Gut health for cognitive function -
This is particularly relevant for men working in high-stress environments where optimal cognitive function is essential for performance. Therefore, paying attention to gut health could be a useful avenue for improving memory and cognitive function in men 4 , 10 , There's growing interest in how the gut's condition can affect mental health, including mood disorders like depression and anxiety.
In particular, researchers are looking at how an imbalance in the gut microbiome can influence our emotional state. Some studies have found that an unhealthy gut can produce substances that affect our mood negatively. These substances can pass through the blood-brain barrier and interact with brain chemicals that help regulate how we feel As previously discussed, one key neurotransmitter for mood is serotonin, most of which is actually produced in the gut.
When the gut isn't healthy—maybe because of diet or stress—it can disrupt the normal production of serotonin. This could lead to feelings of depression or anxiety This topic is especially relevant for men, who may not always seek help for mood issues. Maintaining a balanced gut could offer a way to manage these conditions without the need for medication.
This could be useful for men who are in stressful jobs or who find it hard to discuss their emotional health Current research is encouraging, suggesting that a focus on gut health could offer a way to address mood disorders. By better understanding the links between the gut and the brain, there's hope that new treatments might be developed.
These treatments could help improve both digestive health and mental health in men Diet stands out as the most significant influencer when it comes to the composition of the gut microbiome. Different foods can lead to the predominance of specific microbial community profiles, such as Prevotella, Bacteroides, and Ruminococcus.
Furthermore, the interaction between diet and gut health likely differs between men and women. In addition, external stressors like infections or antibiotics can temporarily disturb the normal gut microbiota.
Factors affecting men's gut microbiome can also include age, lifestyle, and even genetic predisposition. These elements can cause both temporary and permanent changes in gut health.
Stress also plays a unique role in the impact of stress on gut health. The body's autonomic and circulatory systems can carry distress signals to the gut, potentially leading to imbalances known as dysbiosis. Medications, particularly antibiotics, can also interfere with gut health by killing off beneficial bacteria.
Over time, if the gut environment is not balanced, various health issues may arise, including mood disorders. Aging, lifestyle habits, and genetic predispositions further contribute to these changes, making it important to consider a holistic approach to gut health.
Rupa Health offers a selection of tests aimed at evaluating gut health, and among the most notable are the GI-MAP by Diagnostic Solutions and the GI Effects Comprehensive Profile by Genova Diagnostics. While both tests serve the same general purpose—to provide insights into gastrointestinal health—the methodologies, features, and clinical utility of each differ in significant ways.
The GI Effects Comprehensive Profile provides a broader scope, analyzing markers related to digestive function, inflammation, and microbial balance—all factors that can influence systemic health and, by extension, mental clarity and emotional stability.
This test would be particularly useful for men who suspect their cognitive or mood issues may be linked to a more complex interplay of gastrointestinal factors or for those who have co-occurring digestive and systemic conditions.
In the case where a parasitic infection is suspected, make sure you order the three-day profile. On the other hand, the GI-MAP focuses more narrowly on identifying specific pathogens, bacterial infections, and imbalances in the gut.
This test may be more suitable for men who suspect that an infection or specific imbalance in gut flora is impacting their cognitive or emotional health.
Its precision in quantification allows for targeted treatment plans, making it a strong choice for those who desire a more focused approach to improving gut health for the sake of cognitive and mood betterment. A balanced diet rich in fiber, prebiotics, and probiotics emerges as a significant strategy for optimizing gut health.
These components help foster a balanced and diverse gut microbiota, which is beneficial for both cognitive function and mood. Diet for optimal gut health should emphasize plant-based foods, lean proteins, and healthy fats. Overconsumption of processed foods , saturated fats, and artificial sugars should be avoided as they can lead to imbalances in the gut environment.
Managing stress effectively is another essential step for maintaining a healthy gut. Techniques for stress reduction can include mindfulness, meditation, and exercise. Adequate sleep is also fundamental for overall health and particularly beneficial for the gut.
Regular exercise not only aids in stress reduction but also encourages a healthy gut environment. It is also advisable to avoid unnecessary antibiotic usage whenever possible, as antibiotics can disrupt the natural balance of the gut microbiome.
