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Eating Disorders
→ characterized by severe disruptions in eating behavior that affect physical,
psychological, and social functioning.
DSM-5 Criteria for Binge Eating Disorder:
Recurrent episodes of binge eating; on average, at least once a week
for three months
Binge eating episodes include at least three of the following:
eating more rapidly than normal
eating until uncomfortably full
eating large amounts when not hungry
eating alone due to embarrassment about large food quantity
feeling disgusted, guilty, or depressed after the binge
No compensatory behavior is present
Binge-Eating Disorder
– Associated with obesity and history of dieting
Body mass index (BMI) > 30
– Not all obese people meet criteria for binge eating disorder
Must report binge eating episodes and a feeling of loss of control
over eating to qualify
Approximately 2-25% of obese may qualify
– Risk factors include:
Childhood obesity, early childhood weight loss attempts, having been
taunted about their weight, low self-concept, depression, and
childhood physical or sexual abuse
– Equally prevalent among Euro-, African-, Asian-, and Hispanic-Americans
Prognosis of
Binge-Eating Disorder
About 60% (between 25 and 82%) recover
Binge Eating Disorder is the most common and lasts the longest of the three
Eating Disorders
Lasts on average: 14.4 years
Anorexia Nervosa
DSM-5 Criteria:
1. Restriction of behaviors that promote healthy weight; body weight is
significantly below normal
BMI (Body Mass Index) less than 18.5 for adults
2. Intense fear of gaining weight and being fat
Can’t be ‘too thin’
3. Distorted body image or sense of body shape
Feel “fat” even when emaciated
(Amenorrhea not required for diagnosis)
DSM-5 Criteria for Anorexia Nervosa
A. Restriction of energy intake relative to requirements, leading to a
significantly low body weight in the context of age, sex, developmental
trajectory, and physical health. Significantly low weight is defined as a
weight that is less than minimally normal or, for children and adolescents,
less than that minimally expected.
B. Intense fear of gaining weight or of becoming fat, or persistent behavior
that interfere with weight gain, even though at a significantly low weight.
C. Disturbance in the way in which one’s body weight or shape is experienced,
undue influence of body weight or shape on self-evaluation, or persistent
lack of recognition of the seriousness of the current low body weight.
Restricting type
Binge-eating/purging type
DSM-5 Criteria for Anorexia Nervosa
A. Restriction of energy intake relative to requirements, leading to a
significantly low body weight in the context of age, sex, developmental
trajectory, and physical health. Significantly low weight is defined as a
weight that is less than minimally normal or, for children and adolescents,
less than that minimally expected.
B. Intense fear of gaining weight or of becoming fat, or persistent behavior
that interfere with weight gain, even though at a significantly low weight.
C. Disturbance in the way in which one’s body weight or shape is experienced,
undue influence of body weight or shape on self-evaluation, or persistent
lack of recognition of the seriousness of the current low body weight.
Restricting type
Binge-eating/purging type
Physical Changes in Anorexia
Low blood pressure, heart rate decrease
Kidney and gastrointestinal problems
Loss of bone mass
Brittle nails, dry skin, hair loss
Soft, downy body hair
Depletion of potassium and sodium electrolytes
Can cause tiredness, weakness, and death
Medical Sequelae of Anorexia Nervosa
Health complications
• irregular heartbeat
• hypotension (low blood pressure)
• electrolyte imbalances
• infertility
• involuntary hospitalization often required
• approx. 10% of those hospitalized eventually die
• btwn 5 – 8 % die from complications
DSM-5 Criteria for Bulimia Nervosa
A. Recurrent episodes of binge eating. An episode of binge eating
is characterized by both of the following:
1. Eating, in a discrete period of time (e.g. within any 2 hour period), an
amount of food that is definitely larger than what most people would eat in
a similar period of time under similar circumstances.
2. A sense of lack of control overeating during the episode (e.g. feeling that
they cannot stop eating or control what or how much they’re eating).
B. Recurrent inappropriate compensatory behaviors in order to prevent
weight gain, e.g. self-induced vomiting, misuse of laxatives, diuretics or
other medications, fasting, or excessive exercise.
C. The binge eating and inappropriate compensatory behaviors both occur,
on average, at least once a week for 3 months.
Self-evaluation is unduly influenced by body shape and weight
Bulimia Nervosa
Onset late adolescence or early adulthood
90% women
1 – 2% prevalence among women
Typically overweight that led to dieting
Comorbid with depression, PD’s, anxiety, substance abuse, conduct disorder
Suicide attempts and completions higher than in general population but
much lower than in anorexia nervosa
People with Bulimia may have normal BMI or may be overweight
Medical Sequelae of Bulimia Nervosa
Health complications
• unstable weight
• electrolyte imbalance
• dental problems
• cardiac problems
• if medical stabilization is necessary
• from complications
• Mortality rate of 4%
Prognosis of Bulimia
~75% recover
10-20% remain fully symptomatic
Poorer prognosis when depression and substance abuse are comorbid or
more severe symptomatology
Early intervention linked with improved outcomes
A Biopsychosocial Model of Bulimia
. Biological Factors
→ Genetic Factors
→ Disturbances in serotonergic & noradrenergic systems
B. Psychological Factors
→ Negative self-evaluation, low self-esteem
→ Rigid cognitive style, All-or-nothing thinking
Social Factors
→ Cultural norms, emphasis on thinness as the ideal body shape
Certain sports equate body size with ability to succeed
Etiology of Eating Disorders: Genetics
Family and twin studies support genetic link
First-degree relatives of individuals with both disorders more likely to
have the disorder
Higher MZ concordance rates for both anorexia and bulimia
Body dissatisfaction, desire for thinness, binge eating, and weight
preoccupation all heritable
Environmental factors (e.g., family interactions) play an even greater role in
Further research on genetic/environmental interaction is needed
Etiology of Eating Disorders: Neurobiological Factors
Serotonin receptors function abnormally in pts with anorexia and bulimia
Serotonin related to feelings of satiety (feeling full)
Low levels of serotonin metabolites in anorexia and bulimia
—underactive 5HT in AN, 5HT deficit in bulimia prevents sense of
Antidepressants that increase serotonin often effective in treatment
of eating disorders
–perhaps due to comorbid MDD?
Dopamine related to feelings of pleasure and motivation
Pts w/ Anorexia feel more positive and rewarded when viewing
pictures of underweight women
Schematic of Cognitive Behavior Theory of Bulimia Nervosa
Etiology of Eating Disorders:
Gender Factors
Copyright John Wiley & Sons, Inc.
• Objectification of women’s bodies
Women defined by their bodies; men defined by their accomplishments
Societal objectification of women leads to “self-objectification”
Women see their own bodies through the eyes of others
Leads to more shame when fall short of cultural ideals
Aging and changes in life roles (having a life partner, or having children)
associated with decreased eating-disorder symptoms
Etiology of Eating Disorders: Cross-Cultural Factors
Anorexia found in many cultures
Even those not under Western influence
May not include fears of getting fat
In some cultures, higher weight is a sign of fertility and healthiness
As countries become more like Western cultures, eating disorders increase
Bulimia more common in industrialized societies than non-industrialized
Treating Bulimia
Treatment is frequently offered in an eating disorder clinic
The immediate goals of treatment for BN are:
• eliminate binge- purge patterns
• establish good eating habits
• eliminate the underlying cause of bulimic patterns
Programs emphasize education as much as therapy
Prevention of Eating Disorders
Psychoeducational approaches
De-emphasize sociocultural influences
Educate early about the dangers of eating disorders
Dissonance reduction intervention to deemphasize sociocultural
Risk-Factor Approach
Healthy weight intervention to develop healthy weight and exercise
Treating Anorexia Nervosa
B. Medications
→ Serotonin-enhancing medications
C. Psychological Treatments
→ Family therapy
→ Psychodynamic psychotherapy
→ Cognitive-behavioral therapy
Etiology of Eating Disorders: Child Abuse
Self reports of high rates of childhood sexual and physical abuse
Reports of abuse not specific to eating disorders
Also found in other diagnostic categories
Presence of abuse may be too general variable
Age and type of abuse may be more significant
Introduction to Mood Disorders
Depressive Disorders
A. Major Depressive Disorder
B. Persistent Depressive Disorder (Dysthymia)
C. Disruptive Mood Dysregulation Disorder
D. Premenstrual Dysphoric Disorder
E. Substance/Medication-Induced Depressive Disorder
F. Depressive Disorder Due to Another Medical Condition
Bipolar and Related Disorders
A. Bipolar I Disorder
B. Bipolar II Disorder
C. Cyclothymia
D. Bipolar and Related Disorder Due to Another Medical Condition
Defining Major Depressive Disorder
Does the patient meet criteria for a major depressive episode?
e.g. Do they have 5 or more sxs of depression lasting
more than 2 weeks?
• if yes: Is it just one episode? → single episode
Is more than one episode: → recurrent episode
DSM-5 Diagnostic Criteria for Persistent Depressive Disorder (Dysthymia)
A. Depressed mood for most of the day, for more days than not, for at least
two years.
B. Presence, while depressed, of two (or more) of the following:
1. Poor appetite or overeating
2. Insomnia or hypersomnia
3. Low energy or fatigue
4. Low self-esteem
5. Poor concentration or difficulty making decisions
6. Feelings of hopelessness
C. During the 2 year period (1 year for children or adolescents) of the
disturbance, the person has not been symptom free for more than 2 months
at a time.
HHS Public Access
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Clin Psychol Rev. Author manuscript; available in PMC 2018 February 02.
Published in final edited form as:
Clin Psychol Rev. 2016 March ; 44: 125–139. doi:10.1016/j.cpr.2016.02.001.
Shared and unique mechanisms underlying binge eating
disorder and addictive disorders
Erica M. Schultea,*, Carlos M. Grilob,c,d, and Ashley N. Gearhardta
aDepartment of Psychology, University of Michigan, Ann Arbor, MI, United States
bDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT, United States
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cDepartment of Psychology, Yale University, New Haven, CT, United States
dCASAColumbia, Yale University, New Haven, CT, United States
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Scientific interest in “food addiction” is growing, but the topic remains controversial. One critique
of “food addiction” is its high degree of phenotypic overlap with binge eating disorder (BED). In
order to examine associations between problematic eating behaviors, such as binge eating and
“food addiction,” we propose the need to move past examining similarities and differences in
symptomology. Instead, focusing on relevant mechanisms may more effectively determine whether
“food addiction” contributes to disordered eating behavior for some individuals. This paper
reviews the evidence for mechanisms that are shared (i.e., reward dysfunction, impulsivity) and
unique for addiction (i.e., withdrawal, tolerance) and eating disorder (i.e., dietary restraint, shape/
weight concern) frameworks. This review will provide a guiding framework to outline future areas
of research needed to evaluate the validity of the “food addiction” model and to understand its
potential contribution to disordered eating.
