The association between heart failure, cardiovascular disease, and fibrosis with a metabolic marker TMAO is key to preventing and reversing these chronic conditions. TMAO contributes to CVD development by inducing platelet aggregation, foam cell formation and promoting inflammatory responses by activating the NLRP3 inflammasome. Therefore, the close monitoring of this marker and posterior dietary approaches to reduce TMAO are needed to improve our patient’s health.
TMAO as a prognostic marker:
Nowadays, the measurement of TMAO in combination with the NT-proBNP marker can provide enhanced prediction efficiency of death/HF within one year. Furthermore, the current information and limited information do not validate the use of TMAO on acute heart failure, and more information is needed to understand the clinical applications.
On the other hand, studies of TMAO in CHF have more valid information, and its association has in-depth studies. TMAO levels can rise 3.4-fold higher in HF patients when compared to individuals without this condition. This information also suggests that TMAO can predict an increased risk of 5-year mortality, even after adjusting for traditional risk factors.
How to treat elevated TMAO levels:
The answer is always to treat the gut. There is growing evidence showing the relation among gut dysbiosis, high levels of circulating TMAO, and the presence of HF, suggesting a clear gut- TMAO- HF axis.
Our dietary patterns relate closely to our circulating TMAO levels, and nutritional diet therapy has always played a key role in CVD prevention. Besides this, our intestinal microbiota’s composition goes through numerous changes in our life cycle, and dietary interventions can modify its bacterial constituents. Therefore, our western diet, constituted by high animal protein food, saturated fats, and high sugar, provides all the precursors of TMAO and contributes to dysbiosis.
On the contrary, the Mediterranean diet provides a wide array of fresh fruits and vegetables, whole grains, nuts, and a limited quantity of alcohol, eggs, and meat contributes to an optimal gut’s colonization. The Dietary Approaches to Stop Hypertension (DASH) and the Mediterranean diet have a strong association with reducing HF prevalence and preventing secondary cardiac events. Plant-based diets can reduce the risk of developing cardiovascular disease; their components: nuts, vegetables, and whole grains, provide a higher fiber content that promotes a healthy microbiome.
The adverse effects of TMAO on cardiac insufficiency and HF remodeling show that a diet with low choline content (reduced meat and fat) combined with high fiber alleviates ventricular remodeling and improves cardiac function. Finally, these studies conclude that tight monitoring of TMAO levels, reducing meat ingestion, and augmenting the dietary fiber intake can prevent and treat HF by modifying the gut microbiota.
Treating the gut:
The supplementation of probiotics, prebiotics, and fiber is no surprise when treating the gut. Nevertheless, recent studies provide us with specific information on how to improve TMAO levels in patients suffering from cardiac conditions with bacterial strains and phytochemicals.
- Lactobacillus Plantarum: The intervention with this bacterial strain exerts cardioprotective effects by reducing the LV infarction area during ischemia-reperfusion injury.
- Lactobacillus rhamonosus GR 1: The administration of Lactobacillus rhamonosus GR 1 in rats contributes to improving systolic and diastolic parameters. However, these effects were due to the reduction of serum leptin and the increase in taurine levels.
- Lactobacillus Plantarum 299v and Bifidobacterium lactis Bi-07: Supplementation with probiotic Goodbelly to antibiotic-treated mice with myocardial infarction model contributes to the production of short-chain fatty acids (SCFA). Besides, the cardioprotective effects of this combination are due to its impact on reducing TMAO production.
- Bifidobacterium Animalis subsp. lactis (prebiotic): This prebiotic acts by promoting healthy bacteria and reducing TMA’s amount produced by gut microbiota.
- Inulin: Inulin is another prebiotic with a strong association with the production of SCFA, insulin resistance improvement, and reduction of inflammatory markers.
- Allicin: This compound is found in garlic and has antibacterial effects. Nevertheless, it can diminish the amount of TMAO by modulating the gut’s microbiota.
- Resveratrol: A polyphenolic compound found in grapes that exerts cardioprotective effects by shifting the gut’s microbiota composition and reducing TMAO plasma levels.
- Berberine: The phytochemical berberine in combination can modulate the hepatic enzyme FMO3 and reduce the conversion of TMA to TMAO. However, this modulation should be carefully monitored since the inhibition of FMO3 can lead to excessive TMA levels and lead to “fishy odor syndrome.”
TMAO’s role in metabolic conditions is a growing topic, raising questions and producing new answers all the time. The close monitoring of this marker correlates to the gut, metabolic and cardiovascular health. Furthermore, elevated TMAO levels associate with inflammation, which in turn contributes to chronic complications. Therefore, TMAO ensures a new and promising way to prevent heart failure while treating the gut.
In the role of prevention, we need all the help that we can get. Indeed, as technology progresses, new findings allow us to find new inflammatory contributors, which clinicians can monitor closely. The production of TMAO and its harmful effects are associated with the dietary intake of meats, eggs, fish, and dairy. However, this means that we can shift our intake and improve this metabolic marker.- Ana Paola Rodríguez Arciniega, MS
Zhang, Yixin et al. “TMAO: how gut microbiota contributes to heart failure.” Translational research: the journal of laboratory and clinical medicine vol. 228 (2021): 109-125. doi:10.1016/j.trsl.2020.08.007
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Dr. Alex Jimenez DC, MSACP, CCST, IFMCP*, CIFM*, CTG*
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