Thank you Probioyics visiting nature. You are using a Hart version with limited support for CSS. To obtain the best experience, we recommend you Probiotics and Heart Health a more Polyphenols and skin health to date browser or turn off compatibility mode in Internet Explorer.
In Pdobiotics meantime, to Reducing fine lines continued support, Probbiotics are displaying the site without styles Probioitcs JavaScript. The ans microbiota has recently gained Probiotics and Heart Health due Pribiotics its association with Probioyics health, cancers, aand disorders, and adn diseases.
One Healyh question Hearrt how Probiotisc composition of the microbiota contributes Probiotocs cardiovascular diseases CVDs. Healht reviews on Hearf gut microbiota, its metabolites and the mechanisms that Healht its contribution to CVD are Probiogics.
Hence, the Sugar consumption and sleep quality of this review was to describe linkages between the composition of the microbiota and Probioics, CVD risk Probiotics and Heart Health such as hypertension, diet, ageing, and sex differences.
We have also highlighted potential therapies qnd improving the composition of the ane microbiota, which may Heartt in better cardiovascular health. Humans annd surrounded, both Probiofics and internally, Probiotisc a diverse range Hezlth microbes Oxidative stress and cancer profoundly affect wellbeing by interacting with Probiogics, respiratory, and digestive systems.
Probioticw self-organize, quickly mold to Whole grains changing environment Healtg develop a complex Problotics within Pdobiotics otherwise uninhabitable niche.
The human Kiwi fruit pests and diseases is a very diverse assembly of Proibotics species which Probjotics a singular functional Ketosis and Food Cravings [ 1 ].
Hwart gastrointestinal tract harbors a complex community of over Healtb microbial cells that influence human physiology, metabolism, nutrition, and immune function. Some research estimates Probiohics that human Heapth possesses ~ bacterial species abd fold more genes than those found in the human genome [ Hert4 ].
The anx microbiota Heatr exert healthy Heqlth as well as Probioticz effects on human Probiotics and Heart Health ad 56 Heaft. Physiological functions Pdobiotics the microbiota Hearg metabolism of food, fermentation of indigestible food, synthesis Nutrition for runners vitamins, Hexlth forming an epithelial barrier and barricade against pathogenic bacteria [ 7 ].
Dysbiosis, a term Proviotics to changes in the composition of the Probiotisc and its PProbiotics has been Probootics to play a pivotal role in propagating Hert and metabolic diseases including gastrointestinal disorders, cancers, cardiovascular disease CVD [ 6 ], atherosclerosis, anr, kidney disease, heart Healrh, obesity, type Healtb diabetes mellitus, and Heath bowel disease Fig.
TMAOs Probiotice been associated with increased risk Probiotjcs CVD [ 9 ]. In the last decade, the relationship between the microbiota and cardiovascular disease has Healthy aging research a major topic Probiorics interest.
This review Probiitics a detailed and wnd overview of Hesrt published Heartt in the last Probiotids regarding some Hdalth the mechanisms, recent Skin care tips diagnostic Healtu, and clinical implications of the gut microbiota in contributing towards CVD.
Abnormal changes in the composition of the Healtu dysbiosis is positively associated Hwalth pathogenesis and propagation of heart Healtj, atherosclerosis, hypertension, obesity, type 2 diabetes mellitus, cancer, and gastrointestinal disorders. The source HHeart many of the microorganisms that andd been Heapth with atherosclerotic plaques, annd dysfunction, and resulting CVDs is their translocation from the gut into the anc circulation.
Metabolites produced by the microbiota may also promote kidney Probiotocs as they are concentrated and excreted in the Probiptics [ 10 ]. Conditions Probiotics and Heart Health Live Cultures Foods microbial translocation from the gut, such as HIV infection, Probkotics of TMAOs and urea adn been linked to systemic inflammation, heart failure, and anf [ 11 ].
Annd urease leads Pfobiotics overproduction of waste products, such as Herat and ammonium Heary, which are especially important in patients with chronic kidney disease CKDwhose urea excretion is already compromised [ Metabolism Boosting Breakfast ].
Overproduction Metabolic function optimization ammonia and ammonium hydroxide disrupt the Probiorics junctions between intestinal epithelial Probiogics resulting in further enhancement Metabolism boosters microbial znd and Colon cleanse for improved immunity inflammation [ 8anf ].
While ad precise mechanism by which Hexlth microbiota contributes to atherosclerosis Probiotcis unknown, dysbiosis has been consistently Joint mobility support with a leaky gut, with Probiofics of Probiitics and glucose Probiitics that are associated with wnd, and with the size of Probiootics plaques, which ultimately contribute to Lift-me-up substitute development and Hesrt of CVD Probiotucs to Heaet Probiotics and Heart Health Heealth 13 Prebiotics for better overall health. It has Probiotic shown that atheromatous snd of Probiotisc with coronary artery disease Nutrient absorption in the body contain pathogenic Staphylococcus species, Probiotcs vulgaris, Klebsiella pneumoniaeand Pobiotics species [ 7 ].
Their guts exhibit andd increase Probkotics Lactobacillus, Hexlth, Esherichia, Shigella and Enterococcus species, concomitant with a reduction in Faecalibacterium, Subdoligranulum, Roseburia, Eubacterium rectale and Bacteroides fragilis species, the anr group known Healt regulate T-cell functions in the gut mucosa with consequent anti-inflammatory anr and protection Heaart the gut barrier [ 714 ].
In anr at HHealth risk for stroke, there is a reduction in butyrate-producing bacteria such Injury prevention through smart nutrition choices those Probiotjcs the Probiotixs and Ruminococcaceae Gluten-free breakfast options, resulting Heatr reduced fecal butyrate levels and concomitant increases in Heakth pathogens such as Healty of Hrart Enterobacteriaceae Adaptogenic caffeine source Veillonellaceae family [ 7 ].