Probiotic supplementation may also play a role in balancing the gut, thereby potentially enhancing cognitive functions and mood 9. In wrapping things up, it's really comforting to know that our gut health and our brain are so connected, especially for the men in our lives.
If you or someone you love has been wrestling with mood swings, stress, or even just trying to stay sharp mentally, tuning into gut health could be a game-changer. Tests like the GI-MAP and the GI Effects Comprehensive Profile can give you personalized information to help you make the best choices for your body and mind.
Documents Tab. We didn't imagine that they might affect our health. Over the past 15 years, though, we've learned that these gut bacteria are capable of producing substances that affect the cells in our body, because some of those substances are similar or identical to substances that our own cells make.
So, how can bacteria in the gut affect the brain? Substances made by bacteria in the gut can get into the blood, just like nutrients in our food travel from the gut into the blood. Also, certain nerves connect the brain and the gut: bacteria in the gut can send signals through those nerves to the brain.
Finally, gut bacteria can stimulate immune system cells in the wall of the gut, and the immune cells then can send signals though the nerves to the brain. Research in the past decade has found that gut bacteria may influence our emotions and cognitive capabilities.
For example, some bacteria make oxytocin, a hormone our own bodies produce that encourages increased social behavior. Sisodia, PhD, a professor of neurobiology at the University of Chicago. When such genetically modified mice were raised under sterile conditions from birth, they did not acquire gut microbiomes, and their brains showed much less damage at 40 weeks of age than the brains of mice harboring normal mouse microbiomes.
When such mice were raised under normal, nonsterile conditions, they developed normal microbiomes. A course of antibiotics at 2 weeks of age, however, permanently changed the composition of bacteria in their microbiomes.
For male mice, it also reduced the amount of brain damage evident at 40 weeks of age. The protective effects of the microbiome shifts were more pronounced in male mice carrying the APOE3 variant than in those with the high-risk APOE4 variant, possibly because the deleterious effects of APOE4 canceled out some of the protection, the researchers said.
Antibiotic treatment had no significant effect on neurodegeneration in female mice. Further experiments linked three specific short-chain fatty acids — compounds produced by certain types of gut bacteria as products of their metabolism — to neurodegeneration.
All three of these fatty acids were scarce in mice with gut microbiomes altered by antibiotic treatment, and undetectable in mice without gut microbiomes.
I've heard that the bacteria and other germs that live in Gut health for cognitive function intestines Weight loss tips affect our hea,th, Gut health for cognitive function whether we get some brain Guh. Can that be true? If so, how does that happen? It very likely is true. More than a century ago we discovered that bacteria live in our intestines, in our mouth and nose, and on our skin. Indeed, they've been doing so ever since the very first humans walked the earth. Fro Gut health for cognitive functionPreventing diabetes EjtahedSeyed Cognigive SiadatFarshad CogniitiveBagher Larijani; Is There Any Link between Cognitive Impairment and Gut Microbiota? A Systematic Review. Gut health for cognitive function 20 October ; 68 11 : — Methods: A systematic literature search was conducted on PubMed, Scopus, and Web of Science databases up to August The full texts of the papers were analyzed to retrieve the relevant information. Results: Totally, 24 observational studies 14 animal and 13 human studies were included. Most of the animal studies were performed on mouse models of AD.
Gut health for cognitive function -
Dorea longicatena has been reported to be positively associated with BMI and waist circumference [ 43 ]. Meanwhile, higher abundance of Dorea longicatena exists in individuals with circadian rhythm disturbance [ 44 ]. Recent evidence suggests that Dorea might contribute to elevated intestinal permeability [ 45 ].
In general, Dorea longicatena or Dorea may have a negative effect on the maintenance of a healthy gut. Furthermore, the present study revealed that Dorea longicatena and the pathway of formaldehyde oxidation I were positively correlated with IFN-γ.
IFN-γ is an AD-related pro-inflammatory cytokine [ 46 ] and elevated IFN-γ has been reported in AD and other neurologic disorders, such as stroke and multiple sclerosis [ 47 , 48 , 49 ]. These results suggest that inflammation activation plays a key role in the crosstalk between gut microbiome and the central nervous system CNS.
