Comparison of binge-eating disorder and food addiction

Abstract

In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, binge-eating disorder (BED) is classified as episodes of binge eating while not being hungry, eating too fast until feeling uncomfortably full, or eating in solitude with feelings of shame and disgust after eating, without compensatory mechanisms. The controversial disorder food addiction (FA) is characterized by overconsumption, cravings, failure to cut down on amounts of food, and withdrawal and tolerance to overeating. In this narrative review, we aimed to comprehensively characterize and compare BED and FA. We searched PubMed using the keywords “binge-eating disorder” and “food addiction.” We finally included 51 publications according to topic specificity, credibility, the authors’ reputation, and non-bias criteria. BED is characterized by concerns about dietary issues, body shape, and weight as well as depressive symptoms and brooding rumination. FA can be divided into substance addiction and behavioral addiction, which can be differentiated using a list of criteria including hunger, taste, pleasure, function of food, loss of social connections, weight concerns, and awareness about the disorder. Further research is needed to further characterize and distinguish BED and FA.

Keywords

Binge eating disorder food addiction substance addiction behavioral addiction narrative review obesity

Introduction

In the current global obesity epidemic, bariatric surgery is still considered one of the most effective weight loss tools to date. However, a considerable percentage of patients who undergo bariatric surgery will regain the lost weight owing to uncontrolled eating, a minor form of bariatric binge-eating. This underlying psychopathology must be addressed prior to undergoing bariatric surgery. However, because binge-eating disorder (BED) and food addiction (FA) are fairly new additions to the psychiatric literature, it remains difficult to properly categorize these disorders, which share many common features.¹

BED can be considered a newly recognized disorder because it has been recently added to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) and the DSM-V, with some minor changes. BED can be diagnosed on the basis of recurrent binges, where a large amount of food is ingested in a small time window, accompanied by feelings of loss of control, guilt, and shame after the incident, abdominal distension, anxiety surrounding the event, and with no compensation (e.g., laxative use, purging, fasting, excessive exercise). Binge eating is often encountered in patients with bulimia nervosa. The DSM-V further specifies that episodes of BED occur at least once per week for 3 months, and the disorder can be categorized according to severity as mild (1–3 binges/week), moderate (4–7 binges/week), severe (8–13 binges/week), and extreme (≥14 binges/week). Additionally, the remission process can be mapped into partial (one binge/week) and full remission (no bingeing over an extended period of time).²

Addiction is a well-known term, but FA is not officially recognized among addictions. Unlike substances such as drugs and alcohol, foods that can potentially be addictive (as in a hyperpalatable diet with high fat and high sugar) also contain nutritive or caloric value for the body. Because foods can have not only pleasure value but also nutritive value, it is difficult to pinpoint the exact substances that cause FA. For these reasons, the disorder has not yet been officially recognized. However the Yale Food Addiction Scale (YFAS) has shown promising results in measuring FA with symptoms similar to those of other substance addictions (risky use of the substance, social withdrawal owing to substance use, tolerance to the substance, withdrawal symptoms, repeated attempts to quit, and physical and psychological changes). Electroencephalogram studies have shown a correlation between FA symptoms according to the YFAS and substance use disorders, with three or more FA symptoms usually present. It is concluded that FA and alcohol dependence share not only genetic, cellular, and behavioral aspects but also a common neurophysiological substrate.^3–6

Both BED and FA share overlapping features and are fairly newly described. Therefore, it is important to further classify and categorize these disorders to help in treating patients, especially those undergoing bariatric surgery. Therefore, the aim of this narrative review was to provide an overview and comparison of these disorders that can assist physicians in the diagnostic evaluation of eating disorders and addictions.

Methods

In this paper, we focused on BED in relation to FA in the form of a narrative review. We searched PubMed in August 2022 using the keywords “BED,” “BED and food addiction,” and “food addiction” for publications in English and German language (Figure 1). Over 100 papers were identified. We selected only those deemed acceptable for inclusion based on topic specificity, credibility, author reputation, and non-bias criteria.

Figure 1.

Flow chart of literature search and selection.

No ethics approval and patient consent were needed in this comprehensive narrative review. This study was based purely on existing findings published in the scientific literature, together with the authors’ own clinical experience.

Results

The results of our literature search and screening yielded 51 publications that were eligible for inclusion in the present narrative review. Most selected studies were experimental studies as well as systematic literature reviews and meta-analyses.

