Eating ultra-processed foods can rewire your brain's hunger and reward circuits

Eating ultra-processed foods can rewire your brain's hunger and reward circuits

A new brain imaging study shows how ultra-processed foods are reshaping appetite circuits, raising concerns about these everyday products that could rewire our eating habits from the inside out.

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 brain regions of feeding-related brain pieces.

The study results will be published in the journalNPJ -Metabolic Health and Disease.

background

Younger adults and urban residents had the highest ultra-processed food intake—a demographic pattern that persisted even after adjusting for income, education, and physical activity.

Ultra-processed foods are energy-dense products that can provide up to 56% of total calorie intake. Their consumption is increasing rapidly worldwide, mainly due to 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 relationship between ultra-processed food availability, overeating and potential obesity. In this context, animal studies show that the influence of ultra-processed foods on feeding-related brain regions can lead to further overconsumption of these foods.

In the current study, researchers wanted to examine whether ultra-processed food intake alters the structural integrity of the brain and whether these foods exert their effects through metabolic changes associated with obesity or through mechanisms independent of obesity.

Study design

Researchers analyzed data from 33,654 participants in the UK Biobank, a large-scale database and research resource that contains genetic, lifestyle and health data and biological samples from more than 500,000 people.

Study results

Emulsifiers and artificial sweeteners in these foods can directly irritate the intestinal lining and, according to the authors' hypothesis, reach the brain via the intestinal-brain axis.

Analysis of metabolic parameters revealed that ultra-processed food intake significantly reduced blood levels of high-density lipoprotein (HDL) and blood levels of C-reactive protein (CRP; a marker of inflammation), triglyceride and glycated hemoglobin (a measure of glycemia control).

In terms of heart and obesity markers, the analysis found that ultra-processed food intake significantly reduced blood pressure and body mass index (BMI), waist-to-hip ratio and visceral adipose tissue.

Nutrient profile analysis revealed that these food products are associated with increased consumption of total sugars, sodium and saturated fat.

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

Analysis of participants' magnetic resonance imaging (MRI) revealed that ultra-processed food intake was associated with altered tissue microstructure in several brain regions (the nucleus accumbens, hypothalamus, pallidum, putamen, and amygdala) involved in controlling feeding behavior.

Specifically, the study found evidence of increased cellularity - interpreted as gliosis - in the hypothalamus and diffusion MRI metrics indicated decreased 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, decreased HDL levels and increased BMI, which contribute to the observed changes in subcortical feeding-related brain structures or occur independently of these factors.

Investigate significance

Even small daily swaps: every 10% increase in ultra-processed food intake correlated with measurable brain changes, equivalent to two extra chicken nuggets daily.

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

The study also suggests that the observed changes in brain structures could be driven by dyslipidemia, inflammation or obesity caused by these food products. However, the paper notes were small in large size.

The study also recognizes that food additives in ultra-processed foods can alter the composition of the gut microbiota, contributing to immune shutdown and systemic inflammation.

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

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

The 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 may guide food decisions.

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

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

The current study included specific nutrients (total sugars, saturated fat, and sodium) in the primary analysis as confounders that are commonly associated with disease prevalence and may influence eating behavior. The primary analysis also controlled for a large number of other confounding factors that could influence eating behavior.

Therefore, the study results are interpreted as independent of nutrient content, socioeconomic status, physical activity, and smoking and alcohol consumption. However, the causal relationship between ultra-processed food intake and brain structural changes cannot be established due to the observational study design.

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