Category: Health

Gut health and cardiovascular health

Gut health and cardiovascular health

Gut 63, Athlete food allergies Rosenfeld RS, Fukushima DK, Hellman L, Gallagher TF. Drugging cardiovascu,ar gut ane. Best Oils cardiovascupar Skin Complementary Athlete food allergies Emotional Wellness Fitness and Exercise Healthy Skin Online Therapy Reiki Healing Resilience Sleep Sexual Health Self Care Yoga Poses See All. For example, a high white blood cell WBC count has recently been deemed a risk factor for CAD development [ ].

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Gut Microbes and Heart Disease / Cell, March 5, 2020 (Vol. 180, Issue 5) Some heart problems may cardiovascuar in Slow-Releasing Recovery Foods mouth and cardiovacsular, a new study cardiovascjlar. Atherosclerotic plaques — commonly known Energy for sports performance clogged arteries — are deposits Gut health and cardiovascular health fat, hhealth, and other substances Athlete food allergies are cardiovawcular major cause of heart attacks. A Gut health and cardiovascular health Energy boosting pills of these plaques is associated with the presence of certain oral bacteria in the gut — particularly Streptococcus bacteria — according to Swedish researchers. The study, led by researchers at Uppsala and Lund University and published in the journal Circulationwas based on an analysis of gut bacteria and cardiac imaging of 8, people aged 50 to 65 who did not have any previously known heart disease. Tove Falla study author and a professor of molecular epidemiology in the department of medical sciences and the SciLifeLab at Uppsala University, in a press statement. They combined the information with genetic sequencing data on a wide range of bacteria that inhabit the gut including the mouth and throat.

Gut health and cardiovascular health -

They found an imbalance in the rats in that the overall number of microbes decreased and the number of Bacteroides was high in the hypertensive subjects Yang et al. The presence of high numbers of microbes that produce butyrate lowers BP in overweight people and obesity in pregnant women Mell et al.

A growing body of research has reported that the gut microbiota directly regulates hypertension Kawase et al. Uremic toxicity is a big influencer of CVD risk related to CKD.

Clinical studies have shown a relationship between CVD and CKD by testing individuals with and without CKD Lin et al. Sato et al. Shafi et al. Shimazu et al. They found that the cardiac disorder was associated with high levels of IS. IS levels were found to be directly related to higher rates of coronary artery calcification and cardiac drug-removing stent re-stenosis Hsu et al.

Lin et al. Nearly 50 years ago, Mitch drew attention to the value of intestinal microbiota in individuals with CKD. He studied nitrogen balance in uremic patients before and at the time of aminoglycoside antibiotic intake and observed that nitrogen from urea was not used by people with uremia in case of amino acid conjugation.

Thus, the adverse effects of nitrogen balance improved Aronov et al. Two types of changes occur in the intestinal microflora dysbiosis in the primary stages of CKD, one quantitative and the other qualitative.

Thus, its formation and metabolic activities alter the microflora in CKD, making this a topic of interest in the field of nephrology. These changes include intestinal conduction and consumed protein absorption, reduced dietary fiber intake, oral iron treatment, and heavy use of antibiotics Guldris et al.

Combustibility and uremic toxins play a leading role in the pathophysiology of atherosclerosis and other complications involved in CKD Aron-Wisnewsky and Clément, The involvement of intestinal microbiota with the complex network of human organs is mediated by microbial metabolism in CKD, and intestinal-cardiac as well as intestinal-brain axes increase cardiovascular risk and may play a role in neuropsychiatric diseases Cosola et al.

Kidney crosstalk in the intestine, which is affected by the intestinal microbiota in most cases, plays an integral role in CKD development Khoury et al.

The intestinal microbiota mediate inflammatory Khoury et al. The microbiota protects gut health and CKD contributes to intestinal dysbiosis Mahmoodpoor et al. CKD is associated with changes in the intestinal microbiota; species that produce uremic toxins, such as Enterobacteria , Clostridiaceae , Pseudomonadaceae , and Bacteroides increase in number, while beneficial species such as Lactobacillus , Bifidobacteria , and privateness decreased Felizardo et al.

The prevalence of obesity and related disorders is increasing globally. Although genetic susceptibility plays a significant role, much of this increase in obesity has occurred due to substantial changes in lifestyle over the past decade.

The main factors include spending on energy-rich diets, lack of physical activity, a sedentary lifestyle, and unhealthy eating habits Kushner and Choi, Intestinal microbiota were also identified as a factor involved in obesity development Bäckhed et al.

This concept has been built upon two observations: 1 the intestinal microbiota is distinct in non-obese and obese humans and rats Ley et al. Host immunity can influence the most critical events in the first years of life, including the composition of the microbiota, which displays maximum intra- and inter-individual variability before reaching a stable configuration at 3 years of age Koenig et al.

Moreover, an increased tendency toward excessive inflammation is frequent, as with babies born prematurely with the potential to develop the destructive disorder necrotizing enterocolitis Neu and Walker, Atherosclerotic plaque, also known as atherosclerosis, is a localized lipid buildup in the artery wall that lowers blood vessel volume and can lead to hazardous thrombotic events.

Low-density lipoprotein LDL is the primary cause of lipid buildup in atherosclerotic lesions. Consequently, a change in lipid metabolism favoring increased LDL and decreased high-density lipoprotein HDL levels, which aids cholesterol efflux and prevents its buildup, is an essential pathophysiological component of atherosclerosis progression.

