Bulimia nervosa (BN) is a psychiatric disorder characterized by episodic binge eating, purging, and emotional dysregulation. It involves frequent bouts of binge eating that patients believe they are unable to control, followed by compensatory behaviors such as forced vomiting, fasting, the use of laxatives or diuretic and diet pills, or over-exercising. This disorder affects approximately 0.3% of adults in the United States and is much more common in women than in men. Although the exact cause of bulimia nervosa is unknown, it may be caused by disrupted neural processes of self-regulation, taste-rewarding, and body image. Contributing factors include genetic predisposition and the influence of psychosocial and environmental triggers.
People with bulimia experience a decrease in blood flow through the precuneus, the brain region associated with self-consciousness, during food exposure and cravings. It highlights a possible brain mechanism that shifts attention away from negative self-reflection and toward something concrete, such as food, during times of stress. Bulimia symptoms suggest an increased need for stimulation to detect internal states and homeostatic processing, as well as difficulties maintaining internal homeostasis. Symptoms serve to control internal states.
Interoception is defined as the sense of the physiological condition of the body and plays a role in physical and emotional homeostasis. Interoceptive senses include pain, hunger, satiety, taste, sensual touch, heartbeat, breathlessness, and the need to urinate or defecate. Interoception happens automatically and without our conscious awareness. It assesses the body's ability to process stimuli from the interoceptive senses. Interoceptive awareness necessitates metacognitive reflection on one's internal state, which is influenced by interoceptive and exteroceptive integration, conditioning, cognitive patterns, prediction accuracy, and defense mechanisms such as deliberately ignoring internal cues. It’s influenced by higher order cortical processing, which occurs secondary to interoceptive sensory processing.
Deficits in interoceptive neural networks contribute to widespread disturbances in one's ability to track their body, resulting in difficulty detecting hunger and satiety cues, which leads to overeating. Increased pain tolerance may make over-exercise and purging behaviors tolerable, and abnormal taste processing may delay habituation to food rewards, leading to binge eating behaviors. Interoceptive sensory deficits may contribute to body cue-tracking issues and contribute to issues with body image, self-harm, thrill seeking behaviors, and eating regulation problems. Body checking behaviors may be attempts to obtain a sense of one's own body using external stimuli. Risky behaviors or self-harm may be attempts to "feel" the physical state of the body, whereas calorie counting may be an attempt to compensate for hunger and satiety deficits by manually adjusting intake by using cognitive abilities and external stimuli.
The combination of taste, pain, and gastric distention disturbances influences cycles of food restriction and binge eating behaviors, just as taste disturbances can influence food preferences. These changes allow for objectively large amounts of food consumption as well as the ability to tolerate the pain associated with a distended gut. High pain thresholds contribute to over-exercising and the ability to tolerate vomiting.
Serotonin, also known as 5-hydroxytryptophan, is a neurotransmitter that regulates memory, learning, sleep, mood, and appetite. When going without food for longer periods of time, such as while sleeping, there is a significant drop in serotonin levels, which leads to binge eating and increased irritability. When people with bulimia nervosa routinely engage in binge eating episodes, a feedback loop is created that perpetuates the binge-and-purge cycle. They will frequently binge eat in order to increase mood and provide relief from distress. However, the guilt induced by these actions trigger depression and low serotonin levels, leading to further binge eating episodes.
Dopamine is thought of as the “pleasure chemical” due its links with rewarding behaviors and drugs of abuse. Dopamine is involved with reward-motivated behavior and regulates movement, memory, hormones, and sensory processing. Bulimia is associated with lower levels of dopamine and its receptors with binge eating being associated with dopamine release in certain parts of the brain.
Through reward pathways, the hypothalamus serves as the primary appetite regulatory center. It is crucial in orchestrating the body's response to food and hunger. The arcuate nucleus (ARC) suppresses appetite while the lateral hypothalamus stimulates it. The mesolimbic reward pathway promotes pleasure by increasing dopamine release. Food activates the mesolimbic reward system, resulting in pleasure, which activates food-seeking behaviors via cognitive processes.
A Pavlovian conditioning mechanism transforms goal-directed actions into compulsive and stimulus-driven behaviors during binge eating. A key component of habitual responding is the repeated pairing of a reward-associated stimulus with a compulsive seeking behavior. Bulimia is associated with abnormalities in key cognitive domains such as impulsivity and compulsivity, executive function, attention, and decision-making, all of which are primarily mediated by the prefrontal cortex and the striatum. Food impulsivity initially results in pleasure and satisfaction. Compulsivity may develop with chronic substance abuse as an individual's drive shifts from seeking pleasure to seeking relief from distress and the anticipation of obtaining food.
Comments