Fri, Dec-14-18, 12:38
|
 |
Senior Member
Posts: 15,075
|
|
Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
|
|
Cognitive bias? Researchers go into it thinking beef is bad. If they do a study designed to show that TMAO causes bad stuff, and it instead causes good stuff--instead of saying TMAO from beef might not be a bad thing, they say a beefy diet doesn't raise TMAO levels enough.
As to why TMAO might be bad, here's an example;
Quote:
Abstract
Several studies have reported a strong association between high plasma level of trimethylamine N-oxide (TMAO) and atherosclerosis development. However, the exact mechanism underlying this correlation is unknown. In the present study, we try to explore the impact of TMAO on endothelial dysfunction. After TMAO treatment, human umbilical vein endothelial cells (HUVECs) showed significant impairment in cellular proliferation and HUVECs-extracellular matrix (ECM) adhesion compared with control. Likewise, TMAO markedly suppressed HUVECs migration in transwell migration assay and wound healing assay. In addition, we found TMAO up-regulated vascular cell adhesion molecule-1 (VCAM-1) expression, promoted monocyte adherence, activated protein kinase C (PKC) and p-NF-κB. Interestingly, TMAO-stimulated VCAM-1 expression and monocyte adherence were diminished by PKC inhibitor. These results demonstrate that TMAO promotes early pathological process of atherosclerosis by accelerating endothelial dysfunction, including decreasing endothelial self-repair and increasing monocyte adhesion. Furthermore, TMAO-induced monocyte adhesion is partly attributable to activation of PKC/NF-κB/VCAM-1.
|
I think this part;
Quote:
|
These results demonstrate that TMAO promotes early pathological process of atherosclerosis by accelerating endothelial dysfunction, including decreasing endothelial self-repair and increasing monocyte adhesion.
|
is a bit irresponsible. We have to accept that human umbilical vein endothelial cells in a petri dish or somesuch are a good model for arterial endothelial cells in an intact human. At most this suggests a way in which TMAO might etc., rather than demonstrate that it does.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3650111/
Quote:
|
Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis
|
This one does show an increase in atherosclerosis, in apoE deficient mice, when fed carnitine. I haven't read it very carefully, I don't know how tightly this was connected to production of TMAO as such. This paper suggests that production of TMAO by bacteria somehow reduces reverse transport of cholesterol to the liver.
Which explains why I went with the flippant answer. This stuff gets involved, and I haven't fully involved myself with it yet. |