Binge eating disorder; Food addiction; Eating disorders; Substance use disorders
1. Introduction
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It has recently been proposed that “food addiction” may be a contributor to obesity and
eating-related problems (Gearhardt, Corbin, & Brownell, 2009a,b). This hypothesis proposes
that certain foods, such as those high in sugar and fat, may be capable of triggering an
addictive response in individuals with vulnerable characteristics (e.g., reward dysfunction,
impulsivity) (Gearhardt, Davis, Kuschner, & Brownell, 2011). Early evidence in animal and
human studies suggests that high-fat, high-sugar foods may activate reward-related neural
circuitry in a similar manner as drugs of abuse (Gearhardt et al., 2011a; Johnson & Kenny,
2010a). Additionally, behavioral indicators of substance-use disorders, such as loss of
control and use despite negative consequences, have been observed in response to these
Corresponding author at: Department of Psychology, University of Michigan, 2257 East Hall, 530 Church Street, Ann Arbor, MI
48109, United States. eorenste@umich.edu (E.M. Schulte).
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foods (Gearhardt et al., 2009a; Ifland et al., 2009). Although many symptoms of addictive
disorders are behavioral in nature (e.g., consuming more than intended, inability to cut down
on consumption) (American Psychiatric Association, 2013) and behavioral circumstances
may increase addictive potential (e.g., intermittent access, binge patterns of use) (Hwa et al.,
2011; Koob & Le Moal, 2001), the “food addiction” perspective does not reflect a
behavioral addiction or an “eating addiction.” Rather, akin to substance-use disorders, this
framework posits an interaction between the addictive potential of high-fat, high-sugar
foods, behavioral factors that may increase addictive responses (e.g., intermittent, binge
consumption), and an individual’s propensity to develop an addiction (Ahmed, Guillem, &
Vandaele, 2013; Davis & Carter, 2009; Gearhardt et al., 2009a; Gold, Frost-Pineda, &
Jacobs, 2003; Ifland et al., 2015; Ifland et al., 2009).
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The Yale Food Addiction Scale (YFAS) is currently the only validated measure to assess
symptoms of “food addiction” (Gearhardt et al., 2009b). The YFAS is a 25-item self-report
questionnaire that applies the diagnostic criteria for substance-use disorders to consumption
of certain foods (see Table 1). The YFAS provides two scoring options: a symptom count (a
sum of the seven diagnostic criteria) and a diagnostic threshold that reflects the criteria for a
substance dependence diagnosis (the presence of three or more symptoms plus clinically
significant impairment or distress). The YFAS has good internal consistency ranging from α
= .76–.92 (Meule & Gearhardt, 2014) and demonstrates convergent validity with measures
of eating pathology (e.g., emotional eating, food craving) and incremental validity in
predicting binge eating frequency above and beyond existing measures (for a review see
Meule & Gearhardt, 2014) The YFAS has been used to assess “food addiction” in both
community and treatment-seeking samples and has been translated to German, French,
Spanish, and Italian (Granero et al., 2014; Meule & Gearhardt, 2014; Pursey, Stanwell,
Gearhardt, Collins, & Burrows, 2014).
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Though “food addiction” is receiving increased attention, the topic remains controversial
(Avena, Gearhardt, Gold, Wang, & Potenza, 2012; Corsica & Pelchat, 2010; Corwin &
Hayes, 2014; Ziauddeen & Fletcher, 2013). This model posits that certain foods are
addictive akin to substance-use disorders; however, there have been few studies examining
which foods or ingredients in foods may have addictive potential (Corwin & Hayes, 2014;
Ziauddeen & Fletcher, 2013). While initial evidence in animals and humans suggest that
high-fat, high-sugar foods are most associated with behavioral indicators of “food addiction”
(Avena, Rada, & Hoebel, 2008; Johnson & Kenny, 2010a; Schulte, Avena, & Gearhardt,
2015), identifying the potentially addictive agent in these foods is a critical next step in this
line of research. Additionally, it has been suggested that “food addiction” cannot account for
obesity, as only a relatively small percentage of obese individuals meet for YFAS diagnosis
(Corwin & Hayes, 2014; Ziauddeen, Farooqi, & Fletcher, 2012). Thus, there have been
conflicting findings in neuroimaging studies examining whether neural circuits implicated in
addiction are also relevant to obesity (Corwin & Hayes, 2014; Ziauddeen et al., 2012).
However, obesity is a multi-faceted condition that can result from a complex combination of
a number of potential genetic and environmental factors, including for example, physical
inactivity, medication side effects, and sleep problems, in addition to excessive food intake
(Grilo & Pogue-Geile, 1991; Keith et al., 2006; Marcus & Wildes, 2009; Wright & Aronne,
2012). Although “food addiction” is more prevalent in participants with obesity (Flint et al.,
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2014), it has been observed in a range of weight classes (Gearhardt et al., 2009b) and may
explain a unique phenotype of problematic eating behavior. Thus, obesity should not be used
as a proxy for “food addiction” in future behavioral and neuroimaging studies.
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Another important critique is the substantial phenotypic overlap between binge eating
disorder (BED) and definitions of “food addiction.” Both BED and addiction are marked by
loss of control over consumption, continued excess use despite negative consequences, and
repeated, failed attempts to cut down on consumption (Gold et al., 2003). As a result of these
similarities, measures of binge eating and “food addiction” (YFAS) are often highly
correlated, both reflecting and resulting in the difficulty of evaluating and disentangling
potential shared and unique aspects of these different constructs. For example, data from
these types of measures cannot readily be placed in the same statistical model due to multicollinearity concerns (Gearhardt, Rizk, & Treat, 2014).1 YFAS “food addiction” and BED
commonly co-occur, although these constructs do not completely overlap. In samples of
individuals with BED, the frequency of “food addiction” ranges from 42% to 57% and “food
addiction” symptoms predict the frequency of binge eating episodes above and beyond
measures of eating pathology and depression (Gearhardt, White, Masheb, & Grilo, 2013;
Gearhardt et al., 2012). Individuals who meet the criteria for both BED and “food addiction”
exhibit more frequent binge eating episodes, intense cravings, and depressive symptoms than
those with only BED (Davis & Carter, 2009; Gearhardt et al., 2012). Among individuals
who meet the criteria for YFAS “food addiction,” the frequency of BED ranges from 27% to
30% (Davis et al., 2011; Gearhardt, Boswell, & White, 2014). Notably, in community
studies with diverse weight groups, individuals categorized with “food addiction,” but not
BED, report significant levels of impairment and distress, such as depressive symptoms,
impulsivity, and negative affect (Gearhardt, Boswell, & White, 2014). However, by focusing
primarily on the psychometric and phenotypic overlap of “food addiction” and BED, it is
challenging to evaluate whether an addictive process uniquely contributes to some types of
disordered eating or whether “food addiction” is BED slightly reframed.
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We propose the need to move past the use of descriptive similarities and differences to
understand possible relationships between disordered eating, such as binge eating, and “food
addiction.” Examining potential mechanisms underlying problematic eating behaviors may
more appropriately determine whether an addictive process contributes to disordered eating
for some individuals. Thus, there are three goals of this review. First, we review the shared
and unique mechanisms implicated in addictive and eating-related problems to elucidate the
relationship between addictive disorders and BED. Second, we examine how mechanisms
unique to substance-use disorders may relate to problematic eating behavior in order to
evaluate whether a “food addiction” framework may offer a novel understanding of eatingrelated issues. Third, we identify gaps in the literature and provide a theoretical roadmap to
guide future research needed to determine the validity and utility of “food addiction” as a
substance-based addictive disorder.
1For example, a recent study by (Gearhardt, Rizk, et al., 2014) found that YFAS and Binge Eating Scale scores were correlated at .
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2. Shared mechanisms in addictive disorders and BED
Addiction and eating disorder perspectives share a number of proposed mechanisms, which
may contribute partly to the similarities observed between BED and “food addiction”
measures (Gearhardt et al., 2014c). This section will focus on how reward dysfunction,
craving, emotion dysregulation, and impulsivity are relevant contributors to both addictive
disorders and BED.
2.1. Reward dysfunction
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Dysfunction in reward-related processes is one area similarly implicated in theories of
addiction and disordered eating. Addictive substances and high fat/sugar foods appear to
similarly implicate the mesolimbic dopamine system, which has been associated with
wanting and motivation for a substance, and the mu-opioid systems, which are more closely
related to the liking of the sensory experience (Berridge, 2007, 2009; Robinson & Berridge,
1993). The role of reward in addiction has long been discussed beginning in the 1950s and
1960s (Beach, 1957; Eveson, 1962). Specifically, addiction is thought to occur, in part,
because addictive substances trigger hedonically pleasurable effects (Everitt & Robbins,
2005) and cause changes in reward-related neural systems (Dackis & O’Brien, 2001; Koob
& Le Moal, 1997).
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Although there is a consensus that reward dysfunction contributes to the risk of developing
an addiction (Blum et al., 2000; Koob & Le Moal, 2001), there is a debate about whether
hypo- or hyper- response to reward is more problematic. One hypothesis suggests that
individuals with addiction use highly rewarding drugs or behaviors2 as a way to compensate
for a deficient reward system (Blum et al., 2000; Volkow, Fowler, & Wang, 1999). In other
words, these individuals use drugs of abuse to feel a level of reward others experience with
less potent rewards (e.g., social interactions). As a result, individuals with hypo-responsive
reward systems may seek out drugs in order to experience pleasure not achievable through
other means (Reuter et al., 2005). In support of the hypo-reward hypothesis, persons with
addiction exhibit reduced dopamine D2/D3 receptor availability, have less mesolimbic
dopaminergic response to non-drug rewarding stimuli (e.g., money), and are more likely to
have the DRD2 receptor A1 allele (which is associated with less D2-type receptor
availability) (Blum et al., 2000; Reuter et al., 2005; Volkow et al., 1999). However, excess
consumption of drugs of abuse can alter the reward system in a manner that reduces reward
responsivity and D2-type receptor availability (Di Chiara & Bassareo, 2007; Koob & Le
Moal, 1997; Spanagel & Weiss, 1999). Thus, it is unclear whether hypo-responsivity in the
reward system is a cause or a consequence of addictive behaviors.
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In contrast, hyper-reward responses to substance-related cues (e.g., alcohol advertisements,
cigarette packs) are consistently found in addiction (Di Chiara, 1998; Everitt & Wolf, 2002;
Robinson & Berridge, 1993). In other words, the reward system may generally be hyporesponsive, but becomes hyper-responsive to addiction-relevant cues. Individuals with
addictions exhibit elevated activation in reward-related neural circuitry, such as the
2In this manuscript, we will use the terms “substance” or “consumption” for ease of writing, but in the case of gambling this can also
be applied to behavior and engagement in the behavior.
