Sat Fat Killed Mrs. Sprat

[George Che]

This is worth repeating.

One High-Saturated Fat Meal Can Be Bad By JOE MILICIA,
Associated Press Writer Mon Aug 7, 10:52 PMUPDATED 13 HOURS 52
MINUTES AGO

CLEVELAND - Eating just one meal high in saturated fat _ in
this case, carrot cake and a milkshake _ can quickly prevent
"good" cholesterol from protecting the body against clogged
arteries, a small study shows.

The results of the research weren't a surprise to the experts,
but they say the findings reaffirm something that more people
need to understand:

"What we put into our mouth makes a big difference in terms of
our health," said Dr. Charles McCauley, a cardiologist with
Marshfield Clinic in Wisconsin, who reviewed the research but
wasn't involved with the study. "We really have to be very
careful as to how our food is processed and what kind of
ingredients we use."

In the study, at The Heart Research Institute in Sydney,
Australia, 14 people, ages 18-40, ate two meals of carrot cake
and a milkshake one month apart. One meal was high in
saturated fat _ using coconut oil _ and the other was high in
polyunsaturated fat _ using safflower oil.

Saturated fat has long been linked to the buildup of plaque
that can lead to heart attacks and strokes. HDL, the "good"
cholesterol, protects arteries from the inflammation that
leads to artery-clogging plaques. And plaque hurts the ability
of arteries to expand to carry blood to tissues and organs.

The researchers, led by Dr. Stephen Nicholls, a cardiologist
now at the Cleveland Clinic, found that three hours after
eating the saturated-fat cake and shake, the lining of the
arteries was hindered from expanding to increase blood flow.
And after six hours, the anti-inflammatory qualities of the
good cholesterol were reduced.

But the polyunsaturated meal seemed to improve those
anti-inflammatory qualities. Also, fewer inflammatory agents
were found in the arteries than before the meal.

"They're looking at things in terms of real live living," said
McCauley. "Carrot cake. How more real does that get?"

The study appears in the Aug. 15 issue of the Journal of the
American College of Cardiology.

"It's a simple study. Sometimes the best studies are those
that are very straightforward," said Dr. Richard Milani,
head of preventive cardiology at Ochsner Clinic Foundation
in New Orleans.

He notes that the research isn't suggesting that people eat a
steady diet of carrot cake and milkshakes.

However, he said, "given a choice between something with
polyunsaturated fat and saturated fat, please avoid the
saturated fat."

Nicholls said "the take-home, public-health message is this:
It's further evidence to support the need to aggressively
reduce the amount of saturated fat consumed in the diet."

Saturated fats are found mostly in food from animals,
including beef, pork, lard, poultry fat, butter, milk and
cheeses, and some plants, including coconut oil, palm oil and
cocoa butter.

Polyunsaturated fats are found in oils from plants, including
safflower, sesame and sunflower seeds, corn and soybeans, many
nuts and seeds.

Dr. James O'Keefe, a cardiologist at the Mid America Heart
Institute in Kansas City, said Nicholls' study shows "a
really important concept _ when you eat the wrong types of
food, inflammation and damage to the vessels happens
immediately afterward."

Too many people simply are eating the wrong kind of fats,
O'Keefe said.

"Even one meal of a double cheeseburger with fries and a Coke
will mess up your system, let alone a steady diet of it, which
is recipe for disaster," O'Keefe said.

___

On the Net:

American Heart Association: http://www.americanheart.org/

Journal of the American College of Cardiology:
http://www.cardiosource.com/jacc/index.asp

The Heart Research Institute: http://www.hri.org.au/

Copyright 2006 The Associated Press. All rights reserved. This
material may not be published, broadcast, rewritten or
redistributed.

[monty1945]

This is the latest example of what is wrong with the
"nutritional science" establishment these days, as well as
with the mainstream media. Notice that the media reports "play
up" the notion that one meal rich in coconut oil could cause
terrible damage, the kind that leads to heart disease. Aren't
journalists supposed to research such claims before they make
them? If they had just gone to the WHO's web xsgtie, they
would be able to see that peoples who consume diets very rich
in saturated fatty acids (from coconut) have the lowest rates
of not only heart disease, but also cancer, diabetes, etc.
Then there are studies that were done on Asians who ate
"primitive" diets very rich in coconut, had "high
cholesterol," and yet no heart disease. But they don't mention
such on overwhelming evidence. Instead, they are very
impressed by two meals that were consumed by a small number of
people. There is also a condemnation of "saturated fat," even
though this has no meaning. For example, they say that lard
and coconut oil are "saturated fat," yet lard, at 39%
saturated, isn't that much more saturated than chicken when
compared to coconut oil, which is 93% saturated. Thus, those
on coconut oil based diets should be dropping dead like flies,
considering how terribly damaging this report makes coconut
oil seem. Instead, people who consume coconut oil, and not any
oil rich in unsaturated fatty acids, hardly have any incidence
of heart disease. Even in the USA today, there are peoples
like the Amish who eat a "traditional diet" rich in saturated
fatty acids and have much lower rates of heart disease. I have
been purposely packing my body with saturated fatty acids
since 2001 (and avoiding all major sources of polyunsaturated
fatty acids) and have seen many benefits, but have had no
health problems, despite avoiding omega 3 PUFAs nearly
entirely (in other words, I should have signs of "essential
fatty acids deficiency," but instead have only seen various
chronic problems vanish).

