Nutrition 30 (2014) 252–256

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Nutrition
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Review

Neurobiologic basis of craving for carbohydrates

Tamara Ventura M.D., Jaime Santander M.D. *, Rafael Torres M.D., Ph.D., Ana Marıa Contreras M.D.
lica de Chile, Santiago, Chile
Department of Psychiatry, School of Medicine, Pontificia Universidad Cato

a r t i c l e i n f o a b s t r a c t

Article history: Objectives: There is a relationship between emotional disorders, obesity, and craving for carbo-
Received 23 January 2013 hydrates. This relationship complicates the success of treatments aimed at combatting obesity,
Accepted 28 June 2013 which is considered to be the epidemic of the twenty-first century. We conducted a review of the
neurobiologic basis for carbohydrate craving, with the hope that this understanding will enable the
Keywords: design of more efficient therapeutic strategies.
Dietary carbohydrates
Method: We conducted a non-systematic literature search in PubMed using MeSH.
Addictive behavior
Results: Research on the basis of carbohydrate craving is varied, but may be grouped into five main
Biological evolution
Anxiety areas: the serotonergic system, palatability and hedonic response, the motivational system, stress
Eating behavior response systems, and gene–environment interaction.
Neurobiology Conclusions: The models that integrate motivational systems with palatability and hedonic
response studies are the ones that we believe can best explain both craving for carbohydrates and
related addictive phenomena. Research has contributed to a greater understanding of the neuro-
biologic basis of carbohydrate craving. The latter, in turn, contributes to an understanding of the
implications, challenges, and possible therapies that might be put in place to cope with this
phenomenon.
Ó 2014 Elsevier Inc. All rights reserved.

Introduction The scientific literature supports the existence of carbohydrate-

The growing global obesity epidemic and its associated pa-
thologies [1] have focused research on the variables associated
with overeating and the barriers to achieving changes in nutri-
tional habits [2]. Research has ranged from social and cultural
variables, such as the availability of food or the effects of
advertising in childhood [2,3], to attempts at elucidating the
mechanisms associated with the tendency toward excessive
consumption of fats and carbohydrates. Such research also has
suggested the possibility that there may be an addictive pattern
to the consumption of these nutrients under certain circum-
stances [4–6].
We know that emotional factors have become increasingly
important based on associations found among obesity, anxiety,
and mood disorders [5]. Carbohydrates are exceptionally in-
volved in these associations, which has led to further research
into their patterns and roles. Sugar addiction, carbohydrate
craving, and emotional eating have been correlated with obesity
and being overweight. This has led to the establishment of a
strong correlation between obesity, anxiety, and mood disorders
[4–10], all of which have important public health implications.
* Corresponding author: Tel.: þ56 2 27548872; fax: þ56 2 26651951.
E-mail address: jsantan@med.puc.cl (J. Santander).
craving syndrome, in which carbohydrate intake medicates a
dysphoric mood state [8]. This syndrome is defined as a food and
mood disorder, characterized by an irresistible urge to consume
sweets or starchy foods in response to negative moods [9]. The
criteria listed in Table 1 have been proposed to operationalize this
phenomenon [8]. Carbohydrate intake appears to temporarily
improve mood in carbohydrate cravers, whereas individuals who
have no craving for carbohydrates usually complain of fatigue after
eating these foods [9], thus revealing a different relationship with
this nutrient.
However, despite the important role of these relationships,
the underlying neurobiologic mechanisms remain unclear and
have not been directly related to emotional factors. Under-
standing these phenomena potentially could be important for
several reasons. On the one hand, this would allow public health
specialists and clinicians to understand realistically the behav-
ioral changes of individual patients and the general population,
considering how our biology works. On the other hand, this
knowledge would allow specific pharmacologic strategies to be
developed that may lead to more successful outcomes when
dealing with obesity and its consequences.
Given the importance of understanding the neurobiologic
mechanisms underlying the phenomenon of carbohydrate
craving, we aim to review the main neurobiologic hypotheses

0899-9007/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.nut.2013.06.010
 T. Ventura et al. / Nutrition 30 (2014) 252–256 253