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dorsolateral anterior cingulate cortex (dACC) and the orbitofrontal cortex (OFC), in
response to substance-related cues (Engelmann et al., 2012; Goudriaan, de Ruiter, van den
Brink, Oosterlaan, & Veltman, 2010; Yang et al., 2009). These cues can also become highly
salient, as reflected by elevated attention biases for drug-related cues among individuals with
addiction (Field & Cox, 2008; Hester, Dixon, & Garavan, 2006; Lubman, Peters, Mogg,
Bradley, & Deakin, 2000). Greater reactivity to these cues predicts intensity of drug craving
and probability of relapse during quit attempts (Carter & Tiffany, 1999; Janes et al., 2010;
Marissen et al., 2006). Thus, elevated reward sensitivity to addiction-relevant cues appears to
be a major factor underlying addictive disorders.
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Preliminary evidence suggests that reward dysfunction appears to be implicated in “food
addiction.” The only neuroimaging study that has directly examined “food addiction” by
using the YFAS observed patterns in reward circuitry that are also seen in addictive
disorders (Gearhardt et al., 2011a). Individuals endorsing three or more YFAS “food
addiction” symptoms exhibited increased neural activity in reward-related regions when
anticipating a highly processed food (i.e., chocolate milkshake), relative to those who only
endorsed one YFAS symptom (Gearhardt et al., 2011a). This pattern is characteristic of
individuals with addictive disorders with respect to the anticipation of drug rewards
(Martinez et al., 2005; Volkow et al., 2006), which provides evidence that reward
dysfunction may similarly contribute to traditional addictive disorders and “food addiction.”
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Reward dysfunction may also be a relevant mechanism in BED. Since the 1980s, reward
sensitivity and dysfunctional reward responses to highly palatable, highly processed foods
have been proposed as one potential explanation for binge eating (Dum, Gramsch, & Herz,
1983; Fullerton, Getto, Swift, & Carlson, 1985). Individuals prone to overeating may be
driven to eat outside of homeostatic hunger to experience the hedonic, pleasurable effects of
consuming certain foods (Lowe & Butryn, 2007). Though it has been argued that foods
consumed during binge eating episodes vary in nutritional composition (Goldfein, Walsh,
LaChaussee, Kissileff, & Devlin, 1993; Walsh, 2011), some studies have observed that
highly processed foods (e.g., chocolate, French fries) are most frequently consumed when
bingeing (Allison & Timmerman, 2007; Marcus, Wing, & Hopkins, 1988). Additionally, rats
exhibit binge-eating behavior in response to highly processed food, but not to regular chow
(Hagan, Chandler, Wauford, Rybak, & Oswald, 2003). As with drugs of abuse, consumption
of these calorie-dense, nutrient-poor foods appears to activate the mesolimbic dopamine and
endogenous opiate systems, which may be associated with the reinforcing properties of
highly processed foods (Davis et al., 2009; Volkow, Wang, Fowler, & Telang, 2008).
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Akin to addiction, the role of hypo- versus hyper-reward processes in binge eating is also
unclear. Individuals who binge eat may be hypo-responsive to rewards compared to healthy
controls, resulting in these individuals binging on highly processed food to mediate this
reward deficiency (Blum, Cull, Braverman, & Comings, 1996). In support of this hypothesis,
obese individuals with BED exhibit less activation in limbic regions implicated in reward
compared to obese individuals without BED when exposed to monetary rewards (Balodis et
al., 2013a). The presence of DRD2 receptor A1 allele is also linked to compulsive
overeating, which may suggest that reward hyposensitivity is a genetic risk factor for the
development of problematic eating behavior (Blum et al., 2000; Davis et al., 2008).
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However, as with addictive disorders, it is unclear whether reward hyposensitivity is a cause
or effect of BED because excess consumption of highly processed foods may result in
changes to the dopamine system to decrease reward sensitivity (Bello, Lucas, & Hajnal,
2002; Berridge, 2009; Johnson & Kenny, 2010a).
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As demonstrated in addiction, persons with BED appear hyper-responsive to food-related
cues. Individuals with BED compared with overweight and healthy controls exhibit
increased activation in neural regions associated with reward appraisal (such as the OFC) in
response to food stimuli (Schienle, Schafer, Hermann, & Vaitl, 2009; Weygandt, Schaefer,
Schienle, & Haynes, 2012). One study found that binge eating, but not body mass index
(BMI), was associated with increased striatal dopamine release in response to food
stimulation (Wang et al., 2011). Akin to addictive disorders, individuals with BED may
exhibit attention biases to high-calorie foods (Svaldi, Tuschen-Caffier, Peyk, & Blechert,
2010). However, it may be challenging to measure reward-responsiveness to food, as the
reinforcing properties may be greater when individuals who binge eat are in a binge setting
compared to being instructed not to binge eat (Schebendach, Broft, Foltin, & Walsh, 2013).
This suggests that hyper-responsiveness to food cues may vary based on state with increased
responsiveness when bingeing is possible. Although there is limited literature on this topic,
existing studies appear to support a hyper-reward response to food cues for individuals who
binge eat, especially when in a binge setting. Thus, hyper-responsivity to cues appears to be
a common mechanism in BED and addictive disorders.
2.2. Craving
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As with reward dysfunction, craving is implicated in both addiction and BED. Craving is a
central component of addiction (Potenza & Grilo, 2014) that has been added to the
diagnostic criteria for addictive disorders in the DSM-5 and is defined as a “strong desire or
urge to use” (American Psychiatric Association, 2013). In addictive disorders, cravings can
be triggered by environmental cues of the drug and its hedonic effects (“reward craving”) or
by the internal experience of withdrawal symptoms (“relief craving”) (Kilts et al., 2001;
Verheul, van den Brink, & Geerlings, 1999). Triggers of craving (e.g., drug cues) may
produce a dopaminergic release akin to consuming an addictive substance, which can
increase drug-seeking behavior (Volkow et al., 2006; Volkow et al., 2008a). Activation of
reward-related brain regions such as the insula, amygdala, OFC, and hippocampus have been
observed in response to cue-induced craving (Bonson et al., 2002; Childress et al., 1999;
Schneider et al., 2001; Wang et al., 1999). Thus, cravings appear to contribute to
problematic use and compulsive drug seeking and may be related to elevated relapse rates in
addictive disorders (Bottlender & Soyka, 2004; Killen & Fortmann, 1997).
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Craving has also been examined as a potential mechanism in “food addiction.” Food craving
is frequently described as “an intense desire to consume a specific food that is difficult to
resist” (White, Whisenhunt, Williamson, Greenway, & Netemeyer, 2002), and food and drug
cravings appear to activate similar brain regions (Kelley & Berridge, 2002; Pelchat, 2002;
Pelchat, Johnson, Chan, Valdez, & Ragland, 2004; Tang, Fellows, Small, & Dagher, 2012).
Individuals who endorse greater YFAS symptoms of “food addiction” report elevated food
cravings (Davis et al., 2011; Gearhardt et al., 2014c; Meule & Kubler, 2012), particularly for
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high-fat, high-sugar foods (Gearhardt et al., 2014c), but do not have an expectation to be
positively reinforced by consuming the craved foods (Meule & Kubler, 2012). This may
reflect incentive sensitization, a common process in addictive disorders, where individuals
experience a strong wanting or craving for a drug/food reward, but do not necessarily
experience increased liking or pleasure (Berridge, 2009; Robinson & Berridge, 1993). While
research in this area is in its nascent stages, existing evidence suggests that craving may
contribute to “food addiction” in a manner akin to substance-use disorders.
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Similar to addictive disorders, craving may be a relevant mechanism in BED. Craving may
differ across weight categories, and associations between cravings and other clinical
measures may vary across specific groups (White & Grilo, 2005). Notably, obese persons
with BED generally have greater cravings for food and exhibit increased craving prior to
consumption, relative to obese individuals without BED or normal-weight controls (Greeno,
Wing, & Shiffman, 2000; Innamorati et al., 2014; Ng & Davis, 2013; White & Grilo, 2005).
Akin to substance-use disorders, craving in BED may occur in response to food cues (Sobik,
Hutchison, & Craighead, 2005), which may be associated with overeating (Jansen et al.,
2003) or binge eating episodes. For example, Ng and Davis (2013) observed that the level of
craving before food exposure predicted overeating in individuals with BED. Another study
found that craving, even in the absence of hunger, was the best predictor for the onset of
bingeing (Greeno et al., 2000). However, literature in this topic remains limited and further
research is needed to determine whether cue-elicited craving may produce a dopaminergic
response and activate reward-related regions (e.g., insula, OFC), akin to addictive disorders.
Though it has been suggested that sweets (White & Grilo, 2005) and/or fats (Yanovski et al.,
1992) may be implicated in binge eating episodes, future studies should examine which
foods and food attributes (e.g., high-fat, highly processed) are frequently craved. In
summary, craving may be an underlying mechanism in both binge eating behavior and
compulsive drug use.
2.3. Emotion dysregulation
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Emotion dysregulation, or the ineffective modulation of negative affect, is another important
mechanism in both addictive disorders and BED. Negative affect has been associated with
elevated cravings for an addictive substance since the 1960s (Ikard, Green, & Horn, 1969;
Ikard & Tomkins, 1973; Tomkins, 1966). Negative affect can occur in response to a stressor
or physical or psychological withdrawal symptoms, and is linked to increased consumption
of drugs of abuse (Baker, Piper, McCarthy, Majeskie, & Fiore, 2004; Kenford et al., 2002;
Kenny, Chen, Kitamura, Markou, & Koob, 2006; Sinha, 2001; Sinha, Catapano, &
O’Malley, 1999; Sinha, Fuse, Aubin, & O’Malley, 2000). For some individuals, the
substance may be used to cope with negative affect, which may reinforce continued selfadministration (Baker et al., 2004; Brandon, 1994; Li & Sinha, 2008). Neuroimaging studies
have shown that individuals addicted to psychostimulants demonstrate diminished activation
in emotion processing regions (e.g., anterior cingulate cortex) and increased activation in
regions associated with craving (e.g., striatum) in response to stress (Sinha et al., 2005). This
supports the idea that individuals with addictive disorders may crave drugs of abuse in order
to regulate negative emotional states. Further, negative affect appears to be a predictor of
relapse, especially for individuals using drugs to cope (Miller, Westerberg, Harris, &
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Tonigan, 1996; Myers & Brown, 1990; Sinha, Garcia, Paliwal, Kreek, & Rounsaville, 2006)
and when the onset of negative affect is rapid (Shiffman & Waters, 2004).
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Akin to substance-use disorders, emotion dysregulation may contribute to “food addiction.”
As individuals with addiction may utilize drugs in response to strong emotional states (Fox,
Hong, & Sinha, 2008; Li & Sinha, 2008), persons with “food addiction” may consume
certain foods in an effort to regulate emotions. In support of this theory, YFAS symptoms
have been associated with greater endorsement of emotion dysregulation on self-report
questionnaires (Gearhardt et al., 2013b; Gearhardt et al., 2012; Pivarunas & Conner, 2015).
