Wang, G. J., Geliebter, A., Volkow, N. D., Telang, F. W., Logan, J., Jayne, M. C., Galanti, K., Selig, P. A., Han, H., Zhu, W., Wong, C. T., & Fowler, J. S. (2011). Enhanced striatal dopamine release during food stimulation in binge eating disorder. Obesity (Silver Spring, Md.), 19(8), 1601–1608. https://doi.org/10.1038/oby.2011.27 From the research article’s abstract: “Subjects with binge eating disorder (BED) regularly consume large amounts of food in short time periods. The neurobiology of BED is poorly understood. Brain dopamine, which regulates motivation for food intake, is likely to be involved. We assessed the involvement of brain dopamine in the motivation for food consumption in binge eaters. Positron emission tomography (PET) scans with [11C]raclopride were done in 10 obese BED and 8 obese subjects without BED. Changes in extracellular dopamine in the striatum in response to food stimulation in food-deprived subjects were evaluated after placebo and after oral methylphenidate (MPH), a drug that blocks the dopamine reuptake transporter and thus amplifies dopamine signals. Neither the neutral stimuli (with or without MPH) nor the food stimuli when given with placebo increased extracellular dopamine.
Obesity and addiction: neurobiological overlaps
Volkow, N. D., Wang, G. J., Tomasi, D., & Baler, R. D. (2013). Obesity and addiction: neurobiological overlaps. Obesity reviews : an official journal of the International Association for the Study of Obesity, 14(1), 2-18. https://doi.org/10.1111/j.1467-789X.2012.01031.x Review volkow2012 .pdf
Can Food and Addiction Change the Game?
Gearhardt, A. N., & Brownell, K. D. (2013). Can food and addiction change the game? Biol Psychiatry, 73(9), 802–803. https://doi.org/10.1016/j.biopsych.2012.07.024 From the commentary’s text: “Potentially Effective Food-Based Policy Approaches include taxing addictive foods, restricting access, limiting marketing, and eliminating addictive foods from schools.”
Food addiction and body-mass-index: A non-linear relationship
Meule, A. (2012). Food addiction and body-mass-index: a non-linear relationship. Medical Hypotheses, 79(4), 508–511. https://doi.org/10.1016/j.mehy.2012.07.005 From the research article’s abstract: “Excessive food consumption has been recognized to show similarities with substance dependence. Subsequently, it has been proposed that food addiction might contribute to the obesity epidemic. Recent studies using questionnaires for the assessment of food addiction have found statistically significant, but negligible positive correlations with body-mass-index (BMI). Moreover, group comparisons between food-addicted and non-addicted individuals in normal-weight or obese samples did not show differences in BMI. However, the prevalence of food addiction diagnoses is remarkably increased in obese individuals. In the current article, it is suggested that there might be a cubic relationship between food addiction and BMI. Food addiction symptomatology may remain stable in the under- and normal-weight range, increase in the overweight- and obese range, and level off at severe obesity. Empirical data in support of this view are presented.”
Factor Structure and Item Analysis of the Yale Food Addiction Scale in Obese Candidates for Bariatric Surgery
Meule, A., Heckel, D., & Kübler, A. (2012). Factor structure and item analysis of the Yale Food Addiction Scale in obese candidates for bariatric surgery. European Eating Disorders Review, 20(5), 419–422. https://doi.org/10.1002/erv.2189 From the research article’s abstract: “Converging research suggests phenomenological and neurobiological similarities between excessive food consumption and addictive behaviour in substance dependence. Recently, the Yale Food Addiction Scale (YFAS) has been proposed for the assessment of addictive eating behaviour. The German version of the YFAS was administered to obese individuals seeking bariatric surgery (N = 96). Factor structure, internal consistency, and item statistics were analysed. Forty participants (41.70%) received a food addiction diagnosis. The one-factorial structure of the YFAS, which has been found in non-clinical samples, could be confirmed. All but three items had factor loadings >.50. Internal consistency was α = .82. Item analysis revealed that items related to unsuccessful attempts to cut down and consumption despite physical and emotional problems were endorsed by the majority of participants. Findings support the use of the YFAS in clinical populations, while applicability of some items differs between clinical and non-clinical samples.”