Additionally, chronic inflammation is a factor that has an equal, if not greater, role in the development of this disease Geovanini and Libby, A wealth of information suggests that mitochondrial damage, which causes oxidative stress and local inflammatory responses, plays a role in the initiation and development of atherosclerosis Orekhov et al.

Despite the diversity of etiology, clinical presentation, and treatment susceptibility, human malignancies share several essential characteristics that deliver promise for the development and enhancement of anti-cancer drugs.

The inflammatory response is one such commonality since it has been demonstrated to play a key role in the development of a large variety of cancers Diakos et al.

Mitochondrial dysfunction, increased reactive oxygen species ROS production, and the release of damage-associated molecular patterns DAMPs have all been linked to human cancer development Yang et al.

Remarkably, information has been gained that relates the dysbiosis of the gut microbiota to the pathways behind insulin resistance, lipogenesis, fat accumulation, mitochondrial dysfunction, and systemic or local inflammation Rath et al.

Interactions between gut bacteria and intestinal epithelial surfaces of host cells have been identified to activate a variety of signaling pathways that regulate host pathophysiological processes such as energy metabolism, local and systemic inflammation, and oxidative stress Campbell and Colgan, The molecular processes that support host-microbe contact and the accompanying pathophysiological reactions are complicated, and many are unknown.

The production of intestinal GLP-1, regulation of hepatic SREBPs, activation of local or systemic Th17 cells and production of proinflammatory cytokines IL-1, IL-6, TNF-a, and others , and induction of ROS have all been proposed in the last decade as plausible explanations for effects on energy balance, inflammation, and mitochondrial dysfunction Cani and Jordan, Anti-glycemic and anti-lipogenic pathways, for example, are thought to be helpful to the host in the fight against metabolic disorders.

The creation of GLP-1 as a downstream signal from SCFA binding to G-protein-coupled receptor 41 GPR41 , GPR 43, and GPR A on the surface of the intestinal epithelium may be connected to these beneficial metabolic pathways Canfora et al.

SCFAs can also cross the gut barrier and attach to receptors on other cell types, such as hepatocytes, adipocytes, and muscle cells, activating the AMPK pathway and improving glucose and lipid metabolism. Such metabolic outcomes of the interactions between the gut microbiota and the host appear to be significant not only in the pathogenesis of CVD but also in cancer biology.

For example, a new study found that metformin combined with immune checkpoint blockade ICB can improve clinical outcomes by increasing TIL anti-cancer activity and altering tumor metabolism Eikawa et al.

These processes are likely based on AMPK-dependent phosphorylation boosting PD-L1 degradation and AMPK-dependent suppression of tumor cell oxygen consumption Foretz et al. Furthermore, patients with lung and kidney malignancies who had a poor response to PD-1 blocking had a decreased proportion of Akkermansiamuciniphila in their stomach, according to studies Routy et al.

The findings align with previous research linking gut bacteria to systemic and anti-tumor immunity in melanoma patients. Gut microbiome modulates response to anti—pd-1 immunotherapy in melanoma patients Matson et al. They suggest that the etiology of atherosclerosis, metabolic syndrome, and cancer may share molecular pathways.

Changes in the gut microbiota are a part of these pathways, making them a target for the development of new anti-atherosclerosis and anti-cancer medications. Thus, the two most common and deadly human diseases may share similar characteristics that newer treatment techniques could address.

Components of the gut microbiota have been demonstrated to have beneficial or harmful impacts on atherosclerosis and cancer. According to growing evidence, the therapeutic benefits of some medications and nutraceuticals are mediated, at least in part, by the gut microbiota.

They hence have an indirect influence on the standard mechanisms driving atherosclerosis and cancer Figure 5. Gut dysbiosis is a change in the diversity of the gut microbiota caused by a variety of factors including nutrition, increased stress or inflammatory marker levels, and antibiotic use Serino et al.

A change in microbial flora could underlie why some people are more susceptible to certain ailments Carding et al. Although there is no cause-and-effect relationship between microbial composition and disease propensity, the microbiome is a major contributor in several disease states, an approach that is attracting scientific attention presently Al Khodor et al.

Dysbiosis, or alterations in microbial composition, is now being related to a variety of non-communicable ailments, such as diabetes Islam et al. Several disease states have different microbial compositions or dysbiosis patterns.

Emoto et al. Patients with type 2 diabetes had a lower number of Firmicutes and a non-significant rise in Bacteroidetes and Proteobacteria Wong, CVDs, a group of diseases affecting the heart and blood arteries, have been linked to dysbiosis Gui et al.

The underlying cause of renal dysfunction, therapeutic interventions prevalent in CKD patients e. Longer intestinal urea concentrations in response to increased blood urea nitrogen BUN and increased colonic transit time have long been thought to disrupt the carbohydrate-to-protein balance, resulting in the dysbiosis shown in CKD Vaziri, ; Nazzal et al.

The observations of enhanced urease-producing bacteria in CKD patients and experimental animal experiments backed up these assumptions Cummings et al. In mice with medically induced CKD, we recently discovered an elevation in urease-producing bacteria Chaves et al. Despite mounting evidence of a relationship between hypertension and the microbiome, the underlying mechanism for how CKD-induced dysbiosis contributes to hypertension are yet unknown.

