Food addiction was first reported by Randolph [1] in 1956 and refers to the development of addiction-like symptoms associated with one or more foods that an individual consumes frequently and to which they are particularly sensitive. The concept of “food addiction” remained relatively unexplored for a considerable period following its initial conceptualization. Unlike substances known to cause addiction, such as drugs or alcohol, food is a fundamental necessity for survival. However, as research findings increasingly support the idea that specific types of foods, such as processed foods that are energy-dense and high in sugar, fat, and salt, can induce addiction [2], the concept has gained validity. Studies have demonstrated that refined sugar, while not necessary for survival, is abused as a substance, and exerts drug-like effects on the brain [3]. Numerous studies focusing on food addiction have been published in the last decade [4].
The definition of food addiction, as proposed by Gearhardt et al. [5], included the diagnostic criteria for substance dependence outlined in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). Food addiction is defined as a state in which eating behaviors substantially meet the diagnostic criteria for substance use disorders, leading to clinically significant impairment or distress. Although a clear definition or diagnostic criteria have not yet been established, according to numerous subsequent studies, food addiction has been defined as “a chronic and relapsing condition caused by the interaction of many complex variables that increase cravings for certain specific foods to achieve a state of high pleasure, energy, or excitement, or to relieve negative emotional or physical states” [6].
Eating behavior is regulated by the interactions of various neural circuits, including the hypothalamus, dorsolateral prefrontal cortex (DLPFC), amygdala, striatum, and midbrain [7]. Eating behavior is divided into homeostatic food consumption, which is regulated by energy stores and requirements, and hedonic food consumption, which is regulated by reward mechanisms [8]. Hedonic eating refers to the act of consuming food primarily for pleasure, rather than to meet energy requirements. This holds evolutionary significance: for survival, our brains compel us to seek out foods with the highest calorie content. Consequently, when we consume foods rich in fat, salt, and sugar, our brains release dopamine to induce a sense of pleasure [9].
Foods that are highly processed and refined with increased fat, sugar, and salt content to maximize the stimulating taste are called highly palatable (HP) foods. The combination of fat and sugar does not normally exist in nature. However, this pairing, by offering added rewarding effects to both the stomach and brain, tends to promote excessive consumption [10]. Food addiction has been linked to HP food, with studies demonstrating that HP food induces dopamine release in the brain. Additionally, naltrexone reduces consumption and preference for sweet, high-fat foods. Moreover, stimulating the DLPFC diminishes cravings for HP food [8-11].
Two ways are used to examine food addiction: a behavior and a substance. The behavioral perspective argues that no substance has yet been identified in food to cause addiction, such as ethanol in alcoholic beverages or nicotine in cigarettes, and that current research is incomplete, therefore, treating food addiction as an addictive behavior, such as a gambling addiction is reasonable. The substance perspective argues that HP food activates reward circuits in a manner akin to drugs but that certain behavior patterns, such as binge eating, can exacerbate food addiction [3,12]. According to Schulte et al. [12], who supports the “substance” side of the argument, individual risk factors such as genetic vulnerability, the addictive nature of certain foods, such as HP food, and behavior patterns such as bingeing, dietary restraint, and using food in response to negative emotions increase the risk of food addiction.
Binge eating and dietary restraint are common symptoms of eating disorders; therefore, it is reasonable to assume that eating disorders and food addiction are highly correlated. The link between binge eating and addictive disorders is wellestablished. In fact, binge eating overlaps with addiction in terms of diagnostic criteria. Furthermore, substance use disorders are more prevalent in patients with eating disorders than in the general population, and vice versa [13].
However, the therapeutic approach to addiction differs from that for treating traditional eating disorders. Although addiction management focuses on minimizing exposure to substances, treatment for eating disorders centers on addressing the root issue of placing excessive importance on body shape and weight. In this context, dieting is identified as the trigger for binge eating. Standard treatment for eating disorders encourages patients to eat all types of food, as dietary restraint triggers binge eating. When a patient with an eating disorder presents with food addiction, therapists often face conflicts between the aforementioned two approaches.
In this study, we present two patients with restrictive anorexia nervosa who presented to a clinic specializing in treating eating disorders. Anorexia nervosa is characterized by restricted eating and low body weight; binge eating frequently occurs during treatment. We observed that binge eating during recovery differed significantly between patients, with and without food addiction.
This study was approved by the Seoul National University Hospital Institutional Review Board with appropriate informed consent (2310-096-1476).
Case 1 was a 13-year-old female adolescent patient who was referred to the Eating Disorder Clinic for the treatment of anorexia nervosa, restricting type. At the initial visit, the patient was 158 cm tall with a weight of 33.1 kg (body mass index [BMI]=13.3 kg/m2). The patient was discharged from the pediatric ward after 5 days of hospitalization, the day before the outpatient visit.
