Nicole Avena - Hedonic Eating - How The Pleasurable Aspects of Food Can Affect Our Brains and Behavior-Oxford University Press (2015)

Hedonic Eating
Hedonic Eating
How the Pleasure of Food Affects
w
Our Brains and Behavior
Edited by Nicole M. Avena, PhD
3
3
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Library of Congress Cataloging-in-Publication Data

Hedonic eating : how the pleasure of food affects our brains and behavior / edited by
Nicole M. Avena.
p. ; cm.
Includes bibliographical references and index.
ISBN 978–0–19–933045–4 (alk. paper)
I. Avena, Nicole M., 1978- , editor.
[DNLM: 1. Eating—psychology. 2. Hyperphagia. 3. Food Habits. WM 175]
RC552.E18
616.85′26—dc23
2014040915
1 3 5 7 9 8 6 4 2
Printed in the United States of America
on acid-free paper
CON T EN T S
Foreword vii
Marc N. Potenza, Yale University
Preface xi
Nicole M. Avena, Mt. Sinai School of Medicine
Acknowledgments xiii
Contributors xv
1. Introduction 1
Nicole M. Avena, Mt. Sinai School of Medicine
2. Why Do We Eat What We Eat? 9
Kevin Myers, Bucknell University
3. The Brain’s Got a Taste for Good Food 39
Annette Horstmann, Max Planck Institute for Human Cognitive and Brain
Sciences and the University of Leipzig
4. Craving Chocolate? A Review of Individual Differences, Triggers, and
Assessment of Food Cravings 57
Ashley Mason and Elissa Epel, University of California, San Francisco
5. Overeating and Binge Eating 85
Margaret Leitch and Allan Geliebter, Mt. Sinai St. Luke’s Hospital and
Touro College and University System, and University of Calgary
6. Brain-Based Drivers and Consequences of Hedonic Overeating 107
Kyle S. Burger, Pranish A. Kantak, and Abigail J. Sanders, University of
North Carolina at Chapel Hill
7. Food “Liking” and “Wanting”: A Neurobiological Perspective 125
Susana Peciña and Kent Berridge, University of Michigan
8. The Influence of Dieting (Hedonic Deprivation) on Food Intake, How It
Can Promote Hedonic Overeating, and Mindful-Eating Interventions 147
Alexis Conason, Mount Sinai St. Luke’s Hospital
(v)
( vi ) Contents
9. The Modern Food Environment: Changes in Food Quantity and

Quality and Their Impact on Hedonic Eating 163
Wendy M. Stein and Kathleen L. Keller, Pennsylvania State University
10. Food Addiction 185
Emily Sullivan, Alastair Tulloch, Ashley Gearhardt, and Nicole M. Avena,
Mt. Sinai School of Medicine and University of Michigan
Name Index 209

Subject Index 211
FOR E WOR D: T HE C L I N IC A L R EL E VA NC E
OF HED ON IC E AT I NG
M A RC N. POTENZ A*
In recent history, there have been considerable changes in the food landscape.
Compared to prior generations, there is currently a greater availability of food, par-
ticularly in Western societies. With the availability and relatively low cost of food
(as well as other environmental changes such as the amount of energy expended
through more manual forms of labor that may have been more prevalent in the
past than now), there may be differences in the motivating factors underlying food
consumption. In the past, food consumption may have been driven in large part by
the need for restoring energy reserves. While energy restoration probably remains
an important factor in food consumption, it may not be as central in the current
environment as it was previously.1 Given the increases in the prevalence estimates
of obesity and obesity-related complications, understanding the factors motivating
food consumption and relating to increased body mass indices has public health,
policy, prevention, and treatment implications.2
The current environment relating to food, eating, and energy expenditures
has changed in multiple ways, and some of these changes have occurred relatively
rapidly. A culture regarding the consumption of good-tasting food products is cur-
rently present in many societies. So-called foodies exist in many cultures, with “best
foodie cities” being evaluated, ranked, and promoted through media.3 The focus on
and availability of outlets for the consumption of delectable cuisines suggest that
a main factor underlying food consumption in the current environment may be
palatability rather than energy homeostasis, although this point, as it relates to
medically relevant states like obesity, has been recently debated.1,4,5
Given the market of consumers with an appetite for palatable foods and the
modern-day tools for generating palatable foods (with the addition of flavorings
and other items or chemicals), there are highly palatable foods that are widely avail-
able and often relatively inexpensive. These highly palatable foods are frequently
*Dr. Potenza is Professor of Psychiatry in the Child Study Center and of Neurobiology,
Yale University School of Medicine, New Haven, Connecticut. Author for correspond-
ence: Prof. Marc N. Potenza, Yale School of Medicine, Department of Psychiatry, 1
Church Street, Room 726, New Haven, CT 06519; tel. 203-773-3553; fax. 203-737-3591;
E-mail: marc.potenza@yale.edu.
( vii )
( viii ) Foreword
highly caloric, with high sugar and/or fat contents. These characteristics have raised
questions regarding whether the foods themselves may have properties to elicit
subjective and physiological responses akin to those elicited by abused substances,
and whether “food addiction” may be contributing importantly to the increases in
the prevalence of obesity,6 particularly amongst certain subgroups of individuals
like those with binge-eating disorders.7 Of note is that specific food characteristics
may have different impacts on specific individuals; for example, high food palata-
bility may have a greater influence with respect to food consumption in individuals
with poorer impulse control who may have difficulties in regulating portion sizes
or quantities of food consumed.7 Given these and other potential changes in the
food and eating environments, a new look at hedonic eating and its possible conse-
quences is both timely and warranted.
The current volume assembles in a logical manner a set of chapters that cover
multiple aspects of hedonic eating and its possible sequelae. Following an intro-
duction, the chapters cover topics such as the food stimuli that elicit pleasurable
responses, how foods may alter brain structure and function, and how such changes
may relate to eating and other behaviors. The book progresses to discussing over-
eating and potentially related problems and how interventions involving changes
in policy, prevention, and treatment approaches may be realized through consid-
ering food consumption from within a hedonic-eating framework.
In summary, this volume brings together a systematic and thoughtful collection
of chapters that focus on viewing food and eating from a new and clinically rele-
vant perspective. Given the public health impact of obesity and other conditions
associated with overeating behaviors, the book tackles a significant public health
concern. In doing so, it sheds light on issues that are likely to continue to be topical
into the future as we as a society attempt to achieve a balance between pleasure and
health in the current food environment.
ACKNOWLEDGMENTS
This work was supported by National Institute on Drug Abuse (NIDA) grants P50
DA09241, P20 DA027844, and R01 DA035058 and a Center of Excellence grant from
the National Center for Responsible Gaming. The contents of the manuscript were
generated independently from individuals within the funding agencies, and may not
represent the views of the funding agencies. Dr. Potenza reports no conflicts of in-
terest with respect to the content of this manuscript. He has received financial sup-
port or compensation for the following: Dr. Potenza has consulted for and advised
Somaxon, Boehringer Ingelheim, Lundbeck, Ironwood, Shire, and INSYS; has received
research support from the National Institutes of Health, the Veterans Administration,
Mohegan Sun Casino, the National Center for Responsible Gaming, Forest Laboratories,
Ortho-McNeil, Oy-Control/Biotie, Glaxo-SmithKline, and Psyadon pharmaceuticals;
has participated in surveys, mailings or telephone consultations related to drug ad-
diction, impulse control disorders, or other health topics; has consulted for law offices
and the federal public defender’s office in issues related to impulse control disorders;
Foreword ( i x )
provides clinical care in the Connecticut Department of Mental Health and Addiction
Services Problem Gambling Services Program; has performed grant reviews for the
National Institutes of Health and other agencies; has guest-edited journal sections
and journals; has given academic lectures in grand rounds, continuing medical edu-
cation events, and other clinical or scientific venues; and has generated books or book
chapters for publishers of mental health texts.
REFERENCES
1. 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 addic-
tion based on limited data. Nat Rev Neurosci. 2012;13(7):514.
2. Potenza MN. Obesity, food and addiction: emerging neuroscience and clinical and
public health implications. Neuropsychopharmacology. 2014;39:249–250.
3. Ceneviva A. New Haven named top foodie city of 2014; http://wtnh.com/2014/06/16/
new-haven-named-top-foodie-city-of-2014/; Accessed September 23, 2014.
4. Ziauddeen H, Farooqi IS, Fletcher PC. Obesity and the brain: how convincing is the
addiction model? Nature Rev Neurosci. 2012;13:279–286.
5. Ziauddeen H, Farooqi IS, Fletcher PC. Food addiction: is there a baby in the bath-
water? Nature Rev Neurosci. 2012;13:514.
6. Gearhardt AN, Grilo CM, DiLeone RJ, Brownell KD, Potenza MN. Can food be addic-
tive? Public health and policy implications. Addiction. 2011;106:1208–1212.
7. Gearhardt A, White M, Potenza M. Binge eating disorder and food addiction. Curr
Drug Abuse Rev. 2011;4:201–207.
PR EFAC E
Overeating and obesity are on the rise, both in the United States and in other coun-
tries around the world. Despite public health warnings of the dangers of increased
body weight, the availability of diet books and programs, and the stigma associated
with obesity, many people still find it difficult to achieve and maintain a healthy
body weight. While there are many books on the topic of caloric or need-based
eating, obesity and overeating can also result from eating that is not necessarily
driven by hunger. In fact, recent research has discovered that excess food intake is
largely driven by the palatability, or pleasurable taste, of food, and the pleasure de-
rived from eating. This book discusses the pleasurable aspects of food intake that
may cause and perpetuate overconsumption. Broad in its scope, it describes the
various behavioral, biological, and social rewards of food. The chapters will cover
topics ranging from the neurochemistry that underlies food reward, to the hotly
debated concept of “food addiction,” while providing relevant and up-to-date infor-
mation from the current body of scientific literature regarding food reward.
When designing both effective prevention and treatment strategies for overeat-
ing and obesity, it is important to address multiple possible factors that may con-
tribute to their development and maintenance. To date, behavioral treatments
have not shown very much long-term success; however, a better understanding of
the rewarding effects of “hyper-palatable” food may inform and improve current
treatment approaches. The content of this book is aimed at other scientists, medical
doctors, practitioners, and those in the general public who are interested in learning
about the hedonic factors that drive eating and may contribute to pathological eating
patterns. The material covered throughout offers another perspective on the current
understanding of the issues of overeating and obesity rooted in scientific research,
and may provide insights that can inform treatment or prevention strategies.
( xi )
AC K NOW L ED GMEN T S
First and foremost, I would like to thank the contributing authors for their chap-
ters. Each chapter adds a unique contribution to our understanding of Hedonic
Eating, and I am thankful to have had the opportunity to work with such a great
group of colleagues.
I would also like to thank Chris Reid and the team at Oxford University Press for
their patience and enthusiasm for this book.
I would sincerely like to thank Alastair Tulloch for his assistance with organiz-
ing this book. His organization and dedication to this project made it all possible.
Appreciation is also extended to other members of my laboratory (present and
past), especially Susan Murray, Nicole Diaz-Segerra, and Cindy Kroll, for their com-
ments and assistance on several different sections.
And last but not least, I would like to thank my family, Eamon and Stella, for
their patience, support and encouragement in this project (and everything else).
( xiii )
CON T R I BU T OR S
Nicole M. Avena Pranish A. Kantak, B.S.

Assistant Professor, Department Department of Nutrition, University of
of Pharmacology and Systems North Carolina at Chapel Hill
Therapeutics, Icahn School of
Kathleen L. Keller, Ph.D.
Medicine at Mount Sinai
Assistant Professor, Department of Food
Kent Berridge, Ph.D. Science and Department of Nutritional
Professor, Department of Psychology, Sciences, Pennsylvania State University
University of Michigan
Margaret Leitch, Ph.D.
Kyle S. Burger, Ph.D., MPH, RD Assistant Professor, University of Calgary
Assistant Professor of Nutrition,
Ashley Mason, Ph.D.
Department of Nutrition, University
Osher Center for Integrative Medicine,
of North Carolina at Chapel Hill
University of California, San Francisco
Alexis Conason, Psy.D.
Kevin Myers, Ph.D.
Licensed Psychologist and Research
Associate Professor of Psychology,
Associate, Mount Sinai
Psychology Department, Bucknell
St. Luke’s Hospital
University
Elissa Epel, Ph.D.
Susana Peciña, Ph.D.
Associate Professor, University of
Associate Professor of Psychology,
California, San Francisco
Department of Behavioral Sciences,
Ashley Gearhardt, Ph.D. University of Michigan
Assistant Professor, Department of
Abigail J. Sanders, B.S.
Psychology, University of Michigan
Department of Nutrition, University of
Allan Geliebter, Ph.D. North Carolina at Chapel Hill
Mt. Sinai St. Luke’s Hospital, and
Emily Sullivan, B.A.
Department of Psychology, Touro
Mt. Sinai School of Medicine
College and University System
Wendy M. Stein, B.S.
Annette Horstmann, Ph.D.
Department of Nutritional Sciences,
Max Planck Institute for Human
Pennsylvania State University
Cognitive and Brain Sciences and
Integrated Research Treatment Alastair Tulloch, M.S.
Center Adiposity Diseases, Department of Pharmacology,
University of Leipzig Mt. Sinai School of Medicine
( xv )
Hedonic Eating
C H A P T ER 1
w
Introduction
NICOLE M. AV ENA
W hat is the purpose of food? Without a doubt, food is a necessity of life. We need
energy to live, and that energy comes in the form of calories contained in the
foods we consume. These calories are typically found in three primary forms: car-
bohydrates, fats, and proteins. To maintain the appropriate levels of energy that
will allow us to function normally, it has been posited that we should follow a sim-
ple formula, or energy balance equation. This balance of energy takes into account
our basal metabolic requirements, our expended energy from activity, and thermic
energy of food. It is only logical, then, that human beings have evolved with skills
needed to acquire food, and have developed internal signals, whether conscious or
subconscious, designated to either suppress or enhance our desire to eat.
When we look at the timeline of man, it was not all that long ago that hunters
and gatherers roamed the Earth foraging for vegetation and hunting animals to
eat. These individuals expended energy to obtain foods that were not typically ca-
lorically dense. As a result, their expenditure of energy was, on a good hunting day,
in close balance with their consumption. Moreover, the typical diet of hunters and
gatherers was quite different from the diets of today (see Table 1.1).
Over time, many things have changed in our environment that do not solely
influence how we acquire our food. Advances in agriculture and modern farming
techniques have allowed us to grow massive quantities of food with less effort than
was needed in the past. We also now are afforded with the ability to preserve our
foods for consumption at a later time. In addition, our food environment itself has
changed, and will continue to change in dramatic ways. Foods as we know them
today are very different from those of our ancestors, even those from just a genera-
tion or two ago. Today, many of the foods that are consumed are highly processed
combinations of ingredients and chemicals. Food scientists work to create various
combinations of tastes engineered to be desirable, satisfying, and, in most cases,
inexpensive. Foods like corn and wheat are processed and transformed from their
(1)
( 2 ) Hedonic Eating
Table 1.1 NU T R I T IONA L COMPA R ISONS

Ancestral Contemporary Western
Total energy intake More Less

Caloric concentration Very little Much
Dietary bulk More Less
Total carbohydrate intake Less More
Added sugar and refined carbohydrate Very little Much more
Glycemic load Relatively low High
Fruit and vegetables Twice as much Half as much
Antioxidant capacity Greater Lesser
Fiber More Less
Soluble:insoluble Closer to equal Far more insoluble
Protein intake More Less
Total fat intake Equivalent
Serum cholesterol-raising fat Less More
Total polyunsaturated fat More Less
Ratio of ω-6: ω-3 Closer to equal Far more ω-6
Long-chain essential fatty acids More Less
Cholesterol intake More Less
Micronutrient intake More Less
Electrolytes Much more potassium More sodium
Acid-base effect (NEAP) Alkaline Acidic
“Dairy” products Mother’s milk only Considerable
Cereal grains Very little A great deal
Free water intake More Less
Abbreviation: NEAP, net endogenous acid production

Adapted from Eaton SB, Konner MJ, Cordain L. Diet-dependent acid load, paleolithic [corrected]
nutrition, and evolutionary health promotion. The American Journal of Clinical Nutrition, Feb
2010;91(2):295–297. Reprinted with permission from The American Journal of Clinical Nutrition.
original form, and combined with sugars, fats, salt, and other ingredients to yield
low-cost, high-energy foods that line our grocery store shelves.
At the same time that our foods and food environments have evolved, so, too,
has the purpose of food. Aside from being a necessity for life, food has taken on new
purposes. Food is essential for life and health. Yet consumption of excess quanti-
ties of certain types of foods can be detrimental to one’s health. Overeating to the
point at which food intake is causing harm suggests that people are not eating out
of energy needs, but for some other purposes. The ease with which one can procure
food, coupled with the changes in its taste, both of which have been the result of our
modern food engineering, have potentially led food to serve other purposes. Studies
show that people report eating out of boredom, loneliness, as well as sadness,1–4 and
others suggest that people use food to relieve anxiety and alleviate depression.4
There is an old adage that says “Food is the best medicine,” and in many cases we
I ntroduction ( 3)
are seeing this come to fruition in the form of people self-medicating depression
and anxiety with food.
How can food have these powers? The goal of this book is to explore this ques-
tion using the framework of the existing scientific literature on what motivates our
appetite and how these activities intersect with the brain’s reward functions. With
this information, we may be able to better understand the mechanisms that drive
eating for pleasure, and this may be useful when considering treatment for some
cases of overeating and obesity.
Hedonics: The Psychology of Pleasure
Hedonic psychology, or the study of the psyche of happiness, pleasure, and

well-being, is a relatively new field in a discipline that has a history of focusing
on abnormal behaviors (e.g., mental illnesses). In recent years, there have been
new movements to study hedonic psychology, and the closely related field of posi-
tive psychology. 5,6 Hedonic or positive psychology has been applied to thinking
about a variety of concepts, from moral and economic decisions, to issues in the
workplace.7
Hedonic psychology is essentially the study of pleasure. However, from a basic
science standpoint, we know relatively little about the construct of pleasure. From a
neurobiological perspective, pleasure is something that is difficult to define and as-
sess, especially in laboratory animal models. Furthermore, it seems that “pleasure”
is often defined as synonymous with terms like “pleasantness” and “happiness,”
which actually may have different meanings and in an experimental setting be
measuring different things.8 Rozin nicely defines pleasure as “a positive experi-
enced state that we seek and that we try to maintain or enhance.”8 Here, “hedonic”
will be defined in this way, and used interchangeably with “pleasure.”
What Is Hedonic Eating?
Pleasure comes in many forms, and we derive pleasure from many different sources.
Pleasure can be found from a career, companionship, or an athletic event, just to
name a few examples. While the primary purpose of food is to provide us with
the calories and nourishment needed to subsist, the basic biology of food intake is
closely tied to pleasure for several reasons. First, we need food to survive; so eating,
particularly when one is hungry or starved, is inherently reinforcing. Second, since
humans are omnivores, we have to learn to eat in ways that will provide the appro-
priate balance of nutrients available amid an array of food choices. Thus, we derive
momentary and medium-term health rewards for finding, and eating, nutritious
foods.9 Third, in modern times in particular, we are seeing that food serves pur-
poses other than energy needs. People may eat for reasons that are not calorically
driven. People eat out of social pressure (such as when you are coaxed into taking a
taste of a friend’s meal), or even out of boredom or loneliness.10
+100%
Sweet
Pleasant
+50%
Sou
Unpleasant
r
–50%
Salt
Bitter
–100%
Stimulus Concentration
Figure 1.1:
The preponderance of “pleasant” or “unpleasant” judgements in relation to the
concentration of taste solution. Ordinate axis gives percentage “pleasant” minus percentage
“unpleasant.” The abscissa is proportional to concentration, the full length of the baseline
standing for 40% cane sugar, 1.12% tartaric acid, 10% NaCl, and 0.004% quinine sulphate
(by weight).
Reproduced from Pfaffmann C. The pleasures of sensation. Psychological Review. Jul 1960;67:253–268. All
content is in the public domain.
In addition, our brains are developed to perceive certain tastes that are pleas-
urable. Our gustatory sense for sweet taste is innately hedonically positive (see
Fig. 1.1).11 Hedonic responses to mixtures or tastes are not easy to predict. For
example, combinations of sweet and fat have an optimal level,12 but that level is
not the maximum for each, as one might suspect. Furthermore, studies of taste
combinations that are more like what is seen in the foods humans tend to eat sug-
gest that there is a lot of variability in pleasantness ratings among individuals.13
Moreover, whether or not a food is considered to be pleasurable depends on the
context in which it is presented. The internal context of hunger may be the pro-
foundest mediator. Foods that might otherwise be unappealing to an individual
can be extremely rewarding and pleasurable to consume if one is hungry. In con-
trast, if one is sated, foods that would be appetizing and desirable to consume
might be viewed as less appealing. When we are ill, we may not desire foods that we
would normally like to eat. The point here is that a given food can be pleasant or
unpleasant, depending on our internal state.14
External factors also have a profound impact on the hedonic valence of a food.
Simple information about healthy food aspects can sometimes increase the desire
for a certain food: low-fat labels or other indications of improving health may
increase the “liking” of these foods. Moreover, information-based expectations of
how a food tastes (e.g., whole milk versus skim milk) affects a food’s valence.
Social influences also play a role in valence, including (but not limited to) beliefs,
I ntroduction ( 5)
culinary traditions, eating in the presence of others, and the establishment of

family food rules. Social facilitation of increased food intake is a particularly
important aspect of these social influences. Lastly, the physical environment,
which encompasses food availability and accessibility, also affects food hedon-
ics. Limiting access to certain foods (usually highly palatable foods) will often
shift people’s food choices to another food. Whether factors occur internally or
externally, the hedonic value of food clearly changes, leading to the concept of
hedonic eating.
“Hedonic eating” is a relatively new term. It is derived from the concept of hedo-
nism, which by definition is the doctrine that pleasure or happiness is the sole or
chief good in life. Hedonic eating is a form of eating in which one eats for pleasure
rather than for energy needs. The desire to eat solely to reproduce the pleasurable
feelings associated with particular foods activates the reward circuits of the brain,
the details of which will be described in this volume. While scientific research on
the endogenous motivating factors associated with hedonic eating is incomplete,
the existing literature provides a convincing argument that hedonic eating is not
only prevalent in today’s society, but significantly contributes to the overall health
of our population as well. Most importantly, hedonic eating is associated with the
pandemic issue of obesity.
Obesity and Hedonic Eating
In the United States and throughout the world, we are in the middle of an uncere-
monious proliferation of unhealthy weight gain. The United States is facing obesity
rates of 34.9%, and over two-thirds of the American population are overweight.15
One of the contributors of this upward trend in obesity is thought to be hedonic
eating, or in this case, overeating. Individuals typically overeat highly processed
foods filled with empty calories from added carbohydrates and fats. Chronic ex-
posure to such foods often causes drastic changes in our brain’s reward circuitry
and may lead to bingeing behaviors and a net positive energy balance. Ongoing
research is striving to understand the reward processes associated with the rapidly
changing food environment and how targeting these complex networks may pre-
vent and treat obesity. Despite the novelty of the concept of hedonic eating and its
association with obesity, researchers around the world are studying how to resolve
and overcome this pandemic. This book explores the relationships between hedonic
eating and our environment, our neural processes, and our behaviors from the per-
spective of experts in the fields and subjects directed linked to hedonic eating, par-
ticularly with regard to obesity.
OVERVIEW OF THE REST OF THE BOOK
The purpose of this book is to review the literature on various topics that relate
to the concept of hedonic eating. Throughout this book, eating for pleasure as
opposed to energy needs will be discussed and contrasted, especially regarding

the associations between hedonic eating and maladaptive behaviors and health
complications.
• Chapter 2 discusses learned responses to tastes and flavors, which generally steer
choice and promote the intake of calorically dense foods. A thorough understand-
ing these learning mechanisms helps explain specific ways that the modern food
environment promotes overeating.
• Chapter 3 will discuss the neural circuitry that underlies reward-related food in-
take. It will discuss the complex systems regulating the motivational value of
food and obesity-associated alterations in many of its components, making the
argument that it is likely that hedonic responses to food are no longer adjusted in
accordance with homeostatic needs in obesity.
• Chapter 4 reviews literature addressing how food cravings differ across a variety
of individual differences, as well as environmental, biological, behavioral, and
psychological triggers of food cravings. This chapter also reviews measures and
methods commonly used to assess food cravings.
• Chapter 5 will describe the construct of “hedonic overeating.” It will define what is
meant by “overeating,” and describe the psychobiological factors that contribute
to excessive food intake. It analyses the early theories of eating motivation, the
bases of pleasure-driven eating, and how intermittent excessive consumption of
highly palatable foods can reduce inhibitory control, perpetuating cyclical over-
eating habits.
• Chapter 6 will discuss the reported effects of overeating on brain reward sys-
tems and examine possible hedonic eating risk factors, brain-based predictors
of weight gain, correlates of eating behavior, and neural consequences of weight
gain and obesity.
• Chapter 7 reviews the identification of brain reward substrates of food pleasure
and desire, and how food becomes “liked” and “wanted” as well as how these two
systems interact with hunger and satiety mechanisms to influence eating. This
chapter also details how dysfunction of “wanting” and “liking” systems might
lead to overeating.
• Chapter 8 will focus on some of the research examining the effects of diet-
ing behaviors involving hedonic deprivation. It also provides an argument for
mindful eating, which has shown efficacy at reducing overeating behaviors and
managing weight in a sustainable way without the negative effects commonly
associated with weight-loss dieting.
• Chapter 9 will discuss the modern food environment that exists in many indus-
trialized societies and how specific aspects of this environment may influence
our food choices. This chapter will discuss artificially enhanced foods, food ad-
vertising, and other food cues that can pervade modern societies.
• Chapter 10 will discuss the current scientific literature that suggests many
neurochemical and behavioral commonalities between overconsumption of pal-
atable foods and drug addiction, using data from both preclinical and neuroim-
aging studies.
I ntroduction ( 7)
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Psychology. New York: Russell Sage; 1999.
8. Rozin P. Preadaptation and the puzzles and properties of pleasure. In: D Kahneman,
Diener E, Schwarz N, eds. Well being: The Foundations of Hedonic Psychology. New
York: Russell Sage; 1999:109–133.
9. Rozin P, Schulkin J. Food selection. In: Stricker EM, ed. Handbook of Behavioral
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C H A P T ER 2
w
Why Do We Eat What We Eat?
K EV IN M Y ER S
E very August on the rugged high coast of Sweden, the balmy fragrance of sea-
shore and spruce forest is overtaken by a pungent mixture redolent of rotten
eggs, rancid butter, sweat, and ripe fish. It hisses from bulging cans that are pried
open for the annual festival of Surströmming, a soured herring beloved in the re-
gion. “Soured” is a bit euphemistic. Aggressive anaerobic fermentation swells the
cans with hydrogen sulfide and butyric and propionic acids. Tourists snap pho-
tos of uncontrollable grimaces (or worse) triggered by their cautious first bites.
In 1991, a German court hearing a landlord–tenant dispute ruled the aroma of
Surströmming so offensive that it constitutes a nuisance beyond what neighbors
could be reasonably expected to tolerate. Yet many Swedes joyfully gobble up the
fish at summertime parties in an animated affirmation of neighborly fellowship
and national pride.
At the same time of year, market stalls throughout Southeast Asia are piled high
with a heavy, melon-sized fruit called durian. The thick husk studded with spikey
thorns offers visual warning of what is to be found within. Though descriptions of
its intense, complex flavor usually combine terms like sweet, custardy, and caramel
with rotten onion, garbage, turpentine, sewage, and putrid meat, many people snack on
it daily and concoct it into sauces, cakes, pastries, ice cream, and drinks. Particularly
rare cultivars are featured in dishes at exclusive restaurants in Bangkok and Kuala
Lumpur. But not everyone is enamored with durian. It disgusts enough people that
passenger airlines forbid carrying it on board. Signs in the Singapore metro system
prohibit smoking, explosives, and durians.
In my own small town—the very picture of Americana, nestled in the heart of
Pennsylvania farm country—I always offer my out-of-town guests (especially col-
leagues interested in the psychology of food preferences) our peculiar regional spe-
cialty. Scrapple is a congealed breakfast loaf made by rendering the bits left over
after hog butchering. It reflects the early Pennsylvania German settlers’ rather
(9)
utilitarian approach to nutrition. In years, I do not recall ever watching an adult

taste scrapple for the first time who liked it. But to many of us who grew up in this
area, it is the taste of home, and we miss it when we are away for too long.
What accounts for these striking differences in how individuals evaluate the
tastes and flavors of foods? The tremendous diversity in food preferences reflects
a fundamental feature of the sensory-evaluative processes that govern food
choice: experience-dependent plasticity. Humans (and the rats and mice we use
to model the biopsychological building blocks of our behavior) have migrated to
occupy nearly every ecological zone on the planet. Thus individuals are born into
habitats containing such dissimilar collections of flora and fauna that it would be
impossible for any meaningful food-recognition and -evaluation mechanism to be
instinctively wired in by our genetic instructions. Sensitivity to experience early in
development brings preferences roughly in line with what one can expect to find
routinely in one’s macro-environment, or the “food system,” which Rozin describes
as the “massive, behind the scenes” cultural prearrangement from which one is
even capable of choosing.1 Each individual’s unique history of experiences shapes
his or her affective responses to the tastes, flavors, textures, and appearance of
various foods.
Plasticity in food preferences reflects our evolutionary history as generalist
omnivores. There are no nutritionally complete foods, so variety is essential. A few
basic taste sensations from sugars, starches, fats, and proteins only allow rough
assessment of caloric content. Even then, people are fairly inaccurate at judging
the energy density of foods.2,3 There are no universal sensory labels for many es-
sential nutrients, and many potential toxins exist at low levels, so relying on in-
nate taste recognition would be infeasible. Experience with a food is necessary to
transform sensory properties that were not innately attractive into “labels” for the
food’s quality.
The most obvious way that liking for a food affects its intake is by influenc-
ing which foods are selected, especially when procurement costs are relatively low.
Meta-analysis shows that across a wide range of foods, experimental manipula-
tions of palatability predictably change relative preference. For any two foods, the
difference between palatability ratings generally predicts the difference in how
much participants will eat of each one.4 But it would be a mistake to view palata-
bility as the sole determinant of preference. Highly liked foods are often eaten in
small quantities or avoided altogether out of concern for health, weight gain, or for
complex ethical or religious reasons. Thus it is essential to recognize that “liking”
is but one influence on choice and intake. Moreover, causal links between liking
and consumption are almost always bidirectional. In some situations, availability
or cost strictly dictates what is to be eaten, and in turn, sheer familiarity with those
foods establishes liking.
A second way hedonics influence intake is through the dynamic changes in palat-
ability during a meal. Initial exposure to sight, smell, or taste triggers a sensitizing,
“appetizer” effect in proportion to palatability,5,6,7,8 including preparatory digestive
responses and accelerated eating rate. But during a meal, food typically becomes
increasingly unpalatable. This reflects in small part a physiological feedback effect
W hy D o W e E at W hat W e E at ? ( 11 )
from gut satiation signals9,10; gut signals, however, are not absolutely necessary.
Oral exposure to a food’s sensory properties causes specific, habituation-like
decreases in the hedonic evaluation of the flavor, and also willingness to work for
more of that food.11,12 The palatability decrement becomes one causal factor in meal
cessation, and accumulates across meals when the same food is eaten on successive
occasions.13 Thus hedonic evaluation comes to influence one’s choice of foods and
also influences the dynamic control of motivational switching between eating and
other behaviors.
THE IMPORTANCE OF HEDONICS IN THE PSYCHOLOGY

OF TWENTY-FIRST CENTURY EATING
Choice and intake are intrinsically bound up with hedonic evaluation of food’s sen-
sory attributes—the pleasures of tasting, smelling, and feeling food as it is con-
sumed. Understanding hedonic influences becomes especially important now that
technologized food production brings an increasing variety and ease of access to
foods that are specifically designed with sensory appeal in mind. It will always be
difficult to elucidate a causal role of palatability per se in eating patterns, since pal-
atability is neither a physical property of a food nor a fixed response tendency of
the individual, but rather an interaction between the food, the external context,
and internal signals for current physiological state.14,15,16 Nonetheless, virtually all
acts of eating generate some degree of sensory pleasure.
This is illustrated by the fact that many people will pay an equivalent price for
artificially sweetened versions of liked foods or drinks. Operant studies show a
powerful reinforcement effect of non-nutritive sweeteners,17 which can exceed
that of cocaine,18 demonstrating that caloric consequences are not necessary for
sweet taste to maintain food-seeking behavior. Since the spending on artificially
sweetened products like diet soda is not offset by compensatory increased spending
on calories in ordinary foods,19 a behavioral economic perspective suggests that
people, at least “health conscious” ones, are often willing to pay a caloric cost to
obtain sweetness per se.
The importance of sensory pleasure is further illustrated by consequences of
removing it. Nutrients infused intravenously or via nasogastric tube (therefore not
tasted, chewed, or swallowed) are generally less satisfying. In studies of healthy
volunteers, tube-fed participants still consume near-normal meals when permit-
ted to do so.20 In long-term clinical cases, tube-fed individuals become preoccupied
by food cravings.21 Healthy volunteers who consumed nothing for several days ex-
cept a sweet, nutritionally complete drink experienced cravings caused by lack of
sensory variety.22 During a chocolate craving, it is only the tasting, smelling, and
eating of chocolate, rather than its post-ingestive effects, that satisfy the craving.23
Thus, not only will people pay a significant cost to obtain taste pleasure, but nutri-
tional repletion without oral stimulation is unsatisfying, and sensory deprivation
can powerfully stimulate interest in food and evoke mental imagery of food’s desir-
able sensory characteristics.
Understanding hedonic processes is necessary for insights into why individuals

are more or less affected by the modern food environment. People differ in their pre-
ferred amount of sensory stimulation in daily life, known as “sensation-seeking.”
But sensory novelty, complexity, and pleasure can come from both food and
non-food sources, and people differ in the importance of eating as their main
source of that sensory stimulation. Some people describe eating as one of the most
pleasurable activities available, while others would gladly opt to take daily nutri-
tion pills instead of eating at all.24 This is likely to be a developmentally plastic trait,
since it varies across cultures in a manner consistent with prevailing local attitudes
about diet.25
Individual differences in hedonic processes have become a main focus of
research because of the provocative but sometimes contradictory evidence linking
food hedonics to overeating and obesity. Although it is undoubtedly true that a typ-
ical person is inclined to eat more when a given item of food is made to taste better,
it is not clear whether or not obese people perceive food as tasting better in general,
nor whether such differences play a causal role in obesity. Obese individuals may
experience more pleasure from sweetness than do lean individuals, especially when
compared to pleasure derived from non-eating activities.26 Other methods have
linked obesity to sensory preferences for fat and sweet-fat mixtures27,28 or inversely
to liking fruits and vegetables.29 But in contrast, there is also evidence that obese
eat more because they experience less reward from food.30,31 It also needs to be de-
termined whether differences in subjective pleasure from food act as a preexisting
causal factor in overeating, or instead are established by a history of overeating.
Unravelling the complex links between hedonic evaluation, diet history, and weight
status is now a major focus of research on the obesogenic effects of the modern food
environment.
STIMULUS ATTRIBUTES IN FOOD HEDONICS

Sweetness and Fat
Scientific and everyday conversations about food enjoyment and preference usually
begin with sweetness and fat, and for good reason. As biologically significant mac-
ronutrients, sugars and fats are laden with intrinsic positive value and contribute
directly to palatability. Sweet–fat combinations have especially potent appeal to
many.27,32
The pleasure of sweet taste is generally regarded as “hard-wired” at the
start. For newborns, sugar stimulates mouthing and characteristic hedonic fa-
cial expressions,33,34 and has calming, pain-relieving effects. 35 This is seen prior
to any nursing experience,36 and even in infants delivered prematurely.37 Infant
rats respond to sweet taste with vigorous mouthing and swallowing, with a linear
concentration-response function evident by the time they are six days old.38,39 Even
in the womb, embryonic rats respond positively to saccharin.40 While response to
sweet tastes can change with experience, prior experience eating sweet foods does
not appear to be necessary for infants to regard sugar as palatable.
Liking for sweetness is highest during childhood and declines throughout ado-
lescence.41 By adulthood, individual differences are evident both in sensitivity to
detecting sweetness and in liking different amounts of sweetness,42 due in part
to early feeding experiences. For example, higher average sweet-liking among
African-Americans has been linked to the cultural practice of providing infants
with sweetened water, as that practice increases sugar-liking in infancy and later in
childhood, regardless of ethnicity.43,44 Parent–child interactions later in childhood
also have an effect, ironically such that stricter parental restriction of sweets is
associated with children’s subsequent choice of higher sweetness levels.45
Despite the presumably innate origins of sweet-liking, large cultural and ge-
ographic differences are evident. In economically advanced countries, sugar
consumption per capita varies nearly twenty-fold, ranging from 3.3 kilograms an-
nually in South Korea, to 64.4 kg in Israel.46 The United States (33.1 kg) is near the
median, and East Asian countries (Japan, Hong Kong, Taiwan) are consistently the
lowest. Cross-cultural patterns in taste-liking are generally not a consequence of
basic differences in taste detection or intensity perception, but rather in prefer-
ence,47 and tend to parallel the frequency of exposure to foods.48 Sweet-liking is
largely food-specific, since children learn through exposure that sweetness is ap-
propriate in some foods but not others.49
Like sugar, fat also contributes to food palatability. The sensations that make fat
palatable are less well defined, but include gustatory, olfactory, and somatosensory
inputs.50,51,52 Rats avidly consume mineral oil emulsions or diets adulterated with
petroleum jelly,53,54,55 which shows subjectively positive properties independent of
nutritive value, much like the non-caloric sweeteners. Also like sweetness, there
are wide individual differences in fat-liking. This becomes evident in childhood and
may be linked to children’s nutritional or weight status. Children’s fat intake cor-
relates with liking, but perhaps more importantly, with their parents’ adiposity.56
This suggests a possible link in the familial transmission of weight status.
It is sometimes assumed that the perceived palatability of fat is innate, like
sweetness, but the evidence for that is rather ambiguous. Animal studies that
can carefully monitor the development of sweet and fat responses show that they
differ in several important respects. First, fat palatability emerges much later in
the pre-weaning period53,57,58 and increases with maturation, unlike sweet-liking,
which is initially high. The central dopaminergic circuits that mediate intake stim-
ulation by sugars and fat in adulthood are sensitive to sucrose at a much earlier
age than to fat.59,60 Also, the shape of the concentration-response function differs
substantially from that for sugars. In sham-feeding studies of oral reward, intake of
sweet solutions increases monotonically as a function of concentration. In contrast,
the function for corn oil has an inverted-U shape.55
Another curious feature is that infant rats are capable of detecting and perceiv-
ing fat well before the time they start treating it as palatable. Ten-day-old pups,
which do not hedonically respond to fat ingestion, do respond to fat taste in other
ways, such as ultrasonic vocalization61 and anti-nociceptive responses.62 Even
younger pups learn to prefer odors paired with intraoral infusion of corn oil.63
Thus, unlike for sugar, which is palatable as early as sweet can be tasted, for infants
(at least in animal models used for these studies), there may be a period where fat
is detectable and possibly rewarding in some respects, but not especially palatable.
Ultimately, while sugar and fat are calorie sources that form the foundation
of food-liking, the evidence all suggests that responses to sugar and fat have dif-
ferent origins, and that fat palatability may depend more on early experience. Since
infants rely on nursing as their sole source of nutrition and hydration, it is feasible
that ubiquitous experience may be critical in establishing fat palatability.
Flavor
Something puzzling about food choice and hedonics is that, despite claims about
the prepotency of sugar and fat palatability’s stemming from our evolutionary his-
tory, the fact is people almost never routinely consume plain sugar or fat, either
alone or in combination. The closest thing—cake frosting—may feature in binge
eating episodes, but is never routinely consumed on its own by healthy people, and
is actually made more attractive by adulteration with vanilla or other flavorings
that have no intrinsic biological significance. As a treat, white chocolate (almost en-
tirely sugar and fat) is considered a poor substitute for true chocolate, which differs
physically only due to cocoa, which adds complexity of flavor and aroma but has no
intrinsic nutritional value to justify its appeal. In fact, pure cocoa on its own would
be initially repellent to naïve individuals due to its inherent bitterness. Considering
sweet beverages like sodas or fruit drinks, without the proprietary blend of flavor-
ings that turns carbonated sugar-water into cola, or the squirt of lemon that makes
it lemonade, most consumers would just opt for “plain” water or nothing at all, not
unflavored sugar-water. Thus it is genuinely insufficient to view intrinsic palata-
bility provided by sweetness and fats as sufficient to drive preference. There needs
to be more. People like and seek the complex contributions of flavor in foods.
Flavor refers to the perceptual experience created by synthesis of the simpler
oral sensations—the basic tastes combined with odors, and also the trigeminal
touch senses in the mouth which convey a food’s textural, temperature, and chem-
ical irritants like hot pepper. The olfactory system can detect and discriminate
an extraordinarily wide range of distinct odors,64 far outnumbering the few basic
tastes, and thus the volatile odor molecules released from a food contribute much
to its unique flavor, and experimental study of flavor perception usually manipu-
lates odorants. Odors can be detected from a distance, making them useful for food
identification, but they also contribute to flavor during chewing and swallowing
by traveling a retronasal route. When oral sensations and odors synthetically com-
bine, it creates the perceptions that people mistakenly think of as “taste,” because
the brain refers the experience to the mouth.
This perceptual confusion about the taste vs. olfactory components of food
flavor demonstrates the top-down nature of flavor perception that results from
learning. Odors commonly encountered in the context of food flavorings are typi-
cally perceived as having taste attributes. For instance, the vanilla and strawberry
odors seem “sweet,” and lemon “sour,” although nothing inherent in the odorants
triggers coding of those taste characteristics. Adding one of those “sweet” odors
as a flavoring in a sugar solution causes people to perceive the solution as signifi-
cantly sweeter. Yet “non-sweet” odors of similar intensity do not produce this ef-
fect, nor do “sweet” odors enhance the perceived intensity of a non-sweet solution
like salt.65,66 Exposure to some odor-based food flavors is so consistent that it is
probably impossible to experience familiar food odors as they “truly” are, because
these inevitably and automatically call up compound memory representations of
other food attributes.
In contrast to the well-established hedonic or aversive responses to basic tastes
like sweetness and bitterness, most food flavors are not strongly attractive or
aversive until experience makes them so. Since odors are a primary constituent
of food flavor, the development of olfactory perception is instructive. Newborns
have a fairly well-developed capacity for olfactory perception (see reviews67,68) and
do show autonomic reactions and behavioral orienting to many odors. But they do
not typically respond with the same behavioral indicators of hedonic valence to
food-related odors that adults would give, even though infants are clearly capable
of showing such reactions to basic tastes.69 When infants encounter odors like va-
nilla in novel situations, responses are correlated with prior exposure,70 suggest-
ing the critical role of early experience in establishing their attractiveness. Positive
and negative hedonic reactions do begin to emerge in infancy, but not until later in
childhood does the intensity and valence of hedonic responding resemble that of
adults.68,71
Though largely experience-dependent, there are some direct genetic contribu-
tions to individual differences in food evaluation. Most seem to work through
basic taste perception, and broadly speaking, the twin and family studies suggest
the biggest influence is on liking for macronutrient tastes generally (e.g., sweet-
ness), not liking for specific food items.72 Heritable variation in the taste receptor
gene TAS2R38 and in anatomical differences in taste papillae morphology shapes
food preference indirectly, such as by reducing liking and discouraging vege-
table intake among individuals who are especially sensitive to the bitter tastes
in vegetables,73 and by influencing perception of and liking for fat sensation.74,75
Sensitivity to some food-related odors does differ due to variation in some olfac-
tory receptor genes, and this may influence acceptability for some foods.76 Among
the very few known examples of genetic differences in evaluation of a specific
food, cilantro is an interesting case, because opinions about cilantro are so polar-
ized. Variation in a chromosomal region that encodes several olfactory receptors is
strongly correlated with perception of cilantro as either “herbal” or “soapy.”77 But
these genetic differences largely cause different people to perceive things differ-
ently, and therefore cannot explain the more common scenario wherein different
people may agree on how a food tastes and simply have opposite reactions in how
much they enjoy it.
In summary, olfactory stimulation is a major input into food flavor perception
and is what enables rather fine discriminations between the flavor characteristics
of a very wide array of actual or potential foods. Consistent with our evolutionary
history as generalist omnivores, hedonic evaluation of flavor is not predetermined,
and is mostly shaped by experience. So what sorts of experience in particular are

most critical and influential?
DETERMINANTS OF PREFERENCE
Prenatal Experience
Experience shapes preference from the time that the olfactory and gustatory sys-
tems become functional in utero. Animal models have established the importance
of prenatal olfactory learning for normal development. In rats, odors present in
amniotic fluid guide orienting and nipple attachment in the critical minutes after
birth.78 For humans, olfactory memories formed from prenatal experience are
retained after birth, as neonates can behaviorally discriminate the odor of their
own mother’s amniotic fluid from that of unfamiliar women.79 Volatile odor and
flavor compounds in the food that a pregnant woman eats appear in the amniotic
fluid and alter its odor.80
Flavor exposure in utero produces lasting changes in appetitive and hedonic
reactions to those flavors after birth. Animal studies that allow strict control of
the maternal diet have demonstrated this effect in several species,81,82,83 and it
is observed in humans as well. Newborn infants born to mothers who routinely
consumed anise-flavored foods and drinks while pregnant exhibit more positive
facial expressions, mouthing, and sucking when tested with anise odor.84 In an-
other study, infants whose mothers had been randomly assigned to consume carrot
during pregnancy reacted more positively to carrot-flavored cereal at the age of
four months.85 Importantly, these studies find shifts in infants’ facial reactivity to
the target flavor, indicating effects on hedonic evaluation.
As a means for transmitting food acceptance across generations, prenatal
flavor-learning arguably represents the first and most basic way that local culture
identifiably shapes individual habits and preferences. These early effects are especially
important because even subtle shifts in the valence and vigor of flavor responsive-
ness will affect the mother–infant dyad during postnatal feedings, amplifying and
perpetuating initial tendencies. Yet the biopsychological mechanisms underlying this
learning are unknown. Exposure of the still-immature olfactory circuitry during fetal
development may direct its connectivity during a unique sensitive period. But there is
little evidence that responses to flavors experienced in utero are qualitatively different
in form or function from memories acquired after birth (e.g., Menella et al. 200185).
Another possibility is that simple familiarity habituates innate neophobic responses.
In animal studies, prenatal exposure to a flavor of the weaning foods does reduce be-
havioral and physiological indicators of stress during the weaning period.86
But since fetal rats are also capable of learning aversive flavor associations,87
it is possible that something more elaborate than simple familiarity is occurring.
Dietary odors appearing in utero come to elicit ingestion-specific facial affective
responses, as opposed to general orienting responses, which implicates neural sys-
tems involved in appetite specifically, rather than a general recognition memory.84
This may represent a form of operant learning in which the odor/flavor cue comes
to elicit motor responses that are innately triggered by nutrient influx, especially
plasma glucose that would follow a maternal meal.
Neonatal Experience
Immediately after birth, the mother continues to provide experiences preparing

the infant to recognize and accept foods of the local environment, since flavor com-
pounds of the maternal diet are also transmitted via milk. Infant behavior while
nursing shows that they can perceive and are affected by the changing flavor char-
acteristics of milk.88,89 Specific flavors consumed by the mother at this stage subse-
quently elicit more hedonically positive reactions in solid foods at weaning.85
For non-human mammals, nursing is the obligate source of nutrition for new-
borns. But for humans, the availability of manufactured infant formulas creates
a distinct point of developmental divergence for some, since formula feeding
produces lasting effects of its own. One main difference in the experience of
formula-fed infants is reduced sensory variety. Though manipulating the sensory
variety of formulas has not been studied experimentally, effects of reduced variety
are likely, since duration of breastfeeding (which provides variety) is inversely cor-
related with food neophobia and picky eating later in childhood.90,91 Experimental
studies in nursing rats and in older children demonstrate that early variety expo-
sure does increase later acceptance of novel foods.92,93
Another effect of formula feeding comes from the specific sensory character-
istics of the chosen formula. Soy- and hydrolysate-based formulations are more
bitter and sour-tasting and some have odors that are unpleasant to adults. Infants
fed these formulas show decreased aversive reactions to cereals adulterated with
sour or bitter tastes, and increased acceptance of sour or bitter foods and drinks
later on. This early experience also alters childhood preferences for vegetables that
share taste or odor characteristics of the formula.94,95,96
Thus, in some ways, breastfed and formula-fed infants have fundamentally
different experiences, but in each case, sensory experience has lasting effects on
preference. But the effects are complex, since some experiments find more positive
hedonic reactions but reduced intake, at least in short-term test sessions that soon
follow the initial flavor exposure.95,97 Those investigators have proposed this may
be an early form of sensory-specific satiety. Some aspects of learned responding to
the flavor may immediately generalize to other contexts, while other aspects may
take more time to transfer. This is interesting because this is one example of how a
developmental analysis reveals a possible dissociation between aspects of appetite
control that would not necessarily be obvious later in development.
Childhood
Repeated exposure to flavors prenatally and postnatally serves as a bridge to inde-

pendent food evaluation; thus, maternal food choice functionally serves as a filter
that narrows the whole range of possible foods to a smaller, “proven safe” category
that can guide acceptance. After children’s transition to solid foods, parents still
largely control the food environment, and parents’ decisions and behaviors sur-
rounding food continue to be the primary determinant of experience (reviewed in
Savage et al. 2007 and Anzman et al. 201098,99).
As the scope of children’s eating experience gradually expands, previous effects
of early exposure continue to be influential, since familiarity explains most of the
variance in self-described food preferences among younger children,100 and adding
a familiar flavor is an effective way to induce acceptance of a novel food.101 But ex-
perience with foods also begins to incorporate more complex social and cognitive
dimensions. For instance, children begin to internalize cultural notions of appropri-
ateness that make particular foods more or less preferred at different times of day.102
One new influence at this stage is that caregivers begin incorporating foods
into instrumental contingencies, presenting foods either as tasks to complete or
as rewards to earn. Commonly children are instructed to eat a less desirable food
to earn a more desirable food. These strategies usually do not produce the results
caregivers intend.103 Making a reward contingent on eating a particular food does in-
crease intake of that food, but it typically also decreases actual liking for it. Likewise,
using a food as a reward for a task increases liking for the food while potentially re-
ducing intrinsic motivation for the task. Decreased liking for an already disliked
food (e.g., vegetables) that must be eaten to gain a liked food (e.g., dessert) may be
mediated by a perceptual contrast effect between the two. A mental comparison to
the anticipated dessert makes vegetables seem even less appetizing. A more useful
strategy appears to be using non-food rewards or social rewards for eating less-liked
foods, which can better maintain increased preference for specific vegetables.104
Another important new source of influence is interaction with non-family adults
and peers. As children mature, eating increasingly becomes a social activity involv-
ing explicit information exchange and subtler social modeling. In a variety of species,
food preferences are transmitted socially,105 and in humans, social modeling is seen
in experiments using adult and peer-aged models. Simply observing another person
eating a specific food increases a child’s acceptance of it106 and can induce children
to select that food over another that was initially more preferred.107 However, these
social effects may be rather short-lived on their own.108 The power of social mod-
eling probably arises because it produces the initial experience of eating a food that
is sufficient to begin establishing familiarity effects and the opportunity for other,
more durable learning processes that can eventually lead to robust preference.
Associative Conditioning: Flavor-Flavor Learning
Much work on food preferences has focused on infancy and childhood because of the
profound importance of the experiences occurring when circumstances relevant to
eating are largely still novel and there is the most to be learned. Nonetheless, spe-
cific types of associative learning experience can and do continue to modify likes
and dislikes throughout life.
Flavor-flavor conditioning (hereafter, “F-F conditioning”) can occur when a flavor