Further, individuals with elevated YFAS symptoms report that they are often motivated to
consume highly processed foods in an effort to cope with negative emotions (Joyner,
Schulte, Wilt, & Gearhardt, 2015). This preliminary work suggests that emotion
dysregulation may be a mechanism implicated in “food addiction.” Future research could
utilize advanced methodologies as ecological momentary assessment to dissect the process
of how certain emotional states may trigger consumption of highly processed foods among
individuals reporting YFAS “food addiction” symptoms and whether these patterns parallel
precipitants of drug use in persons with substance-use disorders.
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Emotion dysregulation has been proposed as a relevant mechanism in BED since the 1990s
(Greeno et al., 2000; Grilo, Shiffman, & Carter-Campbell, 1994; Heatherton & Baumeister,
1991; Mussell et al., 1996; Stice, Akutagawa, Gaggar, & Agras, 2000; Telch & Agras,
1996). The experience of negative affect may induce cravings for highly processed foods
and often precedes overeating (Grilo, Shiffman, & Wing, 1989) and specifically binge-eating
episodes (Berg et al., 2014; Goldschmidt et al., 2014; Greeno et al., 2000; Telch & Agras,
1996). Binge eating, as substance-use, has long been suggested as a coping mechanism for
intense emotional states (McManus & Waller, 1995; Nasser, Gluck, & Geliebter, 2004). In
support of this hypothesis, Ranzenhofer et al. (2014) observed that interpersonal problems
predict loss-of-control eating episodes, a potential precursor to BED, in adolescent girls.
Ansell, Grilo, and White (2012) reported that interpersonal problems are associated with
binge eating in women and that these effects were statistically mediated by negative affect.
Additionally, Whiteside et al. (2007) found that emotion regulation deficits were the
strongest predictor of binge eating above gender, restriction, and shape and weight concerns.
Research is needed to examine whether the neural correlates of negative affect are similar
among individuals with BED and substance-use disorders. As seen in addictive disorders, it
appears that binge eating may be an attempt to cope with negative affect.
2.4. Impulsivity
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Impulsivity is another mechanism underlying both addictive disorders and BED. Impulsivity
refers to responding to internal or external stimuli in an unplanned manner, with little regard
for potentially negative consequences that may result (Moeller, Barratt, Dougherty, Schmitz,
& Swann, 2001). The role of impulsivity in addictive disorders started receiving attention in
the 1950s (Lolli, 1951; Zimmering, Toolan, Safrin, & Wortis, 1951). While impulsivity may
be a risk-factor for whether an individual develops an addiction, chronic substance use may
also lead to worsening executive control deficits throughout the course of the addiction (de
Wit, 2009). Addicted individuals typically show dysfunction in brain regions associated with
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impulsivity during decision-making tasks (Hester & Garavan, 2004; Hester, Lubman, &
Yucel, 2010) and are impaired at delaying gratification of rewards (Hoffman et al., 2008;
Monterosso et al., 2007). Thus, impulsivity may explain maladaptive decision-making in
addiction where individuals engage in behavior that is rewarding in the short-term (e.g., drug
use), despite being detrimental to them in the long-term (e.g., health problems, interpersonal
difficulties). Importantly, impulsivity has been linked to higher rates of relapse in addictive
disorders (Doran, Spring, McChargue, Pergadia, & Richmond, 2004; Miller, 1991).
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Impulsivity may also be implicated in “food addiction.” Previous studies have found that
YFAS “food addiction” symptoms are associated with attention-based impulsivity, marked
by a faster response time to food cues (Meule, Lutz, Vogele, & Kubler, 2012), negative
urgency, reflecting the tendency to act impulsively while experiencing negative mood states
(Murphy, Stojek, & MacKillop, 2014; Pivarunas & Conner, 2015), and a lack of
perseverance in tasks (Murphy et al., 2014). In the only neuroimaging study of YFAS “food
addiction,” individuals reporting three or more YFAS symptoms exhibited decreased
activation in inhibitory neural systems when consuming a highly processed food reward (i.e.,
chocolate milkshake), relative to persons endorsing one or fewer symptoms (Gearhardt et al.,
2011a). Thus, akin to substance-use disorders, impulsivity may be a relevant mechanism in
“food addiction” and warrants further empirical examination.
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Impulsivity has also been discussed as an important mechanism in BED beginning in the
1990s (McManus & Waller, 1995; Mitchell & Mussell, 1995). Previous studies have found
that individuals who binge eat demonstrate deficiencies in impulsivity, have trouble focusing
attention, make risky decisions, and are poor at utilizing feedback to guide future behavior
(Mobbs, Iglesias, Golay, & Van der Linden, 2011; Svaldi, Brand, & Tuschen-Caffier, 2010).
It has also been suggested that impulsivity plays a role on the initiation of binge cravings
(Dawe & Loxton, 2004; McManus & Waller, 1995). Similar to addictive disorders, binge
eaters are also less successful at delaying gratification of rewards (Davis, Patte, Curtis, &
Reid, 2010; Manwaring, Green, Myerson, Strube, & Wilfley, 2011). Thus, as seen in
addiction, a maladaptive decision-making process may occur in individuals with BED,
where the short-term reward of highly processed food is chosen instead of long-term health
benefits. Schag et al. (2013) observed that individuals with BED exhibited impulsive eye
movements in response to food stimuli. Neuroimaging studies suggest that individuals with
BED have greater activation of executive control regions during a cognitive-control task,
suggesting a maladaptive decision-making process (Balodis et al., 2013b; Gearhardt,
Boswell, & Potenza, 2014). Akin to addictive disorders, high levels of impulsivity may also
have implications in treatment of BED and rates of relapse. Several studies have found that
impulsive children are more likely to binge eat and are less successful in treatment programs
(Nederkoorn, Braet, Van Eijs, Tanghe, & Jansen, 2006; Nederkoorn, Jansen, Mulkens, &
Jansen, 2007). Therefore, impulsivity appears to be a mechanism implicated similarly in
substance-use disorders and BED.
3. Summary of shared mechanisms
In summary, addiction and binge eating share a number of proposed mechanisms. For both
of these disorders, individuals may exhibit elevated reward responsivity to relevant cues and
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may act compulsively in the presence of these cues to satisfy intense cravings. Cravings may
also be triggered by negative mood states, in which the drug or food may be used to regulate
emotions. Finally, impulsivity has been identified as a shared mechanism underlying both
substance-use disorders and BED and may have implications for continued administration
and relapse.
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Collectively, these shared mechanisms likely contribute to the behavioral and biological
similarities between binge eating and traditional addictive disorders (Cassin & von Ranson,
2007; Gearhardt, White, & Potenza, 2011; Gold et al., 2003). Notably, smokers with BED
are more likely to have a substance-use disorder than non-smokers with BED (White &
Grilo, 2006), which provides further evidence for similar processes underlying BED and
addiction at least in some persons or subgroups. If addictive disorders and BED are both
explained in part by shared mechanisms, we propose that it may be plausible that an
addictive process may be contributing to binge eating for some individuals. In support,
preliminary evidence suggests that reward dysfunction, craving, emotion dysregulation, and
impulsivity may all also contribute to “food addiction,” as measured by the YFAS. However,
it is challenging to disentangle BED and “food addiction” given the high degree of
phenotypic overlap and these common mechanisms. There is evidence that individuals who
experience “food addiction,” but who do not meet criteria for BED or other eating disorders,
exhibit clinically significant levels of pathology and eating-related concerns (Gearhardt,
Boswell, & White, 2014). Further, individuals with an eating disorder diagnosis who also
meet for YFAS “food addiction” have particularly severe levels of pathology (Gearhardt,
Boswell, & White, 2014). Thus, the assessment of “food addiction” appears to provide
clinically relevant information to the study of disordered eating. In order to further evaluate
whether an addictive process may explain problematic eating behavior in some individuals,
it is essential to examine mechanisms unique to an addiction perspective (e.g., withdrawal)
and traditional eating disorder approaches (e.g., shape and weight concerns).
4. Unique aspects of addiction perspectives
We now review several core mechanisms of substance-use disorders: the importance of the
substance, withdrawal, and tolerance. We evaluate whether these processes may contribute
to problematic eating behavior in a manner similar to addictions. If certain foods share
features with drugs of abuse and may be capable of triggering addictive responses in some
individuals, this would provide support for the validity and utility of a “food addiction”
4.1. Importance of the substance
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An addiction framework posits that an addictive substance (e.g., nicotine) or behavior (e.g.,
gambling) interacts with individual risk factors (e.g., genetic predisposition, personality
characteristics) to trigger an addictive process. Without exposure to the addictive substance,
an individual at risk will not develop an addiction. Thus, the addictive substance or behavior
is an essential aspect of the problematic behavior. Drugs of abuse are altered from their
natural state to contain an increased concentration (or dose) of the addictive agent and to
increase the rate in which the addictive agent is absorbed into the system (Barnett, Hawks, &
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Resnick, 1981; Henningfield & Keenan, 1993). For example, coca leaves have little
addictive potential when chewed (Hanna & Hornick, 1977), but when they are refined into
cocaine and consumed by nasal insufflation, they become highly addictive (Verebey & Gold,
1988). Further, addictive substances may be capable of producing neuroplastic changes in
brain regions responsible for processing rewards and making decisions (Koob, 1992;
Leshner, 1997). These changes in the mesolimbic dopamine system and prefrontal cortex
may perpetuate self-administration (Chang, Alicata, Ernst, & Volkow, 2007; Volkow &
Fowler, 2000). In other words, an individual’s brain may become “hijacked” by the addictive
substance, resulting in compulsive consumption despite negative consequences (Volkow &
Wise, 2005).
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Highly processed foods (e.g., pizza, chocolate, chips) may share characteristics with drugs
of abuse, as they are altered from their natural state to include higher concentrations of fat
and/or refined carbohydrates like sugar or white flour, and the rate in which the refined
carbohydrates are absorbed into the system is rapid (Gearhardt, Davis et al., 2011). For
example, a minimally processed food, such as a banana, contains natural sugars but would
be expected to have little or no addictive potential compared to a candy bar, which is
processed to contain increased levels of fat and rapidly absorbed sugars.
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Additionally, highly processed foods may also be capable of causing neuroplastic changes in
reward-related brain regions that contribute to behavioral indicators of “food addiction”
(Bello et al., 2002; Berridge, 2009; Johnson & Kenny, 2010b), although research on this
topic is in its nascent stages. Rats who consume a diet of highly processed foods, such as
cheesecake, experience downregulation in the dopamine system, akin to using drugs of
abuse (Johnson & Kenny, 2010b). Notably, binge-prone rats only exhibit addictive-like
responses to foods high in fat and sugar (e.g., Oreo Double-Stuf cookies) and not chow
(Boggiano et al., 2007; Klump, Racine, Hildebrandt, & Sisk, 2013). Animal models suggest
that sugar may be most closely associated with “food addiction,” as rats with intermittent
access to sugar exhibit binge eating, enhanced motivation to obtain the substance (which
may model craving), cross-sensitization, and withdrawal when the sugar is removed (Avena
et al., 2008b) (for a review see Avena, 2010). In humans, Stice, Burger, and Yokum (2013a,
2013b) observed that a high-sugar milkshake strongly activated reward-related regions.