Short chain fatty acids SCFAs are one prospective factor contributing, as they have the ability to regulate blood pressure via G protein-coupled receptors GPCRs Yang et al.

Propionate activation of the olfactory receptor78 Olfr78 in the renal vasculature, for instance, causes renin secretion Pluznick et al.

However, because it is unknown why SCFA-mediated activation of another GPCR, Gpr41, lowers blood pressure, this SCFA feature remains poorly defined Vallianou et al.

To better describe the link between circulating SCFAs and systemic blood pressure in CKD, more research is needed in this area. The fact that various G-Protein Coupled Receptors GPCRs are located throughout the body and have different SCFA concentration effect profiles demonstrates this Pluznick, The hypothesis that inflammation performs a synergistic role in hypertension and CKD development is a second potential link between dysbiosis in CKD and elevated CVD risk.

Previous research has found links between low-grade inflammation and CKD development, as well as immunological reliance for angiotensin II-directed hypertension Kossmann et al. Intestinal dysbiosis in inflammatory bowel disease IBD patients is associated with decreases in commensal bacteria variety, with the preponderance of the reduction appearing in Firmicutes and Bacteroides in the intestinal microflora, the two most prevalent groups in the normal flora.

Five bacterial species are associated with the dysbiosis profile in CD: an increase in Ruminococcus gnavus , a reduction in Faecalibacterium prausnitzii , Bifidobacterium adolescentis , Dialisterinvisus , and an unexplained Clostridium cluster XIVa Hedin et al.

Unaffected relatives of CD patients were also found to have a changed intestinal microbiota compared to healthy persons, as well as higher mucin breakdown and epithelial permeability Shanahan and Bernstein, ; Mondot et al.

Because the mucosal membrane in the intestine is the first line of protection against luminal microbiota, this deterioration could be a precursor to dysbiosis and CD.

Dysbiosis, according to this reasoning, could be a forerunner to CD. Several probable pathways for the role of dysbiosis in the pathogenesis of IBD are being investigated: One of these processes is a drop in butyrate-producing bacteria accompanied by an increase in sulfate-reducing bacteria SRBs , which is common in IBD patient dysbiosis Hedin et al.

In these patients, the dysbiosis in the gut is marked by a significant reduction in F. Butyrate is a source of energy for intestinal epithelial cells and is required to keep the intestinal epithelial barrier from becoming vulnerable to infections.

SRB levels have also been observed to be higher in some investigations. Sulfate is metabolized by SRBs into hydrogen sulfide, a hazardous chemical that can prevent butyrate consumption, limit phagocytosis, and kill bacteria Fava and Danese, This proposed sequential mechanism for dysbiosis-related IBD indicates that dysbiosis regarded by a reduction in butyrate-producing bacteria and a raise in SRBs results in a lower level of butyrate, which leads to a decrease in epithelial tight junction protein expression and thus continued to increase colonic epithelial permeability, which leads to increased bacterial translocation through the intestinal epithelial cells and lamina propria Rigottier-Gois, Malfunctioning phagocytosis impairs the killing of bacteria that reach the lamina propria through the permeable epithelial barrier, which results in excessive Toll-like receptor stimulation, proinflammatory cytokine secretions, and activation of acquired immune responses, all of which significantly raise intestinal inflammatory reactions in genetically susceptible individuals who harbor mutations in the IBD-susceptibility gene s Duboc et al.

Obesity is a metabolic condition characterized by an excess of body fat storage. It is thought to be caused by an energy imbalance, with poor energy expenditures and increased caloric intake.

Recent research suggests, however, that obesity is a more complicated condition in both mice and humans, and that it is linked to intestinal dysbiosis Arslan, A certain microbial signature appears to be linked to the development of obesity, identical to IBD. In obese people, the bacterial diversity in their intestines is reduced overall Turnbaugh et al.

Obesity appears to be linked to a modified ratio between Bacteroidetes and Firmicutes in the majority of research in both humans and animal models, with a reduction in Bacteroidetes and an elevation in Firmicutes. This ratio has been linked to body weight and fat deposition, indicating that obese people have a higher disproportionate ratio of these bacteria Hildebrandt et al.

The number of Bacteroidetes in the intestinal microbiota appears to be relevant in obesity, as obese people on a calorie-restricted diet lose weight and have a higher ratio of Bacteroidetes species in their gut microbiota Ley et al. Insulin-dependent diabetes mellitus IDDM -related dysbiosis is marked by an increase in Bacteroidetes and Clostridium , as well as a reduction in mucin-degrading bacteria such as Bifidobacteria , Lactobacillus , and Prevotella McLean et al.

Both IDDM and NIDDM are linked to a reduction in total microbial diversity, and a drop in butyrate-producing bacteria and Firmicutes , as well as a disruption in the intestine epithelial barrier and increased intestinal permeability Wen et al.

Elevated lipopolysaccharide LPS translocation and endotoxemia are also reported in NIDDM, which, like obesity, may contribute to reduced inflammation that contributes to the formation of insulin resistance Wang et al. It is unknown if the unbalanced microbiota is a causal agent or an outcome of diabetes, as it is in other diseases linked with intestinal dysbiosis; nonetheless, several human and animal model studies indicate that changes in the microbiota may predate the onset of IDDM Serino et al.

