File Name: stress eating and the reward system .zip
Miguel Alonso-Alonso, Stephen C.
The changes in eating patterns that have occurred in recent decades are an important cause of obesity. Food intake and energy expenditure are controlled by a complex neural system involving the hypothalamic centers and peripheral satiety system gastrointestinal and pancreatic hormones. Highly palatable and caloric food disrupts appetite regulation; however, palatable foods induce pleasure and reward. The cafeteria diet is such a palatable diet and has been shown consistently to increase body weight and induce hyperplasia in animal obesity models.
Moreover, palatable high-fat foods such as those of the cafeteria diet can induce addiction-like deficits in brain reward function and are considered to be an important source of motivation that might drive overeating and contribute to the development of obesity. The mechanism of neural adaptation triggered by palatable foods is similar to those that have been reported for nondrug addictions and long-term drug use. Thus, this review attempts to describe the potential mechanisms that might lead to highly palatable diets, such as the cafeteria diet, triggering addiction, or compulsion through the reward system.
Currently, an important cause of obesity has been observed to be related to changes in eating patterns that have occurred in recent decades [ 1 ]. The daily consumption associated with so-called Western diets consists of highly palatable and caloric food [ 2 ], and such diets have become a habit that has led many individuals to develop obesity [ 3 ].
Recent studies using the cafeteria diet as an experimental model of obesity with or without associated chronic stress have shown that animals exposed to this diet became obese and exhibit important changes in lipid profiles, endocrine appetite markers, and the development of hyperphagia [ 4 , 5 ]. Food intake and energy expenditure are thought to be controlled by complex neural systems, and the hypothalamus has been recognized as the center of homeostatic regulation for review see [ 6 ] ; however, palatable foods, such as those of the cafeteria diet, can lead to impairments of normal appetite regulation [ 7 ].
In addition, palatable food disrupts appetite regulation and induces pleasure and reward. Excessive consumption of palatable energy-dense food can lead to a profound state of reward hyposensitivity that is similar to that of drug abuse that can lead to the development of compulsive-like eating [ 8 ].
Based on recent evidence that suggests that nondrug addictions might lead to neural adaptations similar to those that have been reported with long-term drug use, this review attempts to describe the putative mechanisms that might lead to the triggering of addiction or compulsion by highly palatable diets, such as the cafeteria diet, through the reward system. Food control is a complex mechanism that involves the appetite, motivation, and energy demands of the organism and these aspects can be modified by food availability and exposure.
The central nervous system detects a wide variety of peripheral neural and humoral markers, and this complex neural network receives endocrine and hormonal inputs. Hormones, such as leptin, insulin, pancreatic polypeptide PP , amylin, ghrelin, cholecystokinin, glucagon-like peptide GLP-1 , and oxyntomodulin, coordinate food intake through signaling and modulation in orexigenic and anorexigenic neurons for review see [ 9 ].
These markers reflect gastrointestinal functions and energy needs, including taste, which is a central factor in decision-making related to feeding behavior, and the olfaction. Both functions are capable of discriminating features such as odor, texture, and temperature and participating in the choice of food to be ingested [ 10 ].
The homeostasis regulation and maintenance of stable body weight depend on the integration of these signals and on the ability to respond appropriately through modulation of energy expenditure and food intake [ 11 ].
Hypothalamic centers control food intake and weight gain and are part of a complex of neuroregulatory interactions that include the peripheral satiety system gastrointestinal and pancreatic hormones and a large-scale central neural network [ 12 ]. The importance of the hypothalamus in energy homeostasis was first suggested by classic lesioning experiments performed rodents, and subsequent studies suggested the roles of hypothalamic nuclei, such as the arcuate nucleus ARC , paraventricular nucleus PVN , ventromedial nucleus VMN , dorsomedial region DMV , and lateral hypothalamic area LHA , in energy homeostasis [ 13 ].
The blood-brain barrier BBB adjacent to the ARC region serves as the interface of the peripheral metabolic signals and the brain. While the DMV area is the region of satiety, the LH nuclei are the main controllers of feeding responses [ 14 ]. Damage to the hypothalamus, particularly the lateral and dorsomedial hypothalamus, disrupts feeding behavior [ 15 ].