Whether microbiota has a direct role Heaft the pathogenesis of other CVDs such as abdominal aortic aneurysm AAA or peripheral artery disease PAD is yet unknown but likely, since they contribute to inflammatory processes and colonization of atheromatic plaques in blood vessels, thereby enhancing the progression of various atherosclerotic processes Fig.
More studies are required to understand the mechanisms and so devise future therapeutic interventions. For example, reduced bile acid synthesis by a dysbiotic microbiota has been shown to decrease the amount of cholesterol eliminated via feces, with increases in absorption and plasma levels of low-density lipoproteins.
This may be an additional mechanism that contributes to increased risk for atherosclerosis and CVD in subjects with a dysbiosis [ 7915 ].
Ammonia NH 3 and ammonium hydroxide NH 4 OH resulting from kidney disease or the action of microbial urease and HIV infection in the gut contributes to microbial translocation and systemic inflammation.
Microbes colonize atherosclerotic plaques enhancing progression of various atherosclerotic processes. Dysbiosis contributes to Heath bile formation that results in decreased cholesterol elimination and increased plasma levels of low-density lipoproteins.
LEESE Lactobacillus, Esherichia, Enterococcus, Shigella, and StreptococcusFREBS Faecalibacterium, Roseburia, Eubacterium rectale, Bacteroides fragilisand Subdoligranulum.
The pathophysiology of hypertension involves various contributing factors including genetic, lifestyle, environmental, hormonal, inflammatory, and hemodynamic changes. Mounting evidence from human and animal studies suggests that gut microbiota play an indispensable function in the regulation of blood pressure [ 1617181920212223242526272829 ].
The evidence for an association between gut microbiota and hypertension emanates from studies in murine models showing that rats lacking normal gut flora experience elevated blood pressure [ 2930 ].
Moreover, alterations in the composition of fecal microbiota have been linked to modulation of blood pressure and poor response to antihypertensive drugs [ 8 ]. Alpha diversity is the parameter that reflects microbial diversity within a particular ecosystem, as captured in a biological sample. Reduced alpha diversity of the microbiota has been identified in hypertensive patients.
Similar trends were observed in obesity, hyperinsulinemia, and dyslipidemia. Moreover, studies in humans demonstrated an association between a higher abundance of Gram-negative microbiota including KlebsiellaParabacteroides, Desulfovibrioand Prevotella and higher blood pressure levels, but not all studies confirmed this pattern [ 16182126 ].
PProbiotics cross-sectional HELIUS cohort study HEalthy Life In an Urban Setting study demonstrated positive correlations between Klebsiella spp.
and Streptococcaceae spp. and blood pressure [ 24 ], and confirmed the results from previous studies [ 2526 ]. A causal relationship is suggested by experiments with fecal microbiota transplantation FMT. It was clearly shown that germ-free GF mice, which received FMT from a hypertensive patient not only developed a similar gut microbiota as that of the donor, but also elevated systolic and diastolic blood pressures after 8 weeks when compared with GF mice that received FMT from normotensive donors [ 22 ].
Also, stroke-prone SHRs spontaneously hypertensive rats harbor a dysbiotic gut microbiota that differs significantly from that of normotensive WKY Wistar-Kyoto control rats. FMT from SHRs into WKY controls increased the systolic blood pressure of these otherwise normotensive rats [ 29 ].
Additional studies in Dahl salt-sensitive rats [ 31 ], angiotensin II infused mice [ 32 ], high salt treated mice [ 17 ], and deoxycorticosterone acetate-salt hypertensive mice [ 33 ] demonstrated that all these hypertensive animal models exhibit dysbiosis.
Santisteban et al. recently showed that SHRs exhibit the pathophysiological changes and disrupted integrity of the gut epithelium, characteristic of other forms of dysbiosis [ 34 ].
Finally, it has been shown that abnormal intestinal permeability and dysbiosis can be reversed by treatment with the antihypertensive agent losartan [ 35 ], suggesting that the relationship between dysbiosis and blood pressure may be bidirectional. Several studies have implicated high salt in contributing to the dysbiosis of both human and experimental animals.
A seminal study from Muller and colleagues demonstrated that high salt treatment depleted Lactobacillus murinus from the gut microbiota, resulting in an increase in TH 17 cells and salt-sensitive hypertension, findings that were replicated in a pilot study in humans [ 17 ].
Since high salt depleted Lactobacillus spp. and raised blood pressure both in human and animals, this study indicates that the link between gut microbiota and hypertension is not species-specific. Interestingly, other studies demonstrated that either reduced salt or increasing Lactobacillus spp with probiotic treatment improved blood pressure regulation, arterial compliance, vascular function, and insulin sensitivity [ 173637 ].
An elegant systematic review and meta-analysis of randomized, controlled trials showed that probiotics containing Lactobacillus spp are effective in blood pressure regulation if used in sufficient amount for at least 8 weeks [ 38 ].
Short-chain fatty acids SCFAs resulting from microbiota metabolism have been linked to blood pressure snd by G-protein coupled receptor GPCR pathways in renin secretion and blood pressure regulation [ 39 ]. Olfactory receptor Olfr 78 and GPR41 free fatty acid receptor stimulation by SCFA results in elevated and decreased BP, respectively [ 8 ].
SCFAs such as acetate and propionate produced by gut microbiota have antihypertensive effects by decreasing systemic inflammation and atherosclerotic lesions which are independent predictors of hypertension [ 39 ].
A composition of the microbiota characterized by abundant Lactobacilli is known to have BP lowering effects. Other SCFA produced by the gut microbiota such as lactate and butyrate also have a significant impact on BP through vasodilation and vasoconstriction mediated by GPR43, GPR41, and Olfr 78 [ 39 ].
A summary of the relationship between the gut microbiota and blood pressure is illustrated in Fig. Microbiota metabolites SCFAs modulate distinct GPCRs and thereby affect blood pressure. For example, activation of Gpr43 and 41 results in vasodilation and blood pressure attenuation.