Although IFN-γ and microglial activation have been generally linked to inflammatory stimuli in the CNS, the presence of IFN-γ in the blood is not necessarily associated with chronic inflammation [ 50 ]. Thus, our findings need to be verified by more mechanistic studies. Besides systemic inflammation, the pathways involved in glucose metabolism and mitochondrial dysfunction have also been related with AD pathology [ 51 , 52 ].
Glycogen is critical in energy and glucose metabolism [ 53 ]. Enrichment of microbial pathways of glycogen biosynthesis and degradation among participants with poor cognition in the present study may reflect the essential role of these unbalanced metabolic processes in cognitive disorders.
Another pathway enriched in participants with cognitive impairment is the formaldehyde oxidation. Prior investigations have revealed that endogenous formaldehyde accumulation is mainly stimulated by aging, stroke, diabetes, and oxidative stress [ 54 , 55 ].
Recent studies also support that formaldehyde exposure exhibits adverse effects on cognitive function [ 54 ]. Therefore, gut microbiota may be involved in the regulation of formaldehyde oxidation that eventually affects cognition.
In this study, we identified several key metabolites associated with cognitive impairment, of which methylglutaric acid is considered to be neurotoxic through early activation of an oxidative stress response [ 56 ] and increasing the potential for neurodegeneration in rats [ 57 ].
Another key metabolite L -phenylalanine identified is a precursor of catecholamines including dopamine and is essential for biosynthesis of these neurotransmitters [ 58 ]. Moreover, the concentration of L -phenylalanine has been found to be significantly lower in the plasma of AD patients compared to that of healthy controls [ 59 ].
There are several limitations in this study. First, the observational nature of this study makes the results subjected to the influence of potential residual confounders, and the statistically significant differences found in our analysis can only suggest associations of these multi-omics features with the outcomes.
Further experimental studies or clinical trials are required to verify these findings and prove the causality. Second, this study includes only Chinese participants and thus the results may not be generalizable to other ethnic populations. Finally, although we have adjusted for the lag time 1.
A major strength of the present study is that our findings are replicated across three independent populations from different regions in China. Furthermore, the findings based on questionnaire information i. Overall, the present study provides important evidence supporting the close association of gut microbiome with cognitive impairment and alterations of brain structure.
The identified cognition-related gut microbial taxonomies, pathways or serum metabolites may potentially contribute to the development of interventions or drug targets for dementia and cognitive decline in the future. Other data described in the article will be made available upon request by bona fide researchers for specified scientific purposes via contacting the corresponding authors.
Patterson C. World Alzheimer report Google Scholar. Bateman RJ, Xiong C, Benzinger TL, Fagan AM, Goate A, Fox NC, et al. N Engl J Med. Article CAS PubMed PubMed Central Google Scholar. Livingston G, Huntley J, Sommerlad A, Ames D, Ballard C, Banerjee S, et al. Dementia prevention, intervention, and care: report of the Lancet Commission.
Article PubMed PubMed Central Google Scholar. Ghaisas S, Maher J, Kanthasamy A. Gut microbiome in health and disease: Linking the microbiome—gut—brain axis and environmental factors in the pathogenesis of systemic and neurodegenerative diseases.
Pharmacol Ther. Article CAS PubMed Google Scholar. Harach T, Marungruang N, Duthilleul N, Cheatham V, Mc Coy KD, Frisoni G, et al. Reduction of Abeta amyloid pathology in APPPS1 transgenic mice in the absence of gut microbiota.
Sci Rep. Vogt NM, Kerby RL, Dill-McFarland KA, Harding SJ, Merluzzi AP, Johnson SC, et al. Article CAS Google Scholar. Liu P, Wu L, Peng G, Han Y, Tang R, Ge J, et al.
Brain Behav Immun. Article PubMed Google Scholar. Li B, He Y, Ma J, Huang P, Du J, Cao L, et al. Alzheimers Dement. Arnoriaga-Rodriguez M, Mayneris-Perxachs J, Burokas A, Contreras-Rodriguez O, Blasco G, Coll C, et al. Obesity impairs short-term and working memory through gut microbial metabolism of aromatic amino acids.