Further, pharmacology used to treat alcohol-related problems by blocking opioid response
(i.e., naloxone) has also been associated with reduced consumption of ultra-processed foods
in binge eaters (Drewnowski, Krahn, Demitrack, Nairn, & Gosnell, 1995). Additionally, in
the only neuroimaging study of “food addiction,” individuals with elevated YFAS symptoms
exhibit neural responses akin to other addictive disorders in response to cues and
consumption of a highly processed food (Gearhardt et al., 2011a).
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One study has examined which foods are most likely to be implicated in “food addiction” in
humans (Schulte et al., 2015). Schulte et al. (2015) asked participants to complete the YFAS
then rate how likely they were to experience YFAS symptoms with 35 nutritionally diverse
foods. Highly processed foods, with added fat and refined carbohydrates were identified as
the most problematic. Foods with a high glycemic load (which reflects a faster speed of
absorption of carbohydrates and a greater blood sugar spike) were especially problematic for
individuals endorsing “food addiction” symptoms on the YFAS. Thus, like with drugs of
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abuse, the rapid speed of absorption of rewarding ingredients may make highly processed
foods particularly triggering for susceptible individuals. Laboratory studies with direct
observations and measurements of eating behavior and reward response are needed to
confirm and extend these preliminary findings. Though more research is needed, if highly
processed foods cause similar biological and behavioral changes as drugs of abuse, this
would support applying an addiction perspective to problematic eating behavior in some
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If certain foods are capable of triggering addiction-like changes in the brain, it would
challenge one core tenet of traditional eating disorder treatment models such as cognitivebehavioral therapy (CBT) (Fairburn, 2008; Grilo & Mitchell, 2011) which states that there
are no “bad” or “forbidden” foods. CBT perspectives on eating disorders emphasize
individual differences (e.g., shape and weight overconcern, excessive or rigid dietary
restraint, mood regulation difficulties, poor self-esteem) as factors that serve to either lead to
and/or maintain problematic eating behaviors (Fairburn, 1995, 2008; Grilo & Mitchell,
2011); in such models, how individuals under- or over-eat (in the case of BED) is a key
aspect but that the types of food consumed less importance (Fairburn, 1995, 2008; Grilo &
Mitchell, 2011) In contrast, an addiction perspective suggests that some foods (or how some
foods are processed) may trigger the reward system in a manner that makes it more
challenging for at-risk individuals to moderate their consumption (Gearhardt, Davis et al.,
2011). Thus, it is possible that certain foods may not merely be “bad” foods per a common
cognitive bias in CBT models but may actually possess chemical properties that make them
more difficult to eat in a controlled manner for both cognitive and neurobiological reasons.
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Importantly, exposure to addictive substances does not universally trigger compulsive
consumption, and individual differences (e.g., genetics, patterns of consumption, personality
factors) play an important role in who becomes addicted. For example, 90% of people
consume alcohol (an addictive substance) during their lifetime, but only 5–10% of
individuals develop alcohol dependence (American Psychiatric Association, 2000; Grant,
1997). However, there are many individuals with subclinical addictive-like responses to
alcohol, which emphasizes the broad public health implications of classifying alcohol as an
addictive substance. Similarly, if some foods have an addictive potential, it is unlikely that
all or most people would develop a clinical-level of “addiction.” It is also probable that other
individuals would experience subclinical addictive-like responses to certain foods, which
increases the scope of potential public health initiatives (Gearhardt, Grilo, DiLeone,
Brownell, & Potenza, 2011). It is likely that individual differences associated with addiction
risk (e.g., impulsivity, family history of addiction) will interact with the potentially addictive
nature of certain foods to trigger “compulsive” eating in some, but not all, individuals. In
summary, for some cases of BED, mechanisms associated with dietary restraint or shape and
weight concerns may precipitate binge-eating behavior. For others, highly processed foods
may result in reward-related, neuroplastic changes in the brain and trigger an addictive
process for at-risk individuals. This highlights the necessity of a mechanism-focused
approach to understanding problematic eating behavior and for whom each mechanism may
be most applicable.
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4.2. Withdrawal and tolerance
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Withdrawal and tolerance are unique markers of an addictive process that may provide
insight into craving and relapse. Withdrawal is defined in the DSM-5 as the development of
physiological or psychological symptoms in response to abstinence or decreased
consumption of a substance (American Psychiatric Association, 2013). Though physical
withdrawal symptoms were previously considered a core component of addiction, they are
no longer a mandatory characteristic of an addictive disorder, as withdrawal from drugs such
as cocaine and behavioral addictions such as gambling result in minimal physical symptoms
(Brower & Paredes, 1987; Rosenthal & Lesieur, 1992; Weddington et al., 1990).
Psychological withdrawal symptoms, such as preoccupation and anxiety, are considered
more universal across addictive disorders and are predictive of relapse rates (Kenford et al.,
2002; West, Hajek, & Belcher, 1989).
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Animal-model researchers have observed opioid-like withdrawal symptoms following
addictive-like consumption of sucrose (Avena, Rada, & Hoebel, 2009). When sucrose is
removed from the diet, rats experience anxiety, teeth chattering, and more aggressive
behavior (Avena, Bocarsly, Rada, Kim, & Hoebel, 2008; Galic & Persinger, 2002). No
previous studies have examined withdrawal symptoms in humans for highly processed
foods. However, individuals who cut back on high-sugar foods (e.g., dieters) may exhibit
metabolic changes in response to food cues, such as a decrease in blood sugar, and this may
trigger cravings (Herman & Mack, 1975). Similar physiological changes can occur in
response to cues for individuals with addictive disorders, which also results in strong
cravings (Gearhardt et al., 2009a). Further, individuals experiencing problematic eating
behavior anecdotally report withdrawal-like symptoms to carbohydrates (Gearhardt et al.,
2009a; Pelchat, 2002). Thus, it is plausible that some individuals may experience withdrawal
symptoms to highly processed foods. We are unaware of any prior studies that have
investigated whether individuals endorsing YFAS “food addiction” symptoms develop a
withdrawal in response to cutting down on high-fat/high-sugar foods, and this is an
important area that requires further examination.
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Similar to withdrawal symptoms, tolerance is another unique component of an addiction
perspective. Tolerance is characterized by 1) the need to consume increased amounts of a
substance to experience the desired, hedonic effects or 2) the diminished effect of a constant
dose over time (American Psychiatric Association, 2000). Reductions in reward-related
neural pathways over time in response to a constant dose of a substance may model the
development of tolerance. This has been demonstrated in traditional addictive disorders
(Nestler & Malenka, 2004; Volkow, Fowler, Wang, Baler, & Telang, 2009). Importantly, a
recent study observed that frequent ice-cream consumption was associated with reduced
striatal responsivity during the receipt of an ice-cream based milkshake, which is consistent
with the development of tolerance (Burger & Stice, 2012). Behavioral indicators of tolerance
have also been explored. Spring et al. (2008) observed that a beverage high in carbohydrates
became less effective at reducing self-reported dysphoric mood in obese individuals after
repeated administration. No studies to date have investigated whether individuals with YFAS
“food addiction” symptomology exhibit greater tolerance to the consumption of high-fat/
high-sugar foods. The lack of empirical examination of withdrawal and tolerance is a
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significant gap in understanding how addiction-specific mechanisms may contribute to
eating-related problems and an essential next step for evaluating the validity of the “food
addiction” concept.
In summary, exploring whether withdrawal and tolerance contribute to binge eating behavior
is important for evaluating the “food addiction” hypothesis because these components are
unique to an addiction framework. There is no existing research examining the association
of “food addiction” or BED with these mechanisms. If symptoms of withdrawal and
tolerance contribute to eating pathology this would provide evidence that an addiction
framework has unique explanatory power for BED. It is likely that while addiction
mechanisms may be relevant for certain individuals with BED, the unique aspects of the
eating disorder framework may be important for others.
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5. Unique aspects of eating disorder perspectives
We now describe mechanisms implicated in eating disorders like BED and discuss why
these processes would not be considered causal factors in the “food addiction” model. If
mechanisms unique to a traditional eating disorder perspective explain BED but not “food
addiction,” this would suggest that these two phenotypes do not overlap completely.
5.1. Restraint
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Eating disorder models have long held that inappropriate (e.g., extreme or rigid) dietary
restraint is a causal antecedent to binge eating (Fairburn & Harrison, 2003; Herman &
Polivy, 1990; Howard & Porzelius, 1999; Polivy & Herman, 1985; Telch & Agras, 1993).
Restraint was initially thought to be an intentional attempt to reduce calories below a
biological “set point” of consumption (Herman & Mack, 1975; Nisbett, 1972). However,
individuals reporting high levels of restraint often do not appear to be biologically deprived
of calories (Lowe, 1993), suggesting that restraint may be more cognitive in nature. The
perspective of cognitive restraint posits that a high level of restraint is indicative of an
individual forming rigid dietary rules due to concerns about shape or weight (Herman &
Polivy, 1980). In support of cognitive restraint, measures of restraint (e.g., Restraint Scale)
appear to be associated with the utilization of rigid dietary rules (Herman & Polivy, 1980)
but have not been related to biological factors such as acute or long-term caloric intake
(Stice, Cooper, Schoeller, Tappe, & Lowe, 2007; Stice, Fisher, & Lowe, 2004; Stice, Sysko,
Roberto, & Allison, 2010). Further, restrained eaters may exhibit increased food
consumption following challenges to their cognition, such as a high-calorie preload (Polivy,
1976; Spencer & Fremouw, 1979) or tasks that engage cognitive resources (Bellisle & Dalix,
2001; Lowe & Kral, 2006; Ward & Mann, 2000).
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More recently, restraint has been re-conceptualized by some as a reflection of hedonic
hunger, or a perceived, cognitive deprivation for highly palatable foods despite meeting
biological caloric needs (Lowe & Butryn, 2007; Lowe & Levine, 2005; Markowitz, Butryn,
& Lowe, 2008). Hedonic hunger, as measured by the Power of Food Scale (PFS), is related
to increased food craving, and greater consumption of highly processed food (e.g.,
chocolate) (Lowe & Butryn, 2007). Scores on the PFS are higher in obese individuals with
BED (relative to those without the diagnosis) and higher PFS scores are associated with
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binge eating severity in BN (Lowe & Butryn, 2007; Witt & Lowe, 2014). Although scores
on various restraint measures do not appear to be related to objectively measured caloric
deprivation (Stice et al., 2007; Stice et al., 2004; Stice et al., 2010), restraint is associated
with increased hedonic hunger (Lowe et al., 2009). Thus, dietary restraint may reflect, in
part, perceived deprivation for highly palatable foods associated with hedonic hunger.