In fact, as AHA spokesman Dr. Richard Stein stated explicitly
several months ago, only oxidized cholesterol is a problem,
and polyunsaturated fatty acid-rich oils will contribute to
cholesterol oxidation, while coconut oil will not. Lard,
however, is a potential problem because it is only 39%
saturated. Few Americans consume a fat source that is very
saturated, like coconut oil, but instead in most studies of
Americans, the difference between the "high saturated fat"
group and the low one is minimal. Generally speaking,
Americans who consume a lot of lard are unhealthier than those
who consume more fish, but this is related to cooking
techniques and socio-economic factors. Bruce Fife, in his
book, "Saturated fat may save your life," pointed out that one
study found that those who consumed fried fish had a higher
risk of heart attacks than anyone else. This is why you should
boil meat an d eggs, and avoid powdered eggs and dairy, as
well as homogenized dairy.

So why are they making these ridiculous claims, leaving aside
their ignorance of the scientific literature with which they
are supposed to be experts? A major problem is that today
most such studies examine "markers" only, which means that if
the markers are based upon flawed assumptions, the results
may be worse than useless. As in this case, the results may
in fact mislead people into doing the opposite of what is
really healthy. A common example of this is the use of serum
cholesterol. If a food raises serum cholesterol (almost all
of these kinds of studies are short term, keep in mind), it
is said to "raise" the person's "risk" of heart disease.
However, since it is now known that only oxidized cholesterol
can do this, such a study is nearly worthless. Moreover, as
Ancel Keys himself discovered, a serum cholesterol level
lower than about 200 means a higher risk of dying from other
things, such as shock due to trauma as well as cancer. But
the mainstream media fails to report this, though the voices
of a few journalists who are competent are sometimes heard
dimly (see Thomas
J. Moore's book, "Heart Failure," for example.

Now I'll take a look at one of these reports: "according to
the research, eating a meal high in polyunsaturated fat, a
healthier form of fat, can increase the anti-inflammatory
properties of HDL, helping to protect the inner lining of the
arteries, called the endothelium, from plaque buildup"

How can (polyunsaturated fatty acids) PUFAs increase the
"anti-inflammatory" properties of HDL? Inflammation is
possible due to PUFAs, not saturated fatty acids (SFAs), which
act to block prostaglandin production. Inflammatory molecules
are made from PUFAs directly. A statement as baldly stupid as
this is impossible not to laugh at, but I'd be curious to know
exactly what is being claimed. SFAs might lower HDL, though my
HDL rose once I began to eat large amounts of coconut product,
but HDL is only "good" if the cholesterol is more oxidized
than it should be, because only oxidized cholesterol will
build up in plaque, if the plaque forms at all (they are
assuming it will). I do agree that if you fry steaks in lard
and eat one every day you are likely to damage your arteries,
but here they fed people a cake made with coconut oil (did
they use other oils too?
- they don't tell us that), and are claiming that it reduced
"the ability of the body's 'good' cholesterol, or
high-density lipoproteins (HDL), to protect the inner lining
of the arteries from inflammatory agents that promote the
formation of artery-clogging plaques." Exactly how is this
the case? What "marker" are they measuring? Was HDL reduced?
That is the most likely possibility. This kind of thing
often happens when the body has to deal with less stress.
For example, if you are young and healthy, and if you eat a
meal rich in food that acts as oxidizing agents, the levels
of at least some antioxidants in your body will rise, but
that does not mean that this food is "healthy." It means
that you body is capable of dealing with it in the short
term. In the long term, severe damage will occur, though it
is conceivable that if you supplemented your diet with the
right amounts of the right antioxidants you could prevent at
least some of the damage from occurring. If you eat a food
that puts less stress on your body, then the levels of
certain substances will be lowered, and that is "good," not
"bad." The way to determine what the scientific reality is,
of course, is to see which group of people (or experimental
animals) lives longer if fed particular diets. I have
challenged those who disagree with me to do an experiment on
rats, which usually don't live more than a few years,
"loser" to pay for all expenses. One group of recently
weaned rats would be fed a diet of 30% canola oil and fish
oil, while the other group would get 30% coconut oil (my
choice of brand). Everything else would be consistent with a
"normal" lab rat diet. No extra antioxidants would be given
to any of the rats, just basic vitamins and minerals. If the
coconut oil fed rats, "deficient" in "essential fatty acids"
and loaded up with "dangerous" saturated fatty acids, live
at least as long as the other group of rats, you pay for all
expenses; but if the rats fed the "heart healthy"
canola/fish oil diet rats live at least 10% longer, then I
will pay for the expenses. If the results are somewhere in
between we split the costs.

Here's another quotation from the report: "the saturated fat
meal had reduced the ability of the endothelium to expand the
arteries in order to increase blood flow. The researchers
determined this by using a blood pressure cuff to restrict
blood flow and then monitoring the body's response." They
appear to be assuming that one wants one's arteries to be
expanded, which is not something I want. I had an MRA not long
ago, and there was no sign of any plaque buildup. My blood
flow is fine, and I would not want it to be "expanded" in any
way. They don't tell the reader that "expansion" occurs due to
chemical reactions that can be dangerous, especially over the
long term. Coconut oil can indeed act as an inhibitor of
biochemical activity, but not in any dangerous way, unless
perhaps a person's arteries were so clogged up already that
he/she needed powerful medication in order to "expand" them.
Notice that they used a blood pressure cuff to artificially
restrict blood flow. If your arteries were all cuffed up
somehow, then it may be a good idea to refrain from eating
large amounts of coconut oil, but you should probably be much
more concerned with how you could live for more than a very
short amount of time in this condition.