Food addiction (FA)

Merriam-Webster defines addiction as a “compulsive, chronic, physiological or psychological need for a habit-forming substance, behavior, or activity having harmful physical, psychological, or social effects and typically causing well-defined symptoms (such as anxiety, irritability, tremors, or nausea) upon withdrawal or abstinence.“⁷ After its addition to the DSM-V, it is now accepted that addiction can be divided into substance (e.g., alcohol, opioids) and behavioral (e.g., gambling, internet) addictions, which have similar symptoms and consequences such as loss of social connections, repeated attempts but failure to cut down on use or consumption, and irritability when not being able to go through with the action.^8–10

FA remains a controversial disorder that is not yet officially recognized. FA might also comprise substance and behavioral addiction. According to her experience in clinical practice with a large subgroup of obese patients, Bak-Sosnowska wrote that the “differential criteria for BED and FA in the context of causes and treatment of obesity” could distinguish patients who were “addicted to the act of eating itself” rather than to the specific type of food ingested. This suggests that certain people crave quantity rather than a specific substance within the food, which naturally brings about a two-fold problem. Through habituation, individuals seeking a specific substance within a food could develop a behavioral pattern or addiction and over time, individuals who originally sought quantity rather than a particular substance could become dependent on a certain substance (e.g., sugar) within the food that was unknown to them.¹¹

Animal studies have shown that sucralose (sweetener with nutritive value) given orally causes dopamine efflux in the ventral striatum whereas glucose (hedonistic ingredient, generally preferred by animals) given intragastrically causes dopamine release in the dorsal striatum. This illustrates a definite distinction between pleasure arising owing to taste versus caloric and nutritive value in different brain regions.^12–14 Tellez et al. hypothesized that sweetness rather than the nutritive value will lead to bingeing when given intermittent access to it.¹⁵ It is generally believed that the consumption of sugar causes dopamine release in the mesolimbic system, further causing the subject (in these studies, mice) to specifically seek out sugar. Potentially, the switch from the ventral (which would be cue-driven) to the dorsal striatum (which would be outcome-driven) could be responsible for the formation of habits regarding seeking out a specific substance.^13–18 Dopamine is produced in anticipation of reward and opioids as confirmation of ingestion of the actual substance.^13,18 Furthermore, sugar-bingeing rodents exhibited withdrawal symptoms similar to those of opioid withdrawal after administration of the opioid antagonist naloxone, including anxiety, teeth chattering, forepaw tremor, and head shaking when the anticipatory reward was not met with the actual reward (release of opioids).¹⁶ Lenoir et al. best elucidated the addictive nature of sugar in his famous study where rodents chose saccharin over cocaine.¹⁷ Of all other potential causes of substance FA, sugar has been shown to cause bingeing patterns, withdrawal symptoms, craving, and sensitization.^13,18 However, in studies by Heinsbroek et al. as well as Gianotti et al., rodents exhibited a higher motivational drive for heroine; the rodents viewed heroine as an essential item and food as a “luxury” item. Despite this, approximately 50% of rodents in the study by Gianotti et al. showed a preference for food, but the preference was for food pellets rather than sucrose, which is often used in other studies. This is a highly interesting finding as food pellets would not be generally considered palatable, yet some animals showed a preference for the pellets; this will be discussed in greater detail below.^19,20

The “reward deficiency theory” lays the ground for the notion that dopamine release will occur regardless of whether a food is hyperpalatable, especially because taste is ultimately subjective; this balances dopamine levels in the brain in dopamine-deficient individuals. The fact that taste is individual was observed in mice lacking glucagon-like peptide 1 receptor, which increased sensitivity to umami flavor and decreased sweetness sensitivity. The anticipatory reward of dopamine could still potentially be met with the actual reward of opioid release if certain hedonic hotspots were already present (as a reinforcement).^13–19

We can therefore hypothesize that habits are created when strengthening and repeating the expected reward and its dopamine release is met with the actual reward and its opioid release, thereby creating habituation and switching from the ventral striatum (outcome-driven) to the dorsal striatum (cue-driven). Varying degrees of personal sensitivity can be observed among certain individuals who are more cue-reactive than others.¹³

Preliminary neuroimaging studies have compared the consumption of hyperpalatable food and food cues in individuals diagnosed with FA and healthy control groups. Differences have been identified in the brain reward circuits of these two groups, particularly in regions such as the nucleus accumbens, amygdala, insula, orbitofrontal cortex, and striatum. Additionally, differences have been identified in the hypothalamus, which regulates eating behaviors. Like most addictive behaviors, FA is driven by mood and impulsivity. Hypothalamic–pituitary–adrenal (HPA) axis functioning can be negatively affected by chronic stress and might lead to an increased desire to immediately consume hyperpalatable food.⁶

Binge-eating disorder (BED)