(the conditioned stimulus [CS]) is consumed along with another taste or flavor that
is already hedonically significant (the unconditioned stimulus [US]). For example, a
novel flavor may itself may be neither liked nor disliked, but when it occurs in a pal-
atable dessert, it may become associated with the dessert’s sweet taste, and the flavor
CS will be more positively evaluated when encountered again. Evaluation can also
shift negatively when the CS flavor is paired with an unconditionally aversive US-like
bitterness.
There are numerous studies demonstrating this effect in rats.109,110,111,112,113
Human studies have shown, for example, increased liking for a non-sweet herbal
tea flavor after it was previously consumed with sugar,114 and decreased liking for
a specific fruit flavor after it was consumed in an unpleasant, soapy-tasting mix-
ture.115 F-F conditioning appears to be a specific instance of the learning process
more generally called “evaluative conditioning,” which makes it resemble the un-
conscious shifts in emotional responses and feelings of attraction or disdain that
can be produced by advertising, political propaganda, and even some interpersonal
processes.116,117
Human studies of F-F conditioning as a whole suggest that it is easier to produce
negative shifts for flavors paired with aversive US’s than to produce positive shifts
with sweet pairing.118,119 An adaptive account based on negativity bias in evalua-
tive conditioning more broadly120 does make some sense for food learning, since
poison avoidance would be a pressing concern for survival, but that is unlikely to
completely explain why positive F-F conditioning is more difficult in humans, since
F-F preferences with sweetness are robust and easy to produce in rat experiments.
It may be important for F-F conditioning studies to distinguish effects on per-
ception from effects on liking. Pairing a flavor with sweetness can cause the flavor
itself to be perceived as sweet, but that would not necessarily cause a person to like
it better. Preexisting differences in sweetness-liking do predict the direction and
strength of hedonic shifts for a sweet-paired odor.121 Learning may also be moder-
ated by cognitive or personality factors, like dietary restraint. One study found that
learned preference shift for a flavor paired with eating a sweet candy was attenuated
in restrained eaters.122 It could be that restrained eaters did not perceive the candy as
pleasurable, or that eating it triggers concerns about dieting that interfere with con-
ditioning. Thus, as a general principle, perception and evaluation of a flavor is altered
by sensory associations with other tastes or flavors that have accompanied it, but
there are clear individual differences in the case of positive conditioning (especially
with sweet tastes). Further work on this topic could benefit from extending studying
positive F-F conditioning with a range of positive US’s other than sweetness.
Associative Conditioning: Flavor-Nutrient Learning
Another associative learning process that shapes preference reflects the value
of Pavlovian conditioning for using sensory cues to predict impending, biolog-
ically significant events. Since a food’s flavor is always experienced before its
post-ingestive effects, associations between specific flavors and nutrients sensed

in the gut or post-absorptively make flavors a useful guide to food choice and the
amount consumed—or at least that would be the function for animals and our
human ancestors searching for nutrition in an environment where foods were of
variable quality. Flavor-nutrient conditioning (hereafter “F-N conditioning”) is a
Pavlovian learning process in which evaluation of a food’s flavor (the CS) is altered
because of its history of pairing with post-ingestive nutritional effects (US’s).
Most of our understanding of F-N conditioning is based on work with laboratory
animal models. Conditioning typically involves a novel CS flavor of modest initial
acceptability, or even one that would be initially disliked. Consumption of that CS
is accompanied by intragastric or intraduodenal infusion through a catheter of a
nutrient such as glucose, the US. The purpose of this flavor+infusion method is
to separately manipulate what is detected in the gut from what is tasted in the
mouth, so that the flavor is becoming associated with the post-ingestive actions of
the nutrient rather than its own inherently attractive taste (i.e., F-F conditioning).
In alternating sessions, a different flavor is accompanied by plain water infusion, to
control for simpler effects like mere exposure. With experience, rats and mice gen-
erally show dramatically increased attraction to that flavor paired with nutrient in-
fusion, and strongly prefer it in a choice relative to the unpaired flavor, even when
it is no longer accompanied by the nutrient.
F-N conditioning occurs rapidly. In fact, several experiments show that posi-
tive preference shift for a flavor paired with nutrition can be learned in a single
trial.123,124 Prior to this finding, it was already clear that one-trial learning could
occur for flavors paired with long-delayed illness, but unlike aversion learning,
F-N conditioning involves post-ingestive US events that onset rapidly, within the
first few minutes of a meal. Soon after the first bite, food begins emptying from
the stomach into the duodenum, and various sensors there respond to its macro-
nutrient content. This detection is psychologically significant. In studies where
rats or mice are accustomed to consuming a solution accompanied by intragastric
water infusion, the first time a new flavor is accompanied by nutrient infusion,
they accelerate intake within minutes and end up consuming a significantly larger
meal.125,126,127 That positive feedback response to nutrients arriving in the gut is not
merely a general stimulation of appetite. Rather, it reflects specific enhancement
in evaluation of the accompanying flavor.125 If the flavor is removed and replaced
with a different one, rats no longer are inclined to continue consuming it. In other
words, within minutes of a flavor accompanied by nutrition, rats already act as if
that flavor seems “better” because of it.
There are several other attributes of F-N conditioning that underscore its im-
portant role. F-N conditioning is probably involved early in development, such as
increased preference for flavors experienced in mothers’ milk, as F-N conditioning
has been demonstrated in pre-weanling rats.128 Preferences acquired through F-N
conditioning are enduring and long-lasting.123,129 Preference shifts produced by F-N
conditioning can be strong enough that rats will begin avidly consuming an ini-
tially aversive taste or flavor (e.g., bitterness, vinegar) that they would have other-
wise avoided.123,130
The rewarding US signal (or signals) supporting F-N conditioning stems from
physiological effect of nutrients, but it is important to recognize that reward is not
a detection of calories per se, because different nutrients are not equally effective.131
Glucose and maltodextrin in particular support the strongest and most rapid pref-
erence learning, with fructose being relatively ineffective. Fat can produce learned
flavor preferences, but when equated for calories with glucose, post-ingestive re-
ward signals from fat are weaker, onset more slowly, and require more experience
to shift flavor preferences.124,132,133
Extensive work by Sclafani and colleagues aimed at identifying the precise
site of nutrient detection that supports F-N conditioning has made use of sur-
gical deafferentations, genetic knockouts of nutrient-sensitive receptors, and
non-metabolizable nutrient analogues. The transduction mechanisms and afferent
pathways have proven difficult to isolate, though pre-absorptive detection in the
proximal intestines through a still-unknown signaling pathway appears to be im-
portant (see Sclafani & Ackroff 2012134 for a complete account of this line of work).
There may also be secondary, longer-delayed mechanisms of post-ingestive reward,
since portal glucose infusion also activates brain areas relevant to food reward and
preference evaluation.135 This is consistent with behavioral evidence that rats ap-
pear to be affected by at least two phases of post-ingestive events in F-N condi-
tioning: a rapid-acting signal affecting flavor perception and evaluation within the
early minutes of a meal (thus presumably pre-absorptive), and then a longer-delayed
signal or signals arising late in the meal or after its cessation.136
The speed of acquisition and powerful, lasting effects on choice and intake all
suggest that F-N conditioning may play an important role in overeating by steering
choice towards more energy-dense foods and by stimulating increased intake once
they are obtained. But does learning a F-N association produce a true hedonic shift,
causing that flavor to be perceived as more palatable? Though this has often been
a presumed mechanism when preference behavior is so robust, the answer to this
question should not be taken for granted. An alternative, for instance, could be
that a flavor has become more capable of capturing attention and eliciting approach
from a distance, thus leading to meal initiation without necessarily eliciting more
pleasure.
The most direct evidence for a hedonic shift in F-N conditioning comes from
taste-reactivity measurements.137,138 One study found that pairing a minimally
sweet flavor with a post-ingestive nutrient reward produced a positive shift in he-
donic taste reactivity that was comparable in magnitude to increasing the sweet-
ness of a solution from 3% to 16% sugar. Other studies have shown the same pattern
of changes in lick microstructure seen when making a sugar solution sweeter.139
Some human studies also show an apparent palatability effect, especially for fla-
vors associated with the satisfaction of hunger.140,141 In several experiments with
children, the young participants begin to place a flavor higher in a rank-ordering of
different flavored foods after they have experienced that flavor paired with added
calories.142,143
But the evidence for positive hedonic shifts in F-N conditioning is not en-
tirely straightforward. In one study,144 participants reported increased liking for
a distinctive flavor in sorbet after previously experiencing that flavor in a drink

containing sucrose (sweet and caloric). But participants trained with the flavor
in a drink with maltodextrin (caloric but not sweet) did not show the same
pleasantness-increase, even though F-N conditioning was still evident as increased
consumption of the flavored sorbet. This suggests F-N conditioning can produce
a hedonic shift under some circumstances, but a hedonic shift is not necessary to
stimulate increased intake. That interpretation concurs with the animal literature.
Some rat studies have found positive taste-reactivity shifts, but other studies have
found large increases in intake and preference without any apparent taste-reactivity
change.145 A common factor across the sorbet study with human participants and
in the rat taste-reactivity studies may be that positive hedonic shifts were only evi-
dent when a sweetened CS flavor was followed by caloric consequences. In any case,
we can conclude that F-N conditioning can shape food intake and meal size through
both hedonic and non-hedonic processes, though more work is necessary to under-
stand why a hedonic shift only sometimes occurs.
The work on F-N conditioning in animal models produces such robust effects
on flavor evaluation and on meal patterns, and there are enough examples of F-N
conditioning in human experiments, that it is difficult to doubt that this is a funda-
mental influence in human food preference. But reliably producing and describing
F-N conditioning effects with human participants in controlled studies has been
challenging, and some studies fail to detect effects. There are a number of reasons
this may be. First, people already have extensive exposure to different foods and
established likes and dislikes for flavors. Conditioning is likely to be much less
effective with familiar flavors. It is also theoretically debatable whether “liking”
should be the main dependent variable, since animal experiments sometimes
find effects on choice and intake without liking. To the extent that liking is in-
volved, the self-report response scales commonly used have dubious psychometric
properties.146
Another possibility involves developmental changes. There are several clear
demonstrations of F-N conditioning in children (reviewed in Birch 1999147). It
is easier to test children with novel foods and flavors for which they have few
prior associations. But, as mentioned previously, from an ecological and adaptive
perspective, early childhood is a critical time for learning. There may therefore
be gradual reductions in plasticity in the neural circuitry involved in F-N condi-
tioning after childhood. It is widely accepted that such maturational constraints
occur in other domains of human learning, like language acquisition.148 But there
are no obvious developmental reductions in the F-N learning abilities of labora-
tory animals.
Additionally, there may be individual differences in F-N conditioning that are
unaccounted for. One study trained participants with two differently flavored des-
serts, with the flavors corresponding to differences in energy density. Only partici-
pants who were low in dietary restraint subsequently rated the high energy-paired
flavor as better tasting. Restrained eaters showed no evidence of differential condi-
tioning.149 It is unclear if some aspect of dietary restraint made those participants
less sensitive to the caloric consequence, or made them respond differently to it.
But either way, it shows that cognitive factors may impair or interfere with effects
of F-N conditioning.
Some conceptual proposals are more speculative, but warrant serious consider-
ation, especially with regard to the limits of animal models for human nutritional
psychology. Some have questioned whether F-N conditioning should be as influen-
tial in governing human appetite as it is in animals, or, at least whether it should
operate in the same way, given major shifts in the organization of eating behavior
that coincide with the advent of human culture.150 For instance, the invention of
cooking offered proto-humans considerable advantages, which depended to some
degree on mental capacity for advanced planning. Cultural changes that allow more
intentional control over the food environment and eating occasions may mark a
quantum leap that required a fundamental shift in controls of choice and meal
size to incorporate explicit decisions about future states, such as expected satiety,
rather than lower-level, more automatic associative shifts in immediate evaluation
of foods’ sensory attributes.151 Thus perhaps an aim of research on flavor-nutrient
conditioning in humans should be to study its effects on more complex beliefs and
attitudes about foods, like expectations that a food will be “satisfying,” or its eco-
nomic utility, rather than sensory enjoyment as such.
Another possibility is that, for most adult humans living in the modern food en-
vironment, the processes underlying acquisition of new F-N associations are simply
little used and poorly rehearsed. This would be consistent with the evidence that
F-N conditioning is easier to produce in children, but that adults still can learn F-N
preferences under some circumstances. It may be the case that in the modern food
environment, beyond the foundational preferences learned in childhood, there re-
mains little opportunity or even need to learn new preferences in adulthood. There
are at least two observations about modern eating that support this idea.
First, for most people most of the time, we really only encounter foods of fairly
high quality. Unlike our ancestors (and in spite of the dubious claims of many
“natural” health gurus), we do not need to be concerned that a food from the su-
permarket will poison us, nor that we will fail to get enough calories. The current
public concern about industrial sugar production stems from the fact that foods
are usually likely to have more calories than we expect them to. If one is selecting
from a wide range of (mostly processed) foods, there is little need to learn to prefer
one food over another based on its nutrient content because it would be nearly im-
possible to self-select a diet that failed to provide adequate calories. The real risk is
the potential adverse effect of overconsumption, but it is not clear the basic mecha-
nisms of F-N conditioning are sensitive to that input. Second, the ubiquity of eating
opportunities means there is very little cost to getting too few calories on any one
occasion, since another meal is usually available for relatively little cost in money
or effort. Thus there is less need to remember which flavors signal the biggest nu-
tritive payoff.
If true, this by no means diminishes the importance of F-N conditioning in food
preference. The totality of the evidence shows that F-N preferences are readily
learned in childhood, which is when most foods are first encountered and when
many long-lasting habits are established, and those preferences can be modified in
adulthood. Ultimately, these proposals attempt to address why F-N conditioning

experiments in adults obtain mixed or weak results relative to the animal models.
This suggests research on animal models of F-N conditioning should incorporate
experimental manipulations that model specific features of the modern food envi-
ronment, and effects of that environment on basic learning processes.
LOOKING FORWARD: APPLICATIONS TO THE MODERN

OBESOGENIC ENVIRONMENT
The ways that food preferences—of cultural groups, of families, of individuals—are

fundamentally shaped by learning reflect the challenges and constraints on food
availability during our evolutionary history. Now, the propensity to overeat and
maintain extra weight is commonly viewed as resulting from the mismatch be-
tween our inherited tendencies for coping with scarcity, and the new, biologically
bizarre circumstances in which high-calorie food is easy to come by. Thus it becomes
important to identify the ways in which the learning mechanisms that promoted
adaptive control of food recognition, choice, and meal size in ancestral environ-
ments are affected by dietary excess.
Features of the Modern Food Environment
There are several important features of the modern food environment that pose
a challenge. Many modern foods are not grown or produced so much as they are
“designed,” and this process is aimed at maximizing inherent palatability. The
global food manufacturing enterprise uses techniques of chemistry, engineering,
psychology, and mathematics to produce formulations that optimize consumer en-
joyment. The vast scale of food production and retailing makes food less expensive
than ever before. Even though people are buying and eating more food, it repre-
sents only 15% of Americans’ spending, compared to over 40% in the 1960s.152
Doubly problematic is that food processing, which adds sugar and fat, also makes
foods cost less per calorie.153 Food is also easier to obtain. Shelf-stable processed
foods can be purchased ahead, allowing people to keep a pantry full of snacks and
meal items in their homes at any given time. Fast food restaurants and supermar-
kets have proliferated, and many are now open 24 hours a day. With this combina-
tion of low cost and high accessibility, the time and effort needed to stop whatever
you are doing to have a snack is often minimal. Food now has more sensory variety
than ever before. The Kellogg brothers developed corn flakes in 1894 as part of the
bland, abstemious diet Dr. John Harvey Kellogg prescribed for moral well-being.
The company bearing their name now offers about 55 varieties of breakfast ce-
real. Finally, reminders of food are ubiquitous, as advertising continually makes us
aware of food’s sensory attributes and availability.
Given that we are endowed with a learning system that steers choice and pro-
motes intake of foods with flavors that predict positive caloric consequences, and
is tuned to pick out environmental cues that predict food availability, this combi-
nation of factors creates problems. One claim is that, at least for some people, this
pattern of experience makes foods “drug-like,” resulting in a syndrome of learned
physiological and behavioral adaptations that resemble drug addiction, especially
in regard to the excess attention paid to food cues, compulsive food-seeking, and
subjectively experiencing loss of control over intake. To evaluate the usefulness of
this framework, it may be instructive to consider what it means to be a “drug.” Drugs
of abuse that are consumed recreationally for their desirable sensory, perceptual,
and emotional effects are in that category specifically because they directly, pow-
erfully, and supernormally stimulate brain circuitry that would ordinarily process
“natural” rewards: the taste of a berry, a flirtatious display from a potential mate, a
friendly embrace, a sip of water on a hot day. We should expect that neural circuitry
for processing such stimuli should be tuned in sensitivity to the range of stimulus
intensity it would ordinarily handle. But drugs, being “supernormal” stimuli, stim-
ulate an exaggerated version of the ordinary response patterns. That is, drugs are
drugs because they are like food, only more so. It is fitting to view modern food sim-
ilarly. Modern foods are like foods, only more so, especially in the sensory cues that
drive hedonic evaluation and preference. First, there are beyond-natural levels of
added sugars and fat, the fundamental stimuli for palatability. Second, added fla-
vors and flavor enhancers mean that the sensory cues that become learned signals
for post-ingestive consequences are themselves more salient.
As will be discussed in detail in the subsequent chapters of this book, the sen-
sory and nutritional characteristics of modern foods, especially within the con-
text of ubiquity and convenience, may for some individuals contribute to a pattern
of neurobehavioral responses in motivation, attention, affect, and memory that
results in escalating intake, craving, compulsive seeking, and loss of control that
is commonly recognized as addiction. Research on the fundamental motivational
drivers of both appetite and substance abuse have much of value to share with each
other, recognizing that (like with drugs) these consequences ultimately stem from
an extensive history of learning experiences.
Interactions with the Modern Food Environment
There are currently two main perspectives on how the modern food environ-
ment interacts with the learning mechanisms governing food choice, especially
flavor-nutrient learning, that can contribute to overeating. At first they appear to
offer potentially contradictory explanations for overeating, though it is possible to
reconcile them.
Supporting the Preference Learning Systems
The first main view is that overeating is the predictable consequence of the food
preference learning systems’ doing what they are supposed to do. This view is con-
sistent with the idea that these learning mechanisms function to steer choice and
promote intake of calorically dense options, but also, importantly, to anticipate

post-ingestive consequences so as to simultaneously trigger adaptive physiolog-
ical preparations in digestion and metabolism that enable the organism to cope
with such large meals.154 In this view, it could be said that learning functions too
well in the modern food environment that offers more opportunities to encounter
nutrient-dense foods. The appearance, smell, taste, and flavor of preferred foods,
established by prior learning experiences described previously, come to direct both
appetitive and evaluative responses. These stimuli attract, hold attention, and
elicit approaches leading to increased choice of calorically dense foods specifically.
The increased palatability from sugar and fat is influential on its own, but also
establishes conditioned responses to the initially arbitrary flavors in the food. F-F
conditioning and F-N conditioning act to enhance palatability, which serves both
to stimulate vigorous eating and promote cephalic responses that prepare the di-
gestive system for nutrient influx, delaying satiation and enabling rapid deposition
of ingested fuels.
Obscuring the Preference Learning Systems
A different view of food–environment interactions is that certain aspects of the

modern food environment prevent learning from working as it should. Most of the
research on preference learning has focused on the ways learning promotes choice
and increased intake of calorically dense foods. But this second view proposes that
sensory cues for nutrient density also enable individuals to appropriately adjust
and limit their intake in response to anticipated nutrient loads, to avoid overcon-
sumption and, ultimately, the physiological costs of chronic positive energy bal-
ance. Modern overconsumption, according to this view, occurs in part because
aspects of the modern food environment make sensory cues routinely uninforma-
tive or unreliable.155
Flavor-nutrient learning can only occur to the extent that specific sensory cues
reliably correspond to post-ingestive consequences. But modern food processing
can explicitly uncouple flavor–nutrient links, using added flavors, flavor enhanc-
ers, non-caloric sweeteners, thickeners, and textural manipulations. When a
sensory cue sometimes does and sometimes does not predict post-ingestive conse-
quences, it is no longer useful for anticipatory adjustments in physiology or beha-
vior. Impairment would be especially pernicious if one’s early life experience was
characterized by sensory-nutrient consistency, with a maturing appetite control
system that comes to rely on such high-fidelity information, only then to have that
ability degraded as one’s food world expanded. This could be increasingly common-
place for modern children raised with mostly wholesome, minimally processed
foods early on, who then later discover sodas, processed snacks, and other sources
of sensory entertainment.
Much of the work stemming from this view has focused on the effects of incorpo-
rating non-nutritive artificial sweeteners into one’s habitual diet, since sweetness
is an especially salient sensory cue that is intentionally manipulated in modern
foods.156 Artificial sweeteners allow consumers to obtain sweetness without added
calories or other physiological effects of sugar. Presumably, considerable effort by

food product designers is devoted to making the sugar-sweetened and artificially
sweetened versions of snack foods similar in their flavor and texture, though the
artificially sweetened versions may represent anything from a modest to a dra-
matic reduction in calories, thus potentially obscuring the sensory–nutrient link
that would be otherwise informative for frequent consumers. The same may be-
come true for a range of other sensory attributes as advances in food technology
permit creation of various treats whose rich flavors and textures disguise the ab-
sence of expected calories.
There is a variety of circumstantial evidence consistent with the notion that
a history of consuming non-nutritive sweeteners is associated with disturbances
in appetite. In functional magnetic resonance imaging (fMRI) studies, habitual
diet-soda consumers showed a more complete pattern resembling sugar inges-
tion when tasting saccharin, unlike non-consumers, for whom saccharin activated
fewer taste-reward areas than real sucrose.157 Use of non-caloric sweeteners of all
forms (not just sodas) is associated with attenuated amygdala response to sugar
taste.158 Amygdala activation could be interpreted as indicating perceived biolog-
ical relevance of a stimulus, so a reduction is consistent with the proposal that
artificial-sweetener history changes the consequence-signaling value of sweetness.
Compared to non-consumers, people who routinely consume diet soft drinks expe-
rience less stimulation of appetite by a sweet taste, which has been interpreted as a
weakened learned expectation of energy consequences.159
These studies of artificial sweetener consumption, however, must rely on
self-selected samples, whose habits and histories with weight and diet must cer-
tainly differ in various other ways, making it impossible to infer causality. This
makes animal studies of diet history especially useful. These studies have shown
ways that sensory-nutrient inconsistency is problematic for weight maintenance.
One study exposed rats to chow diets with varied flavors added. For different
groups, the flavors sometimes did and sometimes did not correspond to different
energy densities. Rats gained significantly more weight when flavor–energy rela-
tionships were unpredictable.160 This study did not involve sweeteners, but still
demonstrated the principle that some salient sensory property that is informative
about nutritive consequences can be protective against overweight. Another line of
research comparing rats reared with repeated exposure to non-caloric sweeteners
to those with only exposure to nutritive sugars paradoxically found greater weight
gain with non-caloric sweeteners. The effect on weight gain appears to be due to
reduced satiating effectiveness of sweetness, as rats failed to reduce their intake of
a test meal after a sweet preload with caloric or non-caloric sweeteners.161,162 The
effects persist after non-caloric sweeteners are removed from the diet, suggesting a
lasting effect on learned responses.
Combining Perspectives
It may at first seem that these two views offer different, contradictory explanations
for the obesogenic influence of learning in the modern food environment. Is it that
successfully learning about flavor–nutrient relationships (which would have been

essential for adaptation to a lean environment) now drives excess energy intake
when the environment provides an unnatural surplus? Or is it that the inconsistent
nature of the modern, processed food supply confuses and prevents appropriate
learned adjustments in behavior and physiology and in coping with excess energy?
These theories are both feasible and in fact complementary, to the extent that these
experiences affect different aspects of eating behavior. The learned responses to
sensory cues that predict post-ingestive consequences reflect the joint contribution
of two opposing response tendencies: preferential choice and enhanced evaluation
stimulates intake, but learned anticipatory satiation responses put the brakes on
intake.163,164 The modern food environment could inadvertently be acting to pro-
mote the former of these while preventing the latter.
An environment that provides occasional links between specific sensory
cues and post-ingestive nutritional consequences may be sufficient to establish
increased seeking, preferential choice, and positive evaluation of those cues, even if
those links are irregular. Enhanced preference for a flavor paired with nutrients can
be learned in a single trial, and it remains fairly resistant to extinction even after
only minimal training experience.123 But the learned, intake-limiting effects of sa-
tiation expected to follow a learned flavor cue appear to extinguish fairly rapidly
when post-ingestive consequences do not consistently occur.165 Thus the modern
food environment could be doubly problematic by providing situations where the
correspondence between sensory cues like flavors, sweetness, texture, and caloric
consequences is reliable enough to maintain learned intake-promoting responses,
but not reliable enough to maintain learned intake-limiting responses.
CONCLUSION
At the core of appetite, beneath layers of cognitive, emotional, and sociocultural

elaboration, the biopsychological controls of food choice are tied to hedonic eval-
uation of food’s sensory attributes, including the basic tastes of nutrients and
complex flavors. But how individuals evaluate and respond to different foods is
diverse enough that in just about every cuisine there’s something savored by locals
that seems repulsive to visitors. The range of food acceptability stretches so far
that staple foods in some diets are simply rejected as non-foods by outsiders (e.g.,
insects, blood, beef). But it is not even necessary to traverse wide cultural or geo-
graphic distances to document these differences. On a local scale, looking casually
at one’s own family, friends, and neighbors makes the idiosyncratic and individual-
ized nature of food preference evident.
All of this diversity reflects the predominant role of experience in shaping pref-
erence. The environment is influential from the time that gustatory and olfactory
systems are functional in utero. Through experience, which can be as simple as mere
exposure, and broad enough to encompass associative, cognitive, and social influ-
ences, the sensory properties of food become labels for its identity, quality, and suit-
ability to meet nutritional needs. Bottom-up coding of a food’s physical properties
elicits stored memories of prior experiences, and this information is integrated

with signals about current bodily states. Although there are innate influences (e.g.,
the early response to sweetness), the power of learning is demonstrated by the fact
that, in contests between innate responses and learning, learning typically wins.
Culture and individual experiences modify the inherent liking for sweet taste, and
individuals acquire liking through exposure and conditioning for tastes that would
be otherwise aversive.
Learning systems form the nexus between the environment and food hedon-
ics, and therefore become especially important in our efforts to understand how
the modern food environment leads to overeating. The major shifts in how food
is made, distributed, and marketed, and the concomitant changes in food variety,
composition, and availability can be expected to have several effects on appetite
through learning mechanisms that evolved to promote adaptive behavior in a very
different environment. On one hand, learning to like flavors that signaled food
quality enabled individuals to cope with environments where quality was variable,
but this now acts to promote selection of foods that are of unnaturally high quality
(in terms of caloric density, at least). At the same time, some aspects of the mod-
ern environment may fool these learning mechanisms by providing inconsistent,
unreliable information about foods’ sensory properties, and those failures may
particularly impair appropriate cessation of eating. In sum, why we eat what we
eat is generally explained by what we learn about what we eat. Why many people
are now eating so much can be attributable both to what we learn and to what we
fail to learn.
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C H A P T ER 3
w
The Brain’s Got a Taste
for Good Food
A NNET TE HOR STM A NN
THE LOVE OF FOOD
“La bonne cuisine est la base du véritable bonheur.” [Good food is the foundation of gen-
uine happiness.]
Auguste Escoffier
“There is no sincerer love than the love of food.”

George Bernard Shaw
With these two quotes, it becomes immediately evident that our relationship to
food is at least twofold: Food makes us feel good, and, therefore, we love food. This
chapter will elucidate the mechanisms in our brains that mediate this intimate re-
lationship, together with a discussion of possible causes for the rise in overweight
and obesity rates immanent within these processes.
Energy intake is essential for survival of the organism. Thus, the identifica-
tion, memorization, and acquisition of energy-providing resources are processes
that possess a high priority. In order to ensure sufficient energy intake, several
mechanisms have evolved at the level of the brain, which shall be introduced and
discussed in the following sections. This chapter will start with introducing the
way the brain senses food, both in the environment and inside the body. Then, the
motivational aspects related to eating behavior and their neural correlates shall be
explained, along with the brain’s neurotransmitter system mainly associated with
motivation. Finally, mechanisms influencing the motivation to eat and their cen-
tral nervous system implementation will be elucidated.
( 39 )
THE CENTR AL PROCESSING OF FOOD: VISUAL

INFORMATION, TASTE, ODOR AND TEXTURE
The brain senses food and its different physical properties at various stages during
the process of eating: before ingestion, in the oral cavity, and in the gastrointestinal
tract. In the following discussion, the way this information is conveyed by different
sensory pathways and integrated in various areas of the brain shall be explained.
Remote Sensory Information: Sight and Smell of Food
Food, as it appears in the outside world, conveys remote information to visual and
olfactory sensory modalities, which are processed via different sensory pathways in
the brain. The sight of food activates visual receptors in the retina, whose informa-
tion is relayed via the thalamus to primary and secondary visual areas in the occip-
ital and temporal lobes. In parallel, a subcortical route conveys visual input to the
amygdala,1 a region thought to provide information about the behavioral relevance
of stimuli. From both of these sites, information is projected to the orbitofrontal
cortex (OFC),2 a multimodal region. Ortho-nasal odor information—information
entering the nose through the nostrils—is conducted from the primary olfactory
neurons to the olfactory bulb, from whence information is transduced to central
piriform and entorhinal cortices. Direct connections then pass on the information
from the piriform to the posterior OFC. 3 Thus, from these two sensory modalities,
information about food in our environment converges in the OFC. Here, associa-
tions between this information and the learned properties of the food, such as taste
and nutritional value, enable the computation of a corresponding motivational
value. This is further adjusted in relation to homeostatic signals in the anterior
insula, and subsequently, food-seeking and ingestion is either promoted or discour-
aged accordingly. These two senses, vision and olfaction, are primarily responsible
for identifying food4 and predicting the rewarding properties of food.
Information from the Oral Cavity and the Gastrointestinal Tract
When the food is ingested, it additionally conveys information about its taste, tem-
perature, texture, viscosity, and nutritional value. The sense of taste helps the or-
ganism identify nutrients and toxins (e.g., sweet taste signals calories, salty taste
signals electrolytes, savory taste signals proteins, and bitter taste signals the exist-
ence of possible toxins).5 When taste information is combined with somatosensory
and retronasal olfactory inputs from the oral cavity, the percept of flavor emerges,
which is an integrated multimodal representation, mostly unique to different food
items. Examples would be flavors like banana, coffee, and chocolate.
Taste quality and its associated nutritional value have been shown to stably
evoke specific affective reactions.6 Sweet taste, signaling the availability of val-
uable calories from carbohydrates, provokes an automatic appetitive reaction,
T he B rain ’ s G ot a T aste for G ood F ood ( 41 )
which can already be seen in newborns. In contrast, bitter taste, signaling pos-
sible toxins, evokes an automatic aversive reaction.7 Recent studies indicate that
neural responses to taste stimuli of different qualities seem to be amplified in
obese compared to lean subjects. Both subject groups were given different taste
stimuli: sucrose, which is usually perceived as pleasant; quinine HCl, an aversive
taste stimulus; and high-calorie, vanilla-flavored nourishment solution, a complex
taste of high palatability. In obese subjects, activation in response to all these taste
stimuli was stronger—not only in cortical areas processing taste information and
generating a subjective value representation (i.e., insular and adjacent opercula cor-
tices, anterior cingulate cortex, and OFC), but also in subcortical areas coding the
affective value of stimuli (i.e., amygdala, nucleus accumbens, and dorsal striatum).8
The texture of food is represented independently from taste or odor in the pri-
mary taste cortex of the anterior insula and in the adjacent mid-insular cortex,
where the neural signal changes in proportion to logarithmic changes of viscos-
ity.9 Oral fat is also represented in the anterior insula’s primary taste cortex, the
mid-insula, and OFC. In addition, oral fat activates the hypothalamus and the
anterior cingulate cortex. This region in the anterior cingulate cortex is exclusively
activated by fat and sucrose, and not by viscosity, suggesting a region coding the
hedonic aspects rather than the physical properties of fat.9 Activity in these areas
and, importantly, in the amygdala correlates with the fat concentration of food.10
All of the aforementioned signals are integrated in the anterior insula and the
adjacent mid-portion of the frontal operculum. Here, information about the sight,
taste, odor, and texture of food is merged with visceral information from the gut.11
These brain areas commonly provide information about the available food choice
and the homeostatic state of the body, making it possible to compute the need to in-
gest the available food choice. Lastly, after ingestion, humoral and visceral signals
from the gut are relayed back to the anterior insular cortex and the hypothalamus
to update homeostatic state information.
INCENTIVE SALIENCE
Animals, including humans, are equipped with limited central-processing re-

sources. To overcome this limitation, attention has to be preferentially allocated
to items with a high relevance to survival (e.g., energy sources or possible dangers).
Salience is a concept that describes the property of an item that makes it stand out
from its neighboring items due to differences in at least one physical feature. These
features could be, for example, color, orientation, size, pitch, and velocity. The brain
prefers to process items that possess high salience. A special case of salience is in-
centive salience, where the salient property of an item is not a physical feature but
is constructed via its learned reward-predicting value and, hence, can be seen as
a cue-triggered, motivational, “wanting” attribute given by the brain. Items with
high incentive salience command attention, induce approach behavior, and are
easily detected in the environment. Importantly, incentive salience can be modu-
lated powerfully by the physiological state of the body. Normally, a cue predicting
food will have high incentive salience when one is hungry, and low if one is sated12
(i.e., it is dependent on one’s current homeostatic state). This modulation facilitates
the processing of currently relevant information, thereby helping meet the present
needs of an organism. In this context, a distinction between general “liking” and
“wanting” signals can be made: “liking” corresponds to a general pleasantness esti-
mation, whereas “wanting” describes the current desirability or motivational value
(e.g., of a food item).12 In obesity, it has been hypothesized that these two signals
are no longer distinct, but that decisions are being made predominantly on the
basis of the “liking” signal. But before these mechanisms are discussed in more de-
tail, the pathways by which information about food is processed in the brain shall
be introduced.
THE APPETITIVE BR AIN NETWORK
Neural activity in several brain areas translates the motivation to eat into ac-
tion. This so-called appetitive network (Figure 3.1) is able to generate arousal,
provide attention to food-predicting cues, and implement learning and memory
of the nutritional value and availability of food. Furthermore, it is able to weigh
effort costs against food reward, thus providing absolute decision values, and it
integrates information about short- and long-term energy stores with the avail-
able energy choices.13 Neural activity within the whole network responds to food
cues and is heavily modulated by peripheral signals and homeostatic status due to
its intimate connections to the hypothalamus,14 the brain’s primary homeostatic
center. Importantly, all regions of the network receive dopaminergic input from the
brainstem.
The amygdala and posterior OFC provide the current incentive value of food
items.15 The amygdala attributes values to sensory stimuli and relays this infor-
mation on to the OFC and ventromedial prefrontal cortex (PFC), which in turn
compute an absolute decision-value from the costs associated with obtaining the
food and the value signal assigned by the amygdala.16–20 Anterior insular cortex
and the central part of the frontal operculum provide a higher-order multisen-
sory representation of food items, and this information is integrated with cur-
rent homeostatic state.6 The anterior insula seems to be necessary to the act
of learning about the relationship between the multisensory representation of
food and its nutritional value. Therefore, it possibly mediates the conditioning to
food cues. The striatum provides the link between motivational state and action,
since it plays a crucial role in incentive learning and motivated behavior. 21–23
After an incentive motivational state is generated, it provides the propensity
to act accordingly, therefore facilitating motivated behavior. The appetitive
network can be modulated by inhibitory activity in the dorsal medial PFC and
lateral PFC (e.g., in order to adhere to dietary plans or to inhibit inappropriate
behavior such as eating from a buffet before it is opened). 24,25 For obese subjects,
decreased inhibitory control in the presence of highly palatable food (but not in
general) has been demonstrated, 26 suggesting inappropriate downregulation of
Dorsal
Striatum
Insula
Orbitofrontal
Cortex
Amygdala
Nucleus
Accumbens
Figure 3.1:
Areas of the human brain activated in response to palatable food or food-associated cues.
The orbitofrontal cortex and amygdala encode information related to the subjective
incentive value of food. The insula and frontal operculum convey a higher-order
multisensory representation of food and integrate this information with the current
hedonic state. The nucleus accumbens and dorsal striatum, which receive dopaminergic
input from the ventral tegmental area and substantia nigra, regulate the motivational and
incentive properties of food. The lateral hypothalamus may regulate rewarding responses to
palatable food and drive food-seeking behaviors. These brain structures act in a concerted
manner to regulate learning about the hedonic properties of food, shifting attention and
effort towards obtaining food rewards and regulating the incentive value of environmental
stimuli that predict availability of food rewards.
Adapted from Kenny PJ. Reward mechanisms in obesity: new insights and future directions. Neuron.
2011;69(4):664–679. Reprinted with permission from Elsevier.
the appetitive network, specifically in the food context. Incentive salience and
the motivation to eat are critically dependent on activity in the dopaminergic
system, one of the brain’s major neurotransmitter systems, which shall be intro-
duced in the next section.
THE BR AIN’S DOPAMINERGIC SYSTEM
Many researchers suggest that the dopaminergic system plays an important role
in mediating incentive salience and cue-induced appetitive behavior. For example,
positron emission tomography (PET) studies have shown that the neurotrans-
mitter dopamine is involved in the regulation of feeding27,28 and is indeed released
within the striatum in proportion to the degree of pleasure experienced while
eating. Here, the brain’s major dopaminergic structures that are important for the
control of eating behavior, the role of different dopamine receptors, and alterations
of the dopaminergic system in obesity will be described.
Dopaminergic Pathways
The dopaminergic system comprises three main pathways in the brain.

