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Food addiction: true or false?

Joyce A. Corsica and Marcia L. Pelchat


Department of Behavioral Sciences, Rush University
Medical Center, Chicago, Illinois, USA
Correspondence to Joyce A. Corsica, PhD, Department
of Behavioral Sciences, Rush University Medical
Center, 1653 W. Congress Pkwy, Chicago, IL 60614,
USA
Tel: +1 312 942 2002; fax: +1 312 942 4990;
e-mail: joyce_corsica@rush.edu
Current Opinion in Gastroenterology 2010,
26:165169

Purpose of review
Food addiction has been implicated as a putative causal factor in chronic overeating,
binge eating, and obesity. The concept of food addiction has been controversial
historically due to definitional and conceptual difficulties and to a lack of rigorous
scientific data.
Recent findings
Support for the food addiction hypothesis comes from alterations in neurochemistry
(dopamine, endogenous opioids), neuroanatomy (limbic system), and self-medication
behaviors. Foods identified as having potential addictive properties include sweets,
carbohydrates, fats, sweet/fat combinations, and possibly processed and/or high salt
foods. Eating topography has been identified as a necessary factor in neural pathway
changes that promote addiction-like properties in response to some foods. A recently
developed food addiction scale shows promise in identifying food addiction.
Summary
Recent findings have strengthened the case for food addiction. These findings may
serve to validate the perception of food addiction in patients and inform
psychoeducational, cognitive-behavioral, and/or pharmacological treatment for chronic
food cravings, compulsive overeating, and binge eating that may represent a phenotype
of obesity. Screening for food addiction has the potential to identify people with eating
difficulties that seriously compromise weight management efforts. Future research
should include a focus on human food addiction research; evaluating the impact of
treatment on underlying neurochemistry; and prevention or reversal of food addiction in
humans.
Keywords
compulsive eating, craving, eating topography, food addiction, self-medication
Curr Opin Gastroenterol 26:165169
2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
0267-1379

Introduction
Many people report addiction-like symptoms related to
eating, including strong food cravings and loss of control
over eating, that are described as barriers to weight loss
[1,2]. Although the concept of food addiction has been
popular in the lay population for many years, it has
generated significant controversy in the scientific community. However, a recent flood of research strongly
suggests that addiction-like processes may underlie
intake regulation difficulties in some people and contribute to obesity.

Behavioral dependence criteria


In diagnostic terms, addiction is now referred to as substance dependence. The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) [3] defines substance dependence as three or more of the following seven
0267-1379 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

symptoms occurring within 1 year: tolerance, withdrawal


symptoms, substance taken in larger amounts or for a
longer duration than intended, attempts to cut back,
excessive time spent pursuing, using, or recovering from
use, reduction or discontinuation of important activities
because of use, and continued use despite adverse consequences. It is noteworthy that physiological dependence
(tolerance and withdrawal symptoms) is not required for a
dependence diagnosis; therefore, the diagnosis of dependence can be based on behavioral criteria alone.
Based on these criteria, binge eaters and many chronic
overeaters and emotional eaters would meet the criteria
for substance (food) dependence. Recently, Ifland et al.
[4] and Corwin and Grigson [5] have illustrated clear
parallels between dependence criteria and frequently
reported problem eating behaviors. Food-specific expressions of the substance dependence criteria (adapted from
[4]) might include:
DOI:10.1097/MOG.0b013e328336528d

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166 Nutrition

(1) Tolerance
(2) Withdrawal symptoms
(3) Taking in larger amounts or for a longer duration
(4) Attempts to cut back
(5) Excessive time spent pursuing, using, or recovering
from use
(6) Reduction/discontinuation of important activities
because of use
(7) Continued use despite consequences

Starting out with a single cookie, gradually increasing to several or a whole box
Habitually eating to relieve depression, anxiety, and other emotional states;
unpleasant physical sensations when cutting back on carbohydrates
Intending to eat a single serving but instead eating a whole package; binges
extending several hours
Frequent attempts to eat correctly (e.g., avoid overeating or eating certain foods)
that can only be maintained for a short period of time
Frequent thinking about food, planning intake, preparing, and/or resting or sleeping
after excessive intake
Eating instead of spending time with friends; feeling too sick after overeating
to do anything
Overeating in spite of overweight, physical illness, and/or distress about overeating

Recalling that only three criteria would be necessary for a


dependence diagnosis, it is clear that many people with
dysregulated eating, particularly those with binge eating
disorder, would meet criteria for food addiction if it is
conceptualized under the same criteria.