Factor Structure and Item Analysis of the Yale Food Addiction Scale in Obese Candidates for Bariatric Surgery
Meule, A., Heckel, D., & Kübler, A. (2012). Factor structure and item analysis of the Yale Food Addiction Scale in obese candidates for bariatric surgery. European Eating Disorders Review, 20(5), 419–422. https://doi.org/10.1002/erv.2189 From the research article’s abstract: “Converging research suggests phenomenological and neurobiological similarities between excessive food consumption and addictive behaviour in substance dependence. Recently, the Yale Food Addiction Scale (YFAS) has been proposed for the assessment of addictive eating behaviour. The German version of the YFAS was administered to obese individuals seeking bariatric surgery (N = 96). Factor structure, internal consistency, and item statistics were analysed. Forty participants (41.70%) received a food addiction diagnosis. The one-factorial structure of the YFAS, which has been found in non-clinical samples, could be confirmed. All but three items had factor loadings >.50. Internal consistency was α = .82. Item analysis revealed that items related to unsuccessful attempts to cut down and consumption despite physical and emotional problems were endorsed by the majority of participants. Findings support the use of the YFAS in clinical populations, while applicability of some items differs between clinical and non-clinical samples.”
Rationale and consequences of reclassifying obesity as an addictive disorder: neurobiology, food environment and social policy perspectives
Allen, P. J., Batra, P., Geiger, B. M., Wommack, T., Gilhooly, C., & Pothos, E. N. (2012). Rationale and consequences of reclassifying obesity as an addictive disorder: neurobiology, food environment and social policy perspectives. Physiology & behavior, 107(1), 126—137. https://doi.org/10.1016/i.physbeh.2012.05.005 Review allen2012 .pdf
Further developments in the neurobiology of food and addiction: Update on the state of the science
Nicole M. Avena, Jessica A. Gold, Cindy Kroll, Mark S. Gold, Further developments in the neurobiology of food and addiction: Update on the state of the science, Nutrition, Volume 28, Issue 4, 2012, Pages 341-343, ISSN 0899-9007, https://doi.org/10.1016/j.nut.2011.11.002. Review article
Dual roles of dopamine in food and drug seeking: the drive-reward paradox
Wise R. A. (2013). Dual roles of dopamine in food and drug seeking: the drive-reward paradox. Biological psychiatry, 73(9), 819—826. https://doi.org/10.1016/i.biopsych.2012.09.001 Review wise2013 .pdf
Obesity and the brain how convincing is the addiction model?
Ziauddeen, H., Farooqi, I. S., & Fletcher, P. C. (2012). Obesity and the brain: how convincing is the addiction model? Nature Reviews Neuroscience, 13(4), 279–286. doi:10.1038/nrn3212 An increasingly influential perspective conceptualizes both obesity and overeating as a food addiction accompanied by corresponding brain changes. Because there are far-reaching implications for clinical practice and social policy if it becomes widely accepted, a critical evaluation of this model is important. Weexamine the current evidence for the link between addiction and obesity, identifying several fundamental shortcomings in the model, as well as weaknesses and inconsistencies in the empirical support for it from human neuroscientific research. At the outset, it is important to acknowledge that the food-addiction literature has largely adopted the clinical model of addiction as defined by the DSM-IV. Although this model has clinical validity, in the addiction research literature it has been supplemented, and to an extent superseded, by powerful neurobiological models that have decomposed the clinical syndrome in terms of its core cognitive processes and their possible neural substrates (BOX 1). This approach, which is based on a growingunderstanding of the neurobiology of addiction, is welcome and — as we discuss — may offer new ways of identifying overlap between obesity and addiction. However, this article is primarily concerned with theexisting arguments in favour of addiction as a model for obesity, arguments that draw on clinical definitions. ziauddeen2012 .pdf