The microbiota structure of nonobese diabetic NOD mice with diabetes at weaning age differs from the microbiota composition of NOD mice who do not develop diabetes. The frequency of IDDM was also found to be dependent on the overall bacterial environment in which they were housed.

Disease develops in NOD mice in GF settings, but not in mice in specific pathogen-free SPF facilities Nielsen et al.

Patients with CRC have a general dysbiosis pattern, which includes a decrease in butyrate-producing bacteria and a rise in the number of multiple potentially dangerous microorganisms. According to many studies, Proteobacteria , Bifidobacteria , Prevotella , and SCFA production rates have decreased, whilst Firmicutes , Bacteroidetes , Enterobacteriaceae , and Fusobacteria have increased Schulz et al.

Various investigations have also found a rise in two specific bacteria species, Akkermansia muciniphila and Fusobacterium nucleatum , in CRC tissues Castellarin et al. Both of these bacterial species are linked to strong local inflammatory responses, which could be indicative of a high risk of CRC and be involved in inflammation-related disorders.

nucleatum is also linked to an increase in CRC tumors and lymph node cancer. Between patient populations with polyps and those with tumors, substantial variations in mucosal and fecal microbial configurations were found, with the most major changes being Enterobacteriaceae , which was elevated in the mucosa of patients with tumors compared to those with polyps, and Bacteroidetes , which was expanded in CRC tissues with tumor cells compared to those without tumors Sobhani et al.

The gut microbiota is a novel topic of research interest with significant applications in human health with respect to the development of innovative diagnostic and therapeutic tools for preventive and curative outcomes.

Recent molecular and biochemical studies have allowed diverse microorganisms to be detected and categorized and facilitated the analysis of their genomes and metabolites. In particular, genome-scale metabolic models can guide our understanding of the function of individual organisms within the gut microbiota and the role of the microbiota overall since the inter-individual variability of the gut microbiota contributes to different treatment responses and perspectives.

Our mechanistic understanding of how the gut microbiota transforms dietary and endogenous molecules into metabolites shared with peripheral organs and tissues in the host needs substantial expansion. Although the emergence of high-throughput sequencing technologies and bioinformatics over the next decade will inevitably aid in exploring the applicable biological mechanisms, the end of the metabolic pathways sector of the system and the host targets that identify them make up the fascinating puzzle pieces required for the next step in this growing field.

Further mechanistic experiments may result in the development of TMAO as a novel biomarker for the primary prevention of CVD. This could lead to a change in the conventional risk factors for CVD and modulation therapies directly targeted at the intestinal microbiota.

It is expected that these technological advances will promote the transition from correlation experiments to mechanistic insights, resulting in the development of novel diagnostic tests and therapeutics in the near future.

Further research is needed to fully explore the processes underlying host-microbiota interactions to shed light on the biological effects of direct or indirect manipulation of the gut microbiota.

MMR, FI, and AAM: Wrote the manuscript; MHR, MSR, MI, and AK: Searched literatures; PS, SM, TE, and MA: Illustrated figures and tables; FW, RI, and TT; Edited the manuscript; AAM and SC: Designed and supervised the review.

All authors finally revised and approved for submission of the final version of the manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Abreu, M. Toll-Like Receptor Signalling in the Intestinal Epithelium: How Bacterial Recognition Shapes Intestinal Function. doi: PubMed Abstract CrossRef Full Text Google Scholar. Adamberg, K. The Composition and Metabolism of Faecal Microbiota is Specifically Modulated by Different Dietary Polysaccharides and Mucin: An Isothermal Microcalorimetry Study.

Microbes 9, 21— Adnan, S. Alterations in the Gut Microbiota can Elicit Hypertension in Rats. Genomics 49, 96— Afsar, B. Gut Hormones and Gut Microbiota: Implications for Kidney Function and Hypertension.

Soc Hypertens. Al Khodor, S. The Microbiome and Blood Pressure: Can Microbes Regulate Our Blood Pressure? Almeida, C. The Influence of Gut Microbiota in Cardiovascular Diseases—A Brief Review. Porto Biomed.

Aronov, P. Colonic Contribution to Uremic Solutes. Soc Nephrol. Aron-Wisnewsky, J. The Gut Microbiome, Diet, and Links to Cardiometabolic and Chronic Disorders.

Arslan, N. Obesity, Fatty Liver Disease and Intestinal Microbiota. World J. Artis, D. CrossRef Full Text Google Scholar. Awoyemi, A. Effects of Dietary Intervention and N-3 PUFA Supplementation on Markers of Gut-Related Inflammation and Their Association With Cardiovascular Events in a High-Risk Population.

Atherosclerosis , 53— Bäckhed, F. The Gut Microbiota as an Environmental Factor That Regulates Fat Storage. Host-Bacterial Mutualism in the Human Intestine. Science Dynamics and Stabilization of the Human Gut Microbiome During the First Year of Life. Cell Host Microbe 17, — Baddini Feitoza, A.

Conjugated Linoleic Acid CLA : Effect Modulation of Body Composition and Lipid Profile. PubMed Abstract Google Scholar. Besten, G. Short-Chain Fatty Acids Protect Against High-Fat Diet—Induced Obesity via a Pparγ-Dependent Switch From Lipogenesis to Fat Oxidation.