Dopaminergic input comes from neurons in the substantia nigra pars compacta
(SNpc) and the ventral tegmental area (VTA), both located in the midbrain. The
nigrostriatal pathway delivers dopaminergic input from the SNpc to the dorsal stri-
atum. This pathway seems to be mostly associated with motor control and the for-
mation of automatic stimulus–response links such as habits. Information within
the mesolimbic pathway travels from the VTA to the nucleus accumbens (NAc) in
the ventral striatum, from whence it is relayed to the limbic system (i.e., the amyg-
dala, hippocampus, and PFC). The mesocortical pathway provides direct dopamin-
ergic input from the VTA to the frontal cortex.
Gray matter volume in dopaminergic structures (i.e., the NAc, OFC, hypo-
thalamus, striatum, and dorsolateral PFC) has been shown to be associated with
markers of obesity in young healthy subjects,29 indicating a relationship between
obesity and the layout of the dopaminergic system. The function of dopaminergic
signaling in the context of incentive salience is at least twofold. On one hand, it sig-
nals the potential availability of a reward, as when a prediction is made from cues
available in the environment (e.g., the sight of highly palatable food). On the other,
dopamine signals the receipt of a reward (e.g., after ingestion of highly palatable
food). Over the course of learning the associations between environmental cues
and rewards, dopaminergic signals shift with respect to their timing in different
brain regions. Animal studies showed that prior to learning, dopamine neurons
in the VTA and the SNpc respond to unexpected reward with an increase in firing
rate, triggering phasic dopamine release in the ventral striatum.30 After learning,
this signal was shifted backwards in time to the onset of a reward-predicting cue.
When the expected reward was not delivered, the neurons responded with a dip
in their firing rate at the estimated onset time of the expected reward. This signal
has become known as a negative prediction error, signaling the difference between
an expected and a received outcome in case the outcome is worse than expected.
The described increase in firing rate in response to an unexpected reward is analo-
gously termed a positive prediction error. Together, dopaminergic prediction errors
encode the difference between expected and actual outcomes. Thus, they enable us
to learn through experience, detect violations of expectations, and, hence, ensure
efficient behavioral adaptation. For obese subjects, it has been shown that positive
prediction errors following unexpected taste rewards are accompanied by dimin-
ished brain responses in the striatum, insula, OFC, and dorsolateral PFC. 31
To test the role of the dopaminergic system in learning of taste-related predictions,
brain responses to reward-predicting cues as well as to the receipt of a taste reward
were measured using functional magnetic resonance imaging (fMRI), a non-invasive
neuroimaging technique. Activation in dopaminergic regions of the midbrain (i.e.,
the VTA and SNPc, amygdala, striatum, and OFC) was indeed associated with the
anticipation of a primary taste reward.32 The OFC was the only region that was still
activated by reward receipt after the learning of cue–reward associations, supporting
its assumed function in coding the subjective pleasantness of rewards.
Dopamine Receptors
The effect of dopamine release on neurons depends crucially on the type of receptor
it activates. At least five subtypes are organized in two general families of receptors
(dopamine 1—D1; etc.): D1-like receptors mediating activation of the postsynaptic
cell, and D2-like receptors mediating inhibition. Receptors D1 and D5 belong to the
former family, and the D2, D3 (NAc), and D4 receptors to the latter. D1 and D2 recep-
tors are much more abundant in the brain than receptor subtypes D3–D5.33
D1 and D2 receptors are critically involved in learning and memory processes
mediated by the striatum and PFC. 34 D1, D2, and D3 receptor subtypes are involved
in reward and reinforcement mechanisms. For example, the activation of D2 recep-
tors mediates the drive to seek further drug reinforcement, and activation of D1
receptors seems to be sufficient in that it attenuates further drug-seeking behav-
ior in animal experiments. D3 -receptor activation seems to enhance the rewarding
properties of drugs. 33 In obese subjects, a blunted activation in the dopaminergic
dorsal striatum during consumption of palatable food items has been observed, 35
comparable to similar effects seen in drug addiction. 36 Since a negative relation-
ship between D2/D3 receptor availability in the striatum and markers of obesity
has been observed, this blunted response to food might depend on attenuated
dopaminergic transmission in the striatum of these individuals. 37,38
Genetic variation that is affecting the layout of the dopaminergic system has
repeatedly been shown to influence food reinforcement and intake, increased risk
for obesity and macronutrient preference, and the power of brain responses to food
cues for predicting weight gain. Single nucleotide polymorphisms (SNPs) are the most
commonly observed genetic variations. SNPs are DNA sequence variations in which
a single nucleotide—adenine (A), guanine (G), thymine (T), or cytosine (C)—in the
genome differs between people. One well-studied SNP in the dopaminergic system is
the TaqA1 variant, located just downstream of the dopamine D2 receptor gene. This
SNP is associated with low dopamine D2 receptor density in healthy subjects,39 pos-
sibly influencing the efficacy of dopaminergic transmission. For example, differences
in reinforcement learning, especially in learning from errors, have been shown to
depend on dopamine D2 receptor-associated SNPs in normal-weight subjects.40,41
Diet-Induced Obesity and Its Effects on Central

Dopaminergic Signaling
A long-standing question about the significance of obesity-associated alterations in

dopaminergic signaling is the one regarding cause or consequence: Are differences
within this system a precursor and, subsequently, a risk factor for overeating, or a con-
sequence of long-term increased food intake? Due to limited experimental possibili-
ties of investigating this question directly in humans, most longitudinal data on this
topic stem from animal experiments. When rats gain weight through diet-induced
obesity, several alterations in dopaminergic signaling have been observed. The
extracellular dopamine level in the NAc is reduced, and dopamine release in ventral
striatum becomes specific to high-fat food. Electric stimulation or stimulation with

amphetamine yield an attenuated dopamine response in these rats.42
After prolonged feeding of a high-fat/high-sugar (HFHS) diet, D2-receptor
messenger RNA (mRNA) is upregulated in the dorsal striatum and D1-mRNA is
downregulated in the NAc of animals prone to obesity, but not in animals resis-
tant to obesity. The latter effect persists even after withdrawal from HFHS diet.
A decrease in D2/D3 receptor availability in the striatum of rats with diet-induced
obesity seems to depend on the fat–carbohydrate ratio and is influenced by the
motivational aspects (i.e., the hedonic value) of a HFHS diet, since it has been
reported that these changes preferentially occur in animals that are free to choose
a high-calorie diet.43,44
In line with these observations in animals, obesity-associated alterations in the
dopaminergic system of humans have been identified. While there seems to be no
difference between lean and obese subjects regarding dopamine transporter avail-
ability in the striatum, in morbidly obese subjects, a lower striatal binding potential
for D2/D3 receptors has been observed repeatedly.37,45,46 These findings have been
discussed extensively in the framework of the “hyper- vs. hyposensitivity to reward”
theory.47 The lower dopamine-receptor availability in the striatum of obese subjects
might be interpreted as a physiological adaptation to dopamine overstimulation
with high-energy food: obese subjects might have shown higher reward sensitivity
before they became obese. High reward sensitivity is associated with a high dopa-
mine release. To counteract permanent overstimulation with dopamine, dopaminer-
gic transmission is downregulated over time by a decrease in dopamine receptors.
This, however, also decreases dopaminergic transmission after reward receipt, lead-
ing to an attenuated food reward response of the brain. This is thought to lead to a
“reward deficiency” in obese subjects, which, according to the theory, they are try-
ing to compensate for by overconsumption of food with a high reward value (e.g.,
high-calorie food).
By comparing dopamine release in the striatum after ingestion of sucrose to
that after ingestion of sucralose, a calorie-free artificial sweetener, a study revealed
that striatal dopamine increases in mice blind to sweet taste. Thus, dopamine also
increases in response to calorie ingestion independently from dopaminergic signal-
ing following the sight, smell, taste, and texture of highly palatable food. A com-
parable mechanism is hypothesized to be effective in humans. This signal might
additionally contribute to the decrease in motivational value of food rewards after
ingestion, and, consequently, to meal cessations.
PREDICTORS OF MOTIVATIONAL VALUE
The motivational value of food items is determined by a variety of factors, such as

the physical properties of the food, the organisms’ homeostatic state, and influ-
ences from the environment. In the following sections, the relationship between
these factors and the central nervous system’s representation of a food’s motiva-
tional value are introduced.
Gradual Devaluation Through Consumption
Dynamic changes in motivational value are thought to contribute to the acute

control of eating behavior (e.g., promoting food-seeking or cessation of a meal).
Repetitive consumption of a specific food item will lead to a downscaling of its mo-
tivational value and, in consequence, will inhibit actions that would lead to over-
consumption.48–50 After selective satiety has been induced, it is accompanied by a
reduced response to specific taste stimuli in the medial PFC (specifically in men),
amygdala, and hypothalamus (specifically in women).51 This mechanism may be
weakened in obesity: behavioral sensitivity to reward devaluation has been demon-
strated to decrease with increasing body mass index (BMI).50 If subjects ingest more
energy than they would usually eat, brain responses to pictures of food with a high
hedonic value are attenuated in visual and parietal areas as well as in the hippo-
campus.52 Regions that dynamically track the positive motivational value of taste
stimuli are the central operculum (primary taste cortex), the medial OFC, and the
subcallosal region. Activity in these regions decreases in accordance with ratings of
the subjective pleasantness of taste stimuli during a selective satiation procedure.
In contrast, activity increases in the lateral OFC and lateral inferior frontal gyrus
with increasing aversion to the devalued taste stimulus.
Environmental Influences
Food choice and eating behavior are affected by environmental factors such as
stress.53 Stress is known to shift behavioral control from being goal-directed
to habitual actions in subjects who are vulnerable to the deleterious effects of
stress.54,55 This possibly also shifts food-choice towards options with a high affec-
tive value. To test the effect of stress on brain responses to food, women were stimu-
lated inside an fMRI scanner with a highly palatable milkshake, representing sweet,
high-calorie “comfort food.” The level of chronic stress the women experienced dur-
ing daily life boosted the reactivity of the right amygdala to milkshake stimulation.
Acute emotional stress additionally modulated responses in the right amygdala and
OFC,56 possibly increasing the motivational value of highly palatable food under
stress or emotional discontent. The role of the amygdala in stress-induced eating
might, in addition, be moderated by genetic factors. Over the past several years,
some common genetic polymorphisms have been identified that influence pheno-
types such as eating behavior and obesity. A possible link between genetic variation
and these phenotypes is a differential central nervous system processing of food
and its associated reward value.
One candidate system for mediating this link is the central melanocortin
system. It is, among others, responsible for the acute regulation of satiety and
feeding behavior and the integration of long-term appetitive signals. Mutations
within the gene encoding the melanocortin-4-receptor lead to massive hyper-
phagia and severe, monogenic, early onset obesity. A SNP mapping downstream
of the melanocortin-4-receptor gene, putatively influencing function and/or
expression levels of the melanocortin-4-receptor, is associated with disinhib-

ited and emotional eating behavior and human obesity. 57–63 In addition to eating
behavior, genetic variation at this site has been shown to be associated with
alterations in gray matter volume of the OFC and amygdala/hippocampus, thus
indicating possible alterations in central processing of the rewarding properties
of food.64 Moreover, in line with observations of this polymorphism’s impact
on eating behavior and obesity risk, this effect was gender-dependent: the
effect of the SNP on brain structure was more pronounced for women than for
men. Together, these data might indicate a central nervous system pathway for
stress-induced eating.
Nutritional Value and Homeostatic State
The incentive salience of food items is modulated by several factors. First, prop-
erties of the food item itself contribute to its motivational value, including its
visual properties, taste, and viscosity; these serve as a proxy for the food’s calorie
content and composition of macro- and micronutrients. This translation from
nutritional to motivational value may be mediated by the amygdala and OFC.
Functional connectivity between the amygdala and OFC is modulated by the
calorie content of food stimuli. If subjects are presented with high-calorie food
items, functional connectivity between these brain regions is higher than when
the subjects are watching low-calorie food items.65 Interestingly, obese subjects
do not show a modulation of connectivity between the amygdala and OFC that
is dependent on calorie content of food stimuli. This might reflect an attenu-
ated tuning of motivational value according to nutritional value. Furthermore,
regions related to reward anticipation and habit learning (i.e., the dorsal stri-
atum), seem to be automatically activated in obese women following visual stim-
ulation with highly palatable food stimuli.
Second, under normal circumstances, homeostatic state is a powerful modulator
of incentive salience. Refraining from eating for a longer period of time enhances
the subjective pleasantness of food images.66 This effect seems to be especially pro-
nounced in women, and in addition, influenced by food category, especially sweet
foods. The motivational value of sweet food items, which possess a high incentive
salience, seems to be least affected by homeostatic state compared to other cat-
egories, so their motivational value remains high compared to other food items,
regardless of subjective satiation. Hence, the motivational value of sweets might
be dominated by their hedonic value and be mostly unaffected by changes in ho-
meostatic state, therefore facilitating overeating. OFC as well as visual areas show
higher responses to visual food cues during hunger, possibly reflecting a higher
behavioral relevance of these cues when energy is needed.67 Furthermore, hunger
modulates the explicit reward evaluation of food stimuli and is associated with ac-
tivity changes in the OFC, posterior cingulate cortex, basal ganglia, visual areas,
and the insula. Studies investigating the interaction between homeostatic state and
the calorie content of stimuli have shown that hunger boosts activity specifically in
response to high-calorie stimuli in the ventral striatum, amygdala, anterior insula,

medial and lateral OFC, and visual areas.68,69 Moreover, fasting enhanced the sub-
jective appeal of high-calorie more than low-calorie food items, and the change in
appeal bias towards high-calorie food items was positively correlated with medial
and lateral OFC activation. From an ecological point of view, these food items have
the highest nutritional value and are therefore best suited to quickly satisfy present
homeostatic needs.
Homeostatic state can be experimentally manipulated by inducing a state of
mild hypoglycemia, where blood glucose is lower than optimal and, hence, the drive
to consume high-calorie food is high. Another method of manipulation is to in-
duce euglycemia, with normal blood sugar levels signaling no acute need for energy
intake. When people evaluate food stimuli in these different homeostatic states,
the distinction between “liking” and “wanting” becomes apparent. Liking ratings
are not affected by changes in homeostatic state, while wanting ratings are signif-
icantly higher in the hypoglycemic state.70 This differential motivational value is
associated with higher activity in the medial PFC in the euglycemic state and higher
activity in the limbic system and striatum in the hypoglycemic state during evalua-
tion of food stimuli. In overweight and obese subjects, this modulation through ho-
meostatic state seems to be compromised. Higher circulating glucose levels predict
greater medial PFC activation in subjects with normal weight, but this response
was absent in obese subjects. These findings demonstrate that circulating glucose
modulates neural stimulatory and inhibitory control over food motivation and sug-
gest that this glucose-linked restraining influence is lost in obesity.
Furthermore, high-calorie food images yield BMI-dependent activations in re-
gions associated with taste information processing (i.e., the anterior insula and
lateral OFC), motivation (i.e., OFC), emotion, and memory functions (i.e., the
posterior cingulate), independently of the homeostatic state. Accordingly, higher
brain reactivity in areas mediating motivational and attentional salience to pic-
tures of high-caloric food items has been shown to be predictive of less success
in a weight-loss program. Together, these findings indicate that hunger selectively
biases the appetitive brain network towards high-calorie food, and that this mech-
anism is no longer efficient in obese individuals.
GUT–BR AIN COMMUNICATION, HORMONES, AND

MODULATION OF MOTIVATIONAL VALUE
There are several peripheral hormones that are able to influence the state of central
nervous regions controlling eating behavior.71 Because of the multitude of those
signals, three of them shall be introduced exemplarily in this chapter.
Leptin, a hormone secreted by adipocytes, signals the level of peripheral energy
stores to the brain. Its level is roughly proportional to the amount of fat stored
in subcutaneous and visceral adipose tissue. Congenital leptin deficiency causes
feelings of constant subjective hunger and, in consequence, severe obesity. Leptin
substitution in those patients modulates neural activation in striatal regions,
suggesting that leptin acts on neural circuits governing food intake to diminish the
perception of food reward while enhancing the response to satiety signals gener-
ated during food consumption. Obese subjects, however, seem to be resistant to the
modulating effects of leptin.72
Ghrelin is an orexigenic hormone (i.e., a hormone promoting food intake) that
regulates meal initiation. Ghrelin levels rise up to the moment a meal is initiated
and correspond with the level of reported hunger. During food intake, ghrelin lev-
els fall quickly, possibly contributing to meal cessation. High levels of ghrelin have
been shown to potentiate dopamine signals associated with food intake in the NAc
of rodents.73 When ghrelin was administered peripherally to healthy human volun-
teers, it increased brain activity in response to food pictures in the amygdala, OFC,
anterior insula, and striatum, all areas implicated in encoding the incentive value
of food cues. Moreover, the effects of ghrelin on the amygdala and OFC response
were correlated with self-rated hunger ratings.74
Glucagon-like peptide (GLP)-1, a peripheral gut hormone that is secreted in re-
sponse to the presence of nutrients in the small intestine, contributes to satiety
via modulation of brain activity. Infusion of ghrelin has been shown to reduce
responses to food stimuli in the amygdala, insula, caudate, NAc, OFC, and pu-
tamen.75 Furthermore, peripheral administration of a GLP-1 analogue decreases
subjective hunger and is associated with increased connectivity between the hypo-
thalamus and the rest of the brain.76
In conclusion, by modulating the hedonic and incentive responses of the brain
to food-related cues, peripheral metabolic signals such as leptin, GLP-1, and ghrelin
are able to regulate food consumption.
CONCLUSION
Food intake is essential for survival; consequently, complex and extraordinarily ef-
fective mechanisms have developed on the level of the brain to ensure sufficient
energy intake. These processes guarantee that high-energy food is preferred in gen-
eral and, moreover, is perceived as pleasant. A complex brain network, consisting of
evolutionarily old subcortical and relatively young cortical areas, provides the basis
for the efficient control over the motivation to eat and its adaptation in response
to homeostatic signals from the body. Incentive salience is important for the mo-
tivation to eat and is modulated through the physical properties of food such as
visual appearance, taste, smell, and nutritional value, but also through the homeo-
static state of the body, or situational factors such as the level of stress experienced.
Central to motivation, learning, and reward in the context of food is the dopamin-
ergic system of the brain, which seems to be altered in obesity. This system is linked
to the humoral system of the body, which is able to modulate hedonic and incentive
responses of the brain to food-related cues, probably by altering the dopaminergic
system’s state. Recognizing both the complex systems regulating the motivational
value of food and obesity-associated alterations in many of its components, it
becomes clear that, in obesity, hedonic responses to food are no longer adjusted
in accordance with homeostatic needs because of differential brain responses of a

complex system. Animal data suggest that alterations in the dopaminergic system
may represent a consequence of obesity rather than a predisposition to it. Thus, in
addition to prevention strategies that are attempting to avoid the development of
obesity, approaches to restoring the normal signaling of the dopaminergic brain
system might be most promising to tackle obesity.
ACKNOWLEDGMENTS
The author is grateful to Anja Dietrich, Monique Horstmann, Jana Kube, and
Dr. Claudia Sikorski for valuable comments and suggestions on earlier versions of
the manuscript. The author’s work is supported by the Integriertes Forschungs- und
Behandlungszentrum (IFB) Adiposity Diseases, Federal Ministry of Education and
Research (BMBF), Germany, FKZ: 01E01001 (http://www.bmbf.de) and the German
Research Foundation (DFG) (http://www.dfg.de), Project 1052A5 “Neurocognitive
Models of Behavioral Control in Obesity” within the framework of the Collaborative
Research Center (CRC) 1052 “Obesity Mechanisms.”
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C H A P T ER 4
w
Craving Chocolate?
A Review of Individual Differences, Triggers,
and Assessment of Food Cravings
A SHLEY M A SON A ND ELISSA EPEL
F ood cravings are ubiquitous in the modern human experience, yet they appear
to differ between people in many ways. Are one person’s cravings qualitatively
and biologically similar to another’s? What makes some people’s cravings so strong,
irresistible, and chronic, leading to, for example, finishing the box of chocolates,
despite their strongest intentions not to do so?
Food cravings are a common experience among the majority of people strug-
gling with regulating their eating, and a major barrier to diet adherence.1 Although
food cravings play a critical role in what many researchers now refer to as “com-
pulsive eating” or “food addiction,”2 food cravings are reported among individuals
who do and do not meet criteria for DSM-IV (Diagnostic and Statistical Manual of
Mental Disorders, Edition IV) eating pathology—from individuals trying to lose a
few pounds, to those who describe an excessive drive to eat causing undesirable
weight gain. Behavioral and biological overlaps between food and drug addiction, 3
and emerging data linking increased food cravings to greater insulin resistance
among obese individuals,4 underscore the potential utility of food cravings as an
intervention target in the treatment of obesity.
Better understanding of food-craving experiences—individual differences
in intensity and frequency, contextual triggers, and how craving is conceptual-
ized and assessed—would shed light on mechanisms that underlie problematic
and reward-based eating in response to food cravings. This, in turn, would better
clarify targets for intervention.5 In this chapter, we examine food cravings along
different dimensions. We first discuss definitions and prevalence of food cravings.
( 57 )
Obesogenic Long-term
Shorter Term:
Environment adaptations to
Food craving
triggers reward
Increased responsivity
Long Term: More frequent non-homeostatic
Predispositions Metabolic health
& intense food eating in
to experience decline
cravings response to food
food cravings cravings Obesity
Figure 4.1:
This chapter reviews the effects of predispositions to experience food cravings and food
craving triggers on food craving triggers and predispositions to experience food cravings on
food craving experiences. Make the decision, craving experiences.
We then review individual differences in, and common triggers of, food cravings,
with a special focus on the roles of stress and mood. As shown in Figure 4.1, there
are longer-term individual predispositions to experience and indulge in food crav-
ings, and shorter-term common triggers that may interact with these predisposi-
tions. Last, we review methods used to assess food cravings and close with a brief
overview of future directions.
DEFINITIONS AND PREVALENCE
Food craving is most often defined as an intense desire or longing to eat a specific
food.6,7 Studies report a wide range of food-craving prevalence, with rates as high
as 90%–100% of individuals sampled reporting food cravings of some type.1,8–10
People vary in the intensity of their food cravings; in one study, among women be-
tween the ages of 18 and 45, approximately 58% reported ever having experienced
a food craving, and of these, 42% of young and 21% of middle-aged women reported
having had moderate-to-strong and strong cravings.11
Food craving fits into Berridge’s “food reward framework” as a type of wanting,
or appetitive motivation to seek out a particular food, which differs from liking,
or the pleasure derived from eating a particular food.12 Although liking may play
a crucial role in the development of a motivational (wanting) state, individuals
with pathologically elevated levels of wanting in the form of food cravings (due
to predisposition or adaptation) may be at greater risk of overeating in a food-rich
environment.13 Thus, the motivational state of wanting dictates food-craving expe-
riences that lead to overeating and the resulting overweight state.
C raving C hocolate ? ( 59 )
Food craving differs from hunger in terms of specificity: Although a variety of

foods may satisfy one’s hunger, an arguably narrower repertoire of foods may sat-
isfy one’s food craving.14 Some researchers assert that “craving a food differs from
simply deciding, for example, to have a certain food for dinner—unless that decision
is based on a desire so strong that you would go out of your way to satisfy it.”15, p. 355
In humans, food cravings are generally for calorically dense, highly palatable foods
that are often high in fats and sugars;8,16,17 however, cross-cultural data suggest that
food cravings can be culture-specific.18–20 For example, surveys of North Americans
indicate food cravings for pizza, ice cream, chips, pies, and especially chocolate;19,21
whereas surveys of Japanese populations report cravings for rice and sushi to be
most common.18,22 Greater craving intensity is strongly associated with greater in-
take of sweet and high-fat foods.8 Accordingly, some researchers have posited that
food cravings may be considered a conditioned expression of hunger: in one study,
women instructed to eat chocolate only when hungry reported increased chocolate
cravings over a two-week period, whereas chocolate cravings decreased among par-
ticipants instructed to only eat chocolate when sated.23
INDIVIDUAL DIFFERENCES IN FOOD CR AVINGS

Sex and Age Differences
Food cravings vary greatly according to a number of individual differences, and
sex differences are among the most commonly examined factors. Several studies,7,24
though not all,15 have supported the popular notion that women experience more
frequent or more intense food cravings than men.1,7 More women (91%) than men
(59%) report ever having experienced a chocolate craving,25 and 45% of women
report regularly experiencing chocolate cravings.20 Qualitatively, women tend to
crave sweet foods more often, whereas men tend to crave savory foods more often.26
Some data suggest that men and women indulge their food cravings equally often,
but may experience indulgence differently. For example, in one study women re-
ported more tiredness, boredom, and depression when indulging their cravings,
whereas men reported more happiness and relaxation upon indulging their crav-
ings.24 Although men and women report reduced cravings as they age, this reduc-
tion is more pronounced for women, with 100% of young women and 70% of young
men reporting experiences of food or drink cravings, and 66% of older women
and 62% of older men reporting these experiences.1,15 Thus, in older age, men and
women are similar in the frequency with which they experience food cravings.
Overweight Status
Relative to normal-weight people, overweight and obese people report more fre-
quent and intense cravings for highly palatable food (high-fat, high-sugar), and will
work harder in laboratory tasks for food.8,27,28 Weight gain impacts hormone and
peptide action (e.g., leptin and insulin resistance) that can shape reward-seeking
behavior by increasing food cravings and decreasing satiety.29,30 Additionally,

repeated exposure to highly palatable foods upregulates dopamine release and
downregulates dopamine-receptor sites (D1, D2) in the nucleus accumbens.31 The
decreased activation of D1 and D2 receptors may blunt individuals’ sensitivity to
experiences of neural reward, and increase the frequency of and indulgence in food
cravings, especially in the case of sugar.32 (See elsewhere in this chapter for a dis-
cussion how hyper- and hypo-responsivity to reward can be conceptualized as oper-
ating in tandem to exacerbate overeating.) This in turn may make it more difficult
for overweight individuals to adhere to and benefit from lifestyle interventions
targeting weight loss. This hypothesis fits with data collected from participants in
the Diabetes Prevention Program lifestyle intervention, which targeted overweight
adults with impaired glucose tolerance, a likely result of overeating calorically
dense, highly palatable foods. In this sample, greater food cravings at baseline were
associated with more previous weight-loss attempts, greater binge-eating severity,
less weight-loss efficacy, and greater non-adherence to a low-fat diet. Baseline food
cravings did not predict successful weight loss, and unfortunately the authors did
not report data addressing changes in cravings. 33,34
Surgical obesity treatment and lifestyle modifications targeting weight loss
have both resulted in reduced food cravings. Although bariatric surgery requires a
non-trivial amount of lifestyle modification, findings hint that food cravings can
be reduced by weight loss in itself, or changes in gut peptides, and not solely by
the behavioral change that is generally required for weight loss. In one study, 44
obese individuals received obesity surgery that resulted in a 20% weight loss by
six months post-surgery. These participants reported significant reductions in the
frequency of cravings for sweet, starchy, and high-fat foods, including high-fat fast
food, at six-month follow-up.35 Another study examined self-reported changes in
eating behavior in 40 patients 12 months after bariatric surgery, and reported sig-
nificant reductions in food cravings.36
Studies of diet interventions for obese individuals also report that reductions in
weight coincide with reductions in food cravings. In an analysis of 270 participants
assigned to either a low-carbohydrate or a low-fat diet, participants in each group
evidenced similar weight loss over time, and both groups reported similar reduc-
tions in food cravings for carbohydrates, sweet-tasting food, and fast-food fats, at
two-year follow-up.16 Thus, bariatric surgery and lifestyle interventions for weight
loss suggest that reducing body fat in a variety of ways may lead to decreased food
cravings.
Food cravings probably play a role in the subtype of obesity characterized by
high reward drive.37 To better assess subclinical, more normative levels of disor-
dered eating behavior, we developed the Reward-based Eating Drive (RED) scale,
which gauges individuals’ trait-like tendencies to eat in response to factors presum-
ably reflecting strong reward drive—feeling a lack of control over eating, lacking
satiety response, and feeling preoccupied with food.38 We have found that, among
overweight women, those who endorse greater reward-based eating drive also ex-
perience greater daily food-craving intensity, based on naturalistic daily reports.39
Brief self-report assessment measures such as RED may help to identify individuals
at greater risk for problematic food cravings, which is an important symptom to

address in weight-loss interventions and prevention of obesity.
Eating Disorders and Compulsive Eating
Compared to normal eaters, individuals with disordered eating patterns report

more intense food cravings when exposed to food cues.40 Data have indicated that
individuals who periodically binge eat,41,42 or who meet criteria for binge-eating
disorder,43 bulimia,44 or night eating syndrome,42,45,46 report more frequent or in-
tense food cravings. Bulimia, and to a lesser extent, binge-purge type anorexia, are
associated with an increased drive to eat, which correlates with food cravings.47,48
One recent review of food cue processing among individuals diagnosed with eating
disorders such as anorexia, bulimia nervosa, or eating disorder not otherwise speci-
fied, concluded that individuals with eating disorders evidence attentional biases
for food cues across different experimental paradigms.49 A full discussion of the
complex associations among disordered eating and food cravings is beyond the
scope of this chapter, and we refer the interested reader to recent reviews on this
topic.50,51
Dietary Restraint
Broadly, dietary restraint, or restrained eating, refers to the tendency to restrict food
intake consciously with a goal of weight maintenance or reduction. Dietary re-
straint is commonly assessed in various self-report measures, such as the Revised
Restraint Scale,52 Three-Factor Eating Questionnaire,53 and the Dutch Eating
Behavior Questionnaire. 54 Food-craving experiences (frequency, and type) do not
tend to score higher on self-report measures of dietary restraint, 55 and self-reports
of dietary restraint do not appear to predict weight gain over time.56
Dietary restraint, however, may be an important characteristic in terms of re-
ward drive. In laboratory reactivity situations, individuals with higher dietary
restraint report more intense food cravings and greater appetitive responses
upon exposure to food cues. This may help explain why many individuals who
report higher dietary restraint are more likely to fail in achieving a weight-loss,
diet-related goal: People with high restraint may be more likely to eat in response
to food cravings.57 For example, in one study wherein women restricted carbohy-
drate or protein intake for a three-day period, the authors found that individu-
als assigned to the carbohydrate-restriction condition who also reported greater
dietary restraint reported greater cravings for carbohydrate during the restriction
period. Similarly, among women deprived of chocolate for three days, those who
reported greater dietary restraint (relative to those who reported lower dietary re-
straint) ate significantly more chocolate after the deprivation period.58 Thus, data
suggest that trait-like dietary restraint may increase food cravings, but only in re-
sponse to observable cues.
How might we explain why longitudinal and cross-sectional data do not show
that higher dietary restraint is contemporaneously or prospectively associated with
increases in weight?55,56,59 At present, the literature is lacking a complete picture
of the factors that determine successful long-term restraint. Recent data suggest
that dispositional self-control moderates an association between increased die-
tary restraint and increased appetitive responses to food cues. In one study, indi-
viduals high in both dispositional self-control and restrained eating had normal
body mass indices (BMIs), whereas women low in dispositional self-control and
high in restrained eating had overweight BMIs.60 Of note, the authors reported
cross-sectional associations and called for longitudinal studies to understand how
associations between self-control and dietary restraint affect weight over time.
These findings are reminiscent of data that have differentiated between rigid and
flexible dietary restraint. Rigid dietary restraint reflects an “all-or-nothing” atti-
tude toward dieting, characterized by excessive self-control of eating behavior that
is often punctuated by failures, which are then difficult for individuals to over-
come when resuming their diet. In contrast, flexible dietary restraint reflects a
more balanced approach that is more forgiving of lapses that are not as difficult
for individuals to overcome in resuming their diet. One recent study reported that
food cravings mediated an association between rigid restraint (but not flexible
restraint) and perceived self-regulatory success in dieting, suggesting that rigid
restraint decreases perceived dieting success via increased food cravings. In this
study, flexible restraint predicted perceived dieting success.61
Indeed, restrained eaters who are successful in controlling their body weight
report fewer cravings for highly palatable food,62 and although this may be due
to greater levels of dispositional self-control, there are other possibilities. Some
restrained eaters may be more self-aware of their difficulties with eating in re-
sponse to food cravings, and may use this self-knowledge to be more effective in
reducing environmental cues that trigger food cravings, rather than directly sup-
pressing thoughts or responses when cravings occur. For example, several studies
have documented that simple environmental changes, such as moving a candy
dish as few as two meters further from one’s work desk or placing candy in an
opaque dish, decreases wanting for and consumption of that candy.63,64 In con-
trast, restrained eaters who attempt to suppress thoughts about foods that they
crave tend to eat more of this food, suggesting that for these individuals, dietary
restraint does contribute to weight gain.65 Similarly, relative to individuals with
lower dietary restraint, individuals with higher dietary restraint ate significantly
less chocolate before a thought-suppression task and more chocolate after the sup-
pression task.66
Implications of these data are that, although dietary restraint may promote mal-
adaptive eating behavior (especially in response to food cues), dietary restraint can
also be adaptive when paired with high trait self-control. Thus, we cannot interpret
the impact of high dietary restraint on eating behavior without the context of other
individual differences. Additionally, it is important to consider rigid and flexible
restraint as differentially affecting eating behavior. Researchers assessing dietary
restraint should do so in tandem with assessments of self-control, self-regulation
capacities, and the types of strategies individuals use to address cravings in real-life
situations. Moreover, researchers should be aware that, rather than restrained
eating leading to problematic eating behavior, it may well be the case that individu-
als who gain weight subsequently attempt to restrain their eating. That is, rather
than playing a mechanistic or causal role, restrained eating may be a marker for
tendencies to overeat.59
Sensitivity to Reward
Researchers agree that abnormalities in the pathways that shape the neural expe-
rience of reward in response to eating can disrupt normative eating patterns; how-
ever, these abnormalities may follow from a variety of situations. Researchers have
pointed to behavioral pathways (e.g., repeated overeating), genetic influences (e.g.,
the TaqIA A1 allele), biological factors (e.g., dopamine-receptor site availability),
and conditioning processes (e.g., emotional memories linking food intake to pos-
itive affect) as potential causes of such abnormalities. What sorts of abnormali-
ties might underlie a dysregulated reward system that leads people to eat in ways
that promote obesity and other metabolic consequences? Here, we review models
of hypo- and hyper-responsivity to food reward in the context of obesity, and how
food cravings fit within each model. We then review the recently posited dynamic
vulnerability model that incorporates both models.
Hypo-Responsive Model of Neural Reward
The hypo-responsive theory reflects the reward deficiency syndrome model and sug-
gests that obese individuals experience less neural reward in response to eating, po-
tentially due to sluggish neural reward circuitry, and therefore overeat in an effort
to counteract this deficiency.67 Certain genetic predispositions, such as presence of
the TaqIA A1 allele, have been associated with decreased neural reward responsiv-
ity, decreased reinforcement valuation of food, and increased weight gain.27,68 It is
also possible that overconsumption of highly palatable food downregulates dopa-
minergic activity, resulting in reduced neural experience of reward.69 It is unclear
what role, if any, food cravings may play in this profile. While this model focuses
on overeating behavior as a causal factor in neural adaptation, it may be that the
blunted response to eating is preceded by an excessive reward drive and associ-
ated food cravings that motivate individuals to seek highly palatable food in the
first place. Further research should utilize longitudinal designs to assess temporal
associations between food-craving intensity, neural reward circuitry, and subjec-
tive reports of wanting and liking.
Hyper-Responsive Model of Neural Reward
The hyper-responsive theory reflects the reinforcement sensitivity model of sub-

stance abuse, and posits that obese individuals are more sensitive to the rewarding
aspects of eating, and therefore eat more to heighten their experience of re-
ward.70,71 Self-report measures of general reward sensitivity that have been com-
monly used in research on eating behavior include the Physical Anhedonia Scale,72
the Sensitivity to Punishment and Sensitivity to Reward Questionnaire (SPSRQ),73
and the Behavioral Activation System (BAS) component of the Behavioral
Inhibition System (BIS)/BAS scales.74 Greater reward sensitivity, as indexed by
these self-report measures, has been associated with higher BMI and greater trait
food craving.70,75
A growing body of literature highlights important distinctions between the
hyper-responsivity to reward when anticipating versus when consuming palat-
able food. Incentive salience theory suggests that anticipatory and consummatory
reward have temporal associations that lead to increases in the reinforcement
value of food. This increased valuation leads to increased anticipatory reward
(i.e., motivated craving, or wanting) and decreased consummatory reward (i.e.,
hedonic pleasure, or liking).76 These increases in anticipatory reward, or moti-
vated craving, may lead to greater food intake, suggesting that individuals condi-
tioned to experience greater anticipatory reward may be at a heightened risk for
weight gain.77
Dynamic Vulnerability Model of Neural Reward
Burger and Stice78 recently proposed an integration of evidence for each the
hyper- and hypo-responsive models of neural reward, theories of anticipatory and
consummatory reward, and conditioned behavior that shapes the reward experi-
ence. They proposed that individuals at risk for obesity might initially experience
hyper-responsivity to reward in response to eating, which leads to subsequent over-
eating. Repeated overeating (1) increases the reinforcing value of food and strength-
ens conditioned associations surrounding eating; and (2) dampens dopaminergic
action in response to food intake. These two processes form a positive feedback
loop that maintains overeating so as to experience a dopamine-driven neural re-
ward experience. Behavioral responses to food cravings are key components in this
developmental model, given their importance in initiating and maintaining condi-
tioned food cues. Findings suggest that this model may more accurately depict how
the associations between reward responsivity and eating behavior change.78
TRIGGERS OF FOOD CR AVINGS
A biopsychosocial model (e.g., Rogers & Smit, 2000) of food craving posits im-
portant roles for conditioning, dieting status and dietary restraint, food en-
vironment, health behavior (e.g., sleep), biological factors (e.g., hormones and
nutrient deficiencies), and psychological factors (e.g., stress and mood) in trig-
gering food cravings. Below, we review empirical support for several of these
triggers.
Pavlovian Conditioning
The pairing of consumption of a given food with a rewarding consequence

increases the incentive value of a given food. This incentive valuation, or rendering
of certain food cues as highly desirable, results from a Pavlovian conditioning
process.79 According to this conditioning model, the development of a craving for
a given food requires familiarity with this food and the rewarding consequences
of ingesting it, meaning that individuals do not crave highly rewarding novel
foods. This behavioral model maps onto dopamine action, which is considered to
be a primary determinant of food-seeking behavior80 and is discussed in depth
elsewhere in this volume (Chapter 3). Briefly, eating stimulates dopaminergic re-
lease, and over the course of repeated pairings of eating with an environmental
cue, that environmental cue alone may come to stimulate dopamine release. Upon
observing and attending to this cue, dopamine may then bind to D2 receptors in
the nucleus accumbens and stimulate strong motivational states of wanting, or
food craving (for a review, see81). Therefore, researchers have recommended that
individuals who endorse problematic craving-related eating limit the places in
which they eat, and the activities in which they engage while eating, in order to
reduce the development of environmental cues to eat. A person attempting to lose
weight, or avoid future weight gain, might consider bypassing the delicious smells
wafting from a local bakery while walking to work, and might try to avoid the
office kitchen until he or she can be reasonably certain that the morning dough-
nuts have vanished.
Dieting Status and Diet Interventions
Data addressing the impact of dieting on food-craving experiences are mixed. Here,
we refer to “dieting” as the state of currently being on a diet, rather than dietary
restraint, which is most often not correlated with actual caloric intake and there-
fore not reflective of dieting status.82–84 The “deprivation hypothesis” holds that
individuals will more often crave the foods they are deprived of, and short-term
laboratory data support this hypothesis. In one study, women deprived of carbohy-
drate or protein for a three-day period reported increased cravings for these macro-
nutrients during the restriction period.85 More studies, however, report that dieting
in the form of low-calorie diets or macronutrient restriction (e.g., low-carbohydrate
or low-fat diets) can reduce the frequency and intensity of food cravings.86–88 In
one study that assigned individuals to either a low-carbohydrate or a low-fat diet
regimen, individuals reported reductions in food cravings specifically for the mac-
ronutrient they were assigned to limit.16 Similarly, diet interventions that instruct
individuals to restrict caloric intake also lead to reductions in food cravings.88
In addition to reducing food cravings, diet interventions may reduce the fre-
quency with which individuals “give in” to their food cravings: prior to a six-month
diet intervention, overweight women reported “giving in” to their cravings 64%
of the time, and following the intervention, they reported “giving in” 27% of the
time, and this reduction was unrelated to the amount of weight lost.10 Data high-
lighting associations between dieting status and food cravings tend to suggest
that dieting may reduce the frequency and indulgence of food cravings, which
theoretically should be critical to the regulation of eating. However, the status of
simply being on a diet introduces many other vulnerability factors that prevent
weight loss maintenance over time: a recent review of prospective studies examin-
ing the impact of dieting status on future weight gain found that 75% (15) of the
reviewed analyses found a positive association between currently dieting and pro-
spective weight gain.56 Thus, while short-term dieting status may be helpful for
reducing cravings, dieting behavior is notoriously difficult to maintain. Food crav-
ings may play a key role in individuals’ inabilities to maintain successful weight
loss, as some research has indicated that those who successfully maintain their
weight loss report using coping strategies that do not involve eating in response
to food cravings.89,90
Food Environment
The modern food environment is oft-termed “obesogenic” due to the widespread

availability of food and drinks that are calorically dense, non-nutritious, highly
palatable, and often highly processed. 91,92 We are constantly surrounded by ex-
ternal cues to eat when not in a state of energy depletion, and these cues af-
fect our eating behavior even when we do not consciously attend to them. 93–95
This environment is surely a mismatch for humans’ innate response patterns
to the biological need to eat. Researchers have argued that in the context of the
modern food environment, homeostatically based hunger and satiety cues play
a lesser role in determining eating behavior than environmental cues to eat. 96
Sounds, colors, food packaging, smells, plate shape, lighting, socializing, and a
myriad of other environmental factors influence motivations to eat by inhibit-
ing physiological cues of caloric deficit and suggesting alternative reasons for
consumption.97
Individual differences, such as reward processing, impulsivity, and dietary
restraint,98,99 shape attention to cues indicating the availability of highly palatable
food and also render certain individuals more susceptible to the influence of these
cues on eating behavior.70 In one study, overweight individuals, relative to lean
individuals, reported greater increases in the desire to eat pizza when exposed to
the sight and smell of pizza.100 Another study found that food cues can exert larger
effects on the eating behavior of individuals who report greater dietary restraint.
Researchers presented restrained and unrestrained eaters with smells and ver-
bal descriptions of pizza, and found that restrained eaters reported more intense
cravings than unrestrained eaters.98 Individuals who report greater susceptibility
to the impact of living in a food-abundant environment as indexed by the Power
of Food Scale101 experience stronger food cravings in response to environmental
food cues and endorse increased desire to eat when in the presence of highly palat-
able food.102
Sleep Deprivation and Disorders
The past two decades have seen a wealth of data linking dysregulated sleep to
weight gain and overweight and obese status.103,104 Sleep deprivation and disrup-
tion can alter diurnal rhythms of appetite-regulating hormones operating in endo-
crine and metabolic pathways in ways that increase caloric intake. Few studies,
however, have specifically unpacked how sleep affects food cravings. In a sample of
adolescents, greater daytime sleep (for any reason, such as napping to compensate
for insufficient nocturnal sleep) was associated with greater total food cravings,
as indexed by a food-craving inventory.105 In another study, men deprived of sleep
(from ten hours per night to four hours per night) reported increases in desire for
high-carbohydrate, sweet, salty, and starchy foods, as well as changes in the pep-
tides that regulate hunger, specifically, decreased leptin and increased ghrelin.106
Similarly, in a study of individuals with obstructive sleep apnea (OSA), which leads
to reduced or disrupted nighttime sleep, individuals with greater disease severity
selected dinner items off of a menu that were higher in fat and carbohydrate content
(e.g., French fries) than those with lesser disease severity.107 If sleep curtailment is a
causal factor that increases food cravings, increasing sleep time should reduce crav-
ings. Indeed, recent intervention data show that increasing bedtime duration to 8.5
hours each night resulted in decreased cravings for salty and sweet foods, such as
cake, candy, cookies, and ice cream.108 In sum, a growing literature suggests that
sleep restriction may increase cravings, and that interventions targeting increased
sleep duration may reduce food cravings.
Hormones
Gender differences in food cravings implicate non-trivial roles of sex hormones

in eliciting craving experiences. Under normal conditions of reproductive cycling,
pre-menopausal women undergo increases in estrogen and progesterone during the
periovulatory and midluteal phases, with a peak estrogen level at ovulation that is
followed by a drop in estrogen and progesterone. The ovarian hormone hypothesis
of food cravings suggests a direct link between hormonal shifts and food cravings
such that women experience more food cravings during the luteal phase.109 Data
do not uniformly support this hypothesis, with some reporting no differences in
craving across the menstrual cycle.93 The majority of studies, however, appear to
report an impact of the menstrual cycle on food cravings. In one study, nearly 68%
of women reported chocolate cravings around the time of menstruation.110 Women
report food-craving experiences to be a core component of premenstrual syndrome
(PMS),111 and those diagnosed with premenstrual dysphoric disorder(PMDD) en-
dorse more cravings during the luteal phase.112
Furthermore, there is a significant decrease in chocolate cravings between
pre- and post-menopausal women, although this difference is probably not large
enough to support a purely hormonal explanation for chocolate cravings.113
Laboratory studies have yet to manipulate sex hormones to impact food cravings.
Furthermore, estradiol, a common component of oral contraceptives, has not been

found to be significantly associated with frequency of food cravings,114 and oral
contraceptives have not been found to alter food cravings across the menstrual
cycle.115,116 Thus, while there are often small main effects of cycle and menopausal
status across women on cravings, it appears that only a subgroup of women are par-
ticularly vulnerable to problematic hormone-related cravings—such as those with
Premenstrual dysphoric disorder (PMDD). The individual differences that predict
which women are more sensitive to hormone-induced cravings are unknown.
Nutrient Deficiencies and Orosensory Experience
Though popular, the hypothesis that food cravings result from nutrient deficien-
cies has garnered little empirical support. For example, one hypothesis is that
chocolate, an oft-craved food among women, may restore magnesium during
menstruation.7 Others suggest that carbohydrates may increase brain serotonin
levels117 and that sweet foods may restore blood glucose levels.118 Data, however,
do not appear to support these nutrient deficiency hypotheses. One study fed
women variations of chocolate, including an orally ingested capsule of cocoa with
cocoa equivalent to a serving of chocolate, an actual chocolate bar, or a serving
of white chocolate, which lacks commonly cited pharmacological components of
chocolate (e.g., theobromine, magnesium). This study design allowed research-
ers to disentangle the orosensory components of eating chocolate—the smells,
texture, and tastes—from the nutritional content of cocoa, so that they could
better understand if cocoa was indeed craved due to a nutritional deficiency. Data
indicated that cocoa capsules did not satisfy chocolate cravings, white chocolate
partially satisfied chocolate cravings, and chocolate itself reduced chocolate crav-
ing. The authors concluded that although aroma, sweetness, texture, and calories
may lead to satisfaction of chocolate cravings, the lack of reduction in chocolate
cravings following ingestion of the cocoa capsules fails to provide evidence for
pharmacological effects in the satisfaction of chocolate cravings.119 In another
study, young adults eating a monotonous, though nutritionally adequate diet (a
single sweet nutritional supplement beverage) reported sizeable increases in food
cravings relative to when they consumed a varied diet at baseline.15 This, too, sug-
gests that the orosensory components of eating play a key role in the satisfaction
of cravings.
In contrast to the idea that decreasing a nutrient will lead to increased craving
for it, some data show that food cravings for restricted foods decrease in the context
of diet interventions (e.g., decreased carbohydrate cravings on a low-carbohydrate
diet).120 Additionally, food cravings are often for nutrient-poor foods (e.g., pizza, ice
cream).1,7 In sum, it has been difficult to demonstrate an association between nu-
tritional deficiencies or macronutrient compositions and increased food cravings
in laboratory settings, and data thus far suggest that food cravings may primarily
arise due to orosensory factors and dietary monotony.
One emerging theory hints that the gut microbiome may play a role in eating
and obesity. Researchers have hypothesized that gastrointestinal microbes may
stimulate cravings for foods that either enhance their survival or suppress their
competitors; a fascinating concept, but one that awaits experimental data in
humans.121
Stress, Mood, and Food Cravings
Stress has powerful effects on eating behavior, but we know little about the mech-
anisms linking stress to experiences of and indulgence in food. To complicate
things, stress can dampen the appetite and hedonic response to stimuli including
food,122–124 although here we focus on the more common pattern of stress-enhanced
appetite. Stress may increase the intensity or frequency of cravings, particularly for
people with eating issues in a broad sense—such as obesity, high dietary restraint,
emotional eating, or dysregulated eating behavior. Could the effects of stress on
overeating and weight gain be in part due to increases in the reward value of food
and the intensity of cravings under stress? Here we review what is known about
associations between stress, food craving, and eating.
Stress can increase incentive salience and cravings for substances.125 It appears
that stress can also increase the rewarding value of food.126–128 However, as is com-
monly the case with the multifaceted constructs of acute and chronic psycholog-
ical stress, stress more often strengthens the association between vulnerability
factors and resulting behaviors, rather than increasing the behaviors across the
board. Acute stress, such as exposure to a laboratory stressor, affects people differ-
ently depending on their level of chronic or daily stress. Acute stress differentially
impacts individuals’ appetites, with some individuals reporting decreased appetite
and some reporting increased appetite. A growing body of data suggests that these
differential effects may depend in part on levels of background chronic stress and
biological predispositions (e.g., level of hypothalamic-pituitary-adrenal [HPA] axis
responsiveness) or appetitive predispositions to engage in dysregulated eating pat-
terns in times of emotional chaos.
To date, the most dramatic effects of stress on reward drive have been shown in
non-human animals. For example, rats presented with highly palatable food tend
to eat beyond their homeostatic needs. Rats conditioned to binge eat through cyclic
caloric restriction (which may be thought of as an analogue to dietary restraint in
humans), however, eat significantly more highly palatable food when administered
an acute stressor (footshock).129 Administering the opioid antagonist naloxone to
these rats blocks this effect, which suggests that binge eating in rats with histories
of caloric restriction is mediated by the opioidergic system. Data have shown that
this pattern of neural adaptation is robust, and that rats conditioned to binge (via ca-
loric restriction and stressor exposure) will withstand greater aversive stimuli (e.g.,
stronger footshock) in order to obtain a food reward.130 Thus, conditioned eating
in response to stress appears to be a robust response that is likely to be difficult
to extinguish—we are unaware of rodent designs that have successfully reversed

