Can discrimination increase obesity?

In a recent article published in Journal of nature mental health, The researchers examined neural reactivity to unhealthy and healthy food cues and gut metabolites to elucidate potential mechanisms linking discrimination and obesity.

Discrimination exposure influences unhealthy processing of food signals: Crosstalk between the brain and the gut.
Study: Discrimination exposure influences unhealthy processing of food signals: Crosstalk between the brain and the gut. Image credit: ilona.shorokhova/


Table of Contents

Genetics, diet, exercise, and psychological factors contribute to obesity and obesity-related morbidities, and the prevalence of obesity is widespread among all minority subgroups in the United States (US). However, few studies have directly examined the role of discrimination in the etiology of obesity.

Bidirectional interactions of the brain and gut involve the vagus nerve, neurotransmitters, immune-inflammatory mechanisms, microbial metabolites, and hypothalamic signaling.,Pituitary-adrenal axis.

However, the brain-gut-microbiome (BGM) system is of most importance when studying the potential link between obesity differentiation and subsequent stress responses.

In response to discrimination-related stress, it potentially activates brain reward and cognitive control networks, deactivating frontal executive modulation and potentiating brain activity in limbic regions, leading people to crave energy-dense, unhealthy foods. Are motivated to eat.

Similarly, stress disrupts glutamate metabolism, altering gut metabolites through oxidative stress, glutamatergic excitotoxicity, and inflammation, which are all mechanisms responsible for neuronal damage.

Glutamate’s role in executive control and reward processing is also highly relevant to the processing of food signals.

about the study

In the current study, researchers recruited 107 individuals (87 women) from Los Angeles and collected data regarding their age, gender, race/ethnicity, body mass index (BMI), socioeconomic status (SES), and diet. .

In addition, they provided samples for fecal metabolomics, clinical and behavioral measures, and functional magnetic resonance imaging (fMRI).

The team used the Everyday Discrimination Scale (EDS) to assess past experiences of unfair treatment. Based on the average EDS score, they categorized participants into high and low discrimination risk (EDS > 10 and EDS ≤ 10).

They used two-way analysis of variance (ANOVA) to examine the interaction between high versus low discrimination groups and American versus non-American diet on BMI.

The researchers asked all participants to complete a food-cue task in an fMRI scanner, where they made neural responses to images of five types of foods: unhealthy salty, unhealthy sweet, healthy salty, healthy sweet, and non-food (control. ).

They could view each picture for three seconds and respond from 0 to 10, indicating their intention to eat those foods.

Next, the researchers analyzed the entire brain.

To bring groups (across all five contrasts) they combined them to develop discrimination-related food-cue region of interest (ROI) masks and conduct a structural equation model (SEM) analysis.

A subgroup of 62 participants provided fecal samples, which helped the researchers compare 12 metabolites from the glutamate pathway between high versus low discrimination groups using generalized linear modeling.

Furthermore, they conducted multiple linear regression analyzes to evaluate discrimination-induced effects on brain signal changes in the food-cue ROI mask (composite).

In these statistical analyses, the researchers adjusted for all covariates, including BMI, age, sex, race, diet, and SES. Additionally, they corrected multiple analytical comparisons using the false discovery rate (FDR) method outlined in the Benjamini–Hochberg procedure.


Unhealthy sugar-containing foods have rewarding and analgesic nature, and frontal-striatal regions regulate eating behavior in response to the reward and pleasurable aspects of food.

In this study, the authors noted that unhealthy food cues caused greater activation in the aforementioned brain regions, e.g., insular and orbitofrontal cortex.

In contrast, brain regions involved in craving and executive control, the frontal pole, middle frontal gyrus, and superior frontal gyrus, respond to healthy food cues.

EDS scores are positively correlated with greater responsiveness to unhealthy sweet and salty foods and healthy eating. High versus low discrimination groups showed greater willingness to eat unhealthy foods (P = 0.048 and 0.174).

Furthermore, the authors noted that greater differentiation led to the excretion of greater amounts of glutamate metabolites, n-Acetylglutamate and n-Acetylglutamine is involved in studies evaluating obesity pathophysiology.

Studies have also shown the role of these metabolites in glutamate pathways associated with oxidative stress and inflammation.


Overall, the results showed a complex relationship between discrimination and brain-gut changes, especially when evaluating the brain’s response to unhealthy sweet food cues.

Brain-targeted treatments (for example, brain stimulation) may attenuate the overactive food-reward system or enhance frontal control. Thus, it can be used as a neuromodulatory tool to normalize altered brain circuits associated with discrimination risk.

Similarly, probiotic supplements or a Mediterranean diet with anti-inflammatory benefits may help treat disrupted glutamatergic pathways.

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