As defined by the International Classification of Diseases 11th Revision (ICD-11), BED is characterized by the ingestion of an abnormally large quantity of food in a specified time window with feelings of loss of control, the absence of compensatory mechanisms (e.g., laxative use, purging), missing an association between BED and other disorders that would explain the phenomenon (e.g., Prader–Willi syndrome, major depressive disorder), anxiety surrounding the event, and feelings of guilt and shame.²¹

Patients with BED tend to have concerns about their weight, shape, and body to a great extent, although they do not participate in the compensatory mechanisms observed in patients with bulimia nervosa. Stice et al. subdivided patients with BED into a dietary subcategory and dietary/depressed subcategory.²² The dietary subgroup exhibited increased levels of body dissatisfaction (comparing the current situation to an ideal, perfect image of self), checking body status (by pinching fat, weighing themselves, or taking other measurements), avoidance behaviors (such as wearing loose clothing or avoiding places of “judgment“ such as swimming pools), and idealization of thin bodies and perfectionism.^23–25 It was further shown that patients with BED display cognitive bias regarding attention (focusing on disagreeable rather than agreeable areas), memory (focus on weight and shape-related content in speech), and interpretation (wrongly interpreting information).²⁵ Alongside a high level of impulsivity (negative impulse control) and cue-reactive attention, these biases are believed to lead to bingeing.^13,26 Patients with BED also show a high level of brooding rumination (excessively thinking about weight and shape in a pessimistic fashion) rather than reflective rumination (thinking about finding solutions). The dietary/depressed subgroup exhibits the same mental dietary preoccupation, with additional features such as increased interpersonal sensitivity, negative urgency, alexithymia, and lower emotional regulation strategies. It is therefore believed that rumination regarding body, weight, and shape, together with bad mood, bottles up within patients who have BED until a certain “trigger“(such as in the case of realistic body image versus ideal body image) leads to a binge, which causes short-term relief upon giving in to the urge; however, this relief is quickly replaced by feelings of disgust and shame after the event.^22,27–29

Binge eating as such might be genetically determined to a certain extent; specific vulnerabilities are shown to be risk factors for the development of binge eating. This can be observed in Prader–Willi syndrome, for example, where polymorphism of the CYFIP1 (cytoplasmic FMR1-interacting protein 2) protein leads to hyperphagia. Another example is deletion of the CSNK1E (casein kinase 1 epsilon) gene, which also increases bingeing episodes.^30–32 Moreover, women tend to have a higher risk of BED, which has been hypothesized to be owing to the action of progesterone and particularly estrogen. This is interesting because estrogen is linked to the inhibition of food intake and body weight regulation in a cyclical pattern. However, a study by Babbs et al. showed that exposure to 2-hydroxyestradiol in ovariectomized rats led to escalating bingeing patterns over time. Chronic exposure to 2-hydroxyestradiol has therefore been referred to as “learning to binge,“ which is believed to be owing to the inhibited degradation of dopamine and/or its enhanced D2 receptor actions.^33–35 Furthermore, Hildebrandt et al. demonstrated hypofunction in the dorsolateral striatum of female mice with chronic binge eating.³⁶

Another factor affecting binge episodes is stress. Stress has long been shown to affect eating behavior in rodents, which is tightly linked to the HPA axis. This has been especially demonstrated with higher levels of plasma corticosterone and increased expression of corticotropin-releasing factor mRNA in the paraventricular nucleus of the hypothalamus in rodent models. This is hypothesized to increase the craving and urge for hyperpalatable foods rich in sugar and fat. A study by Mena et al. showed that overfeeding carbohydrates might be a consequence of activation of the prefrontal cortex by stress.^6,13,35

To mimic or bring about binge eating, most animal models make use of previous food restriction, limited access to palatable food (provided on only one day in a week), intermittent access to the food when provided (e.g., only on Mondays, Wednesdays, and Fridays for 2 hours), or stressors such as the forced swimming test to mimic loss of control or frustration and rewards in the form of palatable foods rich in sugar and fat. However, sometimes regular food pellets or chow can serve as the reward, which would not be traditionally termed palatable food; yet several studies have shown that rodents can have preferences for and/or binge-like episodes with these foods.^37,38

Despite a vast body of literature on the neurobiological basis of BED, differentiation between BED and FA has rarely been made in previous studies. Most studies compare cravings and withdrawal symptoms owing to hyperpalatable foods with an opioid-related addiction.^13,38 These comparisons are generally more relevant to FA rather than BED. Moreover, patients with BED tend to overeat to ease mental afflictions (dietary and/or depressive symptoms), as mentioned above, rather than seeking out a specific substance or taste. Although no conclusions can yet be made, even regarding the similar underlying neurobiological bases of these disorders, the clinical manifestations of BED and FA clearly vary (see Table 1).^{2,11,22,24,39–42}

Table 1.

