Towards a Translational Approach to Food Addiction: Implications for Bulimia Nervosa

Abstract

Purpose of Review In recent years, the food addiction hypothesis of loss-of-control eating has gained traction in the field of eating disorders. In particular, the neural process of food addiction plays a dominant role in the recently formulated "addictive appetite" model of bulimia nervosa and binge eating disorder. Nonetheless, several components of the food addiction hypothesis, including the presence of withdrawal and tolerance effects, as well as the proposition that some foods possess "addicting" properties, remain highly controversial. In response, the current review synthesises existing evidence for withdrawal and tolerance effects in people with bulimia nervosa. Recent Findings The recent development of a validated tool to measure withdrawal from highly processed foods will aid in measuring withdrawal symptoms and testing hypotheses related to withdrawal in the context of food addiction. We subsequently describe preclinical and human evidence for a central insulin-and dopamine-mediated pathway by which recurrent loss-ofcontrol binge eating is maintained in bulimia nervosa. Summary Evidence in populations with bulimia nervosa and loss-of-control eating provides preliminary support for the role of food addiction in the maintenance of bulimia nervosa. Future longitudinal research is needed to develop a clearer profile of illness progression and to clarify the extent to which dysregulation in glucose metabolism contributes to food craving and symptom maintenance in bulimia nervosa.

Separating the Signal from the Noise: How Psychiatric Diagnoses Can Help Discern Food Addiction from Dietary Restraint

“…The mesolimbic dopaminergic circuit is clearly affected by both highly palatable foods and diet-induced obesity similar to exposure to drugs of abuse [ 92 ]. Recent review articles have discussed highly processed foods (often high in glycemic index) as impacting neurohormonal and inflammatory signaling pathways in ways that create a vicious cycle of impulsivity, compulsivity, FA, and EDs [ 93 , 94 , 95 ]. The Regulatory Model of Addictive Vulnerability (RMAV) proposes that susceptibility to addictive disorders is linked to how well an individual’s regulatory system responds to challenges, also referred to as allostasis [ 96 ].…”

Brain Correlates of Eating Disorders in Response to Food Visual Stimuli: A Systematic Narrative Review of FMRI Studies

“…The alternation between the two phases of BN and OCD is configured in both disorders as a mechanism for maintaining symptomatology in a vicious cycle [ 133 , 134 ]. In addition, it appears that BN individuals develop a form of addiction to tempting food [ 135 , 136 ], which may explain the hyperactivity of the medial PFC.…”

Clinical Considerations of Ultra-processed Food Addiction Across Weight Classes: an Eating Disorder Treatment and Care Perspective

“…Treatment professionals should discuss the issue of fat shaming in society [ 135 ]. Move toward a low glycemic carbohydrate diet (e.g., beans and high-fiber whole grains) given that high glycemic carbohydrates (e.g., refined grains and added sugars) can interact with mesolimbic dopamine systems that heighten food cravings and may lead to loss of control [ 45 , 136 ]. Identifying individual trigger foods that should be avoided can be helpful.…”