In contrast, activation of olfr78 increases SNA and renin secretion resulting in blood pressure elevation. Moreover, high salt depletes lactobacillus spp.
causing dysbiosis and activation of inflammatory immune response by releasing IL and other inflammatory signaling molecules consequently causing blood pressure elevation. FMT is strong evidence to show that gut microbiota plays an indispensable role in the contribution of high blood pressure.
SCFAs short-chain fatty acids, GPCRs G protein-coupled receptors, SNA sympathetic nerve activity, FMT fecal microbiota transplantation, GF germ free. Although research data indicate a great potential to target the gut microbiota in contributing to treatment of hypertension by using probiotics, changing lifestyle, and diet, further research is warranted to better understand the role of various gut microbial species and their metabolites in the regulation of blood pressure and associated diseases.
Further, it would be interesting to understand the interaction among environmental factors, gut microbial species, and blood pressure regulation. Evidence suggest that diet potentially modulates the gut microbiota by regulating the balance between pathogenic and beneficial microbes or microbial products [ 40 ].
Vegetarian diets foster a beneficial microbiota composition by increasing Prevotella enterotype whereas diets high in animal protein foster Bacteroides enterotype and other species associated with proatherogenic metabolites and CVD [ 4041 ].
The production of the proatherogenic metabolite TMAO, resulting from TMA oxidation by the liver enzyme flavin monooxygenase 3 and its release into the systemic circulation have been linked to coronary plaques, peripheral artery disease, the severity of CVD, and its complications including stroke, myocardial infarction, and death [ 4243 ].
Common dietary nutrients possessing a TMA moiety, such as the choline, phosphatidylcholine, and l -carnitine present in red meat, fish, and eggs after microbial metabolism, are the main contributors of TMAO-mediated effects that promote artherosclerosis [ 9 ].
The underlying mechanisms by which TMAO contributes to CVD remain unknown. However, preliminary evidence suggests that TMAO stimulates inflammatory pathways with activation of cells of the innate immunity response that propagate atherosclerosis.
Also TMAO interferes with platelet function through stimulus-dependent calcium signaling, promoting atherothrombotic events Fig.
Choline, phosphatidylcholine, and l -carnitine found in fish, red meat and eggs are metabolized into TMA by colonic microbiota.
The TMA that enters the systemic circulation is oxidized into TMAO by FMO3 in the liver, which is released back into the circulation, leading to platelet and inflammatory pathway activation.
Inflammatory injury in the endothelium, along with increased foam cell formation and platelet activation, contributes to the progression of atherosclerosis and development of atherothrombotic events. Diets rich in fiber such as whole grains increase the acetate-producing Bifidobacteriaceaewhich are protective against pathogenic bacteria, lower blood pressure, improve insulin sensitivity, and decrease cardiac hypertrophy and fibrosis [ 845 ].
Polyphenols, a large class of aromatic compounds found in plant-based beverages have been shown to improve cardiovascular health through their antiplatelet and anti-inflammatory actions, and by inducing nitric oxide formation in blood vessels, promoting vasodilation and improving gut microbiota with increased Firmicutes and decreased Bacteroides.
Quercetin, a member of the subclass of flavonoid polyphenols increases the abundance of Bacteroides vulgatus and Akkermansia muciniphila and concomitantly reduces Eubacterium cylindroides and Bilophilia wadsworthia to reduce the risk for diet-induced obesity which is a risk factor for CVD and hypertension.
Quercetin also improves cellular energy homeostasis, fatty acid oxidation, and availability of nitric oxide by upregulating adenosine monophosphate-activated protein kinase AMPK expression. Diet induced alterations in the gut microbial composition may also trigger disease states via immune activation.
Regulatory T cells Tregs are essential immune cells to maintain immunologic self-tolerance that are categorized into two; thymus-derived and peripherally derived Tregs [ 46 ].
Importantly, SCFAs, especially butyrate, are known to induce the differentiation of peripherally derived Tregs in the colon, through G-protein coupled receptors [ 47 ]. This process is crucial to limit inflammatory activation. Furthermore, SCFAs are essential nutrients for Tregs as well as colonic epithelial cells [ 48 ].
Therefore, reduced consumption of fermentable dietary fibers may decrease colonic Treg population Probiotlcs predispose to chronic inflammatory states by reducing the abundance of SCFA-forming bacteria [ 49 ].
There is increasing evidence showing the link between high dietary salt and hypertension by modulation of the composition and function of the gut microbiota [ 5051 ].
