Pai, N., Vella, S. L., & Richardson, K. (2014). Is food addiction a valid phenomenon through the lens of the DSM-5? Australian & New Zealand Journal of Psychiatry, 48(3), 216-218. https://doi.org/10.1177/0004867413512384 From the research article’s abstract: “The concept of food addiction (FA) continues to gain traction with support from many researchers. This letter is written in response to the claim that FA is overhyped in the media with weak scientific evidence. We believe there is sufficient scientific evidence to support the acknowledgment of FA in the DSM-5 and to further investigate its potential existence. We agree that more research is needed; however, we also believe it is important to consider FA as a possible diagnosis so that we can offer effective treatment options rather than doubting its existence and not offering potentially beneficial therapies.”
Attentional and motor impulsivity interactively predict ‘food addiction’ in obese individuals
Meule, A., de Zwaan, M., & Müller, A. (2017). Attentional and motor impulsivity interactively predict ‘food addiction’ in obese individuals. Comprehensive Psychiatry, 72, 83–87. https://doi.org/10.1016/j.comppsych.2016.10.001 From the research article’s abstract: “Impulsivity is a multifaceted construct and constitutes a common risk factor for a range of behaviors associated with poor self-control (e.g., substance use or binge eating). The short form of the Barratt Impulsiveness Scale (BIS-15) measures impulsive behaviors related to attentional (inability to focus attention or concentrate), motor (acting without thinking), and non-planning (lack of future orientation or forethought) impulsivity. Eating-related measures appear to be particularly related to attentional and motor impulsivity and recent findings suggest that interactive effects between these two facets may play a role in eating- and weight-regulation. One-hundred thirty-three obese individuals presenting for bariatric surgery (77.4% female) completed the BIS-15 and the Yale Food Addiction Scale (YFAS) 2.0, which measures addiction-like eating based on the eleven symptoms of substance use disorder outlined in the fifth version of the Diagnostic and Statistical Manual of Mental Disorders. Sixty-three participants (47.4%) were classified as being ‘food addicted’. Scores on attentional and motor impulsivity interactively predicted ‘food addiction’ status:
Food Addiction: Its Prevalence and Significant Association with Obesity in the General Population
Pedram, P., Wadden, D., Amini, P., Gulliver, W., Randell, E., Cahill, F., Vasdev, S., Goodridge, A., Carter, J. C., Zhai, G., Ji, Y., & Sun, G. (2013). Food addiction: its prevalence and significant association with obesity in the general population. PLoS One, 8(9), e74832. https://doi.org/10.1371/journal.pone.0074832 From the research article’s abstract: “Background: ‘Food addiction’ shares a similar neurobiological and behavioral framework with substance addiction. However whether, and to what degree, ‘food addiction’ contributes to obesity in the general population is unknown. Objectives: to assess 1) the prevalence of ‘food addiction’ in the Newfoundland population; 2) if clinical symptom counts of ‘food addiction’ were significantly correlated with the body composition measurements; 3) if food addicts were significantly more obese than controls, and 4) if macronutrient intakes are associated with ‘food addiction’. Design: A total of 652 adults (415 women, 237 men) recruited from the general population participated in this study. Obesity was evaluated by Body Mass Index (BMI) and Body Fat percentage measured by dual-energy X-ray absorptiometry. ‘Food addiction’ was assessed using the Yale Food Addiction Scale and macronutrient intake was determined from the Willet Food Frequency Questionnaire. Results:
Is Obesity an Addiction?
Kenny, P. J. (2013). The food addiction. Scientific American, 309(3), 44–49. https://doi.org/10.1038/scientificamerican0913-44 From the research article: “Obesity, it seems, is not caused by a lack of willpower. And it is not always caused by an imbalance in hormones. In some cases at least, obesity may be caused by hedonic overeating that hijacks the brain’s reward networks. Like addictive drugs, overeating creates a feedback loop in the brain’s reward centers—the more you consume, the more you crave, and the harder it is for you to satisfy that craving. But does that make hedonic eating an addiction? Drugs of abuse, such as morphine, stimulate the brain’s reward systems the way food does. Yet the similarities do not end there. When morphine is injected into the striatum of rats, it triggers bingelike overeating, even in rats that have been fed to satiety. This response shows that morphine and other opiates mimic the effects of neurotransmitters (brain chemicals) such as endorphins that are naturally produced in the brain to stimulate feeding behaviors.
Is Obesity an Addiction?
Kenny, P. J. (2013). The food addiction. Scientific American, 309(3), 44–49. https://doi.org/10.1038/scientificamerican0913-44 From the feature article’s text: “The more you consume, the more you crave, and the harder it is for you to satisfy that craving. obesity may be caused by hedonic overeating that hijacks the brain’s reward networks.”