Finally, here's an example of the ridiculous "definition" of
"saturated fat" I mentioned above: "Saturated fats are found
in both animal and plant products, and typically are solid at
room temperature. Examples include butter, lard and palm oil."
Note that chicken fat is about 30% saturated while typical
vegetable shortening is about 31% (source: http://www.drlam.c-
om/A3R_brief_in_doc_format/2002-No3-FatandCholesterol.cfm),
while the "saturated fat" lard is 39% saturated and coconut
oil (the kind I use is) is 92%. If you look in most cook
books, with typical recipes used in countries like the USA,
the saturated fatty acid content is very similar, even for
vegetarian dishes. Only if chocolate, cream/butter, or coconut
is used do the dishes have much higher SFA content. And again,
if coconut fat was so bad, where are the raw demographic data
to support this notion? Why does the data support the opposite
conclusion in the strongest possible way? Fortunately, now
there is more than enough molecular-level evidence to
demonstrate beyond any doubt that cholesterol oxidation is the
main problem in "heart disease," and if you'd like to see some
of it, you can read my free essays at:

http://groups.msn.com/TheScientificDebateForum-

Source for the quoted passages above: http://www.docguide.com-
/news/content.nsf/news/852571020057CCF6852571C4004B8124

[David R. T]

In article <ncadnRUq2eDeXkXZnZ2dnUVZ_vqdnZ2d@comcast.com>,
George Cherry <GWCherryHatesGreenEggsAndSpam@alum.mit.edu>
wrote:

>One High-Saturated Fat Meal Can Be Bad

>CLEVELAND - Eating just one meal high in saturated fat _ in
>this case, carrot cake and a milkshake _ can quickly prevent
>"good" cholesterol from protecting the body against clogged
>arteries, a small study shows.

This is interesting work - most work on the cardio effects of
fats looks at the amounts of HDL, LDL or triglycerides
produced, not on changes in their effects.

Still, I think theres somewhat less here than meets the eye.
We already knew that fats were heart-friendsly in this order
(from most to least): PUFA (and omega-3 > omega-6) MUFA Sat
Fat Trans fat.

The article showed another way that Sat fat is less good than
PUFA. That doesn't show that it's bad per se. In particular,
the article doesn't provide any support for the view that one
should get their calories from carbs, instead of sat fat.

DRT

[Ron Peters]

David R. Throop wrote:

> This is interesting work - most work on the cardio effects
> of fats looks at the amounts of HDL, LDL or triglycerides
> produced, not on changes in their effects.

> Still, I think theres somewhat less here than meets the eye.
> We already knew that fats were heart-friendsly in this order
> (from most to least): PUFA (and omega-3 > omega-6) MUFA Sat
> Fat Trans fat.

> The article showed another way that Sat fat is less good
> than PUFA.

http://www.sciencedaily.com/releases/2005/01/050128224527.htm
presents the theory that saturated fats induce a molecular
mechanism in the liver that increases cholesterol and
triglycerides.

> That doesn't show that it's bad per se. In particular, the
> article doesn't provide any support for the view that one
> should get their calories from carbs, instead of sat fat.

The digestive system seems to me optimized for moderate
density foods. We could probably survive fairly well on a low
carb diet, but our digestive system might have problems. I
shared an apartment with a guy who had his intestines
shortened to appendicitis and he had a terrible time with
(awful) waffles.

--
Ron

[monty1945]

I agree that most SFAs will raise serum cholesterol (if
consumed in large enough amounts, of course), but not that
this is a "bad" effect (unless you have a diet rich in food
that acts as oxidizing agents, which I do not), and I also
agree with Ancel Keys' point in his "Seven Countries" book
that in an adult, healthy human man, the 200-220 serum
cholesterol range is usually best for overall mortality. I
went from a serum cholesterol of 131 on a low-fat vegan diet
to 206 on my present diet, and I'm very satisfied with the
benefits I've seen from this change. However, here is an
interesting point: my brother eats a typical American diet,
though he may eat more "junk food" than most, since he eats at
"fast food" restaurants often. His diet would be considered
"high" in saturated fat in most studies done on Americans, and
yet my diet is much higher in percentage SFAs by far, and at
least a bit higher in cholesterol. We both had basic blood
tests within about a month of each other, and the big
difference was that his TGs were very high, while mine were at
the low end of normal, so keep in mind that when they say that
"saturated fat" does this or that they are talking in terms of
broad generalizations, and they are not talking about people
like me, who eat a large amount of SFAs and non-oxidized
cholesterol, but very low in unsaturated fatty acids at the
same time. These generalizations reflect socio-cultural bias,
as there is more than enough evidence from Asians who consume
huge amounts of coconut products for them to realize that what
they are saying (especially the "saturated fat causes heart
attacks" mantra) makes no sense at all, and cannot possible be
accurate (though they would need to define "saturated fat"
before one could even begin a scientific investigation).

Now to the person who said that unsaturated fatty acids are
"heart healthy," my question to you is, have you read any of
the literature on oxidized cholesterol? And also, do you
realize that PUFAs can contribute to cholesterol's oxidation
to a large degree, while a highly saturated fat source like
coconut oil does not?