Food intake and energy metabolism are regulated by a complex interaction between orexigenic and anorexigenic neuropeptides in the ARC of the hypothalamus and peripheral tissues. The hypothalamic nucleus receives inputs of several peripheral hormones including leptin; for example, the arcuate nucleus of the hypothalamus and the area postrema of the nucleus tractus solitarius express leptin receptors and are important regions of appetite control and food ingestion.
Leptin is a hormone that is synthesized and released by adipose tissue and acts as food control in the ARC of the hypothalamus. The combined effect of the actions of leptin suppresses appetite and contributes to the maintenance of energy homeostasis for review see [ 17 ]. Another important hormone that is related to food control is ghrelin.
This hormone is produced by the stomach, hypothalamus ARC and infundibular nucleus , and pituitary gland. In addition to acting on dietary control, both leptin and ghrelin are involved in the reward system [ 17 , 18 ].
Leptin receptors are also found in the mesolimbic pathway in the reward-associated ventral tegmental area VTA and the substantia nigra [ 19 ]. Thus, leptin influences the hedonic aspects of feeding and interacts with the mesolimbic-dopaminergic system, which is known to regulate arousal, mood, and reward for review see [ 17 ] , while ghrelin stimulates dopamine neurons in the ventral tegmental area VTA and promotes dopamine turnover in the nucleus accumbens of the ventral striatum, which is part of the major central reward pathway for review see [ 18 ].
Accordingly the balance between food control centers and peripheral signals determines appetite and energy expenditure and influences the reward system. Palatable foods with high fat and sugar contents are associated with increased food intake [ 7 , 20 ]. Palatable foods alter the behavior of experimental animals. In a study of obese rats with histories of extended access to palatable food, the rats were found to continue to eat palatable food even in the presence of a noxious light cue that predicted the delivery of an aversive foot shock [ 7 ].
Moreover, mice that have previously had access to a palatable high-fat diet spend more time in an aversive environment to obtain the palatable food than do mice with no prior experience of the diet [ 21 ]. Highly palatable foods activate the reward system to affect feeding behavior [ 22 ]. From evolutionary perspective, these foods that are high in fat and sugar are more attractive because they can be quickly converted into energy [ 23 ].
The consumption of these foods over a long period of time can be compared to drug addiction [ 24 ] mainly because these foods generate progressive increases in food intake [ 25 ] that lead to a phenomenon that is comparable to the adaptation triggered by drugs [ 26 ].
In addition, the macronutrients of the palatable food can stimulate the brain reward systems independently of their caloric value [ 27 ]. High levels of consummatory behavior are induced by drugs abuse such as cocaine or nicotine despite the fact that these drugs are devoid of caloric or nutrient value [ 28 ]. Extended access to palatable high-fat food, such as the cafeteria diet, can induce addiction-like deficits in brain reward function that are thought to be important sources of the motivation that might drive overeating and contribute to the development of obesity [ 8 ].
The cafeteria diet is one of many animal obesity models and involves a palatable diet that uses the human foods, such as biscuits, wafers, condensed milk, sausages, and soft drinks. These foods have high sugar, salt, and spice, contents that make them highly palatable, and palatability is critical for determining food preference [ 29 ]. Moreover, this diet has been shown to consistently increase body weight, induce hyperphagia, and alter the metabolic factors related to the metabolic syndrome cluster [ 2 , 4 — 6 , 20 , 30 , 31 ].
Indeed, this diet is one of the factors that has contributed to rapid increase in obesity over the past thirty years [ 32 ]. The cafeteria diet mimics modern patterns of human food consumption and was adapted from a diet that is also known as the Western diet and was previously described by Estadella et al.
Preference for the cafeteria diet over standard chow has been shown in studies with obesity models [ 2 , 32 , 33 ]. Furthermore, the cafeteria diet, along with other palatable diets, acts on many neurotransmitter systems and can lead to changes in the reward system [ 2 ]. Brain regions, such as the lateral hypothalamus LH , nucleus accumbens NAc , ventral tegmental area VTA , prefrontal cortex PFC , and amygdala, are activated in response to palatable food.