Similarities and differences between binge eating and food addiction.

Similarities	Differences
Eating a large quantity of food in a short amount of time	Patients with BED typically exhibit episodes of disturbed behavior whereas patients with FA tend to show a continuous pattern of disturbed behavior
Difficulty controlling urges; feeling craving or an urge to eat that seems impossible to control	Patients with BED tend to eat so as to ease mental afflictions because giving in to the compulsion induces a short-term lived sense of pleasure; patients with FA desire a particular substance or quantity (overeating)
Absence of hunger before a binge takes place	Patients with BED are often concerned about their body weight and shape and are usually quite self-aware about body proportions and food portion sizes; patients with FA tend to deny or project their disordered behavior as a psychological defense mechanism
Overindulgence in food, long past hunger	Patients with BED overeat in solitude during their free time whereas patients with FA neglect social connections to overeat or even overeat in the presence of others
Short-term improvement in mood after a binge	Patients with BED tend to favor situations that prevent binges whereas patients with FA can exhibit aggressive or anxious behavior when they cannot binge
Abdominal distention/bloating after a binge; ingestion of food even though the patient is aware of its adverse effects	Patients with BED do not exhibit typical addiction symptoms whereas patients with FA show tolerance and withdrawal symptoms, as well as the neglect of social connections, abandonment of other activities, and other symptoms
Trying to quit the behavior but ultimate failure to do so	Patients with BED tend to feel guilt or shame after bingeing whereas patients with FA do not
Physical/psychological/social consequences	–
Emotional instability	–
Increased impulsivity	–

BED, binge eating disorder; FA, food addiction.

Discussion

As laid out above, BED and FA involve a variety of overlapping symptoms and behaviors, such as overindulgence in food long past hunger, absence of hunger to begin with, short-term improvement of mood after indulgence, abdominal distension after overeating, cravings, trying to quit but failing, physical/psychological/social consequences, emotional instability, and increased impulsivity.⁴⁰

Bak-Sosnowska provided a distinction between BED and FA based on 13 factors: course, hunger, taste, pleasure, function of eating, lack of food, other activities, other people, awareness, feeling guilty, body concern, body mass, and the typical symptoms of addiction. With respect to the course of the disorder, patients with BED tend to exhibit episodic patterns of behavior (recurrent attacks) whereas patients with FA show continuously disordered behavior. Furthermore, hunger is absent in both cases, but patients with FA will crave particular foods, according to Bak-Sosnowska; however, someone addicted to the behavior of eating larger quantities of food (behavioral FA) rather than a particular substance (substance FA) would not necessarily crave a specific food but would care instead about the quantity of food presently available. A distinction on the basis of taste can also be made, which suggests that patients with BED do not care about the taste of the food ingested but rather about the quantity; this further suggests that patients with FA will select specific items according to a preferred taste. This latter finding is also supported by the study of Tellez et al. where rodents showed a preference for sweetness rather than nutritive value.^11,15 Interestingly, Goodman et al. also showed that groups with greater sweet preference had more episodes of binge-eating behavior.⁴¹ This is valid, but it should be added that even in the case of behavioral FA, quantity rather than taste will be valued. The rodent data are still unclear in terms of “glucose/sucrose/fructose use disorder.” Hildebrandt et al. have provided sufficient evidence at least for classification of “eating addiction” as a behaviorally based addiction rather than a “food addiction” as in chemical dependence.³⁹

Regarding the function of eating, binge eaters will eat to ease mental tension (surrounding weight, shape, failed perfectionism) whereas in the case of food addicts, foods only serve a hedonic purpose.^11,22,24 This hedonism would hypothetically be the same in substance addiction and behavioral addiction. The same can be said about the “lack of food.“ Patients with BED will interpret situations without access to food as positive and those with FA will respond to such “threats“ with anger, aggression, and irritability. In terms of other activities, Bak-Sosnowska stated that overindulgence in foods occurs in patients with BED during their free time whereas patients with FA will cancel plans and give up social connections so as to overeat. This would also hypothetically be the same in substance and behavioral addiction, as is true in most addictions.^9,42 However, the presence of other people during such binges/attacks/events do not matter to food addicts (because they do not experience the same amount of guilt and shame as do patients with BED) whereas binge eaters prefer solitude during these occurrences. Like in most addictions, patients with FA are unaware or unwilling to admit to their problem and will deny, project, and wrongfully assess the actual extent of their psychopathology. In contrast, their counterparts with BED are quite aware of the abnormally large portion sizes and other aspects of their addiction.¹¹ As mentioned in the definition of BED above, binge eaters will feel substantial feelings of guilt and shame after a binging event, unlike food addicts who experience no consequences in terms of their mood or self-esteem as long as the system of self-delusion remains active. Another distinguishing feature is binge eaters’ concern over the shape and weight of their body as well as commonly having increased body mass, which has been reported in several studies, notably by Stice et al.^22,24,43 However, patients with FA commonly do not care about or admit to having increased body mass and generally show a lack of concern regarding their body shape. Finally, the most distinguishing features present in FA but lacking in BED are typical symptoms of addiction, which can be measured using the YFAS.^11,42

