The Vicious Cycle of Starvation and the Brain
Anorexia Nervosa (AN) is one of the most lethal psychiatric conditions, but is the brain dysfunction we see in those affected a root cause of the illness or a devastating consequence of starvation? For decades, this chicken-or-egg question has puzzled scientists and clinicians alike. The answer, emerging from cutting-edge neuroimaging research, is complex: it appears to be both. The malnourished brain becomes both a casualty and a collaborator in the progression of anorexia, trapped in a cycle where the very organ needed for recovery is compromised by the illness itself.
Understanding this relationship isn't just academic—it's crucial for developing more effective treatments and offering new hope to those affected.
2%
of body weight
20%
of daily calories consumed by the brain
75%
showed improvement with HD-tDCS treatment 4
The human brain is a mere 2% of our body weight, yet it consumes approximately 20% of our daily calories. When deprived of essential fuel, it begins to falter, and structural changes follow.
Advanced neuroimaging techniques, particularly Magnetic Resonance Imaging (MRI), have allowed scientists to peer inside the living brain to document these changes. What they've found is a pattern of significant brain tissue loss, primarily affecting the gray matter.
Gray matter forms the brain's outer layer and is packed with neurons responsible for everything from complex thought to emotion regulation. In AN, widespread cortical thinning occurs—essentially, a shrinking of this critical brain tissue 6 . This thinning is most pronounced in the frontal lobes and insula, regions vital for decision-making, emotional regulation, and self-awareness 6 . Simultaneously, the ventricles—fluid-filled cavities in the brain—enlarge, and the volume of cerebrospinal fluid increases, putting additional pressure on the already vulnerable neural tissue 6 .
These structural changes are not without functional consequences. They are linked to the cognitive difficulties often seen in AN, including problems with concentration, memory, and inflexible thinking 6 .
Visual representation of cortical thinning and structural changes in anorexia nervosa
To untangle cause from consequence, scientists have begun studying the brains of children with different types of restrictive eating disorders. A pivotal 2025 study in Nature Mental Health did exactly this, comparing children with Early-Onset Anorexia Nervosa (EO-AN) to those with Avoidant/Restrictive Food Intake Disorder (ARFID) and typically developing children .
This design was ingenious. Both EO-AN and ARFID groups had similarly low body weight, but their psychological drivers were different. While AN is driven by body image distortion and fear of weight gain, ARFID involves a lack of interest in food or sensory aversions, without the body image component 2 . By comparing them, researchers could isolate brain changes due to low weight from those specific to AN's psychology.
Early-Onset Anorexia Nervosa with body image distortion and fear of weight gain.
Participants: 124 children
Avoidant/Restrictive Food Intake Disorder without body image issues.
Participants: 50 children
The results were striking. The children with EO-AN showed a widespread and pronounced pattern of cortical thinning across the brain compared to their healthy peers . In contrast, the children with ARFID, despite being just as underweight, did not show this cortical thinning. Instead, they exhibited reduced intracranial volume and gray matter 2 .
This key difference suggests that the cortical thinning in anorexia is not a simple result of being underweight. If it were, both groups would have shown similar patterns. The distinct "neurological signatures" point to different underlying brain mechanisms for these disorders 2 . The study concluded that in anorexia, approximately half of the cortical thinning could be linked to rapid weight loss, implying other factors specific to the AN psyche account for the rest 2 .
| Brain Structure Metric | Early-Onset Anorexia Nervosa (EO-AN) | Avoidant/Restrictive Food Intake Disorder (ARFID) |
|---|---|---|
| Cortical Thickness | Widespread and significant thinning | Preserved thickness |
| Gray Matter Volume | Lower total volume | Reduced volume |
| Intracranial Volume | No significant difference | Reduced volume |
| Primary Driver of Changes | Combination of low BMI and disorder-specific psychology | Primarily low BMI, with distinct ARFID-specific mechanisms |
Data from landmark study comparing EO-AN and ARFID patients 2
Understanding this complex illness requires a sophisticated array of tools. The following table details some of the key resources and technologies driving this field forward.
| Tool or Resource | Function in Anorexia Research |
|---|---|
| Magnetic Resonance Imaging (MRI) | Provides high-resolution images of brain structure to measure volume, cortical thickness, and identify alterations. |
| High-Definition tDCS | A non-invasive brain stimulation technique being trialed to modulate neural activity in circuits involved in AN. |
| Animal Models | Helps isolate the effects of undernutrition from psychological factors, allowing for the study of metabolic mechanisms. |
| ENIGMA Consortium | A global collaboration that pools brain imaging data from hundreds of patients, increasing statistical power. |
The evidence points to a vicious, self-sustaining cycle.
Some research suggests that pre-existing abnormalities in brain structure or function may create a biological vulnerability to developing AN 1 .
The malnourished brain becomes more rigid, anxious, and fixated—perfectly tailored to sustain anorexic behaviors 5 .
Metabolic and endocrine changes triggered by undernutrition exacerbate reward abnormalities, anxiety, and depression, solidifying the disease 5 .
Starvation directly causes brain damage. The brain is being starved of the nutrients it needs to maintain its structure and function, leading to the documented shrinkage 6 9 . This state of "brain dysfunction" can then perpetuate the illness. The malnourished brain becomes more rigid, anxious, and fixated—perfectly tailored to sustain anorexic behaviors 5 . Metabolic and endocrine changes triggered by undernutrition can further exacerbate reward abnormalities, anxiety, and depression, solidifying the grip of the disease 5 .
On the other hand, some research suggests that pre-existing abnormalities in brain structure or function may create a biological vulnerability to developing AN 1 . For instance, alterations in brain regions responsible for taste, reward, and emotional processing might explain the food avoidance behaviors central to the disorder 6 . Some functional neuroimaging studies have found abnormal functioning in frontal, limbic, and striatal regions that may persist even after recovery, hinting at a potential trait-based, or endophenotype, vulnerability 1 .
Perhaps the most hopeful finding in this field is that much of the brain damage appears to be reversible. Research shows that with weight restoration, brain volume can return, gray matter can be rebuilt, and the gaps between cortical folds can shrink back to normal size 2 6 . This recovery can happen relatively quickly, with studies noting increased brain tissue thickness after just partial weight restoration over three months 6 .
This promise of neurological recovery underscores the critical importance of early intervention. The degree of brain shrinkage has been correlated with the duration of the illness, making timely treatment essential 6 .
Emerging therapies are now targeting the brain directly. A preliminary 2025 trial from Orygen researchers used High-Definition Transcranial Direct Current Stimulation (HD-tDCS)—a non-invasive brain stimulation technique—to target the inferior parietal lobe in adults with AN 4 . This small study found that 75% of participants receiving the active treatment showed clinically meaningful improvements in both symptoms and BMI, offering a promising glimpse into a future where we can directly support neural circuitry to break the cycle of anorexia 4 .
The question of whether brain dysfunction is a cause or consequence of anorexia nervosa is no longer an either/or proposition. The relationship is a complex, bidirectional feedback loop. A brain that may be vulnerable from the start is then profoundly injured by starvation, and that injury, in turn, locks in the disordered behaviors. The groundbreaking research comparing young patients with different eating disorders is finally helping us pull these threads apart.
While the shadow of potential permanent damage exists, especially in chronic cases, the overwhelming message from the science is one of hope and resilience. The brain possesses a remarkable capacity to heal. With ongoing research, earlier treatment, and novel therapies that target both the mind and the brain, recovery is not just a possibility—it is a reachable goal.