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The Addiction Potential of Hyperpalatable Foods


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Scientific interest in "food addiction" continues to grow due both to neurobiological and behavioral similarities between substance dependence and excessive food consumption. An important next step is to examine the addictive potential of highly processed foods. In this paper, we explore addiction-related changes in the modern food environment (e.g., increased potency, elevated speed of absorption), examine the historical and modern understanding of addictive substances as applied to hyperpalatable foods, and outline shared factors that increase the public health costs of both addictive drugs and certain foods.
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140 Current Drug Abuse Reviews, 2011, 4, 140-145
1874-4737/11 $58.00+.00 © 2011 Bentham Science Publishers
The Addiction Potential of Hyperpalatable Foods
Ashley N. Gearhardt*,1, Caroline Davis2, Rachel Kuschner1 and Kelly D. Brownell1
1Yale University, New Haven, CT, USA
2York University, Toronto, Canada
Abstract: Scientific interest in “food addiction” continues to grow due both to neurobiological and behavioral similarities
between substance dependence and excessive food consumption. An important next step is to examine the addictive
potential of highly processed foods. In this paper, we explore addiction-related changes in the modern food environment
(e.g., increased potency, elevated speed of absorption), examine the historical and modern understanding of addictive
substances as applied to hyperpalatable foods, and outline shared factors th at increase th e public health costs of both
addictive drugs and certain foods.
Keywords: Food addiction, food environment, high fructose corn syrup, obesity, substance dependence, withdrawal.
Although the concept of food and addiction is receiving
widespread attention from the popular media, and is woven
into popular language and culture as seen with terms such as
“chocoholic” and “carbohydrate craving”, it has become
credible in the scientific community only recently [1-4].
Since 2006 there has been an exponential increase in the
number of academic publications relating to this topic (Fig.
1), due in part to a shift in persp ective to the view that
addictions should be reframed as unusually strong and
maladaptive desires to ingest a substance or engage in a
behavior despite negative consequences [5, 6].
Fig. (1). Number of publications containing the words “food
addiction” obtained from the Web of Science database, and plotted
for the years 2000-2010.
The term ‘food addiction’ might be seen as an oxymoron
since eating is quintessentially necessary for our health and
survival. We argue the opposite - that many of the highly-
processed foods in modern diets that damage health are more
similar to drugs of abuse than to the natural energy resources
people consumed historically (Table 1). Humans evolved to
prefer foods high in fat, sugar, and salt, but in the quantities
*Address correspondence to this author at the Yale University Department
of Psychology, 2 Hillhouse Ave., New Haven, Connecticut 06511, USA;
Tel: 415-265-9484; Fax: 203-432-7172; E-mail:
and availability these ingred ients now occur in processed and
refined foods, they appear to have an abuse potential similar
to addictive drugs like cocaine and alcohol [7-9].
A growing body of research has identified many
similarities between conventional addiction disorders and
excessive consumption of calorie-dense foods. Presently
many of the studies on the additive potential of certain foods
are based on examinations of rats exposed to sugar, fat, or
highly processed foods [3, 10]. The eating behavior of rats
may provide an especially useful analogue for human food
consumption, as both rats and humans are omnivores who
have developed the ability to ingest a diverse array of foods
[11]. For both rats and humans the dopamine and opioid
neural circuitry implicated in drug addiction is also
associated with the motivation for food and food-related
reward [12, 13]. It has also been demonstrated that rats given
sugar, fat, or highly processed foods exhibit reward-related
neural changes seen in drug addiction, as well as the
behavioral signs of withdrawal, tolerance, and continued use
despite negative consequences [3, 10]. Scientific evidence of
the parallels between substance use and food consumption in
humans is also building. For example, drug and food
cravings foster similar patterns of neural activation in the
brain’s mesocorticolimbic pathways [14]. Further, genetic
(i.e., DRD2 Taq1A allele) and personality factors (i.e.,
elevated reward responsivity) linked with addiction have
also been implicated in obesity and binge eating disorder
[15]. Moreover, individuals who endorse symptoms of food
addiction as indicated by the Yale Food Addiction Scale are
more likely to exhibit patterns of craving-related neural
activation in response to food cues and disinhibition-related
neural activation during palatable food consumption [16].
Examining how hyperpalatable substances have addictive
properties is an important next step in evaluating the validity
of the food and addiction construct. This may be especially
true for understanding the utilityof an addiction perspective
in preventing and treating diet-related disease and obesity. In
this paper, we will explore addiction-related changes in the
modern food environment, examine the historical and
modern understanding of addictive substances, and outline
shared factors that increase the public health costs of both
addictive drugs and certain foods.
2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010
Yea r
The Addiction Potential of Hyperpalatable Foods Current Drug Abuse Reviews, 2011, Vol. 4, No. 3 141
Table 1. Similarities Between Hyperpalatable Foods and
Addictive Drugs
1. Activate dopamine and opioid neural circuitry
2. Trigger artificially elevated levels of reward
3. Absorbed rapidly into the blood stream
4. Alter neurobiological systems
5. Cause compensatory mechanisms that result in tolerance
6. Combined with additives to enhance rewarding properties
7. Elicit cue-triggered cravings
8. Consumed in spite of negative consequences
9. Consumed in spite of a desire to cut down
10. Impact disadvantaged groups to a disproportionate degree
11. Cause high public health costs
12. Exposure in utero can result in long-term alterations
Prior to examining the addictive potential of food, it is
useful to consider what constitutes a food. A wide-variety of
substances is consumed for sustenance, as well as pleasure,
and definitions of what is considered a food varies based on
cultural definitions. For example, insects are a staple of diets
in some regions (e.g., China) [17], but they are not
commonly eaten in the Western world. Further, the
increasing prevalence of chemicals, flavor enhancers and
lab-developed compounds in the food supply has led to the
question of whether ultraprocessed foods should no longer
be called food and should instead be relabeled as food-like
products [18]. To add another layer of complexity, alcohol
(which is typically considered an addictive substance) is a
natural product of ripe fruits, may be a standard part of a
hunter-gather diet, and provides calories and some nutrients
in a similar manner as substances classified as food [19].
Although no one definition is able to succinctly capture the
complexity of this topic, in the current review we use the
term food to reference caloric items that are consumed as
part of the Western diet (i.e., might be purchased at a grocery
store) with special attention given to macronutrients that are
frequently manipulated during food processing, like fat and
sugar. Although alcohol may fall under this definition, in the
current paper we include ethanol-containing products in the
category of substances traditionally considered addictive.
The food environment has changed drastically, which has
resulted in foods with increasingly addictive-like properties.
In the pre-industrial era humans survived on a diet that was
minimally processed, high in protein, grains, and produce,
and relatively low in salt [20]. Foods that had greater caloric
value through elevated sugar and fat content, such as berries
and animal protein, were relatively scarce. As an adaptation
to motivate consumption of calorically dense foods, we
evolved to find foods high in sugar and fat more hedonically
rewarding than foods low in these substrates [20]. As
industrialization occurred and food-related technology
evolved, the environment changed from one with limited
access to calorie-dense foods to one of abundance with
artificially elevated levels of fat, sugar, salt, caffeine and
flavor enh ancers in the meals we eat [21].
Many highly processed foods have been altered in a
similar manner as addictive drugs. Both the elevated potency
of a substance, and its rapid absorption into the bloodstream,
increase a substance’s addictive potential [22]. Many drugs
of abuse derive from plant materials that are refined into
highly concentrated substances (e.g., grapes into wine; the
coca leaf into cocaine). As a result of processing, these
substances became more potent and the active ingredients is
more quickly absorbed into the bloodstream. For example,
when the coca leaf is chewed or stewed as tea, it produces
only mild stimulation and is thought to have little addictive
potential [23]. Further refinement provides a more potent
drug in the form of cocaine and crack, which is hedonically
very rewarding, quickly absorbed, and highly addictive [24].
