics including age, sex, height in centimetres, weight in kilograms, and ethnicity, we assessed participant's weight stigma (i.e., anti-fat prejudice, weight bias). We also included simple measures to assess whether the manipulations affected beliefs about the causes of obesity and weight gain and loss and a food addiction condition manipulation check. All participants received all of the measures summarized below.

### 2.4.1. Weight Stigma

To measure weight stigma we used the Anti-Fat Attitudes Test (AFAT), a psychometrically sound measure that has been widely used in the field to measure weight bias [31]. The AFAT is a 13-item scale comprised of three subscales assessing dislike of "fat people" which assesses antipathy towards people perceived to be "fat" (Dislike: 7 items, e.g., "I really don't like fat people much"), fear of becoming fat (Fear of Fat: 3 items, e.g., "I worry about becoming fat"), and belief that excess weight is due to a lack personal willpower (Willpower: 3 items, e.g., "Some people are fat because they have no willpower"). Participants indicate their agreement to items using a scale ranging from 0 = *very strongly disagree* to 9 = *very strongly agree*. The mean of the subscale items is used for analyses. Previous work has identified that the 'fear of fat' subscale functions as a measure of personal body image rather than weight stigma toward others per se, with one of the items lacking face validity, so this subscale was not analysed in the present study [32]. Cronbach's alpha's for the dislike and willpower subscales were good in the present sample: α = 0.87 and α = 0.79, respectively.

### 2.4.2. Belief in the Food Addiction Explanation

The food addiction support index (FASI) [24] was used to assess participant beliefs in, and support for, the food addiction explanation for eating, obesity, and weight gain, following exposure to the food addiction vs. diet and exercise news articles (manipulation). Participants responded to the five-item FASI (e.g., "Obesity should be treated as an addiction"), using a five-point scale ranging from 0 = *strongly disagree* to 4 = *strongly agree* with items summed to form a scale total from 0 to 20. Cronbach's alpha's in the present experiment was α = 0.83.

### 2.4.3. Belief in Diet and Exercise for Weight Control

Two items from the dieting beliefs scale [33] that directly capture beliefs about exercise and dieting for the control of weight were used to assess the following exposure to the food addiction vs. diet and exercise news article (manipulation). Specifically, participants were asked to indicate their agreement using a six-point scale ranging from 1 = *not at all descriptive of my beliefs* to 6 = *very descriptive of my beliefs* to the statements "By restricting what one eats, one can lose weight" and "By increasing the amount that one exercises, one can lose weight". The two items were combined to form a score ranging from 1 to 12, with higher scores indicating greater belief that diet and exercise are responsible for weight control and obesity.

### *2.5. Food Addiction Manipulation Check*

To assess whether participants attended to the information in the food addition article, we asked a short question assessing recall for a specific piece of information in the food addiction article. Specifically, we asked participants to identify via a multi-choice recognition response (four answer options) "Who first introduced the term Food Addiction?" Participant responses were coded as either incorrect = 0 or correct = 1.

### *2.6. Procedure*

Upon entering the experiment via a web-link to the host university's Qualtrics research platform, participants in both experiments were provided with the title and description of the study, and then were asked to provide consent to participate. To limit bias in sampling and responding, the study used deception in the advertising and description of the experiment. Participants were told that the experiment was interested in how cognitive information processing styles affect public opinion on a range of political, health, and social issues and that researchers were interested in how people deal with being saturated by the wide range of media messages they receive via TV, computer, and mobile devices.

Participants first answered demographic questions before being presented with one of the two news articles (FAM condition vs. diet/exercise condition) or no article for those in the control group for Experiment 2. To enhance the authenticity of the experiment guise, a large set of distractor questions taken from measures assessing experiential and analytical thinking styles [34] were interspersed in the outcome and manipulation measures. These measures asked participants whether they enjoy the process of thinking deeply about issues, and they have been used successfully elsewhere [35]. Finally, participants were presented with the outcome and manipulation measures. The experiment took approximately 22 min on average to complete. Ethical approval for the study was sought and provided by the host university's Human Research Ethics Committee (Project ID: 8912).