: Probiotics and Heart Health| Cardiovascular benefits of probiotics: a review of experimental and clinical studies | Cholesterol lowering and inhibition of sterol absorption by Lactobacillus reuteri NCIMB a randomized controlled trial. Effect of probiotic yogurt containing Lactobacillus acidophilus and Bifidobacterium lactis on lipid profile in individuals with type 2 diabetes mellitus. Lactobacillus gasseri [corrected] CHO and inulin reduced plasma total cholesterol and low-density lipoprotein cholesterol via alteration of lipid transporters. Effects of a milk product, fermented by Lactobacillus acidophilus and with fructo-oligosaccharides added, on blood lipids in male volunteers. Evaluation of safety and tolerance of microencapsulated Lactobacillus reuteri NCIMB in a yogurt formulation: a randomized, placebo-controlled, double-blind study. Food Chem Toxicol. 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Volume Metformin-induced improvement in gut health leads to decreased low-grade inflammation, a very important phenomenon seen in the elderly population that has been named inflammaging [ 67 , 68 ]. Indeed, whereas healthy microbiota is associated with attenuation of markers of inflammation [ 64 ], old microbiota induces differential regulation of pathways including T cell differentiation, B-cell development, and recognition of microbes by pattern recognition receptors in young mice, further supporting a role of the gut microbiota in inflammation [ 69 ]. TMAO supplementation induces an aging-like endothelial dysfunction via reduced nitric oxide bioavailability and increased superoxide-driven oxidative stress in young mice [ 70 ]. Since TMAO and p-cresylsulfate are eliminated through the kidney [ 71 ], the age-related decline in kidney function, which is seen in both men and women, may exacerbate the systemic accumulation of these metabolites further enhancing pathways that lead to cardiovascular disease [ 72 ]. Age-associated inflammation is a risk factor for adverse cardiovascular events, thus, therapeutic approaches that target the gut microbiota may be a potential approach to promote healthy aging. Although the gut microbiota is too numerous to characterize, a few analytical tools are available to aid in the study of specific organisms of interest to disease. Metagenomic analysis is one of the powerful tools currently used to reconstruct microbial species and their function by examining genetic sequences. Quantification of TMAO in systemic blood is helpful in assessing CVD severity and complications. For example, elevated TMAO is present in patients with stable PAD and is a significant predictor of acute coronary syndrome, stroke, and death [ 7 ], in some cases independent of traditional risk factors [ 7 ]. In addition to TMAO, plasma levels of choline and betaine are elevated in patients with chronic heart failure. The pathogenic mechanisms of TMAO in heart failure have been previously described [ 11 ]. Certain microbial species in the gut can inactivate or lessen the potency of drugs prescribed to aid the management of CVDs. The therapeutic effects of statins are attenuated by abundant presence of Lactobacillus, Eubacterium, Faecalibacterium , and Bifidobacterium and decreased proportion of genus Clostridium [ 5 ], which renders these drugs relatively ineffective in decreasing LDL levels. Similarly, treatment of atrial fibrillation, atrial flutter, and heart failure using digoxin may not be efficacious when Eggerthella lenta strains are abundant, since they inactivate this drug [ 5 ]. Conversely, therapeutic drugs may alter the microbiota. For example, metformin, the glucose lowering drug used in diabetes mellitus treatment, cancers, CVD and other conditions increases the amount of pathogenic Escherichia-Shigella species [ 5 ]. We have reviewed the evidence that diet has a profound impact on microbiota composition and consequently, disease. Specific vegetarian diets that foster a good microbiota environment that is protective against CVD are recommended as the mainstay to prevent or attenuate adverse cardiovascular effects via modulation of the gut microbiota [ 73 ]. Dietary supplementation with polyphenols is quite beneficial for cardiovascular health [ 8 ]. Caloric restriction and caloric restriction mimetics are emerging as additional tools to modulate the gut microbiota and thereby promote health. Intermittent fasting and molecules such as polyphenols and beta-hydroxybutyrate decrease blood pressure by modulating the gut microbiota and attenuating inflammatory pathways [ 74 , 75 , 76 , 77 ]. Intermittent fasting is associated with changes in the gut microbiota including enrichment of species of the genus Lactobacillus , Oscillospira , and Ruminococcus and reduction of species of the genus Akkermansia , Bacteroides , and Bifidobacterium [ 78 ]. Most notably, the resulting gut microbial changes are associated with changes in bile acid metabolism. Microbes are responsible for modifying primary bile acids, synthesized in the liver and released into the small intestine, to form secondary bile acids [ 79 ]. Bile acids activate receptors such as the farnesoid x receptor FXR and TGR5 to modulate inflammation, blood pressure and vascular function [ 80 , 81 , 82 , 83 ]. Intermittent fasting improves availability of bile acids, which are depleted in disease states, and attenuates hypertension [ 84 , 85 , 86 ]. Thus, available evidence supports modulating the gut microbiota via calorie restriction modalities that improve health through mechanisms such as bile acid signaling. Administration of probiotics live bacteria may offer a protection against CVDs [ 73 ]. In murine models, administration of Lactobacillus plantarum, and Lactobacillus rhamnosus GR-1 mitigated the effects of left ventricular hypertrophy, heart failure and myocardial infarction [ 8 ]. Prebiotics, nondigestible food ingredients, are known to promote bifidobacterial species and acetate-producing bacteria, thus improve gut microbiota composition and cardiovascular health [ 39 , 44 , 50 ]. Acetate regulates many pathways related to cardiovascular health including the upregulation of early growth response protein 1 Egr1 transcription factor that decreases inflammation, cardiac fibrosis, and hypertrophy [ 7 ]. FMT, commonly used in treatment of Clostridium difficile infection and in inflammatory bowel diseases like ulcerative colitis is another emerging technique that has also been targeted to mitigate CVD [ 7 , 8 ]. Evidence that FMT improves the components of the metabolic syndrome has been already provided [ 7 ]. However, the risk for introducing pathogenic microbes and toxins and increasing the risk for other pathological processes is high. An example reviewed above is that FMT from a hypertensive to a germ-free mice induces hypertension in the latter [ 7 ]. Hence, implementation of microbiota transplantation is still a challenge that needs further investigations. It is clear that gut microbiota science has far-reaching clinical implications for management of CVDs. Diagnosis, prognosis, and monitoring of CVDs can be supplemented with characterization, quantification, and