Cell Metab. The gut microbiome in neurological disorders. Lancet Neurol. Zhang ZQ, He LP, Liu YH, Liu J, Su YX, Chen YM. Association between dietary intake of flavonoid and bone mineral density in middle aged and elderly Chinese women and men.
Osteoporos Int. Katzman R, Zhang MY, Ouang Ya Q, Wang ZY, Liu WT, Yu E, et al. A Chinese version of the mini-mental state examination; impact of illiteracy in a Shanghai dementia survey. J Clin Epidemiol. Popkin BM, Du S, Zhai F, Zhang B. Cohort profile: the China Health and Nutrition Survey—monitoring and understanding socio-economic and health change in China, — Int J Epidemiol.
Folstein MF, Folstein SE, McHugh PR. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. Perneczky R, Wagenpfeil S, Komossa K, Grimmer T, Diehl J, Kurz A.
Mapping scores onto stages: mini-mental state examination and clinical dementia rating. Am J Geriatr Psychiatry. Brandt J, Welsh KA, Breitner JC, Folstein MF, Helms M, Christian JC. Hereditary influences on cognitive functioning in older men.
A study of twin pairs. Arch Neurol. Miao Z, Lin JS, Mao Y, Chen GD, Zeng FF, Dong HL, et al. Erythrocyte n-6 polyunsaturated fatty acids, gut microbiota and incident type 2 diabetes: a prospective cohort study. Diabetes Care.
Sun S, Wang H, Tsilimigras MC, Howard AG, Sha W, Zhang J, et al. Does geographical variation confound the relationship between host factors and the human gut microbiota: a population-based study in China. BMJ Open. Yu Q, McCall DM, Homayouni R, Tang L, Chen Z, Schoff D, et al.
Age-associated increase in mnemonic strategy use is linked to prefrontal cortex development. Pirlich M, Hofer C, Weise CM, Stockert A, Thone-Otto A, Garthe A, et al. Hippocampal gray matter volume in the long-term course after transient global amnesia.
Neuroimage Clin. Tzourio-Mazoyer N, Landeau B, Papathanassiou D, Crivello F, Etard O, Delcroix N, et al. Automated anatomical labeling of activations in SPM using a macroscopic anatomical parcellation of the MNI MRI single-subject brain.
Varela RB, Valvassori SS, Lopes-Borges J, Mariot E, Dal-Pont GC, Amboni RT, et al. Sodium butyrate and mood stabilizers block ouabain-induced hyperlocomotion and increase BDNF, NGF and GDNF levels in brain of Wistar rats. Kim S. ppcor: an R package for a fast calculation to semi-partial correlation coefficients.
Commun Stat Appl Methods. PubMed PubMed Central Google Scholar. Start T. Gephi Tutorial Quick Start [Online]. Saji N, Niida S, Murotani K, Hisada T, Tsuduki T, Sugimoto T, et al.
Analysis of the relationship between the gut microbiome and dementia: a cross-sectional study conducted in Japan.
Stadlbauer V, Engertsberger L, Komarova I, Feldbacher N, Leber B, Pichler G, et al. Dysbiosis, gut barrier dysfunction and inflammation in dementia: a pilot study.
BMC Geriatr. Frost F, Kacprowski T, Ruhlemann M, Pietzner M, Bang C, Franke A, et al. Long-term instability of the intestinal microbiome is associated with metabolic liver disease, low microbiota diversity, diabetes mellitus and impaired exocrine pancreatic function.
Dey N, Soergel DA, Repo S, Brenner SE. BMC Gastroenterol. Cattaneo A, Cattane N, Galluzzi S, Provasi S, Lopizzo N, Festari C, et al. Association of brain amyloidosis with pro-inflammatory gut bacterial taxa and peripheral inflammation markers in cognitively impaired elderly.
Neurobiol Aging. Smith PM, Howitt MR, Panikov N, Michaud M, Gallini CA, Bohlooly YM, et al. The microbial metabolites, short-chain fatty acids, regulate colonic Treg cell homeostasis. Zhou Y, Wang Y, Quan M, Zhao H, Jia J.