[Susan]

x-no-archive: yes

George Cherry wrote:
> This is worth repeating.
>
>
> One High-Saturated Fat Meal Can Be Bad By JOE MILICIA,
> Associated Press Writer Mon Aug 7, 10:52 PMUPDATED 13 HOURS
> 52 MINUTES AGO
>
> CLEVELAND - Eating just one meal high in saturated fat _ in
> this case, carrot cake and a milkshake _ can quickly prevent
> "good" cholesterol from protecting the body against clogged
> arteries, a small study shows.
>
> The results of the research weren't a surprise to the
> experts, but they say the findings reaffirm something that
> more people need to understand:
>
> "What we put into our mouth makes a big difference in terms
> of our health," said Dr. Charles McCauley, a cardiologist
> with Marshfield Clinic in Wisconsin, who reviewed the
> research but wasn't involved with the study. "We really have
> to be very careful as to how our food is processed and what
> kind of ingredients we use."
>
> In the study, at The Heart Research Institute in Sydney,
> Australia, 14 people, ages 18-40, ate two meals of carrot
> cake and a milkshake one month apart. One meal was high in
> saturated fat _ using coconut oil _ and the other was high
> in polyunsaturated fat _ using safflower oil.
>
> Saturated fat has long been linked to the buildup of
> plaque that can lead to heart attacks and strokes. HDL,
> the "good" cholesterol, protects arteries from the
> inflammation that leads to artery-clogging plaques. And
> plaque hurts the ability of arteries to expand to carry
> blood to tissues and organs.
>
> The researchers, led by Dr. Stephen Nicholls, a cardiologist
> now at the Cleveland Clinic, found that three hours after
> eating the saturated-fat cake and shake, the lining of the
> arteries was hindered from expanding to increase blood flow.
> And after six hours, the anti-inflammatory qualities of the
> good cholesterol were reduced.
>
> But the polyunsaturated meal seemed to improve those
> anti-inflammatory qualities. Also, fewer inflammatory agents
> were found in the arteries than before the meal.
>
> "They're looking at things in terms of real live living,"
> said McCauley. "Carrot cake. How more real does that get?"
>
> The study appears in the Aug. 15 issue of the Journal of the
> American College of Cardiology.
>
> "It's a simple study. Sometimes the best studies are those
> that are very straightforward," said Dr. Richard Milani,
> head of preventive cardiology at Ochsner Clinic Foundation
> in New Orleans.
>
> He notes that the research isn't suggesting that people eat
> a steady diet of carrot cake and milkshakes.
>
> However, he said, "given a choice between something with
> polyunsaturated fat and saturated fat, please avoid the
> saturated fat."
>
> Nicholls said "the take-home, public-health message is this:
> It's further evidence to support the need to aggressively
> reduce the amount of saturated fat consumed in the diet."
>
> Saturated fats are found mostly in food from animals,
> including beef, pork, lard, poultry fat, butter, milk and
> cheeses, and some plants, including coconut oil, palm oil
> and cocoa butter.
>
> Polyunsaturated fats are found in oils from plants,
> including safflower, sesame and sunflower seeds, corn and
> soybeans, many nuts and seeds.
>
> Dr. James O'Keefe, a cardiologist at the Mid America Heart
> Institute in Kansas City, said Nicholls' study shows "a
> really important concept _ when you eat the wrong types
> of food, inflammation and damage to the vessels happens
> immediately afterward."
>
> Too many people simply are eating the wrong kind of fats,
> O'Keefe said.
>
> "Even one meal of a double cheeseburger with fries and a
> Coke will mess up your system, let alone a steady diet of
> it, which is recipe for disaster," O'Keefe said.

I can't believe shit like this can still be published.

The most hormonally active part of the meal, the one that effs
up metabolism, is the sugar and starch.

Any study of protein and sat fat in the absence of such
dietary garbage has found only lipid improvements and
reduced CVD risk.

Susan

[Ron Peters]

Susan wrote:

> Any study of protein and sat fat in the absence of such
> dietary garbage has found only lipid improvements and
> reduced CVD risk.

http://www.oilseed.org/pdf/am_2006_materials/Coronacion_Text_-
Only.pdf shows the growing use of coconut and palm kernel oil.

http://www.cdc.gov/diabetes/statistics/prev/national/figbyage-
.htm shows the increasing incidence of diabetes for all
various age groups.

It sure looks like the consumption of saturated fats is
driving the increase in diabetes.

--
Ron

[monty1945]

Ron:

How do you explain millions of Asians using large amounts of
coconut oil and yet having very low rates of diabetes? Again,
you are assuming that "saturated fat" has a definition that is
useful, if not precise, when the reality is the opposite.

Are you aware of Nobel Prize winning scientist Housssay's
animal experiments? He showed that lard is very dangerous in
the "diabetes" context, but that coconut oil is not.

How do you explain this? My explanation is consistent with the
recent molecular-level evidence, while you are just using the
old terminology, which is now obviously inaccurate. Have you
ever read through a cook book that has the nutritional
information included with the recipes? Compared to an Asian
diet rich in coconut, the American diet is much lower in SFAs
as a percentage of daily calories, especially now that highly
unsaturated oils are being used in just about everything. Lard
used to be around 60% or more SFAs, yet now it is not even 40%
SFAs. It is no longer a "saturated fat" by any reasonable
person's definition, and yet it is still the most common
"saturated fat" used in American experments.

Are you aware, Ron, of the experiments showing how dangerous
meat is when cooked in certain ways? This is how they get the
"saturated fat"/diabetes correlation that you refer to, along
with socio-economic factors (that is, poor people eat more
pork rinds, processed meat, etc., and also see their doctors
less often, sleep less, drink more alcohol, etc.). Moreover,
in some experiments, they correlate higher SFA consumption
with diabetes, but they don't mention that the people are
consuming more PUFAs and other dangerous substances. Do you
understand, Ron, that the scientific method requires that all
potentially relevant factors must be rigorously controlled for
in experiments? Fortunately, I was trained in evidence
analysis, so I can "see through" all the tricks being played,
whether or not they are being played intentionally or not. I
went from having high glucose numbers (not far from
"pre-diabetic") to being on the low side of "normal," by
switching from a vegan diet with hardly any SFAs, a lot of
fiber, etc., to one loaded with SFAs an non-oxidized
cholesterol (but very little PUFAs).