Many highly palatable foods follow a similar process that
results in the quicker absorption of sugar and a higher level
of reward. For example, corn is a frequently consumed
starchy vegetable that has been part of the human diet for
centuries. With technological advances, corn was refined
into high fructose corn syrup (HFCS) – a highly
concentrated and very sweet simple carbohydrate, which is
not found in natural foods that comprise most traditional
diets [25].
In the past 40 years or so, HFCS has been added to a
large variety of processed products, such as soft drinks,
baked goods, and cereals. Indeed, our consumption of this
simple sugar has increased exponentially – from about 4 to
12% of our daily caloric intake in a few generations [26]. In
this capacity, the special physiological properties of fructose
render it similar to other drugs of abuse. The most direct
parallels are seen between fructose and alcohol because the
two are biochemically and evolutionarily congruent. Ethanol
is simply the fermented byproduct of fructose [27] and can
have some health benefits when consumed in small doses.
For example, not only is ethanol an energy resource due to
its caloric content, but it may also serve as a stimulant to
further feeding. Given that ethanol is associated with the
valuable nutrients found in ripe fruit, Dudley [19] suggested
that a short-term advantage of ethanol might be to increase
the rate of food intake, which, in turn, would increase blood-
ethanol content and foster further consumption. Similarly,
HFCS provides the body with calories needed to maintain
functioning. Thus, consuming either HFCS or ethanol in
small doses may provide some benefits.
However, as both HFCS and ethanol are legal, relatively
cheap, widely available, and socially sanctioned in most
Western cultures, they are frequently consumed to excess.
When taken in large quantities, HFCS and alcohol may cause
biological changes that encourage further problematic use.
Excessive alcohol consumption causes mesolimbic
dopamine down-regulation, which fosters increased intake,
pronounced cravings, continued use despite negative
consequences and physical withdrawal symptoms during
periods of abstinence [28]. High fructose consumption tends
to promote insulin resistance and chronic hyperinsulinemia,
and this occurs largely through its capacity to induce
increased release of triglycerides in th e liver [29]. We have
142 Current Drug Abuse Reviews, 2011, Vol. 4, No. 3 Gearhardt et al.
also learned that the metabolic impact differs substantially
depending on the type of sugar that is consumed. For
instance, the monosaccharide fructose raises triglyceride
levels and lowers high-density lipoprotein, whereas glucose
does not have these effects [30]. Fructose also blunts leptin
signaling thereby promoting sensations of hunger and
activation of the reward pathways creating a desire for
consumption independent of energy needs [31] – a
phenomenon that is directly comparable to what occurs when
alcohol is used excessively [27]. This seems to occur
because HFCS bypasses the insulin-driven satiety system. In
other words, while glucose stimulates the release of insulin,
decreasing the desire to eat, fructose has this effect to a very
weak degree [31]. Therefore, ingesting elevated amounts of
either ethanol or fructose can result in biological changes
that promote overconsumption.
Another consequence of processing for both food and
drugs of abuse is that the refined substance is combined with
additional products to enhance its rewarding properties. The
tobacco plant, for example, is harvested and processed into a
form that can be either inhaled as smoke, or ingested as a
result of chewing. Although the nicotine in the tobacco plant
is the main active ingredient, the tobacco industry has added
hundreds of additional ingredients to enhance the flavor and
aroma of the product, speed absorption into the lungs, and
increase cigarette shelf life [32]. The resulting tobacco
product is significantly more rewarding and addictive than
unprocessed tobacco.
A similar process occurs with hyperpalatable foods.
HFCS is not consumed on its own, but is combined with
other ingredients, such as sweeteners, fat, salt, flavor
enhancers, and caffeine. For ex ample, a frosted chocolate-
fudge Pop Tart combines HFCS with refined flour, sugar,
oil, salt, cocoa, flavor enhancers, and preservatives. In total,
the resulting product has approximately 37 ingredients.
Thus, similar to cigarettes, the substance that results from
processing is often significantly more rewarding than
minimally processed foods.
In addition to the increased levels of hedonic reward, the
processing of foods may also result in other addiction-related
changes, such as tolerance and cue-reactivity. For example,
individuals have a tendency to consume greater quantities of
foods they find palatable, as evident in the ever increasing
portion sizes of highly processed foods [33]. The
consumption of food, especially in large quantities, increases
the level of glucose into the bloodstream, which disrupts the
homeostasis of the biological system [34]. As a
compensatory mechanism, the pancreas begins to secrete
cephalic insulin in response to food-related cues or at the
beginning of food consumption to allow the body to tolerate
greater levels of food ingestion [34]. Similarly, ingestion of
drugs of abuse also stresses the body and biological
responses occur to compensate for these disruptions, which
increases the body’s tolerance to the addictive substance
[35]. Thus, the body adapts to the ingestion of either food or
drugs of abuse in a manner which results in higher levels of
tolerance. The development of elevated tolerance may then
drive even more problematic levels of consumption.
Addition ally, consump tion of sugar or addictive drugs can
result in elevated dopaminergic activation in response to
related cues, which is associated with an enhanced
motivation to seek out the substance (i.e., wanting) without a
corresponding increase in the hedonic pleasure received
during consumption of the substance (i.e. liking) [36, 37].
The sensitization of dopaminergic activity to cues may result
in cue-triggered cravings playing a large role in both
problematic eating and drug-taking behavior. In summary,
the elevated hedonic nature of highly processed foods may
initially encourage overconsumption, but other factors (e.g.,
increased tolerance, elevated wanting) may also drive
addictive-like eating behavior.
Like the food environment, the conceptualization of an
addictive substance has changed throughout history. In the
19th century, substances that are now classified as addictive
were commonly consumed as a part of daily life. For
example, heroin was an ingredient in over-the-counter tonics
for both children and adults, cocaine was included in Coca-
Cola, and alcohol was consumed as an alternative to
contaminated water [38]. In the late 1800s and early 1900s,
public concern about these substances grew, and some, like
heroin and opium were thought to be a threat to societal and
personal wellbeing [39]. As the impact of these substances
on the body and brain became more evident in the latter part
of the 20th century, the list of problematic drugs increased.
Nevertheless, the classification of what constitutes an
addictive substance has often been controversial. Frequently,
the substance at the center of debate has been associated with
some central features of addiction (e.g., escalating use,
inability to stop despite problems), but lacks other typical
addiction markers. For example, cocaine is associated with
almost no physical withdrawal symptoms, which created
controversy about its addiction potential until the late 1980s
[40]. The addictive nature of tobacco was also the focus of
debate, in part due to its lack of a strong intoxication
syndrome [41].
Hyperpalatable foods are also associated with some of
the factors that once caused cocaine and tobacco’s addictive
nature to be debated. Although there is evidence that sugar
consumption is associated with pronounced physical
withdrawal symptoms in animals [3], evidence of withdrawal
from hyperpalatable foods in humans is largely anecdotal
and based on reports of people experiencing headaches,
elevated cravings, irritability, and temperature dysregulation
while dieting [42]. Like cocaine, the limited exploration of
food-related withdrawal in humans has increased skepticism
about the addictive nature of highly processed foods [43].
Moreover, in a similar manner as tobacco, consumption of
highly processed foods does not result in an obvious
intoxication syndrome. However, the level of intoxication
triggered by an addictive substance does not directly
correlate with the degree of negative consequences. Tobacco
is currently the number one cause of preventable death in the
United States despite the lack of an intoxication syndrome
[44]. The greater public health cost associated with tobacco
is partly because of the ease of accessibility, increased social
acceptability, heavy marketing practices, and low cost [21].