Food cravings, mood, and behavior


Although craving is not a part of the formal criteria for
substance dependence, the two are clearly associated.
Cravings are also associated with binge eating [6] and
notably; food craving activates the same areas of the brain
involved in drug craving [7]. One of the most frequently
reported food cravings is carbohydrate craving, which has
recently undergone detailed scientific re-examination. In
a recent series of studies, Corsica and Spring [8] and
Spring et al. [9] investigated whether purported carbohydrate craving could be verified and demonstrated
in aAhighly controlled experimental environment. In a
double-blind, placebo controlled trial they found that
when rendered dysphoric, carbohydrate cravers reported
a greater reduction in dysphoria and food cravings following carbohydrate ingestion (versus a taste, texture, and
calorie matched high protein alternative). Perhaps more
importantly, participants chose to ingest the carbohydrate
far more often than the taste-matched placebo, demonstrating the salience of the improvement. These findings
demonstrate that for carbohydrate cravers, carbohydrates
seem to have an almost medicinal value in women who
crave them.
Spring et al. [9] extended the model to examine the
addiction potential of carbohydrates in women who crave
them. Examining the fit with physiological dependence
criteria, they analyzed liking, sensitivity, and tolerance to
carbohydrates. The authors found that liking increased
over time (indicating sensitization) and reduction in
dysphoria decreased significantly over time (suggesting
tolerance to the mood effect). They concluded that the
combination of increased liking for carbohydrates in the
context of decreased mood effects paralleled other
addiction processes, and strongly suggested that carbohydrates indeed have abuse potential for women who
crave them.

The origins of such food cravings are unknown. In both


studies, the use of a taste and calorie-matched high
protein placebo ensured that the improved mood and
decreased craving was not due to hedonics, palatability,
or caloric ingestion, but more likely, underlying neurochemical changes that promote mood improvement and
reduce food cravings. Previous research has shown that
food cravings can be induced by repeatedly eating a
specific substance when hungry [10]; thus, it is also
possible that carbohydrate craving is the natural sequela
of repeatedly choosing high carbohydrate (perhaps vending machine-type) snacks in response to mid-afternoon
hunger.

Neurochemistry in food addiction


A great deal of evidence suggests a similarity in the
neurochemical response to drugs and to food. Both palatable food and drugs appear to activate the same mesolimbic dopamine reward system in the brain in human
and animal models [11,12,13]. Moreover, in humans,
PET studies have shown that both obese and drugdependent individuals have significantly lower dopamine
receptor levels, and further, there is an inverse relationship between D2 receptor density and BMI [14]. This is
suggestive of decreased sensitivity in the reward system
in the obese. However, whether this is a cause or an effect
is unknown at this time: it is possible that this is a
preexisting condition that promotes overeating; however,
it is similarly possible that this is a result of repeated
overstimulation of this neuronal system.
Stoeckel et al. [15] have provided preliminary evidence
suggesting that the limbic system in obese women may
be hyperresponsive to food rewards. Using functional
MRI (fMRI), they investigated the activation of the
reward system in response to pictures of high-calorie
(e.g., pizza) and low-calorie (e.g., fish) foods in obese
and normal weight women. They found that obese
women exhibited significantly greater activation in a
number of regions of the brain (including the amygdala,
nucleus accumbens, ventral striatum, medial prefrontal
cortex) in response to high calorie foods as compared with
normal weight women. These areas of the brain are

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Food addiction: true or false? Corsica and Pelchat

thought to influence the motivational effects of food cues.