Table 1 preference for carbohydrates in the diet [11]. Furthermore, in-

Carbohydrate*-craving syndrome criteria [8]
 Cravings during the afternoon or at night to eat sweets or starchy
foods at least four times a week.
 Eating carbohydrates in the afternoon or night at least four times
a week, supported by records.
 Carbohydrate craving that occurs in conjunction with dysphoria,
which is relieved by eating these foods.
* A carbohydrate is defined as a food consumed between meals that has a
carbohydrate to protein ratio of  6:1.
that explain carbohydrate craving, and link carbohydrate crav-
ings with related phenomena, such as emotional eating and
obesity, from a neurobiologic perspective.
Methods
A focused review of the available literature was conducted by using the
database www.pubmed.org. The MeSH tool was used and the search matrix
included the terms stress, carbohydrates, dietary carbohydrates, food, emotional
eating, addictive behavior, and evolution. By combining these terms, 2187 articles
were found, of which some studies were selected according to the objectives of
this review.
Results
We found dispersed information from different lines of
research on carbohydrate craving. We then categorized these
findings into five groups that had similar research lines. The
serotonergic hypothesis is presented first because it is the first
hypothesis to emerge and the one that has received the most
attention in the literature. The hypotheses that follow are pre-
sented in terms of the degree to which they focus on physical
consumption variables, thus beginning with palatability and
ending with environmental aspects. A summary of these hy-
potheses is given in Table 2.
Serotonergic hypothesis
Brain serotonin is an important regulator of appetite, mood,
and preference for certain macronutrients, among its other
functions. Low levels of serotonin stimulate appetite and a
creases in brain serotonin improve mood levels in individuals
who are vulnerable to stress [11].
The serotonergic hypothesis proposes that carbohydrate
intake associated with states of anxiety is an attempt at self-
treatment, given the increase in brain serotonin that occurs af-
ter carbohydrate intake [11]. The behavioral expression of this
hypothesis is the craving for carbohydrates that an individual
experiences within an episode of anxiety. After this macronu-
trient is consumed, the individual’s emotional state improves.
It has been observed that during acute stress there is an in-
crease in serotonergic neuronal activity due to increased plasma
levels of cortisol and beta-endorphins [12]. An increase in sero-
tonin regulates the hypothalamic–pituitary–adrenal (HPA) axis,
which participates in stress adaptation [13]. If this continues over
time, the use of serotonin exceeds its synthesis capacity, which
has been associated with the depletion of tryptophan (Trp), the
precursor of serotonin synthesis, and with depressive mood
levels [12]. Changes in brain serotonin are mainly due to the
availability of Trp in the brain. Serotonin synthesis is known to
increase due to carbohydrates and to decrease or remain unal-
tered from proteins in the diet [10]. In fact, it has been observed
that Trp levels after a meal rich in carbohydrates and low in
protein tend to increase along with serotonin, due to a 42% rise in
brain Trp compared with diets rich in protein and low in car-
bohydrates [14].
Based on the serotonergic hypothesis, it is inferred that other
means of increasing brain serotonin levels may constitute po-
tential treatments for obesity in individuals with anxiety. The use
of serotonin, including fluoxetine, in rats with a history of food
restriction under stress, was shown to decrease compulsive
eating (binging). However, the effect was not the same in rats
with a history of food restriction that were not under stress [5].
Controversy exists regarding the serotonergic hypothesis
because some studies show conflicting results as to whether
increased brain serotonin induced by a diet rich in carbohydrates
effectively translates into a change of affective state and appetite
[11,15,16]. Moreover, the positive effects on mood of increased
brain serotonin induced by a carbohydrate-rich diet occur in
patients suffering from anxiety due to carbohydrate craving, late