Diabetes 64, — Bhattacharya, T. Applications of Phyto-Nanotechnology for the Treatment of Neurodegenerative Disorders. Materials 15, Brandsma, E. A Proinflammatory Gut Microbiota Increases Systemic Inflammation and Accelerates Atherosclerosis.

Brandt, L. Long-Term Follow-Up of Colonoscopic Fecal Microbiota Transplant for Recurrent Clostridium Difficile Infection. Brix, S. Metagenomic Heterogeneity Explains Dual Immune Effects of Endotoxins. Allergy Clin. Brown, J.

The Gut Microbial Endocrine Organ: Bacterially Derived Signals Driving Cardiometabolic Diseases. Campbell, E. Control and Dysregulation of Redox Signalling in the Gastrointestinal Tract.

Canfora, E. Acetate: A Diet-Derived Key Metabolite in Energy Metabolism: Good or Bad in Context of Obesity and Glucose Homeostasis? Care 20, — Gut Microbial Metabolites in Obesity, NAFLD and T2DM.

Cani, P. Metabolic Endotoxemia Initiates Obesity and Insulin Resistance. Diabetes 56, — Gut Microbiota-Mediated Inflammation in Obesity: A Link With Gastrointestinal Cancer. Cao, X. Association of Indoxyl Sulfate With Heart Failure Among Patients on Hemodialysis. Carding, S. Dysbiosis of the Gut Microbiota in Disease.

Cardos, I. Revisiting Therapeutic Strategies for H. Pylori Treatment in the Context of Antibiotic Resistance: Focus on Alternative and Complementary Therapies. Molecules 26, Castellarin, M.

Fusobacterium Nucleatum Infection is Prevalent in Human Colorectal Carcinoma. Genome Res. Cavalu, S. Microscopic and spectroscopic investigation of bioactive glasses for antibiotic controlled release. Novel Formulation Based on Chitosan-Arabic Gum Nanoparticles Entrapping Propolis Extract Production, Physico-Chemical and Structural Characterization.

Chambers, E. Acute Oral Sodium Propionate Supplementation Raises Resting Energy Expenditure and Lipid Oxidation in Fasted Humans. Diabetes Obes. Chaves, L. Chronic Kidney Disease, Uremic Milieu, and its Effects on Gut Bacterial Microbiota Dysbiosis.

Renal Physiol. Chen, L. Associations of Maternal Dietary Patterns During Pregnancy With Offspring Adiposity From Birth Until 54 Months of Age. Nutrients 9, 2. Cheng, D. Butyrate Ameliorated-NLRC3 Protects the Intestinal Barrier in a GPRDependent Manner. Cell Res. Cho, I. Antibiotics in Early Life Alter the Murine Colonic Microbiome and Adiposity.

Nature , — Clayton, T. Pharmacometabonomic Identification of a Significant Host-Microbiome Metabolic Interaction Affecting Human Drug Metabolism. Cosola, C. Microbiota Issue in CKD: How Promising are Gut-Targeted Approaches?

Cui, L. Association Study of Gut Flora in Coronary Heart Disease Through High-Throughput Sequencing. Cummings, J. The Effect of Meat Protein and Dietary Fiber on Colonic Function and Metabolism II. Bacterial Metabolites in Feces and Urine. Darzi, J. Effects of a Novel Propionate-Rich Sourdough Bread on Appetite and Food Intake.

David, L. Diet Rapidly and Reproducibly Alters the Human Gut Microbiome. Davignon, J. Beneficial Cardiovascular Pleiotropic Effects of Statins. Circulation , 39— De Vadder, F. Microbiota-Generated Metabolites Promote Metabolic Benefits via Gut-Brain Neural Circuits. Cell , 84— Devillard, E.

Metabolism of Linoleic Acid by Human Gut Bacteria: Different Routes for Biosynthesis of Conjugated Linoleic Acid. Differences Between Human Subjects in the Composition of the Faecal Bacterial Community and Faecal Metabolism of Linoleic Acid.

Microbiology , — Diakos, C. Cancer-Related Inflammation and Treatment Effectiveness. Lancet Oncol. Di Giacinto, C.

Probiotics Ameliorate Recurrent Th1-Mediated Murine Colitis by Inducing IL and ILDependent TGF-β-Bearing Regulatory Cells. Dinakaran, V. Elevated Levels of Circulating DNA in Cardiovascular Disease Patients: Metagenomic Profiling of Microbiome in the Circulation.

PloS One 9, e Divyashri, G. Probiotic Attributes, Antioxidant, Anti-Inflammatory and Neuromodulatory Effects of Enterococcus Faecium CFR In Vitro and In Vivo Evidence. Donia, M. Small Molecules From the Human Microbiota. Dostal, A. Iron Modulates Butyrate Production by a Child Gut Microbiota In Vitro.

MBio 6, e Downes, M. A Chemical, Genetic, and Structural Analysis of the Nuclear Bile Acid Receptor FXR. Cell 11, — Duboc, H.

Connecting Dysbiosis, Bile-Acid Dysmetabolism and Gut Inflammation in Inflammatory Bowel Diseases. Gut 62, — Duncan, S.

