Open Access
Open Peer Review

This article has Open Peer Review reports available.

How does Open Peer Review work?

Food addiction as a new piece of the obesity framework

  • Jose Manuel Lerma-Cabrera1,
  • Francisca Carvajal1, 2 and
  • Patricia Lopez-Legarrea1Email author
Nutrition Journal201615:5

https://doi.org/10.1186/s12937-016-0124-6

Received: 27 October 2015

Accepted: 9 January 2016

Published: 13 January 2016

Key words

Obesity food addiction neuropeptides palatable food binge eating

Introduction. Obesity today

Obesity has become a major public health burden worldwide due to the huge social and economic impact derived from its related comorbidities [1]. Excessive body weight has been estimated to account for 16 % of the global burden disease [2] and according to World Health Organization estimates, over 600 million adults are obese worldwide Obesity is described as a multi-etiological disorder and several factors have been shown to be involved in its onset and development [1]. Despite the important progression in the study of obesity, prevalence rates continue to increase, suggesting that additional elements must be involved in the pathogenesis of this disease. Moreover, even if weight loss programs are effective, keeping the weight off continues to be an almost insurmountable challenge [3]. In this context, new theories are arising regarding food intake. Understanding obesity as a food addiction is a novel approach that has garnered considerable attention. Some studies have shown an association between mood and the overall dietary pattern including specific nutrients [4]. Recent research also shows that palatable and high calorie food may have addictive potential. Subjects chronically eat some foods in amounts larger than needed for staying healthy, which shows a loss of control in food behaviour [5]. Additionally, a 40 % prevalence of food addiction has been shown in obese individuals seeking bariatric surgery [6]. All these traces indicate that there may be a potential relationship between behaviour and weight gain.

New theories about obesity: obesity as food addiction

In recent years, there has been an increase in scientific evidence showing both neurobiological and behavioral relationships between drugs and food intake. Basic research using animal and humans models has shown that certain foods, mainly highly palatable foods, have addictive properties. In addition, exposure to food and drugs of abuse have shown similar responses in the dopaminergic and opioid systems. These similarities between food and drugs have given rise to the hypothesis of food addiction.

Food intake and brain reward circuits

The dopaminergic system is involved in a large number of behaviors including reward processing and motivated behavior. Thus, all drugs of abuse increase the extracellular concentration of dopamine (DA) in the striatum and associated mesolimbic regions [7]. Di Chiara’s group has extensively showed that addictive drugs (e.g. amphetamine and cocaine) increase extracellular DA in the nucleus accumbens (NAc), a primary site for reinforced behaviors [7]. Likewise, microdialysis has shown that exposure to rewarding food stimulates dopaminergic transmission in the NAc [8].

Furthermore, neuroimaging studies show that our brain response is similar in the presence of food and drug abuse: increased cell activation in the NAc, the brain’s pleasure center [911]. Neuroimaging studies in humans have also shown similarities between obesity and addiction. For example, both obesity and addiction are associated with fewer D2 dopamine receptors in the brain [12, 13], suggesting that they are less sensitive to reward stimuli and more vulnerable to food or drug intake. Thus, for example, individuals with the largest body mass index (BMI) had the lowest D2 values [13].

Specifically, this reduction in striatal D2 density correlates with reduced metabolism in cerebral areas (prefrontal and orbitofrontal cortex) that exert inhibitory control over consumption [12]. Thus, obese subjects show greater activation of reward and attention regions than normal weight subjects do in response to palatable food images versus control images [14, 15]. This observation suggests that a deficit in reward processing is an important risk factor for the impulsive and compulsive behaviors showed by obese individuals. Taken together, these data could explain why in obesity and drug addiction the consummatory behaviors persist despite negative social, health and financial consequences. All these neurobiological data suggest that obesity and drug addiction may share similar neuroadaptive responses in brain reward circuits or action mechanisms.

