Saturated fat prevents coronary artery disease? An American paradox

It is an article of faith that saturated fat raises LDL cholesterol and
accelerates coronary artery disease, whereas unsaturated fatty acids have
the opposite effect (1, 2). One of the earliest and most convincing studies
of the better efficacy of unsaturated than of saturated fat in reducing
cholesterol and heart disease is the Finnish Mental Hospital Study conducted
in the 12 y between 1959 and 1971. In this study, the usual
high-saturated-fat institutional diet was compared with an equally high-fat
diet in which the saturated fat in dairy products was replaced with soybean
oil and soft margarine and polyunsaturated fats were used in cooking. Each
diet was provided for 6 y and then the alternate diet was provided for the
next 6 y (3). After a comparison of the effects of the 2 diets in both men
and women, the incidence of coronary artery disease was lower by 50% and 65%
after the consumption of polyunsaturated fat in the 2 hospitals.

In this issue of the Journal, Mozaffarian et al (4) report the opposite
association. They found that a higher saturated fat intake is associated
with less progression of coronary artery disease according to quantitative
angiography. How can this paradox be explained? In food-frequency
questionnaires, saturated fat intake is more precisely estimated than is
total fat. If saturated fat is more precisely estimated, it will associate
more strongly in statistical analyses with the outcome variable, even though
other variables-such as total fat or carbohydrate-could be more relevant
physiologically. We believe that these possibilities deserve a closer look.

Unlike the diet used in the Finnish Mental Hospital Study, the diet
described by Mozaffarian et al was low in fat, averaging 25% of energy. The
study subjects were women with coronary artery disease: most were
hypertensive, many had diabetes (19-31%), their body mass index (kg/m2)
ranged from 29 to 30, and their lipid profile indicated combined
hyperlipidemia (triacylglycerol concentration: 200 mg/dL; HDL-cholesterol
concentration: 40-50 mg/dL; above-average LDL concentration: 135-141 mg/dL);
these characteristics are consistent with the metabolic syndrome. In
addition, two-thirds of these women were taking sex hormones. The importance
of each of these points is addressed below.

What are the effects of a low-fat, high-carbohydrate diet in comparison with
those of a higher-fat, lower-carbohydrate diet? The response differs by the
2 main types of hyperlipidemia: simple hypercholesterolemia and combined
hyperlipidemia. In our studies of simple hypercholesterolemia in men, a fat
intake 25% of energy and a carbohydrate intake 60% of energy was
associated with a sustained increase in triacylglycerol of 40%, a decrease
in HDL cholesterol of 3.5%, and no further decrease in LDL in comparison
with higher fat intakes (5). In contrast, a low-fat diet in persons with
combined hyperlipidemia caused no worsening of triacylglycerol or HDL, but
intakes of fat 40% of energy and of carbohydrate 45% of energy for 2 y
were associated with a lower triacylglycerol concentration at a stable
weight (6). In the subjects of Mozaffarian et al, a greater saturated fat
intake paralleled a total fat intake, which ranged from 18% to 32% of energy
in the first to fourth quartiles. Modest favorable trends in triacylglycerol
and HDL-cholesterol concentrations were observed with higher fat intakes.

Triacylglycerol and HDL-cholesterol concentrations are stronger predictors
of coronary artery disease in women, whereas the LDL-cholesterol
concentration is a stronger predictor in men (7). Because VLDL
triacylglycerol secretion and removal rates in healthy women are double
those of men (8), conditions impairing lipoprotein removal would be expected
to exaggerate the hyperlipidemic response in women as compared with that in
men (9). This sex difference is seen with the development of diabetes. The
increment in lipids is greater in women than in men and is associated with a
greater increment in coronary artery disease risk in women than in men (9).
Similarly, the development of insulin resistance and obesity is associated
with a greater lipoprotein increment in women than in men (10). The
exaggerated decreases in HDL- and HDL2-cholesterol concentrations observed
with the consumption of a low-fat Step II diet in women but not in men
appear to be another facet of this effect (11).

The failure of female sex hormones to prevent coronary artery disease has
been a great disappointment (9). This effect might also be due to an
estrogen-induced increase in lipoprotein entry against a fixed or impaired
rate of lipoprotein removal, as might be expected in women with the
metabolic syndrome and coronary artery disease.

Would saturated fat still be bad for anyone? Not necessarily. The effect of
saturated fat and cholesterol ingestion in the form of 4 eggs/d for 1 mo in
obese, insulin-resistant subjects is 33% of that seen in lean,
insulin-sensitive subjects, likely because of diminished cholesterol
absorption (12). Thus, the classic effects of saturated fat as compared with
those of unsaturated fat seen in the Finnish Mental Hospital Study are
likely blunted in the subjects of Mozaffarian et al, whereas the effects of
low fat and high carbohydrate intakes on triacylglycerol and HDL-cholesterol
concentrations appear to be exaggerated by the interactions of female sex,
exogenous sex hormones, and the metabolic syndrome. A major effect on
cardiovascular disease risk would be the result of hypertriglyceridemia and
low HDL-cholesterol concentrations, which are attenuated by an increase in
saturated fat intake itself or in total fat intake, for which saturated fat
is a more statistically stable surrogate (4).