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Dieting may also influence eating behavior and be associated with disordered eating. While
restraint appears to reflect a cognitive, perceived deprivation of highly palatable foods,
dieting – in contrast – is associated with decreased caloric intake for weight loss (Allen,
Byrne, & McLean, 2012). Dieting prospectively predicts future weight gain (Lowe et al.,
2006; Lowe, Doshi, Katterman, & Feig, 2013; Stice, Cameron, Killen, Hayward, & Taylor,
1999) and may be a proxy for an individual’s vulnerability for problematic eating behavior
and past problems with eating regulation (Lowe, 2015). Individuals who diet for weight loss
tend to endorse high levels of restrained eating, but the behavior of restrained eaters may
vary based on whether the individual is currently dieting (Lowe, 1993, 1995). For example,
restrained dieters reduce their food intake following a high-calorie preload (Lowe, 1995),
which may be a response to a direct threat to weight-loss efforts. This contrasts restrained
non-dieters who overeat after a high-calorie preload, perhaps due to a violation of rigid
dietary rules (Polivy, 1976; Spencer & Fremouw, 1979).
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Dieting for weight loss appears to be a relevant factor in BED, and data from retrospective
self-report suggest that individuals with BED have histories of frequent dieting attempts and
weight fluctuations although importantly dieting appears to precede binge eating in only
about 50% of those who develop BED (Grilo & Masheb, 2000; Hilbert et al., 2014; Mussell
et al., 1995; Reas & Grilo, 2007; Spurrell, Wilfley, Tanofsky, & Brownell, 1997). Fasting
seems to predict binge eating across diverse weight and disordered eating groups (Stice,
Davis, Miller, & Marti, 2008) and caloric restriction is associated with increased brain
activity in regions associated with attention and reward processing in response to food cues
(Stice et al., 2013a, 2013b).
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While dieting may be a risk factor for binge eating in some individuals, binge eating
precedes dieting in others (Grilo & Masheb, 2000; Hilbert et al., 2014; Reas & Grilo, 2007;
Spurrell et al., 1997). In BED, those who report bingeing before dieting may have an earlier
onset of binge behaviors and endorse lower levels of restraint than those who diet first
(Spurrell et al., 1997). Although retrospective/prospective studies and CBT models suggest
that dieting and restraint increase the risk of binge eating and eating disorders for some
individuals (Fairburn, Cooper, & Shafran, 2003; Grilo & Masheb, 2000; Herman & Polivy,
1990; Spurrell et al., 1997), controlled intervention studies have challenged this idea in some
respects for certain patient groups. Specifically, behavioral weight loss treatments, which
decrease caloric intake, have been shown to effectively reduce binge eating behavior and
eating disorder pathology in obese patients with BED (Grilo, Masheb, Wilson, Gueorguieva,
& White, 2011; Wilson, Wilfley, Agras, & Bryson, 2010). Further, a carefully designed
study demonstrated that a low-calorie diet (e.g., 1000 kcal/day) coupled with behavioral
therapy does not appear to induce increased binge eating behavior (Wadden et al., 2004).
Thus, in at least some circumstances, behavioral weight loss and low-calorie diets do not
appear to increase the frequency of binge eating episodes or worsen BED symptoms.
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An alternative understanding of restraint and dieting behaviors is that they are strategies
utilized to overcome one’s personal vulnerability for weight gain and obesity (Agras, 2010;
Lowe, 2015; Lowe et al., 2013). Thus, some individuals may be vulnerable to shape and
weight ideals and engage in dietary restraint to maintain their weight (Lowe & Levine,
2005). Consistent with this idea, weight concern/importance may prospectively predict the
onset of dieting and disordered eating behavior (Loth, MacLehose, Bucchianeri, Crow, &
Neumark-Sztainer, 2014). However, other individuals may be vulnerable to a food’s hedonic
properties and employ dietary restraint to counteract the rewarding nature of the food (Lowe
& Butryn, 2007). Notably, individuals with BED exhibit lower levels of restraint than
persons with BN, but binge-eating frequency is similar (Grilo et al., 2009; Wilfley,
Schwartz, Spurrell, & Fairburn, 2000), which suggests that are mechanisms other than
restraint contributing to BED.
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Multiple pathways likely interact to result in the development of binge eating. Consistent
with this idea, one prospective study demonstrated that body dissatisfaction interacts
differently with depressive symptoms and dieting to increase the risk of disordered eating
(Stice, Marti, & Durant, 2011). Further, models of binge eating that include both dieting and
affect-related difficulties as contributors to bingeing behavior seem to most appropriately
represent potential pathways to the development of BED (Allen et al., 2012). Thus, dietary
restraint may be one contributing component to binge eating in combination with multiple
other risk factors. Addiction-related mechanisms may be another relevant factor that
interacts with dietary restraint to increase risk for BED.
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Though dietary restraint as a putative underlying, causal mechanism for BED is unique to
eating disorder models, restraint is not absent in addiction. Notably, the restraint behaviors in
BED are not successful (Howard & Porzelius, 1999), which parallels the substance
dependence criteria of being unable to cut down or abstain from use, despite the desire to do
so (American Psychiatric Association, 2000). Repeated, unsuccessful attempts to cut back
on consumption or quit occur as part of an addiction (Best, Ghufran, Day, Ray, & Loaring,
2008; Fagan et al., 2007), and substance-related restraint, or attempts to cut down, has been
measured in addictive disorders (Collins & Lapp, 1992; Ruderman & McKirnan, 1984).
Further, the abstinence violation effect, where an individual excessively uses a substance
after experiencing a lapse in restraint, is often applied to BED (Grilo & Shiffman, 1994), but
originated from the addiction literature (Marlatt, 1979). Thus, for some persons with BED,
dietary restraint may be a consequence, rather than a cause, of binge eating behavior (Grilo
& Masheb, 2000; Reas & Grilo, 2007). For some individuals, restraint may be the failed
attempt to control addictive-like consumption of highly rewarding, calorie-dense foods.
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Dietary restraint may be a strategy for overcoming one’s personal vulnerability for weight
gain in an obesogenic environment (Lowe, 2015; Lowe et al., 2013). While some individuals
may be vulnerable to shape and weight ideals, others may have a propensity to develop an
addictive-like response to hedonically pleasurable, highly processed foods and engage in
dietary restraint after bingeing in an effort to avoid weight gain. Since restraint may be
associated with perceived deprivation of these foods (Lowe & Levine, 2005), individuals
who find these foods especially rewarding or “addictive” may experience hedonic
deprivation more acutely, which may increase their risk for engaging in extreme dietary
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restraint to combat binge eating and weight cycling. This pattern of alternating between
periods of binge eating and dietary restraint may lead to addiction-like changes in the brain,
such as sensitization of the dopamine system (Avena et al., 2008b; Hyman, Malenka, &
Nestler, 2006; Robinson & Berridge, 1993). Thus, for some individuals, dietary restraint
may be used as an attempt to overcome weight gain related to a propensity for developing
addictive-like eating in response to highly processed foods.
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Relatedly, YFAS symptoms of “food addiction” have been associated with greater weight
cycling (e.g., repeated loss and regain of twenty pounds or more), earlier age of first diet,
and time spent dieting (Gearhardt, Boswell, & White, 2014). While some studies have found
an association between YFAS symptomology and a measure of dietary restraint, others have
not (Gearhardt, Boswell, & White, 2014; Gearhardt et al., 2013b; Gearhardt et al., 2012). In
some cases, “food addiction” appears to be related to dieting and restraint, though the nature
of this relationship is poorly understood, as the existing studies are cross-sectional or
retrospective. Thus, it will be necessary to examine whether dieting and restraint may play
some causal role in the development of “food addiction” or whether dietary restraint/dieting
might develop in response to an individual’s propensity to consume highly processed foods
in an addictive manner. Further, future work should evaluate whether alternating between
periods of restriction and excess consumption of highly processed foods may create an
intermittent pattern that, akin to substance use disorders (Berridge & Robinson, 1995;
Robinson & Berridge, 2001), exacerbates addictive-like responses.
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In summary, restraint and dieting may be causal mechanisms for some individuals with
BED, as posited by traditional eating disorder models. In others, restraint may be linked with
binge eating, but it may reflect attempts to resist biologic drives towards obesity (Agras,
2010; Lowe, 2015; Lowe et al., 2013) and/or attempts to manage an addictive response to
highly processed foods. Additional longitudinal research is needed to understand how an
individual’s personal vulnerabilities (e.g., shape/weight concern, propensity for addiction)
may interact with binge eating to result in disordered eating behavior. Future studies might
also examine whether periods of intermittent restraint or fasting (followed by episodes of
binging) may contribute to addiction-related neural sensitization in humans.
5.2. Shape and weight concerns
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In addition to dietary restraint, shape and weight concerns may be antecedents or risk factors
for BED (Fairburn et al., 1998; Killen et al., 1996). This refers to the overvaluation of an
individual’s own shape and/or weight (Hrabosky, Masheb, White, & Grilo, 2007). Though
not a DSM-5 diagnostic criterion for BED, it has been suggested that shape and weight
concerns represent a core psychopathology of eating disorders and may play a key role in
the maintenance of binge eating and associated eating pathology (Fairburn et al., 2003).
Overvaluation of shape and weight may prospectively predict the onset of binge eating for
some individuals (Allen, Byrne, McLean, & Davis, 2008; Killen et al., 1994; Loth et al.,
2014; Sonneville et al., 2015; Stice, Presnell, & Spangler, 2002). Additionally, high reports
of body dissatisfaction appear to greatly increase the risk for disordered eating behavior
(Stice et al., 2011), especially in early adolescence (Rohde, Stice, & Marti, 2015). While
shape and weight concerns may precede eating problems for some, others may experience
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elevated shape and weight concerns due to negative outcomes such as weight gain associated
with bingeing. Binge eaters who report shape and weight overvaluation present with more
severe eating psychopathology and depression than binge eaters without the characteristic
(Grilo, 2013; Grilo et al., 2008; Grilo, Masheb, & White, 2010; Sonneville et al., 2015). This
underscores the idea that shape and weight concern is an important contributor to the
trajectory of BED, though, akin to restraint, it may be a causal mechanism for some
individuals but a consequence of bingeing for others.
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The idea that shape and weight concerns may precipitate and/or maintain problematic eating
is not characteristic of an addiction perspective. If one were to attempt to conceptualize
overvaluation of shape/weight from an addiction perspective, it might perhaps be speculated
that such shape and weight concerns develop as problematic eating continues. For example,
it is logical that smokers would have higher rates of concern about lung cancer because they
are at higher risk due to their addiction. Similarly, “food addiction” has been associated with
elevated shape and weight concerns in cross-sectional research (Gearhardt, Boswell, &
White, 2014; Gearhardt et al., 2013b; Gearhardt et al., 2012; Schebendach et al., 2013),
which may be related to the increased risk of weight gain linked to greater levels of highly
processed food consumption. In a parallel manner, from such a perspective, binge eating
might be associated with greater shape and weight concerns because binge eating increases
risk of future weight gain or obesity. However, studies with BED (Grilo et al., 2008) and
other eating disorder groups with binge-eating behaviors (Grilo et al., 2009), have
consistently demonstrated that overvaluation is not associated with either BMI or obesity
(i.e., it appears to reflect a subjective cognitive feature unrelated to body weight). Thus,
shape and weight concerns appear to be related to both binge eating and YFAS “food
addiction” symptomology, however, longitudinal and experimental studies are needed to
develop an improved understanding of these associations.