conditioned binge eating.
Human laboratory data also underscore impacts of acute stressors on food
cravings and the consumption of highly palatable food. Several paradigms have
exposed women to acute stress so as to examine changes in cortisol, food cravings,
and eating of “comfort food” (which is often highly palatable) in response to the
stressor. In one study, women who evidenced higher cortisol reactivity in response
to an acute standardized stressor ate more calories from comfort foods after the
stressor, and reported eating more sweet foods,131 but this study did not examine
interactions with chronic stress or other eating-relevant moderators. A few re-
cent studies have characterized women by level of chronic stress, which appears
to heighten sensitivity of the reward center and increase appetitive drive. In one
study, women endorsing higher (relative to lower) chronic stress at study intake
evidenced blunted cortisol responses to an acute stressor and reported significantly
more emotional eating.132 Similarly, another study assessing eating in response to
an acute stressor found that women who reported greater trait emotional eating
and who evidenced a blunted cortisol in response to the acute stressor ate signif-
icantly more comfort food after the stressor task.133 In contrast, another study
reported that greater chronic stress was associated with greater trait-level food
craving after an acute stressor, but only for women who showed an increased, rather
than a blunted, cortisol response.134
On the surface, these studies suggest two phenotypes—that women who have
hyper- or hypo-responsive HPA activation may experience more frequent or intense
cravings for highly palatable food after an acutely stressful experience. Why might
these women evidence different patterns? Stress-induced increases in cortisol are
thought to induce increases in appetite—and thus it is not surprising that high reac-
tivity can increase the drive to eat palatable food.131,135,136 In contrast, chronic stress
coupled with repeated overconsumption of highly palatable food suppresses HPA
reactivity, turning the drive to eat palatable food into a habit-based behavior.137
Animal models suggest that chronic stress and intermittent access to highly palat-
able food may instantiate neural adaptations that more tightly couple the eating,
the reward system, and HPA axis activity. Thus the hypo-responsive profile may be
a proxy for people who have undergone neural adaptation to chronic stress. That
is, as described above, a greater motivational drive for highly palatable food may in
turn lead to a downregulated HPA axis. In this way, cortisol reactivity may prove
an integral puzzle piece in understanding neuronal adaptations to chronic stress.
Laboratory stress studies find that biological (cortisol reactivity), behavioral
(eating in response to stress), and stress-related (chronic stress) factors may render
individuals more susceptible to eating in response to food cravings. Thus, under-
standing individuals’ phenotypes as indexed by self-reported stress-related eating,
chronic stress, and trait food craving, as well as objective measures of cortisol re-
activity to acute stress and of eating in response to acute stress, will further eluci-
date associations between stress, food cravings, and eating. Future research should
expand upon the laboratory and short-term animal and human laboratory studies
in order to create and test longitudinal models of associations between stress, food
cravings, and eating in response to food cravings.
Although a body of literature has laid the groundwork for unpacking associations
between stress and food cravings, associations between mood disorders and food
cravings are less abundant. One study reported that, across a large sample of under-
graduates, greater negative affect was associated with greater intensity of cravings,
but only for those who self-identified as “carbohydrate cravers.”9 Several studies
have manipulated state emotions, such as positive and negative affect, to better un-
derstand associations between food cravings and food consumption. These studies
may offer clues about how mood affects food craving and incentive salience of food.
People who identify as “emotional eaters” show greater neural responsivity when
anticipating and consuming palatable food, but only when induced to experience
negative mood.138 In contrast, non-emotional eaters evidenced reduced activa-
tion in the reward system when induced to experience negative mood (relative to
a neutral mood). Studies in rats and humans have demonstrated that induction of
depressive mood can increase chocolate cravings.139 Among women with bulimia,
greater negative affect was associated with greater neural reward activation when
anticipating palatable food, suggesting that negative affect may prime the reward
drive in these women. In contrast, women’s neural activation in response to con-
suming palatable food was uncorrelated with affect.140 In another study of bulimic
women, negative affect was a more potent trigger of cravings that led to a binge
episode than was biological hunger. Furthermore, cravings alone did not typically
lead to binges, but cravings in the context of negative affect did.141 Similarly, obese
people exposed to a negative mood induction, or a relived favorite food cue, both
evidenced greater corticolimbic-striatal activation, a motivation-reward region of
the brain. Activation in this area mediated an association between insulin sensi-
tivity and food craving, suggesting that improving insulin sensitivity and reducing
reactivity to food- and stress-related cues may improve eating behavior in the con-
text of obesity.4 These studies support the idea that negative affect can increase
neural reward drive and the experience of strong cravings.
FOOD-CR AVING ASSESSMENT
Food cravings are a common experience, and may or may not lead to overeating. It
is critical to assess them in ways that will allow us to identify risk factors that pre-
dict the problematic overeating that may result without intervention. Once these
patterns of habitual eating in response to food cravings have already developed,
reversal of the neural, metabolic, and behavioral patterns that promote weight gain
is very difficult to achieve and maintain. Here we review commonly used measures
and suggest study conditions in which they are most applicable.
Pelchat (2002)158 asserts, “Craving, as a psychological experience, is best meas-
ured by self report” (p. 350). There are several self-report methods of measuring
food cravings (for reviews, see120,142). Most self-report measures of food crav-
ings assess either state or trait food craving. “State food craving” refers to food
cravings in response to specific, momentary situations, psychological states, or

physiological states, and these measures can be repeatedly administered over
the course of various interventions. “Trait food craving” refers to aspects of food
craving that are stable within an individual across time and situations, and are
less likely to change over time. Whereas state measures of food craving may elu-
cidate changes in food cravings due to study manipulations, trait measures of
food craving may be more useful in predicting outcomes related to eating beha-
vior and food choice.
The original Food Craving Questionnaires (FCQ) for each state (FCQ-S) and trait
(FCQ-T) food craving143 ask respondents to think of a specific food that one craves
while completing the measures, and have been subsequently modified to reflect
general trait food cravings (G-FCQ-T144); they also target specific foods, such as
chocolate.145 Variations of the FCQ have been validated in several languages, such
as German, Spanish, and Korean.146–148 Authors of the original FCQ-T and FCQ-S
found that participants’ scores on the FCQ-S differed considerably across fasting
and sated states, whereas participants’ scores on the FCQ-T did not.143 Furthermore,
all nine subscales within the FCQ-T correlated with measures of hunger and dis-
inhibited eating, as indexed by the Three-Factor Eating Questionnaire (TFEQ),53
while only one of five subscales within the FCQ-S correlated with both hunger and
disinhibited eating on the TFEQ. Thus, the state and trait versions of this scale ap-
pear to tap distinct facets of food craving.
Self-report inventories of commonly craved foods, such as the Food Craving
Inventory, are often administered pre- and post-interventions, and are designed
to measure changes in food craving as a function of an intervention. Food-craving
inventories also allow the assessor to conceptualize the respondents’ cravings in
terms of broad categories, such as sweets, starches, and fats. This type of scale is
probably most helpful for understanding the specific types of cravings an indi-
vidual is having, and for tailoring specific interventions.
Alternatives to multi-item, validated measures of food craving include face-valid,
individual items asking respondents to rate their craving intensity using visual an-
alogue or Likert scales. For example, in one study targeting reductions in food crav-
ings by using imagery techniques, the authors used a single-item craving intensity
measure, asking participants to rate the intensity of their cravings on a ten-point
Likert scale.149 Assessing cravings qualitatively may also yield rich data: Dressler
and Smith used open-ended questions to interview women living in low-income
environments about their food cravings, and found that overweight/obese and
lean/normal-weight reported that health and cost were significant determinants
of food choices, respectively.150
Assessing food cravings in terms of individuals’ relationship to the experience
of cravings may index individuals’ abilities to experience, but not act on, food crav-
ings. A novel measure of food-craving experience, the Food Craving Acceptance
and Awareness Questionnaire (FAAQ) was developed to assess acceptance of
food-craving experiences and the extent to which individuals attempt to control
these experiences.151 The psychological ability to experience food cravings and
not act on them may prove critical for healthy eating and weight loss, although no
large-scale studies have tested this. Juarascio and colleagues reported that, among
a sample of 29 overweight or obese women enrolled in a weight-loss program,
greater acceptance of food-craving experience as indexed by the FAAQ predicted
greater weight loss.151
In addition to self-report measures of cravings that are generally completed
before and after given interventions, recent investigations of food cravings have
turned to ecological momentary assessments (EMA) as a method of capturing
food-craving experiences in real time. For example, Berkman and colleagues
(2014) developed a text-messaging program that allows individuals to receive and
respond to text messages asking them about their experiences of hunger, craving,
and eating.152 This methodology may be more sensitive to acute changes in sit-
uational (state) food cravings and allow researchers to understand the daily im-
pact of interventions. Additionally, EMA of food cravings allows the assessment
of transient craving experiences in the context of social, behavioral, or environ-
mental antecedents of cravings, as well as the aftermath of craving experiences
(i.e., whether one satisfied the craving, waited for it to pass, or responded in some
other fashion).
In sum, researchers should employ diverse methodologies when assessing food
cravings. Food cravings are not static traits, but dynamic experiences that unfold
in very specific contexts with sensitive timeframes. Trait craving assessments
may reveal important individual differences that indicate who will benefit from
particular interventions. State craving assessments, such as food inventories and
measures of frequency and intensity, would allow researchers to ascertain impacts
of interventions with more sensitive information. Such measures would allow
researchers to unpack how, for example, weight-loss protocols alter cravings for
particular foods, or alter the frequency or intensity with which individuals expe-
rience food cravings. EMA methodologies enable fine-grained analyses targeting
associations between food cravings and a variety of daily events, such as exposure
to food cues while spending the day at a bakery café with friends, or during an
argument with a spouse. Using a multimethod approach to assess food cravings,
and tailoring the measures of food craving to answer key research questions about
food cravings, will undoubtedly increase our knowledge of how food cravings im-
pact health.
CONCLUSION
When does a craving become pathological, putting one at risk of repeated

overeating and obesity-related metabolic dysregulation? The modern food en-
vironment, replete with easily accessible, highly palatable food, can promote
persistent overeating in response to food cues in certain individuals. Here we
have emphasized that frequent and intense food cravings may play a key role
in the growing obesity epidemic and are thus critical to investigate as potential
targets of intervention. Furthermore, cravings may potentiate or otherwise

significantly affect eating-disorder symptomology;141 thus they are implicated
in the development of obesity and eating disorders, pointing to potential for
prevention.
Cravings are a key component of addiction processes, and are experienced by
chronic dieters, individuals with clinical eating disorders (e.g., bulimia and binge
eating), and individuals who do not identify their behavioral responses to food
cravings as contributing to their overweight. Each of these patterns is alarming
and must be attended to. Chronic unsuccessful dieting may lead people to seek
treatment that involves dietary, behavioral, and emotional supports, such as
Weight Watchers,153 and individuals with eating disorders may be less likely to
seek treatment. Overweight individuals who frequently experience and indulge
food cravings and are either not aware that, or do not believe that, their eating
in response to food cravings may contribute to their overweight status, may be
at heightened risk for obese status over time. Therefore, it is critical to identify
people at risk for overeating in response to food cravings and to develop inter-
ventions that target behavioral responses to food cravings and triggers for food
cravings.
Most lifestyle interventions that address food cravings identify obesity as
the target outcome variable; however, some researchers have begun targeting
food cravings as an independent study outcome. The past decade has witnessed
a surge in behavioral treatments for food cravings, including mindfulness and
acceptance-based treatments,86,102,154 cognitive and behavioral treatments,98,155
nutritional interventions,16,88 and suggestions for possible environmental
interventions.156,157
We have found that a ten-item self-report assessment of reward-based eating
drive to eat predicts daily cravings39 as well as weight gain over time. 38 Other
craving measures appear helpful in predicting how people fare in weight-loss
programs. Here we have reviewed many factors that put one at risk for more
food-craving experiences (see Figure 4.1). Better understanding of how these psy-
chological, behavioral, and neurobiological constructs shape cravings will allow
us to develop targeted interventions for craving-related eating behavior. Chronic
stress and dysregulated HPA axis responsivity appear important in laboratory
studies, and may be key players in identifying a risk profile for reward-based
eating, especially in times of high negative affect. It appears that interventions
for reward-based eating that target behavioral responses to cravings are not only
warranted but also are necessary to curb the tide of obesity. Future research will
hopefully shed further light on the types of cravings that lead to overeating, and
how to prevent and reduce them.
ACKNOWLEDGMENTS
The authors are grateful to Michael A. Cohn for his feedback on chapter drafts
and to Carmen Montagnon for assisting with literature reviews. The first author’s
preparation of this chapter was supported by National Center for Complementary

and Alternative Medicine (NCCAM; 5T32AT003997).
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C H A P T ER 5
w
Overeating and Binge Eating
M A RGA R ET LEI TCH A ND A LL A N GELIEBTER
O ur current food environment offers unlimited choices of foods, many of which

are both high in energy density and low in nutrient content.1 Due in part to
the omnipresence of hyper-palatable food, engineered to deliver maximal oral
pleasure, global obesity rates have risen dramatically within the past thirty years,2
which the World Health Organization has referred to as one of the most serious
health crises of the twenty-first century. Obesity is the result of an excess con-
sumption of calories3–6 relative to energy needs. While overeating hyper-palatable
food can be viewed as hedonic excess, unlike other drives for reward such as drugs
or gambling, eating is unique, as food is required to live. Therefore, the complex in-
terplay between homeostatic and hedonic mechanisms within the brain to regulate
feeding has become the focus of intense study.
One of the most important, but least understood, aspects of obesity is how
metabolic factors act in concert with environmental factors (e.g., food cues, social
influences) to perpetuate overeating. The interplay between homeostatic, hedonic,
and inhibitory systems helps determine the amount of food consumed during a
meal and the duration of the meal. Homeostatic eating is guided largely by the
hypothalamus in response to energy depletion, whereas hedonic eating is guided
by the rewarding aspect of food via signaling in the limbic system. Inhibition of
further hedonic intake is modulated by the dorsolateral prefrontal cortex to re-
strain eating.7 Adequate food for sustenance is now common in most industrial-
ized nations, which minimizes the importance of eating in response to homeostatic
needs.8 Overeating relative to energy needs leads to deposition of excess adipose
tissue and other physiological sequelae, which may further impede control of one’s
eating behavior.9 Chronic overeating is often driven by reward and pleasure and
by lack of inhibitory control.10–12 A current research focus is on the interaction be-
tween hedonic and homeostatic systems to help improve inhibitory control.13
( 85 )
We will describe the psychobiological factors that contribute to excessive

food intake, beginning with early theories of eating motivation, the bases of
pleasure-driven eating, and how intermittent excessive consumption of highly pal-
atable foods can reduce inhibitory control, perpetuating cyclical overeating habits.
CHANGES TO THE FOOD ENVIRONMENT
Obesity results largely from overeating relative to the organism’s energy needs.14
The availability of hyper-palatable foods (high-sweet and/or high-fat15), the media
stream of food-related imagery and food cues, and the increased availability of
foods low in fiber and protein are major factors in the global obesity epidemic.16
The decision to eat is the result of a complex interaction between environ-
mental and psychological factors (for reviews, see Blundell & Gillett 200117), but
underlying this is the biological regulation of food intake by hunger and satiety
signals. Peripheral nerves, mainly those in the digestive tract in concert with adi-
pose tissue, communicate to the brain, and the brain itself also recognizes signs of
energy depletion. Neurons within the hypothalamus receive signals from periph-
eral organs or act in response to environmental food cues, which may override real
physiological hunger signals and lead to excess caloric intake. Daily food intake can
be characterized by meal frequency and timing, and meal composition, which vary
greatly across individuals. Psychological states and traits such as impulsivity,10,18
stress,19,20 and depression21 also influence eating behavior.
In the past decade, much progress has been made in identifying the neural cir-
cuits that control the exchanges between homeostatic drives versus emotional and
hedonic aspects. Growing evidence suggests that obesity results from an imbalance
in the brain’s response to rewarding stimuli.9 Excessive consumption of highly pal-
atable foods can also contribute to decreased sensitivity to food reward.14 Given
the increasing frequency of consuming foods outside the home,22 the increasing
portion sizes,23 and the increased processing of corn and soy derivatives,24 it is not
surprising that there has been an marked increase in body mass index (BMI) within
both developed25 and developing countries.26
The current obesity epidemic indicates that our eating is no longer confined by
metabolic needs.27,28 The neural pathways within the corticolimbic structures of
the brain are primarily responsible for emotionally based, pleasure-driven eating,
whereas metabolic systems within the brainstem and hypothalamus are primarily
engaged in determining energy intake and balance. Dysfunctional interaction be-
tween the corticolimbic structures and the hypothalamus can lead to overeating
and obesity.
EARLY THEORIES OF EATING MOTIVATION
Early models of eating behavior emphasized the body weight set-point and its con-
trol by genetic factors.29–32 Nisbett (1968) proposed that body weight was regulated
O vereating and B inge E ating ( 87 )
by a thermostat-like mechanism to readjust weight following large changes to a

person’s genetically predetermined set-point. The hypothalamus regulates appe-
tite by receiving and sending signals to increase energy intake in depleted states
and to reduce intake when energy stores are in excess. The neuronal mecha-
nisms involved include the orexigenic neuropeptide Y/Agouti-related proteins,
which stimulate intake, and the anorexigenic pro-opiomelanocortin/cocaine and
amphetamine-related transcript neurons in the arcuate nucleus of the hypothal-
amus, which reduce intake. These systems communicate energy depletion or re-
pletion via projections from the arcuate nucleus to other hypothalamic nuclei
(paraventricular, dorsomedial, ventromedial, and lateral nuclei).
Short- versus Long-Term Appetite Control
Short-term control of appetite can be described by a satiety cascade. 33 The affec-

tive reactions to taste (i.e., the cephalic phase) provide indications of a food’s en-
ergetic value and can initiate an early satiety response. 34 The stomach then senses
the quantity of food via mechanoreceptors, which communicate to the brain and
also influence the rate with which the stomach empties into the small intestine.
Emptying is inversely related to the energy content of the meal, triggering the re-
lease of more satiety peptides from the small intestine, such as cholecystokinin
(CCK), glucagon-like peptide (GLP-1), and peptide YY.35 The volume and energy con-
tent of a meal, as well as levels of satiety peptides, contribute to the sense of full-
ness.36 However, long-term homeostatic signals also contribute to the regularity
with which one experiences hunger. 37 Peripheral hormones related to body energy
stores, including leptin and insulin, and possibly ghrelin, influence long-term
hunger signals. Hormones can also interact to produce more pronounced feelings
of satiety; for example, interactions between leptin and the satiety peptides, CCK
and GLP-1. Insulin has been shown to modulate the effect of CCK,38 and GLP-1, ac-
tivated by nutrients, can stimulate insulin release.39
The set-point model has evoked much scientific debate,40 particularly in light
of the obesity epidemic. The high rates of obesity in children and adolescents are
unlikely to be a result of dysfunctional regulation of the hypothalamus or impaired
leptin or melanocortin signaling,41 and more likely to be due to increases in the
availability of high-energy palatable foods that can override regulation via hypo-
thalamic control. While set-point theory can help explain well-regulated appetite
in lean individuals,42 it cannot account for the increased incidence of obesity in re-
cent years.43
CONDITIONED OVEREATING
Potent food cues contribute to overeating and highlight the psychological and neu-
rocognitive components that contribute to eating even in the absence of hunger.
Potent environmental cues can override physiological satiety signals, and one of the
earlier models of cue-induced conditioned eating was developed by Weingarten.44

After experimenters paired a tone or light (conditioned stimulus: CS+) with the pre-
sentation of a food cup, energy-restricted rats learned to go to the food cup as soon
as the light was turned on. This behavior persisted even when the rats were then
placed in an ad libitum eating condition, showing that a CS+ could elicit eating, even
in a sated state.
Petrovich et al.45 demonstrated the importance of an extended neural net-
work that responds to food-related stimuli, which includes the amygdala,46 me-
dial prefrontal cortex, and lateral hypothalamus.47 Inputs to the hypothalamus
from both the amygdala and medial prefrontal cortex link conditioned stimuli
to appetitive action. Since the lateral hypothalamus plays a major role in regu-
lating energy balance, the information from both the amygdala and prefrontal
cortex concerning food cues may help override satiety signals. Communication
between lateral hypothalamic orexin neurons and the mesolimbic dopamine
system has been implicated in mu-opioid–induced food intake 48 and reinstate-
ment of drug-seeking.49
Neuroimaging technology has provided researchers with observational tools to
explore the impact of food cues on lean and obese individuals. Rothemund et al. 50
used functional magnetic resonance imaging (fMRI) to assess responses to pictures
of high-calorie and low-calorie foods, and neutral images following a 1.5-hour fast.
In obese (vs. lean) individuals, the high-calorie cues led to increased activation in
the dorsal striatum, anterior insula, claustrum, posterior cingulate, and lateral or-
bitofrontal cortex (OFC). The dorsal striatum is involved in reward anticipation and
habit learning, the anterior insula and lateral OFC are involved in taste processing
and motivation, and the posterior cingulate is involved in emotion as well as mem-
ory functions.51Thus, a CS+—a picture of a food—led to greater relative activation
in obese individuals, especially in cortical areas beyond the hypothalamus.
Interestingly, gender differences have been found in the responses of obese
individuals to food-related imagery.52,53 Using fMRI, Geliebter et al. (2013) found
that obese women had greater neural activation in areas involved in emotional and
cognitive processing compared to obese men,54 which may be a factor in the higher
incidence of disordered eating behavior among women.
NEUR AL BASIS OF PLEASURE-DRIVEN FEEDING
Environmental cues can have a profound effect on motivation to eat. For example,
even brief exposure to food cues can lead to increased reported hunger,55–57 and
conditioned responses in the cephalic phase57–60 which includes the release of in-
sulin61,62 and changes in salivation,63 heart rate, and gastric activity,64 all of which
enhance the motivational drive and physiological preparation for the consumption
of food. Differences in anticipatory responses to cues may play an important role
in distinguishing individuals who are prone to overeating.65 Overeating, especially
binge eating, and other disorders of hedonic excess, such as drug addiction, share
a feeling of loss of control and craving.66 Thus, anticipatory responses to cues to
overeating9, such as increase in cephalic phase response, appear to be driven more

by hedonic than homeostatic factors.
Liking versus Wanting
Berridge & Robinson provided a model67 for understanding motives to eat for
pleasure versus eating for need, by invoking differences between “liking” and
“wanting.” Liking is the expression of positive emotional affect in response
to pleasurable, rewarding reactions to a stimulus. These expressions can be
observed even in decerebrated rats,68 and in babies after tasting a sucrose solu-
tion.69 Liking is associated with neural circuits in the hindbrain, including the
nucleus accumbens (NAc), ventral pallidum, and limbic forebrain. Mu-opioid
receptors, which are located in the olfactory bulb, the NAc, several layers of
the cerebral cortex, and some nuclei of the amygdala, each play a role in eating
for pleasure. Injection of D-Ala, 2 N-MePhe,4 and Glyolenkephalin (DAMGO, an
opioid peptide) into the NAc elicits voracious food intake, particularly of sweet
and high-fat food.70 In humans, when opioid receptors were blocked, food was
rated as less pleasant in taste.71–73
Berridge74–76 suggests that wanting is a dissociated process from liking and is
based on the motivation to obtain a reward, as in drug addiction. As with liking,
wanting is hypothesized to have both an explicit, conscious aspect and an implicit,
unconscious aspect. According to Berridge and Robinson,67,75 “wanting is a motiva-
tional, rather than an affective component of reward. Its attribution transforms
mere sensory information about rewards and their cues (sight, sounds, and smells)
into attractive, desired, riveting incentives.” The neurophysiological components
of wanting are conveyed within the dopaminergic projections from the ventral
tegmental area (VTA) to the NAc, a pathway of the mesolimbic dopamine reward
system.77,78
Repeated stimulation of the dopaminergic system (e.g., by drugs) may lead to in-
creasingly compulsive behavior in pursuit of a reward, and can produce sensitization
of the wanting process27,79–82 while liking remains unchanged.83,84 Although many
individuals, both normal and overweight, realize that they should not buy or con-
sume high-energy, dense, pleasant-tasting foods, many obese participants overall
show greater brain-reward responsivity to stimuli associated with pleasant-tasting
foods high in sugar and fat.85 The increased motivation for foods with a high incen-
tive value can override the rational response and result in eating for pleasure rather
than from need27,86 (see this relationship in Figure 5.1).
Dopamine and Feeding
Dopamine plays a key role in maintaining compulsive eating habits. Feeding, like
other rewarding activities, elicits an increase of extracellular dopamine within the
NAc,87 which may be the basis for the euphoric sensation felt upon experiencing a
food Metabolic System

intake
Organs C
Tissues
HYP Cells
Glucose Molecules food
Peptides intake
Fatty Acids
Amino Acids Organs
Neurohormones HYP Tissues
Glucose Cells
sex Peptides Molecules
food Fatty Acids
B work Amino Acids
family Neurohormones
sex nature PFC
food friends NAc
work community VTA/SN Amygdala
tool-making Hippocampus
family Dorsal Striatum
nature PFC sports Dopamine
music Motor Complex
friends NAc
community Amygdala dance
VTA/SN
Hippocampus crafts
tool-making Dorsal Striatum art
sports Dopamine Motor Complex
music
dance
crafts Reward System
art (reward, aversion, salience, learning)
Figure 5.1:
Food intake can be related to basic hypothalamic mechanisms (A), and to the dopamine
reward system (B); which combined can be conceptualized as the two parts of a “bow tie” (C).
Adapted with permission from an unpublished presentation, courtesy of Dr. John Doyle.
reward. If a person consumes rewarding substances excessively, the sporadic flux of

extracellular dopamine may lead to receptor downregulation, which contributes to
tolerance by decreasing the number of functional cell surface receptors.88 The down-
regulation of receptors may lead to even greater consumption to obtain the same
rewarding sensation. A consistent finding is that both obese and drug-dependent
individuals have a reduction in dopamine 2 (D2) receptor availability,87 although it
is not yet clear to what extent this is causal or consequential.89
There appears to be a systemic “hypo-responsivity” in reward centers that
co-occurs with food cue–specific “hyper-responsivity.” With repeated exposure to
hyper-palatable foods, initially the result of hyper-responsivity to food cues, do-
pamine receptors become downregulated,90–92 leading to greater cue responsivity
to palatable foods.93 Similarly, one finds increased “wanting” occurring simulta-
neously with decreased “liking”94 in addiction,95 as with compulsive, habitual
overeating.
Several hormones and neuropeptides involved in energy homeostasis influence
the dopamine reward pathway.96,97 Dopamine release is associated with an increase
in homeostatic orexigenic signals in the VTA, while anorexigenic signals inhibit
dopamine firing and decrease dopamine release.98 Moreover, neurons in the VTA
and/or NAc express GLP-1, which enhances sensitivity to insulin,99 ghrelin,100,101
leptin,102,103 insulin,104 and orexin,105 which help guide energy balance. Thus, identi-
fication of hormones that act in concert with dopamine has become a focus for the
identification of pharmacological targets in obesity research.
Stimuli associated with primary rewards can acquire motivational potency and
trigger a pervasive desire for that reward by their ability to activate the mesolimbic
system.106 Current models of drug addiction propose that drug-related cues and
paraphernalia trigger drug-seeking behavior by eliciting hyperactivity in a net-
work of areas, such as the VTA, NAc, amygdala, OFC, and ventral pallidum.81,107
Hyper-rewarding substances (e.g., illicit drugs) increase extracellular dopamine
within the NAc shell.108 This surge in dopamine within the NAc shell can also be
seen with consumption of hyper-palatable food, unlike during regular feeding,
when the dopamine response fades as the food loses its novelty.109
OPIOIDS AND OVEREATING
In addition to increasing dopamine in the NAc shell, overeating and binge eating
stimulate release of endogenous opiates,110–113 which can lead to opioid receptor
downregulation. Addicts in withdrawal often overeat highly palatable food, partic-
ularly sugar, which may result in obesity and glucose dysregulation,111 suggesting
that sugar acts as a proxy for the rewarding effects of opiates.114
It has been suggested that chronic dieting sensitizes opioid receptors, and thus
primes the brain for binge eating.115 Repeated bouts of excessive sugar intake de-
crease encephalin messenger RNA (mRNA) in the NAc and enhance mu-opioid
receptor-binding in the NAc shell, cingulate, hippocampus, and locus coeruleus.
Compared to regular chow-fed controls, rats that are bingeing on sugar are also
sensitive to the effects of opioid antagonists (i.e., naloxone), which can lead to
withdrawal-like behavior. Anti-craving treatments used for opiate addiction, such
as naloxone and buprenorphine, may have applications in treating obesity and
binge eating.116 A combination drug (Contrave) of naltrexone (long-acting nal-
oxone) and bupropion (antidepressant) has recently been approved by the Food and
Drug Administration (FDA) for treatment of obesity117,118 A novel approach for dis-
covering new pharmacological treatments includes exploration and identification
of gene markers shared by opiate addiction and binge eating.119
GABA and Glutamate Receptors
Animal studies have led the way in the use of baclofen, a gamma-aminobutyric
acid (GABA)-B agonist, which reduces intake of high-fat diets,120,121 but not nec-
essarily of sweet foods. In human clinical trials, baclofen to treat binge eating has
produced some positive results by reducing binge meal size.122 Animal data sug-
gest that the drug would be best used for those who over-consume high-fat foods
rather than sweets. Other drugs like topiramate, which activate GABA-A recep-
tors, selectively inhibit 2-(aminomethyl) phenylacetic acid/kainite (AMPA/kainite)
glutamate receptors, which in turn can suppress binge eating.123 A drug combina-
tion recently approved by the FDA for treating obesity is Qsymia (topiramate and
phentermine).124
Hypothalamic Pituitary Adrenal (HPA) Axis
Stress can elicit a desire for palatable food,125 and palatable food has been shown to
blunt activation of the hypothalamic pituitary adrenal axis.123,126,127 (For a review,
see: Adam & Epel 2007.128) Overeating may reduce the intensity of stress,112,129 which
reinforces the eating behavior and makes it difficult to extinguish.113 Chronic diet-
ing and stress often antecede overeating and binge eating in clinical and nonclinical
populations.130 Goldfield et al. (2008) found that individuals reporting high stress
and binge-type eating worked harder for food rewards131 than those who did not.
Targeting stress hormones may be a novel way to treat binge eating. Nociceptin/
orphanin has anti-stress properties, and despite its tendency to stimulate appe-
tite, it may still prove useful, by reducing stress as an indirect way to reduce binge
eating.132
BINGE-EATING DISORDER
Binge-eating disorder (BED) can occur independently of obesity.133 Binge eating

is a fairly common aberrant eating behavior and is also a component of bu-
limia nervosa. BED occurs in about 0.7–4% of the general population, and in
30% of the obese subjects in behavioral weight loss programs.134 There are
common features in the etiology and biology of binge eating and substance
abuse,135 and both share such traits as impulsivity and compulsivity.136 In
BED, disturbances have been noted in several neurotransmitter systems, in-
cluding dopamine, opioids, serotonin, GABA and glutamate receptors, and the
hypothalamic-pituitary-adrenal axis, and thus BED represents a good target for
pharmacological agents.
According to the Diagnostic and Statistical Manual of Mental Disorders 5th Edition
(DSM-5), binge episodes are characterized by the consumption of more food in a
discrete period of time than would normally be consumed under similar circum-
stances. There is a subjective sense of loss of control, and there may be feelings of
depression or panic.137 There may also be feelings of distress when palatable foods
are not available, and intense craving for these foods. Those with BED are more
likely to eat when tired, anxious, depressed, or irritable in order to escape a negative
mood state138 and to reduce stress.20
Animal models have shown that dependence or addiction to natural food sub-
stances, such as sugar, can occur.139,140 For example, Hoebel et al. maintained rats
on a schedule of daily 12-hour food restriction followed by 12-hour access to a 25%
glucose or 10% sucrose solution and rodent chow.80,141 (The 10% sucrose solution
mimics the sweetness of many soft drinks.) The animals quickly became sensitized
to the rewarding effects of sugar, and after a few days on this schedule, their daily
intake of sugar increased to resemble binge-like behavior within the first hour of
access. These rats also showed increased motivation and pressed a lever repeat-
edly to obtain more sugar, even following two weeks of abstinence, compared to
before the training schedule.142 It appears that intermittent access is key to shaping
binge-eating behavior in animals. Additional evidence of addictive-like behaviors

are the withdrawal-like symptoms following administration of the opioid recep-
tor antagonist naloxone, including teeth chattering, forepaw tremor, and head
shakes.143
Although the neurobiology of binge eating in humans is poorly understood,
it has been shown that obese binge eaters show more activation to food cues in
frontal and prefrontal cortical areas than do non-binge eaters.144,145 In a recent
investigation of obese binge and non-binge eaters matched for weight, differences
were found in extracellular dopamine in the caudate in response to food cues.146
Such abnormalities in striatal dopamine neurotransmission are also noted in other
compulsive behaviors, driven by excessive hedonic motivation.
Antecedents to Binge Eating: Stress, Food Restriction,

Hyper-Palatability
Hoebel et al. have suggested that the increase in dopamine in response to

hyper-palatable foods may override the depressed or negative mood due to food
restriction. In BED, “forbidden foods” (typically palatable foods) are often con-
sumed during a binge.147,148 The accompanying surge in dopamine may make these
foods even more reinforcing to individuals in a state of energy depletion. Refined
sugars and flours, saturated fats, and high sodium levels, are common ingredients
of highly palatable foods,149 which may act like drug primers.138,150,151 In the pre-
disposed brain, just a small amount of a preferred food may lead to relapse150 and
excessive caloric intake. Food deprivation and restriction can increase subsequent
food intake in both animals140,152 and humans.153,154 Stress can also increase an ani-
mal’s vulnerability to binge-type eating.155 For example, both acute foot shock and
food deprivation can each contribute to overeating.155 After repeated cycles of stress
and food restriction, one stress episode elicited a 53% increase in intake compared
to controls.155 In humans, dieting has also been shown to increase the risk of binge
eating and overeating in non-clinical populations, and to prolong binge-eating epi-
sodes in those with either bulimia nervosa or BED.156,157
Dopamine and Inhibition
For many people, maintaining normal weight relies on the ability to refrain from
eating in multiple circumstances, which often fails in those with BED.45,158 Positron
Emission Tomography (PET) has shown lower striatal D2-receptor availability in
obese, relative to lean, men in a food-restricted state and following intravenous
glucose.91,159 Imaging studies have also revealed reduced availability of striatal D2
receptors in a variety of drug addictions, which can persist for months after detoxi-
fication.95 Furthermore, those with BED have significant increases in extracellular
dopamine in the presence of food cues.146 The reduction in D2 receptors is associ-
ated with decreased activity in prefrontal regions involved in reward recognition
(i.e., OFC),160 error detection (i.e., anterior cingulate cortex),161 and future planning
(i.e., dorsolateral prefrontal cortex).162 Since compulsive behavior is associated with
impairments in the OFC and anterior cingulate cortex,163 impaired dopamine activ-
ity in these regions may underlie the behavior patterns in addiction and disorders
such as BED.
Brain imaging suggests that structural and functional changes in the brain re-
gions associated with inhibitory control are impaired in obesity.90 A negative correla-
tion between gray matter and BMI has been found in elderly women using magnetic
resonance imaging (MRI),164 and other studies have shown significant decreases in
blood flow to the prefrontal cortex in overweight participants.165 Successful dieters
show a pattern of greater activation in areas associated with inhibitory control (dor-
solateral prefrontal cortex and OFC) following a meal compared to non-dieters.166
A similar pattern is seen in lean versus obese participants, in which the prefrontal
cortex exerts greater inhibitory control on limbic and paralimbic areas, such as the
insular cortex, OFC, and hippocampus.167
Disinhibition and Low Satiety Phenotypes
Behavioral risk factors associated with obesity include patterns of eating and
food selection15 that favor consumption of palatable, energy-dense foods.168
Meta-analyses have shown positive associations between scores on the Three
Factor Eating Questionnaire-Disinhibition subscale (TFEQ-D) and BMI. In
a study of 2,509 adults, it was found that the TFEQ-D scale was most predic-
tive of high BMI, with overweight women having the highest TFEQ-D scores.169
Individuals with a high TFEQ-D score are more drawn to energy-dense,169
rewarding foods,170 have a reduced satiety response to a meal when overfed171
and exhibit greater impulsivity.172,173 “Low satiety phenotype” (LSP) individuals
cannot fully recognize their appetite sensations, prior to or shortly after con-
suming a meal,174 which together with an increased sense of anxiety can promote
overeating.175Ghrelin is a peptide hormone that increases hunger, and is often
a precursor to meal initiation.176 Ghrelin administration stimulates feeding in
both animals177 and humans,178 with maximum effect observed within the first
hour of food intake. Somewhat surprisingly, obese individuals,179 and even more
so those with BED,180,181 have lower levels of fasting ghrelin, which may be due
to downregulation from overeating. Following a meal, ghrelin levels decline, but
they decline less in obese and BED individuals, which may contribute to greater
intake167–169 and reduced satiety, as obese subjects remain sensitive to the orexi-
genic effects of ghrelin.182
Stress can also raise ghrelin levels in both obese binge eaters and non–binge eat-
ers.183 The rise in ghrelin in response to stress may contribute to increased vulner-
ability to emotional eating in the obese and in those with BED.184 Moreover, obese
individuals also have larger stomach capacities than lean individuals,185 and among
obese individuals, those with BED have still larger capacities, which may further
contribute to reduced satiety and greater meal consumption.186
CONCLUSION
Consummatory behaviors are driven by energy need and emotional desire, and they
are terminated by adequate inhibitory control. Research in drug- and obesity-related
work has identified psychobiological processes that contribute to disorders of he-
donic excess. As with other examples of hedonic excess, overeating can be charac-
terized by greater sensitivity to reward, paired with inadequate inhibitory control.
In the case of obesity, this may be intensified by repeated failed attempts at dieting
to modify one’s eating behavior, followed by periods of overeating. Increased reward
responsivity to food cues may occur soon after a calorie-restricting regime,187 and
dieting can increase reward responsivity to food cues.188 Recent evidence suggests
that reward-related neural signaling may be activated in concert with inhibitory
signaling65,189 during periods of caloric restriction. The simultaneous activation of
these systems may exhaust both of them, and help explain why a lapse of inhibitory
control in unsuccessful dieters is often accompanied by excessive consumption of
“forbidden” foods.190,191 Prodromal risks for developing chronic overeating habits
may include low basal dopamine,192 which may further contribute to increased im-
pulsivity, another marker for a tendency towards overeating.193 Both food restric-
tion and stress can contribute to bouts of overeating.
Given the similarities between addictive behavior and binge eating, aspects of
therapies for addiction may be helpful in managing overeating.194 Figure 5.1 illus-
trates both homeostatic and hedonic aspects of reward, and is particularly relevant
to overeating behavior. Unlike total abstinence in treatment of substance abuse,
one cannot abstain from eating. In line with strategies to treat addiction, future
public health strategies may be aimed at limiting the availability and amounts of
highly palatable food,195 and also using stress-reduction to help reduce overeating
episodes.196
Despite our growing understanding of the motivation to overeat, more studies
are needed on interactions between appetite-related hormones and dopamine,
stress-reduction to treat overeating and binge eating, and improved pharmacolog-
ical as well as nutritional and behavioral interventions to reduce energy intake.
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C H A P T ER 6
w
Brain-Based Drivers and
Consequences of Hedonic
Overeating
K Y LE S. BURGER , PR A NISH A . K A N TA K ,
A ND A BIGA IL J. SA NDER S
E xcess adiposity tissue of those who are overweight or obese, defined as body
mass index (BMI) greater than 25.1, is related to higher risk for atherosclerotic
cerebrovascular disease, coronary heart disease, cancer, hyperlipidemia, hyperten-
sion, and diabetes mellitus. Collectively, excess weight is estimated as contributing
to as many as 300,000 annual deaths in the United States alone.1,2 In its simplest
terms, excess adiposity is achieved when an individual is habitually in a positive
energy balance resulting from hyperphagia (excess food intake), and/or decreased
energy expenditure or decreased metabolic rate. The determinants of eating beha-
vior are thought to involve parallel systems that interact with the external food
and social environments to influence food intake.3,4 Homeostatic mechanisms are
primarily directed by appetitive hormones (e.g., leptin and ghrelin) that are reflec-
tive of the body’s energy stores and act on hypothalamic and brain stem circuitry to
stimulate or inhibit feeding in an effort to maintain energy balance and a healthy
weight. However, as is evidenced by the prevalence of overweight and obese indi-
viduals, this homeostatic system of energy balance can fail. More recently, theo-
rists posit that neuropsychological abnormalities, such as aberrant reward-related
responses to food stimuli, override homeostatic processes, thereby contributing to
weight gain (e.g., Lutter & Nestler, 20093).
Known to direct motivated behavior, brain regions in the mesolimbic and meso-
cortical pathways (i.e., reward circuitry) have become the primary focal point of
research into hedonically driven food intake. For example, dopamine neurons in the
substantia nigra pars compacta have been implicated in motor control, and project
( 107 )
to the dorsal striatum; while dopamine neurons in the ventral tegmental area are
thought to be more implicated in motivation, reward, and aversion, and project to
the nucleus accumbens, ventral pallidum, medial prefrontal cortex, amygdala, and
hippocampus.5 Interestingly, optogenetic and pharmacological manipulation of do-
paminergic neurons in mice facilitated positive reinforcement during food-seeking
behavior, prompted hyperphagia, and increased preferential intake of high-fat and
high-sugar foods.6–8 While it has been suggested dopamine signaling does not di-
rectly mediate the pleasure achieved from food intake,9 dopamine signaling may
play the primary role in encoding novelty of stimuli, the reinforcement value of
food, as well as reward-based learning.6,9–12 However, in humans, eating palatable
food causes dopamine receptor–binding in the dorsal striatum, with the amount
correlating with self-reported pleasantness ratings of the food.13,14 This suggests
dopamine may also be related to subjective valuation of food pleasure in humans.
Rapidly evolving human neuroimaging techniques, such as functional magnetic
resonance imaging (fMRI) and positron emission tomography (PET), have provided
valuable insights into the brain’s reward circuitry implicated in eating behavior.
Despite these advances, some of the most prominent theories of aberrant neural
responses to food and obesity appear to be in conflict. For example, obesity has
been described as a problem characterized by both hyper- and hypo-responsivity
of the regions within the reward circuitry.15–17 Similarly, it has been suggested that
these opposing physiological signals may operate in tandem to increase intake,
but are specific to a particular type of stimulus (i.e., the response to predictive cue
versus actual receipt of a palatable tastant18).
Although the exact reward mechanisms that are perturbed in obesity are be-
coming better characterized, the foremost shortcoming of the present literature
base is the lack of ability to directly draw inferences regarding the causality of the
observed effects. As such, we are currently unable to concretely differentiate be-
tween innate neural risk factors driving initial hedonic overeating, and neuroad-
aptive processes and consequences resulting from habitual consumption of highly
palatable foods. In this chapter, we briefly examine theoretical risk factors that
may predispose individuals to pursue hedonic behaviors; in particular, overeating.
We then summarize human neuroimaging and complementary animal research
that highlights our understanding of the interplay among the neural response to
food stimuli, eating behavior, and weight regulation.
PREDISPOSING RISK FACTORS FOR HEDONIC OVEREATING