### *2.7. Analysis*

Chi-squared (*X*2) and t-tests were used to assess whether randomisation resulted in balanced groups based on gender, age, and body mass index (BMI). Because weight stigma scores were not normally distributed in either experiment, we adopted a two-step transformation to normalise the data [36]. Subsequent normality checks showed the data to have no issues with skewness or kurtosis. ANCOVAs accounting for age, sex, and BMI as covariates were used to test for significant mean group differences on the dislike and willpower weight stigma measures. A Chi-squared test assessed accurate recognition of the food addiction originator in a probe question (manipulation check). ANOVA was also used to examine whether there were any differences on the manipulation measures (i.e., FASI, dieting/exercise beliefs, and food addiction article attention; i.e., who was the originator of food addiction term). We report adjusted means (M) and standard deviations (SD) along with *F* and *p*-values (significance was set at 0.05) for all primary outcomes.

### **3. Results (Experiments 1 and 2)**

### *3.1. Preliminary Analysis Experiment 1*

Preliminary analyses (*X*<sup>2</sup> and *t*-tests) assessing whether randomisation resulted in balanced groups on demographic characteristics showed there were no significant differences between groups for sex, age, or BMI scores (all *p* values > 0.27). A higher proportion of participants in the food addiction condition (61%) correctly recalled the name of the originator of the term food addiction than did those in the diet and exercise condition (39%, *X*<sup>2</sup> = 23.663, *p* < 0.0005).

### *3.2. Experiment 1 Food Addiction vs. Diet and Exercise*

ANCOVA found significant group difference for the 'dislike' weight stigma measure: *F*(4,525) =7.675, *p* = 0.006. Participants exposed to the FAM explanation had significantly lower dislike of "fat people" (M = 1.82, SD = 1.46) scores than did the participants in the diet and exercise condition (M = 2.13, SD = 1.70). Similarly, participants in the FAM group endorsed significantly lower willpower stigma scores (M = 4.29, SD = 205) than participants in the diet and exercise explanation group (M = 4.68, SD = 1.97; *F*(4,525) = 5.393, *p* = 0.021), indicating that those in the FAM condition were less likely to attribute excess weight to a lack of personal willpower.

We examined whether there were differences between groups in the posited beliefs about the causes of weight control and obesity (i.e., FASI, dieting/exercise beliefs). There were statistically significant group difference on FASI scores. Participants receiving the FAM explanation for obesity and weight control had greater belief in the FAM explanation for obesity and weight control (FASI) (M = 14.57, SD = 3.78) than participants receiving the traditional diet and exercise explanation (M = 13.66, SD = 3.80; *F*(4,525) = 8.823, *p* = 0.003). There was not a statistically significant group difference for the dieting and exercise beliefs measure (FAM, M = 8.60, SD = 2.04; diet and exercise M = 8.50, SD = 2.03; *F*(4,525) = 0.100, *p* = 0.75).

### *3.3. Preliminary Analysis Experiment 2*

Preliminary analyses (*X*<sup>2</sup> and *t*-tests) assessing whether randomisation resulted in balanced groups on demographic characteristics showed there were no significant differences between groups for sex, age, or BMI scores (all *p* values > 0.46). A higher proportion of participants in the food addiction condition (58%) correctly recalled the name of the originator of the term food addiction than did those in the diet and exercise condition (42%; *X*<sup>2</sup> = 15.047, *p* < 0.0005).