Preliminary validation of the Yale Food Addiction Scale for children
Gearhardt, A. N., et al. (2013). Preliminary validation of the Yale Food Addiction Scale for children. Eat Behav, 14(4), 508–512. https://doi.org/10.1016/j.eatbeh.2013.07.002 From the validation study’s abstract: “If highly processed foods also have addictive potential, children may be more susceptible to this effect than adults due to neural and psychological vulnerabilities.”
Stress and addiction
Hildebrandt, T., & Greif, R. (2013). Stress and addiction. Psychoneuroendocrinology, 38(9), 1923–1927. https://doi.org/10.1016/j.psyneuen.2013.06.017 From the research article’s abstract: “Appetitive behaviors such as substance use and eating are under significant regulatory control by the hypothalamic-pituitary adrenal (HPA) and hypothalamic pituitary gonadal (HPG) axes. Recent research has begun to examine how these systems interact to cause and maintain poor regulation of these appetitive behaviors. A range of potential molecular, neuroendocrine, and hormonal mechanisms are involved in these interactions and may explain individual differences in both risk and resilience to a range of addictions. This manuscript provides a commentary on research presented during the International Society of Psychoneuroendocrinology’s mini-conference on sex differences in eating and addiction with an emphasis on how HPG and HPA axis interactions affect appetitive behaviors in classic addictions and may be used to help inform the ongoing debate about the validity of food addiction.”
Relationship of food addiction to weight loss and attrition during obesity treatment
Lent, M. R., Eichen, D. M., Goldbacher, E., Wadden, T. A., & Foster, G. D. (2014). Relationship of food addiction to weight loss and attrition during obesity treatment. Obesity, 22(1), 52–55. https://doi.org/10.1002/oby.20512 From the research article’s abstract: “The relationship between food addiction (FA) and weight and attrition outcomes in overweight and obese adults participating in weight loss interventions were prospectively examined in this study. Participants were 178 adults (51.2 ± 11.7 y, 36.1 ± 4.8 kg/m²) in one of two outpatient weight loss treatment programs for approximately 6 months. The Yale Food Addiction Scale (YFAS) assessed FA diagnosis and symptom count. The relationship between FA and weight loss and attrition was assessed. After controlling for treatment arm, gender, and baseline weight, there was no effect of FA status on weight loss (P = 0.17) or attrition (P = 0.37). Similarly, baseline FA symptom count was not associated with weight loss (P = 0.14) or attrition (P = 0.10). Neither FA status nor symptom count affects weight loss or attrition during weight loss treatment.”
An Introduction to the Special Issue
Small, D. M., & DiLeone, R. J. (2013). An introduction to the special issue. Biological Psychiatry, 73(9), 799-801. https://doi.org/10.1016/j.biopsych.2013.03.007 From the research article’s abstract: “It has long been acknowledged that there are overlapping neural circuits for food and drugs of abuse. In particular, regions of the brain and intracellular signaling cascades implicated in processing the reinforcing effects of food also appear to regulate the consumption of addictive drugs (1–3). What is being ardently debated is whether overlapping substrates imply that food is, or can be, addictive (4,5). This is a critical question because it is attractive to use the addiction framework to jump-start and guide our understanding of how neural circuits of reward and self-control might contribute to understanding overeating and the obesity epidemic. However, the price of adopting an inappropriate framework is high, as it might steer research toward evaluating mechanisms that have been shown to be critical for addiction at the expense of those that are unique to obesity and perhaps key to understanding overeating.”
Does a Shared Neurobiology for Foods and Drugs of Abuse Contribute to Extremes of Food Ingestion in Anorexia and Bulimia Nervosa?
Kaye, W. H., Wierenga, C. E., Bailer, U. F., Simmons, A. N., Wagner, A., & Bischoff-Grethe, A. (2013). Does a shared neurobiology for foods and drugs of abuse contribute to extremes of food ingestion in anorexia and bulimia nervosa? Biological Psychiatry, 73(9), 836–842. https://doi.org/10.1016/j.biopsych.2013.01.002 From the research article’s abstract: “Is starvation in anorexia nervosa (AN) or overeating in bulimia nervosa (BN) a form of addiction? Alternatively, why are individuals with BN more vulnerable and individuals with AN protected from substance abuse? Such questions have been generated by recent studies suggesting that there are overlapping neural circuits for foods and drugs of abuse. To determine whether a shared neurobiology contributes to eating disorders and substance abuse, this review focused on imaging studies that investigated response to tastes of food and tasks designed to characterize reward and behavioral inhibition in AN and BN. BN and those with substance abuse disorders may share dopamine D2 receptor–related vulnerabilities, and opposite findings may contribute to “protection” from substance abuse in AN.