In conclusion, the hypothesis-generating report of Mozaffarian et al draws
attention to the different effects of diet on lipoprotein physiology and
cardiovascular disease risk. These effects include the paradox that a
high-fat, high-saturated fat diet is associated with diminished coronary
artery disease progression in women with the metabolic syndrome, a condition
that is epidemic in the United States. This paradox presents a challenge to
differentiate the effects of dietary fat on lipoproteins and cardiovascular
disease risk in men and women, in the different lipid disorders, and in the
metabolic syndrome.



http://www.ajcn.org/cgi/content/full/80/5/1102

This is nothing new. Read some of my posts. Search this group for
montygram. Even AHA spokesman are saying now that oxidized cholesterol
is the problem, and PUFAs can oxidize cholesterol, but saturated fatty
acids cannot. However, there is a big difference between lard and
coconut oil, though both are called "saturated fat." Coconut oil is
92% saturated, and so is very healthy. Lard is at least 60%
unsaturated, and so should be avoided (it also has no antioxidant
protection). Do not cook any food with cholesterol in it while exposed
to air (boiling is okay). Avoid baked goods that contain eggs, cheese,
milk, etc. - this is very bad stuff. Here are a couple of many studies
making this point:

Oxidized LDL contains inflammatory PAF-like phospholipids.
Trends Cardiovasc Med 2001 Apr-May;11(3-4):139-42
Marathe GK, Prescott SM, Zimmerman GA, McIntyre TM.


Department of Pathology, University of Utah, Salt Lake City, Utah, USA.



Atherosclerosis has an underlying inflammatory component. Oxidation of
low-density lipoprotein (LDL) particles to modified forms promotes
atherogenesis by supplying cholesterol and through the oxidative
generation of agents that activate macrophages, smooth muscle and
endothelial cells. A primary target of oxidizing compounds, derived
from cigarette smoke, dietary sources, exuberant inflammatory cell
responses and normal cellular metabolism among other sources, are the
esterified polyunsaturated fatty acids in the phospholipid shell that
surrounds the insoluble lipids of the lipoprotein core. One type of
phospholipid oxidation product mimics the structure of the potent
inflammatory mediator platelet-activating factor (PAF), and these
oxidation products activate the PAF receptor found on platelets,
monocytes and leukocytes. Production of such PAF mimetics is, in
contrast to the physiologic generation of PAF, uncontrolled. PAF
mimetics and other phospholipid oxidation products are found in
atherosclerotic lesions or even in blood after exposure to cigarette
smoke. Here we summarize our data describing the structure, activity
and metabolism of the PAF-like lipids found in atherogenic LDL
particles.


Ital Heart J 2001 Dec;2(12):867-72
Low-density lipoprotein oxidation.


Iuliano L, Micheletta F, Violi F.


Istituto di I Clinica Medica Universita degli Studi La Sapienza
Policlinico Umberto I Viale del Policlinico, 155 00161 Roma.


Free radical mediated oxidation of low-density lipoproteins (LDL),
which has been extensively studied in the last two decades, plays a
central role in the development of the atherosclerotic plaque.
Oxidation involves the lipid moiety of LDL in a chain reaction
mechanism. In the initial phase, free radicals preferentially attack
highly oxidizable polyunsaturated fatty acids. Subsequent recruitment
of other molecules includes cholesterol and phospholipids. The process
of oxidation is counteracted by antioxidants present in LDL.
By-products formed during oxidation of LDL lipids, which may have
biological activity, react with amino acid residues of the LDL protein
backbone with the consequent modification of chemical and immunological

properties responsible for cellular receptor shift. Oxidation-altered
apolipoprotein B of oxidized LDL is, in fact, recognized by the
macrophage scavenger receptor responsible for foam cell formation. The
mechanism of LDL oxidation and the impact on atherogenesis are
discussed.

cardarch wrote:

I dont get what is happening here.

What's happening is scientists finally noticed that carb levels
count, so they are redoing large numbers of studies to see if
fat is a problem when not combined with high carb.

I thought there was much research
to show that saturated fat in the diet turns to LDL cholesterol which
is largely responsible for creating the inflammation in arteries that
causes plaque to form that causes arteriosclerosis.

All of which was studied using high carb food plans. And so
they demonstrated that high-carb plus high-fat together is
a problem. You could have asked either low carbers or low
fatters that question and gotten the answer long ago.