One distinct feature that has not yet been addressed is the occurrence of sleep disturbances in BED and FA. This characteristic raises the question of whether sleep disturbance leads to binge-like behavior (top-down) or binge-like behavior leads to sleep disturbance (bottom-up-approach). Sleep disturbance itself is often reported to lead to greater impulsivity and loss of inhibitory control, even more so in cue-reactive individuals who have greater motivation to engage in these behaviors or in individuals who are trying to maintain abstinence from certain substances. This is also seen in sleep-deprived animals where sleep loss leads to a greater likelihood to overeat.^44–45 However, binge eaters have been shown to more commonly possess the evening chronotype, in which the individual tends to get up later and go to sleep later and to more commonly complain of chronic insomnia. Additionally, binges generally tend to occur in the later hours, usually between 5 pm and midnight, which might also lead to disruption of the normal circadian rhythm and higher levels of impulsivity.^44,46 Velazquez-Sanchez et al. showed that high impulsivity was among the strongest predictors of FA-like behavior toward palatable food in male Wistar rats.⁴⁷ There is limited research available on the relationship between sleep disturbance and FA. However, some studies suggest that sleep problems may be associated with an increased risk for developing addictive eating behaviors, including FA.^44,47 Research has shown that sleep disturbances such as insomnia and sleep apnea can increase the risk of overeating and binge eating behaviors. Additionally, some studies have found that individuals with FA report poorer sleep quality and more sleep-related problems than those without FA.^46,48–50 It is important to note that the relationship between sleep disturbances and FA is complex and likely influenced by a variety of factors, including genetic predisposition, environmental factors, and comorbid conditions such as depression and anxiety. Therefore, further research is needed to better understand the relationship between sleep and FA, as well as to develop effective interventions for individuals struggling with this condition.

The subtle differences between BED and FA are of key importance to physicians because treatment strategies mainly depend on the underlying psychopathology. Patients with BED might benefit from cognitive behavioral therapy (CBT), which can help them deal with dietary-, body-, and shape-related mental preoccupations (acceptance-based mirror exposure, non-directive body image therapy). CBT might also be implemented in behavioral FA. Individuals with FA in relation to substances might need to eliminate the addictive substances from their diet, which will be very difficult if it is unclear which substance(s) are responsible for the addictive behavior (as in a hyperpalatable diet), as well as the issue regarding food being not only pleasurable but also nutritive.

Regarding pharmacotherapy, lisdexamphetamine dimesylate (LDX) is the first medication to be approved by the US Food and Drug Administration (FDA) for the treatment of adults with BED. LDX is a central nervous system stimulant used to treat attention-deficit hyperactivity disorder. The pharmacologically active dextroamphetamine released from LDX hydrolysis inhibits reuptake of dopamine and norepinephrine (NE) from the synaptic cleft and simultaneously enhances the release of dopamine, NE, and serotonin. By regulating these neurotransmitter systems that are involved in regulating appetite, hunger, and eating behaviors, it is hypothesized that LDX might reduce pathological overeating and can serve as a novel and efficacious pharmacologic treatment in acute BED. Although the drug is approved by the FDA for the treatment of BED, theoretically owing to its effect at the neurotransmitter level, it could also have an effect in FA. However, the warning for Vyvanse (LDX) is clear: the drug should not be used in individuals with an addictive disorder owing to high abuse potential in the amphetamine class of drugs.⁵¹ The study of drugs to combat FA is still relatively new. Although several drugs are being studied for this purpose, it may be some time before specific medications are available to target FA.²⁹

Conclusion

BED and FA overlap to a large degree but also possess distinguishing features. The distinction in FA between substance and behavioral addiction should be further researched, as well as the distinction between FA and BED. Such evidence will help physicians in the diagnosis and treatment of patients with these disorders.

Footnotes

Declaration of conflicting interests

The authors declare no conflict of interest.

Funding

This study did not receive any specific grant from funding agencies in the public, commercial or non-profit sectors.