The role of nutrition neuropeptides in addiction

The idea that neuropeptides involved in metabolic regulation are also involved in modulating the neurobiological responses to drugs of abuse has received a great deal of attention in recent literature [16, 17]. Several studies have shown that exposure to drugs of abuse significantly alters the functionality of numerous neuropeptides systems. On the other hand, compounds that target these neuropeptides systems play an important role in modulating the neurobiological responses to drugs of abuse. For example, the melanocortins (MC) and orexins system, which plays an important role in food intake, is also involved in drug use. Moreover, the brain expression of these neuropeptides is altered after drug binge-like consumption [1820] or palatable substances (caloric and non-caloric) [21]. Central administration of Agouti-related peptide, an MC antagonist, activates midbrain dopamine neurons and induces consumption of fat enriched foods [22]. Taken together, this data could explain why some kinds of food are so often overconsumed.

Regulatory mechanisms for food intake can be homeostatic –biological need– but also hedonic [23]. This idea is supported by the fact that people continue eating even when energy requirements have been met. However, it is noteworthy that these systems (hedonic versus homeostatic) are not mutually exclusive, but will have multiple interconnections [24]. Homeostatic regulators of hunger and satiety, such as ghrelin, leptin and insulin, could mediate between the homeostatic and hedonic mechanisms of food intake influencing the dopaminergic system [25, 26]. Leptin is perhaps the most widely studied biological factor in relation to food intake control. Although it is secreted by the adipose tissue, leptin receptors are expressed on midbrain dopamine neurons [27]. Leptin infusion into the tegmental ventral area, a reward system brain area, decreases food intake and inhibits the activity of dopamine neurons [28]. Thus, current evidence suggests that mesolimbic dopamine pathways could mediate the effect of leptin on food intake.

Therefore, theories of “food addiction” indicate that certain highly processed foods can have a high addictive potential and may be responsible for some cases of obesity and eating disorders [29, 30]. Recently, it have been shown that subjects showing a compulsive overeating consume higher amounts of some macronutrients (fats and proteins) compared with non-food-addicted subjects [31, 32]. It is well established that hyperphagia induced by consumption of fat enriched food and refined sugars is influenced by mesolimbic and nigrostriatal dopaminergic inputs. For example, consumption of highly palatable food, especially sugar, entails the release of endogenous opioids in the NAc [33, 34] and activates the dopaminergic reward system [35]. In addition, the rats exposed to intermittent access to sugar solution show some components of addiction such as escalation of daily sugar intakes, withdrawal signs, craving and cross-sensitization to amphetamine and alcohol [36]. These data suggest that certain foods are potentially rewarding and can trigger addictive-like behaviors in laboratory animals and humans.

How to evaluate food addiction

As mentioned before, obesity is a heterogeneous disease influenced by multiple factors. This review has shown how an addictive process may play a role in binge eating and obesity. Thus, food addiction could be a factor contributing to overeating and then to obesity. However, for the scientific community the concept of food addiction is still a controversial topic [5, 37, 38]. One of the arguments to question the validity of food addiction hypothesis is that although neurobiological studies have identified shared brain mechanisms of food and drugs, there are substantial differences too [37]. Also, the pattern of brain activation of obese individuals and binge-eaters compared with controls is inconsistent [38]. Finally, other critical remarks argue that most of the studies that support the existence of food addiction are restricted to animal models [5]. Bearing in mind this criticism, future research is required to more extensively study the validity of food addiction in humans. Therefore, to evaluate this hypothesis of “food addiction” and its contribution to eating disorders it becomes necessary to have valid and reliable instruments to operationalize food addictive behaviors.

A tool to identify individuals showing symptoms of “dependence” to certain foods has been recently developed. Gearhardt and cols. elaborated in 2009 the Yale Food Addiction Scale (YFAS) [39]. This scale has been used in most of the research related to the concept of food addiction and has been translated into several languages, such as, French, German, Italian, Spanish or Dutch. The instrument is a 25-item questionnaire grouped under criteria that resemble the symptoms of substance dependence as outlined in the Diagnostic and Statistical Manual of Mental Disorders IV. The scale includes items that assess specific criteria, such as loss of control over consumption, a persistent desire or repeated unsuccessful attempts to quit, continued use despite physical and psychological problems, and clinically significant impairment or distress, among others. The most common symptoms of food addiction are loss of control over consumption, continued use despite negative consequences, and inability to cut down despite the desire to do so [40].

