From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.cardiology,sci.med
Subject: Re: dietary fat & cardio deaths: quality not quantity
Date: 21 Jan 2005 20:04:39 -0800
Message-ID: <1106366679.106920.217530@c13g2000cwb.googlegroups.com>

COMMENT:

It's way too complicated a subject to discuss fully. The short form
(which I can't do justice, so this is only approximate) is that
vascular aging per se in absense of atherosclerosis can be studied in
animals like the rat that don't get atherosclerosis or hypertension on
standard diets. As they age, you can see standard "successful aging"
which thickens the artery lining "intima" a bit, and causes the main
wall "media" to expand and lose some elasticity. None of these things
is enough to cause increases in pressure. Actually, what typically
happens is diastolic pressure drops and systolic pressure remains the
same, so that pulse pressure (systolic minus diastolic, or upper number
minus lower one) increases a little without any hypertension. This
happens as blood pressure characteristics come to be set by the large
arteries and their characteristics in advanced "healthy" aging, as
opposed to being set by small artery tone.

This is pretty much what happens in humans in the absense of disease,
with aging. It's what is seen in undeveloped countries in people on a
very low fat diet, who never get atherosclerosis or hypertension.
Normal aging is a pulse pressure of 40 at age 40 and about 60 at age
80. Anything above a pulse pressure of around 80 at 80 usually means
there's some artery damage by more than healthy aging.

By what? Well, hypertension itself, and diabetes, both cause worse
intimal thickening and worse elasticity, so it looks like aging
changes, but worse.

Atherosclerosis, a local fatty-tumor-like injury disease disease in
blood vessels, has many causes, but starts with injury to the intima
due to flexion or hypertension or chemical causes. You see it where
arteries flex a lot, like the neck, the groin or knee, or in the
bouncing heart. It starts with infiltration of the intima with foamy
lessions, which eventually coalese into plaques.These are generally
non-concentric and bulge into the artery from one side. This does NOT
in an of itself increase the pressure. If blood can't go through, it
just doesn't. Systemic pressure increases per se (systolic and
diastolic increases) are due to disease mechanisms of other types,
occuring in the smaller arteries, NOT due to disease like
atherosclerosis in larger arteries. These pressure increases in turn
cause damage (intimal thickening and loss of elasticity) in larger
arteriies, as above, but cause and effect are in the direction
indicated. The pressure increases cause the thickening in large vessels
but not the reverse (the thickening and elasticity loss per se causes
increased pulse pressure, but NOT hypertension). Similarly,
hypertension also causes atherosclerosis, but NOT the other way around
(with the exception occasionally of lessions in kidney arteries which
directly cut off the kidney blood pressure sensing mechanisms, and can
result in high blood pressure that way-- but this is rare and generally
isn't the way it happens).

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: soc.culture.indian,alt.fan.jai-maharaj,misc.health.alternative,
	sci.med.cardiology,sci.med
Subject: Re: Blueberries lower LDL cholesterol better than statin drugs
Date: 27 Jan 2005 16:01:13 -0800
Message-ID: <1106870473.303658.218160@f14g2000cwb.googlegroups.com>

Arteriosclerosis is not a disease but a general wastebasket term for at
least 3 varieties of a hardening of the arteries by some pathological
mechanism. It's not a very useful term, since even normal aging hardens
arteries somewhat by making them thicker and less elastic. However this
normal aging process is not normally considered arteriosclerosis.

Atherosclerosis is named for atheroma-- a sort of Greek gruel. The junk
in the center of placques reminded somebody (Virchow?) of that. Risk
factors are the usual ones for heart disease.

For descriptions of the less common kinds of arteriosclerosis, which
are arteriolar sclerosis (which affects small vessels and has
hypertension as main risk factor), and also for the Monckeberg
arteriosclerosis which involves calcification of larger arteries and
looks horrible on X-ray but actually isn't clinically all that
important, see:

http://www.well-net.com/cardiov/arterios.html