J Alzheimers Dis. Guo M, Peng J, Huang X, Xiao L, Huang F, Zuo Z. Gomez-Arango LF, Barrett HL, McIntyre HD, Callaway LK, Morrison M, Dekker Nitert M, et al. Increased systolic and diastolic blood pressure is associated with altered gut microbiota composition and butyrate production in early pregnancy.
Salomaki-Myftari H, Vahatalo LH, Ailanen L, Pietila S, Laiho A, Hanninen A, et al. Neuropeptide Y overexpressing female and male mice show divergent metabolic but not gut microbial responses to prenatal metformin exposure.
PLoS One. Xu J, Bjursell MK, Himrod J, Deng S, Carmichael LK, Chiang HC, et al. A genomic view of the human-Bacteroides thetaiotaomicron symbiosis. Jing Y, Yu Y, Bai F, Wang L, Yang D, Zhang C, et al. Effect of fecal microbiota transplantation on neurological restoration in a spinal cord injury mouse model: involvement of brain—gut axis.
Dayama G, Priya S, Niccum DE, Khoruts A, Blekhman R. Interactions between the gut microbiome and host gene regulation in cystic fibrosis. Genome Med. Rodriguez J, Hiel S, Neyrinck AM, Le Roy T, Potgens SA, Leyrolle Q, et al.
Discovery of the gut microbial signature driving the efficacy of prebiotic intervention in obese patients. Dugger BN, Dickson DW. Pathology of neurodegenerative diseases.
Cold Spring Harb Perspect Biol. Evans TE, Adams HHH, Licher S, Wolters FJ, van der Lugt A, Ikram MK, et al. Subregional volumes of the hippocampus in relation to cognitive function and risk of dementia. Zhornitsky S, Chaudhary S, Le TM, Chen Y, Zhang S, Potvin S, et al. Psychiatry Res Neuroimaging.
Heger IS, Deckers K, Schram MT, Stehouwer CD, Dagnelie PC, van der Kallen CJ, et al. Associations of the lifestyle for brain health index with structural brain changes and cognition: results from the Maastricht study.
Allin KH, Tremaroli V, Caesar R, Jensen BAH, Damgaard MTF, Bahl MI, et al. Aberrant intestinal microbiota in individuals with prediabetes. Mortas H, Bilici S, Karakan T. The circadian disruption of night work alters gut microbiota consistent with elevated risk for future metabolic and gastrointestinal pathology.
Chronobiol Int. Chen P, Starkel P, Turner JR, Ho SB, Schnabl B. Dysbiosis-induced intestinal inflammation activates tumor necrosis factor receptor I and mediates alcoholic liver disease in mice.
Zheng C, Zhou XW, Wang JZ. Transl Neurodegener. J Immunol. Yilmaz G, Arumugam TV, Stokes KY, Granger DN. Role of T lymphocytes and interferon-gamma in ischemic stroke. Heesen C, Nawrath L, Reich C, Bauer N, Schulz KH, Gold SM. Fatigue in multiple sclerosis: an example of cytokine mediated sickness behaviour?
J Neurol Neurosurg Psychiatry. Lee SH, Kwon JY, Kim SY, Jung K, Cho ML. Interferon-gamma regulates inflammatory cell death by targeting necroptosis in experimental autoimmune arthritis. Su M, Naderi K, Samson N, Youssef I, Fulop L, Bozso Z, et al. Mechanisms associated with type 2 diabetes as a risk factor for Alzheimer-related pathology.
Mol Neurobiol. Gibson GE, Karuppagounder SS, Shi Q. Ann N Y Acad Sci. Shulman RG, Rothman DL. Annu Rev Physiol. Tong Z, Han C, Luo W, Li H, Luo H, Qiang M, et al. Aging-associated excess formaldehyde leads to spatial memory deficits. Tan T, Zhang Y, Luo W, Lv J, Han C, Hamlin JNR, et al.