ORCID iD

Dragana Ratković

References

Ivezaj

Barnes

Cooper

, et al. Loss-of-control eating after bariatric/sleeve gastrectomy surgery: Similar to binge-eating disorder despite differences in quantities. Gen Hosp Psychiatry 2018; 54: 25–30. PMID: 30056316 PMCID: PMC6245943 DOI: 10.1016/j.genhosppsych.2018.07.002.

DSM-5 Child Mental Disorder Classification. NIH National Library of Medicine, NCBI Bookshelf. [Internet]. [cited 2022 Aug 13]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519712/.

Hasin

O’brien

Auriacombe

, et al. DSM-5 criteria for substance use disorders: recommendations and rationale. Am J Psychiatry 2013; 170: 834–851. PMID: 23903334 PMCID: PMC3767415 DOI: 10.1176/appi.ajp.2013.12060782.

Potenza

MN.

Non-substance addictive behaviors in the context of DSM-5. Addict Behav 2014; 39: 1–2. PMID: 24119712 PMCID: PMC3858502 DOI: 10.1016/j.addbeh.2013.09.004.

Horsager

Færk

Lauritsen

, et al. Validation of the Yale Food Addiction Scale 2.0 and estimation of the population prevalence of food addiction. Clin Nutr 2020; 39: 2917–2928. PMID: 31983504 DOI: 10.1016/j.clnu.2019.12.030.

Food addiction [Internet]. Food Addiction - an overview. ScienceDirect. [cited 2022 Sep 14]. Available from: https://www.sciencedirect.com/topics/medicine-and-dentistry/food-addiction.

Addiction definition [Internet]. Merriam-Webster. [cited 2022 Sep 14]. Available from: https://www.merriam-webster.com/dictionary/addiction.

Estévez

Jáuregui

Sánchez-Marcos

, et al. Attachment and emotion regulation in substance addictions and behavioral addictions. J Behav Addict 2017; 6: 534–544. PMID: 29280395 PMCID: PMC6034944 DOI: 10.1556/2006.6.2017.086.

Zou

Wang

D’Oleire Uquillas

, et al. Definition of substance and non-substance addiction. Adv Exp Med Biol 2017; 1010: 21–41. PMID: 29098666 DOI: 10.1007/978-981-10-5562-1_2.

10.

Petry

Zajac

Ginley

MK.

Behavioral addictions as mental disorders: to be or not to be?

Annu Rev Clin Psychol 2018; 14: 399–423. PMID: 29734827 PMCID: PMC5992581 DOI: 10.1146/annurev-clinpsy-032816-045120.

11.

Bąk-Sosnowska

Differential criteria for binge eating disorder and food addiction in the context of causes and treatment of obesity. Psychiatr Pol 2017; 51: 247–259. PMID: 28581535 DOI: 10.12740/PP/OnlineFirst/62824.

12.

Domingos

Sordillo

Dietrich

, et al. Hypothalamic melanin concentrating hormone neurons communicate the nutrient value of sugar. elife 2013; 2: e01462. PMID: 24381247 PMCID: PMC3875383 DOI: 10.7554/eLife.01462.

13.

Novelle

Diéguez

Food addiction and binge eating: lessons learned from animal models. Nutrients 2018; 10: 71. PMID: 29324652 PMCID: PMC5793299 DOI: 10.3390/nu10010071.

14.

Johnson

Kenny

PJ.

Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci 2010; 13: 635–641. PMID: 20348917 PMCID: PMC2947358 DOI: 10.1038/nn.2519.

15.

Tellez

Han

Zhang

, et al. Separate circuitries encode the hedonic and nutritional values of sugar. Nat Neurosci 2016; 19: 465–470. PMID: 26807950 PMCID: PMC4767614 DOI: 10.1038/nn.4224.

16.

Colantuoni

Rada

McCarthy

, et al. Evidence That Intermittent, Excessive Sugar Intake Causes Endogenous Opioid Dependence. Obes Res 2002; 10: 478–488. PMID: 12055324 DOI: 10.1038/oby.2002.66.

17.

Lenoir

Serre

Cantin

, et al. Intense Sweetness Surpasses Cocaine Reward. PLoS One 2007; 2: e698. PMID: 17668074 PMCID: PMC1931610 DOI: 10.1371/journal.pone.0000698.

18.

Avena

Rada

Hoebel

BG.

Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev 2008; 32: 20–39. PMID: 17617461 PMCID: PMC2235907 DOI: 10.1016/j.neubiorev.2007.04.019.

19.