Now there is the Mozaffarian study of postmenopausal women with
coronary disease. They respond well to a high fat diet especially high
saturated fat because it creates higher HDL. Is it because these women
already have compromised cardiovascular systems and are obese?

A high-fat medium-protein low-carb diet is very good at
improving cholesterol numbers. That's been quite consistent
in around 80% of folks doing Atkins and similar low carb
plans.

What are we to believe?

That scientists have started studying stuff other than variations
on low fat and have started producing results that are already
in bunches of low carb books.

One thing I'd hesitate to believe - studies that conclude that low
fat is unhealthy. It should only be unhealthy when plenty of
junk products with "low fat" on the label that substituted extra
carbs for the lower fat. Studies should show that either low
fat or low carb work and are healthy, but that they work in
different ways and grant different health benefits.

"cardarch" wrote in message
ups.com...
I dont get what is happening here. I thought there was much
research
to show that saturated fat in the diet turns to LDL cholesterol
which
is largely responsible for creating the inflammation in arteries
that
causes plaque to form that causes arteriosclerosis. It seems like
the
Not correct. All forms of cholesterol are actually members of the
alcohol family of substances. This particular form of alcohol is
not soluble in water (the basis of our blood). Cholesterol is an
absolutely necessary component of every cell in our bodies.

Our livers manufacture the majority of the cholesterol (and break
down and dispose of the "used" stuff) in our blood stream. Yes. A
little can be added by diet, but it's not like you eat a stick of
butter or pork fat and chunks of "fat" end up in your arteries.
Only digested fats in the form of EFA's can cross the intestinal
barrier. Consequently all of the 'anti-fat' or anti-saturated fat'
propaganda is a fraud at best, and tragedy at worst. Our bodies
absolutely need fats. They are the only material that's absolutely
essential for cellular construction and/or repair. Makes ya wonder
how the fraud of "eat low-fat" lasted so long...and the permanent
damage it caused...think: ADD/ADHD...while considering that your
brain and nerve cells are more than 80% fat...

Further; there is no such thing as "good" vs. "bad" cholesterol.
That's simply a propaganda piece put out by folks that want your
drug dollar. Nor is there a single study that's ever found a
connection to "out of balance" cholesterol levels and heart disease.
Not a one! Nor is there any study that demonstrates that your serum
cholesterol levels are the cause of arteriosclerosis. That damage,
seems to be caused primarily by out of control insulin levels (among
other factors). The cholesterol that ends up in there was simply
put there as a patch, by the body cells, to try to fix things.

Every cell absolutely, positively MUST get some cholesterol each
day, else it dies (or won't be created). In fact, IIRC; cholesterol
is so important that every cell in your body except your brain cells
can manufacture some of their own. Since cholesterol isn't soluble
in blood, it needs another vehicle to get it to where it's going.
It does this by getting inside of a lipoprotein globule (think:
submarine). The "bad" LDL transports cholesterol from your liver to
your outlying tissues. The "good" HDL transports it back from the
cells that used it to the liver where it either gets reprocessed or
excreted as bile. That's just the flip side of the same job. How
one got to be "good" and the other "bad" is something only a PR
agency could know.

There is very little that varying the fat content of your diet can
do to change your cholesterol levels. If you ingest less (a
relatively small fraction to begin with), then your liver simply
cranks up the generation mechanism and makes more. The various
statin drugs can and do lower/alter cholesterol levels...but at the
cost of other less desirable side-effects. The biggest thing that
can effect your cholesterol levels is exercise. The next best
thing, given that your liver manufactures it from it's favorite
"food" or "feed-stock" (read: glucose), is reduce your intake of
carbohydrates. And that is, after all, why most of us are reading
here...right?

8 year study of women reported in the Journal of the American
Medical
Association showed that lowering fat in the diet didnt do anything
for
the cardiovascular health of the women although they didnt
differentiate between types of fat and the women didnt stick to
the low
fat diet and it was all self reported. So...that study doesnt
hold
water. Now there is the Mozaffarian study of postmenopausal women
with
coronary disease. They respond well to a high fat diet especially
high
saturated fat because it creates higher HDL. Is it because these
women
already have compromised cardiovascular systems and are obese?
What
are we to believe?
Believe that your body is doing its best to give you a long and
healthy life. And for that long and healthy life, eat and enjoy
plenty of fats and oils along with your veggies, fruits, and meats
of all kinds; and eschew carbohydrates. Add to that some exercise,
and you'll be on your way to the best outcome your personal version
of a body can deliver. All the rest is "BS" at best.

So, enjoy an egg fried in butter, and lard in your pie crusts
instead of trans-fat laden "shortening" (the only "shortening" it
does is to your life-span). I could go on...but I'm getting
hungry...(:-o)!


