Eating ultra-processed foods may rewire your brain’s hunger and reward circuits

A new brain imaging study reveals how ultra-processed foods reshape appetite circuits, raising concerns that these everyday products could be rewiring our eating habits from the inside out.

Study: Ultra-processed food consumption affects structural integrity of feeding-related brain regions independent of and via adiposity. Image Credit: Rimma Bondarenko / Shutterstock

A team of researchers at McGill University and the University of Helsinki analyzed the UK Biobank data and found that high ultra-processed food intake is associated with adverse metabolic and adiposity profiles and changes in the microstructure of feeding-related brain regions.

The study findings are published in the journal NPJ Metabolic Health and Disease.

Background

Ultra-processed foods are energy-dense products that can contribute up to 56% of total calorie intake. Their consumption is rapidly increasing worldwide, mainly because of their convenience, affordability, and palatability.

High intake of ultra-processed foods can potentially increase the risk of various non-communicable diseases, including cardiovascular, metabolic, and cerebrovascular diseases. These foods are also associated with a higher risk of cognitive impairment (dementia).

Recent clinical evidence establishes a causal link between ultra-processed food availability, overeating, and potential obesity. In this context, animal studies indicate that the impact of ultra-processed food on the feeding-related brain regions can lead to further overconsumption of these foods.

In the current study, researchers aimed to explore whether ultra-processed food intake alters structural brain integrity and whether these food products exert their effects through obesity-related metabolic changes or through mechanisms independent of obesity.

Study Design

The researchers analyzed data from 33,654 participants in the UK Biobank, a large-scale database and research resource containing genetic, lifestyle, and health data and biological samples from more than 500,000 individuals.

Study Findings

The analysis of metabolic parameters revealed that ultra-processed food intake can significantly reduce blood levels of high-density lipoprotein (HDL) and increase blood levels of C-reactive protein (CRP; a marker of inflammation), triglyceride, and glycated hemoglobin (a measure of glycemic control).

Regarding cardiac and obesity markers, the analysis revealed that ultra-processed food intake can significantly reduce blood pressure and increase body mass index (BMI), waist-to-hip ratio, and visceral adipose tissue.

The nutrient profile analysis revealed that these food products are associated with increased consumption of total sugar, sodium, and saturated fatty acids.

These observations collectively highlight the association of ultra-processed food intake with a range of cardiometabolic, anthropometric, and dietary measures.

Impact of Ultra-Processed Food Intake on Brain Structure

The analysis of participants’ magnetic resonance imaging (MRI) scans revealed that intake of ultra-processed foods is associated with altered tissue microstructure in multiple brain regions (the nucleus accumbens, hypothalamus, pallidum, putamen, and amygdala) that are involved in controlling feeding behavior.

Specifically, the study found signs of increased cellularity—interpreted as gliosis—in the hypothalamus, and diffusion MRI metrics suggested reduced cellularity and increased extracellular space in the nucleus accumbens, putamen, and pallidum.

Notably, the study found that UPF intake was associated with increased CRP levels, reduced HDL levels, and elevated BMI, which might contribute to the observed changes in subcortical feeding-related brain structures or occur independently of these factors.

Study Significance

The study links high ultra-processed food intake to altered metabolic markers, increased obesity, and changes in brain regions involved in feeding behavior via adiposity-related pathways and independent mechanisms. For example, hypothalamic changes were mediated by BMI, whereas changes in the nucleus accumbens and pallidum occurred independently of adiposity and were partly linked to inflammation and dyslipidemia.

The study also suggests that the observed changes in brain structures might be driven by dyslipidemia, inflammation, or adiposity caused by these food products. However, the paper notes these effects were small in magnitude.

The study also acknowledges that food additives in ultra-processed foods may alter gut microbiota composition, contributing to immune dysregulation and systemic inflammation.

The study’s observations on brain structural alterations suggest a reduction in the number of cell bodies and an increase in the volume of extracellular space, which are characteristic features of a neurodegenerative process that can lead to neuroinflammation.

Researchers have mentioned that neuroinflammation is likely to play a role in ultra-processed food-induced changes in eating behavior. They also mention the possibility of a bidirectional relationship wherein ultra-processed food intake increases the desire to eat more such foods by influencing the brain’s reward center (nucleus accumbens) through inflammation, independent of BMI.

Researchers have also highlighted the involvement of the pallidum, another brain region associated with reward processing and motivation, in this bidirectional relationship, which they believe can guide food-related decisions.

The study’s compelling findings include structural changes in the amygdala and thalamus related to ultra-processed food intake. The amygdala plays a pivotal role in regulating feeding behavior related to reward, and the thalamus is associated with emotional and motivated behaviors, such as fear and reward-seeking.

Most studies investigating the health effects of ultra-processed foods highlight the contribution of nutritional factors, such as low dietary fiber content and high saturated fat, sugar, and sodium content.

The current study included specific nutrients (total sugar, saturated fat, and sodium) in the primary analysis as confounding factors that are commonly linked with disease prevalence and can influence eating behaviors. The primary analysis was also controlled for a large number of other confounding factors that might influence eating behavior.

Therefore, the study findings are interpreted to be independent of nutrient content, socioeconomic status, physical activity, and smoking and alcohol consumption. However, the causal association between ultra-processed food intake and brain structural alterations cannot be established because of the observational study design.