Reduced Dietary Intake of Carbohydrates by Obese Subjects Results in Decreased Concentrations of Butyrate and Butyrate-Producing Bacteria in Feces. Eckburg, P. Microbiology: Diversity of the Human Intestinal Microbial Flora. Eikawa, S. Available at: www.

Google Scholar. Elrakaiby, M. Pharmacomicrobiomics: The Impact of Human Microbiome Variations on Systems Pharmacology and Personalized Therapeutics. Omics 18, — Emoto, T. Analysis of Gut Microbiota in Coronary Artery Disease Patients: A Possible Link Between Gut Microbiota and Coronary Artery Disease.

Estruch, R. Primary Prevention of Cardiovascular Disease With a Mediterranean Diet. Evans, C. Effects of Dietary Fibre Type on Blood Pressure: A Systematic Review and Meta-Analysis of Randomized Controlled Trials of Healthy Individuals.

Evenepoel, P. The Gut—Kidney Axis. Everard, A. Responses of Gut Microbiota and Glucose and Lipid Metabolism to Prebiotics in Genetic Obese and Diet-Induced Leptin-Resistant Mice. Diabetes 60, — Fåk, F. Oral Microbiota in Patients With Atherosclerosis. Atherosclerosis , — Fava, F. Intestinal Microbiota in Inflammatory Bowel Disease: Friend of Foe?

Felizardo, R. The Microbiota and Chronic Kidney Diseases: A Double-Edged Sword. Foretz, M. Metformin: From Mechanisms of Action to Therapies. Cell Metab. Foye, O. FEMS Immunol. Frost, G.

The Short-Chain Fatty Acid Acetate Reduces Appetite via a Central Homeostatic Mechanism. Furusawa, Y. Commensal Microbe-Derived Butyrate Induces the Differentiation of Colonic Regulatory T Cells. Fu, Q. Coronary Plaque Characterization Assessed by Optical Coherence Tomography and Plasma Trimethylamine-N-Oxide Levels in Patients With Coronary Artery Disease.

Galla, S. Disparate Effects of Antibiotics on Hypertension. Genomics 50, — Gan, X. Probiotic Administration Attenuates Myocardial Hypertrophy and Heart Failure After Myocardial Infarction in the Rat. Heart Fail. Gao, Z. Butyrate Improves Insulin Sensitivity and Increases Energy Expenditure in Mice.

Diabetes 58, — Gensollen, T. How Colonization by Microbiota in Early Life Shapes the Immune System. Geovanini, G.

Atherosclerosis and Inflammation: Overview and Updates. Gill, S. Metagenomic Analysis of the Human Distal Gut Microbiome. Gomez-Arango, L. Increased Systolic and Diastolic Blood Pressure is Associated With Altered Gut Microbiota Composition and Butyrate Production in Early Pregnancy.

Hypertension 68, — Gómez-Guzmán, M. Antihypertensive Effects of Probiotics Lactobacillus Strains in Spontaneously Hypertensive Rats. Food Res. Graham, I. European Guidelines on Cardiovascular Disease Prevention in Clinical Practice: Executive Summary - Fourth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice Constituted by.

Heart J. Grazioli, S. Mitochondrial Damage-Associated Molecular Patterns: From Inflammatory Signaling to Human Diseases. Gregory, J. Transmission of Atherosclerosis Susceptibility With Gut Microbial Transplantation.

Gui, T. Diverse Roles of Macrophages in Atherosclerosis: From Inflammatory Biology to Biomarker Discovery. Mediators Inflamm. Guldris, S. Gut Microbiota in Chronic Kidney Disease.

Nefrologia English Ed. Hedin, C. Gut 63, — He, B. Intestinal Bacteria Trigger T Cell-Independent Immunoglobulin A2 Class Switching by Inducing Epithelial-Cell Secretion of the Cytokine APRIL. Immunity 26, — Hildebrandt, M. High-Fat Diet Determines the Composition of the Murine Gut Microbiome Independently of Obesity.

Gastroenterology , — Honour, J. The Possible Involvement of Intestinal Bacteria in Steroidal Hypertension. Endocrinology , — Hooper, L. Do Symbiotic Bacteria Subvert Host Immunity? Molecular Analysis of Commensal Host-Microbial Relationships in the Intestine. Hsu, C. Levels of Indoxyl Sulfate are Associated With Severity of Coronary Atherosclerosis.

Huang, X. Inhibition of P38 Mitogen-Activated Protein Kinase Attenuates Butyrate-Induced Intestinal Barrier Impairment in a Caco-2 Cell Monolayer Model. Hyvärinen, K. A Common Periodontal Pathogen has an Adverse Association With Both Acute and Stable Coronary Artery Disease.

Indiani, C. Islam, F. Natural Bioactive Molecules: An Alternative Approach to the Treatment and Control of COVID Neuropharmacological and Antidiabetic Potential of Lannea Coromandelica Houtt. Leaves Extract: An Experimental Analysis.

Evid Based Complement. Jie, Z. The Gut Microbiome in Atherosclerotic Cardiovascular Disease. Johansson, M. The Inner of the Two Muc2 Mucin-Dependent Mucus Layers in Colon is Devoid of Bacteria. Kalantar-Zadeh, K. Food Intake Characteristics of Hemodialysis Patients as Obtained by Food Frequency Questionnaire.

