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The Gut and Heart Connection
Published in Mark C Houston, The Truth About Heart Disease, 2023
There are many products and chemicals produced by the bad bacteria in the gut. One of these is called trimethylamine N-oxide (TMAO) which comes from compounds (such as meat and eggs) that contain choline, phosphatidyl choline, and carnitine and is associated with a higher risk for CHD and MI. However, a type of fatty acid called short-chain fatty acid (SCFA) such as butyrate, propionate, and acetate, improve gut and colonic health, insulin resistance, diabetes mellitus, high cholesterol, hypertension, and CHD. In addition, bile acids are important in glucose metabolism, cholesterol and fat metabolism, and in obesity regulation.
Gut Microbiota—Specific Food Design
Published in Megh R. Goyal, Preeti Birwal, Santosh K. Mishra, Phytochemicals and Medicinal Plants in Food Design, 2022
Aparna V. Sudhakaran, Himanshi Solanki
The plant proteins have a positive correlation on intestinal homeostasis. The animal-based proteins are linked to the development of atherosclerosis. Meat and egg are loaded with L-carnitine and phosphatidylcholine that are converted to trimethylamine by the gut microflora and further to its oxide form (into trimethylamine oxide—TMAO) in the liver [39, 68]. In case of milk proteins (casein and whey rich in branched-chain amino acids (BCAAs): valine, leucine, and isoleucine), it was reported to prolong the age-related changes in the gut flora [79]. It also enhances the healthy Lactobacillaceae/Lactobacillus and decreases the abundance of Clostridiaceae/Clostridium in the gut [50].
The Role of the Microbiota and the Application of Probiotics in Reducing the Risk of Cardiovascular Diseases
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Raquel Bedani, Susana Marta Isay Saad
Trimethylamine-N-oxide (TMAO). It is an intestinal microbial co-metabolite that has drawn a lot of attention as both biomarker for CVD risk and a promoter of atherothrombotic diseases, which have supported the link between the gut microbiota and CVD (Brown and Hazen 2018). In this sense, the control of TMAO pathway could be considered as a promising target for CVD drugs focused on intestinal microbiome (Brown and Hazen 2018).
Novel variants and haplotypes of human flavin-containing monooxygenase 3 gene associated with Japanese subjects suffering from trimethylaminuria
Published in Xenobiotica, 2019
Makiko Shimizu, Hiromi Yoda, Narumi Igarashi, Miki Makino, Emi Tokuyama, Hiroshi Yamazaki
The 787 potential trimethylaminuria sufferers were diagnostically assessed by determining the percentage of total urinary trimethylamine and trimethylamine N-oxide excreted as trimethylamine N-oxide under daily food intake. The concentrations of trimethylamine and trimethylamine N-oxide in urine were determined by gas chromatography using a flame ionization detector (Yamazaki et al., 2004). Briefly, the trimethylamine concentration in the urine was directly analyzed by headspace gas chromatography after the addition of 10 M NaOH to urinary samples and preheating to 95 °C for 20 min. Trimethylamine N-oxide concentrations were calculated by subtracting the concentration of free trimethylamine from that of total trimethylamine (free trimethylamine plus trimethylamine N-oxide) after chemical reduction of trimethylamine N-oxide to trimethylamine by TiCl3. Intra- and inter-assay variations for free and total trimethylamine concentrations were within 5% under the present conditions (Yamazaki et al., 2004). The detection limit for trimethylamine concentration was 0.01 µg/mL of urine.
Flavin-containing monooxygenase 3 (FMO3): genetic variants and their consequences for drug metabolism and disease
Published in Xenobiotica, 2020
Ian R. Phillips, Elizabeth A. Shephard
Variation in the gut microbiome has been linked to several disease states. As trimethylamine N-oxide is a metabolite of a gut-microbiome-derived molecule (trimethylamine), its plasma concentration may reflect changes in gut microbiome composition. Thus, elevated plasma concentrations of trimethylamine N-oxide may be a consequence of changes in the gut microbiome, which in turn could be an underlying cause or effect of the disease. In either case, trimethylamine N-oxide would be a biomarker, rather than a causative factor of the disease.
Gut microbes and metabolites as modulators of blood-brain barrier integrity and brain health
Published in Gut Microbes, 2020
Aimée Parker, Sonia Fonseca, Simon R. Carding
Trimethylamines: are metabolites produced from gut microbial metabolism of dietary choline, lecithin, carnitine and trimethylamine-N-oxide (TMAO) that are present in foods such as eggs, nuts, dairy products, meat, and fish. Choline is degraded into trimethylamine (TMA), which is converted in the liver by flavin-containing monooxygenases (FMOs) into TMAO, and demethylated into dimethylamine and methylamine.51 Gut-derived TMA is generated by bacteria of the genera Anaerococcus, Clostridium, Escherichia, Proteus, Providencia, and Edwardsiella.52 The presence of TMAO in human brains indicates its ability to cross the BBB.53 TMAs have been associated with both beneficial and detrimental health effects. High plasma levels of TMAO have been associated with increased risk of colorectal cancer54 and with risk of developing atherosclerosis and cardiovascular disease via effects on cholesterol metabolism.55 This is of interest regarding neurodegenerative diseases including AD and vascular dementia, in which cardiovascular disease and altered cholesterol metabolism are strongly associated with increased risk. In individuals with a hereditary defect in FMO3, bacterial TMA production contributes to the symptoms of trimethylaminuria (TMAU) or fish-odor syndrome.56 Therapy with archaebiotics and attempting to modulate the gut microbiota by administering specific strains of TMA metabolizing Archaea has been proposed as a treatment for cardiovascular diseases and TMAU. The methanogen, Methanomassiliicoccales can reduce TMA concentration in the gut by converting it to methane, thus decreasing the production of TMAO from TMA in the liver.57,58 TMAO’s beneficial effects include reducing endoplasmic reticulum stress and lipogenesis in adipocytes, increasing insulin secretion in pancreatic islets, and attenuating diet-induced impaired glucose tolerance.59,60 Again, by extension, such therapies may also be beneficial in protecting against neurodegenerative disease as diabetes which is another dementia-associated risk-factor. More specific to AD, TMAO has also been shown to restore the ability of mutant tau protein to promote microtubule assembly61,62 with microtubule disassembly and neuron death being hallmark pathological features of AD.63 In addition to its potential use as an AD biomarker,64 TMAO may also have a therapeutic effect in AD and other protein-misfolding conditions, by preferentially hydrating partially denatured proteins to correct folding defects and entropically stabilizing native conformations.65,66