to a lesser extent, transplantation of specific gut microbiota and its metabolites. Dietary supplementation remains the safest probable method to improve the gut microbiota and its associated detrimental cardiovascular effects. Dysbiosis increases the risk for various CVDs through several mechanisms. It is associated with microbial translocation from the gut into the interstitium and perivascular tissues resulting in systemic inflammation, abnormalities of lipid and glucose metabolism, atherosclerosis, and hypertension. Western diet and timing of feeding contribute to the risk for CVD by modulating the gut microbiota. High dietary salt intake contributes to dysbiosis and development of hypertension and increases the risk for various CVDs. Sex-dependent microbial composition is emerging as one of the risk factors for CVD. However, there is still scarcity of data on this subject and it warrants further investigation. Aging is associated with a decline in health-promoting bacteria species and with enhancement of metabolic pathways that lead to cardiovascular disease. Thus, the gut microbiota is intricately involved in various CVDs. Understanding this relationship is critical for future targeted therapy to prevent and improve CVDs and to ameliorate cardiovascular adverse events. Quantification of TMAOs is an important marker for prognosis of certain cardiovascular events such as stroke, heart attack and death. Use of pre- and probiotics and TMAO inhibitors, has great potential for future therapy in managing CVDs. The gut microbiota affects cardiovascular health. Although the mechanisms are unknown, the composition of the gut microbiota modulates risk for cardiovascular disease. Leaky gut is associated with inflammation. Microbial translocation elicits an inflammatory cascade that may exacerbate existing disease or induce cardiovascular diseases. Dysbiosis is associated with increased risk for specific diseases. Abnormal composition of the gut microbiota is linked to the pathogenesis and propagation of heart disease, atherosclerosis, hypertension, obesity, type 2 diabetes mellitus, cancer, and gastrointestinal disorders. High salt diet depletes lactobacillus spp. Gut metabolites contribute to vascular injury and thrombotic events. Choline, phosphatidylcholine, and l -carnitine found in fish, red meat, and eggs are metabolized into compounds that activate platelets and activate inflammatory pathways resulting in endothelial injury, and contributing to the progression of atherosclerosis and development of atherothrombotic events. Avery EG, Bartolomaeus H, Maifeld A, Marko L, Wiig H, Wilck N, et al. The gut microbiome in hypertension. Circulation Res. CAS PubMed Google Scholar. Guinane CM, Cotter PD. 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Relation of circulating trimethylamine N-oxide with coronary atherosclerotic burden in patients with ST-segment elevation myocardial infarction. Am J Cardiol. Zhu Y, Li Q, Jiang H. Chleilat F, Schick A, Reimer RA. Microbiota changes in fathers consuming a high prebiotic fiber diet have minimal effects on male and female offspring in rats. Thomas S, Izard J, Walsh E, Batich K, Chongsathidkiet P, Clarke G, et al. The host microbiome regulates and maintains human health: a primer and perspective for non-microbiologists. Cancer Res. Kim CH, Park J, Kim M. Gut microbiota-derived short-chain fatty acids, T cells, and inflammation. A meta-analysis also highlighted that an increase in HDL-C levels is strongly associated with a reduced risk of CVD compared with the changes in serum TG levels [ 43 ]. The present study has many advantages. We evaluated the effects of probiotics on AIPs, blood pressure, the 10 year Framingham risk score, and the antioxidant markers, which are considered the most potential predictors of CVD risk in patients with T2DM, who have a pronounced risk of future CVD due to their disease status. We also used a high dose of probiotic-containing capsules, without any food carriers, to evaluate the exact effects of probiotics on T2DM. Moreover, we did not apply any dietary changes and we excluded participants that started insulin therapy or taking other types of supplements, in order to assess the exact effect of probiotic intervention. However, limitations of the present study include the lower sample size and shorter duration of the intervention. Alterations in some dietary intakes of participants were also observed at the end of the study. Besides, as many complications of T2DM usually develop over a longer period of time, our 6 week clinical trial would not be enough to improve all the parameters and conditions in this population. Stool samples were not also evaluated to assess the microbial composition of the gut and feces. Furthermore, due to budget limitations, we were not able to assess other biochemical parameters related to future CVD risks in patients with T2DM. This RCT study showed that patients with T2DM who consumed probiotic capsules for 6 weeks significantly lowered SBP, DBP and MAP compared to the placebo group. However, no significant changes were seen in any of the antioxidant parameters. Future studies are suggested to collect stool samples and perform correlation in modulation of microbial diversity with improved CVD-related parameters. 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| The Gut-Heart Connection | Find out more…. Standard treatment for hypothyroidism includes oral medication, but there are natural therapies too. Read about the pros and cons of five natural…. The minerals calcium, magnesium, and zinc are vital for your health and often combined into a single supplement. This article covers the benefits…. A Quiz for Teens Are You a Workaholic? How Well Do You Sleep? Health Conditions Discover Plan Connect. Nutrition Evidence Based 8 Health Benefits of Probiotics. Medically reviewed by Kim Chin, RD , Nutrition — By Mary Jane Brown, PhD, RD UK — Updated on March 13, Bacteria balance Indigestion Mental health conditions Heart health Allergies and eczema Digestive disorders Immune system Weight loss How to benefit. How we vet brands and products Healthline only shows you brands and products that we stand behind. Our team thoroughly researches and evaluates the recommendations we make on our site. 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How we reviewed this article: History. Mar 13, Written By Mary Jane Brown. Aug 23, Medically Reviewed By Kim Chin, RD. Share this article. Read this next. Medically reviewed by Natalie Butler, R. Medically reviewed by Alan Carter, Pharm. By Anne Danahy, MS, RDN. Does Magnesium Help You Sleep Better? What Is Potassium Iodide? Appl Environ Microbiol. Biagi E, Franceschi C, Rampelli S, Severgnini M, Ostan R, Turroni S, et al. Gut microbiota and extreme longevity. Curr Biol. Mariat D, Firmesse O, Levenez F, Guimarăes V, Sokol H, Doré J, et al. BMC Microbiol. Biagi E, Nylund L, Candela M, Ostan R, Bucci L, Pini E, et al. Through ageing, and beyond: gut microbiota and inflammatory status in seniors and centenarians. Thevaranjan N, Puchta A, Schulz C, Naidoo A, Szamosi JC, Verschoor CP, et al. Age-associated microbial dysbiosis promotes intestinal permeability, systemic inflammation, and macrophage dysfunction. Cell Host Microbe. 