Anorexia nervosa (AN) is a serious psychiatric condition defined by extreme food restriction, a pathologically low body weight, and an intense fear of gaining weight. AN carries one of the highest mortality rates among all psychiatric disorders due to the profound physiological and functional consequences that chronic starvation imposes on the central nervous system. Understanding how this process alters the brain is crucial for grasping the complex nature of the illness and recovery challenges.
Structural Alterations in Brain Volume
Severe malnutrition causes measurable changes in brain structure, primarily manifesting as a reduction in overall brain volume. This reduction affects both gray matter and white matter tissues. Gray matter shows a significant decrease in volume, sometimes correlating with the duration of starvation.
These structural changes result from the body diverting resources away from non-essential functions to preserve survival during energy deprivation. The substantial loss of brain volume is attributed to the depletion of fat, protein, and water content within the brain tissue, not the permanent loss of neurons.
This volume loss is often reversible, particularly in younger patients. With successful weight restoration and sustained nutritional rehabilitation, gray matter volume begins to increase, often returning to healthy levels. Prompt treatment is important for minimizing the long-term impact of the illness.
Neurochemical and Metabolic Disruption
The brain has high metabolic demands, and chronic energy deprivation profoundly disrupts its internal chemistry and energy supply. The central nervous system relies almost exclusively on glucose for fuel. Starvation alters how the brain acquires and uses this primary energy source, which can impair functions like attention and memory.
Starvation also disrupts hormonal signaling systems. Leptin (satiety signal) drops dramatically, while ghrelin (the hunger hormone) often rises. Cortisol, a stress hormone regulated by the HPA axis, is chronically elevated in acute illness. This elevation can suppress appetite and motivation to eat, reinforcing restrictive behaviors.
The balance of neurotransmitters is significantly altered. Serotonin, which regulates mood, anxiety, and obsessive thoughts, is dysregulated in AN. Starvation may temporarily lower anxiety by decreasing serotonin activity, creating a negative feedback loop where restriction feels calming. Conversely, in a non-starved state, individuals may have serotonin overproduction, linked to heightened anxiety and emotional distress.
Dopamine, central to reward processing and motivation, is also implicated. Alterations in the dopamine system affect how a person responds to pleasure and reward, including food and social interactions. This dysregulation may contribute to the ability of individuals with AN to resist eating and find less pleasure in typically rewarding activities.
Impact on Cognitive Function and Decision Making
The structural and chemical changes translate into noticeable impairments in cognitive function and decision-making. Executive functions—the mental skills needed to plan, focus attention, and manage tasks—are often compromised during the acute phase of AN. Patients frequently exhibit cognitive rigidity, a difficulty in shifting thought patterns, which contributes to the illness’s inflexible, rule-bound behaviors.
Reward processing is also functionally altered, seen in the brain’s response to food and non-food rewards. Individuals with AN may show a muted neural response to food cues, or even an activated response to punishment. This altered reward circuitry may help sustain self-starvation by diminishing the natural drive to seek and consume energy.
A core symptom is persistent body image distortion, which stems from misinterpreting sensory information. Brain imaging shows altered activity in the parietal and frontal cortex, involved in spatial self-perception. This impairment may explain why the brain fails to accurately update the perception of body size despite visual evidence of emaciation. Difficulties with decision-making involving risk and reward are also observed, sometimes linked to reduced volume in the orbitofrontal cortex during acute illness.
Brain Recovery and Long-Term Outcomes
The prognosis for structural changes in the brain is favorable with nutritional restoration. The reduction in gray matter volume, associated with acute malnutrition, typically begins to reverse quickly once a healthy body weight is achieved and maintained. Long-term weight recovery normalizes overall brain volume and cortical thickness.
The timeline for full recovery of both structure and function varies widely, and not all neurocognitive traits fully resolve. While physical volume may restore, characteristics like heightened anxiety, perfectionism, or cognitive rigidity may persist after weight normalization. This suggests these differences may be predisposing factors or long-lasting effects. Sustained weight restoration is paramount, as relapses can interrupt the healing process.