The link between high meat
consumption and cardiovascular disease (CVD) is sometimes described as resulting
from the increased intake of saturated fats and cholesterol content, originating
from the meat. However, in a recent study led by the David Geffen School of
Medicine at the University of California, analysis of a collection of studies
suggested that there is no association between saturated fat intake and CVD,
rather other factors are responsible. There have been several studies surrounding
this, thus allowing a better understanding in the possible causes and biological
pathways that may lead to cardiovascular related diseases.

Here, in this study, the
metabolism of intestinal microbiota was explored, and more specifically, its
metabolism of L-carnitine, a nutrient found in red meat. It was demonstrated
that the L-carnitine, a trimethylamine (TMA), can be metabolised by the
microbiota to produce trimethylamine-N-oxide
(TMAO), a molecule that can accelerate the process atherosclerosis in mice. Atherosclerosis
is the condition where plaque builds up inside the arteries, and this can lead
to CVD’s, as well as the increased risk of blood clots and the restriction of
blood flow and oxygen to vital organs.

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The study itself presented
several findings. When omnivorous subjects were compared against vegan and
vegetarian subjects, it was observed that the omnivores produced more TMAO –
various experimental procedures were carried out to help determine this result.
Both the omnivorous and vegan/ vegetarian subjects were given large amounts of
L-carnitine – an estimated 180 mg of L-carnitine in a steak, as well as a
capsule containing d3-carnitine. An increased concentration of d3-TMAO was
observed in the plasma and urine of the omnivorous subjects over 24 hours,
whilst the TMAO concentrations for the vegans remained at an undetected level.
Then, in a separate procedure, stable subjects were administered to have varied
plasma carnitine concentrations, reflecting varied levels in the risk of developing
atherosclerosis. When the TMAO concentration was adjusted, however, no
association was observed – this was incredibly important, as it suggested the
direct association of a TMAO- dependant pathway that led to increasing risk of atherosclerosis.

In the experimental procedures
that involved mice, subjects were given L-carnitine supplementation. Analysis
of data from the beginning of the procedure suggested zero detection of plasma
d3-TMAO production, however after several weeks of observations, the very same
mice had developed the ability to produce the d3-TMAO. This production was then
seen to accelerate atherosclerosis. However, in the pathway where the
intestinal microbiota was supressed, the formation of the TMAO did not occur,
thus highlighting the importance of the intestinal microbiota in metabolising
the TMA to TMAO.

In conclusion, the results of
the study suggest the importance of exploring the properties of metabolites
associated with gut microbiota, and recognising the potential role it can play
in the overall health of an individual. The main limitation of this study was
that the mice model data may not correlated with human data. Despite this, the results
have been important in creating links and recognising important developments –
for example, intestinal microbiota may contribute to the already established
link between high levels of meat consumption and CVD’s, and the importance of TMAO,
which can be seen as an atherosclerosis risk-substrate. Further exploration of
this molecule and its pathway may present new venues into the likely causes and
possible treatments for atherosclerosis, and its associated cardiovascular