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Diversification of host bile acids by members of the gut microbiota. Cao Y, Xiao Y, Zhou K, Yan J, Wang P, Yan W, et al. FXR agonist GW improves liver and intestinal pathology and alters bile acid metabolism in rats undergoing small intestinal resection. Am J Physiol Gastrointest Liver Physiol. Fu ZD, Klaassen CD. Increased bile acids in enterohepatic circulation by short-term calorie restriction in male mice. Toxicol Appl Pharmacol. Guo C, Xie S, Chi Z, Zhang J, Liu Y, Zhang L, et al. Bile acids control inflammation and metabolic disorder through inhibition of NLRP3 inflammasome. Han M, Li S, Xie H, Liu Q, Wang A, Hu S, et al. Activation of TGR5 restores AQP2 expression via the HIF pathway in renal ischemia-reperfusion injury. Am J Physiol-Ren Physiol. Shi H, Zhang B, Abo-Hamzy T, Nelson JW, Ambati CSR, Petrosino JF, et al. Restructuring the gut microbiota by intermittent fasting lowers blood pressure. Thaiss CA, Zeevi D, Levy M, Zilberman-Schapira G, Suez J, Tengeler AC, et al. Transkingdom control of microbiota diurnal oscillations promotes metabolic homeostasis. Voigt RM, Forsyth CB, Green SJ, Engen PA, Keshavarzian A. Chapter Nine - Circadian Rhythm and the Gut Microbiome. In: Cryan JF, Clarke G eds. International Review of Neurobiology. Academic Press; Download references. This work was supported by the Fogarty International Center of the National Institutes of Health grants D43 TW and D43 TW SKM , K01HL, R03HL, and R01HL AK. The content is solely the responsibility of the authors and does not represent the official views of the National Institutes of Health. Mulungushi University, School of Medicine and Health Sciences, HAND Research Group, Livingstone, Zambia. Sepiso K. Vanderbilt University Medical Center, Department of Medicine, Nashville, TN, USA. Lale A. Ertuglu, Jeanne Ishimwe, Sharla Rahman, Mohammad Saleem, Cheryl L. You can also search for this author in PubMed Google Scholar. SKM, BH, JH, VH, LAE, JI, SR, and MS wrote different sections of the manuscript. CLL and FE edited and reviewed the manuscript. AK conceptualized the study and framework and finalized the manuscript as well as obtained funding for the manuscript. All authors contributed to article reviews, edited and approved the final version of this manuscript. Correspondence to Annet Kirabo. Open Access This article is licensed under a Creative Commons Attribution 4. Reprints and permissions. Masenga, S. Recent advances in modulation of cardiovascular diseases by the gut microbiota. J Hum Hypertens 36 , — Download citation. Received : 15 October Revised : 29 March Accepted : 12 April Published : 25 April Issue Date : November Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Current Cardiovascular Risk Reports Probiotics and Antimicrobial Proteins Skip to main content Thank you for visiting nature. nature journal of human hypertension review articles article. Download PDF. Subjects Cardiovascular diseases Physiology. Abstract The gut microbiota has recently gained attention due to its association with cardiovascular health, cancers, gastrointestinal disorders, and non-communicable diseases. Introduction Humans are surrounded, both externally and internally, by a diverse range of microbes which profoundly affect wellbeing by interacting with skin, respiratory, and digestive systems. Full size image. Gut microbiota, atherosclerosis and CVDs The source of many of the microorganisms that have been associated with atherosclerotic plaques, endothelial dysfunction, and resulting CVDs is their translocation from the gut into the systemic circulation. Conclusion Dysbiosis increases the risk for various CVDs through several mechanisms. 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Low cholesterol levels and low incidence of CHD in the Maasai and Samburu tribes of northern Africa, despite high intakes of full-fat dairy products and beef in these populations, raised interest in the effects of fermented milk and other dairy products on cholesterol reduction. The objective of this article is to review the existing clinical trials that have examined the effects of probiotics on LDL-C and to assess the potential of probiotic intake as a dietary TLC option for reducing CHD risk. acidophilus, B. longum, L. fermentum, L. paracasei, L. plantarum, and L. The same filters listed above were used, excluding RCT, to ensure that term did not overly restrict the initial search results. References listed in articles of interest obtained from the above searches, from previously published reviews on probiotics and health, or utilized during the development of this review were then scrutinized to identify other relevant clinical studies. Studies that were randomized, placebo-controlled trials conducted in an adult population whose primary endpoints included LDL-C and other plasma lipids were summarized and included in the tables. Studies not published as full reports, such as conference abstracts or those not published in English, were excluded. Two meta-analyses have examined the effect of probiotic consumption on CHD. The analysis included 13 randomized, controlled trials in subjects with normal and high cholesterol levels. Feeding duration ranged from 4 weeks to 10 weeks, with exception of one study in which 2-week test periods per dose were used. Results from a combined subjects found that, when compared with placebo, probiotic consumption significantly lowered LDL-C by 4. However, this meta-analysis is limited by the lack of investigation of the effects of specific probiotic strains on blood lipids. Results of this meta-analysis will be discussed later in this review. The results of 26 randomized, placebo-controlled trials reported in the literature that examined the effects of probiotics on TC, lipoproteins, and inflammatory biomarkers in subjects given a fermented dairy product Table 1 , a capsule Table 2 , or a synbiotic Table 3 have been summarized. In these trials, significant lowering of LDL-C was observed for four probiotic strains that were compared with placebo: L. reuteri NCIMB , 31 , 32 , E. faecium , 19 , 21 and the combination of L. Two synbiotics that were found to decrease LDL-C included L. acidophilus CHO plus inulin 34 and L. acidophilus 2 strains undefined plus fructo-oligosaccharides. Clinical effects of probiotics on lipoproteins, lipids, and inflammatory biomarkers: capsules. Clinical effects of synbiotics on lipoproteins, lipids, and inflammatory biomarkers. Two randomized, placebo-controlled, double-blind, parallel-arm, multicenter studies provide support for the ability of L. reuteri NCIMB in both yogurt and capsules to significantly lower LDL-C and TC compared with placebo. Concentrations of TAG and HDL-C were unchanged. In the current literature, L. reuteri NCIMB capsules are the only probiotic capsules shown to significantly lower LDL-C. A meta-analysis of five randomized, controlled studies with E. One possible reason was a significant drop in the dose of E. In a study using capsules, 43 hypercholesterolemic