How a Small GLP-1 Study Became a Misleading Media Narrative
Content Note: This post discusses eating behaviours, “food noise,” loss-of-control eating, weight-loss medications, and bariatric surgery. It also references the clinical term “obesity,” because it appears directly in the published study. I do not use this term to describe people or their worth, only to reflect the language used by the researchers.
Terminology Note: Throughout this post, I quote the study’s wording where necessary, including terms like “obesity” and “loss-of-control eating.” These are medical categories used in the paper, not labels I apply to individuals. My own work is weight-inclusive and trauma-informed.
Last week, I came across a Reuters article with the headline “Eli Lilly weight-loss drug appears to suppress binge-eating signal, small study finds.” The drug in question was tirzepatide. You may know it by its brand names Mounjaro and Zepbound. They are GLP-1/GIP medications prescribed for type 2 diabetes and weight management.
As someone who works with people healing their relationship with food and body, I was curious to read more. After reading the Reuters piece, I went on to read the full journal article published in Nature Medicine.
What surprised me wasn’t the existence of the research itself, but how inaccurately and confidently the findings were reported. That kind of reporting is especially harmful for people already navigating shame, fear, or confusion around their eating patterns.
The Reuters article claimed that the study suggested “…a role for future versions of Mounjaro or other GLP-1 drugs in treating certain eating disorders.”
That framing is where things start to unravel.
The paper does include a general, forward-looking scientific reflection that understanding how incretin-based drugs interact with brain reward circuits could help broaden their therapeutic scope in the future (potentially including conditions related to dysregulated eating).
But this conclusion wasn’t drawn from the study’s results. It was not presented as evidence that tirzepatide treats eating disorders, nor as a clinical claim. It was a speculative comment about future neuroscience research directions.
That nuance was lost entirely in the headlines.
So let’s walk through what the study actually did, what the media reported it did, and why the gap between the two matters.
What the Nature Medicine study actually examined
This study was not about binge eating disorder. It was not about bulimia. In fact, it wasn’t about any eating disorder at all.
It was also not designed to test tirzepatide as a treatment for any eating disorder or compulsive eating condition.
Instead, it was a rare, scientifically fascinating look at what happens in the brain during moments of severe food preoccupation. What many now call “food noise.”
The researchers studied three women who were classified in the paper as having severe, treatment-resistant obesity following bariatric surgery and later weight regain. All three experienced distressing food preoccupation and frequent episodes of loss-of-control eating.
Importantly, the study did not classify these episodes as binge eating disorder. After bariatric surgery, stomach capacity is drastically reduced, meaning people physically cannot eat the “objectively large amount of food” required by DSM-5 criteria.
This creates a diagnostic grey area.
Someone may eat until they’re uncomfortably full, eat large amounts when they’re not physically hungry, and feel intense guilt or distress afterwards. These experiences can feel profoundly out of control. But because the DSM requires an “objectively large amount of food” for a binge-eating diagnosis, episodes like these are not always recognised as binge eating disorder, even when the person’s lived experience is deeply distressing.
Nonetheless, this nuance was completely lost in the media reporting.
To study what the brain was doing during these episodes, researchers measured electrical activity directly in the nucleus accumbens. The nucleus accumbens is the deep brain region involved in reward, motivation, urges, and compulsive behaviours.
This allowed them to monitor brain activity in real-time during moments when participants felt calm versus intensely preoccupied with food.
This kind of direct brain recording is very rare in humans.
The brain signal the researchers were looking for
The researchers focused on a slow, low-frequency electrical pattern in the nucleus accumbens. Earlier research had linked this pattern to moments when someone feels overwhelmed by food thoughts.
The Nature Medicine study confirmed this pattern:
Surged during moments of severe food noise
Stayed low during calmer moments
This created a measurable neural marker of food preoccupation.
There is no evidence that this neural pattern reflects binge eating, bulimia, or any eating disorder. It simply appeared when participants were in a state of intense food preoccupation.
What happened for Participants 1 and 2
Participants 1 and 2 were not taking GLP-1 medications. Responsive deep brain stimulation (rDBS) was used to reduce their episodes of food preoccupation.
Over time:
Their food-preoccupation episodes decreased
The low-frequency biomarker reduced or disappeared
These improvements remained stable throughout the study period
These two cases are genuinely scientifically important. But they never became headlines.
I suppose “brain stimulation reduces food noise in two people” doesn’t sell quite like, “weight-loss drug appears to suppress binge-eating signal”
Participant 3: the only person taking tirzepatide
This is where the media fixated and where nuance completely disappeared.
Participant 3 was the only person in the entire study taking tirzepatide (originally prescribed for type 2 diabetes). Although she was already on the medication at the start of monitoring, she was likely on a low, sub-therapeutic dose.
GLP-1 medication doses are always started low and slowly increased.
This lower dose didn’t appear to be strong enough to meaningfully affect appetite, reward pathways, or “food noise.” This explains why she continued to experience food preoccupation during the early part of the study.
However, things changed after her dose increased.