Hyperresponsivity of this neural mechanism may have
been appropriate and adaptive when food was scarce, but
in the modern environment can clearly create difficulties
with intake regulation [16].

Eating topography
As a substance that releases opioids and dopamine, sugar is
thought to have addiction potential [17]. In studying the
potential for sugar addiction in animals, Avena et al. [17]
found that it may not be the substance in and of itself that
promotes addiction, but rather the combination of the
substance (in this case, sugar) with a specific eating style.
This was demonstrated in a series of models in which rats
were first exposed to a palatable substance, then access to it
was restricted, and then the substance was provided, but on
a limited basis. This restriction/exposure pattern promoted
binge eating and neuronal changes suggestive of addiction
(similar to those induced by drugs of abuse) indicating that
certain foods are capable of promoting addiction-like
behavior and neuronal change under certain conditions.
Taken together, several lines of evidence now suggest that
palatable food is probably not addictive in and of itself
[7,11,1820]. Instead, it is the manner in which the
food is consumed (i.e., restriction plus overeating/binging)
that appears to create an addiction-like process. This
eating topography hypothesis provides strong evidence
for combined behavioral and neurochemical components
of a food addiction process in animals. It is unknown at this
time whether the same model might apply to humans.
However, it is worth considering that the restriction/overeating pattern demonstrated in the eating topography
findings may have a human parallel in binge eating, night
eating, emotional eating, and even diet cycling. Further
research with human individuals is needed to elucidate the
applicability of these findings to human models of
food addiction.

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external food sensitivity (as measured by the Dutch Behavioral Questionnaire) and with increased hunger after
exposure to appetizing images. This suggests that less
efficient connectivity among relevant brain regions might
represent a neuronal marker for vulnerability to develop
abnormal behavior, including food craving and overeating.
Although this study has not yet been done in people who
are obese or who are addicted to food, this is an area for
future investigation. With additional supporting research,
it is possible that measuring differences in the magnitude
of responses may help to determine an individuals risk for
disordered eating and obesity.

New hypotheses
Two new but untested conceptual models of food addiction have recently been hypothesized. The refined food
addiction model [4] suggests that high concentrations of
sugar, refined carbohydrates, fat, salt, and caffeine are
addictive substances, and that foods containing these
ingredients are consumed in a manner consistent with
generally understood concepts of addictive behavior
found in the DSM-IV-TR. Similar to drugs of abuse,
the substances may not be addictive until they are
extracted and concentrated by modern industrial processes, and combinations of these foods may enhance
their potentially addictive power. The salted food hypothesis [23], purports that salt acts as a mild opiate
agonist that promotes overeating and weight gain via
stimulation of opiate and dopamine receptors in the
brains reward and pleasure centers. In a small prospective study of individuals withdrawing from opiates, the
authors observed a significant increase in fast-food intake
(and a 57% weight gain). Unfortunately, the study
design prevents the drawing of any conclusions supporting salt as the putative addictive component, as a similar
case could be made for increased fat or processed food
intake (both of which may be found in combination with
high salt in fast food). Both new hypotheses would
benefit from further scientific investigation.

Neuroanatomy
Pelchat [7] has highlighted how external stimuli, particularly environmental cues, can modulate food seeking and
food intake through learning mechanisms. External food
sensitivity (susceptibility to environmental cues) may
serve as a predisposing factor in food cravings and food
intake, as the sight, smell, or suggestion of food can serve as
a potent eating trigger in those who are susceptible. Moreover, external food sensitivity is associated with overeating
and greater preference for appetizing foods [21]. Recently,
Passamonti et al. [22] used fMRI to examine the neurological correlates of external food sensitivity in normal
weight humans. They found that viewing appetizing versus bland foods produced changes in connectivity among
the ventral striatum, amygdala, anterior cingulate, and
premotor cortex that were strongly correlated with both