Studies using the YFAS have found that patients scoring high in the scale show more frequently binge eating episodes [22, 41, 42]. In turn, prevalence of food addiction diagnosed using YFAS was 5.4 % in general population [31]. However, food addiction increased with obesity status range between 40 % and 70 % in individuals with binge eating disorder [42], compulsive-overeating [43] or bulimia nervosa [6]. Furthermore, individuals with high food addiction scores were found to have comparable responses when viewing food images as individuals with drug dependence viewing drug cues. They showed elevated activation in reward circuitry (anterior cingulate cortex, dorsolateral prefrontal cortex and amygdala) in response to food cues and reduced activation in inhibitory regions (medial orbitofrontal cortex) in response to food intake [29].

Interestingly, the prevalence of food addiction was positively related to measures of adiposity (e.g. body fat, BMI) [31, 44]. These data suggest that food addiction is likely an important factor in the development of human obesity and that it is associated with the severity of obesity from normal to obese individuals. In fact, obese people showing a worse weight loss response to treatment [41] and greater weight gain after undergoing bariatric surgery [45] obtain higher YFAS scores. Thus, weight-loss treatments should consider the role of food addiction as a psychological factor underlying difficult weight management situations.

On the other hand, some personality traits, such as impulsivity, have been associated with alcohol and drug misuse [46]. In the context of food addiction, recent research has demonstrated that obese individuals scoring high in YFAS were more impulsive and displayed greater emotional reactivity than obese controls [22]. These findings suggest that a food addiction construct shows a psycho-behavioral profile similar to conventional drug abuse disorders.

However, although food addiction constructs exists, it is highly unlikely that all foods have addictive potential. Manufacturing industries have designed processed foods by adding sugar, salt, or fat, which can maximize the reinforcing properties of traditional foods (fruits, vegetables). The high palatability (hedonic value) that this kind of processed food offers, prompts subjects to eat more. Thus, certain processed food may have a high addictive potential and be responsible for some eating disorders such as obesity [30, 40]. Although there is little evidence in humans, animal models suggest that processed food is associated with addictive-like eating. For example, Avena and cols. showed that excessive intake of sugar causes neurochemical (increased release of dopamine and acetylcholine in NAc) and behavioral (increased intake of sugar after a period of abstinence and cross-sensitivity to drugs of abuse) signs of dependence [47]. These findings suggest that overconsumption of highly processed food, but not standard rat chow, produce some addictive-like characteristics. Also, it has been shown that overconsumption of palatable food triggers down-regulation of striatal D2 receptors expression in the same way that drugs do [48], which suggests that obesity and drug addiction may share an underlying hedonic mechanism, as noted above.

Nevertheless, not everyone exposed to palatable food environments develops obesity. Knowing the biological and/or behavioral motives or reasons why people eat highly palatable foods could help explain the susceptibility or resilience with respect to obesity. Thus, by identifying why people begin to eat these kinds of food it could be possible to design appropriate “personalized” treatments to combat obesity. The Palatable Motives Eating Scale (PEMS) is a validated and robust scale to identify motivations for eating highly-palatable foods [49]. The scale allows detecting motives for eating tasty food: social (e.g., to celebrate a special occasion with friends), coping (e.g., to forget about your problems), reward enhancement (e.g., because it gives you a pleasant feeling) and conformity (e.g., because your friends or family want you to eat or drink these foods or drinks). Moreover, PEMS have a good convergent validity with YFAS scores. It makes it possible to evaluate different food addiction constructs. While the YFAS probes the consequences of consuming highly palatable foods, the PEMS probes the motives for such consumption.

Two examples of scales (YFAS and PEMS) to evaluate food addiction have been shown.

Conclusion

As indicated above, obesity has become a major public health problem worldwide. Therefore, finding efficient strategies to fight this disease represents a big challenge for the international scientific community. Studying the possible role of food addiction in humans as an influencing factor in excessive food intake is attracting attention. More so, considering the interesting results obtained with animals. It is known that some cases of excessive food intake do not respond to physiological needs but to a psychological behavioural component that needs to be identified. Finding this component would allow the inclusion of behavioural therapy among the cornerstones of obesity treatment, thus achieving a multidisciplinary approach in accordance to the multifactorial origin of the obesity. This more realistic grasp may allow applying effective treatments, leading not only to greater weight loses, but also to a better chance of keeping the lost weight off. YFAS and PEMS tools offer a rigorous way to evaluate whether an addictive process contributes to certain eating disorders, such as obesity and binge eating. However, further research is needed in order to evaluate the food addiction hypothesis and its relationship to eating disorders. It is necessary to study the effect of psychological, behavioral, cognitive and physiological factors in the food addiction construct. In any case, certain foods (fatty, sugary and salty) have shown to have an addictive potential, thus implying the possibility of preventing and treating obesity.

