All articles tagged with #gut brain axis
A Porto-led study with 200 healthy adults found correlations between higher psychopathy scores and certain gut bacteria (Allisonella, Prevotella, Cloacibacillus evryensis), suggesting a biological footprint beyond brain-based models. The researchers caution the results show correlation, not causation, and peer review is pending.
A small, first-of-its-kind study from University of Porto suggests a link between gut microbiota and psychopathic traits: stronger psychopathy scores correlated with higher abundances of Allisonella, Prevotella, and C. evryensis and lower levels of T. vincentii. The findings are correlational and based on a small, self-reported sample, so causality cannot be established; authors caution that further, cross-regional research is needed to understand the microbiome–brain connection and potential bidirectional effects.
A small, non-peer-reviewed study from the University of Porto reports a correlational link between specific gut and oral bacteria (Allisonella, Prevotella, and C. evryensis) and psychopathic traits in 200 adults. The researchers caution that the study is correlational with a small sample and potential biases, so causality cannot be established and results may vary by geography or self-report biases; more research is needed to explore how the gut microbiome might influence extreme behavior, if at all.
In an early Translational Psychiatry study, researchers analyzed 200 healthy adults and found that higher levels of certain gut and oral bacteria (Allisonella, Prevotella, Cloacibacillus evryensis) correlated with stronger psychopathic traits, while Treponema vincentii showed a negative association. The work does not show causation and is not yet peer-reviewed, but suggests microbiota could serve as biomarkers for psychopathic traits and potentially influence behavior via inflammation or neurotransmitter pathways like GABA.
A US study published in Nature Communications suggests that signals from the digestive system, carried by the vagus nerve, can influence memory formation in rats, linking dietary choices to how the brain encodes memories.
A USC-led rat study shows a nutritious meal triggers a gut-to-brain signal via the vagus nerve that boosts acetylcholine release in the medial septum and hippocampus, strengthening memory-related brain activity; fats and sugars intensified the effect while a Western junk-food diet early in life weakened it. The effect depends on intact vagal afferents and septal acetylcholine neurons, and may not translate directly to humans, but points to gut-brain targets and vagus nerve stimulation as potential therapies—though further research is needed and the study used male rats only.
A rat study shows the vagus nerve senses gut state during eating and triggers acetylcholine release in the brain, supporting attention and memory; disrupting this pathway impairs cognitive signaling, and a Western-style high-fat/high-sugar diet may further weaken it, offering clues about diet-related cognitive decline and aging-related diseases like dementia.
Researchers propose a Trigger–Gateway–Hub–Effector framework showing how gut dysbiosis and microbiota-derived signals may disrupt the intestinal barrier, ENS signaling, and gut motility, contributing to constipation; therapies aiming to rebalance the microbiota, modulate immune or neural responses, or protect enteric neurons—via probiotics, prebiotics, or fecal transplants—are being explored, though human mechanistic data remains limited and evidence is moderate.
A nutritionist argues that gut health starts with regulating the nervous system rather than relying on probiotics, explaining that chronic stress and a dysregulated nervous system disrupt digestion via the gut–brain axis and the vagus nerve. She suggests switching to a parasympathetic “rest and digest” state and using techniques like diaphragmatic breathing, eating in a relaxed environment, getting 7–9 hours of sleep, and regular exercise to improve digestion and reduce inflammation. Probiotics and supplements can help, but may not suffice if stress remains high; persistent issues should be evaluated by a healthcare professional.
A 2024 Nature Communications twin study found that daily prebiotic supplements (inulin or FOS) added to a protein powder improved memory test scores in people over 60, prompting the PRECODE trial at Wageningen to test three fibers—chicory inulin, resistant dextrin, and seaweed polysaccharide—over 26 weeks. Early data from 36 twin pairs show modest cognitive gains and subtle gut microbiome changes (notably more Bifidobacterium), with results expected in 2027. Researchers view these inexpensive, over-the-counter fibers as a promising, safe approach to supporting brain health during aging.
The article discusses how gluten-related conditions, especially celiac disease, may affect sleep via GI symptoms, systemic inflammation, and nutrient absorption, with mixed evidence on whether a gluten-free diet improves sleep. It notes that sleep quality can improve for some individuals on a gluten-free diet if calories and nutrients are adequate, but improvements are gradual and influenced by factors like stress or iron/magnesium/B vitamin status. Clinicians are advised to consider sleep hygiene and dietary factors when advising patients on gluten-related issues, while recognizing that more research is needed on the gluten-sleep relationship.
A University College Cork study shows coffee reshapes the gut microbiome and gut-brain axis, with certain bacteria thriving in coffee drinkers; decaf improves memory, sleep, and mood, while caffeinated coffee enhances attention and lowers inflammation, indicating coffee’s benefits go beyond caffeine and may affect mood, recovery, and cognitive function—useful insights for athletes, though individual microbiomes vary.
A study from the University of Birmingham and University of Oxford found that prucalopride, a laxative used for constipation, improved performance on tests of focus, attention, planning, short- and long-term memory, and emotional cognition in 50 participants with depressive episodes. Participants (aged 18–40) received 2 mg of the drug or placebo for 7–10 days, with cognitive assessments before and after; the drug acts on the 5HT4 serotonin receptor in the gut-brain axis, suggesting potential new treatment avenues for cognitive symptoms of depression.
In mice, the GLP-1 drug liraglutide reduces depressive-like behavior not by acting in the brain, but by accumulating in the gut where it promotes Lactobacillus delbrueckii. This bacterium increases levels of the endocannabinoid 2-AG via diacylglycerol, dampening stress-related brain activity. The antidepressant effect disappears if the gut microbiota is depleted, indicating a microbiome-dependent, brain-receptor–independent mechanism. The findings suggest potential for targeted probiotics to treat depression in obesity/diabetes, though human trials and sex-inclusive studies are needed.
A large, continuous-spectrum GWAS of anxiety symptoms (693,869 European-ancestry participants) identified 74 genetic loci (39 new) and revealed notable genetic overlap with irritable bowel syndrome (r≈0.57) and modest overlaps with coronary artery disease and migraine. The study estimates about 6% of anxiety symptom variation is explained by common variants, with the rest shaped by environment and gene–environment interactions; researchers caution that correlations do not imply causation and emphasize methodological advances (dimensional analysis) and the need for more diverse datasets. It complements clinically diagnosed anxiety genetics work and highlights gut–brain axis as a key area for future research.