Assessment of food addiction


Momentum in the study of food addiction is also found in
the area of assessment with the recent publication of the
Yale Food Addiction Scale (YFAS) [2]. The 21-item selfreport measure identifies signs of addiction to foods
(primarily high-fat and high-sugar), with a focus on paralleling the substance dependence criteria in the DSMIV-TR. Preliminary data suggested that this is a valid and
reliable tool for detecting eating patterns that are similar
to behaviors seen in the classic areas of addiction.
The development of this scale also yielded useful data on
the rate of probable food addiction as measured by the
YFAS. In this primarily normal weight undergraduate

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168 Nutrition

sample, 11.4% met criteria for food addiction. This new


measure should help to facilitate empirical research on
the concept of food addiction, perhaps at the same time
increasing confidence in the methodological rigor of food
addiction studies.

2 Gearhardt AN, Corbin WR, Brownell KB. Preliminary validation of the Yale
 Food Addiction Questionnaire. Appetite 2008; 52:430436.
Introduces a new food addiction measure, with 21 items and good preliminary
validity and reliability in a college sample. This measure awaits validation in other
populations (e.g., obese, eating disorders).

Conclusion

4 Ifland JR, Preuss HG, Marcus MT, et al. Refined food addiction: a classic
 substance use disorder. Med Hypotheses 2009; 72:518526.
Proposes a refined food addiction model based on a literature review by
addiction topic and clinical lay observations. Provides a good linkage of dependence criteria with food addiction symptoms. The overall model remains to be
tested.

So, is food addiction true or false? If we define food


addiction using the same criteria as substance dependence, then recent behavioral and neurobiological evidence increasingly points to true. It appears that the
behavioral criteria for dependence are met by people
with chronic overeating, compulsive eating, and/or binge
eating. Carbohydrates have demonstrated abuse potential (sensitization and tolerance) in female carbohydrate
cravers, which may be the result of learned behavior and/
or neurochemistry. Recent evidence suggests behavioral
and neural pathway changes that may be induced by
specific eating topography, including self-medication,
restriction/binge pattern, or eating certain foods while
hungry. External food sensitivity, learned behaviors, and
biological predisposition all may contribute to food addiction-type symptoms.
Although it seems that a strong case for food addiction is
being established, it is important to note that due to its
multifactorial nature, obesity in and of itself should not be
considered to constitute an addiction to food. The food
addiction hypothesis supports a model of heterogeneity
in obesity conceptualization, such that food addiction
might best be considered a phenotype of obesity.
Whether a cause (preexisting risk factor) or an effect
(overstimulation) is not yet known.
Our hope is that further scientific study may serve to
validate the perception of food addiction in some patients
and inform psychoeducational, cognitive-behavioral, and/
or pharmacological treatment for chronic food cravings,
compulsive overeating, and binge eating that may
represent a phenotype of obesity. Screening for food
addiction has the potential to identify people with eating
difficulties that seriously compromise weight management efforts. Future research should include a focus on
human food addiction research; evaluating the impact of
treatment on underlying neurochemistry; and prevention
or reversal of food addiction in humans.

References and recommended reading


Papers of particular interest, published within the annual period of review, have
been highlighted as:

of special interest
 of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (pp. 183184).
1

Bjorvell H, Ronnberg S, Rossner S. Eating patterns described by a group of


treatment seeking overweight women and normal weight women. Scand J
Behav Ther 1985; 14:147156.

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington DC: American Psychiatric Association;
2000.

Corwin R, Grigson P. Symposium overview. Food addiction: fact or fiction.


J Nutr 2009; 139:617619.

Cepeda-Benito A, Fernandez MC, Moreno S. Relationship of gender and


eating disorder symptoms to reported cravings for food: construct validation
of state and trait craving questionnaires in Spanish. Appetite 2003; 40:47
54.