The patient started dieting 6 months before her visit when she weighed 52 kg. At first, she ate regularly and exercised, but gradually began to eat less, losing 19.5 kg in 5 months. Although her weight reduced to 30.8 kg; she limited her intake to less than 500 calories due to the fear of weight gain. She weighed herself and examined her body daily. The patient had been amenorrheic for 3–4 months. She was admitted to the pediatric department and gained 2.3 kg in 5 days. After discharge from the hospital, the patient visited the clinic for evaluation and treatment of anorexia nervosa.
Therapeutic intervention and progress noteAt the beginning of the treatment, eating behaviors were addressed using Cognitive Behavior Therapy for Eating Disorders (CBT-E) to structure eating and educate the patient. As is the case with most young patients, this patient was receptive to education. Once the meals were structured, we increased the size and diversity of the food. Gradually, she was able to consume sugary and fatty foods that she had previously avoided. Two months after the visit, the patient ate three meals regularly, and her weight recovered to 40.6 kg. After 5 months, her weight returned to 46.4 kg and she resumed menstruation. Her food intake remained stable, and her weight was maintained between 48 and 52 kg (BMI=19.2–20.9 kg/m2) for more than 6 months when the treatment was terminated (Fig. 1). The total treatment duration was 1 year and 3 months.
Therapeutic interventions included psychopharmacotherapy and family therapy, in addition to CBT-E. The patient was medicated with escitalopram and olanzapine and maintained at 10 mg of escitalopram and 2.5 mg of olanzapine.
Binge eating patterns in the recovery phaseBinge eating begins at some point of recovery in most patients with anorexia nervosa [14]. This patient began to experience increased appetite, overeating, and binge eating after 2 months of treatment. After overeating, due to fear of weight gain, she engaged in self-harming behaviors, such as wrist cutting and self-hitting. She also forced her mother to consume the same amount of food.
The patient’s self-monitoring record displayed heightened fear and anxiety correlating with an escalation in the quantity of food consumed and the frequency of binge eating. Controlling behaviors, such as eating mostly low-calorie foods, holding off on eating high-calorie foods for as long as possible, and prolonged hesitation before eating were observed (Tables 1-3 and Supplementary Tables 1
Case 2 was a 15-year-old female adolescent patient who visited the Eating Disorder Clinic for treatment of anorexia nervosa, restricting type. At the initial visit, the patient was 162 cm tall and weighed 36 kg (BMI=13.7 kg/m2). The patient had a history of 3 months of psychiatric treatment, including 2 weeks of hospitalization. The patient visited the clinic wanting to continue treatment at a specialized eating disorder facility.
She had maintained a slim physique since elementary school through continuous ballet training. She started dieting in her second year of middle school when she noticed weight gain. At first, she curtailed snacks but gradually reduced her food intake to extreme levels, losing 15 kg in a year. Concerned about her condition, her parents admitted her to the pediatric psychiatric unit of a university hospital, for 2 weeks. She was then referred to the clinic for evaluation and treatment of her eating disorder.
Therapeutic intervention and progress noteAt the beginning of treatment, we attempted to establish a regular eating pattern. Based on the principles of the CBT-E, three regular meals, and two to three snacks were recommended, and the patient was encouraged to choose the type of food she ate. Initially, the patient ate cookies and ice cream as snacks, but gradually, all meals and snacks consisted of sweet foods. After a few weeks of observation, she was binge eating sweet foods, and her craving for sweet foods became intense. The uncontrolled intake led to increased conflict between the patient and her mother and an escalation in self-injury, such as picking the skin and self-hitting was observed. A 1-week inpatient hospitalization was used to manage binge eating and regulate the consumption of sweet foods. After discharge, we intervened to reduce the intake of sweet foods.
Her weight recovered to 43.8 kg at 4 weeks, 46.9 kg at 8 weeks, 49.9 kg at 12 weeks, 50 kg at 6 months, and 55 kg at 7 months, and she maintained 56–57 kg (BMI=21.3–21.7 kg/m2) for 1 year (Fig. 2). In addition to CBT-E, interpersonal psychotherapy, family therapy, and individual psychotherapy for the patient’s mother, and medication was administered. During the treatment period of 20 months, the primary medicines used were fluoxetine 20–40 mg and fluvoxamine 5–150 mg with doses escalating as needed, and naltrexone was also added during the treatment course. For sleep control, lorazepam and trazodone were administered over time. The treatment is ongoing.
The patient presented with binge eating episodes occurring once a week after treatment at a previous institution. A few days after the initial appointment, her mother contacted the clinic to report that she was binge eating every day and asked for advice. Subsequently, binge eating has continued, and the patient has become obsessed with sweet foods. As binge eating occurs in many patients with anorexia nervosa, we educated the patient and her parents that eating the foods she had been avoiding is normal. However, the number of snacks consumed continued to increase, and the patient felt addicted to them.
