X-Message-Number: 13436
Date: Mon, 27 Mar 2000 23:16:09 -0500
From: mgdarwin <>
Subject: atherosclerosis and sugar

Doug Skrecky writes in response to George Smith:

From: Doug Skrecky <>
Subject: Stroke mortality, heart disease question

In Message #13417 "George Smith" <> wrote:

>> I have been given to understand that there may be a direct coorelation
>> between the increased incidence of heart disease in general to the
>> introduction of refined sugar in the diet of that culture.

>You may suspect that cardiovascular disease is a modern phenonmena.
>If that is the case, I would like to confirm that your suspicion is
>probably correct. The most primitive peoples appear to have a zero
>incidence of both ischemic heart disease, and stroke. I'm currently
>researching up this interesting fact, and will report on it further. 
>Sugar is not the villian, but it is not entirely clear what is. The
>case for the usual suspects (like animal fat) is surprisingly weak, 
>but several overlooked micronutrients look like they may be able to
>explain the lack of cardiovascular disease in primitives.

Thomas Donaldson argues that most primtive peoples do not live long enough
to develop atherosclerosis and Doug rebuts him.

Well, regardless of whether I wanted to or not, I've become an expert on
the subject. (If you define expert as being invited to speak all around the
world at legitimate medical conferences to intensivists, anesthesiologists
and cardiologists...)

The simplest answer is that the process is mulifactorial and NOT uniform.
In even in the highest risk populations there are subsets of people with
very high HDL/LDL levels who age blissfully into their 90's (or die of
something else first) and do not have a trace of atheroma. Apropos of
centenarians, I've seen a couple of their autopsies and their aortas, even
at the areas of maximal turbulence (= mamimal intimal injury = most likely
site for atheromas) are clean, as are their carotids and smaller caliber
vessels.

Animal fat (saturated fat)  DOES play a very significant role in
atherosclerosis whether Doug wants to believe it or not. The open question
is to what extent oxidized versus unoxidized fats contribute, as well as
co-factors.

As to ancient cultures not having atherosclerosis this so much balderdash!
A few months ago I spent quite some time face to face with Ramses II, the
Egyptian Pharoha whose massive egocentric building campaign lead Shelley's
to write his famous poem King Ozymandias (the 36 meter solid-block pink
granite collossus of Ramses at the Ramasseum was toppled in the great
earthquake of 27 BCE). 

 What was interesting was to look at the radiographs of his entire body; he
died somewhere between his mid 80's and late 90's probably from sepsis
secondary to a dental abcess that perforated his braincase. So extensive is
his atherosclerotic disease that his entire coronary tree is visible as a
calcified artifact. Ditto his femoral vessels!  I could even clearly
delineate his popliteal arteries bilaterally. His descending aorta looks
like a section of clay pipe. Both carotids and their external branches are
also visible due to calcification.

Surgar cane is a major internal crop in Egypt today; it was introduced
about 25 years ago :-). The only source of "sugar" Ramses and his similarly
athrosclerotic cohorts had was honey (mostly fructose) and fermented sugar
residues in wine. What they *did* have in abundance was meat, lots of
surplus calories, and probably rancid polyunsaturates in their diets. Not
to mention a sedentary lifestyle.

We see atherosclerosis frequently in primitive polulations such as those at
the Bahariya Oasis. Of the thousands of well preserved Graeco-Roman mummies
there, only 105 have been examined so far (they are doing it VERY carefully
and very thoughtfully). The community of 30,000 or so people at  Bahariya
had periods of severe malnutrition as indicated by interruption in bone
growth. They were agricultural people who lived largely in peace near the
end of the Roman empire. They have a ratio of atherosclerosis in the
population that survived past age 50 of about 45%. This is very close to
what it is in developed Western countries today.

It should also be noted that the Chinese noblewoman Madame Li, preserved so
well for nearly 2 thousand years in a mercurial liquid *died* of an acute
MI following a meal during which she consumed pork and  watermelon (some
very well preserved watrermellon seeds were recovered from her stomach
contents). There was no refined sugar around in any of these places.

Similarly, some native subsaharan hunter-gatherer populations also develop
atherosclerosis, albeit at a much decreased rate from that of affluent
nations.

So, what is the cause? The short answer is that we don't fully know. Deaths
from atherosclerotic disease began to decline sharply in the United States
well before dietary changes to reduce fat intake or public education
campaigns began. In fact, the best correlate is the introduction of the
synthetic antioxidant food preservatives (BHA and BHT) into foodstuffs
which, within a few years of approval,  correlates with a sharp downwad
trend in cardiovascular mortality which continues to this day.