Hyperpalatable foods are also ubiquitous, socially
acceptable, highly marketed, and inexpensive [21] and their
public health consequences are enormous. Furthermore,
despite the lack of an intoxication syndrome, ingredients in
The Addiction Potential of Hyperpalatable Foods Current Drug Abuse Reviews, 2011, Vol. 4, No. 3 143
highly processed foods appear to have reinforcing properties
on par - or possibly exceeding - drugs of abuse. For example,
Lenoir and colleagues [45] found that cocaine-addicted rats
will choose saccharin, a calorie-free sweetener, over cocaine
in a forced choice task, which led to the conclusion that the
rewarding properties of sweetness may surpass that of drug
Although hyperpalatable foods may differ in some ways
from the typical conceptualization of addictive drugs, they
share many features with traditionally addictive substances.
First, highly processed foods and drugs of abuse are both
capable of triggering cravings [14, 46]. Second, consumption
of highly processed foods and drugs of abuse can both be
associated with compulsive overuse in the face of severe
negative consequences [42]. And finally, in some individuals
there is evidence of chronic relapse and an inability to cut
down consumption of both substances [42]. Thus, while
highly processed foods may not be associated with a clear
intoxication syndrome, and evidence of withdrawal is just
now building, there are significant areas of overlap with
conventional addiction disorders.
In addition to nosological debates, the application of an
addictive label has also been mark ed by societal controversies.
For individuals, stigma is often associated with a substance
dependence diagnosis. The stereotype of persons with addiction
as weak-willed and untrustworthy can be a barrier for those
thinking of seeking treatment and may result in occupational
and social discrimination [47]. In contrast, the conceptualization
of addiction as a disease has also led to more widespread
support for those seeking treatment for substance use disorders,
increased insurance coverage for addiction, and greater funding
for addiction-related research [47]. Similarly, applying an
addiction perspective to food may increase weight stigma or
conversely may lead to greater support for the treatment of
eating-related problems. Addictive substances have also been
linked to questions of social justice. Certain addictive
substan ces (e.g., crack-cocaine)have been linked to
underprivileged groups (e.g., urban poor, African-Americans),
which have resulted in stricter legal consequences for the use of
these drugs relative to other substances [48]. Further, at-risk
groups have often been disproportionally targeted for the
marketing of legal drugs. For example, primarily African-
American neighborhoods in metropolitan areas have a higher
density of tobacco billboards and magazines designed for
African-American readers are more likely to contain cigarette
advertisements [49]. Currently, food-related problems, such as
obesity, are impacting minorities and economically
disadvantaged groups in disproportionately high numbers [50].
As with tobacco, advertisements for potentially addictive foods
are specifically designed to appeal to these demographics and
fast-food restaurants are more prevalent in poorer
neighborhoods [51, 52]. The historical relationship of addiction
with social issues may prove informative in considering the
burden of potentially addictive foods on disadvantaged groups.
Although addictive substances appear to be somewhat
heterogeneous in nature (i.e., varying levels of withdrawal,
intoxication, etc.), the addiction rubric has been useful in
identifying substances that are likely to be consumed
excessively despite negative consequences and to result in
clinical levels of impairment/distress. Ultraprocessed foods
appear to share many of the characteristics of addictive
substances and excessive consumption of these foods is
already associated with some clinical disorders (e.g., binge
eating disorder). The consequences of potentially addictive
foods, like drugs of abuse, will also likely extend beyond
clinically significant disorders. Widespread use of addictive
substances often results in steep public health costs due in
part to sub-clinical problematic use. For example, alcohol
consumption is prevalent in America, but only 5-10% of
alcohol users develop alcohol dependence during their
lifetime [53]. Despite the relatively low rates of dependence,
alcohol is the third leading cause of preventable death in the
United States, partially as a result of accidents and health
conditions caused by sub-clinical alcohol use [44]. Highly
processed foods may have a similar impact on public health
by triggering problematic use in individuals that do not
exhibit clinically disordered eating. Moreover, ingredients in
highly processed foods are implicated in health problems
beyond elevated body mass index. For example, research
suggests that HFCS relative to sucroseis more likely to cause
adipose fat in the abdominal region, increase circulating
triglyceride levels, and result in metabolic syndrome [31,
54]. If hyperpalatable foods are capable of driving
widespread overeating and metabolic dysfunction to a degree
that impacts health, this may partially account for the high
public health cost of excessive food consumption [44].
Protective factors against the development of addictive
behaviors are also on the decline in the current food
environment. Addictive substances consumed in the context
of cultural and religious rituals appear to be less likely to be
abused (e.g., [55]). If it is only socially appropriate to
consume a substance in a specific context, social mores may
restrain substance use and only a limited number of cues
may be linked with the substance, which could result in
fewer triggers for use. In a similar vein, food consumption
has traditionally been linked with the experience of eating in
a social or cultural context. For examples, meals were
frequently eaten with family or friends while seated at a table
and snacking between meal times was not a common
practice. The current trends in food consumption find people
eating more frequently in isolation, in a variety of setting
(e.g., the car, at a work desk, in front of th e television), and
snacking regularly between meals [56]. The uncoupling of
food consumption for social/cultural settings may also
increase the likelihood that highly processed food
consumption will result in an addictive behavior.
Additionally, the frequency and the duration of one’s
exposure to an addictive substance, as well as early age of
substance use [57], increases the likelihood of becoming
addicted [58]. There is some evidence that the same dosing
effects may also apply to food high in sugar, fat and salt.
While drug experiences typically begin during adolescence
or early adulthood, direct exposure to processed and highly
palatable food normally begins within the first few years of
life. Indeed, recent research indicates that these influences
can occur in utero and can substantially modify the fetal
genome [59]. For instance, maternal consumption of a high-
fat diet during pregnancy can induce long-term alterations in
dopamine and opioid gene expression and preference for
palatable foods in animal offspring [60]. In addition, there is
144 Current Drug Abuse Reviews, 2011, Vol. 4, No. 3 Gearhardt et al.
evidence that children of obese mothers are at increased risk
for insulin resistance and subsequent obesity and metabolic
dysfunction [61]. Therefore, the early age of exposure to
processed foods and the chronic nature of its consumption
may increase the consequences of potentially addictive
In summary, although highly processed foods differ from
the traditional conceptualization of addictive drugs in some
ways, such as the lack of intoxication, the degree of overlap
is significant and compelling. In addition to neurobiological
and behavioral similarities, hyperpalatable foods and
addictive substances both trigger artificially high levels of
reward, cause biological compensations that result in
tolerance, and become linked with associated cues. Factors
that increase the addictive potential of substances, such as a
lack of cultural context, frequent consumption and early age
of use, are also relevant to highly processed foods. Further,
the components that increase the public health consequences
of alcohol and nicotine are also present in the modern food
environment, such as the ease of accessibility, increased
social acceptability, heavy marketing and lower cost of high-
calorie foods. Due to the similarities between highly
processed foods and addictive drugs, successful policies in
reducing the impact of addictive drugs may also be useful in
combating food-related problems. For example, tobacco
consumption was significantly reduced in the United States
when effective individual treatments were comb ined with
tobacco-focused interventions, such as barring cigarette
machines, increasing taxes and limiting marketing. Similar
interventions have been proposed in response to the obesity
epidemic, such as reducing nutrient-poor foods in school
vending machines, implementing a soda tax and reducing
marketing of high-calorie foods to children [62,63]. Given
the similarities between highly processed foods and tobacco,
these approaches may also prove effective in reducing the
public health consequences of excess food consumption.
