Brain Imaging Study Redefines the “Fussy Eater” Narrative

For years, children with avoidant/restrictive food intake disorder (ARFID) have been dismissed as merely "fussy eaters." However, research from the University of Aberdeen has revealed that ARFID is linked to measurable differences in brain structure, offering new insights into the neurodevelopmental roots of this misunderstood eating disorder.

The study was published in the Journal of Child Psychology and Psychiatry.

Understanding ARFID and its impact

ARFID is an eating disorder that has often been mischaracterized as extreme fussy eating. However, the reality of ARFID is far more complex.

Officially recognized in 2013, ARFID is distinguished by selective and restrictive eating behaviors that impair a person’s ability to meet nutritional needs. Unlike other eating disorders, like anorexia nervosa or bulimia nervosa, ARFID is not driven by concerns about body image or weight. Instead, it arises from distinct factors such as sensory sensitivities, lack of appetite or a fear of adverse outcomes like choking or vomiting.

“Many people may experience fussy eating at some point in their lives, while individuals with ARFID experience severe health and psychological consequences resulting from their disordered eating,” said lead author Dr. Michelle Sader, a research fellow at the University of Aberdeen.

The reported prevalence rates vary, ranging between 0.3%–17.9% in global populations. ARFID’s impact also extends beyond physical health, often interfering with social relationships and activities. For example, individuals with ARFID may struggle to eat in social settings, participate in family meals or maintain adequate energy levels for daily functioning. Children with the disorder may fail to meet critical developmental milestones, and adults can experience severe nutritional deficiencies.

“Although the condition can develop at any age, some children experiencing the disorder may not enter puberty because they aren’t able to eat a wide enough range of foods to meet their nutritional needs. There is a significant impact on their lives. This might mean they can’t eat out or at school or work for example,” said Tom Quinn, director of external affairs at Beat, a UK-based eating disorder charity.

Despite its profound effects, ARFID remains less well-researched compared to other eating disorders. Earlier studies have mostly focused on functional aspects of the disorder, such as how it affects food-related behaviors and caloric intake, but investigations into its neurobiological underpinnings have been scarce.

“Previous research has highlighted that ARFID exhibits adverse physiological effects similar to restrictive eating disorders such as anorexia nervosa, but it is regarded as far less dangerous and thus less important to tackle,” said Sader.

Prior neuroimaging studies, while limited, have provided some clues. Research has shown alterations in brain regions associated with appetite and sensory processing, including the orbitofrontal cortex (OFC) and anterior insula. Yet, these studies were either small-scale or lacked control groups, leaving large gaps in understanding the structural neural basis of ARFID.

“Since the introduction of the ARFID diagnosis in 2013, no structural neuroimaging studies have been conducted in ARFID or ARFID-like populations,” said Sader.

Brain structural differences in ARFID

The study utilized data from the Generation R cohort, a large population-based study from the Netherlands, comprising 1,977 children aged 10 years. Of these, 121 children displayed ARFID symptoms. Sader and the team compared brain structures between children with and without ARFID symptoms using advanced MRI techniques to examine cortical thickness, surface area and volume.

The researchers observed an increase in cortical thickness in the frontal and superior frontal cortices of children with ARFID symptoms – areas that are critical for cognitive flexibility, otherwise known as the ability to adapt thoughts and behaviors in response to changing environments or stimuli.

“Our findings demonstrate that children presenting with symptoms of ARFID showed significantly greater cortical thickness in certain areas of the brain compared to those without ARFID symptoms. These brain regions are associated with executive function and are particularly important for anticipation of conflict and inhibition control,” said Sader.

While no differences in brain volume or surface area were detected, the increased cortical thickness suggests that ARFID may be linked to developmental disruptions, such as altered synaptic pruning. This is a normal process during childhood and adolescence where unused neural connections are eliminated, ensuring efficient brain functioning. Impairments in this process have been implicated in other neurodevelopmental and psychiatric disorders, including autism, which has a high comorbidity with ARFID.

Developing new treatment strategies for ARFID

“This work assists researcher and clinician understanding of ARFID by identifying brain regions associated with the feeding and eating disorder and has potential to inform on approaches for ARFID treatment, management and support,” said Sader.

“To our knowledge, this is the first structural imaging study associated with ARFID, and findings from this study will act as a foundation for future imaging-related ARFID research,” said co-author Dr. Gordon Waiter, director of the Biomedical Imaging Centre at the University of Aberdeen.

The findings pave the way for new treatment and management strategies. Current interventions for ARFID often focus on addressing immediate nutritional deficits and exposure to a broader range of foods. However, this study suggests that treatments may also need to address neurodevelopmental factors, such as difficulties with impulse control, flexibility and decision-making.

The study also indicates the need for further research to deepen our understanding. While these findings point to significant structural differences in the brains of children with ARFID, it remains unclear whether these differences are a cause or consequence of the disorder. Longitudinal studies will be essential to determine how these structural changes evolve over time.

“While we recognize the importance of the University of Aberdeen’s fantastic research, these statistics also highlight the need for further research to build on these findings. There is much more that we need to learn before we fully understand how best to treat and ultimately prevent ARFID and other eating disorders,” added Quinn.

Reference: Sader M, Harris HA, Waiter GD, Jansen PW, Williams JHG, White T. Neural correlates of children with avoidant restrictive food intake disorder symptoms: large‐scale neuroanatomical analysis of a paediatric population. Child Psychol Psych. 2024:jcpp.14086. doi: 10.1111/jcpp.14086

This article is a rework of a press release issued by the University of Aberdeen. Material has been edited for length and content.