It’s a brutal statistic. Up to half of people treated for anorexia nervosa relapse within a decade. The disorder has a lifetime prevalence of around 4 percent among women, and the stakes are always high. Relapse isn’t just a setback; it’s a return to a state where the body is starved and the mind is trapped.
Why does it keep happening?
New research points to a hormonal tug-of-war that may hold the key. Specifically, scientists are looking at two proteins: ghrelin and LEAP2. Understanding the balance between these two might finally explain the biology of relapse and point toward treatments that go beyond simple weight restoration.
Зміст
The Hormone Battle: Ghrelin vs. LEAP2
To understand why relapse is so common, you have to look at the biology of hunger. Ghrelin is known as the “hunger hormone.” It signals the brain to eat. In a healthy body, ghrelin levels spike before meals and drop after eating, providing a clear feedback loop.
But anorexia disrupts this loop.
A new study tracked 30 women aged 18 to 60 with anorexia nervosa during a four-month refeeding program. Refeeding is the medical process of slowly increasing calorie intake to restore health. The participants provided blood samples at three key moments: before treatment, after four months, and again six months post-discharge.
The results were striking.
When patients were first hospitalized and severely underweight, their levels of LEAP2 —a protein that blocks ghrelin from doing its job—were 20 percent higher than when they gained weight. LEAP2 acts as an antagonist, essentially muting the hunger signal.
Here is the critical finding: The ratio of ghrelin to LEAE2 correlated with impulse control in those who maintained their weight. In other words, the hormonal balance stabilized when the patients stayed healthy.
But in those who relapsed? LEAP2 levels spiked back up.
The animal studies supported this, linking these hormonal shifts directly to nutritional status. It’s not just a psychological struggle. It’s a physiological one.
“In the absence of access to food, thebrain adapts by not expecting as muchreward from food.”
Why This Matters for Recovery
So, how does this lead back to relapse?
Rebecca Boswell, PhD, director of the Princeton Center for Eating Disorders, explains that the brain adapts to starvation by dampening its reward system. Food doesn’t taste as good. Eating doesn’t feel rewarding. It’s a survival mechanism, but it makes recovery incredibly hard because the brain no longer sees eating as a positive activity.
Recovery requires “rewiring” this system. Through exposure to food and weight restoration, the brain must re-learn that eating brings reward. This is where the ghrelin/LEAP2 pathway comes in.
For successful recovery, the body needs to shift out of that protective, muted state. When patients maintain stable weight, the ghrelin/LEAE2 balance supports impulse control. When that balance fails, and LEAE2 rises again, the hunger signals are blocked or distorted. The brain reverts to its starvation mode.
Erin Birely, LCPC, an expert in disordered eating at The Renfrew Center, emphasizes that ghrelin doesn’t cause relapse in isolation. Recovery is complex—biological, psychological, and social factors all intertwine. However, this research highlights a specific mechanism: the body and brain remain deeply connected throughout the healing process. If the biological signal is wrong, the psychological work becomes exponentially harder.
Moving Beyond Weight: The Search for Better Biomarkers
Currently, the primary metric for success in eating disorder treatment is weight. If the scale goes up, the treatment worked. For many, this is insufficient. Weight is just one data point.
The findings on ghrelin and LEAE2 suggest a more nuanced approach is possible.
Boswell describes the potential for using hormonal changes as a biomarker for treatment success. Instead of relying solely on pounds regained, clinicians could measure ghrelin and LEAE2 levels to see if the brain is actually healing its reward pathways.
This could be a game-changer for individualized care.
If a patient’s weight is stabilizing but their hormonal profile still shows signs of starvation mode, the treatment plan might need adjustment before a relapse occurs. It shifts the model from a reactive one—waiting for weight loss to trigger intervention—to a proactive, science-based approach.
“Future work could allow us to consider… changes in hormonal… and cognitive function as indicators of treatmentoutcome.”
The Path Forward
This research doesn’t offer a cure. There’s no new pill on the horizon based solely on these findings. What it does is clarify the biological reality of anorexia. It confirms that the disorder physically alters how the body communicates hunger and reward.
For the millions affected by anorexia nervosarelapse rates, this validation is significant. It’s not a lack of willpower. It’s a mismatch in hormonal signaling that the body struggles to correct.
As treatment models evolve, integrating these biomarkers could mean earlier interventions and more personalized support. But for now, the gap between biological understanding and clinical application remains.
We know the hormones are involved. We see the pattern. The next step is turning that data into a tool that actually sticks.