Abbreviations

DA: 

dopamine

NAc: 

nucleus accumbens

BMI: 

body mass index

MC: 

melanocortins

YFAS: 

Yale Food Addiction Scale

PEMS: 

Palatable Motives Eating Scale

Declarations

Acknowledgements

The present work was conducted thanks to Universidad Autonoma de Chile (DPI 62/2015).

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Centro de Investigacion Biomedica, Facultad de Ciencias de la Salud, Universidad Autonoma de Chile
(2)
Depto de Psicología y Sociología. Facultad de Ciencias Sociales y Humanas, Universidad de Zaragoza

References

  1. Lopez-Legarrea P, Olivares PR, Almonacid-Fierro A, Gomez-Campos R, Cossio-Bolanos M, Garcia-Rubio J. Association between dietary habits and the presence of overweight/obesity in a sample of 21,385 chilean adolescents. Nutr Hosp. 2015;31(5):2088–94.Google Scholar
  2. Hossain P, Kawar B, El Nahas M. Obesity and diabetes in the developing world--a growing challenge. N Engl J Med. 2007;356(3):213–5.View ArticleGoogle Scholar
  3. de la Iglesia R, Lopez-Legarrea P, Abete I, Bondia-Pons I, Navas-Carretero S, Forga L, et al. A new dietary strategy for long-term treatment of the metabolic syndrome is compared with the American Heart Association (AHA) guidelines: the MEtabolic Syndrome REduction in NAvarra (RESMENA) project. Br J Nutr. 2014;111(4):643–52.View ArticleGoogle Scholar
  4. Perez-Cornago A, Lopez-Legarrea P, de la Iglesia R, Lahortiga F, Martinez JA, Zulet MA. Longitudinal relationship of diet and oxidative stress with depressive symptoms in patients with metabolic syndrome after following a weight loss treatment: the RESMENA project. Clin Nutr. 2014;33(6):1061–7.View ArticleGoogle Scholar
  5. Ziauddeen H, Farooqi IS, Fletcher PC. Obesity and the brain: how convincing is the addiction model? Nat Rev Neurosci. 2012;13(4):279–86.Google Scholar
  6. Meule A, von Rezori V, Blechert J. Food addiction and bulimia nervosa. Eur Eat Disord Rev. 2014;22(5):331–7.View ArticleGoogle Scholar
  7. Di Chiara G. Nucleus accumbens shell and core dopamine: differential role in behavior and addiction. Behav Brain Res. 2002;137(1-2):75–114.View ArticleGoogle Scholar
  8. Roitman MF, Stuber GD, Phillips PE, Wightman RM, Carelli RM. Dopamine operates as a subsecond modulator of food seeking. J Neurosci. 2004;24(6):1265–71.View ArticleGoogle Scholar
  9. Hollander JA, Ijames SG, Roop RG, Carelli RM. An examination of nucleus accumbens cell firing during extinction and reinstatement of water reinforcement behavior in rats. Brain Res. 2002;929(2):226–35.View ArticleGoogle Scholar
  10. Roop RG, Hollander JA, Carelli RM. Accumbens activity during a multiple schedule for water and sucrose reinforcement in rats. Synapse. 2002;43(4):223–6.View ArticleGoogle Scholar
  11. Volkow ND, Wang GJ, Tomasi D, Baler RD. Obesity and addiction: neurobiological overlaps. Obes Rev. 2013;14(1):2–18.View ArticleGoogle Scholar
  12. Volkow ND, Wang GJ, Telang F, Fowler JS, Thanos PK, Logan J, et al. Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: possible contributing factors. Neuroimage. 2008;42(4):1537–43.View ArticleGoogle Scholar
  13. Wang GJ, Volkow ND, Logan J, Pappas NR, Wong CT, Zhu W, et al. Brain dopamine and obesity. Lancet. 2001;357(9253):354–7.Google Scholar
  14. Nummenmaa L, Hirvonen J, Hannukainen JC, Immonen H, Lindroos MM, Salminen P, et al. Dorsal striatum and its limbic connectivity mediate abnormal anticipatory reward processing in obesity. PLoS One. 2012;7(2):e31089.View ArticleGoogle Scholar