Future Research Questions:
It is highly unlikely that all foods are equally capable of triggering
an addictive process. What foods have the greatest addictive
potential? What increases foods’ addictive nature (e.g., elevated
sugar, increased fat)?
Does a reduction in the consumption of highly processed foods
trigger a withdrawal syndrome? Do symptoms of withdrawal from
hyperpalatable foods (e.g., anxiety, agitation, physical symptoms)
increase the risk of weight gain or being unable to adhere to a
healthier diet?
Can the implementation of protective factors against the
development of addictive behaviors (e.g., inclusion of consumption
in social/cultural settings, reduced exposure to advertisements) also
reduce problematic food consumption?
Key Learning Objective:
The food environment has changed drastically in a relatively short
period of time. One cause for concern is that foods are now being
processed in ways that increase both their reward potency, as well as
the speed of absorption of fat/sugar into the system. These are two
factors that increase the addictive potential of other substances (e.g.,
coca leaves). This may have increased the likelihood that certain
foods may be capable of triggering an addictive process.
Labeling a substance addictive has been historically controversial.
For example, the minimal physical withdrawal symptoms associated
with cocaine and the lack of an intoxication syndrome linked with
tobacco led to debates about their addictive nature. Hyperpalatable
foods are associated with similar factors, which will likely lead its
addictive nature to be a topic of controversy.
Despite these differences, hyperpalatable foods and addictive drugs
share a number of characteristics. They are both associated with
loss-of-control, continued use despite negative consequences, high
rates of relapse, public health costs and in utero influences. If
evidence of the addictive potential of highly processed foods
continues to build, effective policies for reducing the impact of other
addictive substances (e.g., increased taxation, restricted advertising)
may prove essential in dealing with the obesity epidemic.
[1] Blumenthal DM, Gold MS. Neurobiology of food addiction. Curr
Opin Clin Nutr Metab Care 2010; 13: 359-65.
[2] Volkow ND, Wang GJ, Fowler JS, et al. Overlapping neuronal
circuits in addiction and obesity: evidence of systems pathology.
Phil Trans R Soc Lond B Biol Sci 2008; 363: 3191-200.
[3] Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction:
Behavioral and neurochemical effects of intermittent, excessive
sugar intake. Neurosci Biobehav Rev 2008; 32: 20-39.
[4] Corwin RL, Grigson PS. Food addiction: fact or fiction? J Nutr
2009; 139: 617-9.
[5] Orford, J. Addiction as excessive appetite. Addiction 2001; 96: 15-
[6] Frascella J, Potenza MN, Brown LL, et al. Shared brain
vulnerabilities open the way to nonsubstance addiction: carving
addiction at a new joint? Ann N Y Acad Sci 2010; 1187: 294-315.
[7] Ifland JR, Preuss HG, Marcus MT, et al. Refined food addiction: a
classic substance use disorder. Med Hypotheses 2009; 72: 518-26.
[8] Spring B, Schneider K, Smith M, et al. Abuse potential of
carbohydrates for overweight carbohydrate cravers.
Psychopharmacology 2008; 197: 637-47.
[9] Cocores JA, Gold MS. The salted food addiction hypothesis may
explain overeating and the obesity epidemic. Med Hypotheses
2009; 73: 892-9.
[10] Johnson PM, Kenny PJ. Dopamine D2 receptors in addiction-like
reward dysfunction and compulsive eating in obese rats. Nat
Neurosci 2010; 13: 635-41.
[11] Thibault L, Woods SC, Westerterp-Plantenga MS. The utility of
animal models of human energy homeostasis. Brit J Nutr 2004; 92:
[12] Volkow ND, O’Brien CP. Issues for DSM-V: Should obesity be
included as a brain disorder? Am J Psychiatry 2007; 164: 708-10.
[13] Berridge KC, Ho C-Y, Richard JM, et al. The tempted brain eats:
pleasure and desire circuits in obesity and eating disorders. Brain
Res 2010; 1350: 43-64.
[14] Pelchat ML, Johnson A, Chan R, et al. Images of desire: food-
craving activation during fMRI. Neuroimage 2004; 23: 1486-93.
[15] Davis C, Levitan RD, Kaplan AS, et al. Reward sensitivity and D2
dopamine receptor gene: A case-control study of binge eating
disorder. Prog Neuro-Psychoph 2008; 32: 620-8.
[16] GearhardtAN, Yokum S, Orr PT, et al. Neural correlates of food
addiction. Arch Gen Psychiatr in press.
[17] DeFoliart GR. Insects as human food: Gene DeFoliart discusses
some nutritional and economic aspects. Crop Prot 1992; 11: 395-9.
[18] Pollan M. In defense of food: an eater’s manifesto. New York:
Penguin Press 2008.
[19] Dudley R. Fermenting fruit and the historical ecology of ethanol
ingestion: is alcoholism in modern humans an evolutionary
hangover? Addiction 2001; 97: 381-8.
[20] Eaton BS. The ancestral diet: what was it and should it be a
paradigm for contemporary nutrition? Proc Nutr Soc 2006; 65: 1-6.
[21] Gearhardt AN, Grilo CM, DiLeone RJ, et al. Can food be
addictive? Public health and policy implication. Addiction 2011;
106(7): 1208-12.
[22] Henningfield JE, Keenan RM. Nicotine delivery kinetics and abuse
liability. J Consult Clin Psych 1993; 61: 743-50.
Hanna JM, Hornick CA. Use of coca leaf in southern Peru:
adaptation or addiction. Bull Narc 1977; 29: 63-74.
The Addiction Potential of Hyperpalatable Foods Current Drug Abuse Reviews, 2011, Vol. 4, No. 3 145
[24] Verebey K, Gold MS. From coca leaves to crack: the effects of
dose and routes of administration in abuse liability. Psychiatr Ann
1988; 18: 513-20.
[25] Bray GA. Fructose: should we worry? Int J Obes 2008; 32: S127-
[26] Vos MB, Kimmons JE, Gillespie C, et al. Dietary fructose
consumption among US children and adults: the Third National
Health and Nutrition Examination Survey. Medscape J Med 2008;
10: 160.
[27] Lustig RH. Fructose: metabolic, hedonic, and societal parallels
with ethanol. J Am Diet Assoc 2010; 110: 1307-21.
[28] Melis M, Pillolla G, Perra S, et al. Electrophysiological properties
of dopamine neurons in the ventral tegmental area of Sardinian
alcohol-preferring rats. Psychopharmacology 2009; 201: 471-81
[29] Huang J, Borensztajn J, Reddy JK. Hepatic lipid metabolism. Mol
Pathol Liver Dis 2011; 5:133-46.
[30] Welsh JA, Sharma A, Cunningham SA, et al. Consumption of
added sugars and indicators of cardiovascular disease risk among
US adolescents. Circulation 2011; 123: 249-57.
[31] Bocarsly ME, Powell ES, Avena NM, et al. High fructose corn
syrup causes characteristics of obesity in rats: increased body
weight, body fat and triglyceride levels. Pharmacol Biochem Behav
2010; 97: 101-6.
[32] Rabinoff M, Caskey N, Rissling A, et al. Pharmacological and
chemical effects of cigarette additives. Am J Public Health 2007;
97: 1-11.
[33] Nielson SJ, Popkin BM. Patterns and trends in food portion sizes,
1977-1998. JAMA 2003; 289: 450-3.
[34] Woods SC. The house economist and the eating paradox. Appetite
2002; 38: 161-5.
[35] Stewart J, Badiani A. Tolerance and sensitization to the behavioral
effects of drugs. Behav Pharmacol 1993; 4: 289-312.
[36] Robinson TE, Berridge KC. Incentive-sensitization and addiction.