There is also a connection between the nucleus accumbens NAc and the lateral hypothalamus LH that is important for energy homeostasis for review see [ 7 ]. The LH is also functionally connected to other cortical and limbic brain sites that have been implicated in organizing and directing behavior toward obtaining palatable food. LH damage abolishes the stimulatory effects of NAc manipulations on food intake, while inactivation of the NAc enhances the activity of the LH, particularly LH neurons [ 34 ].
The NAc is a brain region that seems to play a crucial role in behavior related to feeding and drug reward [ 35 ]. This structure is considered to serve as an interface of emotion, motivation, and action based on its numerous inputs from the amygdala, prefrontal cortex PFC , and hippocampus for review see [ 36 ]. The NAc receives information from the brain stem in response to ingested food through a connection with the nucleus of the solitary tract for review see [ 36 ]. The NAc receives information from the brain stem in response to ingested food through a connection with the nucleus of the solitary tract for review see [ 37 ].
It is important to note that nucleus accumbens has been subdivided into medioventral shell NAcs and a laterodorsal core NAcc in accordance with morphological features, and its different projections were studied with tract-tracing methods.
Thereby depending on the specific places of the nucleus accumbens where dopamine transmission is released, different behavioral responses can be triggered [ 38 , 39 ]. In addition, the amygdala is a key structure for the processing of emotions and integrates food-related sensory and physiological signals from the hindbrain and cortex for review see [ 36 ].
The amygdala connects external and internal sensory information with the motivational systems of the brain and sends input to the NAc.
The hippocampus has crucial roles in memory formation and in the control of food intake, while the prefrontal cortex PFC is responsible for higher-order cognitive processing, planning, and decision-making.
The PFC receives input from insular cortical regions that relay gustatory information and has an important influence on NAc signaling. The neurons that connect the brain regions involved in reward behavior are related to many neurotransmitter systems. Moreover, studies have shown that dopamine, endogenous opioids, and serotonin are highly related to drug and food addiction for review see [ 7 ]. Dopamine DA is a neurotransmitter that has been more extensively implicated in the mechanism of drug addiction due to its influence on neuroadaptation and psychostimulant reward process [ 40 ].
Studies employing microdialysis technique showed that addictive substances increase extracellular dopamine DA release in the NAcc [ 37 ] and the changes in dopamine transmission in the NAcs and NAcc in response to appetitive and consummatory behavior motivated by food [ 38 ]. Dopaminergic neurons are located in the midbrain; they send their axons through the medial forebrain bundle and innervate wide regions within the systems while dopaminergic reception and the intracellular signaling are mediated through the two major subtypes of G protein-coupled DA receptors [ 41 ].
It is important to consider that dopamine receptors regulate signaling cascades on cells that can alter the transcription of genes and can trigger neuroadaptative and behavioral changes on brain structures with changes in protein synthesis. This way, the learning theories of addiction postulate that some psychostimulant substances are engaged on molecular mechanisms implicated in learning and memory as D1 receptors and downstream intracellular messenger cascades that may cause synaptic rearrangements.
Likewise, these substances induced dopamine release and may alter learning-related molecular changes by activating common signal transduction pathways. Several studies showed that psychostimulant substances are related to memory consolidation, and it suggests that addiction is due to drug-induced neuroadaptations in reward-related learning and memory processes in the NAcc [ 42 ]. The corticolimbic pathways that are responsible for reward-associated feeding behavior include the ventral tegmental area, insular cortex, anterior cingulate cortex, orbitofrontal cortex [ 13 ], substantia nigra, amygdala, prefrontal cortex, posterolateral ventral striatum globus pallidus and putamen , and anteromedial ventral striatum nucleus accumbens and caudate nucleus [ 17 ].
The mesolimbic and the mesocortical pathways regulate the dopamine DA systems effects on reward-related behavior, and modifications of these systems are associated with the rewarding effects of drugs and food [ 45 ]. Drug abuse and palatable food with high fat and sugar content can significantly activate the DA reward circuitry, and both increase dopamine levels in the mesolimbic system and dopaminergic transmission in the NAc [ 45 ].