Formaldehyde induces diabetes-associated cognitive impairments. FASEB J. Colin-Gonzalez AL, Paz-Loyola AL, de Lima ME, Galvan-Arzate S, Seminotti B, Ribeiro CA, et al. Experimental evidence that 3-methylglutaric acid disturbs mitochondrial function and induced oxidative stress in rat brain synaptosomes: new converging mechanisms.
Neurochem Res. Ribeiro CA, Hickmann FH, Wajner M. Probiotics are microorganisms that provide a health benefit when consumed.
Here's everything you need to know about probiotics. Both probiotics and prebiotics help keep your gut bacteria healthy but serve different functions.
Here are the functions and benefits of each. Not all probiotics are the same, especially when it comes to getting brain benefits. See which probiotics work best for enhancing cognitive function.
Some medical professionals deny that leaky gut exists, while others claim it causes all sorts of diseases. Here's an unbiased look at the evidence. Omega-3 fatty acids are incredibly important for your body and brain.
This article lists 17 science-based health benefits of omega-3s. Having healthy gut bacteria is important for your health. However, many diet, lifestyle and other factors can negatively affect the health of your gut.
Short-chain fatty acids are produced by the friendly bacteria in your gut. They may promote weight loss and provide various health benefits. While they're not typically able to prescribe, nutritionists can still benefits your overall health.
Let's look at benefits, limitations, and more. A new study found that healthy lifestyle choices — including being physically active, eating well, avoiding smoking and limiting alcohol consumption —…. Carb counting is complicated.
Take the quiz and test your knowledge! A Quiz for Teens Are You a Workaholic? How Well Do You Sleep? Health Conditions Discover Plan Connect. Nutrition Evidence Based The Gut-Brain Connection: How it Works and The Role of Nutrition. By Ruairi Robertson, PhD on July 31, How Are the Gut and Brain Connected?
Probiotics, Prebiotics and the Gut-Brain Axis. What Foods Help the Gut-Brain Axis? The Bottom Line. How we reviewed this article: History. Aug 20, Written By Ruairi Robertson. Vogt et al. Furthermore, Zhao and Lukiw et al.
Our findings are consistent with these studies because our patients with more Bacteroidetes had lower logical memory subtest scores, indicating impaired memory function.
The mechanism through which the gut microbiome affects human cognitive functions remains unknown, although animal studies strongly implicate the gut microbiome as a key regulator of the brain and behaviour The functional pathways through which the gut microbiome communicates with the brain, also known as gut—microbiome—brain cross-talk, is a bidirectional, functional communication network between microbes and the brain that comprises neuroendocrine, neural, and neuroimmune signalling pathways Explicitly, three hypothesis have been proposed: 1 a circulation pathway, indicating the transportation of microbial metabolites, toxins, and pro-inflammatory factors; 2 a neuroendocrine pathway, indicating the activation of neuroendocrine cells that can be attributed to microbial metabolites; and 3 a neural pathway, indicating an interaction between the gut microbiome and the autonomic nervous system.
This previous report also showed that an increase in the abundance of a pro-inflammatory gut microbiome taxon and a reduction in the abundance of an anti-inflammatory taxon may be associated with a peripheral inflammatory state in patients with cognitive impairments and brain amyloidosis Another report describing the gut—brain module analysis of faecal metagenomes identified the microbial synthesis of metabolites and suggested a potential role for these metabolites in the onset of depression At present, we do not have sufficient data to identify the underlying mechanism that mediates the association between the gut microbiome and cognitive impairment.
However, potential differences regarding the presence of WMH may represent supporting evidence that cerebral SVD acts as an intermediate between cognitive impairment and the gut microbiome.
Likewise, Ong et al. Further studies examining the association between cerebral SVD and gut microbiome metabolites in the Gimlet study cohort will shed light on this issue. Here, we found other interesting findings. There was an independent association between WMH and the gut microbiome, although other components of cerebral SVD, such as SLI and CMB, did not show such significant differences.
This finding suggests that a potential mechanism regarding the development of WMH may be attributable to the gut microbiome, either directly or indirectly. Further study regarding the association between cerebral SVD and the gut microbiome is warranted.