Addiction 2001; 96: 103-14.
[37] Berridge KC, Robinson TE, Aldridge JW. Dissecting components
of reward: ‘liking’, ‘wanting’, and learning. Curr Opin Pharmacol
2009; 9: 65-73.
[38] Vallee BL. Alcohol in the Western World. Sci Am 1998; 278: 80-5.
[39] Jaffe JH. Footnotes in the evolution of the American national
response: some little known aspects of the first American strategy
for drug abuse and drug traffic prevention. Brit J Addict 1987; 82:
[40] Cottler LB, Shillington AM, Compton WM, et al. Subjective
reports of withdrawal among cocaine users: recommendations for
DSM-IV. Drug Alcohol Depend 1993; 33: 97-104.
[41] Robinson JH, Pritchard WS. The role of nicotine in tobacco use.
Psychopharmacology 1992; 108: 397-407.
[42] Gearhardt AN, Corbin WR, Brownell KD. Food addiction: an
examination of the diagnostic criteria for dependence. J Addict
Med 2009; 3: 1-7.
[43] Drewnowski A, Bellisle F. Is sweetness addictive? Nutr Bull 2007;
32: 52-60.
[44] Mokdad AH, Marks JS, Stroup MF, et al. Actual causes of death in
the United States. JAMA 2004; 291: 1238-45.
[45] Lenoir M, Serre F, Cantin L, et al. Intense sweetness surpasses
cocaine reward. PLoS ONE 2007; 2: 698-708.
[46] White MA, Whisehunt BL, Williamson DA, et al. Development
and validation of the food-craving inventory. Obes Res 2002; 10:
[47] Leshner AI. Addiction is a brain disease, and it matters. Science
1997; 278: 45-7.
[48] Vagins DJ, McCurdy J. Cracks in the system: Twenty years of the
unjust federal crack cocaine law. American Civil Liberties Union
2006; 1-11.
[49] Moore DJ, Williams JD, Qualls WJ. Target marketing of tobacco
and alcohol-related products to ethnic minority groups in the
United States. Ethn Dis 1996; 6: 83-98.
[50] The obesity epidemic in the United States – Gender, age,
socioeconomic, racial/ethnic and geographic characteristics: A
system review and meta-regression analysis. Epidemiol Rev 2007;
29: 6-28.
[51] Grier SA, Kumanyika SK. The context for choice: Health
implications of targeted food and beverage marketing to African
Americans. Am J Public Health 2008; 98: 1616-29.
[52] Powell LM, Chaloupka FJ, Bao Y. The availability of fast-food and
full-service restaurants in the United States: Associations with
neighborhood characteristics. Am J Prev Med 2007; 33: S240-S5.
[53] American Psychiatric Association. Diagnostic and statistical
manual of mental disorders 4th ed. text revision. Washington, DC:
[54] Nakagawa T, Tuttle KR, Short RA, et al. Hypothesis: fructose-
induced hyperuricemia as a causal mechanism for the epidemic of
the metabolic syndrome. Nat Clin Pract Nephrol 2005; 1: 80-6.
[55] Fábregeas JM, González D, Fondevila S, et al. Assessment of
addiction severity among ritual users of ayahuasca. Drug Alcohol
Depend 2010; 111: 257-61.
[56] Rennie KL, Johnson J, Jebb SA. Behavioural determinants of
obesity. Best Pract Res Clin Endocrinol Metab 2005; 19: 343-58.
[57] Dewit DJ, Adlaf EM, Offord DR, et al. Age at first alcohol use: a
risk factor for the development of alcohol disorders. Am J
Psychiatry 2000; 157: 745-50.
[58] Lewinsohn PM, Rohde P, Brown RA. Level of current and past
adolescent cigarette smoking as predictors of future substance use
disorders in young adulthood. Addiction 1999; 94: 913-21.
[59] Heerwagen MJR, Miller MR, Barbour LA, et al. Maternal obesity
and fetal metabolic programming: a fertile epigenetic soil. Am J
Regul Integr Comp Physiol 2010; 299: R711-R22.
[60] Vucetic Z, Kimmel J, Totoki K, et al. Maternal high-fat diet alters
methylation and gene expression of dopamine and opioid-related
genes. Endocrinology 2010; 151: 4756-64.
[61] Catalano PM. Obesity, insulin resistance, and pregnancy outcome.
Reproduction 2010; 140: 365-71.
[62] Brownell KD, Frieden TR. Ounces of prevention – the public
policy case for taxes on sugared beverages. N Engl J Med 2009;
360: 1805-8.
[63] Brownell KD, Farley T, Willett WC, et al. The public health and
economic benefits of taxing sugar-sweetened beverages. N Engl J
Med 2009; 361: 1599-605.
Received: January 26, 2011 Revised: March 22, 2011 Accepted: April 19, 2011
... Binge eating is also highly correlated with substance use disorder as the two disease conditions have a high comorbidity (e.g., binge eaters are more likely to use alcohol and illicit drug compared to controls) [98,99] and share common symptomatology (e.g., an overwhelming desire for food/substances, a feeling of "loss of control" even in the face of adverse consequences, and preoccupation with thoughts of food/substances) [100], risk factors (e.g., increased reward sensitivity, impulsivity, and diminished self-control), and neurobiological underpinnings (e.g., interruptions in the dopaminergic pathways) [99,100]. Therefore, the dopamine-related theories of substance use disorder may also apply to binge eating. ...
... Binge eating is also highly correlated with substance use disorder as the two disease conditions have a high comorbidity (e.g., binge eaters are more likely to use alcohol and illicit drug compared to controls) [98,99] and share common symptomatology (e.g., an overwhelming desire for food/substances, a feeling of "loss of control" even in the face of adverse consequences, and preoccupation with thoughts of food/substances) [100], risk factors (e.g., increased reward sensitivity, impulsivity, and diminished self-control), and neurobiological underpinnings (e.g., interruptions in the dopaminergic pathways) [99,100]. Therefore, the dopamine-related theories of substance use disorder may also apply to binge eating. ...
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Objective Binge eating, a core diagnostic symptom in binge eating disorder and bulimia nervosa, increases the risk of multiple physiological and psychiatric disorders. The neurotransmitter dopamine is involved in food craving, decision making, executive functioning, and impulsivity personality trait; all of which contribute to the development and maintenance of binge eating. The objective of this paper is to review the associations of dopamine levels/activities, dopamine regulator (e.g., dopamine transporter, degrading enzymes) levels/activities, and dopamine receptor availability/affinity with binge eating. Methods A literature search was conducted in PubMed and PsycINFO to obtain human and animal studies published since 2010. Results A total of 31 studies (25 human, six animal) were included. Among the human studies, there were 12 case–control studies, eight randomized controlled trials, and five cross-sectional studies. Studies used neuroimaging (e.g., positron emission tomography), genetic, and pharmacological (e.g., dopamine transporter inhibitor) techniques to describe or compare dopamine levels/activities, dopamine transporter levels/activities, dopamine degrading enzyme (e.g., catechol-O-methyltransferase) levels/activities, and dopamine receptor (e.g., D1, D2) availability/affinity among participants with and without binge eating. Most human and animal studies supported an altered dopaminergic state in binge eating (26/31, 83.9%); however, results were divergent regarding whether the altered state was hyperdopaminergic (9/26, 34.6%) or hypodopaminergic (17/26, 65.4%). The mixed findings may be partially explained by the variability in sample characteristics, study design, diagnosis criteria, and neuroimaging/genetic/pharmacological techniques used. However, it is possible that instead of being mutually exclusive, the hyperdopaminergic and hypodopaminergic state may co-exist, but in different stages of binge eating or in different individual genotypes. Conclusions For future studies to clarify the inconsistent findings, a homogenous sample that controls for confounders that may influence dopamine levels (e.g., psychiatric diseases) is preferable. Longitudinal studies are needed to evaluate whether the hyper- and hypo-dopaminergic states co-exist in different stages of binge eating or co-exist in individual phenotypes. Plain Language Summary Binge eating is characterized by eating a large amount of food in a short time and a feeling of difficulty to stop while eating. Binge eating is the defining symptom of binge eating disorder and bulimia nervosa, both of which are associated with serious health consequences. Studies have identified several psychological risk factors of binge eating, including a strong desire for food, impaired cognitive skills, and distinct personality traits (e.g., quick action without careful thinking). However, the physiological markers of binge eating remain unclear. Dopamine is a neurotransmitter that is heavily involved in feeding behavior, human motivation, cognitive ability, and personality. Therefore, dopamine is believed to play a critical role in binge eating. This review synthesized study findings related to the levels and activities of dopamine, dopamine regulators, and dopamine receptors in the context of binge eating. The primary finding is that most studies that used neuroimaging, genetic, or drug techniques found an altered dopaminergic state related to binge eating. However, the literature is inconsistent concerning the direction of the alteration. Considering the mixed findings and the limitations in study design, future studies, especially those that include repeated measurements, are needed to clarify the role of dopamine in binge eating.