### *3.4. Experiment 2 Food Addiction vs. Diet and Exercise vs. Control*/*No News Article*

ANCOVA found significant group difference for the dislike of 'fat people' weight stigma scores (*F*(5,684) = 5.157, *p* = 0.006). Post-hoc tests showed that participants exposed to FAM explanation had significantly lower dislike of 'fat people' (M = 1.85, SD = 1.57) than participants in the diet and exercise condition (M = 2.23, SD = 1.76, *p* < 0.001). Participants in the diet and exercise condition also endorsed higher weight stigma scores than those in the control condition (M = 1.70, SD = 1.54). There was no significant difference in dislike of 'fat people' scores between the FAM condition and the control group (*p* = 0.56). There was also no significant group difference for willpower weight stigma scores (*F(*5,684) = 0.217, *p* = 0.81), with the FAM, diet and exercise, and control groups having similar mean scores (M = 4.71, SD = 2.05, and M = 4.81, SD = 1.86, M = 4.62, SD = 2.16, respectively).

We examined whether there were differences between groups in the posited beliefs about the causes of weight control and obesity (i.e., dieting/exercise beliefs, FASI). There was no significant group difference for the dieting/exercise beliefs measure (*F*(5,682) = 2.055, *p* = 0.13; diet and exercise condition M = 4.62, SD = 0.95, control condition M = 4.38, SD = 1.06, FAM group M = 4.43, SD = 1.03). We found no statistically significant group difference in FASI scores (*F*(5,680) = 1.764, *p* = 0.17; control M = 14.54, SD = 4.17, FAM M = 15.01, SD = 3.29, diet and exercise M = 13.99, SD = 3.90).

### **4. Discussion**

We examined whether the FAM explanation for weight control and obesity versus the traditional public health messaging around control of diet and exercise would affect weight stigma. Relative to the dominant public health narrative that obesity stems from lack of control over diet and exercise, the FAM explanation resulted in lower weight stigma. In Experiment 1, both dislike of 'fat people' and perceptions that excess weight is a result of lack of willpower were lower in people presented with the FAM explanation. In a second experiment, we introduced a control group that was not exposed to information about obesity or causal models for obesity. Similar to Experiment 1, participants in Experiment 2 who received the FAM explanation for weight control and obesity displayed less weight stigma (dislike of "fat people") than participants in the diet and exercise condition. Importantly, there was no difference between the FAM and control groups in levels of weight stigma. Contrary to Experiment 1, in Experiment 2 there was no significant group difference with respect to perceptions that excess weight is caused by a lack of willpower (blame). The results of these two experiments are consistent with work by Latner and colleagues [25] who reported less stigma following exposure to a food addiction explanation. The results do not appear to support the notion that attaching an addiction label to people with obesity would exacerbate weight stigma. Accordingly, a simple interpretation of the results of both experiments is that the dominant public health messaging around the diet and exercise explanation for weight control and obesity exacerbates weight stigma, but the FAM explanation does not.

We found mixed support for the attribution value model of weight stigma [10]. Analysis of the FASI scores in Experiment 1 suggest that the difference in weight stigma scores between the FAM and diet and exercise conditions was due to changes in participants' attributions about the causes of obesity. However, we found no significant group difference on FASI scores in Experiment 2. Similarly, there was no group differences in participant beliefs about personal control of diet and exercise as a primary cause for obesity and weight control in Experiment 1 or 2. This finding is unexpected, as it was reasonable to predict a decrease in attributions of dieting and exercise as a causal explanation among participants who received the FAM explanation. It is possible that the FAM explanation resulted in less stigma because of a greater understanding of, and/or empathy for, those facing the challenges of weight management when one is addicted to food. As we did not assess constructs related to empathy, it will be important for future work to assess the relationship between perceptions of food addiction and levels of empathy towards people with obesity. It is apparent that those in the FAM condition did not dismiss the notion of diet and exercise as contributors to weight control and obesity. Participants may already have firmly established beliefs about personal control of weight given pervasive societal messages emphasizing this message. However, this possible pre-existing belief did not interfere with participants' abilities to receive and incorporate a different message about the contributors to obesity emphasized in the FAM perspective.