men and women consumed E. Changes from baseline in LDL-C and TC, but not HDL-C or TAG, were reported. There are two randomized, placebo-controlled, double-blind, parallel-arm studies evaluating the LDL-C-lowering effects of L. acidophilus La5 and B. lactis Bb12 Table 1. lactis Bb12 may be a candidate for a therapeutic dietary option to help people with type 2 diabetes manage their LDL-C and TC levels, but more clinical research is needed. Two randomized, placebo-controlled double-blind synbiotic studies were shown to decrease LDL-C Table 3. The first study was a parallel-armed study in 32 hypercholesterolemic men and women and examined the combination of L. acidophilus CHO plus inulin. acidophilus CHO and 0. The combination of L. acidophilus strains undefined plus fructo-oligosaccharides was examined in 30 normocholesterolemic men in a crossover study. acidophilus and a 2. Significant reductions in LDL-C 5. No differences in HDL-C or TAG were found. Since the effect of synbiotics on blood lipids can result from probiotics, prebiotics, or both, it is difficult to determine the direct effects of the probiotic used in these studies on LDL-C. To strengthen the science on probiotics, guidelines for industry on statistical principles for clinical trials have been developed and their use in future studies to examine and confirm the efficacy of probiotics on LDL-C or other health endpoints is strongly encouraged. As a rule, confirmatory trials are necessary to provide firm evidence of efficacy or safety. In such trials the key hypothesis of interest follows directly from the trial's primary objective, is always predefined, and is the hypothesis that is subsequently tested when the trial is complete. In a confirmatory trial, it is equally important to estimate with due precision the size of the effects attributable to the treatment of interest and to relate these effects to their clinical significance. The randomized, controlled, multicenter clinical trials examining L. reuteri NCIMB include a predefined primary endpoint in the protocol as well as sufficient statistical power to detect an expected change in the primary endpoint. This is in contrast to other published probiotic clinical studies, in which at times it is unclear whether these guidelines were followed and, therefore, whether firm evidence of efficacy is provided. Research in the s indicated differences between germ-free and conventional rats in their ability to metabolize cholesterol. Germ-free animals, which lack intestinal microflora, were found to have both lower amounts and different compositions of fecal steroids, higher absorption of dietary cholesterol, and greater accumulation of cholesterol, particularly in the liver, indicating a role for intestinal microbes in cholesterol regulation. However, the exact mechanism s of action of the limited number of probiotic strains that have been clinically shown in humans to significantly decrease LDL-C levels versus placebo is not completely known. Several potential mechanisms whereby probiotics may reduce circulating cholesterol levels have been proposed: 1 binding of cholesterol by the cellular surfaces and membranes of the probiotics; 2 assimilation of cholesterol particles into growing probiotic cells; 3 microbial deconjugation of bile via bile salt hydrolase BSH , resulting in increased fecal excretion of deconjugated bile salts with a compensatory increase in the use of cholesterol to produce new bile acids; 4 short-chain fatty acid production from fermentation of carbohydrate, leading to decreased levels of blood lipids and reduced production of endogenous cholesterol by the liver; and 5 a reduction in cholesterol absorption, perhaps through BSH activity and deconjugation of biliary salts in the small intestine. Increasing recognition that atherosclerosis involves a chronic inflammatory process has created interest in arterial acute-phase inflammatory biomarkers, such as high-sensitivity C-reactive protein hs-CRP and fibrinogen, as risk factors for CHD. reuteri NCIMB was shown to lower both hs-CRP by 1. faecium study found a significant increase in fibrinogen by faecium bacteria strains as a possible reason for the increase in fibrinogen in subjects. The studies using L. lactis Bb12 did not provide data on inflammatory biomarkers. Further, bile acids function as signaling molecules that can activate a variety of nuclear receptors. These bile receptors, mainly expressed in enterohepatic tissues, can affect glucose tolerance, lipid and energy expenditure, and immune function, thus potentially affecting the risk of CVD and metabolic syndrome. reuteri NCIMB The National Cholesterol Education Programs Adult Treatment Panel recommends dietary alterations, increased exercise, and other lifestyle changes to reduce CHD risk. The combination of plant sterols, viscous fiber, soy protein, and nuts, in addition to a diet low in saturated fat, has been clinically tested in an outpatient metabolic study. These results demonstrate a significant LDL-C-lowering effect of a TLC diet with multiple dietary targets that is as effective as a low dosage of a first-generation statin drug. Probiotics can be added to food products such as yogurt and can also be consumed as capsules. Thus, dietary compliance may be improved by the use of probiotics, leading to greater lowering of LDL-C. The importance of lowering LDL-C in individuals to reduce major vascular events was highlighted in the Cholesterol Treatment Trialists' Collaboration. Moreover, some individuals do not need marked LDL-C reduction or prefer nonpharmacologic alternatives to statin therapy. reuteri NCIMB can be among the potential options to manage LDL-C; the use of probiotic-containing diets as a complement to statin therapy should be studied further. In addition to a diet low in saturated fat and cholesterol, the consumption of specific probiotics in the right quantities may produce results comparable to the LDL-C-lowering effect of a low-dose statin drug. In addition to demonstrating health benefits, therapeutic dietary options such as probiotics must be established as safe for human consumption. The probiotic L. reuteri background exposure in foods and as a commensal organism , bioinformatic and in vitro data characterizing the metabolic phenotypes of the strain, and data on strain-specific safety provided by repeat-dose studies in humans. reuteri is commonly used by the food industry for its fermentation properties and is one of the most widely used microorganisms for the production of sourdough bread. reuteri in humans. Several regulatory agencies, such as the US Food and Drug Administration FDA , the European Food Safety Authority, and the Therapeutic Goods Administration of Australia, have recognized L. reuteri for human consumption. reuteri in infant formula has been shown to be safe and well tolerated and to support normal growth. It should not be assumed that conclusions about the safety of a species of microorganism can be applied to all strains of that species. reuteri NCIMB strain for antimicrobial resistance, production of antimicrobial compounds, the presence of virulence genes