... With the dramatic change in the food environment and food practices, the fact that food is processed in ways which increase its potential reward can contribute to the severity of obesity (Pedram et al., 2013), a topic in the sphere of food addiction that has been widely researched in recent years. Especially since 2006, the number of academic publications regarding this topic has been growing rapidly (Gearhardt et al., 2011). Food addiction is widely researched in the Western world, and yet extensive research on adolescent obesity in the Czech environment is lacking. ...
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INTRODUCTION: The Czech Republic records one of the highest prevalence levels of obesity in comparison to other European and world countries. The present study aims to fill a gap in the use of tools in research of food addiction (FA), which is believed to be one factor in the high prevalence of obesity. METHODS: A pen-and-paper study was conducted using a nationally representative non-clinical sample of 3950 adolescents aged 11–19. RESULTS: The FA prevalence rate was 4.1%. Exploratory and confirmatory factor analyses verified a one-factor structure. The reliability corresponded to KR = 0.80, CI95% = (0.79, 0.81), McDonald’s ω = 0.79 (0.86 for continuous scale). The connection between FA and impulsivity was confirmed using Poisson regression and logistic regression, and the prevalence of FA decreases with lower impulsivity. CONCLUSIONS: The study findings suggest that the Czech version of mYFAS 2.0 is a reliable tool for research purposes with regard to the Czech environment. Further research should incorporate additional personality traits to obtain a more comprehensive understanding of the emerging topic of food addiction.
... Both impulsivity and ADHD neurobiology have been associated with lower levels of brain dopamine (DA) signaling (Del Campo et al., 2011;Pattij and Vanderschuren, 2020); contrarily, drug and palatable food intake are known to increase DA neurotransmission in the reward pathways, especially in the nucleus accumbens (NAc) (Gearhardt et al., 2011). Thus, it is suggested that abnormal food intake or drug abuse would be an attempt to compensate for the decreased activation of the brain reward system, as a form of self-medication (Cortese and Vincenzi, 2012;Wilens et al., 2007). ...
Impulsivity, as observed in patients diagnosed with Attention-deficit/hyperactivity disorder (ADHD), can induce dysregulated behaviors such as binge eating and drug addiction. We previously demonstrated that neonatal hypoxia-ischemia (HI) resulted in ADHD-like behaviors in rats and that methylphenidate (MPH) administration (the first therapeutic option for ADHD) reversed these deficits. Here, we aimed at investigating addictive-like behaviors, such as the reward-based feeding behavior (using the BioDAQ monitor) and ethanol consumption (using the IA2BC procedure) in adult animals subjected to neonatal HI and treated with or without MPH. Male Wistar rats were divided into four groups (n = 10–12/group): control saline (CTS), CTMPH, HI saline (HIS) and HIMPH. The HI procedure was conducted at postnatal day (PND) 7 and behavioral analyses between PND 60–90, in which MPH (2.5 mg/kg, i.p.) was administered 30 min prior to each behavioral evaluation (6 sessions in BioDAQ and 12 sessions in the IA2BC protocol). HI animals had a dysregulated feeding intake shortly after eating a small piece of the palatable diet, and MPH reversed this dysregulated pattern. However, when the palatable diet was freely available, MPH stimulated a higher intake of this diet in the first exposure day, and this effect was potentialized in HIMPH rats. Increased ethanol intake was observed in HI rats, and MPH administration alleviated this behavior; contrarily, MPH treatment in control rats induced an increase in ethanol consumption. The present findings give additional support to the relationship between neonatal HI and ADHD but the differential response to MPH in control or HI animals highlights the importance of avoiding indiscriminate use of MPH by healthy individuals.
... Those students who presented worse nutritional patterns, such as skipping breakfast, eating excessive red/processed meats and soft drinks, or overconsuming pastries, presented higher values of food addiction. These findings are in line with the food preferences of people with food addiction; they are more impulsive towards the consumption of foods that are rich in sugars, fats and carbohydrates [28]. However, until now, the associations between different types of meat and food addiction had not been analyzed. ...
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The transition to college is a decisive stage for the acquisition of eating habits that continue into adulthood. The aim of this study is to assess the consumption of healthy elements of the Mediterranean diet in a group of university students and to evaluate whether the consumption pattern was related to sex, Body Mass Index (BMI), food addiction or the amount of physical activity performed. A total of 515 nursing students participated. The Mediterranean diet adherence questionnaire (PREDIMED), the food addiction scale (YFAS 2.0) and the International Physical Activity Questionnaire (IPAQ) were completed. For data analysis, multivariate analysis was performed with multiple linear regression and adjusted for sex, age, and BMI. The results showed that females consumed various types of meats (white/red, processed) in a healthier proportion (p < 0.05). Students that consumed more than one per day (unhealthy) of red/processed meats (mean difference (MD) = −0.49; 95% CI: −0.83; −0.15), soft drinks (MD = −0.82; 95% CI: 82–1.36; −0.27) and pastries (MD = −0.63; 95% CI: −0.97; −0.30) displayed higher food addiction scores. In addition, students who skipped breakfast also scored higher on food addiction (MD = 0.75; 95% CI: 0.31–1.19). Higher values of physical activity were observed in those who presented a healthy consumption of vegetables (MD = 140.86; 95% CI: 72.71–209.02), fruit (MD = 145.78; 95% CI: 69.35–222.21), legumes (MD = 136.46; 95% CI: 60.43–212.50) and nuts (MD = 74.36; 95% CI: 14.23–134.49). Students who consumed more red or processed meats, more pastries and more soft drinks had higher values of food addiction, while those who consumed more vegetables, fruits, legumes, and nuts had more minutes of physical activity per week. These findings invite us to insist on expanding knowledge regarding the health benefits of consuming a Mediterranean-type diet as a whole. The healthy consumption of fish, fruit and legumes should also be emphasized, especially among university students.
... The body of evidence regarding the food addiction construct has been growing in recent years. Food addiction is characterized by excessive consumption of energetically dense, hyper-palatable, and processed foods with characteristics and repercussions similar to substance addiction [12]. Given the complex nature of addictions, food addiction is assessed with instruments designed to reflect this diagnostic criterion for other addictive disorders, such as loss of control over consumption, intense cravings, and continued use despite negative health consequences [13]. ...
