Food Addictions

Genetic contributions to food addiction seem plausible given the fact that addiction has an estimated heritability of 50–70%. Various researchers have described how such genetic factors are at play in the dysmorphic syndromes of Prader-Willi, Cohen, Carpenter, and others, as well as leptin/receptor mutation, β3 AR mutation and the overexpression of neuropeptide Y (NPY). Each one of these genetic syndromes results in obesity and can be seen to exacerbate food addictions in the individuals that are so afflicted. As described later in the neurochemical section, dopamine plays a critical role in addiction. The neurogenetics of dopaminergic receptor supersensitivity and brain reward circuitry continues to emerge. For example, a plethora of animal models are being used to elucidate the role that genetics plays in both animal and human vulnerability to addiction in terms of their responsiveness to food or cocaine.

Obesity Models

Given the importance of examining food addiction in the context of the obesity epidemic, several models of obesity have been used to explore the idea of food addiction. A full, comprehensive review of obesity models is beyond the scope of this chapter. However, diet-induced obesity, in which rodents overconsume a highly palatable, high-fat, sweet diet, or a cafeteria diet, consisting of a variety of highly palatable foods (such as bacon, cheesecake, and peanut butter), is often cited in the food addiction literature. Early studies using a cafeteria diet report opiate-like withdrawal in obese rats when they were administered the opioid antagonist naloxone (Le Magnen, 1990). Compulsive eating behavior has also been noted in obese rats maintained on a cafeteria diet (Johnson & Kenny, 2010), potentially indicating an addictive-like state. Mice that were maintained on a high-fat diet for 6 weeks and then abstained from the diet showed indications of withdrawal symptoms such as anxiety-like behavior as well as enhanced motivation for palatable foods (Sharma, Fernandes, & Fulton, 2013).

“Food Addiction” and Obesity

“Food addiction” as measured with the YFAS relates to higher body mass index (BMI). In nonobese adults, prevalence rates of “food addiction” range between 5% and 15%. Two studies that used a child version of the YFAS in children and adolescents reported prevalence rates between 3% and 7%.12,13 In obese adults, prevalence rates range between 15% and 20% but reach up to 30%–50% in treatment-seeking adults with extreme obesity.14,15 Similarly, 38% of obese adolescents recruited at the beginning of an in-patient weight-loss program were classified as “food addicted.”16 Therefore, although a relationship between “food addiction” and body weight exists, neither can obesity be equated with “food addiction” nor is “food addiction” restricted to individuals with obesity.

Abstract

Food addiction (FA) is loosely defined as hedonic eating behavior involving the consumption of highly palatable foods (ie, foods high in salt, fat, and sugar) in quantities beyond homeostatic energy requirements. FA shares some common symptomology with other pathological eating disorders, such as binge eating. Current theories suggest that FA shares both behavioral similarities and overlapping neural correlates to other substance addictions. Although preliminary, neuroimaging studies in response to food cues and the consumption of highly palatable food in individuals with FA compared to healthy controls have shown differing activation patterns and connectivity in brain reward circuits including regions such as the striatum, amygdala, orbitofrontal cortex, insula, and nucleus accumbens. Additional effects have been noted in the hypothalamus, a brain area responsible for regulating eating behaviors and peripheral satiety networks. FA is highly impacted by impulsivity and mood. Chronic stress can negatively affect hypothalamic–pituitary–adrenal axis functioning, thus influencing eating behavior and increasing desirability of highly palatable foods. Future work will require clearly defining FA as a distinct diagnosis from other eating disorders.