6. Practical implications
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If addiction mechanisms may contribute to problematic eating behavior for some
individuals, this framework may inform new treatments or improve existing interventions.
While research has identified specific psychological (Wilson, Grilo, & Vitousek, 2007) and
pharmacological (Reas & Grilo, 2014, 2015) treatment interventions for BED, even with the
best available treatments (Grilo et al., 2011; Wilson et al., 2010), a sizeable minority of
patients do not achieve remission and most fail to lose clinically meaningful weight.
(Brownley, Berkman, Sedway, Lohr, & Bulik, 2007; Grilo et al., 2011; Vocks et al., 2010;
Wilson et al., 2010), Treatment can be improved further by an improved understanding of
predictors/moderators (Grilo, Masheb, & Crosby, 2012) and of mediators (Kraemer, Wilson,
Fairburn, & Agras, 2002; Wilson et al., 2007). Research on mediators of BED treatments is
lacking and represents a priority for research. Novel treatments that target underlying
mechanisms may increase efficacy. For example, if an intervention designed to reduce
smoking focused on changing the individual’s thoughts and beliefs about cigarettes, but did
not address the cigarettes’ addictive nature, this therapeutic technique would likely have
limited success.
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Future research is warranted to determine whether interventions that target addictive-like
mechanisms may be beneficial for some individuals with problematic eating behavior.
Notably, CBT for BED and addictive disorders already share common features, such as
emotion regulation, trigger identification, and craving management (Gearhardt et al., 2011d).
The greatest point of contention between existing treatments tailored to “food addiction”
(e.g., Overeaters Anonymous) relative to treatment addressing traditional eating disorder
tenets (e.g., restraint) is the role of the food (Gearhardt et al., 2011d). In eating disorder
models, there are no “bad” or “forbidden” foods (Fairburn et al., 2003). However, an
addiction perspective would suggest that some foods have a greater “addictive potential” and
for some individuals, these foods may be capable of “hijacking” neural circuitry (Gearhardt,
Davis et al., 2011) and making it more difficult to regulate eating behaviors and patterns. If
an addictive process contributes to problematic eating behavior for some individuals (or if
highly processed foods create greater challenges to controlled intake for both cognitive and
neurobiological reasons), then perhaps specific interventions utilized in the treatment of
addictive disorders should be evaluated for their utility in addressing “food addiction.” The
assessment of novel treatment approaches may be clinically useful for improving outcomes,
though research is also needed to identify the potential harm of incorporating addiction
intervention perspectives into the treatment of eating problems.
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One major concern regarding treatments for “food addiction” is that the goal of abstinence
from certain foods may be harmful and increase disordered eating behaviors, such as dietary
restraint (Wilson, 1993). Although abstinence-based interventions for problematic eating
behavior, such as Overeaters Anonymous and Food Addicts Anonymous, have been around
since the 1960’s, there has been limited empirical examination of their efficacy (Schwartz &
Brownell, 1995). Due to the potential harm of abstinence-based programs, future research is
needed to examine the utility of this treatment approach as applied to “food addiction.” Until
there is significant empirical evidence of positive treatment outcomes, the identification of
potential contraindications, and the assessment of possible adverse consequences,
abstinence-based treatments for eating should be approached with caution.
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However, there are empirically supported, addiction-focused interventions that do not
require abstinence, such as harm-reduction. Harm-reduction aims to minimize potential
harm associated with addictive substances by focusing on using in moderation and reducing
consumption in high-risk situations (Cheung, 2000; Marlatt, 1996; Marlatt & Tapert, 1993).
For example, a harm-reduction intervention for individuals with alcohol-use disorders would
aim to reduce binge drinking episodes through strategies such as alternating between
alcoholic beverages and glasses of water and monitoring the quantity of alcoholic drinks
consumed (Marlatt, Somers, & Tapert, 1993; Marlatt & Witkiewitz, 2002). Harm-reduction
approaches also focus on tolerating craving and developing alternative coping strategies to
regulate intense mood states (Marlatt, Larimer, & Witkiewitz, 2011). While harm-reduction
strategies are empirically supported for reducing negative outcomes associated with
substance-use disorders (Langendam, van Brussel, Coutinho, & van Ameijden, 2001;
McBride, Farringdon, Midford, Meuleners, & Phillips, 2004; Monti et al., 1999), it is
uncertain whether this intervention would be well-suited for addictive-like consumption of
highly processed foods. Thus, future examination of a harm-reduction approach for treating
“food addiction” may be warranted.
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Another consideration for the utility of “food addiction” in a clinical context is whether the
construct predicts treatment outcomes. We are unaware of previous studies that have
examined if addiction-specific treatments like harm reduction or abstinence-based
interventions are effective in reducing symptoms of “food addiction” or eating-related
problems like binge eating and obesity. However, there have been mixed findings regarding
whether an individual’s endorsement of “food addiction” symptoms predicts outcomes in
treatments for obesity, with some studies finding that “food addiction” was related to less
weight loss (Burmeister, Hinman, Koball, Hoffmann, & Carels, 2013) and others observing
no association with weight loss or attrition (Lent, Eichen, Goldbacher, Wadden, & Foster,
Author Manuscript
The literature regarding the predictive significance of BED for obesity treatment outcomes is
mixed and suffers from methodological limitations, consisting of mostly retrospective and
non-randomized studies, limited further by self-report measures and varying ways of
categorizing “binge eaters” (Wilson et al., 2007). Blaine and Rodman (2007), in a matchedstudy meta-analysis of obesity trials, reported that obese binge eaters, on average, lost
significantly less weight than obese non-binge-eaters (1.3 kg vs 10.5 kg). Such aggregate
findings across studies suggest that BED is a negative prognostic indicator for obesity
treatment, although the comparison strategy and the methodological limitations of many of
the studies suggests caution and need for further research. More recently, Grilo and White
(2013), in the first controlled, prospective study of BED status on obesity outcome
treatment, reported that BED significantly predicted worse eating and depression outcomes
and significantly moderated the effects of anti-obesity medication (orlistat) on weight loss
(i.e., medication added to behavioral therapy enhanced weight losses among non-bingeeaters but not BED).
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Given the mixed findings in the literature, further examination is warranted for how
constructs as “food addiction” and binge eating may predict intervention outcomes for
obesity. However, obesity is not synonymous with “food addiction” or binge eating, and
future research should also focus on identifying which treatments may be most effective for
particular eating-related problems (e.g., harm reduction for the treatment of “food
addiction”) and whether individual characteristics (e.g., impulsivity) may moderate
treatment outcome.
7. Future directions
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Given the unique mechanisms relevant to applying an addiction framework to food (e.g.,
withdrawal), there are six key research directions that are important to further evaluate the
“food addiction” construct (Table 2). First, it is essential to identify the addictive agent in
food to determine which foods or ingredient(s) have an addictive potential. Though animal
models and the only existing study in humans support the role of highly processed foods in
“food addiction” (Avena et al., 2008b; Johnson & Kenny, 2010b; Murray, Tulloch, Chen, &
Avena, 2015; Schulte et al., 2015), the addictive agent(s) is unknown, as are the specific
individual characteristics that may enhance one’s risk of developing “food addiction.” The
absence of a defined addictive agent remains one of the most significant criticisms of the
food addiction hypothesis (Hebebrand et al., 2014; Ziauddeen & Fletcher, 2013). The
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identification of the potentially addictive agent in food is fundamental to the proposal of an
addictive process and should be prioritized in future studies. Second, it is important to
determine whether mechanisms unique to addictive disorders, such as withdrawal and
tolerance, may contribute to addictive-like consumption of certain foods. Third, longitudinal
work is needed in order to understand the temporal relations between “food addiction,”
obesity, binge eating, and BED. The YFAS-C, a measure of “food addiction” symptoms in
children, is associated with elevated BMI (Gearhardt, Roberto, Seamans, Corbin, &
Brownell, 2013), emphasizing the necessity of examining how “food addiction” develops
and relates to other eating-related problems across the lifespan. Further, longitudinal
methodologies used in other fields (Cain et al., 2012; Shea et al., 2004) may help to clarify
further the nature of the associations among the constructs and especially whether the
possible mechanisms described in this review are causal factors or contributors to the
maintenance or course of eating-related problems. Fourth, treatment approaches for
addictive disorders, such as abstinence-based interventions or harm-reduction, should be
evaluated for the treatment of “food addiction.” This is especially important given the
potential for certain addiction-focused treatment approaches to increase restrictive eating
practices. Fifth, there is emerging evidence that YFAS scores may be associated with other
forms of binge eating, such as bulimia nervosa (Meule, von Rezori, & Blechert, 2014) and
anorexia nervosa- binge/purge subtype (Granero et al., 2014). As such, the role of addictionspecific mechanisms in problematic eating behavior should be explored across various forms
of binge eating and disordered eating in future research. Sixth, BED and “food addiction”
are both associated with obesity but do not occur exclusively in obese individuals (Davis et
al., 2011; de Zwaan, 2001; Gearhardt et al., 2009b). However, many of the mechanisms
implicated in addictive disorders and BED (e.g., impulsivity, reward dysfunction) may also
contribute to obesity (Davis & Carter, 2009; Volkow et al., 2008b). Thus, it will be important
to examine whether certain mechanisms are particularly relevant to individuals with both
obesity and compulsive patterns of food consumption.
8. Concluding remarks
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“Food addiction” and BED have significant phenotypic overlap, such as loss of control over
consumption and continued use despite negative consequences. To evaluate whether an
addictive process contributes to problematic eating, increased attention to underlying
mechanisms is warranted. While many mechanisms appear to be shared among BED and
addictive disorders, such as reward dysfunction, craving, emotion dysregulation, and
impulsivity, there are also important differences. For some individuals, dietary restraint and
shape or weight concerns may be causal mechanisms in the development and/or
maintenance of binge eating behavior. However, for others, highly processed foods may be
capable of triggering neuroplastic changes in the brain to result in an addictive-like process.
In conclusion, though “food addiction” and BED share several underlying mechanisms, the
utility of “food addiction” may be most appropriately understood by investigating whether
mechanisms unique to an addiction perspective offer novel explanatory power for
problematic eating in some individuals. Further, a mechanistic approach may contribute to
the development of new intervention approaches to improve treatment outcomes.
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Agras, WS. The Oxford handbook of eating disorders. Oxford University Press; 2010.
Ahmed SH, Guillem K, Vandaele Y. Sugar addiction: Pushing the drug–sugar analogy to the limit.