The perception that weight is determined by the individual's personal control of choices regarding dieting and exercise behaviours is widespread and accepted in society [37]. Belief in this dominant public health model for overweight and obesity is thought to be linked to weight stigma because it infers and/or attributes overweight and obesity to personal responsibility, lack of discipline, and laziness. The FAM explanation for obesity and weight control is garnering attention in several research fields [19,38,39] and is gaining traction in popular culture [40]. Indeed, studies suggest that around 15% of people meet criteria for a food addiction and anywhere from 28–52% of people believe they may be addicted to a food [22–24]. The present findings support suggestions that popular societal messages of blame and personal responsibility for weight may be partly responsible for the prevalence and rise of weight bias [1]. In contrast, an alternative explanation for obesity, the FAM explanation, may have a positive effect of reducing weight stigma. As our studies did not assess attitudes over time, it will be important for future work to examine whether changes in participants' causal attributions for obesity can be maintained following brief interventions or information about alternative contributors to obesity. It is likely that repeated exposure to FAM information and messages would be needed to

sustain shifts in people's perspectives over time, especially in the face of continued and prominent societal messages emphasizing personal behaviours as the primary cause of obesity. Nevertheless, findings from both of our studies suggest that it is possible to shift weight stigma attitudes with a brief intervention emphasizing a FAM narrative for obesity.

Several limitations of this research should be noted. First, study participants were mostly young and female, with a majority who did not have overweight or obesity. Future studies should examine the FAM explanation in a more representative population sample, including those with diverse body sizes. Baseline data on weight stigma variables were not collected, which could otherwise have been included as potential covariates in the analyses. However, the decision not to collect baseline data on these variables was balanced against the importance of maintaining the study's deception, to avoid tipping off participants to the nature of the study and cuing them in the direction of socially desirable responding. Still, future studies could employ within-participant designs to examine potential changes in weight stigma across subjects upon exposure to the FAM model of weight. In addition, future research should explore the longer-term outcomes of public health messages, particularly those delivered in real-world settings.

### **5. Conclusions**

The present study found lower weight stigma after exposure to a food addiction model of weight and greater weight stigma after exposure to a diet and exercise model of weight. While several studies have attempted to reduce weight stigma, with varying success, far more work is needed to address this prevalent and harmful societal problem. The improvement found in weight stigma following an addiction explanation, and the worsening of weight stigma following a diet and exercise explanation, has implications for public health messages about body weight and obesity. The results support the growing popularity of the food addiction model for eating and associated body weight and obesity. Increasing public understanding of the role of a food addiction explanation for eating behaviour and weight may help to alleviate weight stigma, including, potentially, internalised weight bias/self-stigma. At the same time, our research suggests that the current dominant public health message that largely attributes weight control and obesity to lack of personal control of, and responsibility for, diet and exercise needs to be changed as it appears to be supporting weight stigma [41]. Future research is needed to explore ways to modify current public health messaging so that it is not exacerbating weight stigma. Such messaging could describe the interplay between biological (e.g., FAM, genes) and/or environmental factors (e.g., food security, access to healthy and affordable foods, exercise-facilitating living and work environments) contributing to weight, as well as the importance of healthy eating and physical activity for all individuals, regardless of body size.

**Author Contributions:** Conceptualization: K.S.OB., A.C., J.D.R., J.D.L. data curation: K.S.OB., J.D.R., A.B.; formal analysis: K.S.OB., J.D.R.; project administration: K.S.OB., A.C., J.D.R.; supervision: K.S.OB., A.C.; writing—original draft: K.S.OB., J.D.L., Z.V., R.M.P., A.B.; writing—review and editing: K.S.OB., A.B., R.J., J.A.H., Z.V., D.S., D.L. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research received no external funding.

**Conflicts of Interest:** The authors declare no conflict of interest.

### **References**


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