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Download PDF Download PDF Original Article Published: 08 January 2022 Prevalence of food addiction and its association with anxiety, depression, and adherence to social distancing measures in Brazilian university students during the COVID-19 pandemic: a nationwide study André Eduardo da Silva Júnior, Mateus de Lima Macena, …Nassib Bezerra Bueno Show authors Eating and Weight Disorders - Studies on Anorexia, Bulimia and Obesity (2022)Cite this article Metricsdetails Abstract The study’s objective was to determine the prevalence of food addiction (FA) in Brazilian university students and to verify whether there is an association with anxiety, depression, and adherence to the social distancing measures adopted during the COVID-19 pandemic. This is a nationwide cross-sectional study carried out through the application of online questionnaires. Self-reported data on age, sex, economic class, race/skin color, anthropometric data, depression diagnosis, anxiety, modified Yale Food Addiction Scale 2.0 (mYFAS 2.0), and adherence to social distancing measures were collected. 5368 participants were included, with a mean age was 24.1 ± 6.3 years, the majority were female (n = 3990; 74.3%), and the mean BMI in our sample was 24.5 ± 5.3 kg/m2. The prevalence of FA was 19.1% (95%CI: 18.0; 20.0%). An association was observed between FA with depression (PR: 1.60; 95%CI: 1.43; 1.78; p < 0.01), and anxiety (3.13; 95%CI: 2.74; 3.58; p < 0.01), but not with adherence to social distancing measures (p = 0.70). In conclusion, there was a higher prevalence of FA in Brazilian university students. Besides, university students with anxiety, depression, overweight, or obesity and females are more prone to FA.
... The foods and nutrients most often cited as being addictive both within the scientific community and general public include refined carbohydrates (i.e., sugar), salt and/or fat, or combinations of these [8,14,15]. These foods are thought to exceed the rewarding properties of traditional foods, such as vegetables, fruits, and nuts due to the high potency of refined ingredients [16]. ...
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(1) Background: Research suggests that certain foods may have addictive effects; however, no reviews have systematically appraised studies in this area. The aims of this review were to determine the nutrients, foods and dietary patterns associated with addictive eating. (2) Methods: Published studies up to November 2020 were identified through searches of 6 electronic databases. Eligible studies included those in in children and adults that reported dietary intakes of individuals with ‘food addiction’. (3) Results: Fifteen studies (n = 12 in adults and n = 3 in children/adolescents with Yale Food Addiction Scale defined ‘food addiction’) were included. Foods commonly associated with addictive eating were those high in a combination of fat and refined carbohydrates. Generally, intakes of energy, carbohydrates and fats were significantly higher in individuals with addictive eating compared to those without. (4) Conclusions: Due to the heterogeneity in study methodologies and outcomes across included studies, it is difficult to conclude if any specific foods, nutrients or dietary patterns facilitate an addictive process. Further research is needed to elucidate potential associations. However, present addictive eating treatment approaches could incorporate individualised dietary advice targeting foods high in fat and refined carbohydrates.
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Binge eating is increasingly prevalent among adolescents and young adults and can have a lasting harmful impact on mental and physical health. Mechanistic insights suggest that aberrant reward-learning and biased cognitive processing may be involved in the aetiology of binge eating. We therefore investigated whether recently developed approaches to catalyse brief interventions by putatively updating maladaptive memory could also boost the effects of cognitive bias modification training on binge eating behaviour. A non-treatment-seeking sample of 90 binge eating young adults were evenly randomised to undergo either selective food response inhibition training, or sham training following binge memory reactivation. A third group received training without binge memory reactivation. Laboratory measures of reactivity and biased responses to food cues were assessed pre-post intervention and bingeing behaviour and disordered eating assessed up to 9 months post-intervention. The protocol was pre-registered at We found limited evidence of premorbid biased processing in lab-assessed measures of cognitive biases to self-selected images of typical binge foods. Accordingly, there was little evidence of CBM reducing these biases and this was not boosted by prior ‘reactivation’ of binge food reward memories. No group differences were observed on long-term bingeing behaviour, caloric consumption or disordered eating symptomatology. These findings align with recent studies showing limited impact of selective inhibition training on binge eating and do not permit conclusions regarding the utility of retrieval-dependent memory ‘update’ mechanisms as a treatment catalyst for response inhibition training.
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Purpose of Review Hyper-palatable foods (HPF) may exploit our neurobiological propensities to seek and consume rewarding foods. The review highlights evidence from basic behavioral and neurobiological studies in humans on the reinforcing properties of HPF and consequences of repeated HPF consumption over time. The review also addresses HPF within the context of the US food environment. Recent Findings There is reasonably strong behavioral evidence to indicate that HPF may have reinforcing properties that are similar to drugs of abuse. Evidence indicates that healthy individuals may exhibit greater preference for HPF relative to non-HPF and that powerful cues may develop that indicate the presence of HPF as a reward. Preliminary evidence indicates that elevated HPF intake may yield neurobiological consequences for brain reward neurocircuitry. The US food environment provides wide and easy access to HPF. Conceptualized as a substance, HPF exist unregulated in our environment, similar to the tobacco availability in the 1940s. Parallels have been drawn between food and tobacco company practices; a review of industry documents indicates that tobacco companies owned major US food companies since the 1980s, possibly leading the development and proliferation of HPF. Summary There is reasonably strong evidence to indicate that HPF may have powerful reinforcing properties similar to drugs of abuse; however, more longitudinal work is needed. Critical attention to the factors and drivers of HPF proliferation in the US food system is paramount to conceptualizing the presence of HPF in our food environment and in considering strategies to protect the US population’s health.
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Amaç: Bu çalışmada pandemi döneminde bireylerin antropometrik ölçümlerinde ve fiziksel aktivite düzeylerinde meydana gelen değişimlerin yeme bağımlılığıyla olan ilişkisinin incelenmesi amaçlanmıştır. Bireyler ve Yöntem: Çalışmaya 19-65 yaş arası 288 yetişkin birey (248 kadın, 40 erkek) dahil edilmiştir. Çalışma verileri web-tabanlı anket formu yardımıyla toplanmıştır. Anket formu ile bireylerin sosyo-demografik özellikleri ve antropometrik ölçümleri sorgulanmıştır. Bireylerin yeme bağımlılığı durumu Yale Yeme Bağımlılığı Ölçeği ve fiziksel aktivite durumları Uluslararası Fiziksel Aktivite Anketi kısa formu aracılığıyla değerlendirilmiştir. Bulgular: Bireylerin %23.0’ında yeme bağımlılığı vardır. Yeme bağımlılığı olan bireylerin beden kütle indeksi (BKİ) ve bel/boy oranı değerlerinin, yeme bağımlılığı olmayan gruba göre anlamlı olarak daha yüksek olduğu saptanmıştır (p<0.05). Aşırı yeme isteği uyandırdığı için ekmek, simit, pizza/lahmacun/döner, poğaça/açma, patates kızartması, makarna, muz, şeker/şekerleme ve cips gibi besinlerle sorun yaşayan bireylerin oranı yeme bağımlılığı olan bireylerde, yeme bağımlılığı olmayan bireylere göre anlamlı derecede daha yüksek bulunmuştur (p<0.05). Yeme bağımlılığı olan ve olmayan bireylerde pandemi ile fiziksel aktivite düzeyinde anlamlı azalma saptanmıştır (p<0.05). Yeme bağımlılığı olan bireylerde pandemi ile BKİ ve bel/boy oranı değerlerinde anlamlı artış belirlenmiştir (p<0.05). Ayrıca yeme bağımlılığı olan kadın bireylerde pandemi ile vücut ağırlığı ve bel çevresi değerlerinde anlamlı artış saptanmıştır (p<0.05). Sonuç: Çalışmadan elde edilen sonuçlara göre pandemi döneminde yeme bağımlılığı ile antropometrik ölçümler arasında ilişki olduğu ve yeme bağımlılığı durumundan bağımsız olarak bireylerin fiziksel aktivite düzeylerinde azalma olduğu saptanmıştır.