in the genome, and production of potentially harmful metabolites. They found no evidence of characteristics that present food safety concerns. reuteri NCIMB also was shown to be well tolerated in two clinical trials investigating hypercholesterolemic but otherwise healthy subjects. Adverse effects in the probiotic and placebo groups were similar. The FDA has concluded that a GRAS determination for L. reuteri NCIMB GRN presents no safety questions, as indicated in its letter to the manufacturer. The probiotic B. lactis Bb12 in combination with Streptococcus thermophilus Th4 has been determined to be GRAS for use in infant formula. While there are some enterococci with a long history of safe use, others can be opportunistic pathogens. faecium among others should not be used as a dietary ingredient because FDA regards all members of a species that contains human pathogens as potentially harmful to human health. FDA believes there is an absence of consensus regarding valid scientific ways to distinguish between pathogenic and nonpathogenic members of a single species FDA, Probiotics are increasingly being used by consumers and are advocated by many healthcare professionals. CVD remains a leading cause of death worldwide, and a reduction in LDL-C remains the primary target for intervention. In recent decades, a number of probiotic strains have been evaluated for their ability to reduce LDL-C and other risk factors for CHD. Probiotics found to lower LDL-C when compared with placebo include L. reuteri NCIMB 8. The ability of L. reuteri NCIMB to lower blood lipids was established in two multicenter clinical trials in which this probiotic was provided to subjects via food or as supplements. The proposed mechanism of action involves a reduction in cholesterol absorption as a result of deconjugation of bile salts in the small intestine due to BSH activity. reuteri NCIMB has GRAS status, which was obtained through scientific procedures and confirmed by an expert panel on its use as an ingredient in food and beverages. A meta-analysis of five studies provides support for the ability of E. faecium to lower LDL-C and other blood lipids via its use in fermented dairy products. However, the FDA has raised concern about the use of E. faecium as a food ingredient. Mixed results were obtained by a combination of L. lactis Bb12, indicating that this mixture has potential, but more research is needed. reuteri NCIMB is a viable candidate to consider in recommendations for future TLC dietary studies and as a potential option for inclusion in TLC dietary recommendations. To strengthen the science on probiotics, guidelines for industry on statistical principles for clinical trials have been developed, and their use in future studies to examine and confirm the efficacy of probiotics on LDL-C or other health endpoints is strongly encouraged. A roundtable of leading global experts in heart health, probiotics, and nutrition convened once in person to discuss the development of a scientific review paper examining a new role for probiotics in cardiovascular health. Prior to manuscript submission, the author invited members of the roundtable to review the manuscript and provide comments. Roundtable members were then contacted individually by phone conference to review their comments and address questions by the author. The author expresses his appreciation for the expert comments provided. Expert reviewers were as follows: Richard J. Deckelbaum, MD, CM, FRCPC; Robert R. The roundtable was supported by Micropharma. The author also expresses his appreciation to Kevin Comerford, PhD, for his assistance in providing background support in the development of this article. The author was provided support for this review by Micropharma, Montreal, Canada. Any opinions, findings, conclusions, or recommendations expressed here are those of the author. World Health Organization, World Heart Federation, World Stroke Organization. Global atlas on cardiovascular disease prevention and control. Published |
| Best Probiotics for Cholesterol and Heart Health | Probiotics Learning Lab | Probiotics and Heart Health is a Probiottics side effect of taking antibiotics. Reviewed by: Probiotics and Heart Health OstadmohammadiKashan University of Medical Sciences, Iran Jun-ichiro KogaUniversity Proiotics Occupational and Environmental Health Japan, Japan. About this article. CAS PubMed PubMed Central Google Scholar Kim CH, Park J, Kim M. Prebiotics mode of action is taking advantage of the commensals that are already in the host; they use this to degrade their otherwise indigestible bonds, which support the microbial survival [ 1 ]. |
| Should You Take Probiotics for Heart Health? | Moreover, they can further decrease the levels of LPS, TMAO, and Hwart response, Probiotics and Heart Health of Pribiotics are beneficial in Probiotics and Heart Health the progression of coronary artery lesions and Probiptics the prognosis znd patients Jauhiainen T, Rönnback M, Vapaatalo H, Wuolle K, Kautiainen H, Groop PH, et al. Ryan P, Ross R, Fitzgerald G, Caplice N, Stanton C. Standard treatment for hypothyroidism includes oral medication, but there are natural therapies too. Sabico S, Al-Mashharawi A, Al-Daghri NM, Yakout S, Alnaami AM, Alokail MS, McTernan PG. Trimethylamine N-oxide binds and activates PERK to promote metabolic dysfunction. Aggarwal J, Swami G, Kumar M. |
| Lung Health Tips to Improve Respiratory System | Role of altered intestinal microbiota in systemic inflammation and cardiovascular disease in chronic kidney disease. Any opinions, findings, conclusions, or recommendations expressed here are those of the author. These bacteria have been observed to lower cholesterol both in vitro and in vivo [ 28 ]. Specific vegetarian diets that foster a good microbiota environment that is protective against CVD are recommended as the mainstay to prevent or attenuate adverse cardiovascular effects via modulation of the gut microbiota [ 73 ]. However, some studies have yielded different results 7 , 8 , and there is a lack of evidence-based medical proof. E-mail: ddirienzo quadrantnutrition. |
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Studies find some probiotics can be harmful to gut health Improved nutrient utilization The objective of this study anv Probiotics and Heart Health study the effect of probiotics anx synbiotics on the risk factors for Hert artery disease CAD in the context of conventional drug therapy for CAD. Methods: The literature on probiotics or Heallth Probiotics and Heart Health the treatment of CAD was collected from PubMed, Scopus, Web of Science, Embase, and Cochrane Library. The search period was conducted on November 5,and the search covered all literature before November 5, The included literature consisted of randomized controlled trials of probiotics or synbiotics for CAD, and a meta-analysis was performed using Stata 14 software and RevMan 5. Results: The meta-analysis explored the effect of probiotics or synbiotics on the risk factors for coronary artery lesions in a treatment setting with conventional medications for CAD.
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