Table 2
Summary of the main hypotheses that explain carbohydrate craving

Neurobiologic hypothesis Highlights

Serotonergic  Increased brain serotonin improves mood [11].
 Brain serotonin levels depend on the availability of its Trp precursor [14].
 Dietary carbohydrates increase the passage of Trp through the blood–brain barrier, unlike proteins, which alter LNAA [14].
 Faced with anxiety, an individual eats carbohydrates, which increase brain serotonin, thus improving mood [11].
Palatability and hedonic  The pleasurable experience of eating food with high palatability immediately improves mood [17].
response  This occurs in individuals with greater genetic sensitivity to sweet taste through the activation of the endogenous opioid
system [19].
 Faced with anxiety, an individual eats a food with high palatability, activating the hedonic mechanism, which improves
mood [16].
Motivational system  Carbohydrates act in the motivational system in the same manner as abused substances [6].
 This increases dopamine and endogenous opioids, which are associated with a known pleasurable effect, [4] improving mood.
 If this behavior is repeated over time, structural changes in the brain are produced that generate dependence on highly
palatable foods [4,6,23].
Stress response  Faced with anxiety associated with stress, the HPA axis activates [30].
 Highly palatable foods activate the motivational system and reduce the HPA axis, thus regulating the stress system [30].
 Therefore, when faced with anxiety, highly palatable food produces a hedonic reward as well as reducing the state
of anxiety [30].
Gene–environment  Eating is a coping tool to relieve negative emotions.
 The behavior is learned through inadequate parenting and environment [9].
 It also stems from an inability to distinguish hunger from other aversive internal states [9].
 There is greater susceptibility in carriers of the A1 allele of the DRD2 dopamine receptor and carriers of the short allele of
the serotonin transporter gene [33,34].

HPA, hypothalamic–pituitary–adrenal; LNAA, large neutral amino acids; Trp, tryptophan