Generalized Reward Sensitivity and Impulsivity
It has been theorized that individuals with high levels of trait reward-sensitivity
display enhanced activity in brain regions implicated in food reward, and therefore
are at greater risk for hedonic overeating and weight gain.16 Similarly, data-driven
hypotheses indicate that individuals at risk for substance abuse initially experi-
ence greater reward from substance use, increasing the risk for substance abuse.19,20
Similar theories have also implicated lack of cognitive control and/or impulsivity
D rivers and C onsequences of H edonic O vereating ( 10 9 )
with overeating and obesity as well as substance abuse, problem gambling, and
risky sexual behavior.19,21 Despite mounting evidence that reward-sensitivity and
impulsivity are associated with obesity, it remains unclear whether these specifi-
cally relate to overeating or whether they are simply generalized risk factors for any
hedonic behavior.
When it comes to overeating (unlike other hedonic behaviors), individuals in
industrialized nations are consistently exposed to an environment that inundates
individuals with food cues and food consumption is necessary to sustain life. As
a result, nearly all individuals in industrialized nations consume highly palat-
able foods, at least intermittently. Critically, repeated non-intermittent intake of
highly palatable foods is necessary to facilitate weight gain and its associated ad-
verse health consequences. Thus, examining risk factors that are food-specific and
aimed at assessing the transition from experimental/intermittent eating behavior
to habitual eating behavior may prove to be the most useful research in understand
hedonic overeating and weight gain.
Cue-Reward Learning Propensity as a Risk Factor

for Hedonic Overeating
The incentive-sensitization model suggests that hyper-responsivity of reward cir-

cuitry to palatable food cues can result in cravings that prompt overeating.17 While
similar to the aforementioned trait reward sensitivity theory of overeating,16 in-
centive sensitization is defined as a uniquely focused, heightened response to cues
that are associated with a reward, making the cue responsivity contingent on re-
ward learning processes. Classical conditioning animal experiments indicate that
cues need to be paired with a rewarding stimulus (e.g., palatable food) prior to be-
coming salient. Consistent with this, firing of dopamine neurons initially occurs
in response to receipt of a novel palatable food; after repeated pairings of palatable
food intake and cues that signal impending receipt of that food, dopamine neurons
begin to fire in response to reward-predictive cues and no longer fire in response to
food receipt.22–24 Theorists posit that this shift during reward learning reappropri-
ates the predictive value of stimuli where the cue becoming sensitized and thereby
promotes future behavioral responses to predictive cues.25 In animals that readily
attribute incentive salience toward cues during reward learning (sign-trackers), the
reward cues robustly motivate and control behavior.26,27 Given that reward cues di-
rectly inform goal-directed behavior among animals,28 people who show more pro-
nounced reward-cue learning may be at greater risk for habitual reward-seeking
behavior, such as hedonic overeating. In support of this theory, increases in cau-
date response to food-predictive, but otherwise arbitrary, cues occur over repeated
exposures, indicating cue-reward learning in humans29 (Figure 6.1). Those who
exhibited the greatest escalation in ventral pallidum responsivity to cues over re-
peated exposures showed significantly greater weight gain over the following two
years.29 This supports the notion that those who most readily associated cues to
food reward were at higher risk for weight gain.
Figure 6.1:
Average caudate response to arbitrary cue that signaled impending palatable food receipt over
four learning periods (16 total events). The increase in T-value of activity over the learning
periods shows an increase in caudate responsivity over the repeated exposures suggesting
cue-reward learning (r = 0.42; p < 0.05).
Adapted from Burger KS, Stice E. Greater striatopallidal adaptive coding during cue-reward learning and reward
receipt habituation predict future weight gain. NeuroImage. 2014;99:122–128. Reprinted with permission from
Elsevier.
BR AIN-BASED PREDICTION OF WEIGHT GAIN
Prospective studies can provide insight into preexisting risk factors for weight gain
relative to the consequences and maintenance factors associated with obesity. In
support of the incentive salience and cue-reward-learning hypotheses, greater re-
sponse in the ventral striatum and medial prefrontal cortex/anterior cingulate
during exposure to appetizing food images predicted weight gain over a six-month
period.30 Further, individuals who showed greater activation in the orbitofrontal
cortex (OFC) in response to a cue predicting palatable food intake gained weight
over one year. 31 Interestingly, the OFC is thought to play a particularly prominent
role in valuation and representation of rewards such as palatable food.32
Prospective neuroimaging that evaluates the response to palatable food receipt
as a predictor for weight gain has revealed somewhat less consistent results, how-
ever. In cross-sectional studies assessing individuals “at risk for weight gain” (as
defined by having overweight/obese parents), lean “at risk” adolescents showed
greater activity in the dorsal striatum, parietal and frontal operculum (thought to
encode gustatory processes) during food intake when compared to lean adolescents
with lean parents.18 Striatopallidal and midbrain response to milkshake receipt was
positively related to weight gain at one-year follow-up in a sample containing over-
weight and healthy-weight participants33 (Figure 6.2). In a separate study, increased
responses in the dorsal striatum to milkshake receipt also predicted weight gain at
one-year follow-up, but only in individuals with the A2/A2 polymorphism of the
TaqIA allele.34
Collectively, results of these studies support the theory that a high risk for obe-
sity is associated with greater response to food cues in brain regions thought to
encode aspects of motivated behavior, reward, and taste. However, it is less clear
whether the aberrant reward circuitry response to food intake is a robust, innate
D rivers and C onsequences of H edonic O vereating ( 111 )
10 6 2 –2 –6 –10
5
L NAc L VP Hypothal
2
BMI change
0
(kg/m2)
–2 r2 = 0.43* r2 = 0.42* r2 = 0.38*
–40 –20 0 20 40 –20 0 20 40 –50 –20 10 40

PE PE PE
Figure 6.2:
Brain activity correlated with the change in BMI at one-year follow-up. Scatter plots
illustrate the correlation between change in BMI (y-axis) and average parameter estimate
(PE) representing brain activity within all voxels falling in each region of interest (x-axis).
Abbreviations: NAc; nucleus accumbens; VP: ventral pallidum; Hypothal: hypothalamus.
Adapted from Geha PY, Aschenbrenner K, Felsted J, O'Malley SS, Small DM. Altered hypothalamic response to
food in smokers. The American Journal of Clinical Nutrition. 2013;97(1):15–22. Reprinted with permission from
American Society for Nutrition.
risk factor for hedonic overeating and weight gain. Independent replication of
these data is needed to better identify neural predictors of weight gain and onset
of obesity.
BR AIN-BASED CORRELATES OF EATING BEHAVIOR
To critically evaluate the brain-based underpinnings of hedonic overeating, one

can examine the neural correlates of both acute and short-term eating behavior
prior to any influence associated with changes in weight. The relation between
reward circuitry response and acute eating behavior is largely understudied in
humans. However, supported by previous animal models, the few existing human
studies provide evidence that hedonic eating may be associated with varied
responses in brain regions involved in encoding reward. For example, dopamin-
ergic midbrain and medial OFC activity in response to palatable food intake pos-
itively predicted subsequent ad libitum milkshake consumption in the absence of
hunger, 35 indicating the influential role of the reward circuitry in hedonic over-
eating. Further, response in the ventral striatum during exposure to appetizing
1.5
1 r = 0.72
Parameter estimate
[3–30–15]
0.5
–0.5 0 100 200 300 400 500 600

–1 Ad lib milkshake intake (mL)
Figure 6.3:
Positive correlation between blood-oxygen-level dependent (BOLD) response to milkshake
receipt and later ad libitum milkshake intake (r = 0.72; p < 0.05). The scatter plot illustrates
the correlation between parameter estimates representing brain activity in response to
milkshake (y-axis) and ad libitum milkshake intake (mL; x-axis).
Adapted from Nolan-Poupart S, Veldhuizen MG, Geha P, Small DM. Midbrain response to milkshake
correlates with ad libitum milkshake intake in the absence of hunger. Appetite. 2013;60:168–174. Reprinted
with permission from Elsevier.
food images positively predicted ad libitum snack consumption36 (Figure 6.3). In

addition to associations with acute food intake in close proximity to scanning,
studies integrating more naturalistic eating behavior data have further clarified
the brain-based correlates of hedonic eating behavior. A positive relationship was
observed between objectively measured energy intake over a two-week period
and reward circuitry, gustatory and visual processing response during cues pre-
dicting food receipt. 37
In comparison with effects associated with food cues, the relationship be-
tween brain response during food receipt and eating behavior presents a very
different neural response pattern. Frequency of ice cream consumption has
been found to be inversely related to responses in the ventral striatum, insula,
and ventromedial prefrontal cortex during milkshake receipt 38 (Figure 6.4).
Similarly, greater frequency of artificial sweetener use was related to decreased
striatal response during intake of a saccharin (a nonnutritive sweetener) solu-
tion, 39 as well as decreased response in the insula and amygdala during sucrose
solution intake.40 Collectively, these data indicate that regular, repeated con-
sumption of sweetened foods is related to a reduced response during intake of a
similarly sweet tastant.
0 1 2 3 4
Frequency of ice cream consumption
12
r = –0.34
10
r = –0.30
over two weeks
8 Putamen (R)
r = –0.29 6 Putamen (L)
Caudate (R)
4
0
–8 –6 –4 –2 0 2 4 6 8
Striatal responsivity to milkshake intake
Figure 6.4:
Reduced ventral striatal responsivity to milkshake receipt as a function of frequency of
ice cream consumption. The scatter plot illustrates the correlation between frequency
of ice cream consumption over the previous two weeks (y-axis) and parameter estimates
representing brain activity in response to milkshake receipt (x-axis).
Adapted from Burger KS, Stice E. Frequent ice cream consumption is associated with reduced striatal response
to receipt of an ice cream-based milkshake. American Journal of Clinical Nutrition. 2012;95(4):810–817.
Reprinted with permission from American Society for Nutrition.
ABERR ANT NEUR AL RESPONSE

ASSOCIATED WITH OBESITY
The most replicated finding in the neuroimaging of obesity is the elevated neural
response to images of palatable and/or energy-dense foods seen in obese versus
lean humans. These data, however, only represent brain-based correlates associ-
ated with obesity, as they provide no information regarding temporal precedence
of the observed effects. Overweight and obese individuals show significantly
more activity in the striatum, insula, OFC, and amygdala when compared to their
lean counterparts.41–49 These regions were previously implicated in encoding the
reward value of stimuli and consequently influencing goal-directed behavior.50

Furthermore, when exposed to visual food images or cues predicting palatable food
receipt, obese, relative to lean, individuals also consistently show greater activation:
(1) in brain regions associated with visual processing and attention (visual and an-
terior cingulate cortices);
(2) in brain regions encoding stimulus salience (precuneus);
(3) in the primary gustatory cortex (anterior insula, frontal operculum); and
(4) in oral somatosensory regions (postcentral gyrus, rolandic operculum).41–49
In contrast, several studies showed that obese, relative to lean, individuals

exhibited less activity in the reward circuitry in response to receipt of palatable
food.34,49,51–53 Furthermore, data indicate that obese relative to lean adults show both
lower striatal dopamine D2 receptor availability54,55 and lower capacity of nigrostri-
atal neurons to synthesize dopamine.56 These data are supported by animal work
wherein obese, relative to lean, animals have lower basal dopamine levels, lower
dopamine D2 receptor availability, and less ex vivo dopamine release in response to
electrical stimulation in nucleus accumbens and dorsal striatum tissue.57–59
These data indicate that overweight/obese status is related to aberrant neural
responses to food stimuli. Specifically, they are associated with elevated striatal,
gustatory, and attentional responses to anticipatory food cues (e.g., food images and
predictive cues) and decreased striatal responses during consumption. As a result,
these findings support both the hyper- and hypo-reward theories of obesity.15–17
By the nature of study design alone, these cross-sectional data do not allow for the
ability to draw inferences regarding the temporal precedence of weight status and
observed neural effects; therefore, they equally support the notions that the neural
response patterns are (a) an underlying cause of weight gain or (b) a consequence of
habitual overeating and/or obesity.
Neuroendocrine Consequences of Obesity
An increasing amount of data indicate that hormones attributed to homeostatic

mechanisms of food intake—such as leptin, peptide YY (PYY), glucagon-like
peptide 1 (GLP-1), and ghrelin—operate distinctly from, but also influence
aspects of, hedonic eating by moderating the brain’s reward circuitry.60 In sup-
port, the adipokine—leptin—conveys information to the central nervous
system about long-term energy stores and inhibits activity of the appetite
stimulants—neuropeptide Y (NPY) and agouti-related peptide (AgRP)—in the
hypothalamus.61 Leptin may influence hedonically driven food intake through
alteration of mesostriatal dopamine, as leptin receptors are expressed on midbrain
dopamine neurons in the ventral tegmental area (VTA) and substantia nigra.62 Like
dopamine receptor antagonists, leptin inhibits the rewarding properties of sucrose
by inhibiting the activity of dopamine neurons in the VTA, and decreasing food
intake in animals.63,64 Moreover, in individuals with congenital leptin deficiency,
leptin replacement reduces insula and striatopallidal activity and increases pre-
frontal cortex activation in response to images of appetizing foods65,66; changes in
neural activation in these areas are consistent with reduced appetitive drive and
increased inhibitory control in humans. Similar to leptin, the gut hormones PYY
and GLP-1 are implicated in reducing appetite and signaling meal termination. For
example, exogenous administration of GLP-17–36 amide leads to a reduction in appetite
and ad libitum energy intake.67,68 Furthermore, following exogenous administration
of PYY 3–36 and GLP-17–36 amide, in fasted, healthy-weight individuals, reductions in
striatal, insular, and OFC response were observed during exposure to appetizing
food images.69 Lastly, ghrelin is a gastrointestinal tract peptide that acts on the hy-
pothalamic NPY/AgRP orexigenic pathway, promoting the initiation of feeding.70,71
Ghrelin administration in normal-weight individuals leads to increased energy in-
take72,73 and increased response in the striatum, amygdala, OFC, and anterior insula
during exposure to appetizing food images.74 In animals, ghrelin has been shown
to exert an excitatory effect on midbrain dopamine systems75–77 and increase the
reward value of food.78
In sum, these findings demonstrate that appetitive hormones can in-
fluence food intake, in part, by modulating hedonic responses to food and
food cues. This hormonal influence on hedonic eating appears to be true for
both meal initiation (e.g., ghrelin), and satiation signaling (e.g., leptin, PYY,
GLP-1). Importantly, the circulating levels and sensitivity of these peptides
are highly associated with body weight and may underlie many of the observed
cross-sectional effects seen when assessing neural response to food stimuli in
obese versus lean individuals.60
BR AIN-BASED CONSEQUENCES OF WEIGHT GAIN
Only controlled experiments can assess the neuroadaptations associated with

eating behavior and weight change, and they are critical to elucidating the tem-
poral precedence of aberrant brain-activation patterns associated with weight gain
and obesity. One such study revealed that change in adipose tissue and BMI over a
six-month period was positively related to activity in the insula and visual cortex
activity during exposure to appetizing food images, relative to baseline scans.79
Interestingly, weight gain over a six-month period was associated with reduced stri-
atal response to palatable food receipt relative to both baseline and to women who
maintained a stable weight over the six-month period80 (Figure 6.5).
Accordingly, diet-induced obesity in laboratory animals has been associated
with a decrease in the responsiveness of reward sites in the lateral hypothalamus.81
Deficits in reward signaling have also been reported in adult rats that previously
had unlimited access to sucrose or high-fat food during adolescence.82 Additionally,
animals randomized to overeating conditions show downregulation of postsyn-
aptic D2 receptors, reduced D2 sensitivity, reduced dopamine levels and turnover,
and lower sensitivity of reward circuitry to electrical stimulation.81,83–85 The ca-
pacity for reduced dopamine signaling may be a function of the habitual intake of
3.5
4.00 3
2.5
2
1.5
1
0.5
2.00 0
Caudate
0.00
Weight Loss
–2.00 Weight Stable
Weight Gain
Baseline 6-month follow-up
Figure 6.5:
Decreased activation in the caudate in response to milkshake receipt by weight-change
group over a six-month period. Those who gained weight (solid line) showed decreases in
caudate response to palatable food receipt (parameter estimates; y-axis), whereas those
who lost weight (dashed line) or were weight-stable (dotted line) showed slight increases in
response over the six-month period (x-axis).
Adapted from Stice E, Yokum S, Blum K, Bohon C. Weight gain is associated with reduced striatal response
to palatable food. Journal of Neuroscience. 2010;30(39):13105–13109. Reprinted with permission from The
Society for Neuroscience.
high-fat diets, which decrease the synthesis of the gastrointestinal lipid messenger
oleoylethanolamine.86 In support, rats fed a highly palatable, energy-dense diet
manifested a downregulation of striatal D1 and D2 receptors relative to an eucaloric
diet of normal chow; no difference in weight change between the two groups was
observed.87
Reminiscent of the opponent-process theory,88 it has been suggested that
diet-induced reward deficits associated with obesity likely reflect a counteradap-
tive response in food reward circuitries to counteract overstimulation by palatable
food.81 As noted in theories of substance abuse and relapse,89,90 these counter-
adaptive processes may be a function of repeated exposure to particularly highly
rewarding palatable foods,38,91 and are not contingent on obesity or weight gain.
This suggests that the rewarding aspects of food consumed, rather than the en-
ergetic value or weight change, may serve to alter how the brain responds to fu-
ture intake. Specifically, these data indicate that changes in response to food cues
in attention and gustatory regions are positively associated with weight change,
whereas changes in striatal response to food receipt are inversely related to weight
change. The neuroadaptations associated with hedonic overeating and weight gain
presented here are supported by results seen in the cross-sectional and prospective
studies evaluating weight status and eating behavior.
NEUROADAPTATIONS TO BEHAVIOR AL
WEIGHT LOSS EFFORTS
Dieting is defined as the intentional and sustained restriction of caloric intake for
the purposes of weight loss or weight maintenance,92 and is frequently assessed by
dietary restraint questionnaires. Surprisingly, studies using objective measures of
caloric intake indicate that individuals who report efforts to reduce food intake do
not consume fewer calories and may be at an increased risk for future weight gain
(see Stice et al.93 for review). The actions of dieting have been shown to increase
both self-reported cravings for, and the power of, palatable food.94 Not surpris-
ingly, actual dieting is related to increased hunger and possibly greater periods of
caloric deprivation.95 Hunger can enhance palatable food-related activity in the re-
ward circuitry of humans both by experimental manipulation96,97 and by volitional
restriction.98 For example, activity in the ventral striatum, amygdala, insula, and
OFC in response to palatable food images was far greater when human subjects
were hungry rather than well fed.99
There is a possibility that dieting efforts increase the reward value of food, in
part by increasing stress, as being on a low-calorie diet is associated with increased
cortisol and self-reported stress.100 Theoretically, individuals with elevated neg-
ative affect eat in an effort to feel better or provide distraction from their ad-
verse affective state.101 Preference for sweet, fatty, energy-dense foods has been
seen in emotional eaters, and this is thought to occur in order to suppress the
hypothalamic–pituitary–adrenal (HPA) axis.102 In support, there is a relation-
ship between BMI and stress-related activation of the OFC and the right amygdala
during milkshake intake.103 Stress has also been found to increase reward-circuitry
response and decrease prefrontal activity when individuals under chronic stress
are exposed to images of highly palatable foods.104 Lastly, emotional eaters after
negative mood induction show greater reward-related response as compared to
non-emotional eaters during palatable food intake.105
Collectively, these data point toward neuroadaptations that act to protect against
weight loss. Volitional dieting may increase the implicit and subjective reward value
of food, as the individual is calorically restricted. Moreover, the dieting individual
is placed in distress, which further alters reward circuitry. Maintaining caloric
restriction in the face of these barriers may be particularly difficult in individuals
who have previously used food as a coping mechanism. In summary, these neural
counteradaptations to dieting aim to increase food consumption and the suscepti-
bility to dieting failure.
CONCLUSION
Many advances have been made recently in identifying and understanding the
brain systems underpinning hedonic eating as well as the neuroadaptations that
occur in response to habitual consumption of highly rewarding palatable food.
As previously noted, there are prominent similarities in brain systems. Common
adaptive responses are triggered in response to hedonic overeating and addictive

substances.106 However, unlike use and abuse of illicit drugs, the consumption of
food is needed for survival, and considerable consumption of energy-dense and
palatable foods is likely to occur in industrialized nations. Furthermore, cues
and advertisements for these foods are omnipresent in most cultures. Thus, con-
tinuing to increase our understanding about individual risk factors for hedonic
overeating and the neuroadaptive consequences of this behavior are critical to
guiding effective healthy-eating intervention efforts and better informing food
policy legislation.
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C H A P T ER 7
w
Food “Liking” and “Wanting”
A Neurobiological Perspective
SUSA NA PECIÑA A ND K EN T BER R IDGE
S eeing or smelling a delicious food, walking by a place where you once ate some-
thing good, thinking about a tasty food or even imagining something deli-
cious: these are a few things that can powerfully make one “want” to eat, even if not
hungry. Foods and their related cues can activate brain reward mechanisms of food
“liking” and “wanting,” and so determine, to a large extent, whether, what, when,
and how much we eat.1–3 These involve brain mechanisms both of pleasure and of
incentive motivation for food and food-associated cues.4,5 Accordingly, dysfunction
within one or both mechanisms may contribute fundamentally to overeating and
obesity that show characteristics of excessive “wanting” and/or “liking.”2,6–10
How do “liking” and “wanting” systems of food reward contribute to eating and
overeating? Palatable foods (e.g., a tasty cookie) and their associated cues (e.g., the
smell of cookies while being baked) can activate brain systems of pleasure and de-
sire and trigger intense urges to eat.1,11,12 Brain systems of “liking” and “wanting”
evolved to be activated to satisfy metabolic needs, and so may contribute to neces-
sary intake for survival and growth. But in the modern world of abundant palatable
foods and food cues, brain reward systems of “liking” and “wanting” are often ac-
tivated in the absence of metabolic need. The sight of a tasty chocolate cake might
produce an intense desire to eat even if we are not hungry. In such cases, palatable
foods and cue-triggered desire to eat can contribute, not only to eating, but also to
overeating. In a food-rich environment in which foods are ever-present, the temp-
tation to eat is often difficult to resist.
We refer to “liking” brain mechanisms as the brain substrates that are able
to generate objective hedonic reactions to the hedonic impact of a pleasant sen-
sation such as sweetness, which can be detected in behavioral affective reactions
( 125 )
or in neural signals, and are generated mainly by subcortical substrates. Objective

“liking” reactions typically are accompanied by a subjective pleasure or conscious
hedonic feeling of liking, and may need to recruit additional brain circuits. Those
probably include cortical circuits, especially in prefrontal cortex areas such as the
orbitofrontal cortex or insula cortex. Similarly, we refer to “wanting” brain processes
as the brain substrates of incentive salience, which makes foods attention-grabbing,
attractive, sought-after, and desired. Brain mechanisms of “wanting” can be acti-
vated by foods or by food-associated cues, and trigger a desire to eat.1,13
Food-reward systems do not act in isolation to control eating. Rather, they in-
teract with homeostatic brain systems that process signals of hunger and satiety.14
However, food-reward mechanisms can sometimes powerfully override metabolic
signals and generate strong urges to eat even when metabolic needs have been met,
contributing to overeating and obesity (e.g., one can eat a delicious apple pie in the
absence of hunger after a large meal).1,3,15 Understanding the brain mechanisms
that make foods taste so good and food-associated cues so powerful at triggering
urges to eat may open an avenue to identifying preventative measures and clinical
treatments for obesity and related overeating disorders.
HOW DO FOODS BECOME “LIKED”?
Particular foods are especially “liked,” but the taste and smell sensations of all
foods are initially hedonically neutral until brain reward systems actively generate
their hedonic impact. Normally palatable foods can fall to neutral or even become
“disliked” and disgusting if brain hedonic systems are disrupted in that task.
Many sweet tastes, like sugar, are generally perceived as pleasant, and other
tastes that are intensely bitter or overly sour or salty are perceived as unpleasant.
But a “liked” sweet taste can become unpleasant while remaining sweet, also via
psychological revaluation, such as after being paired with illness such as occurs in
taste-aversion learning, a type of Pavlovian conditioning.16–18 Conversely, a “dis-
liked” intensely salty taste (e.g., triple concentration of seawater) can become pleas-
ant if the body lacks sodium, as occurs during “salt appetite.”19,20 And similarly,
although bitter tastes can be especially unpleasant, hedonic plasticity and repeated
cultural experience allow many individuals to find the taste of cranberries, coffee,
beer, and other bitter foods quite pleasant.1 Thus, taste pleasure is not merely a
taste sensation,21,22 but rather, the pleasure is generated by the brain in the moment
of tasting.
How Is Hedonic Causation Identified?
Many brain structures have been found to be activated by pleasurable stimuli, but
compelling evidence for pleasure causation has so far been found for only a few he-
donic hotspots in subcortical structures.9,23–25 We have approached hedonic causa-
tion in our laboratory by searching for brain manipulations that cause an increase
F ood “ L iking ” and “ Wanting ” ( 12 7 )
in psychological and behavioral “liking” reactions to pleasant foods, or other brain

manipulations that cause normally “liked” sweet tastes to become suddenly “dis-
liked.” This has allowed us to identify “hedonic hotspots,” which are small brain
subregions tucked within limbic structures that have special pleasure-amplifying
capabilities compared to the rest of the brain. Hedonic hotspots have been identi-
fied in the nucleus accumbens (NAc) shell and the ventral pallidum (VP), as well
as in deep brainstem regions, including the parabrachial nucleus, in the pons. The
pleasure-generating capacity of the hedonic hotspots in the NAc and the VP in the
base of the forebrain, and in the parabrachial nucleus in the brainstem, has been re-
vealed in part by studies in which microinjections of drugs stimulated neurochem-
ical receptors on neurons within a hotspot, and caused a doubling or tripling of the
number of hedonic “liking” reactions normally elicited by a pleasant sucrose taste
(Figure 7.1). Useful behavioral “liking” reactions that are employed in our studies
to measure food pleasure and its causation are the affective orofacial expres-
sions that are elicited by the hedonic impact of sweet tastes. These facial “liking”
reactions were described originally in human infants by Jacob Steiner26 and ex-
tended to rats by Harvey Grill and Ralph Norgren.27,28 For example, sweet tastes
elicit positive facial “liking” expressions (e.g., rhythmic and lateral tongue protru-
sions that lick the lips, etc.) in human infants and in rats, whereas bitter tastes in-
stead elicit facial “disliking” expressions (e.g., gapes, etc.) (Figure 7.1). Confirming
the hedonic nature, changes in these affective facial reactions specifically track
changes in sensory pleasure induced by hunger or satiety, learned preferences, or
aversion, and brain shifts that alter hedonic impact.27,29–35 Facial “liking” reactions
Hedonic Reactions (sweet)
Aversive Reactions (bitter)
Figure 7.1:
Hedonic and aversive orofacial homologies across species. Top: hedonic tongue protrusion
response to a “liked” taste (e.g., sweet taste) in rat, primate, and human infant.
Bottom: aversive gape response to a “disliked” taste (e.g., bitter quinine).
are homologous between humans and other mammals,26,28,36,37 which implies that
what is learned about brain mechanisms of pleasure causation in animal studies is
useful for understanding pleasure-generation in humans, too.11,22,38–41
Brain Mechanisms of “Liking”: Nucleus Accumbens Medial Shell
The first hotspot discovered was found inside the NAc, a brain structure at the
bottom-front of the brain (Figure 7.2). The hotspot lies in the medial shell subdi-
vision of the NAc; specifically, in a cubic-millimeter volume of tissue in the rostro-
dorsal quadrant of the medial shell.23 In the hedonic hotspot, “liking” for sweetness
can be amplified by microinjections of drugs that mimic endogenous opioid neuro-
chemical signals.
D -Ala 2, N-me-Phe 4, Gly-ol 5 -enkephalin (DAMGO) is a drug that selectively acti-
vates the mu type of opioid receptor, and in the hotspot this appears sufficient
to enhance taste pleasure.11,23,35,42 We have found that DAMGO microinjections
in the hedonic hotspot more than double the usual number of positive “liking”
Opioid ‘Liking’ and ‘Wanting’ Zones

in the Nucleus Accumbens NAcShell
Hedonic Hotspot
‘Liking’ ‘Disliking’
Increase Decrease
Hedonic Coldspot
‘Liking’
Decrease
Diffuse ‘Wanting’
Eating
Increase
Sagittal
Figure 7.2:
Opioid “liking” and “wanting” zones in NAc shell. Opioid hotspots and cold spots in the NAc
(medial shell region shown in sagittal view). Diffuse wanting: entire nucleus accumbens
mediates opioid-stimulated increases in “wanting” for food reward. Hedonic hotspot: only
a cubic-millimeter sized hedonic hotspot in the rostrocaudal quadrant of medial shell
generates increases in “liking” for the same opioid stimulation. Hedonic coldspot: opioid
stimulation of a small hedonic “hotspot” suppresses “liking” reactions to sucrose. Disliking
decrease: reduced “disliking” reactions to quinine.
Based on data from: Pecina S, Smith KS, Berridge KC. “Hedonic hot spots in the brain.” Neuroscientist.
2006;12(6):500–511, and adapted from Pecina S, Smith KS. “Hedonic and motivational roles of opioids in
food reward: implications for overeating disorders.” Pharmacology Biochemistry & Behavior. 2006;97(1):34–46.
Reprinted with permission from Elsevier.
reactions emitted to sucrose taste by rats. “Disliking” reactions to quinine are

never enhanced, but rather are suppressed by mu opioid activation in and around
the hotspot. Thus sweetness pleasure is enhanced, and bitterness displeasure is
simultaneously reduced, by neurochemical stimulation of the hedonic hotspot.23
More recently, findings by Daniel Castro in our lab indicate that kappa and delta
types of opioid stimulation in the medial shell hotspot may also generate hedonic
enhancements in sweetness “liking.”43,44 Hedonic enhancement is especially sur-
prising for kappa opioid stimulation, which is often associated with aversive effects
rather than reward. The ability of kappa stimulation within the NAc hotspot to
enhance hedonic impact shows how unique the rostrodorsal quadrant of the me-
dial shell is for pleasure-generation. The observations show that microinjections
of drugs that selectively stimulate those opioid receptors within the NAc hotspot
effectively enhance hedonic “liking” reactions to sucrose taste, though neither type
of opioid stimulation outside the hotspot at other sites in the medial shell has this
effect. Instead, in a hedonic coldspot in the posterior half of the medial shell, all
three forms of opioid stimulation suppress hedonic reactions to sucrose, apparently
reducing “liking.”43,44
Beyond opioid neurotransmission, endocannabinoid neurotransmitters (nat-
ural brain signals mimicked by marijuana) also appear to magnify “liking” by acting
within the NAc hotspot. Endocannabinoid stimulation in a variety of structures,
including the NAc, has been shown to increase the consumption of palatable food
(equivalent to the “marijuana munchies”).45–47 In our lab, Mahler et al.48 found that
microinjection of anandamide, an endogenous ligand for the cannabinoid receptor
type 1 (CB1), into the NAc hotspot increased “liking” reactions to sucrose taste,
similar to opiod stimulation. These results support the idea that endocannabinoids
probably modulate appetite and intake in large part by modulating the palatability
of food49 (Figure 7.3).
Unique Anatomical Bases of the Nucleus Accumbens Hotspot
What is anatomically special about the NAc hotspot that makes it different from
the rest of the NAc shell? Recent neuroanatomical studies have revealed the ana-
tomical basis of the hotspot’s functional uniqueness. Thompson and Swanson have
shown that the NAc hotspot (rostrocaudal quadrant of the medial shell) receives
specific inputs from a particular region of the infralimbic cortex (homologous to
Brodmann’s area 25 or the subgenual anterior cingulate cortex in humans). 50–52 In
addition, they reported that the NAc hotspot sends outputs in a unique pattern to
restricted subregions of the hypothalamus and VP, different from the targets of
other shell subregions.53 Based on additional mapping of thalamic and prefrontal
cortex connections, Thompson and Swanson concluded that the NAc hotspot was
embedded in its exclusive closed-circuit corticolimbic loop (separate from other
segregated loops passing through different NAc shell subregions) (Figure 7.3).
Zahm and colleagues54 have recently reported other ways in which the NAc
hotspot of the rostral shell differs from the caudal shell, and specifically suggest
that the rostral hotspot shares some connection patterns with the lateral septum.
Thompson and
TS
Swanson, 2010
Z Zahm et al., 2012

Anterior Z
Cingulate Cortex
Prelimbic Cortex Glutamate

Z
Z TS Z
Orbito- Infralimbic Cortex/ Paraventricular
TS Nucleus Glutam
frontral Brodman’s Area 25 ate
Cortex Dopamine
te
Thalamus
ama
Interfascicular
A
B
ut
Gl Nucleus GA
Hotsopt Accumbens Nucleus TS
Glutamate
TS Z Medial Shell TS Hotsopt
Ventral Ventral Parabrachial
Z Pallidum Tegmental Nucleus
G ABA Preoptic Area Z
Area TS
G ABA Z
Z Lateral at e
am
GA
BA Hypothalamus Glut
Gl
am
ut
at e
Figure 7.3:
Mesocorticolimbic circuits for “liking” and “wanting. Neural circuits underlying food
“wanting” and hedonic “liking.” A summary map showing the connections between cortical,
limbic, and midbrain nuclei, with a particular focus on the unique connectivity of the NAc
hotspot and the VP hotspot. Hedonic hotspots are labelled in the NAc and VP. Thompson
and Swanson (TS labelled boxes; 2010) reported that the NAc hotspot is embedded in a
closed-circuit loop, receiving corticolimbic inputs from infralimbic cortex, and projecting
outputs to restricted subregions of the hypothalamus (lateral preoptic area–lateral
hypothalamic transition zone) and rostral VP. These hypothalamo-pallidal afferents then
project to the paraventricular nucleus of the thalamus, which then completes the loop by
sending efferents to the infralimbic cortex. Zahm et al. (Z labelled hexagons; 2012) suggest
additional connectivity in a pattern similar to lateral septum.
Adapted from Richard JM, Castro DC, DiFeliceantonio AG, Robinson MJ, Berridge KC. Mapping brain circuits
of reward and motivation: in the footsteps of Ann Kelley. Neuroscience and Biobehavioral Reviews. 2013;37(9 Pt
A):1919–1931. Reprinted with permission from Elsevier.
These investigators suggested the rostral half of the NAc that contains the hotspot
to be an anatomical transition zone that merges NAc shell features with features of
the lateral septum (again, different from the caudal half of the medial shell, which
they suggest may instead be a transitional zone of the NAc with the extended amyg-
dala, including the bed nucleus of the stria terminalis and central nucleus of the
amygdala).55 While Zahm and colleagues differ from Thompson and Swanson on
some points that remain to be resolved, taken as a whole, both studies provide ini-
tial confirmation that the NAc rostrocaudal quadrant of the medial shell is a rela-
tively distinct anatomical entity as well as a functional hotspot (Figure 7.3).
Ventral Pallidum Mechanisms of “Liking”
The VP is another crucial substrate for the generation of taste pleasure, and has its own
hotspot, contained in its posterior half.20,25,56–58 In the VP hotspot, microinjections of
F ood “ L iking ” and “ Wanting ” ( 131 )
drugs that stimulate neuronal receptors for mu opioid or orexin neurotransmitters

cause increases in “liking” reactions to sucrose, similar to the NAc hotspot micro-
injections.25,59 The special importance of the VP hotspot to hedonic “liking” is also
reflected in the fact that it is the only brain region known thus far where neuronal
death abolishes all “liking” reactions and replaces them with “disliking,” even for
sweetness (at least for a period of several weeks).11,20,25,32,35,57,58,60,61
The NAc and VP are substantially interconnected, with each structure sending
gamma-amino butyric acid (GABA) projections to the other (Figure 7.3). Although
the hotspots may not be directly interconnected anatomically,53 they functionally
interact, and each hotspot seems able to recruit the other in the generation of taste
pleasure. For example, NAc hotspot DAMGO microinjections enhance firing by VP
hotspot neurons to the taste of sucrose in a sustained pattern that appears to code
for the hedonic impact of the sweet sensation.62
HOW DO FOODS BECOME “WANTED”?
Foods become “wanted” when the sight, flavor, or mental representation of the food
or its cue(s) activate brain mechanisms of “wanting,” which involve larger mesocor-
ticolimbic brain circuitry than do the “liking” hotspots, and this activation espe-
cially depends on ascending dopamine projections from the midbrain to the NAc
and other forebrain structures. The process of “wanting” attributes food stimuli
with incentive salience, enhanced attractiveness, making them sought-after, and
likely to be consumed. In other words, they are more salient and desired.4,6,12 When
food cues (e.g., the smell of a cookie, the packaging of a chocolate bar) acquire moti-
vational power, they can trigger intense desire for food. Importantly, cue-triggered
desire for food can override satiety signals and lead to food consumption even when
we are not hungry.6,15
Ordinarily, “wanting” occurs along with other reward components of “liking”
and “learning,” and with subjective desire, but it can be dissociated both from other
components and subjective desire under some conditions. Usually the brain “likes”
the food that it “wants.” But sometimes it may just “want” it.12
Brain Mechanisms of “Wanting”
Contrasting the neurobiology of “wanting” to “liking,” we note that brain sub-

strates for “wanting” are more widely distributed and more easily activated than
substrates for “liking.”57,63–69 The mesolimbic dopamine system is probably the
best-known neural substrate able to enhance “wanting.” Dopamine activation is
evoked by pleasant foods and reward cues.70–78
A causal relationship between mesolimbic dopamine neurotransmission and
“wanting” has been found in experiments that have used the Pavlovian-Instrumental
Transfer test (PIT), a paradigm that better isolates incentive salience mecha-
nisms,79,80 as well as in simple eating. In PIT, a Pavlovian cue (e.g., a sound that
has previously been associated with sugar) triggers a burst of increased efforts to
obtain the associated food (e.g., a rat presses harder and more frequently on a lever
that the rat previously learned could earn it sugar pellets). For example, elevations
of the spurt of “wanting” elicited by a reward cue in PIT have been produced in ordi-
nary rats by amphetamine-induced elevation in dopamine release, and by long-term
drug-sensitization of mesolimbic systems.66,79–81 Similarly, excessive dopamine in
the brains of mutant mice whose gene mutation causes extra dopamine to remain
in synapses (knockdown of dopamine transporter) produces elevated “wanting” for
sweet food reward, as measured in a greater determination to run in a runway to
obtain sugar rewards, but no elevation in “liking” reactions to sweetness.82 Several
neuroimaging studies of humans have similarly found that dopamine levels may
correlate better with subjective ratings of wanting a reward than with pleasure rat-
ings of liking the same rewards.67,83,84
Opioids Increase Food “Wanting,” Not Just “Liking”
While opioids are known for their role in hedonic processes, our mapping studies in
the NAc and VP suggest that opioids might also play a more specific role in incentive
motivational processes above and beyond their effects on palatability, even outside
of hedonic hotspots (Figure 7.2). DAMGO microinjections in the NAc and VP he-
donic hotspots stimulate “wanting” and food intake, as well as enhance “liking.”23,25
However, “wanting” mechanisms can extend far beyond the hedonic hotspots, and
appear to be widely distributed throughout the entire medial shell, and also extend
to the entire NAc core and to parts of other brain structures, including neostriatum
and amygdala, even at sites that fail to enhance “liking” for food.9,22,23,85
The notion that opioids increase appetitive motivational processes above and
beyond their effects on “liking” processes is consistent with many previous find-
ings that opioids stimulate food intake or “wanting” measures throughout a range
of striatal sites, as well as in many other brain areas.86–90 For example, mice lacking
beta-endorphin, enkephalin, or both, show reduced motivation to obtain food
when sated but not when food-deprived,91 while mice lacking the mu opioid recep-
tors show reduced willingness to work for food rewards.92
Importantly, food and food-reward cues are not always attractive, but rather vary
across time in motivation potency. A cue’s power to trigger desire fluctuates espe-
cially when encountered in different physiological brain states (e.g., hunger, satiety,
stress), which may recruit these distributed “wanting” systems in the brain.62,93
FOOD “WANTING” AND “LIKING” SYSTEMS INTER ACT

WITH HUNGER AND SATIETY SYSTEMS
Brain systems of food pleasure and desire dynamically change their response to
food and food-associated cues, depending, among other things, on the organism’s
metabolic states of hunger and satiety. This interaction contributes fundamentally
to food intake control. Hedonic “liking” is enhanced during hunger and decreased
during satiety, a phenomenon called alliesthesia.94,95 Similarly, cue-triggered
“wanting” for food is also enhanced after fasting and decreased during satiety.
Great progress has been made in recent years toward understanding the neural
interactions between food-reward systems and regulatory systems of caloric
hunger and satiety. 3,96–101 Overall, orexigenic signals increase dopaminergic ac-
tivity when exposed to food or food-related cues, whereas anorexigenic signals
inhibit dopamine-firing and decrease dopamine release. So, how does hunger en-
hance food “liking” or “wanting” to make food more tempting and attractive?
There are a number of promising mechanisms, and we briefly present and discuss
several here.
Enhanced Food “Liking” During Hunger: Orexin

Mechanism of Alliesthesia
Hunger increases “liking” for food, and one potential neurobiological candidate
for the interaction might be orexin (hypocretin). Orexin neurons in the lateral
hypothalamus (LH) are implicated both in food reward and in hunger. 2,14,102–111
Anatomically, orexin neurons in the LH project to many forebrain targets, in-
cluding the VP,112 where orexin inputs are especially dense in its posterior half.112
The projection of orexin neurons from LH to posterior VP suggests the possi-
bility that the VP hotspot might also mediate orexin-induced enhancement of
food “liking.”
Recent findings by Chao-Yi Ho in our laboratory have shown that orexin micro-
injections in the VP hotspot can directly potentiate “liking” reactions to sweet
tastes.59 Thus, the posterior VP appears to have an orexin hedonic hotspot, with
boundaries similar to those of the opioid hotspot. These findings suggest that
orexin activation during hunger might directly enhance hedonic “liking” by stimu-
lating neurons in hedonic hotspots, such as the posterior VP.
Are Food Cues More Salient During Hunger?
Hunger can increase the intensity of incentive salience attributed to food cues,
making them more attractive and harder to resist. This hypothesis has found
support from human studies that show that hunger elevates food-cue incentive
salience, both in obese and in normal control subjects as indicated by increased
gaze duration,113 and that hunger increases the sensitivity to visual food cues.114
Interestingly, food cues affect behavioral response inhibition in a “go/no-go” task in
hungry individuals but not in sated individuals, suggesting a higher salience of the
food cues during hunger.115 Similarly, 24 hours of fasting also heightens “wanting”
for food and food-related cues, as revealed by tests that examine food “wanting”
in computerized tasks.116 Together, these findings suggest that food cues might be
more attractive, tempting, and difficult to resist during hunger.
What might be the neurobiological basis of the interaction between hunger sig-
nals and food-cue salience? Besides orexin, another potential candidate might be
ghrelin, a peptide released by the stomach that is elevated by food restriction,116
and the only known gut peptide associated with hunger.117 Recent evidence sug-
gests that ghrelin might be a chief mechanism by which high metabolic need alters
the incentive salience of food.100 In support of this hypothesis, ghrelin has been
shown to enhance the effort to obtain sucrose rewards in operant conditioning
paradigms118 thought to reflect incentive motivation, and to depend on opioid and
dopamine mesolimbic systems. The stimulatory effects of ghrelin are suppressed
by dopamine (D1) receptor antagonists,118 suggesting that ghrelin interacts with
dopamine systems to promote feeding.
Human studies have also revealed that intravenous injections of ghrelin in-
crease the neural responses to food pictures in structures known to be involved in
reward, such as the striatum and the amygdala, as well as the orbitofrontal cortex
and the anterior insula. These findings suggest that ghrelin may stimulate food
consumption by enhancing the incentive properties of food-related cues.119
The potential role of ghrelin as a key metabolic signal of “wanting” for food
reward is supported by the neurobiological interaction between ghrelin and
the mesolimbic dopaminergic system.120 Ghrelin receptors are expressed on
GABAergic and dopaminergic neurons in the ventral tegmental area (VTA) and
substantia nigra,121 and ghrelin is thought to increase food intake several-fold: by
increasing dopamine levels in the NAc,122–125 by activation of dopamine projec-
tions from the VTA to the nucleus accumbens,100 and by activation of D1-like and
D2 receptors in the NAc.100 The interaction between ghrelin and dopamine sys-
tems is most apparent in studies that show that ghrelin-induced food intake is
reduced by the administration of dopamine antagonists. In a study that exam-
ined operant behavior in rats, sucrose-motivated behavior was reduced by the
administration of D1-like and D2-like receptor antagonists in the NAc shell.126
Together, these studies demonstrate the potential role of ghrelin signaling in
food “wanting.” Future studies are needed to determine the exact function by
which ghrelin supports cue-induced feeding.
HOW DO FOOD “WANTING” AND “LIKING” SYSTEMS