Heinsbroek

Giannotti

Mandel

, et al. A common limiter circuit for opioid choice and relapse identified in a rodent addiction model. Nat Commun 2021; 12: 4788. PMID: 34373454 PMCID: PMC8352904 DOI: 10.1038/s41467-021-25080-x.

20.

Giannotti

Mottarlini

Heinsbroek

, et al. Oxytocin and orexin systems bidirectionally regulate the ability of opioid cues to bias reward seeking. Transl Psychiatry 2022; 12: 432. PMID: 36195606 PMCID: PMC9532415 DOI: 10.1038/s41398-022-02161-z.

21.

6B82 Binge eating disorder. ICD-11 for Mortality and Morbidity Statistics [Internet]. World Health Organization. [cited 2022 Aug 13]. Available from: https://icd.who.int/browse11/l-m/en#/http://id.who.int/icd/entity/1673294767.

22.

Stice

Agras

Telch

, et al. Subtyping binge eating-disordered women along dieting and negative affect dimensions. Int J Eat Disord 2001; 30: 11–27. PMID: 11439405 DOI: 10.1002/eat.1050.

23.

Ahrberg

Trojca

Nasrawi

, et al. Body Image Disturbance in Binge Eating Disorder: A Review. Eur Eat Disord Rev 2011; 19: 375–381. PMID: 21341345 DOI: 10.1002/erv.1100.

24.

Stice

Gau

Rohde

, et al. Risk factors that predict future onset of each DSM–5 eating disorder: Predictive specificity in high-risk adolescent females. J Abnor Psychol 2017; 126: 38–51. PMID: 27709979 PMCID: PMC5215960 DOI: 10.1037/abn0000219.

25.

Lewer

Bauer

Hartmann

, et al. Different facets of body image disturbance in binge eating disorder: a review. Nutrients 2017; 9: 1294. PMID: 29182531 PMCID: PMC5748745 DOI: 10.3390/nu9121294.

26.

Kalon

Hong

Tobin

, et al. Psychological and neurobiological correlates of food addiction. Int Rev Neurobiol 2016; 129: 85–110. PMID: 27503449 PMCID: PMC5608024 DOI: 10.1016/bs.irn.2016.06.003.

27.

Dingemans

Danner

Parks

Emotion Regulation in Binge Eating Disorder: A Review. Nutrients 2017; 9: 1274. PMID: 29165348 PMCID: PMC5707746 DOI: 10.3390/nu9111274.

28.

Wang

Lydecker

Grilo

CM.

Rumination in Patients with Binge-Eating Disorder and Obesity: Associations with Eating-Disorder Psychopathology and Weight-bias Internalization. Eur Eat Disord Rev 2017; 25: 98–103. PMID: 28078784 PMCID: PMC5318238 DOI: 10.1002/erv.2499.

29.

Hutson

Balodis

Potenza

MN.

Binge-eating disorder: Clinical and therapeutic advances. Pharmac Ther 2018; 182: 15–27. PMID: 28830840 DOI: 10.1016/j.pharmthera.2017.08.002.

30.

Kirkpatrick

Goldberg

Yazdani

, et al. Cytoplasmic FMR1-interacting protein 2 is a major genetic factor underlying binge eating. Biol Psychiatry 2017; 81: 757–769. PMID: 27914629 PMCID: PMC5386810 DOI: 10.1016/j.biopsych.2016.10.021.

31.

Goldberg

Kirkpatrick

Yazdani

, et al. Casein kinase 1‐epsilon deletion increases mu opioid receptor‐dependent behaviors and binge eating 1. Genes Brain Behav 2017; 16: 725–738. PMID: 28594147 PMCID: PMC6180211 DOI: 10.1111/gbb.12397.

32.

Davis

The epidemiology and genetics of binge eating disorder (BED). CNS Spectr 2015; 20: 522–529. PMID: 26258270 DOI: 10.1017/S1092852915000462.

33.

Babbs

Unger

Corwin

RL.

2-Hydroxyestradiol enhances binge onset in female rats and reduces prefrontal cortical dopamine in male rats. Horm Behav 2013; 63: 88–96. PMID: 23116652 PMCID: PMC3586335 DOI: 10.1016/j.yhbeh.2012.10.010.

34.

Babbs

Wojnicki

Corwin

RL.

Effect of 2-hydroxyestradiol on binge intake in rats. Physiol Behav 2011; 103: 508–512. PMID: 21497615 PMCID: PMC3132134 DOI: 10.1016/j.physbeh.2011.03.029.

35.

Mena

Sadeghian

Baldo

BA.