In the reports in question here, the "journalists" talked
about PUFAs increasing HDL's anti-inflammatory qualities. Can
you explain what this means or can you quote a passage from
the actual study? My guess is that they are talking about an
indirect effect which is something like this: you have
oxidized cholesterol in your body, and if your HDL is not
"high," then there will be a lot of the oxLDL around to cause
damage, which then prompts an inflammatory response, which as
usual, causes symptoms of what people such as yourself
describe as a "disease." Fine, except that coconut oil will
not oxidize cholesterol, so there is no reason to fear
something like coconut oil if you avoid eating oxidized
cholesterol or allowing it to get oxidized in your body (which
is what a high PUFA oil diet will do to you, unless you
supplement massively with antioxidants). Basically, though
they don't realize it, they are assuming that your body will
be damaged by a PUFA-rich diet, and then they think increasing
HDL is "good," along with "expanding" the arteries, though
they seem unaware of non-oxidized cholesterol's protective
role against cancer, shock, "bleeding" strokes, etc.

As is required by science, I am willing to do experiments on
common lab animals to demonstrate my point, if anyone who
truly "believes" that I am wrong and that a diet rich in PUFAs
will result in much better overall mortality is willing to pay
for all expenses if it turns out that he or she is incorrect.
It should not cost more than a couple of thousand dollars.
What are you waiting for? If I am wrong, I will admit it here
and on the other newsgroups I've posted on, and it will not
cost you anything. Moroever, you will have a study that you
know about first-hand and can explain to whoever you want that
it was focused on the factor almost everyone wants to know
about first and foremost: overall mortality; "how long will I
live on that diet?" How about you, Ron?

[monty1945]

Because the reports were of such poor quality, with
statements such as:

QUOTE: Six hours after the saturated fat meal, researchers
found that high density lipoprotein, the HDL or "good"
cholesterol, was less able to control inflammation inside the
arteries. Inflammation is linked with heart disease.

By contrast, the polyunsaturated meal seemed to boost the
anti-inflammatory abilities of HDL. UNQUOTE.

Source: http://www.iol.co.za/index.php?set_id=1&click_id=31&a-
rt_id=qw1155071706744B243

I decided to do some research to try and determine exactly
what they were claiming. The following seems to be the most
likely candidate:

QUOTE: Reduced HDL concentrations appear to be unable to
efficiently eliminate the cholesterol excess at the vascular
wall level, contributing to the onset of the inflammatory
response that typically occurs in the pathogenesis of
atherosclerosis from its earliest stages. UNQUOTE.

Source: http://www.ingentaconnect.com/content/fm/fca/2006/000-
00002/00000001/art00007;jsessionid=328j0ft50s9g1.alice

Thus, it is likely that their results are simply that serum
HDL increased after the high PUFA meal and did not (or
decreased somewhat) after the meal with coconut oil. Note that
we still don't know if they used only coconut oil, as I do
when I bake breads, or if they used it in conjuction with a
very dangerous oil, such as rapeseed. But as I said in the
other posts, with coconut oil only, you don't need very high
HDL, because coconut oil can't do the damage that the highly
polyunsaturated oils do to your arteries. Again, they are
assuming that the damage is going to be done, but this is only
the case because the American diet is now so high in
unsaturated fatty acids (and too low in antioxidant-rich
foods) that they fear low HDL. However, as I said, my HDL
increased substantially (in a way the "experts" say is
impossible, actually) when I began to eat large amounts of
coconut and avoided all major sources of PUFAs. This may have
been due to the fact that I went from a diet with no
cholesterol in it (and a serum cholesterol level of 131) to a
diet rich in non-oxidized cholesterol (and my serum
cholesterol rose to over 200). If you are going to be
persuaded by such a study (that is, feeding a small number of
people two meals), then my experience should probably be
written up as a study as well. As I said in the other posts,
the molecular-level evidence and the raw demographic data
(involving hundreds of millions of people) are in accord, so
why anyone would do anything but laugh at this "study" is
beyond comprehension. However, the results, if they are what
they appear to be, are consistent with the evidence. The
problem is that they are interpreting their findings in a way
that is ridiculous.

[Ron Peters]

monty1945@lycos.com wrote:

> How do you explain millions of Asians using large amounts of
> coconut oil and yet having very low rates of diabetes?
> Again, you are assuming that "saturated fat" has a
> definition that is useful, if not precise, when the reality
> is the opposite.

I don't know that Asians eat large amounts of any kind of fat.

Mech Ageing Dev. 1991 Nov 1;60(3):267-74. has an abstract that
says: "Effect of lard, palm and rapeseed oils life
conservation in aged mice.

Suzuki H, Yamazaki M, Arai S, Nagao A, Terao J.

National Food Research Institute, Ibaraki, Japan.