By contrast, in India, where the diet has always been rich, heart disease
has reached astronomical levels with the mean age for sudden cardiac death
having dropped to between 36 and 38 years of age. The average age of a
bypass (CABG) patient in Bombay is arounf 44 years!  Most good hospitals do
8, 10, even 20 CABGs a day, not including angioplasties and stents! It is
interesting to note that NO synthetic preservatives are allowed in the
diet, and ghee (clarified butter) is a rich source of oxidized cholesterol.
Soimilarly, per capita calorie intake has skyrocked, and exercise has
decreased dramatically. 

Here are some factors which likely come into play in causing
atherosclerosis, not in any order of importance:

1) Heredity (bad HDL/LDL ratios).
2) Excess calorie consumption leading to elevated triglyceride (modest
effect).
3) Agriculture: this means starches and high glycemic index foods and GUM
DISEASE. Periodontal disease is a major cause of C-reactive protein
release, which definitely drives atherosclerosis.
4) Multiple bacterial and viral infections associated with crowded city
(agriculture-mediated) conditions. CMV and chlamydia have both been
implicated in atheromatous plaque formation, particularly in people with
low total cholesterols and good HDL/LDL ratios who would seem to be at low
risk of SCD.
5) While sugar has a bad reputation, many foods, like potatoes, cause much
larger swings in blood glucose and contribute to glycation of vessel
proteins. Glycation of intimal vessel proteins is a major driver of
atherosclerosis in diabetics and probably in normal people too.
6) Agriculture means less protective micronutrients since the people are
locked-into their immediate area and tend to deplete the soil of critical
trace elements with sustained agriculture.
7) Hunter-gatherers don't STORE food. Granaries are an artifact of
civilization. And with granaries come oxidized polyunsaturated fats.
Similarly, storage of "aged" rotten meat ("tenderized" for those of a
delicate disposition) is only possible with agriculture. Indeed, today's
best cuts of beef are "aged" in just this way and are sold in fancy
resturaunts at high prices!
8) Increased iron intake! Once you have heavy-duty access to meat and milk
you have a huge increase in iron. 20% of the population has iron storage
disease as it is (hemochromatosis)!  In fact, the ONLY protective effect of
estrogen on heart disease now appears to be that women menstruate when they
make endogenous estrogen and have far lower serum ferritin levels from the
blood loss!. Indeed, men who regularly give blood have heart disese risks
almost identical to those of pre- and immediately post-menopausal women.
Supplemental estrogen in post-menopusal women appears to confer little if
any protective effect against atherosclerosis and it increases the risk of
cancer. It used to be argued it helped with osteoporosis, but far better
and safer drugs are now available to build bone or stop its loss in post
menopausal women and in elderly men too!
9) Salt and hypertension. Hunter-gatherers are marginal on salt intake.
Civilized peoples prize salt and uniformyly use it to vast excess. A
subfraction of these people develop sodium-mediated hypertension which
definitely contributes to atherosclerosis.

I could go on and on, but the point is, this is a multifactorial disease.
The good news is that the statin drugs dramatically reduce mortality,
morbidity and even the occurrence of atherosclerosis. The statin drugs have
resulted in a big transient dip in the US overall death rate which has
adversely impacted the business well-being of mortuary conglomerates
(stocks deropped big time when the projected death rate fell!). The statins
are squaring the curve along no doubt with supplementation of vitamin E,
folic acid (lower homocysteine levels) and selenium. 

Mevacor (a prototypical statin) was even shown to reduce crdiovascular
death in people not at known risk for it! More recently, the statins have
been shown to have a multiplicity of unexpected effects, including
up-regulatig endogenous nitric oxide in endothelial cells and
down-regulating inducible nitric oxide (NO) in ischemic tissue. That means
more circulation to atherosclerotic tissues, less NO mediated free
radicals, and, if a heart attack or stroke does occur, the infarct size is
smaller in both heart and brain (BTW estrogen DOES decrease brain infarct
size in stroke even when given to male animals within ~2 hours of the
stroke).

My best advice to people with a family history of atherosclerosis is to
start on a statin drug. The newer ones work in very small quantities and
are cheaper, but no one has done the extensive epidemiological studies that
have been done with Mevacor and the earlier statins.

And if there is one thing a cryonicist DOES NOT want to die of it is sudden
cardiac death (half of all first heart attacks are fatal) or worst of all,
a stroke. Especially not a stroke where you survive a few days and your
brain macrophages are gobbling up the injured neurons by the gram.

Mike Darwin

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