Our study has several strengths. First, we systematically assessed the cognitive functions of patients, using a comprehensive geriatric assessment in the setting of the memory clinic. These steps have provided detailed analyses of cognitive function. Second, we found a close and strong association between the gut microbiome and MCI, identified by multivariable analyses and graphical modelling, compared with the relationships between the other risk factors and MCI.
Applying graphical modelling has strengthened our findings. Third, our comprehensive assessment regarding the gut microbiome and MCI may fill the knowledge gap regarding the mechanisms that connect cognitive decline with the gut microbiome.
Finally, because we have established a new relationship and have widened the knowledge of such associations with regard to MCI, our findings may contribute to a better understanding and increased attention being paid to the associations between the gut microbiome and cognitive functions.
Nonetheless, this study has several limitations. A causal relationship between the gut microbiome and MCI could not be established because of the cross-sectional study design.
The small number of patients renders our study at risk of being statistically underpowered. The unequal numbers of patients with MCI and those with NC may also be a potential limitation. Selection bias may exist because this was a single hospital-based cohort.
Furthermore, potentially confounding factors may exist because the gut microbiome is affected by diet 20 , 21 and the presence of complications, such as blood pressure variability and cardiovascular disease Likewise, we plan to assess the nutritional status including the diet pattern in the future study because the Japanese diet pattern can alter the intestinal bacteria and have beneficial effects on humans Assessments of the amyloid-β precursor protein may be useful because this factor suggests inflammatory endothelial dysfunction and the risk of cognitive impairment The specific mechanism through which the microbiome affects cognitive decline has not yet been clarified.
Rather than identifying the roles of specific bacteria, the functional analysis of the gut microbiome as one integrated organ may be more practically useful. Our data indicate both accelerating in the present study and decelerating in a previously published study 5 effects of Bacteroides on cognitive decline.
To date, various risk factors for cognitive impairment have been proposed, such as aging, education years, hypertension, diabetes mellitus, and social factors 1 ; however, the human gut microbiome has not previously been mentioned as a risk factor.
Our findings add the gut microbiome as a new risk factor for cognitive impairment. More importantly, controlling the gut microbiome may represent a possible method for the prevention and intervention of cognitive impairment.
Although this sub-analysis study contains a small number of patients and our analysis is preliminary, our findings provide supporting evidence for a relationship between the gut microbiome and cognitive impairment. Longitudinal assessments of the gut microbiome using next-generation sequencing technology, assessments of the various metabolites produced by the gut microbiome, and assessments of diet patterns should be investigated in future studies to clarify the underlying mechanism that connects the gut microbiome with cognitive function.
We showed that components of the gut microbiome, in particular Bacteroides , may be associated with the presence of MCI in patients without dementia. We speculate that some gut microbiome metabolites could affect cognitive functions through a microbiome—gut—brain axis. Further studies are warranted to examine such relationships.
This study was a sub-analysis of our previously published, single-centre observational study Gimlet study 5. The aim of this study was to investigate the association between the gut microbiome and MCI in patients without dementia. This study complied with the Declaration of Helsinki and was approved by the Institutional Review Board at the National Center for Geriatrics and Gerontology No.
Informed consent was obtained from all patients and their families before participation in this study. The Gimlet study is registered with the UMIN Clinical Trials Registry UMIN Detailed information has been provided in the supplementary file and in the previous report 5.
Patients were also excluded from this sub-analysis if they met the following criteria: 1 had dementia; or 2 were unable to provide sufficient faecal samples to facilitate the analysis of metabolites both now and in the future. Clinical samples and data were provided by the NCGG Biobank, which collects clinical data for research.
In the present sub-study, the patients without dementia were further divided into two categories: MCI and NC. Patients underwent a 1. The presence and components of cerebral SVD were categorised using standards for reporting neuroimaging vascular changes 37 , including SLI, WMH, CMB, and CSS.
Moreover, VSRAD advance software Eisai Co. Increased VSRAD scores suggest the potential presence of AD, as this score reflects hippocampal atrophy, one of the characteristics of the AD brain Patients also underwent N-isopropyl-p-[ I]-iodoamphetamine-SPECT.
After all samples were collected, the gut microbiome was analysed by the TechnoSuruga Laboratory Shizuoka, Japan , using T-RFLP analysis T-RFLP analysis is one of the most well-established and reliable 16S ribosomal RNA-based methods, especially when considering its high throughput and reproducibility.