254 T. Ventura et al. / Nutrition 30 (2014) 252–256
luteal phase syndrome, or seasonal affective disorders, and do
not occur in healthy individuals under normal circumstances.
These effects of diet on affective states are probably due to a
relatively reduced amount of brain serotonin, induced by chronic
stress [13].
Another critical aspect of the serotonergic hypothesis is that it
implicitly assumes that there is a delay between carbohydrate
intake and mood improvement, because this depends on the
entry of Trp through the blood–brain barrier and serotonin
synthesis [17]. The latter is a process that takes at least 60 min
[18], whereas emotional eating immediately affects negative
mood [17]. This temporal dissociation has raised questions about
the validity of this hypothesis.
Palatability and hedonic response hypothesis
Regulation of eating and energy homeostasis includes, in
addition to hunger and satiety signals, factors such as the sense
of reward (or salience) of food, environmental keys, and cogni-
tive factors [16]. This hypothesis proposes that carbohydrate
craving during states of anxiety is due to the salience of this
macronutrient, which calms the emotional state via hedonic
brain response induced through the endogenous opioid system
[17]. The expression of this hypothesis occurs because the indi-
vidual with anxiety eats highly palatable food that lowers his or
her anxiety levels.
Eating chocolate immediately affects a negative mood, but
not a positive or neutral mood. This effect has a short duration
and comes from the palatability of the food [17]. This hypothesis
proposes that, because the effect on mood is immediate, it is
unlikely to be due to the direct effects of the nutrients in neu-
rotransmitters or to the psychopharmacologic effect of the active
ingredients of chocolate, as these are produced 1 to 2 h after
consumption [17].
There is evidence that patients with psychiatric disorders
(mood, anxiety and eating disorders, and premenstrual syn-
drome) have greater hedonic response levels to concentrated
sucrose solutions. This is a stable, innate, and inherited trait that
is at least partly determined by genetic mechanisms in animals
and humans, and is associated with higher hedonic response
levels to sweet tastes, which increases the risk for developing
obesity [19].
There are at least two mechanisms described in the literature
that can determine individual differences in terms of hedonic
response to sweet taste. The first mechanism is related to the
perception of sweet taste. Polymorphisms in the region of the
TAS1R3 gene are associated with a preference for saccharin in 30
strains of mice. Furthermore, it has been shown that variations of
the TAS2R38 gene, are associated with a preference for sweet
foods and beverages in children (5–10 years) and undergraduate
students (mean age: 22). The second possible mechanism is the
opioid system in the brain. This system regulates food intake by
modulating the associated orosensory reward, instead of intake
being modulated by energy needs. Individuals with a greater
taste for sweets have a basally inhibited brain opioid system, and
therefore are more sensitive to the effects associated with con-
sumption of these foods [19].
If the consumption of highly palatable foods is maintained
over time, it can lead to repeated release of endogenous opioids,
which induces hypersensitivity of the opioid receptor. This, in
turn, may perpetuate binge eating of highly palatable foods.
Interestingly, when individuals addicted to exogenous opioids
are in withdrawal, they eat more sugary foods, probably to
replace the action of opiates in the brain [5]. It has even been
suggested that there is a withdrawal syndrome for highly
palatable foods, leading to the emergence of depressive states
that could be relieved by eating these foods again [20].
This hypothesis implies that the use of drugs acting on opioid
receptors, such as naltrexone, naloxone, and buprenorphine [5,
21], could be proposed as a possible treatment for carbohy-
drate craving.
With respect to the critical aspects of this hypothesis, a
distinction has been made between the two components of the
eating reward: the “like” and “want” [16]. The “like” aspect cor-
responds to palatability and depends on the opioid system, the
hedonic component of eating, which means the pleasure derived
from the orosensory stimulation of food. The “want” aspect is
under the control of dopamine and is a serious motivational
component in the desire to obtain food [16]. In our opinion, these
systems are intrinsically connected, thus making this distinction
questionable [22].
Motivation system hypothesis
The motivation system hypothesis posits that an individual
displays craving for carbohydrates when faced with anxiety, and
after consuming carbohydrates, they generate neuronal and
behavioral changes similar to those produced by addictive sub-
stances. This leads to increased cravings, especially when faced
with states of anxiety or anxiety from withdrawal from highly
palatable food. Thus, consumption is perpetuated and the
carbohydrate-craving syndrome comes into being [6,23].
Substance dependence structurally and functionally alters the
brain’s motivational system, which is composed of the ventral
tegmental area (VTA), amygdala, prefrontal cortex, hippocampus,
and nucleus accumbens, among other areas. Once changes have
occurred in the brain, it is known that anxiety, among other
stimuli, increases the craving for consumption. During withdrawal
syndromes it is also common to find symptoms of anxiety that
predispose the patient to repeated substance consumption [23].
A common etiology has been proposed for eating disorders
and substance dependence [24]. In situations where there is
limited and intermittent access to sugar, consumption of sugar
increases levels of dopamine and opioids in the same way as drug
