Anorexia nervosa (AN) is a bio-psycho-social disorder characterized by a low body weight, unhealthy weight loss methods, an obsession with weight and body shape, or self-starvation. The frequently chronic and disabling condition is characterized by irregular feeding patterns and weight regulation, as well as a deviant attitude and perceptions of body weight and shape. This eating disorder leads to an unrelenting obsession with fatness, extreme medical and psychological morbidity, and a standardized mortality rate higher than that of other psychiatric disorders, leading to the second highest mortality rate among adolescents. Although the cause of anorexia is unknown, biological, genetic, environmental, and social factors, as well as neurobiological vulnerabilities, all play a role.
Anorexia may be associated with disruptions in pathways related to feeding behavior modulation, mood, temperament, obsessionality, or impulse control. It could also be caused by primary disruptions in pathways that modulate factors related to body proprioception, resulting in body image distortions. The limbic and cognitive pathways are of particular interest. The limbic pathway is concerned with what is important and rewarding to a person, whereas the cognitive pathway is concerned with what to pay attention to, what to avoid, how to plan, and how to control oneself. They have an impact on appetite, emotion, and thought.
There has been suggested aberrant functioning of parietal somatosensory regions, anxiety-related mesolimbic circuits, and reward-related regions. Along with these processing centers, abnormalities in the prefrontal cortex have been observed, resulting in an impaired ability to identify the emotional significance of stimuli such as hunger signals associated with altered interoceptive awareness or body image disturbance. Increased traffic on these circuits causes anxiety.
Anomalies in the orbitofrontal cortex, which sends signals to the brain to stop eating, increased activity in the dorsal striatum, which is linked to habitual behavior, and a change in the right insula, which processes taste perception and is involved in interoception, or the ability to sense one's own body signals, have all been observed in anorexia. The sensory-hedonic response to taste is coded by the anterior insula, the anterior cingulate cortex, and the orbitofrontal cortex. Changes interfere with the desire to eat. When consuming palatable food, anorexic patients have altered set-points or altered sensitivity for sensory-interoceptive reward processes. The set point simulates a constant state of satiety, limiting reward processing.
Dopaminergic function modulates both reward and affect. It is essential in the processing of reward in reinforcers such as food. Aberration in dopaminergic functioning is seen in obsessive or ritualistic behaviors. In anorexia, the neurotransmitter dopamine is involved in faulty reward processing. Typically, the pleasure of taste makes you want to keep eating it. However, in this case, this fails and breaks down in anorexia. The brain has trouble coding reward and is overly sensitive to punishment. Dopamine release from the dorsal striatum causes anxiety rather than pleasure. In fact, while reward processing brain circuits are "losing," they become more active. Ingestion of highly palatable foods (such as high-sugar foods) may trigger dopamine release and responses similar to those seen with amphetamine use, which are associated with euphoria in people who do not have anorexia. However, in anorexic patients, this release causes the expected endogenous dopamine release but is perceived as highly unpleasant and anxiogenic, which may account for the persistence in self-starvation. If food is anxiogenic, self-starvation reduces anxiety; anorexic individuals find it aversive. Along with dopaminergic findings, serotonergic functioning has been accounted for behavioral rigidity and trait obsessionality in anorexia.
With the etiology of anorexia nervosa still unknown, it is important to explore contributions from genetic and biological factors along with sociocultural influences. Vulnerabilities in certain processing centers, altered appetitive mechanisms, and anomalies of neurotransmitters have been observed in a wide variety of examinations including imaging, genetic, and hormonal or biological studies. The neurobiology behind anorexia nervosa is complex due to a variety of factors and continues to be considered the most deadly psychological illness. It is important to understand the biological vulnerabilities of this illness in order to directly improve treatment and prognosis.
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