Induction of hyperphagia and carbohydrate intake by μ-opioid receptor stimulation in circumscribed regions of frontal cortex. J Neurosci 2011; 31: 3249–3260. PMID: 21368037 PMCID: PMC3131113 DOI: 10.1523/JNEUROSCI.2050-10.2011.

36.

Hildebrandt

Fisher

LaPalombara

, et al. Corticostriatal dynamics underlying components of binge-like consumption of palatable food in mice. Appetite 2023; 183: 106462. PMID: 36682623 PMCID: PMC9974784 DOI: 10.1016/j.appet.2023.106462.

37.

Hildebrandt

Ahmari

SE.

Breaking It Down: Investigation of Binge Eating Components in Animal Models to Enhance Translation. Front Psychiatry 2021; 12: 728535. PMID: 34484010 PMCID: PMC8414642 DOI: 10.3389/fpsyt.2021.728535.

38.

Brown

James

MH.

Binge eating, overeating and food addiction: Approaches for examining food overconsumption in laboratory rodents. Prog Neuropsychopharmacol Biol Psychiatry 2023; 123: 110717. PMID: 36623582 DOI: 10.1016/j.pnpbp.2023.110717.

39.

Hebebrand

Albayrak

Adan

, et al. “Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior. Neurosci Biobehav Rev 2014; 47: 295–306. PMID: 25205078 DOI: 10.1016/j.neubiorev.2014.08.016.

40.

Gearhardt

White

Potenza

MN.

Binge eating disorder and food addiction. Curr Drug Abuse Rev 2011; 4: 201–207. PMID: 21999695 PMCID: PMC3671377 DOI: 10.2174/1874473711104030201.

41.

Goodman

Breithaupt

Watson

, et al. Sweet taste preference in binge-eating disorder: A preliminary investigation. Eat Behav 2018; 28: 8–15. PMID: 29202335 DOI: 10.1016/j.eatbeh.2017.11.005.

42.

Gearhardt

Corbin

Brownell

KD.

Preliminary validation of the Yale Food Addiction Scale. Appetite 2009; 52: 430–436. PMID: 19121351 DOI: 10.1016/j.appet.2008.12.003.

43.

Dingemans

Van Furth

EF.

Binge eating disorder psychopathology in normal weight and obese individuals. Int J Eat Disord 2012; 45: 135–138. PMID: 22170025 DOI: 10.1002/eat.20905.

44.

Mehr

Mitchison

Bowrey

, et al. Sleep dysregulation in binge eating disorder and “food addiction”: the orexin (hypocretin) system as a potential neurobiological link. Neuropsychopharmacology 2021; 46: 2051–2061. PMID: 34145404 PMCID: PMC850561 DOI: 10.1038/s41386-021-01052-z.

45.

Ahrens

Ahmed

OJ.

Neural circuits linking sleep and addiction: Animal models to understand why select individuals are more vulnerable to substance use disorders after sleep deprivation. Neurosci Biobehav Rev 2020; 108: 435–444. PMID: 31756346 DOI: 10.1016/j.neubiorev.2019.11.007.

46.

Kandeger

Selvi

Tanyer

DK.

The effects of individual circadian rhythm differences on insomnia, impulsivity, and food addiction. Eat Weight Disord 2019; 24: 47–55. PMID: 29856005 DOI: 10.1007/s40519-018-0518-x.

47.

Velázquez-Sánchez

Ferragud

Moore

, et al. High trait impulsivity predicts food addiction-like behavior in the rat. Neuropsychopharmacology 2014; 39: 2463–2472. PMID: 24776685 PMCID: PMC4138758 doi: 10.1038/npp.2014.98.

48.

Cassidy

Harvey

Smyth

Examining the relationship between obstructive sleep apnoea and eating behaviors and attitudes: A systematic review. Appetite 2023; 181: 106390. PMID: 36423746 doi: 10.1016/j.appet.2022.106390.

49.

Najem

Saber

Aoun

, et al . Prevalence of food addiction and association with stress, sleep quality and chronotype: A cross-sectional survey among university students. Clin Nutr 2020; 39: 533–539. PMID: 30878156 DOI: 10.1016/j.clnu.2019.02.038.

50.

Borisenkov

Popov

Tserne

, et al. Food addiction and symptoms of depression among inhabitants of the European North of Russia: Associations with sleep characteristics and photoperiod. Eur Eat Disord Rev 2020; 28: 332–342. PMID: 32153116 DOI: 10.1002/erv.2728.

51.

Tarman

DV.

Vyvanse and Addiction. Addictions unplugged: The Power Is Ours [Internet]. 2015 [cited 2023 Feb 7]. Available from: https://addictionsunplugged.com/vyvanse-and-addiction/.