TMAO is metabolized by the liver, and is synthesized from trimethylamine which is produced by the actions of beneficial gut bacteria. Those at risk for heart disease often display high levels TMAO in their blood; exact process that increases plasma TMAO is vague, and the effect of the compound on the circulatory system is uncertain.
Some studies report that TMAO appears to harm the circulatory system such as in 2014 rodent studies conducted at the Medical University of Warsaw that found hypertensive effects of a vasoconstrictor lasted longer in healthy rats that experienced a 10,000% increase in blood TMAO during a two week period. TMAO plasma levels significantly increased after fish and vegetable intake.
Effects of TMAO were evaluated on hypertension and cardiovascular disease, testing the compound for chronic periods of time; and a animal model of hypertension using spontaneously hypertensive rats were used as test model with healthy rats being used as controls.
Once weaned rats were given tap water or a solution containing 333 milligrams per liter of trimethylamine oxide doses to raise TMAO levels by 300-500%. At 6 weeks animals were anesthetized to implant devices to track cardiovascular telemetry; heart rate and mean arterial blood pressure data was collected every week for 9 weeks. After 9 weeks the animals were evaluated for additional in depth recordings of cardiovascular and brain health; and blood samples were taken from their right heart ventricles. After being sacrificed animal arteries, hearts, and kidneys were harvested for histopathological and biochemical analysis, especially in regards to trimethylamine and trimethylamine oxide levels in urine and blood.
Mass spectrometry and chromatography testing showed plasma trimethylamine oxide levels in the hypertensive treated rats to be much higher than the controls by an average of 20%; TMAO increased by 400-500%; and they did not accelerate or aggravate hypertension.
Angiopathy, cardiac hypertrophy, and blood pressure of both groups of hypertensive rate were more or less the same at 16 weeks; those treated with trimethylamine oxide displayed better left ventricular end diastolic pressure, had lower plasma NH2 terminal pro-B-type natriuretic peptide, and their hearts were in better shape with less fibrosis.
60 week animal’s results matched outcomes of younger rats. Water treated animals suffered from hypertensive angiopathy and diastolic heart failure; trimethylamine oxide supplemented animals in contrast proved to be far healthier.
Based on finding the researchers concluded increasing trimethylamine oxide in the body benefits animals with hypertension; and the compound appears to decrease negative effects of hypertension on the heart and circulatory system.