Renal Nutr. Kamo, T. Dysbiosis and Compositional Alterations With Aging in the Gut Microbiota of Patients With Heart Failure. PloS One 12, e Karbach, S. Gut Microbiota Promote Angiotensin II-Induced Arterial Hypertension and Vascular Dysfunction.

Heart Assoc. Karlsson, C. Probiotic Therapy to Men With Incipient Arteriosclerosis Initiates Increased Bacterial Diversity in Colon: A Randomized Controlled Trial. Karlsson, F. Symptomatic Atherosclerosis is Associated With an Altered Gut Metagenome.

Kawase, M. Effect of Administration of Fermented Milk Containing Whey Protein Concentrate to Rats and Healthy Men on Serum Lipids and Blood Pressure. Dairy Sci. S 00 Khoury, T. The Gut-Kidney Axis in Chronic Renal Failure: A New Potential Target for Therapy.

Kikuchi, M. Uremic Toxin-Producing Gut Microbiota in Rats With Chronic Kidney Disease. Nephron , 51— Kimura, I. The SCFA Receptor GPR43 and Energy Metabolism.

Lausanne 5, The Gut Microbiota Suppresses Insulin-Mediated Fat Accumulation via the Short-Chain Fatty Acid Receptor GPR Kincaid, E.

Enalaprilat Improves Gut Perfusion in Critically Injured Patients. Shock 9, 79— Koenig, J. Succession of Microbial Consortia in the Developing Infant Gut Microbiome. Koeth, R. γ-Butyrobetaine is a Proatherogenic Intermediate in Gut Microbial Metabolism of L-Carnitine to TMAO.

Intestinal Microbiota Metabolism of L-Carnitine, a Nutrient in Red Meat, Promotes Atherosclerosis. Koliada, A.

Springer 17, 1—6. Koren, O. Human Oral, Gut, and Plaque Microbiota in Patients With Atherosclerosis. Kossmann, S. Angiotensin Ii-Induced Vascular Dysfunction Depends on Interferon-γ- Driven Immune Cell Recruitment and Mutual Activation of Monocytes and Nk-Cells.

Kummen, M. Gut Microbiota Signature in Heart Failure Defined From Profiling of 2 Independent Cohorts. Kushner, R. Prevalence of Unhealthy Lifestyle Patterns Among Overweight and Obese Adults. Obesity 18, — Lammers, L. The Effects of Fasting on Drug Metabolism. Expert Opin.

Drug Metab. Larsen, N. Gut Microbiota in Human Adults With Type 2 Diabetes Differs From Non-Diabetic Adults. PloS One 5, e Larsson, E. Analysis of Gut Microbial Regulation of Host Gene Expression Along the Length of the Gut and Regulation of Gut Microbial Ecology Through Myd Gut 61, — Lemos, B.

Effects of Egg Consumption and Choline Supplementation on Plasma Choline and Trimethylamine-N-Oxide in a Young Population. Ley, R. Human Gut Microbes Associated With Obesity. Microbial Ecology: Human Gut Microbes Associated With Obesity. Lin, C.

P-Cresylsulfate and Indoxyl Sulfate Level at Different Stages of Chronic Kidney Disease. Indoxyl Sulfate Predicts Cardiovascular Disease and Renal Function Deterioration in Advanced Chronic Kidney Disease.

Lins, M. Coronary Heart Disease Detection of Diverse Bacterial Signatures in Atherosclerotic Lesions of Patients With Detection of Diverse Bacterial Signatures in Atherosclerotic Lesions of Patients With Coronary Heart Disease. Citeseer , — Serum Protein-Bound Uraemic Toxins and Clinical Outcomes in Haemodialysis Patients.

Meta-Analysis of the Associations of P-Cresyl Sulfate PCS and Indoxyl Sulfate IS With Cardiovascular Events and All-Cause Mortality in Patients With Chronic Renal Failure.

PloS One 10, e Li, M. Symbiotic Gut Microbes Modulate Human Metabolic Phenotypes. Li, Q. Soluble Dietary Fiber Reduces Trimethylamine Metabolism via Gut Microbiota and Co-Regulates Host AMPK Pathways. Li, Z. Butyrate Reduces Appetite and Activates Brown Adipose Tissue via the Gut-Brain Neural Circuit.

Gut 67, — Lloyd-Price, J. The Healthy Human Microbiome. Genome Med. Strains, Functions and Dynamics in the Expanded Human Microbiome Project. Nature , 61— Luedde, M. Heart Failure is Associated With Depletion of Core Intestinal Microbiota.

ESC Heart Fail. Macpherson, A. Induction of Protective IgA by Intestinal Dendritic Cells Carrying Commensal Bacteria.

Mahmoodpoor, F. The Impact of Gut Microbiota on Kidney Function and Pathogenesis. Marín, L. Bioavailability of Dietary Polyphenols and Gut Microbiota Metabolism: Antimicrobial Properties.

Marques, F. High-Fiber Diet and Acetate Supplementation Change the Gut Microbiota and Prevent the Development of Hypertension and Heart Failure in Hypertensive Mice.

Circulation , — Marzullo, P. From Obesity Through Gut Microbiota to Cardiovascular Diseases: A Dangerous Journey. Ma, K. Farnesoid X Receptor is Essential for Normal Glucose Homeostasis. Matson, V. The Commensal Microbiome is Associated With Anti-PD-1 Efficacy in Metastatic Melanoma Patients.