Current Opinion in Clinical Nutrition and Metabolic Care. 2013; 16(4):434–439. http://dx.doi.org/
10.1097/MCO.0b013e328361c8b8. [PubMed: 23719144]
Allen KL, Byrne SM, McLean NJ. The dual-pathway and cognitive–behavioural models of binge
eating: Prospective evaluation and comparison. European Child & Adolescent Psychiatry. 2012;
21(1):51–62. http://dx.doi.org/10.1007/s00787-011-0231-z. [PubMed: 22120762]
Allen KL, Byrne SM, McLean NJ, Davis EA. Overconcern with weight and shape is not the same as
body dissatisfaction: Evidence from a prospective study of pre-adolescent boys and girls. Body
Image. 2008; 5(3):261–270. http://dx.doi.org/10.1016/j.bodyim.2008.03.005. [PubMed: 18585990]
Allison S, Timmerman GM. Anatomy of a binge: Food environment and characteristics of nonpurge
binge episodes. Eating Behaviors. 2007; 8(1):31–38. http://dx.doi.org/10.1016/j.eatbeh.2005.01.004.
[PubMed: 17174849]
American Psychiatric Association, A. P. Diagnostic and statistical manual of mental disorders: DSMIV-TR. Washington, DC: American Psychiatric Association; 2000.
American Psychiatric Association, A. P. A. Diagnostic and statistical manual of mental disorders:
DSM-5. 2013. from http://dsm.psychiatryonline.org/book.aspx?bookid=556
Ansell EB, Grilo CM, White MA. Examining the interpersonal model of binge eating and loss of
control over eating in women. International Journal of Eating Disorders. 2012; 45(1):43–50. http://
dx.doi.org/10.1002/eat.20897. [PubMed: 21321985]
Avena NM. The study of food addiction using animal models of binge eating. Appetite. 2010; 55(3):
734–737. [PubMed: 20849896]
Avena NM, Bocarsly ME, Rada P, Kim A, Hoebel BG. After daily bingeing on a sucrose solution, food
deprivation induces anxiety and accumbens dopamine/ acetylcholine imbalance. Physiology &
Behavior. 2008a; 94(3):309–315. [PubMed: 18325546]
Avena NM, Gearhardt AN, Gold MS, Wang GJ, Potenza MN. Tossing the baby out with the bathwater
after a brief rinse? The potential downside of dismissing food addiction based on limited data.
Nature Reviews Neuroscience. 2012; 13(7):514. http://dx.doi.org/10.1038/nrn3212-c1 (author
reply 514).
Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of
intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews. 2008b; 32(1):20–
39. http://dx.doi.org/10.1016/j.neubiorev.2007.04.019. [PubMed: 17617461]
Avena NM, Rada P, Hoebel BG. Sugar and fat bingeing have notable differences in addictive-like
behavior. The Journal of Nutrition. 2009; 139(3):623–628. http://dx.doi.org/10.3945/jn.
108.097584. [PubMed: 19176748]
Baker TB, Piper ME, McCarthy DE, Majeskie MR, Fiore MC. Addiction motivation reformulated: An
affective processing model of negative reinforcement. Psychological Review. 2004; 111(1):33–51.
http://dx.doi.org/10.1037/0033-295X.111.1.33. [PubMed: 14756584]
Balodis IM, Kober H, Worhunsky PD, White MA, Stevens MC, Pearlson GD, … Potenza MN.
Monetary reward processing in obese individuals with and without binge eating disorder.
Biological Psychiatry. 2013a; 73(9):877–886. http://dx.doi.org/10.1016/j.biopsych.2013.01.014.
[PubMed: 23462319]
Balodis IM, Molina ND, Kober H, Worhunsky PD, White MA, Rajita S, … Potenza MN. Divergent
neural substrates of inhibitory control in binge eating disorder relative to other manifestations of
obesity. Obesity (Silver Spring). 2013b; 21(2):367–377. http://dx.doi.org/10.1002/oby.20068.
[PubMed: 23404820]
Barnett G, Hawks R, Resnick R. Cocaine pharmacokinetics in humans. Journal of Ethnopharmacology.
1981; 3(2–3):353–366. [PubMed: 7242115]
Beach HD. Morphine addiction in rats. Canadian Journal of Psychiatry/Revue Canadienne de
Psychologie. 1957; 11(2):104.
Clin Psychol Rev. Author manuscript; available in PMC 2018 February 02.
Schulte et al.
Page 23
Author Manuscript
Author Manuscript
Author Manuscript
Author Manuscript
Bellisle F, Dalix AM. Cognitive restraint can be offset by distraction, leading to increased meal intake
in women. The American Journal of Clinical Nutrition. 2001; 74(2):197–200. [PubMed:
Bello NT, Lucas LR, Hajnal A. Repeated sucrose access influences dopamine D2 receptor density in
the striatum. Neuroreport. 2002; 13(12):1575–1578. [PubMed: 12218708]
Berg KC, Peterson CB, Crosby RD, Cao L, Crow SJ, Engel SG, Wonderlich SA. Relationship between
daily affect and overeating-only, loss of control eating-only, and binge eating episodes in obese
adults. Psychiatry Research. 2014; 215(1):185–191. [PubMed: 24200217]
Berridge KC. The debate over dopamine’s role in reward: The case for incentive salience.
Psychopharmacology. 2007; 191(3):391–431. http://dx.doi.org/10.1007/s00213-006-0578-x.
[PubMed: 17072591]
Berridge KC. ‘Liking’ and ‘wanting’ food rewards: Brain substrates and roles in eating disorders.
Physiology & Behavior. 2009; 97(5):537–550. http://dx.doi.org/10.1016/j.physbeh.2009.02.044.
[PubMed: 19336238]
Berridge KC, Robinson TE. The mind of an addicted brain: neural sensitization of wanting versus
liking. Current Directions in Psychological Science. 1995; 71–76
Best DW, Ghufran S, Day E, Ray R, Loaring J. Breaking the habit: A retrospective analysis of
desistance factors among formerly problematic heroin users. Drug and Alcohol Review. 2008;
27(6):619–624. http://dx.doi.org/10.1080/09595230802392808. [PubMed: 19023771]
Blaine B, Rodman J. Responses to weight loss treatment among obese individuals with and without
BED: A matched-study meta-analysis. Eating and Weight Disorders. 2007; 12(2):54–60. [PubMed:
Blum K, Braverman ER, Holder JM, Lubar JF, Monastra VJ, Miller D, … Comings DE. Reward
deficiency syndrome: A biogenetic model for the diagnosis and treatment of impulsive, addictive,
and compulsive behaviors. Journal of Psychoactive Drugs. 2000; 32(Suppl i–iv):1–112.
Blum K, Cull JG, Braverman ER, Comings DE. Reward deficiency syndrome. American Scientist.
1996; 84(2):132–145. http://dx.doi.org/10.2307/29775633.
Boggiano MM, Artiga AI, Pritchett CE, Chandler-Laney PC, Smith ML, Eldridge AJ. High intake of
palatable food predicts binge-eating independent of susceptibility to obesity: An animal model of
lean vs obese binge-eating and obesity with and without binge-eating. International Journal of
Obesity. 2007; 31(9):1357–1367. http://dx.doi.org/10.1038/sj.ijo.0803614. [PubMed: 17372614]
Bonson KR, Grant SJ, Contoreggi CS, Links JM, Metcalfe J, Weyl HL, … London ED. Neural
systems and cue-induced cocaine craving. Neuropsychopharmacology. 2002; 26(3):376–386.
http://dx.doi.org/10.1016/S0893-133X(01)00371-2. [PubMed: 11850152]
Bottlender M, Soyka M. Impact of craving on alcohol relapse during, and 12 months following,
outpatient treatment. Alcohol and Alcoholism. 2004; 39(4):357–361. http://dx.doi.org/10.1093/
alcalc/agh073. [PubMed: 15208171]
Brandon TH. Negative affect as motivation to smoke. Current Directions in Psychological Science.
Brower KJ, Paredes A. Cocaine withdrawal. Archives of General Psychiatry. 1987; 44(3):297–298.
[PubMed: 3827523]
Brownley KA, Berkman ND, Sedway JA, Lohr KN, Bulik CM. Binge eating disorder treatment: A
systematic review of randomized controlled trials. The International Journal of Eating Disorders.
2007; 40(4):337–348. http://dx.doi.org/10.1002/eat.20370. [PubMed: 17370289]
Burger K, Stice E. Frequent ice cream consumption is associated with reduced striatal response to
receipt of an ice cream-based milkshake. The American Journal of Clinical Nutrition. 2012; 95(4):
810–817. http://dx.doi.org/10.3945/ajcn.111.027003. [PubMed: 22338036]
Burmeister JM, Hinman N, Koball A, Hoffmann DA, Carels RA. Food addiction in adults seeking
weight loss treatment. Implications for psychosocial health and weight loss. Appetite. 2013; 60(1):
103–110. http://dx.doi.org/10.1016/j.appet.2012.09.013. [PubMed: 23017467]
Cain NM, Ansell EB, Wright AG, Hopwood CJ, Thomas KM, Pinto A, … Grilo CM. Interpersonal
pathoplasticity in the course of major depression. Journal of Consulting and Clinical Psychology.
2012; 80(1):78–86. http://dx.doi.org/10.1037/a0026433. [PubMed: 22103955]
Clin Psychol Rev. Author manuscript; available in PMC 2018 February 02.
Schulte et al.
Page 24
Author Manuscript
Author Manuscript
Author Manuscript
Author Manuscript
Carter BL, Tiffany ST. Meta-analysis of cue-reactivity in addiction research. Addiction. 1999; 94(3):
327–340. [PubMed: 10605857]
Cassin SE, von Ranson KM. Is binge eating experienced as an addiction? Appetite. 2007; 49(3):687–
690. http://dx.doi.org/10.1016/j.appet.2007.06.012. [PubMed: 17719677]
Chang L, Alicata D, Ernst T, Volkow N. Structural and metabolic brain changes in the striatum
associated with methamphetamine abuse. Addiction. 2007; 102(Suppl 1):16–32. http://dx.doi.org/
10.1111/j.1360-0443.2006.01782.x. [PubMed: 17493050]
Cheung YW. Substance abuse and developments in harm reduction. CMAJ. 2000; 162(12):1697–1700.
[PubMed: 10870502]
Childress AR, Mozley PD, McElgin W, Fitzgerald J, Reivich M, O’Brien CP. Limbic activation during
cue-induced cocaine craving. The American Journal of Psychiatry. 1999; 156(1):11–18. [PubMed:
Collins RL, Lapp WM. The temptation and restraint Inventory for measuring drinking restraint. British
Journal of Addiction. 1992; 87(4):625–633. [PubMed: 1591514]
Corsica JA, Pelchat ML. Food addiction: True or false? Current Opinion in Gastroenterology. 2010;
26(2):165–169. http://dx.doi.org/10.1097/MOG.0b013e328336528d. [Pub…
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