For several months:
She had almost no severe food-preoccupation episodes
The delta–theta biomarker was nearly silent
This disappearance only occurred after a dose increase.
The paper doesn’t state the exact doses, but it does note that she eventually reached the maximum dose.
The quiet phase eventually ended.
When she reached the highest dose, the biomarker reappeared, signalling that food-preoccupation activity had come back. Her episodes of food preoccupation returned too.
This happened despite her remaining on the maximum dose of tirzepatide.
The study also highlighted a seven-week gap between the biomarker returning and the severe food preoccupation returning.
This suggests the brain adapted first, and the outward behaviour followed.
In comparison to Participants 1 and 2, this short-lived suppression was interesting. It hinted that tirzepatide might temporarily alter reward-circuit activity in some individuals.
But the key-word here is temporarily.
This was not a cure.
It looked much more like tolerance (the brain adapting to the drug’s initial effects).
Where the media coverage went wrong
The Reuters article described the participant as having “a severe binge-eating problem”, despite the study explicitly stating that the episodes were not binge eating.
It then claimed that the trial involved patients being treated for “loss-of-control eating disorders such as binge-eating and bulimia.”
None of this is true.
This was not an eating disorder trial
No participants had bulimia
None had binge eating disorder
The brain signal was never described as a “binge-eating signal”
Taken together, these misstatements reveal how quickly the nuance of the research was lost once the story moved into the media cycle.
1. Oversimplifying “food noise”
The coverage turned food preoccupation into a dramatic psychiatric malfunction that tirzepatide supposedly “switched off.”
But food noise isn’t a disorder; it’s a communication pattern shaped by biology, emotion, stress, trauma, and nervous-system state. Reducing it to a faulty circuit erases the context that gives those experiences meaning.
2. Turning preliminary neuroscience into a “miracle drug” story
The study did not show that tirzepatide cures binge eating, treats binge eating disorder, or suppresses binge-related brain activity.
It showed one participant with a temporary reduction in a food-preoccupation signal that later returned.
3. Suggesting GLP-1 drugs could treat eating disorders
This is an irresponsible leap.
GLP-1 medications can blunt appetite or intrusive food thoughts, but they do not treat the psychological, relational, trauma-linked, or nervous-system drivers of eating disorders.
Framing them as ED treatments risks delaying proper care.
The missing question: why was there food preoccupation?
One of the biggest omissions from both the study and the media coverage was any exploration of why food preoccupation was happening in the first place.
Food noise can emerge from:
metabolic imbalance
chronic restrictionstress and nervous-system activation
emotional coping
trauma
sensory overloadunmet needs
Silencing this signal is not the same as healing what drives it.
The disappearance of food preoccupation was interpreted as “progress,” but for many people, hunger cues and food thoughts are meaningful messages.
Without understanding the cause, we cannot understand the meaning of the change.
What this study does and does not tell us
This study offers a rare window into reward-circuit activity in a very specific, very unusual clinical context.
It shows that GLP-1 medications may temporarily alter activity linked to food preoccupation in some individuals.
But it does not tell us how GLP-1 medications affect:
Binge eating disorder
Bulimia
Trauma-driven eating patterns
Restriction-induced food obsession
Long-term recovery
Nervous-system dysregulation
Neurodivergent eating patterns
Stress-based eating
It also does not replace therapy, relational support, or embodied healing practices.
Silencing a signal is not the same as building safety.
My takeaway
I’m not anti-medication or anti-GLP-1. I am pro-accuracy and pro-context.
People deserve reporting that honours the complexity of human eating, rather than quick, dramatic stories that flatten everything into a narrative about hunger and control.
I appreciate that the scope of the original study was not to explore the causes of food preoccupation, trauma, or nervous-system dysregulation. And I’m aware that my perspective is shaped by my own lived experience and professional work supporting people to heal their relationship with food and body.
That lens makes me particularly sensitive to how easily scientific findings can be misinterpreted in ways that reinforce shame, stigma, or false hope.
We can hold curiosity about emerging research without overstating what it means, without losing sight of the human beings behind the data.
Sources:
Dr Simon Cork, Anglia Ruskin University (ARU. (2025). Expert reaction to weight-loss drugs influencing brain signals linked to food cravings, as published in Nature Medicine. [Online]. Science Media Centre. Last Updated: 17th November 2025. Available at: https://www.sciencemediacentre.org/expert-reaction-to-weight-loss-drugs-influencing-brain-signals-li [Accessed 8th December 2025].
Choi, W., Nho, YH., Qiu, L. et al. Brain activity associated with breakthrough food preoccupation in an individual on tirzepatide. Nat Med 31, 4038–4043 (2025). https://doi.org/10.1038/s41591-025-04035-5
Reuters. (2025). Eli Lilly weight-loss drug appears to suppress binge-eating signal, small study finds. [Online]. https://www.reuters.com/. Last Updated: 17th November 2025. Available at: https://www.reuters.com/business/healthcare-pharmaceuticals/eli-lilly-weight-loss-drug-appears-suppr [Accessed 8th December 2025].
