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