  15. Stice E, Spoor S, Bohon C, Veldhuizen MG, Small DM. Relation of reward from food intake and anticipated food intake to obesity: a functional magnetic resonance imaging study. J Abnorm Psychol. 2008;117(4):924–35.View ArticleGoogle Scholar
  16. Thiele TE, Navarro M, Sparta DR, Fee JR, Knapp DJ, Cubero I. Alcoholism and obesity: overlapping neuropeptide pathways? Neuropeptides. 2003;37(6):321–37.View ArticleGoogle Scholar
  17. Barson JR, Leibowitz SF. Hypothalamic neuropeptide signaling in alcohol addiction. Prog Neuropsychopharmacol Biol Psychiatry. 2016;65:321–9.View ArticleGoogle Scholar
  18. Navarro M, Cubero I, Knapp DJ, Breese GR, Thiele TE. Decreased immunoreactivity of the melanocortin neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) after chronic ethanol exposure in Sprague-Dawley rats. Alcohol Clin Exp Res. 2008;32(2):266–76.View ArticleGoogle Scholar
  19. Lerma-Cabrera JM, Carvajal F, Alcaraz-Iborra M, de la Fuente L, Navarro M, Thiele TE, et al. Adolescent binge-like ethanol exposure reduces basal alpha-MSH expression in the hypothalamus and the amygdala of adult rats. Pharmacol, Biochem Behav. 2013;110:66–74.View ArticleGoogle Scholar
  20. Carvajal F, Alcaraz-Iborra M, Lerma-Cabrera JM, Valor LM, de la Fuente L, Sanchez-Amate Mdel C, et al. Orexin receptor 1 signaling contributes to ethanol binge-like drinking: Pharmacological and molecular evidence. Behav Brain Res. 2015;287:230–7.View ArticleGoogle Scholar
  21. Alcaraz-Iborra M, Carvajal F, Lerma-Cabrera JM, Valor LM, Cubero I. Binge-like consumption of caloric and non-caloric palatable substances in ad libitum-fed C57BL/6 J mice: pharmacological and molecular evidence of orexin involvement. Behav Brain Res. 2014;272:93–9.View ArticleGoogle Scholar
  22. Davis C, Curtis C, Levitan RD, Carter JC, Kaplan AS, Kennedy JL. Evidence that ‘food addiction’ is a valid phenotype of obesity. Appetite. 2011;57(3):711–7.View ArticleGoogle Scholar
  23. Pandit R, de Jong JW, Vanderschuren LJ, Adan RA. Neurobiology of overeating and obesity: the role of melanocortins and beyond. Eur J Pharmacol. 2011;660(1):28–42.View ArticleGoogle Scholar
  24. Lutter M, Nestler EJ. Homeostatic and hedonic signals interact in the regulation of food intake. J Nutr. 2009;139(3):629–32.View ArticleGoogle Scholar
  25. Kenny PJ. Common cellular and molecular mechanisms in obesity and drug addiction. Nat Rev Neurosci. 2011;12(11):638–51.View ArticleGoogle Scholar
  26. Palmiter RD. Is dopamine a physiologically relevant mediator of feeding behavior? Trends Neurosci. 2007;30(8):375–81.View ArticleGoogle Scholar
  27. Elmquist JK, Bjorbaek C, Ahima RS, Flier JS, Saper CB. Distributions of leptin receptor mRNA isoforms in the rat brain. J Comp Neurol. 1998;395(4):535–47.View ArticleGoogle Scholar
  28. Hommel JD, Trinko R, Sears RM, Georgescu D, Liu ZW, Gao XB, et al. Leptin receptor signaling in midbrain dopamine neurons regulates feeding. Neuron. 2006;51(6):801–10.View ArticleGoogle Scholar
  29. Gearhardt AN, Yokum S, Orr PT, Stice E, Corbin WR, Brownell KD. Neural correlates of food addiction. Arch Gen Psychiatry. 2011;68(8):808–16.View ArticleGoogle Scholar
  30. Gold MS, Frost-Pineda K, Jacobs WS. Overeating, binge eating and eating disorders as addiction. Psychiatr Ann. 2003;33(2):117–22.View ArticleGoogle Scholar