Effects of lard, palm and rapeseed oil diets on the survival
and fatty acid composition of liver and brain lipids were
studied in male and female mice for 15 months. Over 80% of
mice fed on lard and rapeseed oil (n-3 PUFA sufficient) diets
survived to the end of feeding trial, however, 60% of male
mice fed on palm oil (n-3 PUFA deficient) diet died before the
end. Although a survival curve in female mice fed on palm oil
diet was similar to that in male, it was not as dramatic as
that of the male. The fatty acid analyses revealed that severe
n-3 PUFA deficiency occurred in the mice fed on a palm oil
diet. Moreover, the fatty acid was more deficient in the male
than in the female. These results suggest that short life in
mice may be caused by n-3 PUFA deficiency and, therefore, the
fatty acid may be essential in enjoying a long life."

They weren't using coconut oil in the test, but were using
palm oil which has more satuated fat than lard but has almost
no omega-3 fatty acids.

It sure loks like omega-3 fatty acids are needed in a small
amount to be healthy and people are unlikely to consume too
much. Omega-6 is also needed in small amounts, but it is easy
to eat large amounts which may result in harm to the liver and
other organs.

--
Ron

[monty1945]

Palm oil is quite different from palm kernel, and in the
context of free radical damage, a poor-quality palm oil is
much more dangerous (palm kernel is much more saturated).
Thus, before any conclusions can be drawn, we would have to
know if the oil was fresh, and there are established tests for
this purpose (Rancimat, for example). In 1948, rats were fed a
diet of not fat, and this mortality problem was not found, so
your conclusion about omega 3s cannot be correct, though it
would not necessarily apply to humans anyway. My great
grandparents lived very long lives and had no source of omega
3s (no flax, no oily fish, no canola oil, no pumpkin seeds, no
walnuts or walnut oil, etc.), and I've consciously avoided
omega 3s for years now, witnessing only benefits from this
decision (along with avoiding any major PUFA source and
packing my body with SFAs and non-oxidized cholesterol). And
as for your ignorance of the demographic data, Ron, do you
realize that you can go to the WHO's web site and look at the
statistics? Yes, Asians generally don't gorge themselves the
way Americans do, but I am talking about saturated fatty acids
as a percentage of daily calories, not total amount. This is
one of the problems with the studies we hear about in the
mainstream media all the time, that is, many or all of the
subjects are eating way too many calories, and as the
scientific method demands, caloric intake needs to be
controlled for, because it certainly can be a factor,
especially on diets high in PUFAs and meat cooked while
exposed to air. And lastly, if this study is correct in terms
of your interpretation of it, why not take me up on my
experiment offer? Fresh coconut oil should really kill off the
rats quickly, according to your way of thinking, even though
Nobel Prize winner Houssay had the opposite results.

[monty1945]

I should mention that while it seems highly unlikely, it is
certainly possible that mice, unlike rats, do need omega 3s,
or perhaps it is that if they are raised on an omega-3 rich
diet that removing it causes problems. The 1948 experiment was
done on rats. It could also be that lifestyle plays a factor -
we don't know how the mice lived during this time period. And
of course I am leaving aside the possibility of outright
fraud, which is not something that is impossible here. In
science, experiments should be repeated by another group of
scientists, and all relevant factors need to be controlled
for, and from this study's abstract it is impossible to know
if they did that or not.

But the interesting point is that if you do believe this study
to be "true," then you should also believe that humans do not
need omega 3s at all, based upon the diet of my great
grandparents and also of my diet for the last few years. Of
course, you could think that I am lying for some reason, but
then all you have to do is your own experiment, as the
literature claims that "EFA deficiency" occurs within about a
month. On my web site, I describe my diet in detail, and I
suggest if you do your own experiment, you document exactly
what you are eating, in what amounts, how it is cooked, etc.
(for example, if you consume dairy, is any of it homogenized?
does it contain carrageenan?).

[Ron Peters]

monty1945@lycos.com wrote:
> Palm oil is quite different from palm kernel, and in the
> context of free radical damage, a poor-quality palm oil is
> much more dangerous (palm kernel is much more saturated).
> Yes, Asians generally don't gorge themselves the way
> Americans do, but I am talking about saturated fatty acids
> as a percentage of daily calories, not total amount.

http://www.unu.edu/Unupress/food/8F152e/8F152E07.htm says that
liquid oils are the major frying oils, especially domestic
cooking, in Japan. However, palm oil has now reached 22% use
in the production of margarine, shortening, and other
processed fats.

The following shows the increasing amount of diabetes in
Japan: "Current trend in prevalence of diabetes mellitus in
Japan, 1964-1992.

Islam MM, Horibe H, Kobayashi F.

Department of Health and Psychosocial Medicine, Aichi Medical
University, Japan.

Prevalence of diabetes mellitus in Japan was investigated
through studying the published reports from 1964 to 1992 by
searching the electronic data base and some leading Japanese
journals following certain inclusion criteria. Out of total 74
retrieved reports, 14 were found eligible for review, some
containing data of multiple community and/or periods and were
converted into total of 40 reports following a predetermined
criteria. Review analysis of only the prevalence of diabetes
was done paying much attention to age range, survey
methodology and response rate. Oral glucose tolerance test
(OGTT) was done in 19 (47.5%) with and in 21 (52.5%) reports
without initial urine and/or blood sugar screening. OGTT was
done using 75, 50, or 100 grams glucose following either Japan
Diabetes Society or WHO criteria. The recent prevalence was
estimated ranging from 9.6-11.9% in both sexes of 40 years or
over, 4.2-13.1% in men and 2.6-12.9% in women. The higher
prevalences were found in and around 1990 and the lower values
in and around 1970. Regression analysis shows the upward trend
of the prevalence of diabetes 2.2% in men (p < 0.01), 1.6% in
women (p < 0.01) by 10 years."