However, DA responsiveness is different among these structures and it depends on hedonic, taste, and novelty stimulus. In addition, single exposure to palatable food in NAcs promptly induces habituation of DA responsiveness, consistent with a role in associative learning. It is important to note that mild food deprivation can impair habituation of NAcs DA responsiveness to palatable food. It has been suggested that DA release in this region is not the cause but consequence of the food reward.
The taste properties of food can have good or bad postingestive consequences which are related to DA release of NAcs after food intake [ 46 ]. It should be noted that dopamine is associated with reward related to food intake and the behaviors required to maintain feeding for survival. These peptides might change the frequencies or patterns of the action potentials generated in the dopaminergic cells of the VTA or induce downstream DA release in the NAc [ 14 ].
Chronic drug abuse induces dopaminergic stimulation that results in impaired inhibitory control, compulsive drug intake, and enhanced emotional reactivity to drugs. Similarly, repeated exposure to high fat and sugar content foods results in compulsive food consumption, poor control of food intake, and food stimulus conditioning [ 48 ].
Midbrain dopamine transmission influences palatable food intake in humans. The dopamine pathway is activated in humans and laboratory animals in response to palatable food and appetitive food-related cues. In addition, leptin, ghrelin, and other regulators of appetite influence the activity of system, which suggests that the midbrain dopamine systems play an important role in palatable food consumption for review see [ 34 ].
Indeed, dopaminergic pathways are heavily involved in the reward system. Dopamine neurons in the VTA send axonal projections to the amygdala, nucleus accumbens, and prefrontal cortex.
The projections of the dopaminergic system from the amygdala and prefrontal cortex to the lateral hypothalamus, as shown in Figure 1 , are directly involved in food control [ 34 ]. The endocannabinoid and opioid systems have wide receptor distributions within the CNS and play important roles in reward-related feeding [ 50 , 51 ].
Morphine has a strong rewarding effect and addiction liability. Moreover, morphine enhances the frequency of the firing of mesolimbic dopamine neurons in the VTA and increases dopamine turnover in the NAc, which confirms the excitatory effects of opioids on the dopamine system [ 55 — 57 ].
Regarding the cannabinoids, evidence suggests that the cannabinoid-1 CB1 receptor has a role in the rewarding aspects of eating. The peripheral administration of CB1 antagonists reduces the intake of palatable sugar in rats [ 58 , 59 ]. Cannabinoid receptor CB1 antagonist administration prevents the orexigenic effect of the endocannabinoid agonist anandamide on food intake [ 60 ].
The changes in eating patterns that have occurred in recent decades are an important cause of obesity. Food intake and energy expenditure are controlled by a complex neural system involving the hypothalamic centers and peripheral satiety system gastrointestinal and pancreatic hormones. Highly palatable and caloric food disrupts appetite regulation; however, palatable foods induce pleasure and reward. The cafeteria diet is such a palatable diet and has been shown consistently to increase body weight and induce hyperplasia in animal obesity models. Moreover, palatable high-fat foods such as those of the cafeteria diet can induce addiction-like deficits in brain reward function and are considered to be an important source of motivation that might drive overeating and contribute to the development of obesity. The mechanism of neural adaptation triggered by palatable foods is similar to those that have been reported for nondrug addictions and long-term drug use.
The reward-based eating drive scale: a self-report index of reward-based eating. Plos One 9 6 : EE, Associations of parental feeding practices and food reward responsiveness with adolescent stress-eating. Appetite , An experimental examination of the effort-reward imbalance model of occupational stress: Increased financial reward is related to reduced stress physiology. Biological Psychology ,
Have you ever found yourself craving certain foods when you are feeling stressed? Stress eating, also known as emotional eating, is eating in response to how you are feeling rather than hunger. The more comforting the comfort food, the better we feel. A habit of stress eating can lead to weight gain and serious health concerns over time. In a study by M. Tyron, researchers discovered that high-sugar foods can also lessen the stress response.
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