CONTRIBUTE TO OVEREATING AND OBESITY?
There is a considerable body of literature demonstrating differences in reward

function between lean and obese laboratory animals, as well as lean and obese
humans.127–130 Food-reward systems are complex and are likely to contribute to
overeating and obesity in a number of different ways. The discussion here will
focus on three fundamental mechanisms: (1) hyper-responsiveness in abnormal
environments; (2) “hyperliking” and “hyperwanting” in overeating and obesity;
(3) food cues becoming more tempting during stress. These mechanisms are prob-
ably not independent from each other and might produce synergetic effects in some
individuals.
Hyper-responsivenes in Abnormal Environments
Normal reward systems can lead to overeating in an abnormal environment; that

is, an environment of abundant food and food cues. Food-reward systems are
essentially “go” systems, and while they can be diminished by hunger and satiety
signals, they are normally never completely “off.”1 In food-rich societies in which
food and food cues are ubiquitous, resisting the temptations of food cues is difficult
for some.
“Hyperliking” and “Hyperwanting” in Overeating and Obesity
Alternatively, overeating can take place as a result of reward dysfunction in the

form of “hyperliking” and “hyperwanting.” At least some obese individuals have
been found to report heightened “liking” for food in several studies. For example,
hedonic ratings for fat have been found to positively correlate with body mass index
(BMI).131,132 Similarly, overweight subjects who tend to consume highly fatty foods
report heightened positive enjoyment reactions to these foods compared to their
lean counterparts who also tend to prefer consuming fatty food.133 Additionally,
heightened hedonic responses for sweet and creamy solutions among Pima
Indians (who are highly prone to obesity) are associated with weight gain in these
populations.134
Obese individuals have also been found to show heightened responses to
food-related cues. For example, obese individuals have higher gaze measures of
incentive salience for food images compared to non-food images, even when they
have recently eaten.113 Similarly, overweight subjects will put forth more effort to
obtain foods and eat and drink more when cued by salient stimuli, like food sights
and smells.135–137 In addition, overweight people salivate more than lean individuals
in response to food-associated cues138,139 even if they do not report greater feelings
of hunger, indicating that brains may over-react to foods in ways that are not neces-
sary consciously detected.
Neurobiologically, pathological overactivation of the opioid or endocannabi-
noid hedonic hotspot in the NAc or VP could cause enhanced “liking” reactions
to taste. Moreover, overactivation of the opioid or dopamine systems could cause
enhanced “wanting” for food and food-related cues. Davis and colleagues have
recently reported that overeaters and obese individuals who are likely to describe
themselves as “compulsive overeaters” are far more likely to carry a genetic combi-
nation that may heighten brain opioid and dopamine signals, and so elevate “lik-
ing” and “wanting” for foods in obesity and binge eating.127 Similarly, Campbell and
Eisenberg have suggested that people with genes that promote elevated dopamine
functioning might similarly experience stronger cue-triggered urges in the pres-
ence of foods and be more prone to develop obesity.140
Consistent with the hypothesis that obese individuals might have enhanced
responsiveness of brain reward systems to palatable food cues and related cues,
neuroimaging studies show that food cues more robustly enhance a desire to eat
and more strongly activate the NAc and neostriatum (CPU) in obese people,137,141–143
possibly even prior to the development of obesity.144,145 In addition, obese subjects
also show greater activation in brain regions associated with visual processing and
attention (i.e., the visual and anterior cingulate cortices and the precuneus) to food
and food-related cues142,143,146–149 as well as to palatable food–related cues.130,150
Dopamine Downregulation?
In apparent contrast with the hypothesis that increased food “wanting” enhances
consumption of highly palatable foods and leads to obesity, other neuroim-
aging studies have found that obese individuals may have lower levels of dopa-
mine D2 receptor-binding in their striatum.151,152 These results originally gave
rise to the “reward-deficiency hypothesis” for overeating, which suggests that a
reward-deficient state leads to compensatory overeating to remedy an anhedonic
state.153 That hypothesis is based, at least implicitly, on the idea that dopamine
mediates the pleasure or “liking” for food, so low dopamine receptors would re-
duce pleasure and produce a reward deficiency. In our view, the idea that dopamine
causes food “liking” is incorrect. However, beyond that issue, there are also reasons
to think that low D2R density is not the preexisting cause of obesity, but instead are
a negative-feedback consequence of excessive reward-activation due to eating pal-
atable foods, and/or of heightened satiety signals resulting from obesity itself. For
example, the downregulation of D2R levels observed in obese individuals can be
reversed by effective weight-loss surgery in obese individuals.154 Also, exposing lab-
oratory animals to especially palatable foods, such as cafeteria diets or “junk food,”
can produce reductions in brain D2R density. More recently, evidence is emerging
that hyper-reactivity of the mesolimbic dopamine system, rather than suppression,
may be more responsible for causing obesity. For example, Kessler and colleagues
have examined changes in dopamine levels in individuals transitioning from nor-
mal weight to mild obesity and found an increase in amphetamine-induced release
of dopamine in striatum, consistent with the notion that early stages of obesity
might be caused by increased reactivity of dopamine neurotransmission.155
Food Cues More Tempting Under Stress
Another way that food “wanting” systems might contribute to overeating and obe-
sity is through interactions with systems of stress. Stress is thought to promote
eating in about 40% or more of the population.156–158 Traditional explanations for
stress-induced overeating have generally focused on the aversive aspects of stress,
and the hedonically soothing effects of eating palatable foods. That is, increases in
eating during stress are traditionally posited to be an attempt at stress reduction by
hedonic “self-medication.”156,157,159
However, data from our laboratory suggest that stress may directly increase
“wanting” for food, without necessarily causing aversive states or needing hedonic
self-medication to power the eating. We found that corticotropin-releasing factor
(CRF) microinjections in the NAc shell directly increased cue-triggered “wanting”

for sucrose, under conditions that ruled out aversive motivational mechanisms or
associations with hedonic self-medication.80 CRF microinjections in the NAc pro-
duced an increase in peaks of “wanting” to obtain a piece of sugar, whenever the
subject was presented with a cue that had been previously associated with that
reward, just as amphetamine microinjections in the NAc increased dopamine levels.
This incentive effect of CRF in NAc may provide a novel explanation for why
stress may enhance cue-triggered bursts of binge eating. The explanation is
that CRF in the NAc makes the sight, smell, sound, or imagination of food more
“wanted,” and more able to trigger an intense “wanting” to eat the associated food.
These results might also explain why stressed individuals might be more likely to
experience strong cravings for rewards and compulsively indulge in pleasurable
activities, such as eating or taking drugs.
CONCLUSION
All eating patterns are controlled intimately by brain mechanisms of food reward.
As described above, while brain mechanisms of food “liking” and “wanting” evolved
under pressures to protect us from scarcity, in the modern world rich in palatable
foods, these brain systems can override metabolic signals and lead to obesity. But
perhaps it is the prevalence of normal weights, rather than obesity, that should
be more surprising in modern societies. Why do some individuals control their
weight in the face of modern temptations while others do not? And what might be
the neurobiological bases of those differences? These questions are just beginning
to be answered, and future research will further help us understand the role of
food-reward mechanisms in normal eating and in eating-related disorders.
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C H A P T ER 8
w
The Influence of Dieting (Hedonic
Deprivation) on Food Intake, How It
Can Promote Hedonic Overeating,
and Mindful-Eating Interventions
A LE X IS CONA SON
S ocietal pressures to maintain an ideal body weight lead many people to diet for
weight loss or weight maintenance. Dieting is largely viewed as a positive and
normative health behavior. Over 50% of young adults report engaging in dieting
behaviors.1 This includes more than half of female adolescents and a quarter of
male adolescents.2 In a sample of college students, 82% reported a desire to lose
weight.3 According to data from the National Health and Nutrition Examination
Survey (NHANES), 53% of young women and 32% of young men ages 20–29 and
57% of women and 39% of men ages 50–59 years old reported trying to lose weight
in the past year.4
Dieting is triggered by dissatisfaction with body shape and size. Body dissatis-
faction often arises from sociocultural pressures to be thin,5 in pursuit of the “thin
ideal” of both beauty and health. One only need turn on the television, read a mag-
azine, or look at fashion models to see that our society values thinness. Our current
standards of beauty are founded on an extremely thin physique. This body type
is unattainable for all but the smallest minority of adult women. The “thin ideal”
exists in parallel with an “obesity epidemic” in the United States. Obese individuals
are highly stigmatized in the United States and face multiple forms of prejudice and
discrimination. Public health campaigns aimed at obesity prevention and interven-
tion often result in increased stigmatization of obese individuals.6 Media coverage
of the “obesity epidemic” emphasizes personal responsibility and presents obesity
as a moral panic that blames the obese individual.7 These societal forces result in
( 147 )
both pressure to be thin to meet the standards of beauty, to avoid stigma and per-
ceived illness, and a fear of becoming fat. These pressures come from a variety of
sources, including media, family, peers, and medical professionals, and may involve
either direct or indirect messages.5 For many people, the solution to cope with these
pressures is dieting to lose or maintain weight.
The distinction between “healthy” weight-loss dieting and disordered eating
is often unclear. Frequency of dieting has been positively associated with mala-
daptive weight-control behaviors such as self-induced vomiting, use of laxatives,
and fasting, as well as binge eating.1 Dieters commonly experience preoccupation
with food, weight, and body shape; increased emotional responsiveness; cogni-
tive distractibility; heightened arousal and arousability; increased neuroticism;
and lower self-esteem.8 These are similar to characteristics frequently observed in
eating-disordered populations.
Dieting typically involves hedonic deprivation. Hedonic deprivation occurs
when dieters deny themselves highly palatable foods that they enjoy eating, in an
effort to lose weight. The most popular weight-loss strategies include low-fat diets,
low-calorie diets, limiting portion sizes, and avoiding eating snacks or desserts.1
Dieting has been defined as the “intentional and sustained restriction of caloric in-
take for the purposes of weight loss or maintenance.”9 However, this definition may
be misleading, since not all dieters successfully restrict caloric intake. In fact, most
dieters do not actually consume fewer calories than non-dieters.9 Research has
found a poor correlation between scores on dietary restraint scales (a commonly
used measure of dieting) and caloric intake.9,10,11 Ironically, dieting is associated
with hedonic overeating and weight gain.1,2,12 Dieting behavior is frequently char-
acterized by periods of food restriction followed by periods of overconsumption.
Weight-loss diets have greater than an 80% failure rate,13 and most dieters find
long-term, sustainable weight loss to be elusive.
While dieting may not lead to caloric deprivation, it does lead to perceived dep-
rivation. Perceived deprivation occurs when people eat less food than they desire
or restrict intake of palatable foods, as is characteristic in hedonic deprivation.
Perceived deprivation occurs despite a state of energy balance14 and without re-
striction of caloric or fat intake.15 There is evidence that perceived deprivation may
induce hedonic overeating. Studies found that perceived deprivation, rather than
energy deficits, trigger binge-eating episodes in women.16
This chapter will review the effects of hedonic deprivation on hedonic overeat-
ing, including proposed mechanisms and theoretical underpinnings. Mindful eating,
an emerging novel ideal, is an alternative to dieting that shows promise in helping
people regulate their eating behaviors. This chapter will focus on restrained eating
and hedonic deprivation, rather than caloric deprivation resulting in energy imbal-
ance, as this is most reflective of real-world dieting behaviors and mindsets. Many
studies on caloric deprivation induce deprivation in a laboratory setting or instruct
participants to either restrict caloric intake or fast. These studies have limited gen-
eralizability because they are not capturing a sample of people who self-impose
restriction, a central characteristic of dieters. In addition, fasting for weight loss is
not a popular real-world dieting strategy. As stated above, most dieters are not in
T he I nfluence of D ieting ( 14 9 )
a state of energy deprivation, but they are in a state of hedonic or perceived dep-
rivation. Hedonic deprivation is very likely to be more characteristic of real-world
dieters than caloric deprivation, and I will focus my attention accordingly in this
chapter.
LONGITUDINAL STUDIES OF DIETING
Longitudinal studies have examined the effects of dieting in naturalistic settings.

Based on this body of research, dieting has emerged as a predictor of weight gain
and disordered eating behaviors. In a three-year longitudinal study (n = 675), Van
Strien et al.12 found that baseline dietary restraint and concern for dieting were
significantly associated with an increase in body mass index (BMI) for females
three years later. This association between restraint and increased BMI in females
was not explained by disinhibitionary or overeating tendencies. These effects were
only found in female participants, not in males. Frequency of dieting and history of
weight cycling predicted increased BMI at three-year follow-up for both males and
females.12 This study used the Restraint Scale17 to prospectively assess restrained
eating. Due to some controversies surrounding the validity of this scale (see dis-
cussion later in this chapter), the authors also included the Dutch Eating Behavior
Questionnaire–Restraint Scale (DEBQ-RS)18 in post-hoc analyses to account for
possible differences in dieting behaviors detected by each scale. Analyses with the
DEBQ-RS yielded similar results. The results from this study support the notion
that dieting is not only an ineffective means of weight loss and weight maintenance,
but can actually have an effect opposite of what the dieter intends to achieve.
A 4-year longitudinal study using data from the Growing Up Today Study
(GUTS) with a large sample size (n = 4,480 females) also showed that frequency of
dieting to control weight was predictive of weight gain, although no single specific
weight-control strategy was significantly associated with weight change.1 There
was a strong association between frequency of dieting and binge eating. Contrary to
the findings by Van Strien et al.19 discussed previously, which found that restrained
eating predicted weight gain independently of overeating, Field et al.1 posit that
overeating may mediate the relationship between dieting and weight gain.1
In a five-year longitudinal study using data from Project EAT-II (n = 2,516),
Neumark-Sztainer et al.2 found that dieting at baseline predicted outcomes related
to obesity and eating disorders at five-year follow-up. For both male and female
adolescent participants, dieting at baseline was associated with over one-half unit
of BMI increase at 5-year follow-up. Dieting predicted increased BMI regardless of
whether or not participants reported engaging in “healthful dieting” or unhealthful
weight-control behaviors. Female dieters had three times the odds of being over-
weight and were at a twofold increased risk for engaging in extreme weight-control
behaviors and reporting an eating disorder at 5-year follow-up when compared
with female non-dieters. The study adjusted for baseline BMI and found that the
results were not simply a result of dieters being a heavier group and more prone to
weight gain to begin with.2
Like the previously discussed studies, a six-year longitudinal study using data
from the Quebec Family Study (n = 537)20 also found an association between
baseline measures of restrained eating, disinhibited eating as assessed by the
Three-Factor Eating Questionnaire,21 and weight gain six years later. Participants
who scored high on restraint at baseline gained over 1 kilogram more than a refer-
ence group, were 26% more likely to gain more than 5 kg at six-year follow-up, and
were 18% more likely to develop obesity, even when controlling for baseline BMI.20
Again, this study supports the notion that dieting predicts weight gain independ-
ently of baseline BMI, indicating that dieting is not simply a proxy for individuals
with a genetic propensity for weight gain.
Studies of monozygotic and dizygotic twins help further sort out the genetic and
environmental effects of dieting. Pietilainen et al.22 assessed Finnish twins (n = 4,129
individuals) from the FinnTwin16 study at ages 16, 17, 18, and 25 years old. Overall,
the risk of becoming overweight by age 25 years old was proportional to the number of
times that a participant had tried to lose weight. The authors concluded that there is
a strong genetic component to weight gain, which supports the notion that dieting is
a reaction to, rather than the cause of, increased weight. BMI at baseline (age 16 years
old) highly significantly and independently predicted the risk of being overweight at
25 years old. However, adjusting for baseline BMI did not change the overall finding,
indicating that dieting also has an effect that is independent of genetic propensity
towards weight gain. Pairs of dizygotic (DZ) twins who both dieted were heavier at all
time points than DZ twins who did not diet. Similarly, in pairs of DZ twins who were
discordant for dieting (when only one twin dieted), the dieting twin was heavier at all
time points than her or his non-dieting co-twin. Twin pairs who dieted had heavier
parents than twins with no dieting history. Again, this supports the notion that par-
ticipants with a history of dieting are genetically predisposed to be heavier. However,
in monozygotic (MZ) twins who were discordant for dieting history, the twin with a
dieting history had a significantly higher BMI than the non-dieting co-twin, despite
having a similar BMI at baseline and sharing the same genetics. These results suggest
a causal relationship (although clinically modest) between dieting and subsequent
weight gain, independent of genetic effects.
In conclusion, the longitudinal research provides evidence that, in naturalistic
real-world settings, dietary restraint and dieting predict weight gain. While dieting
may serve as a proxy for individuals who have a genetic propensity for weight gain, the
research suggests that dieting also has an independent effect on weight gain, above
and beyond identifying individuals with a genetic propensity for weight gain. This se-
gues well to the experimental studies, which may help us gain an understanding of the
mechanisms underlying the relationship between dieting, overeating, and weight gain.
EXPERIMENTAL STUDIES AND THEORETICAL MECHANISMS

Restraint Theory
Restraint theory23 was developed to describe paradoxical eating-regulation behav-
iors observed in laboratory studies of dieting. This theory suggests that dieters
rely on cognitive control, rather than physiological cues, to govern their eating
T he I nfluence of D ieting ( 151 )
behavior. Dieters make rules to control their intake, including specifications of

allowed and forbidden foods. These rules are often vague and only roughly speci-
fied by the dieter. These restrictive norms that dieters impose on themselves lead
to disinhibited eating when the norms are breached.24 Herman and Polivy25 coined
a term, the “what the hell” effect, in which dieters think, “What the hell, I’ve al-
ready blown my diet by eating one slice of pizza (a forbidden food); I might as well
eat the whole pie.” They suggest that dieters are vulnerable to disinhibited hedonic
overeating when their cognitive controls are disrupted by emotions, consumption
of a forbidden food, or the perception of having overeaten. Paradoxically, attempt-
ing to restrict food intake through chronic inhibition of hedonic eating induces ex-
cessive eating and disinhibition of food intake.26
In experimental studies, restrained eaters exhibit “counter-regulation” in re-
sponse to a preload of food. While unrestrained eaters usually compensate for a
caloric preload by eating less, restrained eaters eat more following a larger preload
than after either a small preload or no preload at all.23,27 According to restraint
theory, this occurs because the larger preload has sabotaged the restrained eater’s
diet, which undermines motivation for continued restraint and leads to disinhib-
ited eating.28
In their classic 1975 study, Herman and Mack 23 administered varying levels of
a milkshake preload to dieters (restrained eaters) and non-dieters (unrestrained
eaters). Following the preload, participants were provided ad libitum access to ice
cream. Results indicate that non-dieters reduced later ice cream consumption in
response to larger milkshake preloads, while dieters increased later ice cream con-
sumption in response to larger milkshake preloads. The authors posit that the diet-
ers ate more ice cream due to a perception that their diet had been broken as a
result of consuming the milkshake preload. Once the diet was broken, the dieting
norms no longer applied, and the dieters did not have any means to regulate their
food intake, other than extreme levels of physiological fullness. The amount of ice
cream consumed was the same in the one versus two milkshake preload conditions,
suggesting that one milkshake was enough to break the diet and induce disinhib-
ited eating. In fact, dieters exhibited disinhibited eating in response to even one
ounce of a milkshake preload. This indicates that a dieter’s diet may be broken by
consuming a high-calorie food or a forbidden food, even when the quantity of that
food is small.24
Laboratory studies provide evidence that disinhibited eating can be induced by
the dieter’s perception of preload, rather than the actual energy content of the pre-
load. A study by Herman, Polivy, and Deo28 examined groups of dieters (restrained
eaters) and non-dieters (non-restrained eaters) and manipulated participants’
perceptions of the size of a slice of pizza consumed for the preload in their study.
The actual size of the pizza slice was identical in all conditions. After the preload,
participants were given free access to cookies. Results indicate that dieters (re-
strained eaters) who perceived that they had eaten a larger preload ate more cookies
afterwards than did restrained eaters who perceived that they had eaten a smaller
preload or had no comparison of the size of the preload. In contrast, non-dieters
(unrestrained eaters) regulated their intake by eating fewer cookies after they per-
ceived that they had eaten a larger preload.
In addition to the studies described above, disinhibited eating in dieters (re-

strained eaters) has been elicited in laboratory settings, induced by various factors
such as previous overeating, anticipated overeating, perception of eating some-
thing fattening, feeling emotionally distressed, being intoxicated, devoting mental
resources to other tasks,8 negative affect, ego threats, and exposure to food cues.26
Critique of Restraint Theory and the Three-Factor

Model of Dieting
Lowe29 has critiqued restraint theory and questioned the validity of the Restraint
Scale.23 He argues that the Restraint Scale measures perceived deprivation rather
than actual calorie restriction.30 Lowe14 proposes a homeostatic-hedonic model of
hunger based on the fact that, in most developed countries, people seldom experi-
ence the effects of acute energy depletion. Thus, most food consumption is moti-
vated by factors other than physiological signals of energy depletion. Perceived
deprivation is emotion-based deprivation that stems from eating less than you
want, not from eating less than you need. It is likely that perceived deprivation,
rather than actual energy restriction, leads to hedonic overeating and weight gain. 31
Studies indicate that the Restraint Scale is only minimally related to
self-reported dieting. Most restrained eaters (as classified by the Restraint Scale)
are not currently on a weight-loss diet.30 Differences have been noted between “re-
straint intentions” and “restraint behaviors.” “Restraint intentions” are associated
with more emotional and external eating, while “restraint behaviors” were associ-
ated with less emotional and external eating.32 Self-reported restrained eating is
not associated with sufficient restriction of energy intake to induce an energy def-
icit or engage homeostatic mechanisms,14 indicating that diet-related overeating is
related to hedonic rather than homeostatic mechanisms.
One may argue that the notion of restraint is representative of many real-world
dieters who do not necessarily engage in “successful” calorie restriction but have a
dieting mentality that results in hedonic overeating. Clinically, many people deny
being on a weight-loss diet when directly asked; however, upon further inquiry,
they do report restrictive thoughts about eating, including classification of foods
as good or bad, attempted avoidance of certain foods, feelings of guilt after having
consumed forbidden foods, and patterns of hedonic deprivation and hedonic over-
eating characteristic of restrained eating.
Lowe developed the Three-Factor Model of Dieting29 as an alternative to
Restraint Theory. While he is in agreement that dieting causes overeating,29 Lowe
argues that the Three-Factor Model, rather than Restraint Theory, best describes
the phenomenon. Lowe29 argues that there are three different facets to dieting. The
first factor that Lowe identified is “frequency of dieting and overeating,” which
refers to an individual’s history of dieting and overeating. He argues that this factor,
rather than restrained eating, is what Herman and Polivy observed in their experi-
ments and is most similar to the concept of restrained eating. The second factor
is “current dieting,” which refers to an effort made by an individual at the present
time to restrict caloric intake to lose weight. He argues that these individuals are
in a state of negative energy balance due to calorie restriction. Many people who
are currently dieting have a history of dieting and would be classified as restrained
eaters. However, the converse is not true; most restrained eaters are not currently
dieting. The final factor is “weight suppression” and refers to the maintenance of
weight lost through dieting. Dieters who sustain weight loss would fall into this
category, while those who regain the weight would be restrained eaters. According
to the Three-Factor Model, each factor has a unique influence on eating behavior.
In support of his Three-Factor Model, Lowe conducted research that concluded
that restrained eaters who report current dieting for weight loss regulate their
eating in response to a preload similar to unrestrained eaters.33,34 He proposes that
dieting is a response to—rather than a cause of—hedonically based mechanisms
that drive overeating.30,35 Similarly, Larsen et al.32 proposed that restrained eaters
are individuals with a propensity towards overeating who unsuccessfully attempt
to restrict their intake through restrained eating.32 Lowe advocates that while diet-
ing for weight loss may cause harmful effects for average-weight individuals, it
may be beneficial for overweight individuals in that, while it is unlikely to result in
weight loss, it may slow the rate of weight gain in individuals prone to weight gain.30
Overweight and obese restrained eaters utilize regulatory strategies to consume less
food following a preload when compared to overweight and obese unrestrained eat-
ers, while normal-weight restrained eaters consume more following a preload when
compared to normal-weight unrestrained eaters.36 Thus, weight status may influ-
ence the effects of restrained eating. Lowe criticizes the dieting literature for largely
ignoring an individual’s propensity towards weight gain as a factor in most studies.30
Tomiyama et al.37 also critiqued Herman and Polivy’s methodology. They argue
that the laboratory setting used in Herman and Polivy’s studies does not generalize to
real-world settings, because it would be highly unusual for dieters to be forced to break
their diet and then immediately be forced to eat forbidden foods. In addition, the mar-
keting of the Herman and Polivy studies as taste test studies may have biased partic-
ipant recruitment towards dieters who were willing—and perhaps even looking—for
an excuse to break their diet. Tomiyama et al.37 conducted two studies that used die-
tary self-monitoring to assess the reaction of restrained eaters to diet violations. They
did not find increased overeating in response to diet violations in either study. In fact,
participants compensated for a milkshake preload similar to that used in Herman and
Mack’s original study23 by consuming fewer calories the rest of that day. They argue that
dieters who can control their environment by avoiding tempting foods may be more
successful at compensating for a diet violation over the remainder of their day than
dieters who are forced to break their diet and are then confronted with tempting foods.
CR AVINGS
Does dieting increase cravings? Some researchers propose that food cravings medi-
ate the relationship between dieting and weight gain. Overall, food cravings are a
common occurrence and are not specific to dieters. Studies have found that 97% of
female college students and 68% of male college students reported having experi-
enced food cravings.38 However, cravings exist on a continuum between mild and
extreme, and some types of cravings may be more normative than others.
Hill39 described cravings as hedonic responses to food, characterized by an in-
tense desire directed at a particular food, drink, or taste. Interestingly, some research
concludes that fasting reduces food cravings while dieting may increase or have no
effect on cravings.39 Cravings experienced by dieters are reported as stronger, more
difficult to resist, and slower to disappear than those of non-dieters.39 Monotonous
diet and self-restriction are associated with increased cravings.39 Dieters tend to
report cravings for foods that they attempt to restrict, and they consume these “re-
stricted” foods on 70% of the craving occasions.39
A study by Polivy, Coleman, and Herman40 found that restrained eaters who had
been deprived of chocolate ate more chocolate than restrained eaters who had not
been deprived of chocolate. Unrestrained eaters did not exhibit this rebound ef-
fect. In addition, they found that restrained eaters who were chocolate-deprived
reported more cravings for chocolate than chocolate-deprived unrestrained eaters.
They conclude that dietary restraint moderates both food intake and cravings in
selective food restriction. Vanilla restriction did not seem to have the same effect.40
Coehlo et al.26 examined food cravings in college students who restricted either
complex carbohydrates or protein for three days. Participants reported increased
cravings following carbohydrate and protein restriction, with cravings being spe-
cific to the type of food that had been restricted (e.g., carbohydrate-restricted partic-
ipants reported increased cravings for carbohydrates during the restriction period).
In terms of food intake following the restriction period, carbohydrate-restricted
participants consumed significantly more carbohydrates (croissants) during ad
libitum eating than did either protein-restricted or no-restriction participants.
However, protein-restricted participants did not consume significantly more pro-
tein (chicken). The authors conclude that carbohydrate restriction is associated
with both more carbohydrate cravings and intake, while protein restriction is only
associated with increased protein cravings but not intake.26 This may be related to
the perception of the carbohydrate food selection as forbidden but not the protein
food selection, since previously discussed research has suggested that restrained
eaters are disinhibited by forbidden foods. However, the study did not find any in-
teraction between dietary restraint status and food intake.
Blechert et al.41 deprived regular chocolate eaters from consuming chocolate for
one week while maintaining the rest of the participants’ diets as usual (no other
restrictions). The authors measured physiological eye-blink startle responses to
hedonic deprivation of chocolate. Participants showed reduced startle response
during images of chocolate during deprivation states, which indicates more appe-
titive/approach response and attention allocated to chocolate cues. However, the
chocolate-deprived participants exhibited a similar response to energy-dense,
highly palatable, non-chocolate food cues, suggesting that deprivation of one par-
ticular type of food may generalize to increased responses to other types of highly
palatable foods. Behaviorally, participants liked, wanted, and consumed more choc-
olate compared to energy-dense highly palatable foods when hedonically deprived
of chocolate than when sated with chocolate. This study emphasizes that perceived
deprivation rather than an energy deficit induces hedonic hunger and cravings.41
Some argue that dieters experience greater cravings for high-calorie foods than
non-dieters do, but that these cravings are not accompanied by an increased liking
or enjoyment of these foods. This is similar to the effect seen in drug addiction.42
Hoefling and Strack42 found that restrained eaters exhibited a contradictory pattern
of positive implicit and negative explicit attitudes towards foods with high calorie
content. This suggests that restrained eaters experience a psychological conflict
when confronted with highly palatable high-calorie foods. Restrained eaters are
both impulsively attracted to high-calorie foods, as demonstrated by immediate
activation of hedonic thoughts about calorically dense foods, while simultaneously
negatively evaluating these foods in direct evaluation of attitudes.42 Thus, dieters
experience a push and pull to highly palatable foods, creating an enticing yet forbid-
den attraction.
ANIMAL MODELS OF DIETING
The relationship between hedonic deprivation, dieting, and hedonic overeating in

humans is complex. Results from animal models may help elucidate the effects of
dieting on hedonic overeating and the underlying mechanisms. Corwin, Avena, and
Boggiano43 report on the effect of limited access to highly palatable food in rats.
Rats were provided continuous access to chow and water (not food-deprived), but
were only allowed intermittent sporadic access to a highly palatable food (short-
ening). They found that, when highly palatable food was provided sporadically to
rats, intake increased during the limited access period and was significantly greater
than the intake of rats that had daily access to the highly palatable food. A pattern
of overeating and undereating developed, which was similar to the pattern pro-
posed to occur in human dieters based on restraint theory. Rats with limited access
to the highly palatable food overate on days that the highly palatable food was pro-
vided and underate chow on days when palatable food was not provided. This study
suggests that the unpredictable consumption of palatable food contributes to binge
eating. In humans, dieting mimics this paradigm of intermittent access to palatable
foods through hedonic deprivation followed by hedonic overeating.
Animal studies have also concluded that a history of dieting seems to play a key
role in the relationship between dieting and hedonic overeating. In fact, a history
of dieting may change the way that we react to stress, which in turn may influence
eating behaviors. Pankevich44 found that a history of food restriction produces a
change in the stress neurocircuitry of mice, leading to increased stress sensitivity
and a tendency to over-consume high-fat foods. Mice that were calorie-restricted
had significantly lower levels of leptin, an increased stress response and delayed
stress recovery, and more depressive symptoms and helplessness, compared to
non-calorie-restricted control mice. When mice that had undergone calorie re-
striction were exposed to chronic variable stress and allowed limited access to a
high-fat food, they consumed more calories from high-fat foods than control
mice did, resulting in a higher percentage of total calories from a high-fat diet.
The calorie-restricted mice experienced increases in orexegenic hormones asso-
ciated with motivation to consume calorically dense preferred foods in response
to the high-fat diet, while the control mice experienced a reduction in orexigenic
hormones. This research suggests that a previous experience of dieting increased
binge-eating of high-fat foods under stress. In addition, the mice were physiologi-
cally motivated to consume even more high-fat food in response to the high-fat diet,
creating a self-perpetuating cycle.44 Withdrawal from a high-fat diet increased the
relative stress state and promoted reinstatement behaviors in which mice selected
an aversive environment to access a high-fat diet.45
Rats that were exposed to a history of both dieting and stress ate significantly
more food (30–100% more kilocalories of palatable food), despite the fact that they
were not in a state of energy deprivation, compared with rats who were exposed
either only to history of dieting, only to stress, or to neither condition. The rats
binged on cookies, not chow, consistent with hedonic eating as opposed to meta-
bolic need. Rats with a history of dieting (both that were and were not exposed to
stress) consumed more food than rats without a history of dieting by increasing
their normal chow intake. However, it was only the rats that were exposed to both
a history of dieting and stress that exceeded homeostatically driven overeating by
also consuming significantly more palatable food.43
MINDFUL EATING
Mindful eating is a promising treatment for disordered eating that helps people
eat according to their internal signs of hunger, fullness, and satiation. While diet-
ing activates the hedonic system of eating behaviors, mindful eating activates the
homeostatic system. Mindful eating has been defined as “being aware in the pre-
sent moment when one is eating, paying close attention to the senses, including
physical and emotional sensations.”46 Rather than reliance on external rules,
which easily yield to hedonic overeating when violated, mindful eating utilizes the
body’s innate physiology to guide eating behaviors. Mindful eating can reconnect
us to the internal signals of hunger, fullness, and satiation, from which dieting
disconnects us.
Much of the research on mindfulness and eating behaviors has examined the
effect of general mindfulness interventions, rather than more specifically targeted
mindful-eating interventions. This research indicates that general mindfulness
interventions are effective at treating overeating, hedonic eating, and other disor-
dered eating behaviors. There is also some evidence that general mindfulness may
be effective for weight loss.47 However, one study that examined both general mind-
fulness (“everyday mindfulness”) and mindful eating found that mindful-eating
skills have more influence on eating behaviors than general mindfulness medi-
tation.48 Due to the more specific connection between mindful eating and eating
behaviors, this chapter will focus specifically on studies that examine mindful
eating, not general mindfulness meditation. Review of the general mindfulness
meditation literature and the impact on eating behaviors is beyond the scope of
this chapter.48
There have been few randomized controlled trials investigating the effec-
tiveness of mindful eating.49,50 Most studies used the Mindfulness-Based Eating
Awareness Training (MBEAT) program.51 Kristeller et al.49 examined participants
(n = 150) with symptoms of binge eating who underwent a 12-week MBEAT pro-
gram, a psychoeducational cognitive-behavioral group (PECB), or a waitlist control
group. Both interventions were focused on eating behaviors rather than weight
loss, although they did include discussion of weight management and calorie bal-
ance.49 The MBEAT program was designed to increase mindful awareness of eating
experiences and to decrease mindless or habitual reactivity, through the use of
mindfulness meditation. The program aims to cultivate attention to increase non-
judgemental awareness of internal experiences and automatic patterns related to
eating and reengage the natural physiological processes of eating-regulation.50 The
PECB group served as a comparison group that was known to be clinically effec-
tive. Results indicate that the mindfulness-based intervention was as effective as
the PECB intervention at reducing binge-eating behaviors. Most participants in the
treatment groups who met criteria for binge-eating disorder (BED) at the outset of
the study no longer met criteria at one-month and four-month follow-ups. These
improvements were significantly greater than the waitlist control group. In the
MBEAT group, more meditation practice was significantly associated with greater
weight loss. While there were no statistically significant differences between the
MBEAT and PECB groups, the MBEAT group had larger effect sizes than the PECB
group on indicators of reactivity towards food and food intake, indicating greater
self-regulation and self-control. The authors posit that, if cravings are driven by
anxiety related to abstinence from highly palatable food, the MBEAT program
may serve to regulate the neural processes involved in impulsive responses to food
cravings.
Another randomized control trial examined patients with type 2 diabetes (n =
52) using a version of MBEAT adapted for diabetes (MBEAT-D). The MBEAT-D in-
tervention was compared to a diabetes self-management education (DSME) pro-
gram designed to improve diabetes knowledge, outcome expectations, and self-care.
The MBEAT-D intervention was found to be as effective as the DSME program in
increasing knowledge, outcome expectations, eating-related self-efficacy, cognitive
control over eating, weight loss, and decreasing disinhibition of control, hunger sus-
ceptibility, overeating, and symptoms of depression.50
A smaller (n = 47) randomized control pilot study examined a mindfulness in-
tervention that integrated elements from the MBEAT program, as well as more
general principles of mindfulness. Results of that study indicate that the mind-
fulness intervention was effective at reducing external eating in a group of over-
weight and obese women. Obese women in the mindfulness group also experienced
significant reductions in their cortisol awakening response, indicating a reduction
in stress that was related to decreased abdominal adiposity. Overweight women in
the mindfulness group did not experience these reductions. The mindfulness inter-
vention was also effective for weight maintenance; participants in the mindfulness
group were more likely to maintain weight, while participants in the control group
were more likely to gain weight.52
In an earlier exploratory study with a small sample size (n = 18) of women with
BED, a mindful-eating group intervention was found to be effective in significantly
reducing the frequency and intensity of binge episodes. In addition, participants
reported increased sense of control over eating and increased awareness of hunger
and satiety.53 Another exploratory study with a small sample size (n = 10) of obese
participants found that a six-week mindful-eating intervention designed for over-
weight and obese participants (Mindful Eating and Living, MEAL) resulted in
decreased weight, eating disinhibition, binge eating, depression, perceived stress,
physical symptoms, negative affect, and C-reactive protein while increasing cogni-
tive restraint around eating. The intervention improved eating behavior, psycho-
logical distress, and weight loss in obese participants.
Other studies examined mindful eating in nonclinical samples without using
any interventions. In a nonclinical sample of college students, there was an inverse
relationship between mindful eating and BMI.46 There was no significant relation-
ship between mindful eating and physical activity (but there was a trend towards
a negative relationship), indicating that mindful eating is not simply a character-
istic of those with healthy lifestyles. In a study that examined a nonclinical sample
of South Australian adults, results indicate a significant negative relationship be-
tween mindful-eating behavior and self-reported serving size of energy-dense
foods.48 Together, results of these largely observational studies indicate a positive
relationship between mindful eating and healthy eating behaviors and an inverse
relationship between mindful eating and BMI.
CONCLUSION
The research discussed in this chapter casts doubt on the effectiveness of dieting
for weight loss and weight loss maintenance. While some dieters may be able to ob-
tain a state of negative energy imbalance for a limited time, perhaps under the strict
guidance of formal weight-loss interventions, many dieters practice restrained
eating associated with vacillations between perceived deprivation and hedonic
overeating. Despite the strong societal pressures towards thinness that drive a cul-
tural norm of weight-loss dieting and valiant efforts by many obese and overweight
people to reduce their weight, the “obesity epidemic” persists. It is essential that
we explore non-dieting approaches to weight management and regulating eating
to encourage people to improve their health without a preoccupation with weight
and deprivation. The published literature on mindful eating is limited, not only by
the paucity of studies, but also by methodological limitations, including case study
design, lack of control groups, small sample sizes, and qualitative reports. However,
the few randomly controlled studies that have been published demonstrate prom-
ising results. Mindful eating may be a way for people to control hedonic overeating
and restore homeostatic eating-regulation without dieting.
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C H A P T ER 9
w
The Modern Food Environment
Changes in Food Quantity and Quality and
Their Impact on Hedonic Eating
W ENDY M. STEIN A ND K ATHLEEN L . K ELLER
D iet-related chronic diseases such as cardiovascular disease, type 2 diabetes,

and obesity are the leading causes of morbidity and mortality, contribut-
ing to 62% of deaths worldwide in 2009. This number is projected to increase to
73% by the year 2020.1 The effects of diet-related chronic illnesses far outweigh
those of malnutrition, yet these diseases were nonexistent among our ancestors.
One reason for this is our longer lifespan. The average lifespan of hunter-gathers
was only 35 years,2 while humans today live over twice that long. However, an-
other likely contributor to increased chronic disease rates is diet. Starting around
10,000 years ago, the human species experienced revolutionary changes in food
production. Subsequent to these changes, the advent of modern agricultural prac-
tices made the production of nutritious, energy-dense, and tasty foods easier and
cheaper to attain.
Worldwide increases in obesity rates3 have brought to the forefront serious con-
cerns about the impact of the modern food environment on human health. Without
doubt, there are many advantages to having an efficient global food-production
system. For example, historically, the ability to access highly palatable food sources
was reserved for higher-income countries. Now, poorer countries where malnutri-
tion and hunger were traditionally the greatest concerns are experiencing the nu-
trition transition—a shift from primarily nutrient-deficiency diseases to chronic
diseases fueled by nutrient excess. Increased globalization of the food supply has
not only allowed freer and more rapid movement of food, but it has also hastened
the spread of “Western” styles of food production, promotion, shopping, and
( 163 )
eating. The availability of supermarkets and “megastores” has expanded, with the
most rapid increases seen in developing areas like Latin America, Africa, and Asia.4
Moreover, the food industry has broadened its reach, with prominent companies
like Coca-Cola and McDonald’s now selling a significant number of products out-
side North America.5 Globally, diets have become sweeter and more energy-dense.6
In addition, the foods we eat have become highly processed and less nutrient-dense
than those of our ancestors. Highly palatable foods are more available and acces-
sible today than they have been at any time in history. These rapid environmental
changes have contributed to the increased rates of diet-related diseases seen glob-
ally. Terms like “obesogenic”7 and “toxic”8 have been used to describe the current
environmental conditions.
To truly appreciate the rapidity of these changes, one only has to look back a
few decades. In the 1960s, hunger was a much greater concern than obesity. An
estimated 10 million Americans (5% of the population) were unable to provide suf-
ficient food for their families. The nation was awakened to this issue in the CBS
documentary “Hunger in America” released in 1968, which covered reports on
hunger, malnutrition, and poverty in over 250 counties in 23 states. The results re-
vealed widespread evidence of hunger and inadequate nutrition among the nation’s
poor.9 As a result of this report, in 1969, President Richard Nixon announced the
“War on Hunger,” and the subsequent decade brought changes in policy that in-
cluded the Supplemental Food Program for Women, Infants, and Children (i.e.,
WIC); the expansion of food stamp programs, the National School Lunch Program,
and special nutrition programs for the elderly. A decade later, improvements had
been made, and the evidence of frank malnutrition in the United States declined.10
Just over 40 years later, in 2006, the global prevalence of obesity surpassed that of
malnutrition.11 Paradoxically, malnutrition, hunger, and obesity now occur simul-
taneously due to the widespread availability of cheap, highly palatable foods that
lack essential nutrients.12
In this chapter, we provide an overview of the modern food environment and
its implications for eating behavior and obesity. The changes to the food environ-
ment that have occurred over the past 50 years have contributed to increasing rates
of diet-related chronic diseases on a global level. The primary changes that have
occurred include increases in the quantity of palatable foods available, combined
with simultaneous decreases in the quality of foods and of the diet as a whole. Finally,
we review recent trends to move to specialized diets (e.g., “Paleolithic,” veganism,
organic diets), and we argue that these may be individual- and population-based
attempts to adapt to the overabundance of highly palatable foods in the modern
food environment.
QUANTITY: EVIDENCE THAT THE AMOUNT OF

PALATABLE FOODS HAS INCREASED
Over the past 50 years, both the availability and the accessibility of palatable foods
have increased. Due to improvements in the efficiency of food production, the
T he M odern F ood E nvironment ( 16 5 )
amount of available energy per day has increased by an average of 400 kilocalo-
ries per person since 1969.13 In developed countries like the United States, many
of these calories are in highly palatable, highly processed foods. Because taste is
the most important factor in determining what to eat,14 the abundance of palat-
able foods is a potent motivator of intake. In this section, we discuss three key
changes that have contributed to increases in the quantity of palatable foods in our
diets: the growth of supermarkets, food marketing and promotion, and increased
portion sizes.
Supermarkets
The variety of highly palatable foods available for consumption is heavily influ-
enced by the growth of supermarkets. Prior to supermarkets, consumers bought
foods from small specialty shops that carried specific foods. Meat was purchased
from the butcher, bread from the baker, and vegetables from a produce stand. Shops
were small and local so they could be accessed on foot. The volume of sales at these
establishments was low, making markup on individual goods high. Foods were not
aggressively marketed and promoted by profit-driven companies, therefore choices
closely reflected needs, not wants. The growth of the modern supermarket changed
all this, and for the first time, consumers could have year-round access to a greater
variety of tasty, safe, and affordable foods, all under one roof. As of 2011, super-
markets accounted for about 91% of American food sales.15 In addition, developing
countries like Brazil and China have seen an explosion of supermarkets since the
1990s.16 These trends have increased consumer accessibility to a wider variety of
highly palatable foods and beverages.
By definition, the Food Marketing Institute (FMI) distinguishes “traditional
food retailers” (e.g., supermarkets and grocery stores) from “nontraditional retail-
ers” offering food as well as non-food items (e.g., convenience stores, “supercent-
ers,” and “hypermarkets”). Per the FMI definitions, “grocery stores” are those that
profit $2 million or less per year and occupy smaller spaces than “supermarkets,”
which make over $2 million per year and occupy an average of 20,000 to 65,000
square feet. Supermarkets and grocery stores supply abundant varieties of canned,
frozen, fresh, and prepared foods, while “convenience stores” carry limited selec-
tions including milk, bread, sugar-sweetened beverages (SSBs), and snacks, most
of which are packaged and promoted by the food industry. In the last decade, the
number of even larger markets, called “hypermarkets,” has increased. These estab-
lishments combine sales of clothing, electronics, garden equipment, and health
aids with grocery items. “Supercenters” and “wholesale clubs” (e.g., Sam’s Club and
Costco) have also grown during the last decade, and these stores offer bulk items at
an average of 7.5% less than the same items sold in traditional stores.17 As of 2008,
an estimated 50% of Americans shopped at wholesale clubs.18 While the relation-
ship between buying foods in bulk quantities and eating behavior has not been
fully investigated, there is evidence that the rise in supercenters may be associated
to the rise in obesity.19
Simultaneously with the growth of the supermarket industry, the variety of

products sold at supermarkets has also increased. Over the past 50 years, there
has been a surge in the variety of baked goods, beverages, breakfast cereals, can-
dies, condiments, and dairy products available for purchase. In 2000, the total
number of food products available exceeded 300,000, and the median number
of products carried by supermarkets was nearly 40,000, compared to 26,000 in
the 1990s20 and 14,000 in the 1980s.21 Increases in product variety from 1970 to
2000 contributed to an estimated 24.5% increase in daily calorie intake, of which
9.5% was from refined grains, 9% from added fats and oils, and around 5% from
added sugars.22 A key advantage of increased product variety is that it appeals
to a wider range of consumer preferences.23 However, increased food variety can
lead to excess intake under certain conditions. For example, laboratory studies by
Rolls and colleagues24–26 demonstrate positive associations between food variety
and the amount consumed. Compared to exposure to a single food item, exposure
to a variety of foods within a meal simultaneously (buffet-style meal) or succes-
sively (multi-course meal) is estimated to increase food intake in humans by 14%
to 25%.24,27–32 Moreover, a cross-sectional study by McCrory and colleagues33 found
that after controlling for age and sex, adults who reported consuming a greater
variety of energy-dense foods (i.e., sweets, snacks) over a six-month period had
greater body fat than adults who reported less variety within these food groups.
These findings suggest that greater variety, particularly of energy-dense foods
readily available at the supermarket, might be a contributing factor in the devel-
opment of obesity.
The growth of supermarkets and hypermarkets in many suburban areas has
been causally linked to a reduction in the number of small, family-owned “mom
and pop” stores housed in more urban environments.21 As a result, many urban,
low-income neighborhoods have insufficient access to fresh fruits, vegetables, and
other healthful foods. The term “food desert” has been used to describe a densely
populated, impoverished area with low access to fresh produce. To qualify as a
“low-access community,” at least 500 people and/or at least 33% of the Census
tract’s population must reside more than one mile away from a supermarket or
large grocery store. It has been suggested that because people in these areas shop
for groceries at small convenience stores with little to no access to fresh produce,
they have higher rates of obesity.34 Research has shown that after adjusting for ed-
ucation, income, age, gender, race/ethnicity, and physical activity, the absence of
supermarkets and the availability of convenience stores in the neighborhood was
associated with lower fruit and vegetable consumption and higher rates of over-
weight and obesity.34,35 However, more recent studies have reported that distance
to supermarkets is a weak predictor of obesity and diet quality. 36–39 For example,
in the Seattle Obesity Study, Drewnowski and colleagues38 demonstrated that
proximity to the nearest or most frequented supermarket had no impact on body
weight. After examining the shopping patterns of local consumers, researchers
found that only one in seven consumers reported shopping at the supermarket clos-
est to home. In addition, Cummins et al.40 evaluated the impact of opening a new
supermarket in a “food desert” and saw no effects on reported fruit and vegetable
intake or weight status.
While supermarkets provide consumers with easy access to fresh fruits and
vegetables, they also offer a greater variety of highly palatable pre-packaged and
prepared foods. These competing forces contribute to the struggle consumers face
during their weekly trips to the food store: “Do I go with the apple or the chocolate
bar?” Consumers routinely factor taste, price, convenience, and health into their
food choices,14,41,42 and the weights of these factors are different for each consumer.
For instance, when prioritizing the cost of a meal, people may be enticed to se-
lect cheap, pre-packaged, energy-rich foods (e.g., frozen pizza) that guarantee them
“more bang for their buck” (i.e., less money spent per calorie) and require less time
in the kitchen. Complicating consumers’ ability to make decisions, supermarkets
are staged to encourage sales. Research has shown that the mere, sight, smell, or
taste of food can enhance intake.43 Therefore, the experience of shopping in today’s
supermarket, with its vibrant produce sections, fresh baked goods, and persuasive
messages on packages can be enough to stimulate unplanned food purchases. The
store “planogram,” or model of product placement that maximizes sales, likewise
contributes to the decisions about which foods are placed in consumers’ shopping
carts. A phrase commonly used is “Eye level is buy level,” as products positioned at
eye level are more likely to sell.44 Supermarkets are a key location in the modern
food environment that offer the convenience of one-stop shopping, but in doing so,
they often expose consumers to cues that encourage impulse decisions and facili-
tate overconsumption.
Marketing and Advertising
Along with the increase in food availability and variety at supermarkets has
come a dramatic rise in consumers’ exposure to food products that are heavily
marketed and promoted. Nearly constant exposure to product advertising and
promotion has become the norm—from ads on our smart phones, to pop-ups
on social media, promotions at the supermarket, and billboards on our drive to
work. In the United States and other Westernized countries, food advertising
is ubiquitous. This excessive promotion of foods, particularly for those that are
highly processed, energy-dense, and nutrient-poor, has been labeled as a mod-
ifiable risk factor for chronic disease and is linked to the international obesity
crisis.45–47 Still, research in this area is not conclusive, leading many to question
the extent to which exposure to food advertisements contributes to what and
how much we eat.
The advertising outlet that has garnered the most attention is television (TV),
particularly for its influence on children. While advertisements influence adults,
too, the effects on children are hypothesized to be more deleterious because they
lack the ability to differentiate between ads on TV and real life.48 According to a
2009 report,49 children ages 2–11 years spent about 30 hours per week in front
of a TV. Greater TV viewing time is directly linked to greater food-advertisement

exposure. With the food industry spending close to $2 billion per year marketing
to children,50 it is estimated that children see an average of 10.9 to 12.7 food com-
mercials per day, or between 4,000 to 4,700 per year.51 Food companies use ani-
mated and fictional characters to associate fun, adventure, and fantasy with their
targeted food products.52 These marketing strategies are now employed worldwide,
with promotions for fast food, dairy products, and SSBs rapidly expanding in low-
and middle-income countries.47 While strides have been made to put restrictions on
food advertising directed at children, such as the 2006 Council of Better Business
Bureaus’ Children’s Food and Beverage Advertising Initiative and annual Institute
of Medicine (IOM) workshops, recent data show that 98% of ads are still for nu-
tritionally poor, energy-dense foods that supersede recommended amounts of fat,
sodium, or added sugar.53
Exposure to food advertisements, in any form, influences viewers’ acceptance
of that food. Whether or not this directly leads to increased intake is in question.
Studies conducted in laboratory and school settings have demonstrated mixed
findings.54–57 However, a recent study conducted in Quebec examined the effect
of banning TV ads targeted at children on French-speaking TV networks.58 Using
household expenditure data from 1984 to 1992, the Quebec food-advertisement ban
was associated with reduced fast-food consumption in French-speaking compared
to English-speaking Canadian families. In addition, no differences were observed
between families without children or between families living in provinces without
the ban. These results suggest that reducing exposure to food advertisements on
TV may have an impact on improving eating behaviors in some populations.
Aside from TV, food marketers are branching out to new media outlets, including
websites, video games, and mobile phone messaging. Furthermore, food companies
are spending money on other forms of advertising, such as packaging, direct mar-
keting, and event sponsorship.59 In line with packaging is the concept of “branding,”
or the use of names, symbols, characters, and slogans to create unique, emotional
attachments to a product in hopes that consumers will buy them.60 Researchers
have tested the influence of branding on children’s liking and intake of foods,
demonstrating that some children may be more susceptible to its effects than oth-
ers.54–64 Robinson et al.61 found that 3–5-year-olds preferred food items packaged in
McDonald’s logos compared to plain packaging. In addition, Keller and colleagues62
tested the impact of branding on meal intake in 7–9-year-old children and found
that girls ate about 100 calories more from a meal packaged with McDonald’s logos
compared to plain packaging, while boys ate a similar number of calories in the two
meals. Although the foods and beverages in the meals were the same, these studies
demonstrate the robust impact of branding on children’s food acceptance and intake.
With strong evidence that exposure to food advertising increases acceptance,
and suggestive evidence that this leads to increased food intake and obesity, it is
a concern that food companies have expanded their market share in lower- and
middle-income countries.65 To address these alarming trends, additional research
on effective solutions to mitigate the effects of food advertising in young children
is needed.
Portion Size of Foods
Not only is there a greater variety of foods available for purchase and consumption,
but the quantities of these foods sold and presented to us on a given occasion have
also increased. Eating meals outside the home has become routine in the modern
food environment. The percentage of meals prepared outside American homes, for
instance, has almost doubled since 1970.66 When people do not prepare their own
foods, they increase their chances of being exposed to large portion sizes served at
takeout places, convenience stores, and restaurants. Portion sizes of many fast and
prepared foods are two to eight times larger than the sizes recommended by the US
government,67 and there is evidence that portion sizes might be increasing in some
European countries as well.68,69 The variety of sizes available at fast-food estab-
lishments has also increased over time. Figures 9.1, 9.2, and 9.3, represent how
increases in the size of common food portions affect the amount served to consum-
ers. For example, in 1954, Burger King only sold one size of French fries: the 2.6-oz.
regular. In 2002, the 2.6-oz. small, 4.1-oz. medium, 5.7-oz. large, and 6.9-oz. king
size were available.67 The trend towards introducing large portions to consum-
ers does not appear to be declining, according to recent survey data. There have
been 147 large-size (i.e., “supersize”) portions introduced from 2000 to 2009 for
foods like burgers, pizza, beverages, and candy bars.70 Many of these items contain
nearly half of the recommended number of calories a healthy adult should consume
in a day.
Large portions are a concern because they drive us to eat more without real-
izing how much we are eating. In most short-term studies, exposure to large por-
tions of food increases the amount people eat without affecting self-reported
ratings of fullness. This has been demonstrated with high energy-dense foods like
pre-packaged snack foods,71,72 amorphous entrées,73 unit foods like sandwiches,74
and even healthier options like fruits and vegetables.75,76 Increased intake in re-
sponse to large portions of food has been shown not only in the laboratory, but also
1980s 2000s
2.4 oz. 6.9 oz.