  31. Pedram P, Wadden D, Amini P, Gulliver W, Randell E, Cahill F, et al. Food addiction: its prevalence and significant association with obesity in the general population. PLoS One. 2013;8(9):e74832.View ArticleGoogle Scholar
  32. Schulte EM, Avena NM, Gearhardt AN. Which foods may be addictive? The roles of processing, fat content, and glycemic load. PLoS One. 2015;10(2):e0117959.View ArticleGoogle Scholar
  33. Ragnauth A, Moroz M, Bodnar RJ. Multiple opioid receptors mediate feeding elicited by mu and delta opioid receptor subtype agonists in the nucleus accumbens shell in rats. Brain Res. 2000;876(1-2):76–87.View ArticleGoogle Scholar
  34. Will MJ, Franzblau EB, Kelley AE. Nucleus accumbens mu-opioids regulate intake of a high-fat diet via activation of a distributed brain network. J Neurosci. 2003;23(7):2882–8.Google Scholar
  35. Rada P, Avena NM, Hoebel BG. Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience. 2005;134(3):737–44.View ArticleGoogle Scholar
  36. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20–39.View ArticleGoogle Scholar
  37. Rippe JM. Lifestyle medicine: the importance of firm grounding on evidence. Am J Lifestyle Med. 2014;8:306–12.View ArticleGoogle Scholar
  38. Ziauddeen H, Fletcher PC. Is food addiction a valid and useful concept? Obes Rev. 2013;14(1):19–28.View ArticleGoogle Scholar
  39. Gearhardt AN, Corbin WR, Brownell KD. Preliminary validation of the Yale Food Addiction Scale. Appetite. 2009;52(2):430–6.View ArticleGoogle Scholar
  40. Gearhardt AN, Davis C, Kuschner R, Brownell KD. The addiction potential of hyperpalatable foods. Curr Drug Abuse Rev. 2011;4(3):140–5.View ArticleGoogle Scholar
  41. Burmeister JM, Hinman N, Koball A, Hoffmann DA, Carels RA. Food addiction in adults seeking weight loss treatment. Implications for psychosocial health and weight loss. Appetite. 2013;60(1):103–10.View ArticleGoogle Scholar
  42. Gearhardt AN, White MA, Masheb RM, Grilo CM. An examination of food addiction in a racially diverse sample of obese patients with binge eating disorder in primary care settings. Compr Psychiatry. 2013;54(5):500–5.View ArticleGoogle Scholar
  43. Bégin C, St-Louis ME, Turmel S, Tousignant B, Marion LP, Ferland F, et al. Does food addiction distinguish a specific subgroup of overweight/obese overeating women? Health. 2012;4(12A):1492–9.View ArticleGoogle Scholar
  44. Gearhardt AN, Boswell RG, White MA. The association of “food addiction” with disordered eating and body mass index. Eat Behav. 2014;15(3):427–33.View ArticleGoogle Scholar
  45. Clark SM, Saules KK. Validation of the Yale Food Addiction Scale among a weight-loss surgery population. Eat Behav. 2013;14(2):216–9.View ArticleGoogle Scholar
  46. de Wit H. Impulsivity as a determinant and consequence of drug use: a review of underlying processes. Addict Biol. 2009;14(1):22–31.View ArticleGoogle Scholar
  47. Avena NM, Bocarsly ME, Hoebel BG. Animal models of sugar and fat bingeing: relationship to food addiction and increased body weight. Methods Mol Biol. 2012;829:351–65.View ArticleGoogle Scholar
  48. Johnson PM, Kenny PJ. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci. 2010;13(5):635–41.View ArticleGoogle Scholar
  49. Burgess EE, Turan B, Lokken KL, Morse A, Boggiano MM. Profiling motives behind hedonic eating. Preliminary validation of the Palatable Eating Motives Scale. Appetite. 2014;72:66–72.View ArticleGoogle Scholar

Copyright

© Lerma-Cabrera et al. 2016