--
Ron

[Ron Peters]

monty1945@lycos.com wrote:
> I should mention that while it seems highly unlikely, it is
> certainly possible that mice, unlike rats, do need omega 3s,
> or perhaps it is that if they are raised on an omega-3 rich
> diet that removing it causes problems. ...

It is possible for certain types of fatty acid conversions to
take place in animals. However, there is no known way for
omega-3 fatty acids to be coverted from non-omega-3 fatty
acids in the human body. However, the brain contains large
amounts of DHA, an omega-3 fatty acid, so where can it come
from other than diet?

> But the interesting point is that if you do believe this
> study to be "true," then you should also believe that humans
> do not need omega 3s at all, based upon the diet of my great
> grandparents and also of my diet for the last few years. ...

Unfortunately, personal experiences aren't repeatable. If your
great grandparents only ate seal blubber, they would have had
tremendous amounts of omega-3 fatty acids.

DHA is now being used as a supplement in baby formula with the
blessing of the FDA to help babies with their brain
development.

--
Ron

[monty1945]

Palm oil is an oil that has quite a bit of UFAs, and if it is
poor quality, the lipid peroxiation is almost certainly the
problem. The Japanese diet is a unique one, so I would not
draw any conclusions from it, with the possible exception of
the connection betwen raw/burnt/pickled food and stomach
cancer. The demographic data to look at are the of people who
eat a diet that is very high in PUFAs or SFAs, for example,
and when you do that, with people who eat a lot of coconut oil
but no other fat, yon don't see all these "chronic dieases."
The Greenlanders, on a high omega 3 PUFA diet, on the other
hand, had terrible mortality, and if you go to my site you
will see the evidence for yourself.

Getting back to the mouse study: look at the actual numbers.
About 60% of the mice lived to the target age with palm oil,
whereas the ones with rapeseed oil and lard were at just over
80%. How does this show that omega 3s are absolutely
essential? If they were, it should have been near zero for the
palm oil group. What is interesting is that plam oil is fairly
high in oleic acid (nearly 40%), and this is what olive oil,
said to be the "healthiest" oil by so many "experts" today, is
richest in. Non-refined plam oil is a great source of
antioxidants too. Rapeseed oil is very dangerous, which is why
the "experts" bred the eruic acid out of it to make canola oil
(which is also dangerous in its own way), and of course just
about everyone realizes that lard is unhealthy, though the
reasons differ. This study sounds ridiculous, in terms of the
results, and I would be willing to do my experimental offer
with these oils, that is, one group of newly weaned generic
lab rats get 15% common lard and 15% common rapeseed oil
(meaning off the shelf at a local grocery store), whereas the
other group gets 30% palm oil (my choice of brands). No added
antioxidants, just basic vitamin/mineral supplement, along
with the same protein/carbohydrate chow. Again, the palm oil
group, according to Ron, should have much higher mortality
rates, but if not, you pay for all expenses. Let's sort this
thing out using the scientific method !

[Ron Peters]

monty1945@lycos.com wrote:

> Getting back to the mouse study: look at the actual numbers.
> About 60% of the mice lived to the target age with palm oil,
> whereas the ones with rapeseed oil and lard were at just
> over 80%. How does this show that omega 3s are absolutely
> essential?

I assume that the mice were fed omega-3 fatty acids until they
got on their diet, so I wouldn't expect an immediate effect on
deprivation.

Palm oil and palm seed oil come from the same plant, with the
palm oil being produced in much larger quantities.

The researchers should have had a test group supplementing the
palm oil with omega-3 fatty acids to show whether the life
span difference was due to the high intake of saturated fats
or the low intake of omega-3 fatty acids.

--
Ron

[monty1945]

Yes, this study is very odd, and since the SFA content of lard
can vary tremendously, it is difficult to know what they are
suggesting: do they want people to go on a rapeseed oil and
lard diet?

In any case, I found a study that seems to show what is going
on at the molecular level:

Mol Cell Biochem. 2006 Aug 8; [Epub ahead of print]
Lysophosphatidylcholine induces inflammatory activation of
human coronary artery smooth muscle cells.Aiyar N, Disa J, Ao
Z, Ju H, Nerurkar S, Willette RN, Macphee CH, Johns DG,
Douglas SA. Department of Vascular Biology and Thrombosis,
Cardiovascular and Urogenital Center of Excellence for Drug
Discovery, GlaxoSmithKline, 709 Swedeland Road, King of
Prussia, PA, 19406, USA, Nambi_Aiyar-1@gsk.com.

Lysophosphatidylcholine (LPC) is the major bioactive lipid
component of oxidized LDL, thought to be responsible for many
of the inflammatory effects of oxidized LDL described in both
inflammatory and endothelial cells. Inflammation-induced
transformation of vascular smooth muscle cells from a
contractile phenotype to a proliferative/secretory phenotype
is a hallmark of the vascular remodeling that is
characteristic of atherogenesis; however, the role of LPC in
this process has not been fully described. The present study
tested the hypothesis that LPC is an inflammatory stimulus in
coronary artery smooth muscle cells (CASMCs). In cultured
human CASMCs, LPC stimulated time- and concentration-dependent
release of arachidonic acid that was sensitive to
phospholipase A(2) and C inhibition. LPC stimulated the
release of arachidonic acid metabolites leukotriene-B(4) and
6-keto-prostaglandin F(1alpha), within the same time course.
LPC was also found to stimulate basic fibroblast growth factor
release as well as stimulating the release of the cytokines
GM-CSF, IL-6, and IL-8. Optimal stimulation of these signals
was obtained via palmitic acid-substituted LPC species.
Stimulation of arachidonic acid, inflammatory cytokines and
growth factor release, implies that LPC might play a
multifactorial role in the progression of atherosclerosis, by
affecting inflammatory processes.