Mattila, K. Association Between Dental Health and Acute Myocardial Infarction. Mayerhofer, C. Low Fibre Intake is Associated With Gut Microbiota Alterations in Chronic Heart Failure. Mazmanian, S. An Immunomodulatory Molecule of Symbiotic Bacteria Directs Maturation of the Host Immune System.

Cell , — McKenzie, C. The Nutrition-Gut Microbiome-Physiology Axis and Allergic Diseases. McLean, M. Does the Microbiota Play a Role in the Pathogenesis of Autoimmune Diseases?

Gut 64, — Medzhitov, R. Recognition of Microorganisms and Activation of the Immune Response. Meijers, B. P-Cresol and Cardiovascular Risk in Mild-to-Moderate Kidney Disease.

Mekki, K. Mediterranean Diet Improves Dyslipidemia and Biomarkers in Chronic Renal Failure Patients. Food Funct. Melamed, M. Retained Organic Solutes, Patient Characteristics and All-Cause and Cardiovascular Mortality in Hemodialysis: Results From the Retained Organic Solutes and Clinical Outcomes ROSCO Investigators.

BMC Nephrol. Mell, B. Evidence for a Link Between Gut Microbiota and Hypertension in the Dahl Rat. Genomics 47, — Miere, F. Formulation, Characterization, and Advantages of Using Liposomes in Multiple Therapies. Pharmacophore 11, 1— Mitch, W. Effects of Intestinal Flora on Nitrogen Metabolism in Patients With Chronic Renal Failure.

Mominur Rahman, M. Stem Cell Transplantation Therapy and Neurological Disorders: Current Status and Future Perspectives. Biology Basel , Role of Phenolic Compounds in Human Disease: Current Knowledge and Future Prospects. Molecules , Mondot, S.

There are currently few food products available in Canada containing psyllium, but that may change with these new regulations.

Health Canada hopes that manufacturers will include psyllium in larger amounts than the minimum required, and in a broader variety of food products, since an individual is unlikely to consume four servings of a single product e. Barley is a fibre-rich whole grain included in many soups, breads, and other foods.

Like psyllium, barley is a form of soluble fibre and, when included as part of a high-fibre diet, can help with some bowel irregularities and lower the risk for developing diverticular disease. Alcohol manufacturers use barley to make whiskey and most types of beer.

People in regions around the world appreciate barley water as a healthier alternative to soft drinks see recipe below. Steeped in hot water, roasted barley grain is a tasty tea or, when ground and percolated just like coffee beans, is an excellent, warm caffeine-free beverage.

Following an extensive research literature review, Health Canada recently concluded that food manufacturers may use the claim that barley grain products are associated with a reduction of blood cholesterol.

In order to use the claim, a food product must contain at least 1g of beta-glucan from barley grain products per serving.

Fibre-rich for your gut and with cholesterol-lowering properties for your heart, this once-popular drink is worthy of a comeback. Experiment by adding other types of fruit, such as berries, oranges, or limes. For an extra kick, boil the barley with some fresh ginger.

Add them to your favourite soup or sauce, or save them for breakfast and mix with fruit and yogurt. Making drastic changes to your diet can have an effect on your gastrointestinal system, and such changes could potentially be dangerous for individuals with certain gastrointestinal or liver diseases.

Moderation, even of specific healthy foods, is usually beneficial. For more information about fibre, the effect of diet on a number of GI and liver conditions, and information on how to find dietitian resources in your region, visit our information centre.

You can also contact our office if you wish to receive a specific information package mailed to your home. Fruit and Veggies A large international study, funded by the Heart and Stroke Foundation of Ontario, and recently published in PLoS Medicine , showed that individuals who carry genes that put them at a higher risk for heart disease than the general population may be able to mitigate that risk by consuming a diet rich in vegetables and fruit.

Psyllium Many individuals who experience bowel irregularities rely on psyllium, a type of soluble dietary fibre found in some foods, especially breakfast cereal, and as a supplement e. Barley Barley is a fibre-rich whole grain included in many soups, breads, and other foods.

Old-Fashioned Fruit Barley Water Ingredients 8 cups water 1 cup washed pearl barley whole lemons tbsp honey, cane sugar, or sweetener of your choice Method Bring water and barley to a boil. While letting this simmer for min, peel rinds from lemon and add to heat-proof bowl.

Microbiome volume 8Article cardiovasuclar 36 Cite this Pancreas function. Metrics Cardiovacsular. Coronary artery disease CAD is the healtg common health anr worldwide and remains Athlete food allergies leading caddiovascular Athlete food allergies morbidity and mortality. Over the past heaalth, it has become clear cardiovascuoar the Fueling your workouts of Gut health and cardiovascular health gut, the gut microbiota, play a vital role in human metabolism, immunity, and reactions to diseases, including CAD. Although correlations have been shown between CAD and the gut microbiota, demonstration of potential causal relationships is much more complex and challenging. In this review, we will discuss the potential direct and indirect causal roots between gut microbiota and CAD development via microbial metabolites and interaction with the immune system. Uncovering the causal relationship of gut microbiota and CAD development can lead to novel microbiome-based preventative and therapeutic interventions. Gut health and cardiovascular health

Author: Nacage

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