Study: Feeding gut microbes to nourish the brain: Unravelling the diet–microbiota–gut–brain axis . Image Credit: Ellen Eryomenko / Shutterstock.com The rise in brain disorders is linked to poor diet, while healthy eating supports brain health.
This review highlights the gut-brain axis, where diet influences brain function through gut microbiota, and discusses its potential for treating neuropsychiatric disorders. A recent Nature Metabolism study discusses the diet-microbiota-gut-brain axis, which describes the role of both diet and gut microbiota composition on cognitive and emotional health. Diet and the gut microbiota Diets rich in carbohydrates significantly increase Bifidobacterium levels in the gut microbiome while leading to reduced Bacteroides levels.
Undigested carbohydrates in prebiotics promote the growth of a healthy gut microbiota, thereby benefitting the gastrointestinal (GI) tract. Proteins are the primary source of amino acids, which are key for brain health. Consuming plant-based proteins increases short-chain fatty acid (SCFA) and branched-chain amino acid (BCAA) levels, both of which promote overall health.
Comparatively, long-term consumption of animal-based proteins may adversely impact the gut microbiota. Increased consumption of saturated fats has been associated with cognitive impairment, whereas an inverse effect has been observed for unsaturated fatty acid intake. The quantity and saturation of fat determines the exact effects on the gut microbiota.
Minerals, vitamins, and trace elements are needed for the survival and growth of several gut bacteria. Thus, micronutrient deficiencies could lead to poor cognitive performance and emotional disturbances. Previous studies have also demonstrated the association between mood disorders and the consumption of ultra-processed foods (UPF), with the gut microbiome having a key role in this relationship.
The gut-brain axis and neuropsychiatric disorders The gut microbiota regulates anorexia nervosa (AN), which entails being underweight through compensatory behaviors and/or chronic food restriction. The risk of schizophrenia can also be partially mediated by the gut microbiota due to inflammation induced by maternal or postnatal dietary malnourishment through over- or under-feeding. The ketogenic diet increases the abundance of certain genera, such as Bifidobacterium and Akkermansia.
Increasing the production of ketones through this dietary approach inhibits apoptosis and reduces oxidative stress, which has been therapeutically effective in the management of certain forms of epilepsy. Dietary patterns, specifically those that involve increased consumption of high-fat dairy products, meat, butter, eggs, and refined sugar, are associated with an increased risk of dementia or Alzheimer’s disease (AD). Children with attention deficit hyperactivity disorder (ADHD) exhibit lower serum concentrations of chromium, magnesium, and zinc.
ADHD has also been associated with an increased abundance of Eggerthella and Faecalibacterium. Gut metabolites and their therapeutic potential Several molecular pathways are involved in the bidirectional communication of the diet-microbiota-gut-brain axis, which coordinates cognition and emotion in healthy and diseased states. Bacterial metabolites involved in digestion similarly influence communication between the gut microbiota and the brain.
SCFAs, such as propionate, acetate, and butyrate, produced from microbial fermentation of host-indigestible dietary fibers or microbial protein breakdown are associated with blood pressure regulation, GI function, neuroimmune function, and circadian rhythm regulation. Several studies have shown that the changes in fecal SCFA levels are associated with obesity, Parkinson’s disease (PD), ASD, and chronic psychosocial stress, thus demonstrating the robust role of SCFAs in microbiota-gut-brain axis-related disorders. A reduction in SCFA-producing bacteria in the gut increases the risks of PD.
This has led researchers to investigate the efficacy of propionate treatment, which has been shown to increase dopaminergic cell survival rates in a PD mouse model. Taurine is another microbial metabolite involved in host digestion. In addition to its role in digestive processes, taurine is associated with anticonvulsant, neuroprotective, and cognitive-enhancing properties through its activity as an agonist of glycine , gamma-aminobutyric acid type A (GABAA), and gamma-aminobutyric acid type B (GABAB) receptors in the brain.
Taurine supplementation has a potential therapeutic value for epilepsy, AD, PD, anxiety, and depression. Major gut-associated microbial taxa, such as Bifidobacterium , Lactobacillus , and Bacteroidetes , express bile salt hydrolase enzymes that de-conjugate bile acids from taurine and glycine. Alterations in gut microbiota composition due to an unbalanced diet may induce neuroinflammation and reduce synaptic plasticity as a result of impaired TGR5 signaling and changes in bile acid synthesis.
Commensal bacterial metabolites such as choline, bacteriocins, neuromodulators, bile acids, and SCFAs function as signaling molecules and can modulate microbe-host interactions. These metabolites influence neural signaling and communicate with the brain. Future outlook Additional research is needed to evaluate how chronic food intake influences the microbiota-gut-brain axis.
Longitudinal and multimodal study designs can be used to understand the role of the diet-microbiota-gut-brain axis in the pathogenesis of neuropsychiatric disorders and/or in symptom severity. Furthermore, randomized controlled trials can be conducted to determine whether diet-induced alterations in gut microbiota affect clinical populations. The #diet #microbiota gut–brain axis represents an uncharted frontier for brain health diagnostics and therapeutics across the lifespan.
#Aging New from @jfcryan @NatMetabolism Feeding the microbes #microbiota https://t.co/c1ZjiNBHgf Schneider, E., O’Riordan, K.
J., Clarke, G., & Cryan, J.
F. (2024) Feeding gut microbes to nourish the brain: Unravelling the diet–microbiota–gut–brain axis. Nature Metabolism ; 1-25.
doi:10.1038/s42255-024-01108-6.
