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Subject:
From:
Jim Walsh <[log in to unmask]>
Reply To:
Paleolithic Eating Support List <[log in to unmask]>
Date:
Mon, 6 Aug 2001 10:01:22 +0930
Content-Type:
text/plain
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"Todd Moody [log in to unmask] " wrote:
>
> On Sun, 5 Aug 2001, Jim Walsh wrote:
>
> Concerning asymptomatic CHD, I stand corrected.
>
> > > One of the points that Ravnskov makes, which is often overlooked,
> > > is the fact that the Japanese, who have far fewer heart attacks,
> > > angina, etc., than Americans, are just as atherosclerotic.
> >
> > Do you have any references to his material? I would be interested to read up on this.
>
> As Dori said, his book, _The Cholesterol Myths_, is my source.
> It is profusely documented with references to the literature.
> The point about the Japanese has a citation of: I. Gore, AE
> Hirst, Y. Koseki.  Comparison of aortic atherosclerosis in the
> US, Japan, and Guatemala.  American Journal of Clinical Nutrition
> 7, 50-54, 1959.

Thanks... on my list of "homework"!  :)


> > > Furthermore, plenty of people have heart attacks, fatal and
> > > nonfatal, and angina -- who have little or no measureable
> > > atherosclerosis.
> >
> > Again, I would be interested in references for this. Ischemic
> > events are not unheard of without atherosclerosis, (prinzmetal's
> > angina) but I from my understanding it is very rare. (Around 25%,
> > meaning that 75% *do* have atherosclerosis.)
>
> 25% hardly qualifies as very rare.  If one person in four has a
> heart attack without appreciable atherosclerosis, that's a
> significant chunk of the heart disease population.

Sorry, I didn't explain myself very well. Prinzmetal's angina, (angina
caused by coronary spasm) is rare. Of the (rare) group that experience
prinzmetal's angina, 75% have atherosclerosis. The remaining 25% of that
rare group (sufferers of prinzmetal's angina) would be *more* rare.

The effect of a very small amount of artherosclerotic narrowing (5%) could make the difference between a 50% open or completely closed artery when constricted. So, at best, artheroslerosis severely comlicates vasospasm.


> > > We are indoctrinated to think of "blocked arteries" as the cause
> > > of heart attacks, but it is not so simple.  A heavily plaqued
> > > artery does have reduced blood flow, but in many cases this is
> > > not a problem because the heart develops collateral vascularity
> > > -- additional blood vessels to compensate for the reduced blood
> > > flow.  This is believed to be the reason why heart attacks in
> > > younger men are more likely to be fatal: There has not been time
> > > for much collateral vascularity to develop.
> >
> > Collateral vessels are the bodies attempt to repair the problem
> > (artherosclerosis). It is important to note that the bodies attempt
> > rarely (probably never) manages to keep up with the process of
> > artheroslerosis. (Resulting in a net deficiency of blood flow to
> > the heart muscle.)
> >
> > > The immediate cause of angina and heart attacks is not blockage
> > > of the arteries, but *constriction* of them.
> >
> > In some cases yes, in *many* others, no.
> >
> > Severely narrowed arteries can cause such a deficiency of blood
> > flow to the heart that angina can and does result without vasoconstriction.
>
> Yes.  Here I should distinguish angina and heart attacks.  Even
> in people with advanced atherosclerosis, angina tends to come and
> go, according to exertion, stress, etc.  We don't know about
> angina in animals, but we do know about heart attacks, which are
> difficult to induce by means of atherosclerosis.

However, it is possible to have a heart attack by simply ignoring
angina, and "soldiering on". Under those conditions, the reduced blood
flow to the heart (caused by the artherosclerosis) would eventually
result in some heart tissue dying (heart attack). No blockage or spasm
required.

> > It is also known that an artery suffering from atherosclerosis,
> > does not respond correctly to the chemical released by the body
> > to dialate blood vessles. (They will constrict, even when the
> > body is telling them to dialate!)
>
> I didn't know that.  Very interesting.
>
> > > It is very difficult -- almost impossible -- to cause heart
> > > attacks in animals by diet alone.  To do that, you must stress
> > > them.  Stress hormones cause vascular constriction.
> > > Prostaglandin imbalance causes vascular constriction.  Stimulants
> > > cause vascular constriction (probably by means of the other two).
> >
> > I agree totally that stress is a major player in heart disease.
> > (I believe that I am proof positive of that.) Medical science has
> > great difficulty with "stress" because it is so difficult to
> > objectively quantify.
>
> AMbient levels of stress hormones is one way.  This,
> incidentally, is probably a reason to avoid long-term deep
> ketosis.  The stress hormone cortisol is the signal for
> gluconeogenesis to occur.  If gluconeogenesis has to occur pretty
> much continuously, then this hormone will tend to be elevated
> continuously, which is not a good thing, in my view.

Hmmm... mental note made.

>
> > I also believe that stress will accelerate the growth of artherosclerotic plaques.
>
> Yes.  And stress drives up cholesterol levels very effectively.
>
> > > It is well known, but not much advertised, that the most
> > > significant risk factors for heart disease are not dietary.
> > > We've known about the hard-driven "type A personality" for years,
> > > for example.
> >
> > Agreed.
> > That was me 12 years ago, when I had my first heart attack (at 30 yo).
> >
> > > We know that job satisfaction is a major factor.
> > > We know that divorces, loss of loved ones, and the like are all
> > > risk factors for acute heart disease.  Atherosclerosis may make
> > > us more vulnerable, but it is apparently not a key player.
> >
> > I can't go along with "not a key player".
> >
> > Certainly artherosclerosis is not the "be all and end all" of heart
> > disease, but (IMHO) it is certainly a "key player".
>
> Fair enough.  I was thinking in terms of the "Japanese paradox".
> If they are as atherosclerotic as we are, and yet have much lower
> rates of fatal and non-fatal heart attacks, then the explanation
> of the difference must be something other than atherosclerosis.
> But you're right; I don't want to give the impression that
> atherosclerosis is *irrelevant* to heart attacks either.
>
> > A prime example is myself. If I could snap my fingers right now
> > and make the artherosclerosis disappear from my arteries, I would
> > instantly gain about 80% functionality. I am disabled by the lack
> > of blood supply to my heart, not the scars on my heart, nor
> > vasoconstriction.
>
> I hope that finger-snapping works, and I defer to your more
> direct experience of this.
>
> I'll be going nomail this evening, but maybe we can pick up the
> conversation again in two weeks when I return from vacation.

If this mail catches you before you go, I hope you have a great trip.
(Actually, I hope you have a great trip even if you miss this!)  :)

> I'll be in Austria and Paris, eating much forbidden fruit, no
> doubt.


Bye for now,
Jim.

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