210 cal 610 cal
Figure 9.1:
Change in French fries portion size from the 1980s to 2000s. Adapted from National Heart,
Lung, and Blood Institute (NHLBI) Portion Distortion, 2003.
1980s 2000s
5 cups 11 cups
270 cal 630 cal
Figure 9.2:
Change in popcorn portion size from the 1980s to 2000s. Adapted from NHLBI Portion
Distortion, 2004.
in free-living environments such as restaurants.77 Moreover, both children78 and

adults71–74 are responsive to laboratory manipulations in portion size, and in adults,
these effects have persisted up to 11 days.79 Clearly, increasing the portion sizes of
foods can have a profound influence on the amount we eat.
Portion sizes in restaurants are not the only concern. The size of food packages
sold at the supermarket has also increased.67 This is a concern because people tend
to serve themselves more from larger containers than they do from smaller con-
tainers.80 Further thwarting our efforts to control intake, the sizes of plates, bowls,
and other serving vessels have also increased. Estimates suggest that restaurant
plates in the year 2000 had 44% more surface area than they did in the 1980s.81
Because we add more food to larger plates than we do to smaller plates,82 larger
plates have been hypothesized to contribute to greater intake.
1980s 2000s
6.5 oz. 20 oz.

85 cal 250 cal
Figure 9.3:
Change in soda portion size from the 1980s to 2000s. Adapted from NHLBI Portion
Distortion, 2003.
T he M odern F ood E nvironment ( 171 )
Given these short-term effects, some have posited that increased portions
of food have contributed to the obesity epidemic, 83 but evidence to support this
has been less consistent. According to the Continuing Survey of Food Intake by
Individuals, 1994–1996 and 1998, consumption of larger portions at meals was
positively associated with body weight in some age groups, but not others. 84,85
Furthermore, only a couple of studies have demonstrated differences in re-
sponse to increases in portion size based on weight status, with obese individuals
showing greater increases in intake from larger portions than non-obese indi-
viduals. 86,87 However, most previous work in this area was not powered to test
for individual differences in portion-size response, which may explain the lack of
evidence in this area. Notably, a recent study done with adults in the workplace
showed that exposure to large portions at lunch for six months was associated
with increased weight gain.88
“Supersizing” or value-added marketing has become the norm in the United
States, and several European countries are following suit. Because the cost of
food is cheap relative to the packaging, food companies and restaurants have
used this strategy to increase market share and remain competitive. 89 This has
been effective, as consumers are drawn to products in large packages,90,91 and
they report large portions as a key reason behind restaurant selections. 92 Large
portions offer better value to consumers. Therefore, food companies and restau-
rants that lack reasonably priced large portions are at a disadvantage. However,
the huge popularity of the 100-calorie snack packs suggests that today’s con-
sumers have interests beyond supersizing.93 With new research proposing that
these products might help overweight consumers monitor their intake, 94 it is
likely that portion-controlled products will become even more popular over the
next few years.
QUALITY: DECREASES IN FOOD AND DIET QUALITY
While the relative amounts and accessibility of palatable foods have increased for
the modern consumer, the quality and nutrient-density of these foods have, in
many cases, decreased. In this section, we review how changes in food-processing
and the use of sweeteners have affected food and diet quality.
Processed and Ultra-Processed Foods
The mechanization of food production in the mid–nineteenth century was a critical

factor in decreasing the high rates of hunger and malnutrition that occurred prior
to this time. The term “processed foods” refers to raw agricultural commodities
that have undergone procedures (e.g., washing, cutting, canning, cooking) to alter
them from their natural state.95 Nearly all foods that we eat are processed in some
way. Fruits and vegetables are washed, peeled, sliced, and packaged. Whole grains
undergo milling, rolling, and cracking before they are considered edible. Processing
of foods is essential to ensure a nutritious, safe, and sustainable food supply. In

addition, processing also improves foods’ palatability.96 Nevertheless, a recent study
found that 43% of consumers have negative perceptions about “processed foods,”
and those with higher education tended to rate them less favorably than those with
less education. Processed foods were perceived to be nutritionally inferior and less
safe than “unprocessed” foods. The term “processed” has become synonymous with
“unhealthy,” due in large part to perceptions that processed foods cause obesity.97
Despite this negative view, sales of processed foods have grown globally over the
past three decades, but the rate of change has been most dramatically observed in
lower-income countries.98
Processed foods provide a significant proportion of many of the essential
vitamins and minerals to American consumers. According to the National
Health and Nutrition Examination 2003–2006, processed foods account for
73% of vitamin C, 36% of fiber, and 31% of potassium.99,100 Further investiga-
tions suggest that without enrichment and fortification of foods, a vital com-
ponent of processing, 100% of the population would fail to meet the Estimated
Average Requirement (EAR) for vitamin D, and 75% would not meet this re-
quirement for vitamin A. Fifty percent of the population would have inadequate
intakes of folate and thiamin if not for enrichment and fortification.101 In ad-
dition, without canning, preserving, and freezing, many consumers would be
without fruits and vegetables throughout much of the year. Clearly, processed
foods are an essential part of our food supply that helps many individuals meet
their nutrient needs.
Because most foods that we eat are processed in some form, the term
“ultra-processed” has been proposed to differentiate the more “natural” mini-
mally processed foods from those that are completely manufactured. Monteiro101
argues for a three-group classification to make distinctions between minimally
processed whole foods; ingredients extracted from whole foods (e.g., flours, oils);
and ultra-processed foods that consist of ingredients extracted from whole foods
combined with salt, preservatives, and other additives. These foods include cookies,
pies, candies, cereals, sugary beverages, and packaged meat products like hot dogs.
He argues that ultra-processed foods are created in sophisticated ways to be highly
palatable, and most are aggressively marketed to consumers.102 When consumers
are asked about “processed” foods, these are most likely the types of foods that
come to mind, and they are also the types of foods that are especially problem-
atic, particularly for those who are vulnerable to overeating. There is some evidence
that greater household availability of ultra-processed foods is associated with inad-
equate nutrient intake103 and obesity.104 Additional studies are needed to identify
possible causal links in this relationship, should they exist.
The processing of foods offers benefits that are necessary for maintaining a safe,
affordable, and tasty diet. Yet, there is concern around the sophisticatedly designed
ultra-processed foods that achieve ultimate levels of palatable nutrients and ingre-
dients (e.g., salt, sugar, fat, flavor-enhancers). The optimal levels of palatability
achieved in these foods are far greater than those of any foods our ancestors were
exposed to, and for some, these foods can be difficult to resist. However, the extent
to which highly processed foods contribute to weight gain above and beyond their
energy content has yet to be determined.
Sweetening of the Diet
In addition to greater availability of ultra-processed foods with optimal levels of

palatability, our diets have generally grown sweeter and more energy-dense since
the beginning of the Industrial Revolution.105 Humans are biologically driven to
like sweet-tasting foods and beverages.106 Our ancestors were drawn to these foods
because they contain carbohydrates and energy.107 Yet hunter-gatherers were re-
stricted to consumption of sweet foods like honey only when it was seasonally
available. However, advancements in sweetener production that occurred during
the 1970s have made it possible to economically produce large quantities of foods
that are more palatable than most sweetened foods grown in nature.108 In this
section, we review global consumption trends of added sugars and calorically and
non-calorically sweetened beverages.
The term added sugars is defined as “all sugars used as ingredients in processed
or prepared foods that do not occur naturally in the food” (e.g., lactose in milk or
fructose in fruit).109 The most commonly used added sweeteners in the food in-
dustry are corn syrup, sorghum, cane sugar, high-fructose corn syrup, and fruit
juice concentrate. Over 75% of foods purchased in the United States contain added
sugars.110 From the mid-1970s to the mid-1990s, US consumption of added sugars
increased by 35%.111 However, more recent studies using data from the National
Health and Nutrition Examination Survey 1999–2000 to 2007–2008 suggest that
added sugar intake in American adults and children is decreasing, primarily due to
decreases in intake from SSBs.112
The primary sources of added sugars in the US diet are SSBs, or soft drinks.
Our history with caloric beverages has been relatively brief, considering that the
first soft drink (Coca-Cola) was not introduced until 1886. Today, regardless of
where you live, you can choose from a wide variety of soft drinks, flavored waters,
juice drinks, sports drinks, sodas, energy drinks, and fruit juices. Similar to trends
with added sugars, consumption of SSBs has tended to decrease in nearly all age
groups over the past decade.112 Using a more comprehensive method of categoriz-
ing SSBs that included drinks sweetened after purchasing (e.g., teas, coffee), Miller
and colleagues113 found that Americans ages 2 and over consumed an average of
171 calories of added sugars from SSBs per day in 2007–2008. The highest con-
sumption of added sugars from SSBs was found in adolescent boys and girls, with
energy per day equal to 294 kcal and 194 kcal, respectively. In addition, as reported
by other sources, children’s soda consumption increased with age, while intake of
sweetened, flavored milks decreased with age.113 It is important to note that while
intake of sodas and juices tends to be decreasing among American adults and
children, intake of added sugars from energy drinks, sports drinks, and flavored
waters is increasing.112 These population-based trends in consumption reflect rev-
enues reported from PepsiCo and Coca-Cola, the two most profitable companies
that sell SSBs. Both companies report downward trends in sales of caloric carbo-
nated soft drinks and increases in sales from bottled waters, energy drinks, and
sports drinks.114 These trends support a shift to lower-energy beverage choices in
higher-income countries like the United States.
While higher-income countries are reporting decreases in the consumption of
sugar-sweetened sodas and soft drinks, intake of these beverages has been increas-
ing in developing countries like Brazil and China. For example, in Brazil, sales of
sugar-sweetened carbonated soft drinks increased by 107% and 95% for Coca-Cola
and PepsiCo from 2005–2010, respectively. In addition, sales of fruit and vegetable
juices sold by Coca-Cola in China have increased by 444% from 2005–2010.114 These
trends are likely to drive forward the nutrition transition in these countries. It is
not known if beverage companies are targeting developing countries to make up
for declining sales of SSBs in the United States, although Kleiman and colleagues114
raise this hypothesis.
While it is encouraging to see reductions of added sugar and SSB intake in some
higher-income countries, data suggesting an increase in soda and soft drink con-
sumption in developing countries is concerning.3 Over the next few decades, we are
likely to see greater introduction of ultra-processed, sweet, energy-dense foods in
developing countries, particularly as the food and beverage industry expand sales
to broader and more diverse markets.
IMPLICATIONS AND FUTURE DIRECTIONS
It is not possible to describe the modern food environment without including an

overview of some of the new food trends taking place. The global epidemics of obe-
sity and diabetes have, in part, fueled a strong interest in health, and related to this
have been growing trends to move to more local, sustainable, organic, and mini-
mally processed foods. In many ways, these changes represent the final stage of
the nutrition transition, which Popkin describes as behavioral changes that include
improved dietary quality and reduced “sedentarianism” in order to adjust to the
modern food environment.115 In this section, we provide a short overview of some of
the recent fad diets and food trends that represent individual and population-level
attempts to adjust to the obesogenic food environment.
Food Trends and Diet Fads
The search for the magic combination of supplements, foods, and beverages that
will allow us to eat whatever we want and still lose weight is not new, but over the
past several decades, the number of options available has greatly increased. From
low-carbohydrate to low-fat, vegan, “Mediterranean,” “Paleolithic,” gluten-free,
juice fasts, and cleanses, there are diets to match a variety of consumer interests.116
While these fad diets may not be the quick fix consumers are envisioning, their
demand effects in the marketplace are substantial. In response to the low-fat diet
craze of the 1980s, products with low- and no-fat claims grew from 9.2% in 1989
to over 25% in 1995 and 1996.117 Moreover, in 2004 at the height of the Atkins diet
craze, the percentage of products with the low-/no-carb claims peaked, accounting
for 17% of all new products.117
Over the last decade, low-fat diets have evolved, with more people eating
plant-based fats or following vegetarian/vegan diets. Surveys from consumer
research found that one-third of restaurant chains now offer at least one vege-
tarian entrée,118 and in 2012, nearly half of Americans ate at least one meatless
meal per week, up from 40% in 2007.119
Low-carbohydrate diets have also changed since the publication of Dr. Atkins’ New
Diet Revolution. For example, the eco-Atkins diet, the South Beach diet, the Zone
diet, and the Paleolithic diet all share similarities with the Atkins high-protein/
fat, low-carbohydrate eating plan. Many of these diets suggest limits on saturated
fat and encourage consumption of fruit and vegetables. “Paleolithic diets” advocate
an eating plan thought to be in line with our hunter-gatherer ancestors, suggest-
ing eating meat, fruits, nuts, and eggs, and avoiding grains, legumes, and dairy.
As with most fad diets, whether or not this new trend has any merit is still up for
debate. Related to the low-carbohydrate diet craze is the trend to reduce or elim-
inate intake of gluten, or proteins found in grains such as wheat, rye, and barley.
Nearly one-third of American adults report that they are cutting down on or com-
pletely avoiding gluten in their diets.120 This shift has again led to an explosion of
gluten-free products available in grocery stores, restaurants, and specialty markets.
From 2001 to 2010, the percentage of new gluten-free products increased from 1%
to 12%.117
Other trends on the forefront are the use of locally sourced, organic, minimally
processed foods. Consumers have grown increasingly interested in foods raised lo-
cally, and the presence of farmers markets over the last two decades reflects this
interest. Data from the US Department of Agriculture (USDA) National Directory
of Farmers Markets indicate that there were 1,755 farmers’ markets nationwide in
1994, compared to 8,144 farmers’ markets in 2013.121 In addition, the variety of
organic foods and ingredients sold in supermarkets has also increased. Although
research suggests no major nutritional benefits to eating organic foods,122 a recent
poll found that 58% of consumers preferred organically grown foods to conven-
tional foods because they wanted to support local farms (36%), avoid toxins (34%),
and promote environmental sustainability (17%).123 With many consumers actively
seeking out organic and natural foods, supermarkets have responded by lining these
products on their shelves. Kroger, Giant Food, and Shaw’s all offer corporate-brand
organic or natural products (Naturally Preferred, Nature’s Promise, and Wild
Harvest). In addition, Publix has introduced its GreenWise supermarkets featur-
ing organic produce, meats with no added hormones, and more healthful prepared
foods, along with conventional grocery items.15
Consumers are also taking the initiative to actively play a role in shaping the
food environment, and this has been partly facilitated by rapid online communi-
cation and social media. For example, Kraft Foods has agreed to remove artificial
dyes from their popular macaroni and cheese products for children due to online
petitions with over 348,000 signatures.124 In addition, specialty stores like Trader
Joe’s and Whole Foods do not sell products with artificial flavors, colors, and pre-
servatives, and clearly display this information on their websites.125,126 The tech-
nological advances in communication that have occurred over the last decade have
democratized food production and made it possible for consumers to take a more
active role in changing the food environment.
CONCLUSION
The food environment has undergone drastic changes over the last 50 years. These
changes have increased the quantity of palatable foods available for consumption
while simultaneously decreasing the nutritional quality of these foods, and our
diets as a whole. The growth of supermarkets, food marketing and promotion, and
increased portion sizes have all contributed to increases in the quantity of palatable
foods available for consumption. While the amount and accessibility of palatable
foods have increased for the modern consumer, reliance on food-processing and
the use of sweeteners have decreased the quality and nutrient-density of the diet.
This widespread availability of large portions of sweet, energy-dense, and highly
marketed foods is in direct conflict with our biology. Humans have innate drives to
consume these foods, but insufficient feedback mechanisms for controlling energy
intake. While the United States has been at the forefront of many of these environ-
mental changes, lower- and middle-income countries have been quick to follow. As
a result, developing countries have experienced a rapid nutrition transition, and the
incidence of diet-related chronic diseases has hit peak levels over the last decade.
In response to the environmental changes, there has been an abundance of new
fad diets and food trends that seem to reflect people’s attempts to adjust to the obe-
sogenic food environment. For example, vegetarian, Paleolithic, and gluten-free diets
have gained popularity. Consumers have contributed to changes in food products,
due in large part to organization facilitated by online communication. The demand
for organic, sustainable, minimally processed foods has also increased. Furthermore,
trends for a reduction in SSB and added sugar intake in the US population suggest
small improvements in the quality of food environments, at least in higher-income
countries. However, the possibility that the beverage industry has made up for declin-
ing SSB sales in the wealthier countries by expanding markets in poorer countries
cannot be ignored. Regardless of whether these latest food trends will have an impact
on health, they offer some hope to consumers who are struggling to control intake in
the face of widespread availability of highly palatable foods and beverages.
ACKNOWLEDGMENTS
Primary author Stein was supported by a training grant from the United
States Department of Agriculture, the USDA National Institute for Food and
Agriculture Grant #2011-67001-30117 Program A2121—Childhood Obesity
Prevention: Transdisciplinary Graduate Education and Training in Nutrition and

Family Sciences.
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C H A P T ER 10
w
Food Addiction
EMILY SULLI VA N, A L A STA IR T ULLOCH,
A SHLEY GE A R H A R DT, A ND NICOLE M. AV ENA
T here is a point at which, in some cases, a pleasurable behavior can turn into an
addiction. Drugs of abuse are a classic example of this phenomenon. One nor-
mally initiates drug use (e.g., alcohol, nicotine, or heroin) because of the pleasure
that is derived from it. Underlying factors that belie pleasure-seeking drug use may
include self-medicating or alleviating some other source of angst in a person’s life.
The beginning stages of the drug use are, hence, associated with procuring pleasure.
However, as an addiction to the drug develops, one’s initial pleasure-seeking mo-
tive is thought to transition to an urge to alleviate feelings of withdrawal or dys-
phoria that are caused by the repeated use of the drug.1
A discussion of the hedonic aspects of food leads one to wonder whether, in
extreme cases, the same may happen when a person is overeating food. From an
evolutionary standpoint, food is necessary for survival, and there are innate bio-
chemical processes that reinforce feeding behavior when one is hungry. Similarly,
other “natural” behaviors, such as sexual behavior, are necessary for the survival
of our species, and are thus powerful reinforcers. Some of our ancestors survived
to procreate by spending their time hunting for food and then engaging in oppor-
tunistic bingeing due to lack of refrigeration and the scarcity of their next meal.
However, food is plentiful in the modern-day environment of industrialized coun-
tries, and the “natural” reinforcers have changed in modern society: there are now
highly processed foods with artificially high levels of sugar and fat, and pornog-
raphy is easily available on the Internet. The more potent forms of these natural
reinforcers may begin to have an addictive potential, and the skills that were pre-
viously needed for survival may now lead to detrimental behavior, affecting both
the brain and subsequent feeding behaviors. Thus, there may be an innate drive
to overeat when food is available, and in our present environment, that may mean
that people indulge on a regular basis.2
( 185 )
This drive to consume food is motivated by the release of neurochemicals that

are associated with a feeling of euphoria and pleasure. As described in the next
section, palatable foods (those that are high in sugar, salt and fat) are especially
strong reinforcers, sending these systems intended to motivate food consumption
for survival into overdrive.
Animal studies have shown that the over-consumption of palatable food
induces certain behavioral and reinforcing neurological effects that are similar
to those of addictive drugs, suggesting that they are regulated, at least in part, by
a common biological mechanism. 3 Much like the development of drug addiction,
food addiction may become most apparent in a subset of genetically susceptible
individuals. This may set the biological basis for the development of addictive
overeating. This chapter discusses the current scientific literature, which exam-
ines behavioral and neurochemical commonalities between the over-consumption
of palatable foods and drug addiction, as well as their treatment and implications
for further research.
DEFINITIONS
Palatable Food
If eating were solely controlled by homeostatic mechanisms, everyone would be at
their ideal weights, and eating would be considered a dull but necessary part of
existence, like breathing. However, eating is often a source of pleasure, and both
humans and other animals are prone to eating beyond homeostatic needs if pre-
sented with highly palatable food. Palatable food is defined as food that is calorically
dense, pleasurable, easily converted to fat, and the type of food that people tend to
most frequently over-consume.4 Palatable food is high in sugar (including refined
carbohydrates like white flour), fat, salt, or a combination of these nutrients. Food
palatability is the reason why certain foods elicit additional feelings of reward be-
yond their metabolic content.
Why is palatable food so rewarding? Genetic studies suggest that the neu-
rocircuitry underlying the acquisition and bodily storage of food evolved in
congruence with food scarcity, which promoted survival in times of famine. 5
In this evolutionary milieu, palatable foods, while calorically dense, have typ-
ically been scarce and, through time, became more neurologically rewarding.
Modern developments in the technology and production of food have enabled
the modification and even creation of foods that artificially enhance palata-
bility beyond what is considered natural due to greater sugar, fat, and caloric
value.6 Such highly palatable, calorie-rich foods are easily accessible in the
typical Western diet. This combination of factors may lead to the activation
of reward-mediated neurocircuits, which evolved to reinforce feeding behavior
and which would have been advantageous in times of famine; now, in the con-
text of abundance, this activation presents as a maladaptive desire to engage in
perpetual over-consumption.7
F ood A ddiction ( 18 7 )
Substance Dependence
Substance dependence is characterized as three or more of the following symptoms’

being present within a twelve-month period:
(1) tolerance (increased amount with a corresponding decrease in effect);

(2) withdrawal (negative physical or psychological symptoms arising after depriva-
tion of a particular substance);
(3) loss of control (instances of a greater amount taken over time and for a longer
period than intended);
(4) persistent desire or repeated unsuccessful attempts to quit;
(5) excessive time spent to obtain, use, or recover from its effects;
(6) reduced social, occupational, or recreational activities because of substance use; and
(7) use continues despite knowledge of its adverse consequences.8
While the neurochemical mechanisms of substance dependence are appreciably

studied, research on hedonic overeating and its neurological correlates is still devel-
oping. Animal studies have demonstrated that binge-eating palatable food produces
behavioral and neuronal changes that are distinct from any effects of consuming
palatable food in a non-bingelike manner.9 Such neurological changes are thought to
be similar to those of drug addiction; in fact, the term “food addiction” is used collo-
quially (though its scientific definition is just now emerging) by those who feel they
are addicted to particular (palatable) foods and find it difficult to stop overeating.
Food Addiction
Within the field of medicine, the term addiction is conventionally applied to drugs
of abuse, and though the concept of food addiction has received media attention
in recent years, a scientific diagnosis has not yet been developed. Several clinical
accounts have attempted to determine the “addictive” properties of foods, such as
how this addiction manifests as excessive overeating, feelings of distress when pal-
atable food is not available, and craving for certain foods.10 It is quite clear from
these studies that sugar, fat, and salt have been heavily implicated.9 The manner
in which the palatable foods are consumed also contributes to their addictive
strength, as does the foods’ propensity to induce an addictive-like state following a
restriction/binge pattern of consumption.4 Food addiction is similar to other sub-
stance addictions in that exposure to certain foods produces behaviors and changes
in the brain that resemble an addiction-like state:
(1) a loss of control (i.e., more frequent and/or larger meals during the binge);
(2) withdrawal (i.e., nutritional deprivation that causes neurochemical changes and
depressive effects);
(3) craving (i.e., seeking the reward without necessarily enjoying the food); and
(4) sensitization (greater quantity of palatable food consumed in subsequent binge

episodes).4,11,12
These symptoms of hedonic overeating parallel those described in the Diagnostic

and Statistical Manual of Mental Disorders, 4th Ed. (DSM-IV) for substance abuse and
dependence and demonstrate that food meets the diagnostic criteria for an addic-
tive substance.13
Considering specific molecules that contribute to food addiction, the macro-
nutrient sugar has been implicated as potentially addictive, as it produces similar
behavioral and neurochemical signs of addiction in rats, including, for example,
dopamine and opioid release during withdrawal.3 Along the same lines, fat also
produces results representative of addictive behaviors in laboratory animals and
also induces changes in the brain similar to those of sugar.11,14,15 There is also a
“salted-food addiction” hypothesis, which proposes that salted food acts in the
brain like an opiate agonist, producing a hedonic reward perceived as “flavorful”
or “delicious.” This hypothesis also suggests that opiate-receptor withdrawal is
delineated as “urges,” “craving,” or “hunger” for salted food. Another study found
neuropsychiatric evidence that salted food acts as a mild opiate agonist, driving
overeating and weight gain.16
BEHAVIOR AL EVIDENCE OF ADDICTION

Sugar Addiction Model
Binge-eating is a multifaceted behavior, with emotional and cultural components
that are difficult to model in laboratory animals. Nonetheless, animal models of
binge-eating are integral to understanding the physiological and neurochemical
basis of this behavior. Multiple models of binge-eating are available and of great
interest, as each has its own particular relationship to human behavior, such as
stress-induced eating and fat bingeing.17–19 While chronic binge behavior is not
solely dependent upon the type of food consumed—the mental state of the indi-
vidual (e.g., tired, anxious, depressed, irritable) and the extent of caloric restriction
also contribute to how the individual will interact with palatable food18 —we will
focus on sugar bingeing because, under normal conditions, rats and people have a
pleasurable reaction to the taste of a sugar solution, sugar is ubiquitous in our soci-
ety, and it is associated with the rapid rise in the incidence of obesity.20
Certain pathological patterns of food consumption—consistent overeating,
binge-eating, stress-induced eating, emotional eating—reinforce overeating and
induce patterns of behavior in striking resemblance to those seen in substance-use
disorders. Consequently, there are three indicators of addiction that are demon-
strated using animal models: loss of control (often indicated by bingeing), with-
drawal, and craving.21 In addition, it is thought that behavioral sensitization
underlies some aspects of food addiction.21,22
In the following sections, we will describe the empirical data that suggests
addictive-like brain and behavioral changes using animal models of binge-eating.
The data described below have been summarized in previous reports.3,11
Bingeing
Bingeing, which is defined as an escalation of sugar intake (in this context) during
a narrow time frame, is usually preceded by a period of forced or voluntary restric-
tion.3 The particular sugar-binge model in rodents outlined in the Avena et al. paper3
helps elucidate the behavioral characteristics of binge behavior. In this model, rats
are maintained on a daily 12-hour food-deprivation paradigm, followed by 12-hour
access to a 25% glucose or 10% sucrose solution (similar to the sugar concentration
of a soft-drink) and rodent chow.3 After several days on this schedule, rats begin
to increase their daily intake and binge on sugar during the first hour of access.23
Additionally, the daily feeding patterns change, and the rats eat larger sugar meals
throughout the access period compared with control animals that have unrestricted
access to the sugar solution and chow. These control animals consume an amount
similar to that consumed by the bingeing animals, but their consumption is spread
over 24 hours, and these rats do not engage in bingeing episodes.
In addition to the Avena et al. study, other experiments show that sugar is a more
influential reinforcer of binge behavior than fat or salt, and its intake increases
over time during repeated bouts of exposure.24 Together, these studies demonstrate
that sugar plays a key role in binge behavior.
Withdrawal
Withdrawal becomes apparent in animals when the substance is removed or is chem-

ically blocked. In opiate-dependent animals, withdrawal has clear and well-defined
behavioral signs, such as anxiety (using an open-arm maze), decrease in body tem-
perature, aggression, dysphoria, and behavioral depression (using the forced-swim
test, which measures swimming escape efforts vs. passive floating).25,26
Behavioral characteristics of withdrawal from food have largely been studied
in rats with a history of sugar bingeing. In one study, rats were administered the
opioid-receptor antagonist naloxone, and experienced somatic signs of withdrawal,
such as headshakes, teeth chattering, and forepaw tremors.27 Food deprivation can
also precipitate opiate-like withdrawal signs, as observed in rats when food was
removed for 24 hours.3,27 Therefore, these data strongly suggest that bingeing on a
sugar solution releases opioids in the brain, with resultant neural adaptations that
manifest as a dependency. Other researchers have obtained supportive findings using
similar models of sugar bingeing. For example, signs of anxiety have been reported in
rats with limited access to a high-sucrose diet.28 The mere removal of sugar has been
reported to decrease body temperature.29 Also, signs of aggressive behavior have been
observed during withdrawal of a diet that includes intermittent sugar access.30
Craving
Craving occurs when motivation is enhanced, typically after a period of absti-

nence, to procure an abused substance.1 Following a period of use and subsequent
forced abstinence, animals will take more of a self-administered drug of abuse that
becomes available again, than prior to abstinence.31 Animals will also often persist
in unrewarded operant responding (known as “resistance to response extinction”),
and over time increase their responding for cues previously associated with the
drug.32–34 This increase in motivation to obtain a substance of abuse mimics behav-
iors observed with humans and may contribute to the likelihood of relapse.
When applying the behavioral signs of craving in laboratory animals to food,
sugar-bingeing rats show signs of increased motivation to obtain sucrose: in a
test following two weeks of abstinence from sugar, rats lever-pressed for 23%
more sugar than their initial quantity of sugar before abstinence. 21 However, a
control group with prior half-hour daily access to sugar followed by two weeks of
abstinence did not show this effect. This implies that sugar has a strong motiva-
tional impact that persists through prolonged periods of abstinence, but only in
the context of prior intermittent access to sugar (i.e., 12-hour access, described
above).9
Additionally, as with drugs of abuse, the motivation to obtain sugar appears to
grow with the duration of abstinence. Sucrose-seeking increases during abstinence
in rats with a history of intermittent sugar access for 10 days, which is even greater
after 30 days of sugar abstinence than after one week or one day. This suggests a
gradual emergence of long-term changes in the neural circuitry underlying motiva-
tion as a result of sugar self-administration and abstinence. 35
Sensitization and Cross-Sensitization to

Psychostimulant Drugs and Alcohol
Sensitization is defined as an increase in responsiveness to a repeatedly presented

stimulus. It is the opposite of tolerance, which is a gradual decrease in responsive-
ness, such that more of the substance is needed to produce the same effect. Both
are exacerbated by, and contribute to, binge behavior. 3 Different processes within
the brain systems can simultaneously manifest both sensitization (increase in
dopamine release) and tolerance (decrease in dopamine receptors) (see “Mesolimbic
Dopamine System” section in this chapter). However, tolerance mechanisms are
resolved within days after cessation of drug use, but neural sensitization can last
for years. This theory helps explain why a recovered addict may relapse back into
addiction, even after years of sobriety, particularly with the expectation that no
pleasure will be gained from a momentary relapse.36 Similarly, cross-sensitization,
whereby sensitization to one drug makes an animal susceptible to the effects of
another drug, has been demonstrated. 37,38 This “gateway effect” leads to a subse-
quent increase of another drug or substance.39–44
Intriguingly, sugar-bingeing rats become sensitized to amphetamine. Such ani-
mals are hyperactive in response to a low challenge-dose of amphetamine that has
little or no effect on naïve animals.45 This was observed after eight days of absti-
nence from sugar. The amphetamine had little effect on rats maintained on the sugar
feeding schedule or on any control groups (non-bingeing sugar groups, chow, etc.).
F ood A ddiction ( 191 )
Conversely, rats sensitized to amphetamine show locomotor cross-sensitization

to a small meal of sugar.45 Other laboratories have reported that intermittent su-
crose access cross-sensitizes with cocaine46 and facilitates sensitization to the do-
pamine agonist, quinpirole.47 Collectively, these results support the theory that the
dopaminergic system is sensitized by intermittent sugar access, as evidenced by
cross-sensitization. This is important since enhanced mesolimbic dopaminergic
neurotransmission plays a role in the behavioral effects of sensitization as well as
cross-sensitization.48
When rats binge on sugar and are then forced to abstain, they subsequently
show enhanced intake of 9% alcohol.49 This suggests that intermittent access to
sugar can be a gateway to alcohol use. Others show animals that prefer the sweet
taste of saccharin will learn to self-administer cocaine more readily than usual. 50
The behavioral parallels between drug use and hedonic overeating of palatable
food spurs the question whether palatable food causes molecular adaptations that
further promote consumption. The studies discussed in this chapter suggest that
this is indeed the case. Highly palatable diets frequently cause adaptations in an
individual’s neurobiology, permuting the drive to overeat palatable food away from
voluntary control and into compulsivity.
NEUROCHEMICAL COMMONALITIES BETWEEN DRUG

SELF-ADMINISTR ATION AND HEDONIC EATING
The evidence described above suggests that sugar bingeing can produce behaviors
similar to those observed in drug-dependent rats. Similarly, laboratory animal
studies have been instrumental in advancing our knowledge of the neurochemical
effects of palatable food and how these effects parallel those of drugs of abuse.
Evidence supports the hypothesis that neural systems evolved to motivate and
reinforce foraging and food intake and also to regulate drug-seeking and abuse;
therefore, the neurocircuitry underlying hedonic eating and drug addiction has
many similarities. 3 This section discusses several neurotransmitter systems that
may result in, or perpetuate, hedonic compulsive eating and are also similarly af-
fected by drug abuse: the mesolimbic dopamine system, opioid receptors, orexin,
acetylcholine, and serotonin.
Drugs of abuse typically increase dopamine signaling from nerve terminals orig-
inating in the ventral tegmental area (VTA) onto neurons in the nucleus accumbens
(NAc). The increase in dopamine is thought to occur either by direct action on do-
paminergic neurons (e.g., stimulants and nicotine), or indirectly through inhibition
of gamma-aminobutyric acid (GABA)-ergic interneurons in the VTA (e.g., alcohol
and opiates). A third mediator for drug-induced activation of the VTA dopamine
neurons is the neurotransmitter orexin, which is released by lateral hypothalamic
neurons that broadly innervate much of the brain including the VTA.12 These limbic
regions experience similar neuroadaptations following exposure to both food and
drugs. Such adaptations alter the motivation to obtain these substances, as will be
discussed in detail in the following sections.
Mesolimbic Dopamine System
Dopamine, a neurotransmitter involved in reward and motivation, is released from

neurons in the VTA and the NAc when pleasurable external stimuli are encountered.
The mesolimbic dopamine system reinforces natural behaviors such as eating,
sexual behavior, and socializing, but it is also stimulated by recreationally abused
drugs.51 The activation of this system by both food and drug intake suggests that a
common neural mechanism may underlie the reinforcing value of both substances.
Drugs of abuse can alter dopamine receptors (primarily D1, D2, and D3 receptors)
and dopamine release in the mesolimbic regions of the brain. Drugs like cocaine upreg-
ulate D1 receptors52 and increase D1 receptor binding,53,54 as well as increase D3 recep-
tor messenger RNA (mRNA),55 but also lower the D2 receptor density56 and decrease
D2 receptor mRNA in the NAc of laboratory animals.57–59 Clinical studies also reveal
that D2 receptors are downregulated in cocaine addicts.60–62 Similarly, sugar-bingeing
laboratory animals exhibit increased D1 receptor binding in the NAc,23 decreased D2
receptor binding in the striatum and NAc,23,63 decreased D2 receptor mRNA in the
NAc,64 and increased D3 receptor mRNA in the NAc and caudate-putamen.64
With regard to extracellular dopamine levels, the repeated increase in extracel-
lular dopamine upon recurring exposures is a hallmark of drugs that are abused.65
Palatable food consumed in a bingelike manner continuously releases dopamine in
the NAc, resembling a pattern comparable to that seen in drugs of abuse, which do
not show a blunted release in the NAc upon repeated exposure.9,24,66 In contrast, the
dopamine response to bland or “normal” food fades out after repeated exposure.67
“Priming,” in this context, occurs when a stimulus/stressor reduces extracellular
dopamine levels in the NAc, subsequently exacerbating the potency of a substance
(e.g., drugs or food). This phenomenon is well documented in drugs of abuse, in
which abstinent drug users are primed to desire or relapse with small quantities of
a respective drug.68 With palatable food intake, energy deprivation primes rats to
binge-eat because the accompanying dopamine surge within the NAc when food is
reintroduced is sustained, reinforcing the reward of the palatable foods.24,69 Stress
is another primer for binge-eating and can trigger binge-eating palatable and un-
palatable foods, though less potently than a history of dieting.9
Moreover, in the limited access model, in which laboratory animals have con-
tinuous access to chow and water at all times but are given sporadic, time-limited
access to palatable food to simulate binge conditions, rats consume significantly
more palatable food than the control group. This behavior stems from the repeated
release of dopamine, which exacerbates the dopaminergic mechanisms involved in
sustaining bingeing behaviors.70 Together, these studies suggest that binge episodes
disrupt dopamine signaling, promoting the bingeing and addictive behaviors.
Endogenous Opioids and Receptors
The opioid system works in concert with the dopaminergic system in both feeding
and reward, and as such, is affected by hedonic overeating in a manner similar to
the effects of drugs of abuse. In response to chronic access to cocaine and morphine,
laboratory animal studies reveal, mu-opioid-receptor binding is upregulated in the
NAc, caudate-putamen, and cingulate cortex. 54,71,72 Moreover, repeated injections
of morphine decrease enkephalin (an endogenous opioid) mRNA in the striatum
and NAc.57,59,73 Using brain-imaging in cocaine-dependent humans, researchers
have observed similar changes.74
Ingestion of palatable foods increases endogenous opioid-receptor binding in
the NAc,75 and significantly decreases enkephalin mRNA in the NAc in labora-
tory animals.64,76 Additionally, a history of binge-eating of palatable food (espe-
cially repeated bouts of excessive sugar intake) may result in opioid-receptor
super-sensitivity in the NAc shell, cingulate, hippocampus, and locus coeruleus.23
Palatable food stimulates opioid release in the hypothalamus, and that may explain
why, in food-deprived, stressed rats, a minimal morsel of palatable food unleashes
binge-eating of bland chow, an effect that does not occur without the palatable food
trigger.18 These studies suggest that “hedonic” binge-eating may be mediated by
opioid-receptor super-sensitivity, which is perhaps the result of repeated endog-
enous opioid release following palatable food intake, and is analogous to opiate
addiction.
Orexin
The lateral hypothalamus (LH) is a fundamental area that bridges homeostatic and
hedonic eating. Orexins, synthesized exclusively in the hypothalamus, are associ-
ated with feeding behavior—specifically, stimulating food consumption (in fact,
“orexin” means “appetite”).77 Recent studies have investigated a role for orexin in
reward-seeking for food and drugs of abuse. Orexin has been implicated in drug
abuse due to the overlapping neural circuitry involved in food and drug reward,78
although the specific mechanisms for behavior remain unclear (though action sites
include such reward-associated areas as the VTA and NAc).79
Activation of LH orexin neurons is strongly linked with strength of preference
for cues associated with drug and food reward. For example, in one study, research-
ers ascertained rats’ preference for morphine, cocaine, food, or no reward, and
then gave rats the option to seek their corresponding preferred reward in a reward
chamber, or to enter an empty chamber. Only conditioned rats that had exhibited
a preference for the food or drug reward–paired chamber showed increased Fos
activation (a marker of neuronal stimulation) in LH orexin cells; rats conditioned
to prefer a “novel object” reward displayed preference behavior, but exhibited no
enhanced orexins.80
Interesting findings have been made with orexin and drug cessation. Following
protracted abstinence from morphine, rats showed decreased preference for food
reward and increased preference for drug reward, which was mirrored by altera-
tions in Fos activation within LH orexin neurons.81 A recently discovered role
for LH orexin neurons within the context of food and drug reward–seeking con-
cerns reinstatement. Chemical activation of LH orexin reinstates an extinguished
drug-seeking behavior that was previously blocked by prior administration of an

orexin-A antagonist. Additionally, administration of the orexin-A peptide directly
into the VTA also reinstated drug-seeking.80
In addition to orexin’s involvement in drug abuse, a neural connection between
NAc and hypothalamic orexin neurons may mediate the rewarding aspects of
palatable food intake.82 Cason et al. found that orexin signaling in the VTA stim-
ulates intake of a rewarding high-fat diet even in sated rats, suggesting that a neu-
ral pathway linking the NAc and LH induces reward-based eating in sated rats.79
Additionally, mice that lack sweet receptors are still able to develop a strong prefer-
ence for sucrose solutions, probably because the orexin neurons that are activated
upon feeding directly stimulate VTA dopamine neurons.12 Indeed, it is hypothe-
sized that dysfunction of the orexin system may be a contributing factor in the
hedonic overeating that leads to obesity.79
Acetylcholine and the Dopamine–Acetylcholine Balance
Acetylcholine (ACh) in the NAc normally increases during a meal and peaks when
feeding stops, which is associated with satiety. Interestingly, the elevated ACh
levels are blunted in underweight rats, inciting slower satiation.83 In the sugar ad-
diction model, rats bingeing on sugar develop a delay in the rise of ACh, which prob-
ably plays a role in the increase in food intake.9,66 The irregularities in other eating
behaviors and drug abuse are quite intriguing. The behavioral signs associated with
drug withdrawal are usually accompanied by alterations in dopamine–ACh balance
in the NAc, in which dopamine decreases while ACh increases. This imbalance has
been shown during chemically induced withdrawal from several drugs of abuse,
including morphine, nicotine, and alcohol.84–86 This neurochemical imbalance in
dopamine–ACh during withdrawal also occurs in sugar-bingeing rats, when they are
given naloxone to precipitate opiate-like withdrawal27 and after 36 hours of food
deprivation.87 Together, sugar binges blunt the release of ACh, which is thought to
reduce the feelings of satiety, but withdrawal increases ACh which, coupled with
reduced dopamine levels, is postulated to create not satiety, but an aversive state
such as that seen during behavioral depression, drug withdrawal, and conditioned
taste aversion.3
Serotonin
Serotonin (5-hydroxytryptamine; 5-HT) is associated with reducing food intake. In

the context of drug and sugar abuse, reduced 5-HT levels are associated with both
depression and compulsive behavior, two disorders that play a role in addictive be-
havior.81 Similarly, laboratory animals with a history of caloric restriction coupled
with intermittent access to palatable food exhibit a 71% reduction of 5-HT in the
rats’ medial prefrontal cortex.88 Succinctly, binge-eating may precipitate 5-HT dys-
regulation, thereby strengthening the addictive urge to overeat.
Neuroanatomy
Neuroanatomy is another point of comparison between the effects of food and

drugs on the brain. In a study using functional magnetic resonance imaging (fMRI)
to determine areas of the brain affected by food craving, activation was found
in the caudate nucleus, hippocampus, and insula, three areas also reported to be
involved in drug craving.89 More recently, tools designed to assess food addiction in
humans, and studies incorporating such tools, provide additional evidence of this
construct.90 For example, using fMRI scanning, individuals with greater food addic-
tion scores have also been shown to have greater activation of motivation-related
brain regions when anticipating highly palatable food, and reduced activation of
inhibitory regions in response to food intake: both characteristics similar to those
of drug-addicted individuals who view and subsequently use a drug.91
CLINICAL STUDIES SUGGESTIVE OF FOOD ADDICTION
In addition to the complementary research from laboratory animal models, there

is strong clinical support for the theory of sugar addiction. Obesity and eating dis-
orders, such as bulimia and anorexia nervosa, recurrently exhibit properties of an
“addiction” in some individuals.92–96 For example, binge-eating and self-starvation,
in certain cases, stimulate endogenous opioid activity.97 This may be an underlying
cause that induces bulimic patients to excessively binge on non-caloric sweeten-
ers,98 which also suggests that these patients derive benefits from sweet orosensory
stimulation. This orosensory trigger of binge-eating is also observed in labora-
tory animal studies that associate the taste of sugar with dopamine release and
an inhibited release of the satiety-associated ACh in the accumbens.99 Finally, the
cross-sensitization between sugar, amphetamines, and cocaine discussed previ-
ously in this chapter provides an explanation for the documented comorbidity
between bulimia and substance abuse.100 This is particularly apparent in drug
addicts who binge-eat during the early recovery period and substitute food for drug
use, effectively satisfying their drug cravings.101
The characterization of food addiction in humans has recently emerged, utiliz-
ing diagnostic criteria for substance dependence (see Table 10.1). The Yale Food
Addiction Scale (YFAS), one of the first psychometrically validated scales used to
target food addiction, identifies feeding behaviors associated with addiction. This
tool brings food addiction into the clinical realm, as it provides a means to identify
those who exhibit addictive-like eating behaviors.102 Higher scores on the YFAS have
been associated with higher body mass index (BMI), more frequent binge-eating,
increased dieting, elevated weight-cycling, greater impulsivity, increased emotion
dysregulation, and greater attentional biases for food.103 In addition to behavioral
studies, human brain-imaging studies support the idea that aberrant eating behav-
iors, including those observed in obesity, may have similarities to drug depen-
dence. Similar to alterations in drug-craving fMRI signals, craving-related changes
in response to palatable foods have been observed.104 Food addiction based on the
Table 10.1 A PPLIC AT ION OF T HE DSM-V SUBSTA NCE-USE DISOR DER S CR I T ER I A
TO FOOD A DDIC T ION
DSM-V Criteria for Substance-Use Relation to Food Addiction