This gets us back to the original point of this thread, that
is, fatty acids and heart disease. I agree with these people
that upon a certain amount of cellular stress, AA will be
released and made into LTB4, which then does the damage that
leads to "heart disease." The question is, what role could
palm oil play here? If palm oil was of very poor quality, it
would cause the kind of stress that start the process, but
since the major stressor is free radical damage/lipid
peroxidation (in the heart disease context, as well as just
about every other disease, in one way or another), the more
saturated the fat source, the less likely it is to do harm.
Cooking methods, however, as well as processing, can change
this theoretical formula substantially, which is why I insist
on choosing the "saturated" fat source if anyone were to take
me up on my experimental offer.

In any event, the evidence is clear, and there is more just
about every day. For example, the following addresses how free
radicals appear to play a key role in "diseases" that were
previously attributed to "bugs:"

http://www.sciencedaily.com/releases/2006/08/060809232944.htm

[Ron Peters]

monty1945@lycos.com wrote:

> This gets us back to the original point of this thread, that
> is, fatty acids and heart disease.

http://www1.wfubmc.edu/articles/Focus+on+Atherosclerosis gives
a good summary as of 2003 which says:

"But Rudel and his colleagues decided to test various dietary
fats to see if LDL and HDL levels in fact predicted what went
on inside the coronary arteries. "When we looked in the
coronary arteries, the monounsaturated-fat-fed animals had
just as much atherosclerosis as those fed saturated fat and
only the polyunsaturated-fat-fed animals had less."

"Meanwhile, John Parks, Ph.D., professor of comparative
medicine, was pursuing fish oil, which reduced coronary artery
atherosclerosis in monkeys. Parks found that fish oil
facilitated conversion of LDL from a solid to a liquid state.
"Our hypothesis was this might facilitate removal of LDL from
the arterial wall or wherever it happened to be trapped."

"Fish oil compared to saturated fat or other kinds of more
atherogenic fats repeatedly has been shown to reduce
atherosclerosis," Parks said.

"When they fed monkeys monounsaturated fat, cholesterol oleate
accumulated in the arteries. Tests of extracellular material
in the arteries confirmed that it was cholesterol oleate."

"Meanwhile, Parks was focused on LCAT, which operates in the
bloodstream. The LCAT enzyme attaches linoleic acid - the
predominant fatty acid in vegetable oil - to the cholesterol
particles to make cholesterol linoleate. Earlier studies in
people of Scandinavia had shown that increased cholesterol
linoleate led to less coronary heart disease. The researchers
documented the same things in monkeys and found that the two
fatty acids worked in opposition to each other. "When
cholesterol linoleate is high, cholesterol oleate is low,"
Rudel said."

--
Ron

[monty1945]

Well, Ron, you are actually suggesting that the current dogma,
that is, that "monounsaturates" are "heart healthy," is
totally wrong. In any case, this is where the shenanigans are
often played, that is, when they say "saturated fat" did this
or that, what do they mean? What was the source of the
"saturated fat?" And how is it possible that heart disease is
so low in nations that conume large amounts of coconut oil as
percentage of daily calories? The molecular-level evidence
explains it perfectly (lipid peroxidaiton/cholesterol
oxidation). If you get a high quality "polyunsaturated" oil,
such as sesame, it will be rich in antioxidants, and if you
eat it without cooking it, there will be little if any
arterial damage, at least from that choice. On the other hand,
if you get lard and fry food in it, you will do damage to your
arteries. This is usually the reason why they say that
"saturated fat" is so bad, but it's the definition and the way
they categorize things and abstract the phenomena that leads
to this conclusion. Then they say that coconut oil is really
bad, because it is "so saturated," yet this totally flies in
the face of the raw demographic data and also of the studies
that controlled for other variables. I would be willing to be
part of a study, but you would have to find people who eat a
diet exactly like mine, that is, very high saturated fatty
acids (palm oil, lard, and beef tallow would not be permitted,
for example), no or small amounts of meat, only boiled, boiled
eggs, and dairy that is not cooked higher than on the "low"
setting or homogenized. Also, at least small amounts of
berries, prunes, raisins, dark chocolate, and other
antioxidan-rich foods would have to be consumed each day.
Etc., etc. In science, you have to control for all possiblly
relevant variables, and these kinds of people are actually
doing the opposite, that is, they are making all kinds of
assumptions that were never demonstrated experimentally, and
then they use these assumptions to justify not controlling for
all possibly relevant variables.

[monty1945]

Also should have mentioned that the link you provided supplies
no data, so there is no way to examine their claims. And then,
for example with the monkey study they mention, there is no
way to know if the diet fed to them was high in oxidizing
agents. They do talk about oxidized LDL, but in a way that
makes it seem like it is totally new, when in fact I have been
citing stuides of oxidized LDL for a long time on this
newsgroup. They are clearly behind the times, and because they
have preconceptions based on the old flawed studies, I would
not expect much of value from them. What are they likely to
do? They might take one group of people eating a typyical
American diet, too high in calories, too high in PUFAs, also
rather high in SFAs, too high in meat cooked while exposed to
air, and too low in antioxidant-rich foods, and measure their
"risk factor" "markers." Then there will be a second group
that had been eating a similar diet. This second group will be
fed various plant compounds, some of which might have a fair
amount of antioxidants. In any case, a terrible diet will be
replaced by a bad one. