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The Impact of Diet on Gut Microbiota & Brain Function

by Ella

Carbohydrate-rich diets significantly boost levels of Bifidobacterium in the gut while decreasing Bacteroides levels. Undigested carbohydrates in prebiotics support a healthy gut microbiome, benefiting the gastrointestinal (GI) tract. Conversely, proteins, particularly plant-based ones, enhance levels of short-chain fatty acids (SCFAs) and branched-chain amino acids (BCAAs), which are crucial for brain health. Long-term consumption of animal-based proteins may negatively affect the gut microbiota.

Increased intake of saturated fats is linked to cognitive impairment, whereas unsaturated fatty acids have an opposing effect. The impact of fat on the gut microbiota depends on both quantity and type. Essential minerals, vitamins, and trace elements support gut bacteria, and deficiencies can lead to poor cognitive function and emotional issues. Previous research has also highlighted a connection between ultra-processed foods (UPFs) and mood disorders, with the gut microbiome playing a central role.

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The gut microbiota influences anorexia nervosa (AN), characterized by being underweight through restrictive behaviors. It also partially mediates the risk of schizophrenia, which can be exacerbated by maternal or postnatal dietary malnourishment. The ketogenic diet, by increasing genera such as Bifidobacterium and Akkermansia, enhances ketone production, reducing oxidative stress and apoptosis, proving effective in managing certain epilepsy forms.

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Dietary patterns high in fat, dairy, meat, butter, eggs, and refined sugars are associated with an elevated risk of dementia and Alzheimer’s disease (AD). Children with attention deficit hyperactivity disorder (ADHD) often have lower serum levels of chromium, magnesium, and zinc, and exhibit higher levels of Eggerthella and Faecalibacterium.

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The diet-microbiota-gut-brain axis involves several molecular pathways coordinating cognition and emotion. SCFAs like propionate, acetate, and butyrate, derived from the fermentation of dietary fibers and microbial protein breakdown, are linked to blood pressure regulation, GI function, neuroimmune responses, and circadian rhythms. Changes in SCFA levels are associated with conditions such as obesity, Parkinson’s disease (PD), autism spectrum disorder (ASD), and chronic stress, underscoring SCFAs’ role in microbiota-gut-brain axis disorders.

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A decrease in SCFA-producing bacteria raises PD risk, prompting research into propionate’s efficacy, which has shown promise in enhancing dopaminergic cell survival in PD models. Taurine, another microbial metabolite, has potential therapeutic value for epilepsy, AD, PD, anxiety, and depression due to its neuroprotective and cognitive-enhancing effects. It functions through receptors like glycine, GABAA, and GABAB.

Major gut-associated taxa such as Bifidobacterium, Lactobacillus, and Bacteroidetes produce bile salt hydrolase enzymes that modify bile acids. Diet-induced changes in microbiota composition may trigger neuroinflammation and affect synaptic plasticity through altered TGR5 signaling and bile acid synthesis.

Further research is required to explore how chronic dietary patterns influence the microbiota-gut-brain axis. Longitudinal and multimodal studies could clarify the diet-microbiota-gut-brain relationship in neuropsychiatric disorders. Randomized controlled trials should assess whether dietary modifications impacting gut microbiota affect clinical populations.

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