7 Pelchat M. Food addiction in humans. J Nutr 2009; 139:620622.



Review of the food addiction literature focused on dopamine as a neurobiological
substrate of sweet food addiction potential.
Corsica J, Spring B. Carbohydrate-craving: a double-blind, placebo
controlled test of the self-medication hypothesis. Eat Behav 2008; 4:
447454.
The study demonstrated that in carbohydrate cravers, a dysphoric mood induction increases appetite for sweets and starches, and that dysphoric mood is
significantly reduced by the consumption of carbohydrates but not by a protein
placebo. This study eliminated the earlier flaws in the carbohydrate craving
literature.

8


Spring B, Schneider K, Smith M, et al. Abuse potential of carbohydrates for


overweight carbohydrate cravers. Psychopharmacology 2008; 197:637
647.
Used a drug self-administration paradigm to evaluate the abuse potential of
carbohydrates. The authors demonstrated sensitivity and tolerance effects to
carbohydrates, suggesting abuse potential for carbohydrates in carbohydrate
cravers.

9


10 Gibson EL, Desmond E. Chocolate craving and hunger state. Appetite 1999;
32:219240.
11 Avena NM, Rada P, Hoebel BG. Sugar and fat bingeing have notable
 differences in addictive-like behavior. J Nutr 2009; 139:623628.
Describes strong evidence for addiction-like behavioral and neurological alterations in rats that binge on sugar and how these effects differ from those that occur
when rats binge on fat.
12 Lutter M, Nestler EJ. Homeostatic and hedonic signals interact in the regulation of food intake. J Nutr 2009; 139:629632.
13 Small DM, Jones-Gotman M, Dagher A. Feeding induced dopamine release in
dorsal striatum correlates with meal pleasantness ratings in healthy human
volunteers. Neuroimage 2003; 19:17091715.
14 Wang GJ, Volkow ND, Logan J, et al. Brain dopamine and obesity. Lancet
2001; 357:354357.
15 Stoeckel LE, Weller RE, Cook EW, et al. Widespread reward system activation in obese women in response to pictures of high calorie foods. Neuroimage 2008; 41:636647.
16 Volkow ND, Wise RA. How can drug addiction help us understand obesity?
Nature Neuroscience 2005; 8:555560.
17 Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and
 neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev 2008; 32:2029.
This review article summarizes evidence for sugar addiction as demonstrated in the
rat model. Bingeing, withdrawal, craving, and cross-sensitization were each
demonstrated behaviorally, and then related to neurochemical changes in the
brain similar to those that occur with addictive drugs. This provides evidence
suggesting that rats can become sugar-dependent and suggests a model for
human food addiction.
18 Corwin RL, Wojnicki FHE, Fisher JO, et al. Limited access to a dietary fat
option effects ingestive behavior but not body composition in male rats.
Physiol Behav 1998; 65:545553.
19 Puhl MD, Cason AM, Corwin RL, et al. Addiction-like behaviors in rats
previously maintained on a high-fat diet. Appetite 2008; 51:392.

Copyright Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Food addiction: true or false? Corsica and Pelchat


20 Wojnicki FHE, Roberts DCS, Corwin RL. Effects of baclofen on operant
performance for food pellets and vegetable shortening after a history of bingetype behavior in nonfood deprived rats. Pharmacol Biochem Behav 2006;
84:197206.
21 Elfhag K, Tholin S, Rasmussen F. Consumption of fruit, vegetables, sweets,
and soft drinks are associated with psychological dimensions of eating
behavior in parents and their 12-year-old children. Public Health Nutr
2008; 11:914923.

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22 Passamonti L, Rowe JB, Schwarzbauer C, et al. Personality predicts the brains



response to viewing appetizing foods: the neural basis of a risk factor for
overeating. J Neurosci 2009; 29:4351.
Examined the neurological correlates of external food sensitivity in humans using
fMRI. Viewing appetizing versus bland foods produced changes in connectivity
among the human ventral striatum, amygdala, anterior cingulated, and premotor
cortex that were strongly correlated with external food sensitivity.
23 Cocores JA, Gold MS. The salted food addiction hypothesis may explain
overeating and the obesity epidemic. Med Hypotheses 2009; 73:892899.

Copyright Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

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