L8r all,
DustyB

Dusty Bleher wrote:
"cardarch" wrote in message
ups.com...

I dont get what is happening here. I thought there was much
research
to show that saturated fat in the diet turns to LDL cholesterol
which
is largely responsible for creating the inflammation in arteries
that
causes plaque to form that causes arteriosclerosis. It seems like
the

Not correct. All forms of cholesterol are actually members of the
alcohol family of substances. This particular form of alcohol is
not soluble in water (the basis of our blood). Cholesterol is an
absolutely necessary component of every cell in our bodies.

http://en.wikipedia.org/wiki/Cholesterol


Actually, cholesterol (the 'simple chemical') is technically an alcohol
because of an OH group, it is also technically a steroid from the ring
structure part of the molecule, and it has a fatty hydrocarbon or lipid
"tail".
It can be said to be an alcohol and a steroid (ie: a sterol) and a
fatty substance(lipid).

No extra charge for the multiple chemical traits.




Our livers manufacture the majority of the cholesterol (and break
down and dispose of the "used" stuff) in our blood stream. Yes. A
little can be added by diet, but it's not like you eat a stick of
butter or pork fat and chunks of "fat" end up in your arteries.
Only digested fats in the form of EFA's can cross the intestinal
barrier. Consequently all of the 'anti-fat' or anti-saturated fat'
propaganda is a fraud at best, and tragedy at worst. Our bodies
absolutely need fats. They are the only material that's absolutely
essential for cellular construction and/or repair. Makes ya wonder
how the fraud of "eat low-fat" lasted so long...and the permanent
damage it caused...think: ADD/ADHD...while considering that your
brain and nerve cells are more than 80% fat...

Further; there is no such thing as "good" vs. "bad" cholesterol.
That's simply a propaganda piece put out by folks that want your
drug dollar. Nor is there a single study that's ever found a
connection to "out of balance" cholesterol levels and heart disease.
Not a one! Nor is there any study that demonstrates that your serum
cholesterol levels are the cause of arteriosclerosis. That damage,
seems to be caused primarily by out of control insulin levels (among
other factors). The cholesterol that ends up in there was simply
put there as a patch, by the body cells, to try to fix things.

Every cell absolutely, positively MUST get some cholesterol each
day, else it dies (or won't be created). In fact, IIRC; cholesterol
is so important that every cell in your body except your brain cells
can manufacture some of their own. Since cholesterol isn't soluble
in blood, it needs another vehicle to get it to where it's going.
It does this by getting inside of a lipoprotein globule (think:
submarine). The "bad" LDL transports cholesterol from your liver to
your outlying tissues. The "good" HDL transports it back from the
cells that used it to the liver where it either gets reprocessed or
excreted as bile. That's just the flip side of the same job. How
one got to be "good" and the other "bad" is something only a PR
agency could know.

There is very little that varying the fat content of your diet can
do to change your cholesterol levels. If you ingest less (a
relatively small fraction to begin with), then your liver simply
cranks up the generation mechanism and makes more. The various
statin drugs can and do lower/alter cholesterol levels...but at the
cost of other less desirable side-effects. The biggest thing that
can effect your cholesterol levels is exercise. The next best
thing, given that your liver manufactures it from it's favorite
"food" or "feed-stock" (read: glucose), is reduce your intake of
carbohydrates. And that is, after all, why most of us are reading
here...right?


8 year study of women reported in the Journal of the American
Medical
Association showed that lowering fat in the diet didnt do anything
for
the cardiovascular health of the women although they didnt
differentiate between types of fat and the women didnt stick to
the low
fat diet and it was all self reported. So...that study doesnt
hold
water. Now there is the Mozaffarian study of postmenopausal women
with
coronary disease. They respond well to a high fat diet especially
high
saturated fat because it creates higher HDL. Is it because these
women
already have compromised cardiovascular systems and are obese?
What
are we to believe?

Believe that your body is doing its best to give you a long and
healthy life. And for that long and healthy life, eat and enjoy
plenty of fats and oils along with your veggies, fruits, and meats
of all kinds; and eschew carbohydrates. Add to that some exercise,
and you'll be on your way to the best outcome your personal version
of a body can deliver. All the rest is "BS" at best.

So, enjoy an egg fried in butter, and lard in your pie crusts
instead of trans-fat laden "shortening" (the only "shortening" it
does is to your life-span). I could go on...but I'm getting
hungry...(:-o)!


L8r all,
DustyB










--
1) Eat Till SATISFIED, Not STUFFED... Atkins repeated 9 times in the book
2) Exercise: It's Non-Negotiable..... Chapter 22 title, Atkins book
3) Don't Diet Without Supplimental Nutrients... Chapter 23 title, Atkins
book
4) A sensible eating plan, and follow it. (Atkins, Self Made or Other)