INTRODUCTION Previous research has identified reward sensitivity as an important factor that may contribute to the engagement in eating behavior (e.g., binge eating, emotional eating, etc.) and increase obesity risk. In the current study, we conducted a systematic review of the literature to determine the relationships between reward sensitivity, eating behavior, and obesity-related outcomes. The study focused on two commonly used measures of reward sensitivity in the literature: the Sensitivity to Punishment and Sensitivity to Reward Questionnaire (SPSRQ) and the Behavioral Inhibition Scale/Behavioral Activation Scale (BIS/BAS Scale). METHOD We conducted a systematic search to identify studies that analyzed reward sensitivity as a predictor of eating behavior or obesity-related outcomes, and measured reward sensitivity using the SPSRQ or BIS/BAS Scale. The search yielded N=19 total publications included in the review. RESULTS Findings indicated that reward sensitivity, primarily measured by summary scores on the SPSRQ or BIS/BAS Scale, were positively associated with a variety of eating behaviors and obesity-related outcomes with small to moderate effect sizes. Findings were most consistent across studies that examined the association between reward sensitivity and eating behavior outcomes (e.g., binge eating, emotional eating) (r values= .08 to .41; p values < .001 to p < .05) and food consumption outcomes (e.g., palatable food intake) (r values = .21 to .40; p < .001 to p values < .05). Findings were less consistent for food craving and BMI outcomes, and revealed these relationships may depend on individual-level factors and/or environment-related factors, (e.g., food cues). A quality evaluation using the Critical Appraisal Tool for Cross-Sectional Studies (AXIS tool) indicated that most studies were rated as moderate to strong quality (84%). CONCLUSION Findings indicate that elevated reward sensitivity may be a risk factor for engagement in eating behaviors that may increase obesity risk.
Context While general consensus holds that food portion sizes are increasing, no empirical data have documented actual increases.Objective To determine trends in food portion sizes consumed in the United States, by eating location and food source.Design, Setting, and Participants Nationally representative data from the Nationwide Food Consumption Survey (1977-1978) and the Continuing Survey of Food Intake by Individuals (1989-1991,1994-1996, and 1998). The sample consists of 63380 individuals aged 2 years and older.Main Outcome Measure For each survey year, average portion size consumed from specific food items (salty snacks, desserts, soft drinks, fruit drinks, french fries, hamburgers, cheeseburgers, pizza, and Mexican food) by eating location (home, restaurant, or fast food).Results Portion sizes vary by food source, with the largest portions consumed at fast food establishments and the smallest at other restaurants. Between 1977 and 1996, food portion sizes increased both inside and outside the home for all categories except pizza. The energy intake and portion size of salty snacks increased by 93 kcal (from 1.0 to 1.6 oz [28.4 to 45.4 g]), soft drinks by 49 kcal (13.1 to 19.9 fl oz [387.4 to 588.4 mL]), hamburgers by 97 kcal (5.7 to 7.0 oz [161.6 to 198.4 g]), french fries by 68 kcal (3.1 to 3.6 oz [87.9 to 102.1 gl), and Mexican food by 133 kcal (6.3 to 8.0 oz [178.6 to 226.8 g]).Conclusion Portion sizes and energy intake for specific food types have increased markedly with greatest increases for food consumed at fast food establishments and in the home.
The question of addiction concerns the process by which drug-taking behavior, in certain individuals, evolves into compulsive patterns of drug-seeking and drug-taking behavior that take place at the expense of most other activities, and the inability to cease drug-taking, that is, the problem of relapse. In this paper we summarize one view of this process, the “incentive-sensitization” view, which we e rst proposed in 1993. Four major tenets of the incentive-sensitization view are discussed. These are: (1) potentially addictive drugs share the ability to alter brain organization; (2) the brain systems that are altered include those normally involved in the process of incentive motivation and reward; (3) the critical neuroadaptations for addiction render these brain reward systems hypersensitive (“sensitized”) to drugs and drug-associated stimuli; and (4) the brain systems that are sensitized do not mediate the pleasurable or euphoric effects of drugs (drug “liking”), but instead they mediate a subcomponent of reward we have termed incentive salience (drug “wanting”).
During the past few years there has been a new upsurge of interest in insects as food. One factor that may be responsible is an increasing awareness in the western world that insects are traditional and nutritionally important foods for many non-European cultures. Other factors may be increased pride in ethnic roots and traditions, increased concern about environment and overuse of pesticides, and better communication among scientists who are interested in the subject. Edible insects may be closer now than ever before to acceptance in the western world as a resource that should be considered in trying to meet the world's present and future food needs.
Compares the various modes of cocaine use and their relative dependence producing potential and toxicity. The effects of the dose and route of administration are investigated in relation to bioavailability, tolerance development, and serious toxicity. The impact of crack and the practice of cocaine smoking on compulsive cocaine addiction is examined. Topics of discussion include coca leaf chewing; oral, intranasal, and iv administration; smoking coca paste; cocaine freebase smoking; cocaine doses and toxic reactions; and cocaine smoking disorder. The physical and psychological symptoms and symptom list of 32 freebase users are presented. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Summary  The notion that sweetness is ‘addictive’ endures in the scientific literature and in the popular press. The most common targets of food cravings and addictions are energy-dense foods that are sweet, high in fat, or both. In clinical studies, the consumption of sweet and high-fat foods has been selectively reduced by opiate antagonists, suggesting a link between hedonic pleasure response and the brain systems of reward. Recent brain imaging studies have further implicated the dopamine system in mediating the pleasure response to food as well as a range of addictive behaviours. However, suggestions that sugar and fat have a permanent impact on the neurobiology of food preference are in sharp contrast with the view that the vast majority of food addictions are simply a matter of misattribution. Dietary restraint, coupled with ambiguous attitudes towards good-tasting but energy-dense foods, may lead consumers to claim that some aspects of eating behaviour are beyond their control. This distinction between addiction and attribution has implications for obesity-related lawsuits. The chief attraction of addiction theory for the plaintiff’s counsel lies in the claim of diminished personal responsibility and abrogation of free choice. However, sugar and sweets do not appear to meet the current criteria for substance dependence as formulated in the Diagnostic and Statistical Manual of Mental Disorders – Fourth Edition. Examining scientific literature on sweet food ‘addictions’ and their putative links to the obesity epidemic is the topic of this review.
The liver is a major regulator of lipid metabolism in the body. It plays a central role in the synthesis and degradation (oxidation) of fatty acids. Fatty acids serve as an important source of energy as well as energy storage for many organisms and are also pivotal for a variety of biological processes, including the synthesis of cellular membrane lipids and generation of lipid-containing messengers involved in signal transduction [1]. Fatty acids can generally be stored efficiently as non-toxic triglycerides (triacylglycerols/fat), which generate more than twice as much energy, for the same mass, as do carbohydrates or proteins. Accordingly, liver is a key player in energy homeostasis: first, as it converts excess dietary glucose into fatty acids that are then exported to other tissues for storage as triglycerides as lipid droplets [2]; second, under conditions of increase in synthesis and decreased oxidation of fatty acids the liver contributes to the progressive accumulation of excess unspent energy in the form of energy-dense triglycerides in adipocytes of adipose tissue, which provide virtually limitless capacity to store energy and finally, under chronic energy over-load situations the liver may serve as a surrogate reservoir for storing considerable quantities of excess fat, leading to the development of hepatic steatosis and steatohepatitis [3].