The phylum Firmicutes included the Lactobacillales and Clostridium clusters, and the phylum Bacteroidetes included Bacteroides and Prevotella.
First, patients were divided into two groups, according to the presence or absence of MCI, and their clinical characteristics and the compositions of their gut microbiomes were compared using the Wilcoxon rank-sum test and χ 2 test, respectively.
Second, patients were also divided into two groups, either enterotype I and non-enterotype I, or enterotype III or non-enterotype III, to compare their clinical characteristics based on Gimlet baseline data. This division indicated that there were a small number of patients with enterotype II.
Third, multivariable logistic regression models were performed to identify factors that were independently associated with MCI. Last, graphical modelling was generated to illustrate mutual associations among the factors used in the multivariable logistic regression analyses, including traditional risk factors and gut microbiome, to visualize and compare mutual relationships.
Data were analysed using the JMP Livingston, G. et al. Dementia prevention, intervention, and care. Article PubMed Google Scholar. Ganguli, M. Prevalence of mild cognitive impairment by multiple classifications: The Monongahela-Youghiogheny Healthy Aging Team MYHAT project. Am J Geriatr Psychiatry.
Article PubMed PubMed Central Google Scholar. Saji, N. Lancet Neurol. Stower, H. Depression linked to the microbiome. Article PubMed CAS Google Scholar. Analysis of the relationship between the gut microbiome and dementia: a cross-sectional study conducted in Japan.
Sci Rep. Article ADS PubMed PubMed Central CAS Google Scholar. Alkasir, R. Human gut microbiota: the links with dementia development. Protein Cell. Article CAS PubMed Google Scholar. Vogt, N. Sci Rep 7 , Solas, M. Inflammation and gut-brain axis link obesity to cognitive dysfunction: plausible pharmacological interventions.
Curr Opin Pharmacol. Zhao, Y. Front Cell Infect Microbiol 7 , Article PubMed PubMed Central CAS Google Scholar. Wu, S. Nature Communications. Tang, W. Gut Microbiota in Cardiovascular Health and Disease. Article CAS PubMed PubMed Central Google Scholar.
Wang, Z. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Article ADS CAS PubMed PubMed Central Google Scholar. Proportional changes in the gut microbiome: a risk factor for cardiovascular disease and dementia? Hypertens Res. Front Immunol. Cryan, J.
Talking about a microbiome revolution. Nat Microbiol. Welcome, M. Current perspectives and mechanisms of relationship between intestinal microbiota dysfunction and dementia: A review. Dement Geriatr Cogn Disord Extra. Article Google Scholar.
Cattaneo, A. Association of brain amyloidosis with pro-inflammatory gut bacterial taxa and peripheral inflammation markers in cognitively impaired elderly. Neurobiology of Aging. Valles-Colomer, M. The neuroactive potential of the human gut microbiota in quality of life and depression.
Ong, I.
Your fujction is a bustling and thriving alien colony. They number in their trillions cognitivve include thousands of funcction species. Many of fujction microorganisms, including bacteria, archaea and eukarya, were fof long before humans, Safe appetite suppressant evolved alongside funcction Gut health for cognitive function now outnumber our Gut health for cognitive function cells many times over. Indeed, as John Cryan, a professor of anatomy and neuroscience at University College Cork, rather strikingly put it in a TEDx talk : "When you go to the bathroom and shed some of these microbes, just think: you are becoming more human. Collectively, these microbial legions are known as the "microbiota" — and they play a well-established role in maintaining our physical health, from digestion and metabolism to immunity. They also produce vital compounds the human body is incapable of manufacturing on its own. But what if they also had a hotline to our minds?
Und was jenes zu sagen hier?
Ich meine, dass Sie sich irren. Geben Sie wir werden besprechen. Schreiben Sie mir in PM.
Ich meine, dass es das sehr interessante Thema ist. Geben Sie mit Ihnen wir werden in PM umgehen.
Eben dass wir ohne Ihre sehr gute Idee machen würden
Auf jeden Fall.