use does [4,24]. This leads to changes in the expression or avail-
ability of dopamine receptors [3]. The role of glutamate, g-ami-
nobutyric acid, and opioids in the regulation of food intake also
has been demonstrated. This suggests signaling in the nucleus
accumbens on the hedonic component of eating [25,26]. Dopa-
mine also has a role in intake: dopaminergic projections from the
VTA to the nucleus accumbens determine how much of a certain
food will be ingested and by how much satiety or other metabolic
or behavioral needs will be exceeded. This cognitive process is
strongly and constantly stimulated by the modern socioeconomic
environment, generally resulting in increased intake [27].
Bingeing, withdrawal syndrome, and craving for sugar also
have been associated with neurochemical changes in the brain
that also are produced with addictive drugs [4]. The withdrawal
signs appear to be largely determined by opioid withdrawal in
addition to a decrease of dopamine and release of acetylcholine
in the nucleus accumbens [4]. These effects are similar to those
produced by opiates and psychostimulants, although smaller in
magnitude.
Recent evidence has shown that simple exposure to highly
palatable food does not induce behavioral changes or neuronal
pathologic changes in the craving for carbohydrates and the
motivation system. Rather, repeated, intermittent, and excessive
consumption of highly palatable food is required for these
 T. Ventura et al. / Nutrition 30 (2014) 252–256
changes to be established. It has even been seen that when low
palatability foods are eaten in an addictive manner, this had to
have been primed with a highly palatable food [5].
This hypothesis implies that carbohydrate-craving treatment
should be similar to the treatment used in substance depen-
dence, with the sole limitation being that in this case, it is
impossible to completely withdraw from the dependent sub-
stance [28].
Critics of this hypothesis argue that it is not possible to draw
a parallel between substance addiction and “supposed” food
dependence. A disease model is different from a model of
a complex physiological response that may eventually lead to
a somatic disease such as obesity [29].
Stress response hypothesis
The stress response hypothesis posits that glucocorticoids
and noradrenaline, which both participate in stress physiology,
increase their levels after the effect of a stressor, thus mediating
the relationship between anxiety and carbohydrate craving [30].
During acute stress, eating is suppressed due to the anorectic
effect of the corticotropin-releasing hormone. However, this
behavior increases during recovery due to the residual effects of
cortisol. Furthermore, cortisol, during acute stress, increases
available energy levels through lipolysis and gluconeogenesis.
Additionally, as a mechanism to increase energy, glucocorticoids
produce hyperphagia, which ultimately leads to weight gain, as
part of the pathophysiology of obesity [12]. The tendency to gain
weight over time has also been shown in chronic stress, which
may be due to stress-related endocrine changes and behaviors
associated with coping with the situation [12]. It also has been
shown that individuals with high cortisol reactivity consume
significantly more calories and sweet foods while under stress
than those with low reactivity of this hormone [10].
A study in female rhesus monkeys continuously exposed to
stressors verified that they consumed more carbohydrate calo-
ries compared with controls, which was associated with a flat-
tening of the diurnal cortisol rhythm and a greater increase in
serum cortisol when faced with acute separation. These data
support the hypothesis that daily exposure to psychosocial stress
increases the consumption of high-calorie foods [31].
Additionally, it has been found that acute stress reduces food
intake unless there is access to highly palatable food during the
stressful period. This “non-homeostatic eating” has been hy-
pothesized to activate the motivational system and decrease the
activity of the HPA axis, controlling the stress response, as evi-
denced by lower levels of cortisol. That is, the stress activates
dopaminergic neurons and the stress response is controlled after
eating highly palatable food [30]. This is what enables con-
sumption of high palatability foods to continue over time, giving
rise to obesity.
A proper understanding of the mechanisms of the interaction
between the stress system and the motivation system will enable
the eventual development of new therapies to combat obesity
[30].
Gene–environment hypothesis
The gene–environment hypothesis suggests that inadequate
parenting in managing emotions generates carbohydrate craving
in adults as part of the coping response to states of anxiety. This
phenomenon is more common in genetically vulnerable adults.
The distress that induces eating is highly prevalent in obese
adults but has a low prevalence in young children. That is why it
255
has been suggested that most children exhibit the natural
biological response to distress (loss of appetite) because the
normal distress response is associated with physiological re-
actions that are designed to prepare the individual for fight or
flight, thereby suppressing the feelings of hunger and satiety. It
has been suggested that emotional eating can be acquired as a
result of inadequate parenting, which would have lasting effects
on the neurobiologic response to stress. This may include a
hypoactivation of the HPA axis, with reversed neurovegetative
symptoms: hyperphagia and weight gain. These changes usually
do not appear before puberty [18].
A restrictive mother–child feeding style has been associated
with higher levels of consumption in the absence of hunger and
with increased intake of restricted foods when free access to
them is permitted [32].
One study showed that carriers of the A1 allele of the dopa-