As compared to Case 1, in Case 2 the craving for sweetness was significantly greater than the fear of gaining weight. Regret after binge eating and fear of weight gain were also present in Case 2 but played a minor role. The observed behaviors included constant craving for food and excessive consumption, with futile attempts to control them (Tables 4-6 and Supplementary Tables 4
After 1 week of inpatient treatment, binge eating was more controlled than before. She packed lunch for school and tried to eat healthy food. After discharge, we intervened with the types of food she was eating and encouraged her to reduce the sweetness. The frequency and amount of binge eating gradually decreased. However, a few months later, she experienced a series of negative events that led to a resurgence in binge eating. She still consumed excessive amounts of sugar, such as 3–4 chocolates and 3–4 ice creams, at a time.
The patient in Case 1 exhibited a typical recovery process for treating anorexic nervosa, meanwhile, Case 2 exhibited a less common pattern of food addiction. In Case 2, the patient’s self-monitoring record (Tables 4-6 and Supplementary Tables 4
Controversy may arise over whether food addiction occurs solely within the context of eating disorders or represents an independent impairment. Considering the clinical features of food addiction, the particular addiction appears to be distinct from eating disorder diagnoses. In anorexia nervosa or bulimia nervosa, the core pathology is over-evaluation of body shape and weight. In contrast, food addiction tends to revolve around symptoms of addiction to specific foods, making it relatively distinguishable. However, controversy exists regarding whether the clinical features of binge eating disorders, such as excessive food consumption, negative emotions after consumption, and loss of control, overlap with those of food addiction. However, although binge eating is the central symptom of binge eating disorder, not all individuals with food addiction necessarily encounter this. Only 47% of individuals with binge eating disorders met the criteria for a food addiction diagnosis, and 44% of those with food addiction did not meet any eating disorder diagnostic criteria, supporting this distinction [16].
Although eating disorders and food addiction are separate diagnoses, they are closely related. Contributors to food addiction can include individual risk factors such as genetic vulnerability, behavioral patterns, such as restriction or binge eating, and the addictive potential of certain HP foods [12]. A plausible hypothesis is that vulnerable patients may trigger food addiction through extreme dieting, as observed in anorexia nervosa. Additionally, stress-induced binge eating might serve as a catalyst for food addiction, or increased consumption due to food addiction could potentially lead to obesity.
The treatment of the Case 2 patient presented a significant challenge because of the treatment approach for eating disorders, particularly anorexia nervosa, which emphasizes avoiding restrictions on the type or amount of food consumed. The current leading treatment for eating disorders is CBT-E, as outlined by Fairburn [14]. CBT-E acknowledges that many patients transition between different eating disorder diagnoses, recognizing the core pathology that underlies all diagnoses: over-evaluation of shape and weight and their control [14]. The core pathology causes patients to adhere to strict diets, resulting in the development of eating disorders. We aim to be respectful and ensure that patients consume an adequate amount of food, even if their initial choice of meals primarily includes unhealthy options. This is because restricting specific foods or controlling their quantities may trigger the underlying pathology.
Although the aforementioned approach is effective for many patients with eating disorders, it does not seem equally favorable for individuals with food addiction, as in Case 2. When food addiction is present, limiting the consumption of specific foods is necessary. This does not mean dieting but rather implies abstinence from specific foods representing addictive patterns, requiring cautious consideration regarding the exacerbation of eating disorder symptoms. However, as eating disorder treatment aims not for unrestricted eating of any food but for a balanced diet, this is a necessary approach.
The reason why CBT-E does not incorporate an approach that considers the aspect of food addiction may be related to historical factors. In 2003, the DSM-IV eating disorder diagnoses consisted only of anorexia nervosa and bulimia nervosa [10]. Over the past two decades, the consumption and production of HP foods, including those containing refined sugars, have significantly increased. Additionally, the emergence of food delivery services and food consumption trends, such as mukbang, has gained popularity. These changes are believed to directly influence symptoms in individuals with eating disorders.
Given recent trends in food culture among Korean adolescents, such as Maratang, Tanghuru, and mega-sized sugary drinks, incorporating an assessment for food addiction into the diagnosis and treatment approach for adolescent patients with eating disorders can enhance the therapeutic effect. Evaluation may include exploring family dietary habits and using questionnaires, such as the Food Craving Questionnaire and YFAS. If food addiction is suspected, initiating nutritional intervention and education from the early stages of treatment and considering the use of medications, such as naltrexone can be beneficial. Currently, research is sparse with no clear treatment protocol, thus more research is needed.
The online-only Data Supplement is available with this article at https://doi.org/10.5765/jkacap.230069.
Data sharing not applicable to this article as no datasets were generated or analyzed during the study.
The authors have no potential conflicts of interest to disclose.
Supervision: Hyung Jin Choi, Min-Jung Park. Visualization: Younjoo Song. Writing—original draft: Younjoo Song. Writing—review & editing: Hyung Jin Choi, Min-Jung Park.
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