Disorders*
Criterion A: Impaired Control over Substance Use
The individual may take the substance in Unintended hyperphagia; eating despite lack of
larger amounts or over a longer period than hunger; eating until feeling physically ill
was originally intended
The individual may express a persistent desire Dietary restraint; repeated failed attempts to
to cut down or regulate substance use and limit the consumption of particular foods
may report multiple unsuccessful efforts to
decrease or discontinue use
The individual may spend a great deal of time Going out of one’s way to obtain certain foods;
obtaining the substance, using the eating throughout the day; sluggish after
substance, or recovering from its effects overeating
Craving is manifested by an intense desire or Overwhelming urge to consume certain foods;
urge for the drug preoccupied by thoughts of food and eating
Criterion B: Social Impairment
Recurrent substance use may result in Overeating that results in obesity can limit
a failure to fulfill major role obligations at recreational activities and the ability to perform
work, school, or home some aspects of one’s job or household chores
The individual may continue substance use Individuals often get in arguments with loved
despite having persistent or recurrent ones about the amount or way they are eating,
social or interpersonal problems caused or akin to fighting about smoking
exacerbated by the effects of the substance
Important social, occupational, or Professional or social situations may be avoided
recreational activities may be given up or based on food availability (e.g., certain food
reduced because of substance use is absent or fear of overeating foods present).
Also, overeating that leads to obesity can limit
participation in activities
Criterion C: Risky Use of the Substance
Recurrent substance use in situations in Bingeing on sugar despite having diabetes or

which it is physically hazardous another comorbidity that poses an immediate
hazard to one’s health
The individual may continue substance use Food habits are continued despite physical
despite knowledge of having a persistent or health concerns (i.e., diabetes, hypertension,
recurrent physical or psychological problem excessive weight gain, cardiovascular disease) or
that is likely to have been psychological health concerns (i.e., depression,
caused or exacerbated by the substance low self-esteem, eating disorders characterized
by binge-eating)
Table 10.1 (CON T INUED)
DSM-V Criteria for Substance-Use Relation to Food Addiction

Disorders*
Criterion D: Pharmacological Criteria
Tolerance is signaled by requiring a markedly Laboratory animals show escalation of palatable

increased dose of the substance to food intake over time in binge paradigms.
achieve the desired effect or a markedly Humans also report needing greater amounts
reduced effect when the usual dose is of food over time to achieve the same effect,
consumed including reducing negative emotions like
sadness or increasing pleasure
Withdrawal is a syndrome that occurs when Opiate-like withdrawal has been observed in
blood or tissue concentrations of a laboratory animal models. Humans may
substance decline in an individual who had feel irritable, nervous or sad; food is used
maintained prolonged heavy use of the to alleviate negative physical symptoms or
substance emotional problems, and when certain foods
are cut down, physical symptoms occur (e.g.,
headaches, fatigue)
* The severity of one’s disorder may range from mild to severe depending on the number of criteria met,
with two to three symptoms indicating mild severity, four to five suggesting moderate severity, and six or
greater indicating a severe Substance-Use Disorder.
YFAS has also been related to differential response to dopamine agonists and ele-
vated scores on a composite genetic index of higher dopamine signaling.105,106 Thus,
addictive-like eating and drug addiction are both associated with similar dysfunc-
tion in the reward system.
DISCUSSION AND CLINICAL TREATMENT
Hedonic overeating in a disordered manner, such as that manifested in binge-eating

disorder, bulimia nervosa, and some cases of obesity, presents a number of compli-
cations for the medical community because its etiology is not well characterized.
Some experts propose that, given the increasing evidence of neurochemical and
behavioral commonalities between over-consumption of palatable foods and drug
addiction, as well as the urgent need to develop effective treatments to combat obe-
sity and overeating, it is important to consider the effect of chronic exposure to
highly palatable foods on the reward system as a contributing factor to these issues,
as well as a target for treatment.90
Interventions for this effect include the use of pharmacological treatments that
reduce palatability in association with behavioral therapies, which may prove benefi-
cial in diminishing the perceived palatability of foods, thereby reducing food intake.107
Specifically, a neurobehavioral model of treatment suggests that reward-sensitivity
to palatable food drives hedonic overeating only when accompanied by insufficient
inhibitory control. Strengthening inhibitory control, through pharmacological or

other clinical means, could lessen the effect of palatable food on food addicts.108
A number of new treatments for obesity targeting neural areas associated with
food addiction are currently in phase II and phase III clinical trials.109 The majority
of these potential treatment options target the neural pathways and neurotrans-
mitters discussed in this chapter. Specifically: raclopride, buproprion, and anti-
psychotics target the dopaminergic system; naltrexone, naloxone, and nalmefene
target the opioid system; baclofen and topiramate target the GABA-ergic system;
and rimonabant (SR141716) and AM-251 target cannabinoid receptors.110 These
medications are not without risk, and many of these drugs carry significant side
effects, including increased risk for obsessive-compulsive disorder, anxiety, depres-
sion, seizures, suicide, confusion, or memory deficits.109 Details of some of the
aforementioned drugs and their neurochemical effects are outlined below.
Dopamine
Dopamine D2 receptors are consistently associated with food reward and consump-
tion. Differential effects of D2 receptor blockade on palatable food consumption
have been reported. For example, Corwin et al.111 found that the D2 receptor an-
tagonist raclopride selectively attenuated binge-consumption of vegetable fat pre-
cipitated by limited access, while it had no effect on ad libitum intake of the same
food. In rats fed an ad libitum high-fat diet, raclopride reduced consumption of the
high-fat diet at high doses, but increased consumption at lower doses.112 In addition,
the schedule of access to fat varies the effects of D2 receptor blockade: raclopride
was less effective at reducing fat intake in non-deprived rats with intermittent ac-
cess to fat as compared with daily, one-hour access.111,113 By contrast, raclopride has
been shown to attenuate sucrose intake regardless of the access schedule.114
Opioids
Naltrexone, an opiate-receptor antagonist, is used for the treatment of alcohol de-

pendence and is approved by the Food and Drug Administration (FDA); however, its
efficacy is debated.115 Notwithstanding, several animal studies support the efficacy
of opioid antagonists in reducing bingelike food consumption, though under variable
circumstances. Opiate-receptor blockade may be more effective at reducing hedonic
overeating of fat and sugar bingeing,18 which is especially evident with the use of the
opiate-receptor antagonist naltrexone, which exerts its influence on reward-related
areas of the brain (e.g., amygdala) rather than homeostatic-related areas (e.g., hypo-
thalamic paraventricular nucleus).116 Another study suggests that, because opioids
play a role in reward as well as in pleasure, naltrexone reduces short-term palatable
food intake and reduces pleasantness ratings for foods without affecting hunger.89
Finally, fluoxetine (alone and as an adjuvant to naltrexone) effectively reduces the
frequency of binge-eating in case studies and open-label trials.81
Serotonin
Serotonin (5-HT) is involved with hedonic eating by inhibiting food intake.

Individuals with a history of binge-eating behavior have reduced 5-HT transporter
binding; however, after treatment with a selective serotonin reuptake-inhibitor
(SSRI), fluoxetine, 5-HT binding increased significantly.117 SSRIs—such as fluox-
etine and citalopram—which are typically used to treat depression, have demon-
strated efficacy at reducing the frequency of binge behavior, but do not significantly
result in weight loss. However, the serotonin and norepinephrine reuptake-inhibitor
sibutramine is efficacious at reducing both short-term binge frequency and weight.118
In animal studies, fluoxetine attenuates binge-eating of palatable food in rats
with a history of food restriction and sporadic extended access to palatable food.88
Interestingly, fluoxetine also reduces intravenous cocaine self-administration in
rats.119 Serotonin transporter binding is an adaptive mechanism that can be affected
by treatment, and has been shown to reduce binge-eating in short-term studies.
Orexin
Orexin systems are implicated with inciting palatable food- and drug-seeking
behavior when cue-stimulated (even in the absence of reward). Researchers have
observed overlap in the treatment of hedonic overeating and substance abuse with
orexin antagonists (similar treatment for obesity as for alcohol-seeking) in rats.120,121
Specifically, blocking orexin receptor-1 (OxR1) signaling attenuates cue-induced
reinstatement of sucrose-seeking, primarily in food-restricted rats.79 Results from
preliminary studies have implications for humans as well: interference with the
orexin system using an orexin-1 receptor antagonist affects long-term energy bal-
ance via both food intake and weight reduction.121 Orexin systems are valid targets
for the pharmacotherapy of binge-eating.
Ineffective Pharmacological Treatment
The effectiveness of pharmacological interventions may be contingent, to some ex-

tent, upon the macronutrient composition of a binge. For example, an interven-
tion targeting the dopamine system was more effective during a high-fat, low-sugar
meal, and less effective with higher sugar content, especially when the sugar was
consumed within a short amount of time.114 To further illustrate, drugs such as
the GABA receptor agonist baclofen, the D2 receptor antagonist raclopride, and the
opioid-receptor antagonist naltrexone, though effective in reducing intake of mix-
tures with low levels of sucrose but high levels of fat, are ineffective at preventing
bingeing in rats when exposed to both high-fat and high-sugar mixtures.114 This
highlights the importance of a multidimensional treatment approach that limits
both fat and sucrose concentrations in binge foods (or limits access to highly palat-
able foods) in addition to pharmacological treatment.
To date, current treatment options for binge-eating are still poorly estab-
lished, mainly due to the lack of controlled studies in large samples of patients.
Notwithstanding, the data on serotonin and norepinephrine reuptake inhibi-
tors and on anticonvulsants are promising in terms of both efficacy and tolera-
bility. There also exist promising preliminary data that suggest the possibility of
regulating appetite through an interference with the ghrelin system.122 However,
emerging evidence aside, our current understanding in light of binge-eating treat-
ment studies is wanting; no clear treatment protocol has yet been determined for
binge-eating.
NON-PHARMACOLOGICAL TREATMENT
Some individuals hedonically overeat as a form of self-medication to soothe neg-

ative emotional states such as loneliness, boredom, anxiety, depression, anger,
and conflict. Therefore, behavior modification is often a necessary and effec-
tive addition to pharmacological interventions in the treatment of food addic-
tions.6 Indeed, certain behavioral interventions have been useful for both food
and drug abuse; namely, incentive motivation, cognitive behavioral therapy,
and 12-Step programs. 5 Another treatment method with a cognitive orienta-
tion, Rational Recovery (which teaches the addict to dis-identify with the urge
to use or binge), also successfully aids recovery in both substance abusers and
binge eaters.123,124 Notwithstanding the optimal support of any of these treat-
ment methods, treatment of disordered eating may still be a laborious process for
the addict, punctuated by alternating periods of relapse and recovery.90 Clinical
treatment combined with pharmacological treatment may proffer more signifi-
cant, long-lasting changes.
COMBINED PHARMACOLOGICAL AND

NON-PHARMACOLOGICAL TREATMENT
Upon short-term analysis of pharmacological treatments—antidepressant selec-

tive serotonin reuptake inhibitor (SSRI) (fluoxetine) medication, anti-epileptic
medication, and obesity medication—in conjunction with non-pharmacological
treatments—behavioral weight loss and cognitive behavioral therapy—in
attenuating binge-eating and promoting weight loss, findings indicate that
combined treatment is as effective as pharmacotherapy alone at affecting the
likelihood of remission from binge-eating. SSRIs, anti-epilepsy drugs, and obe-
sity drugs were similarly effective at reducing binge behavior.125 Studies also
suggest that while certain pharmacotherapies may reduce the binge behaviors
in the short term, their longer-term effects are unknown. Additionally, while
weight loss may occur with the above-mentioned medication, it is likely to be
insubstantial.125
CONCLUSION
Chronic hedonic overeating of highly palatable foods can alter brain function in
ways similar to drugs of abuse. Long-standing neurobiological research (i.e., posi-
tron emission tomography scans and fMRI imaging) has provided insight into how
drug and alcohol addiction affects brain systems. Building on these studies, which
provided addiction neuroscience models, further research with laboratory animals
has rendered considerable evidence to support the theory that both drugs of abuse
and the consumption of highly palatable foods utilize a shared pathway within the
limbic system to mediate motivated behaviors. Neurologically speaking, palat-
able foods can act like a traditional drug of abuse, altering brain function in ways
similar to drugs, particularly within the mesolimbic dopamine-reward pathway.
Similarly, pharmacological interventions that extinguish drug addiction and crav-
ings can also be effective at reducing binge behavior and palatable food cravings,
though more research is warranted. Notwithstanding great advancements in un-
derstanding the short-term effects of hedonic eating, there is a paucity of long-term
research on food addiction, binge-eating, and its neurobiological effects and treat-
ment. Determining the long-term consequences of diets high in sugar, salt, and fat
on the limbic system and on human behavior will provide insights into the under-
lying causes and treatments of compulsive eating.
ACKNOWLEDGMENTS
The preparation of this chapter was supported by the National Institute on Drug
Abuse grant DA-031230.
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N A ME I N DE X
Atkins, R., 175 Hoefling, A., 155

Avena, N. M., 1–7, 155, 185–208 Horstmann, A., 39–55
Horstmann, M., 51
Berkman, E. T., 73
Berridge, K. C., 58, 89, 125–145 Juarascio, A., 72–73
Blechert, J., 154
Boggiano, M. M., 155 Kantak, P. A., 107–123
Burger, K. S., 64, 107–123 Keller, K. L., 163–183, 168
Kessler, R. M., 136
Campbell, B. C., 135 Kleiman, S., 174
Cason, A. M., 194 Kristeller, J., 157
Coelho, J. S., 154 Kube, J., 51
Cohn, M. A., 74
Coleman, J., 154 Larsen, J. K., 153
Conason, A., 147–161 Leitch, M., 85–105
Corwin, R. L., 155, 198 Lowe, M. R., 152, 153
Cummins, S., 166–167
Mack, D., 151
Davis, C. A., 135 Mahler, S. V., 129
Deo, R., 151 Mason, A., 57–83
Dietrich, A., 51 McCrory, M. A., 166
Dressler, H., 72 Miller, P. E., 173
Drewnowski, A., 166 Montagnon, C., 74
Monteiro, C. A., 172
Eisenberg, D., 135 Myers, K., 9–37
Epel, E., 57–83
Neumark-Sztainer, D., 149
Field, A. E., 149 Nisbett, R. E., 86–87
Norgren, R., 127
Gearhardt, A., 185–208
Geliebter, A., 85–105 Pankevich, D. E., 155
Goldfield, G. S., 92 Peciña, S., 125–145
Grill, H., 127 Pelchat, M. L., 71
Petrovich, G. D., 88
Herman, P. C., 151, 152, 154 Pietilainen, H. K., 150
Hill, A. J., 154 Polivy, J., 151, 152, 154
Ho, C.-Y., 133 Popkin, B. M., 174
Hoebel, B. G., 92, 93 Potenza, M. N., vii–ix
( 209 )
( 210 ) Name Index
Robinson, T. E., 89 Strack, F., 155

Robinson, T. N., 168 Sullivan, E., 185–208
Rolls, B. J., 166 Swanson, L. W. S., 129, 130
Rothemund, Y., 88
Rozin, P., 3, 10 Thompson, R. H. T., 129, 130
Tulloch, A., 185–208
Sanders, A. J., 107–123
Sclafani, A., 21 Van Strien, T., 149
Sikorski, C., 51
Smith, C., 72 Weingarten, H. P., 88
Stein, W. M., 163–183
Steiner, J., 127 Zahm, D. S., 129
Stice, E., 64
SU B J EC T I N DE X
abnormal environments, and anorexigenic signals, and dopaminergic

hyper-responsiveness in, 135 system, 133
acetylcholine, and the dopamine-ACh anti-epilepsy drugs, and treatment of
balance, 194 food addiction, 200
addiction anti-psychotic drugs, and treatment for
behavioral evidence of, 188–191 food addiction, 198
and binge eating, 95 anxiety
clinical treatment of, 197–200 and binge eating disorder, 92
and dopamine reward pathways, 91 as medication side effect, 198
DSM-V criteria for substance use using food to self-medicate, 2–3
disorders, 196, 197 appetite
effects of sugar, 91, 92, 93 appetitive brain network,
and food consumption patterns, 42–43, 43, 49
25, viii and habitual use of artificial
reinforcement sensitivity model, 63–64 sweeteners, 27, 112
and reward sensitivity and impulsivity, short-term vs. long-term control of, 87
108–109 stress-enhanced appetite, 69–70, 117
sensitization and cross-sensitization, artificial sweeteners
190–191 habitual use of, 26–27
see also food addiction and neural response pattern, 112
see also food addiction, treatment of associative conditioning
adiposity and flavor-flavor learning, 18–19
effects of excess adiposity, 107 and flavor-nutrient learning, 19–24
familial transmission of weight and the modern obesogenic
status, 13 environment, 24–28, 29
and food cravings, 59–60
see also obesity baclofen, 91, 198
adolescents bariatric surgery, and food cravings, 60
consumption of soft drinks, 173 Behavioral Activation and Inhibition
FinnTwin16 study, 150 Systems, 64
liking for sweets, 13 behavioral therapies
advertising of food, 167–168 and food addiction, 197–198, 200
African-Americans, hedonic response to and neuroadaptation to weight loss
sweets, 13 efforts, 117
agriculture, modernization of, 1–2 binge eating
alcohol, and sensitization to sugar, 191 antecedents to, 93
alliesthesia, and food “liking,” 133 binge eating disorder, 92–94
anandamide, and activation of hedonic and dopamine signaling, 192
“hotspots,” 129 and food addiction, 187, 189
( 211 )
( 212 ) Subject Index
binge eating (cont.) caloric deprivation, 148, 149

and frequency of dieting, 149, 158 carbohydrates
hypothalamic pituitary adrenal (HPA) low-carbohydrate diets, 175
axis, 92 restriction of, 154
and mindful eating, 157, 158 cardiovascular disease, and ancestral vs.
and opioids, 91–92 modern dietary patterns, 163
sugar addiction model, 188 children
bitter taste, hedonic consumption of soft drinks, 173
nature of, 4, 4, 126 flavor-nutrient conditioning, 22, 23–24
blood-oxygen-level, and food and food advertisements, 167–168
consumption, 112 food evaluation, 17–18
body mass index (BMI) hedonic reactions to food, 15, 127, 127
brain activity and, 111 liking for sweetness, 13
dietary restraint and, 149, 150 Children’s Food and Beverage Advertising
mindful eating and, 158 Initiative, 168
brain chocolate
appetitive brain network, 42–43, cravings for, 68
43, 50–51 and dieting, 154, 155
brain-based consequences of weight citalopram, 199
gain, 115–116, 116 cognitive control of dieting, 150–151
brain-based prediction of weight gain, cognitive side effects of medication, 198
110–111 compulsive eating and food cravings, 61
and changes in body mass index conditioned overeating, 87–88
(BMI), 111 conditioning, associative
correlates of eating behavior, 111–112 and flavor-flavor learning, 18–19
and food-related stimuli, 88 and flavor-nutrient learning, 19–24
hedonic “hotspots,” 126–128 and the modern obesogenic
hypothalamus, dopamine, and hedonic environment, 24–28, 29
eating, 90 conditioning, evaluative, 18–19
hypothalamus and body weight Continuing Survey of Food Intake by
regulation, 86–87 Individuals, 171
and motivational value of food, Contrave, 91
47, 48–49 corticotropin-releasing factor (CRF), 137
neural responses in obesity, 113–115 cortisol, and stress-enhanced appetite,
obesity and changes in inhibitory 70, 117, 157
control, 94 cross-cultural patterns
reward circuitry and hedonic eating, and food cravings, 59
107–108 in taste-liking, 13
reward circuitry and obesity, 5, 86 cue-reward learning propensity, 109,
sensory processing of food, 40–41 110, 110
and stress-induced eating, 47–48, 117
“wanting” and “liking” food, 89, DAMGO
131–132 effect on food “liking” and
see also dopaminergic system of “wanting,” 132
the brain microinjections and hedonic
see also nucleus accumbens (NAc) shell “hotspots,” 128, 131
branding of food products, 168 delta opioids, and activation of hedonic
breastfeeding, and food preferences in “hotspots,” 129, 131
later childhood, 17 depression
bupropion, 91, 198 and binge eating disorder, 92
Subject Index ( 213 )
as medication side effect, 198 and mesolimbic pathways, 192

and mindful eating, 158 and neural response in obesity,
and restricted eating, 155 114–115
using food to self-medicate, 2–3 and reward-predictive cues, 109
deprivation and “wanting” foods, 131–132
hedonic, perceived, and caloric, 148, dopaminergic system of the brain,
149, 158 43–46, 50–51
perceived, 152 and diet-induced obesity, 45–46
sleep deprivation, 67 dopamine receptors, 45
diabetes dopaminergic pathways, 44–45
and ancestral vs. modern dietary and food cravings, 60, 65
patterns, 163 and hedonically driven food
and mindful eating, 157 intake, 108
dietary patterns interaction with ghrelin, 134
of ancestral vs. modern diets, 1–2, 2, orexigenic and anorexigenic
23–24, 28–29, 163–164, 185–186 signals, 133
decreased quality of food, 171–174 repeated stimulation and overeating,
sweetening of the diet, 173–174 89–91, 90, 95
dieting Dr. Atkins’ New Diet Revolution
animal models of, 155–156 (Atkins), 175
and binge eating episodes, 93 drug use, and hedonic overeating
defined, 148 acetylcholine, and the dopamine-ACh
fad diets, 174–176 balance, 194
and food cravings, 153–155 endogenous opioids and receptors,
longitudinal studies of, 149–150 192–193
neuroadaptations to, 117 mesolimbic dopamine system, 192
personal characteristics of dieters, 148 neuroanatomy, 195
related societal pressures, 147 orexin, 193–194
restraint theory, 150–152 parallels between drug use and
Three-Factor Model, 152–153 overeating, 190–191
vs. mindful eating, 156–158 serotonin, 194
and weight loss, 153 DSM-V criteria for substance use
diet interventions, 60, 62–63, 65–66 disorders, 196, 197
disease, chronic, 163, 164, 176 durian, Southeast Asian fruit, 9
disinhibited overeating, 151–152 Dutch Eating Behavior Questionnaire,
disinhibition and low satiety 61, 149
phenotypes, 94 dynamic vulnerability model of neural
disordered eating reward, 64
and pattern of dieting, 149
vs. dieting, 148 eating behavior
dopamine in ancestral vs. modern times, 23–24,
and acute eating behavior, 111, 112 28–29, 163–164
and binge eating disorder, 92 brain-based correlates of, 111–112
and compulsive behavior, 93 determinants of, 107
downregulation vs. hyper-reactivity eating motivation, early theories
of, 136 of, 86–87
and drugs of abuse, 191 environmental cues, 86
and hedonically driven food intake, homeostatic vs. hedonic
107–108 eating, 85
and inhibition, 93–94 mindful-eating skills, 156–158
eating disorders post-ingestive rewards, 21

binge eating disorder, 92–94, 157, 158 processed foods, decreased quality of,
disordered eating vs. dieting, 148 171–173
and food cravings, 61, 71, 73–74 sensory processing of, 40–41
and substance abuse, 195, 201 traditional vs. non-traditional food
endocannabinoid neurotransmitters retailers, 165
activation of hedonic “hotspots,” 129 use as reward in childhood, 18
“hyperliking” and “hyperwanting” of food, “liking” vs. “wanting”
food, 135 in homeostatic state, 49
environmental cues how foods become liked, 126–131
and conditioned overeating, 87–88 how foods become wanted, 131–132
and food cravings, 66 “hyperliking” and “hyperwanting,”
evaluative conditioning, 18–19 135–136
experience-dependent plasticity, 9–10 neural basis of, 89, 125–126, 137
vs. food cravings, 58
facial expressions, and hedonic impact of food addiction
taste, 127, 127–128 and ancestral vs. modern dietary
farmers’ markets, prevalence of, 175 patterns, 185–186
fast-food restaurants, and increased food behavioral evidence of, 188–191
availability, 24 characteristics of substance
fasting dependence, 187
and cue-triggered “wanting” of clinical studies of, 195–197
food, 133 commonalities with drug use, 191–195
and frequency of dieting, 148 DSM-V criteria for substance use
and motivational value of food, 49 disorders, 196, 197
and reduced food cravings, 154 and hedonic overeating, 187–188
fat content and palatable foods, 186
addictive qualities of foods high in patterns of, 25
fat, 188 food addiction, treatment of, 197–201
and palatability of food, 13–14 anti-epilepsy drugs, 200
fatigue, and binge eating disorder, 92 combined treatments, 200–201
FinnTwin16 study, 150 dopamine, 198
flavor fluoxetine, 200
and palatability of food, 14–16 ineffective pharmacological treatment,
and sensory processing of food, 40 199–200
flavor-flavor learning non-pharmacological treatment, 200
associative conditioning and, 18–19 opioids, 198
in modern food environment, orexin, 199
25–27, 28 serotonin, 199
flavor-nutrient learning food consumption
associative conditioning and, 19–24 and blood-oxygen-level, 112
in modern food environment, changes in patterns of, 1, vii
25–27, 28 familiarity and neural response, 113
fluoxetine, 198, 199, 200 increased portion size, 169,
food 169–171, 170
decreased quality of, 171–174 increased product variety, 166
incentive value of, 65 inhibitory control, 94
increased availability of, 164–165, 176 lack of sensory cues, 26
marketing and advertising of, 167–168 modern supermarkets, 167
motivational value of, 46–49 and palatability, xi
product branding, 168 gastrointestinal tract

sensory variety, 11 gut microbiome and food cravings, 69
social influences on, 4–5 and sensory processing of food, 41
Food Craving Acceptance and Awareness genetic variation
Questionnaire, 72–73 and addiction, 91
Food Craving Inventory, 72 body weight set-point, 86–87
Food Craving Questionnaires, 72 dieting and weight gain, 150
food cravings disinhibition and low satiety
assessing, 71–73 phenotypes, 94
definition of, 58 dopaminergic system of the brain, 45
and dieting, 153–155 food evaluation, 15
and eating disorders, 61 “hyperliking” and “hyperwanting” of
ecological momentary assessments food, 135
(EMA), 73 reward value of food, 47
and food addiction, 187, 188, 189–190 stress-enhanced appetite, 70, 74
and mindful eating, 157 weight gain, 110
during nasogastric feeding, 11 ghrelin
neural experience of reward, 63–64 hormonal modulation of eating
prevalence of, 57, 58–59 behavior, 50
progression of, 58 long-term hunger signals, 87
and restrained eating, 61–63 neural response in obesity, 115
sex and age differences, 59 obesity and fasting ghrelin, 94
“trait” vs. “state” food cravings, salience of food cues during
71–72, 73 hunger, 134
triggers of, 64–71 globalization, and shifts in dietary
vs. hunger, 59 patterns, 163–164, 176
and weight status, 59–60 glucagon-like peptide (GLP)- 1, 50
“food deserts,” in urban areas, 166–167 glutamate receptors, and binge
food environment eating, 91, 92
ancestral vs. modern dietary patterns, gluten-free diet, 175
163–164, 176 Growing Up Today Study
flavor and nutrient learning systems, (GUTS), 149
25–27, 28
and food cravings, 66 hedonic deprivation
food trends and diet fads, 174–176 and animal models of dieting,
hyper-responsiveness in, 135 155–156
modern features of, 24–25, 28–29, 86 defined, 148
food evaluation, and genetics, 15 intermittent access to palatable
food preferences food, 155
development in childhood, 17–18 hedonic eating
flavor-flavor conditioning, 18–19 clinical relevance of, vii–ix
flavor-nutrient learning, 19–24 consequences of, 107–108, 117–118
neonatal experience, 17 described, 3–5
prenatal experience, 16–17 determinants of preference, 16–24
food production, democratization of, identifying hedonic causation,
175–176 126–128
food restriction, and binge eating, 93, 189 neural basis of, 88–91
food trends and fad diets, 174–176 neural responses, 113–114
formula feeding, and food and obesity, 5
neophobia, 17 orofacial expressions, 127, 127–128
hedonic eating (cont.) hunger

and post-ingestive rewards of appetitive brain network, 49
food, 21–22 effect on food “liking” and “wanting,”
and reward circuitry of the brain, 86 132–134
social influences on, 4–5 effect on hedonic eating, 4
vs. homeostatic eating, 85 and high incentive salience, 42
vs. mindful eating, 156–158 and palatability of food, 117
hedonic overeating and salience of food cues, 133–134
and animal models of dieting, 155–156 in United States in 1960s, 164
brain-based correlates of, 111–112 vs. food cravings, 59
brain-based drivers of, 107–108, Hunger in America (documentary), 164
117–118 hyper-palatability
disinhibited overeating, 151–152 and binge eating, 93
excessive hedonic motivation, 93 and excess food intake, xi
and food addiction, 187–188 hyper-responsiveness
incentive-sensitization theory of, 109 in abnormal environments, 135
intermittent access to palatable food, hyper-responsive model of neural
155, 156 reward, 63–64
neuroadaptations, 115–116 hypothalamic pituitary adrenal
parallels with drug use, 190–191 (HPA) axis
predisposing risk factors for, 108–109 and binge eating, 92
hedonic overeating, and substance abuse and stress-enhanced
acetylcholine, and the dopamine-ACh eating, 117
balance, 194
endogenous opioids and receptors, impulsivity, and hedonic overeating,
192–193 108–109
mesolimbic dopamine system, 192 incentive-sensitization theory of
neuroanatomy, 195 overeating, 109, 110
orexins and feeding behavior, infants
193–194 neonatal flavor-learning, 17
parallels between, 190–191, 201 olfactory and taste perception
serotonin, 194 among, 15
hedonics prenatal flavor-learning, 16–17
definition of, 3 inhibitory control
importance in twenty-first century and chronic overeating, 85, 95
eating, 11–12 disinhibition and low satiety
stimulus attributes in food, 12–16 phenotypes, 94
homeostatic eating in obese vs. lean subjects, 94
determinants of, 107 insulin, and long-term hunger
homeostatic brain systems, 126 signals, 87
homeostatic state, 41–42, 46, 48–49 Israel, sugar consumption per
and mindful eating, 156–158 capita, 13
vs. hedonic eating, 85
hormones kappa opioids, and activation of hedonic
and dopamine reward pathways, 90 “hotspots,” 129, 131
and food cravings, 67–68
and modulation of eating behavior, leptin
49–50, 67, 87 and hormonal modulation of eating
and neural response in behavior, 49–50
obesity, 115 and long-term hunger signals, 87
and neural response in obesity, nucleus accumbens (NAc) shell

114–115 anatomical characteristics of the NAc
and restricted eating, 155 hotspot, 129–130
and endogenous opioids and receptors,
low-fat diets, 174–175 193, 194
as hedonic “hotspot,” 127, 130,
malnutrition, reduced rates of, 164 130, 131
marketing of food, 167–168 and “hyperliking” and “hyperwanting”
melanocortin system, and stress-induced of food, 135, 136
eating, 47–48 and “liking” foods, 128–130
menstruation, and food cravings, 67–68 and mesolimbic dopamine system, 192
mesolimbic and mesocortical pathways and “wanting” of food, 137
circuits for “liking” and “wanting,” nutrient deficiencies, and food
130, 130 cravings, 68–69
hedonically driven food intake, nutritional value, and appeal of food,
107–108, 131 4–5, 48–49
hedonic overeating and substance
abuse, 192, 201 obesity
mindful eating and aberrant neural responses,
as alternative to dieting, 148, 158 113–115
vs. dieting, 156–158 and ancestral vs. modern dietary
Mindfulness-Based Eating Awareness patterns, 24, 28–29, 163–164
Training (MBEAT), 157 and appetitive brain network, 42–43
mood disorders, and food cravings, 71 and binge eating, 93
motivational states, and food cravings, 58 body weight set-point and, 87
motivational value of food, 46–49, 50 brain-based prediction of, 110–111
mu opioids, and activation of hedonic and changes in inhibitory control, 94
“hotspots,” 129, 131 conflicting theories regarding, 108
dopamine downregulation in, 136
nalmefene, 198 and dopaminergic system of the
naloxone, 91, 93, 198 brain, 45–46
naltrexone, 198 food addiction and consumption, viii
nasogastric feeding, and food cravings, 11 and food advertising, 167–168
National Health and Nutrition and food cravings, 59–60, 73–74
Examination Survey (NHANES), 147, and food “wanting” and “liking”
172, 173 systems, 134–137
National School Lunch Program, 164 health risks of, 107
neonatal experiences, and food and hormonal modulation of eating
preferences, 17 behavior, 50, 51
neostriatum (CPU), and “hyperliking” and “hyperliking” and “hyperwanting” of
“hyperwanting” of food, 136 food, 135–136
neural reward models, 63–64, 108 and increased portion sizes, 171
neuroadaptation and neural experience of
to behavioral weight loss efforts, 117 reward, 63–64
to hedonic overeating, 115–116 neuroendocrine consequences of,
neuroanatomy, and food addiction, 195 114–115
neuroendocrine consequences of obesity, and obesogenic food environment, 66
114–115 and pleasure in eating, 12
Nixon, Richard M., “War on Hunger,” 164 and positive prediction errors, 44
nociceptin/orphanin, 92 and sensory-nutrient inconsistency, 27
obesity (cont.) parallels with drug use, 190–191

and societal pressure to lose weight, predisposing risk factors for, 108–109
147–148 see also hedonic overeating
and substance abuse, 195 see also hedonic overeating, and
and types of food retailers, 165, substance abuse
166–167
and “ultra-processed” foods, 172 palatability
obsessive-compulsive disorder, as and ancestral vs. modern dietary
medication side effect, 198 patterns, 186–187
odors, and palatability of food, 14–15 and dieting efforts, 117, 155
opioids ethnic and cultural examples of, 9–10
activation of hedonic “hotspots,” 128, and excess food intake, xi
128–129, 131 and flavor of food, 14–16
and binge eating disorder, 92 and hedonic overeating, 109, 110
and chronic overeating, 91–92 and increased availability of food,
endogenous opioids and receptors, 164–165
192–193 initial triggers of sight, smell, and
and “hyperliking” and “hyperwanting” taste, 10–11
of food, 135 and overstimulation of reward
and treatment of food addiction, 198 circuitries, 116
and “wanting” foods, 132 of processed foods, 172
orexigenic signals responses in obesity, 113–115
and caloric restriction, 156 vs. nutritional value, 164
and dopaminergic system of the Paleolithic diet, 175
brain, 133 parabrachial nucleus, as hedonic
orexin “hotspot,” 127
and food addiction, 193–194, 199 Pavlovian conditioning, and food
microinjections in ventral cravings, 65
pallidum, 133 Pavlovian-Instrumental Transfer test
and salience of food cues during (PIT), 131–132
hunger, 134 Pennsylvania, Scrapple breakfast food
organic foods and ingredients, in, 9–10
prevalence of, 175 perceived deprivation
orofacial expressions, and hedonic defined, 148
impact of taste, 127–128 and food cravings, 154–155
orosensory experience and hedonic overeating, 152
and food addiction, 195 pharmacological treatments, and food
and food cravings, 68–69 addiction, 197–198, 199, 200
overeating, chronic phentermine, 91
conditioned overeating, 87–88 Physical Anhedonia Scale, 64
disinhibited overeating, 151–152 Pima Indians, hedonic response to
and dopaminergic system of the brain, sweets, 135
89–91, 90 plasticity, experience-dependent, 9–10
and food “wanting” and “liking” pleasure, relationship to food
systems, 134–137 intake, 3–5
hypothalamic pituitary adrenal (HPA) portion size of foods, increase in, 169,
axis, 92 169–171, 170
incentive-sensitization theory of, 109 positive psychology, relationship to
and lack of inhibitory control, 85 hedonics, 3
and opioids, 91–92 post-ingestive rewards of food, 21
poverty, and urban “food deserts,” hedonically driven food intake,

166–167 107–108
Power of Food scale, 66 homeostatic brain systems, 126
preference, determinants of, 16–24 hyper-responsiveness, 135
premenstrual dysphoric disorder (PMDD), “liking” vs. “wanting” food, 125–126
and food cravings, 67, 68 mesocorticolimbic circuits for “liking”
prenatal experience, and food and “wanting,” 130, 130
preferences, 16–17 and obesity, 5
processed foods overstimulation by palatable food, 116
decreased quality of, 171–173 reward-deficiency hypothesis, 136
and increased food availability, 24 reward sensitivity, 46
and modern eating habits, 1–2 reward sensitivity and impulsivity,
produce 108–109
access to healthful variety of, treatment of food addiction, 198
166–167 reward-related responses to food
locally grown, 175 acute eating behavior, 111, 112
Project Eat II, 149 cue-reward learning propensity, 109,
protein, restriction of, 154 110, 110
psychology, positive, 3 familiarity of food, 113
rimonabant, 198
Qsymia, 91
Quebec Family Study, 150 salience
definition of, 41
raclopride, 198 incentive salience, 41–42, 50, 64,
restaurants 69, 126
and increased food availability, 24 salience of food cues during hunger,
portion sizes in, 169, 169–170, 170 133–134
restrained eating salt taste
and attitudes toward forbidden addictive qualities of salty foods, 188
foods, 155 hedonic nature of, 4, 4, 126
and flavor-flavor conditioning, 19 satiation
and flavor-nutrient disinhibition and low satiety
conditioning, 22–23 phenotypes, 94
and food cravings, 61–63, 154–155 effect on food “liking” and “wanting,”
intentions vs. behaviors, 152 132–134
rigid vs. flexible, 62–63 and food palatability, 10–11
vs. dieting, 65 satiety cascade, cephalic phase of,
Restraint Scale, 149, 152 86, 88–89
restraint theory satiety cascade and appetite
critique of, 152–153 control, 87
and patterns of dieting, 150–152 Scrapple, breakfast food, 9–10
Revised Restraint Scale, 61 Seattle Obesity Study, 166
Reward-based Eating Drive (RED) seizures, as medication side effect, 198
scale, 60–61 self-medication, and increased food
reward circuitry of the brain palatability, 2–3
binge eating and drug use, 191 sensation-seeking, and pleasurable
chronic overeating, 86 eating, 12
and dopamine, 44, 45, 90 Sensitivity to Punishment and Sensitivity
eating and chronic stress, 117 to Reward Questionnaire, 64
food cravings, 60, 61, 63–64 sensory processing of food, 40
serotonin effects of, 91, 92

and binge eating disorder, 92 as gateway to alcohol use, 191
and food addiction, 194, 199 in modern diets, 173–174
sibutramine, 199 opiates and effects of, 91
side effects of medications to treat food suicide, as medication side effect, 198
addiction, 198 supermarkets
sight, and sensory processing of food, 40 in developing countries, 164
sleep deprivation, and food cravings, 67 and increased food availability, 24,
smell, sense of 165–167
importance for taste, 14–15 organic foods and ingredients in, 175
and sensory processing of food, 40 portion sizes in, 170
social media, and food environment, “supersizing” of foods, 171
175–176 Supplemental Food Program for Women,
social modeling, of novel foods, 18 Infants, and Children (WIC), 164
societal pressure, for weight reduction Surströmming, Swedish sour herring, 9
and maintenance, 147–148 sweetness
soft drinks, availability and consumption artificial sweeteners, 26–27, 112
of, 173–174 and flavor-flavor learning, 19
sour taste, hedonic nature of, 4, 4 hedonic nature of, 4, 4, 11, 126
Southeast Asia, durian fruit in, 9 palatability of sweetness and fat, 12–14
South Korea, sugar consumption per sweetening of the typical diet, 173–174
capita, 13
stress taste, sense of
binge eating and, 93, 156 and balance of sweet, sour, salt, and
dieting and, 117 bitter, 4, 4
food behavior and, 47–48 importance of smell in, 14–15
food cravings and, 69–71 neurochemical enhancement of,
and food “liking” and “wanting,” 128–129
136–137 orofacial expressions and, 127, 127–128
levels of fasting ghrelin, 94 and sensory processing of food, 40–41
and mindful eating, 158 television advertising, effects on
and restricted eating, 155–156 children, 167–168
stress-enhanced eating, 92, 117 Three-Factor Eating Questionnaire, 61,
substance abuse 72, 94, 150
and binge eating disorder, 92, 93, Three-Factor Model of Dieting, 152–153
95, 201 topiramate, 91, 198
characteristics of dependence, 187
clinical treatment of, 197–200 value-added marketing, 171
DSM-V criteria for substance use ventral pallidum (VP)
disorders, 196, 197 as hedonic “hotspot,” 127, 130, 130
and food addiction, 187–188, 195, 197 and “hyperliking” and “hyperwanting”
and overstimulation of reward of food, 135
circuitries, 116 mechanisms of food “liking,” 130–131
and reward sensitivity and impulsivity, vitamins, and fortification of processed
108–109 foods, 172
sugar
addictive qualities of sugar-sweetened weight gain
foods, 188 and aberrant neural responses,
binge eating and withdrawal, 189–190 113–115
consumption per capita worldwide, 13 benefits of dieting, 153
brain-based consequences of, weight-loss programs and food

115–116, 116 cravings, 73–74
brain-based prediction of, 110–111 weight suppression, 153
and cue-reward learning, 109 weight status, and food cravings, 59–60
weight loss wholesale clubs, and food availability, 165
and mindfulness interventions, 156–158 withdrawal, and food addiction, 189
neuroadaptation to behavioral
efforts, 117 Yale Food Addiction Scale, 195, 197

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Hedonic Eating

Edited by Nicole M. Avena, PhD

Oxford New York

Oxford is a registered trademark of Oxford University Press

Published in the United States of America by

© Oxford University Press 2015

All rights reserved. No part of this publication may be reproduced, stored in

You must not circulate this work in any other form

Library of Congress Cataloging-in-Publication Data

9. The Modern Food Environment: Changes in Food Quantity and

Name Index 209

Nicole M. Avena Pranish A. Kantak, B.S.

Table 1.1 NU T R I T IONA L COMPA R ISONS

Total energy intake More Less

Abbreviation: NEAP, net endogenous acid production

Hedonics: The Psychology of Pleasure

Hedonic psychology, or the study of the psyche of happiness, pleasure, and

What Is Hedonic Eating?

culinary traditions, eating in the presence of others, and the establishment of

Obesity and Hedonic Eating

OVERVIEW OF THE REST OF THE BOOK

opposed to energy needs will be discussed and contrasted, especially regarding

utilitarian approach to nutrition. In years, I do not recall ever watching an adult

THE IMPORTANCE OF HEDONICS IN THE PSYCHOLOGY

Understanding hedonic processes is necessary for insights into why individuals

STIMULUS ATTRIBUTES IN FOOD HEDONICS

and is mostly shaped by experience. So what sorts of experience in particular are

Immediately after birth, the mother continues to provide experiences preparing

Repeated exposure to flavors prenatally and postnatally serves as a bridge to inde-

Associative Conditioning: Flavor-Flavor Learning

Flavor-flavor conditioning (hereafter, “F-F conditioning”) can occur when a flavor

Associative Conditioning: Flavor-Nutrient Learning

post-ingestive effects, associations between specific flavors and nutrients sensed

a distinctive flavor in sorbet after previously experiencing that flavor in a drink

adulthood. Ultimately, these proposals attempt to address why F-N conditioning

LOOKING FORWARD: APPLICATIONS TO THE MODERN

The ways that food preferences—of cultural groups, of families, of individuals—are

Features of the Modern Food Environment

Interactions with the Modern Food Environment

Supporting the Preference Learning Systems

promote intake of calorically dense options, but also, importantly, to anticipate

Obscuring the Preference Learning Systems

A different view of food–environment interactions is that certain aspects of the

calories or other physiological effects of sugar. Presumably, considerable effort by

successfully learning about flavor–nutrient relationships (which would have been

At the core of appetite, beneath layers of cognitive, emotional, and sociocultural

elicits stored memories of prior experiences, and this information is integrated

1. Rozin P. Food choice: An introduction. In Frewer L, Van Trijp H, eds., Understanding

8. Louis-Sylvestre J, Le Magnen J. Palatability and preabsorptive insulin release.

52. Manabe Y, Matsumura S, Fushiki T. Preference for high-fat food in animals. In

116. De Houwer J, Thomas S, Baeyens F. Association learning of likes and dislikes: A

THE LOVE OF FOOD

“There is no sincerer love than the love of food.”

THE CENTR AL PROCESSING OF FOOD: VISUAL

Remote Sensory Information: Sight and Smell of Food

Information from the Oral Cavity and the Gastrointestinal Tract

Animals, including humans, are equipped with limited central-processing re-

THE APPETITIVE BR AIN NETWORK

THE BR AIN’S DOPAMINERGIC SYSTEM

The dopaminergic system comprises three main pathways in the brain.

Diet-Induced Obesity and Its Effects on Central

A long-standing question about the significance of obesity-associated alterations in

striatum becomes specific to high-fat food. Electric stimulation or stimulation with

Name Index 209