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Eating a poor diet might lead to structural brain changes that cause the development of common mental disorders (CMD).
Poor nutrition may lead to brain changes that are consistent with anxiety and depression, according to recent findings published in Nutritional Neuroscience. The study, conducted by researchers at the University of Reading, Roehampton University, FrieslandCampina (Netherlands), and Kings College London, found a reduction in gamma aminobutyric acid (GABA) and elevated glutamate (GLU) in the frontal lobe among individuals with poor quality diets, which may explain the association between nutrition and mental health.
Around 300 million individuals globally are affected by common mental disorders (CMDs), causing subclinical symptoms such as low mood, worry, anxiety, and depressive disorders. CMDs are associated with an impaired prefrontal excitatory/inhibitory (E/I) balance, based on magnetic resonance spectroscopy measurements (1H-MRS), and alter frontal GABA and GLU concentrations. Additionally, abnormalities in grey matter volume (GMV), cortical thickness, and gyrification in the frontal and temporal regions of the brain have also been observed in patients with anxiety and depression.1
According to the recent study, poor diet quality is consistent with reduced GABA and elevated GLU, which are neurometabolites responsible for brain functioning and neuronal excitability regulations. The study authors also observed a reduction of grey matter (GM) in the frontal lobe, a crucial part of the brain involved with mental health. The improper production and activation of GABA and GLU can interfere with the brain’s typical functioning, which could explain the association between diet and mood.1,2
The study authors used multiple methods to determine the associations between diet quality, function and structure of the brain, CMD, and rumination in humans, which is largely misunderstood. Using Mediterranean Diet Adherence Screener (MEDAS) scores, a test to measure adherence to Mediterranean style diets, 30 adults were categorized into high MEDAS score (High MEDAS; > 8, n = 19) and low MEDAS score (Low CT; < 6, n = 19) groups. Additionally, the participants completed other questionnaires, including the Depression and Anxiety Stress scale (DASS) to quantify recent levels of depression, anxiety or stress; the Ruminative Response Scale (RSS) to assess reflection, brooding, and depression-related rumination; and the EPIC Norfolk Food Frequency Questionnaire (FFQ) to estimate habitual food intake.1
To assess function and structure of the brain, the study authors performed 1H-MRS to measure medial prefrontal cortex (mPFC) metabolite concentrations. According to their findings, individuals in the high MEDAS group (M = 4.22, SD = 1.23 institutional units) exhibited higher mPFC GABA levels compared with individuals in the low MEDAS group (M = 3.30, SD = 0.88 institutional units). The high MEDAS group also exhibited lower mPFC GLU levels compared with participants in the low MEDAS group.1
The study authors measured GMV in the right precentral gyrus (rPCG) using full brain voxel-based morphometry (VBM). Participants exhibited no GMV differences amongst both contrasts (low MEDAS > high MEDAS and high MEDAS > low MEDAS). However, individuals in the high MEDAS group (M = 11.40, SD = 0.82), exhibited greater rPCG GMV, which is associated with cognitive function and mental health, compared with individuals in the low MEDAS group (M = 10.62, SD = 0.83). The findings provide insight into the correlation between diet quality and observable changes in brain structure, which could explain the impact of eating habits on CMD.1
Additionally, positive associations were found between RSS scores and mPFC GLU corrected metabolite levels (Corr) (r(25) = 0.320, P = .1), providing valuable insight into the underlying neurochemical mechanisms impacting rumination. The study authors also observed a significant negative correlation between ruminative response scale scores and rPCG GMV (r(25) = −0.5877, P = .003).1
Although the study found some associations between diet quality and CMD, the authors noted the need for further longitudinal analysis to more accurately link the impact of diet on brain chemistry and volume. This is largely due to limitations in the study sample size, the image quality of brain scans, and the inability to identify direct cause and effect associations between diet and brain health.1
The overall findings suggest that adherence to unhealthy diet habits may be associated with neurochemical and morphological alterations in the brain that could result in the development of CMD. These results offer further depth of knowledge into the underlying mechanisms of CMD to expand treatment opportunities for patients, as well as offer them a relatively cost-effective solution for improving their mental health outcomes.