Chuck wrote
(big snip)
The small particles are
> considered the bad guys because they are small enough that they can work
> their way into the intima (the inner layer of an artery or vein) where
> they ultimately show up in arterial lesions. But, AFAIK, no one has
> explained why and how a normal component of the blood should decide to
> take up residence in (and only in) the arterial and carotid arteries.
I don't think this (take up residence in (and only in) the arterial and
carotid
arteries) is what Dr Esselstyn is saying or inferring. Of course these
plaques can develop in an artery feeding your big toe, but that is unlikely to
kill you. When they do develop in your cardiac / carotid arteries, that IS
likely
to threaten your life.
Currently, the major medical interventions to combat that are surgical -
insertion of stents and arterial bypass operations, neither of which are long-
lasting. And the medical profession currently thinks (by and large) that
surgical intervention is the way to go.
Interestingly, there was yesterday a re-broadcast here of a CNN video
featuring a Dr Patel from New York. I didn't see it, but from what I have been
able to ascertain from the internet, he is hanging onto Esselstyn's coat-tails.
Among the important points he makes are that the endothelial cells which
line our arteries are most important. They manufacture nitric oxide, which is
a critically important vasidilator, it prevents white blood cells and platelets
from becoming sticky to form plaque, keeps the smooth muscle cells of
arteries from growing into plaques, and may even diminish existing plaques.
These discoveries won a Nobel Prize in 1998 (Drs Robert F. Furchgott,
Ferid Murad, and Louis J. Ignarro ).
Fat entering the bloodstream damages the endothelial cells, lowering the
nitric oxide concentration, and thus enabling plaques to form.
Brian Swale.
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