mine D2 receptor (DRD2) gene Taq1A polymorphism have
reduced availability of these receptors in the brain. Another
study found that adolescents exposed to adverse experiences
who develop emotional eating carry at least one DRD2 A1 allele.
This suggests that the relationship between adverse experiences
and the development of emotional eating can depend on a
genetic substrate [33]. The short (S) allele of the serotonin
transporter gene (5-HTTLPR) also has been associated with this.
The S allele, compared with the long (L), can give a genotype that
is more susceptible to stress and the consequent emotional
eating [34].
It has been observed that individuals who are both restricted
in their eating and vulnerable to uncontrolled eating are par-
ticularly susceptible to having negative emotions affect their
intake [35].
The gene–environment hypothesis places importance in the
management of obesity to upbringing, emotional education, and
the teaching of coping mechanisms, especially in individuals
with genetic vulnerability.
Discussion
The results of this review, although only focused on carbo-
hydrate craving, allow us to begin to understand the neuro-
biologic mechanisms that individuals and clinicians must
overcome when attempting to achieve behavioral changes to
address the obesity epidemic [1,2].
The first group of studies, which focus on the role of the
serotonergic pathways, link mood levels with a disposition to
seek carbohydrates [11,12]. These studies also imply a lapse in
time between carbohydrate consumption and the effects on
mood that are inconsistent with reports that symptoms of anx-
iety subside [17,18]. In short, although the serotonergic hypoth-
esis is attractive because it relates the consumption of
carbohydrates with an appetite for carbohydrates and with some
psychiatric conditions, it does not allow for a proper under-
standing of the carbohydrate-craving phenomenon.
Alternatively, the association of mechanisms underlying pal-
atability with an intense hedonic response that reinforces the
motivational systems is in agreement with the rapid changes in
emotional symptoms observed after consumption of carbohy-
drates [16,17,19]. Such association also may be compatible with
the eventual reinforcement of sugar consumption, which would
lead to cravings and potentially addiction [5,6]. It must be added
that the normal response to stress further enhances the hedonic
response following carbohydrate consumption, enhancing be-
havioral reinforcement under conditions of stress [12,30,33]. In
other words, it is necessary to consider at least these lines of
256 T. Ventura et al. / Nutrition 30 (2014) 252–256
research: palatability and hedonic response, motivational sys-
tems, and stress systems, in order to gain further understanding
of the complexity of the system.
On the one hand, it also must be taken into account that
human have evolved in an environment with a relative scarcity
of resources [2,36], where obtaining vital resources is a key
objective. In this regard, identifying the most efficient nutrients
is a fundamental adaptive capacity [2,36]. Their consumption
triggers a pleasurable response, which, by acting on motivational
systems, will seek repetition, as with everything else that is
biologically desirable. Thus, carbohydrate craving appears to be
part of a biologically conducive system. If we add stress response,
which also is evolutionarily selected through phylogeny, the
power of this aforementioned circuit increases, probably because
of the possibility of quickly storing available energy resources in
order to face aversive stimuli [2,36]. Consequently, we can posit
that the carbohydrate-craving mechanism for maintaining
emotional homeostasis could have been evolutionarily selected
due to its environmentally adaptive functions.
Of course, there are certain genes that might increase
vulnerability to this phenomenon. For example, it could be
suggested that individuals with higher reactivity to cortisol or
the carriers of the A1 allele of the dopamine DRD2 receptor [33]
or the S allele of the serotonin transporter gene [34] could be
more vulnerable to presenting a craving for carbohydrates, this
effect being amplified in the presence of psychiatric disorders.
As a result of this review, it is clear that carbohydrate craving
involves systems that were neurobiologically selected thr-
oughout our evolutionary history to sustain life. It is for this
reason that confronting this phenomenon will require much
more from clinicians and public health specialists than mere
indications or restrictions that will be difficult to sustain in an
environment of a plentiful food supply. Long-term education
campaigns could be required to encourage people to change
their habits, creating a culture that is able to modulate or modify
people’s spontaneous behavior [1,2,28]. Moreover, research
opens the door to the use of pharmacologic strategies both to
trick palatability systems, with carbohydrate substitutes, for
example, and to decrease hedonic response, acting on opioid or
other pathways [5,21].
We understand that this review has a number of limitations;
for example, it does not cover other foods that have been shown to
be the subject of potential abuse and dependence, like fat and salt
[6]. Although research in this area is under development, it has
been possible to illustrate the complexity of the carbohydrate-
craving phenomenon and the potential neurobiologic barriers to
overcome in order to achieve substantial changes in people’s
nutritional behavior. We hope that future advances in the study of
neuroscience associated with carbohydrate craving may help
clarify the hypotheses described here because they are comple-
mentary. Therefore, new findings should offer greater coherence
to the models currently under development.
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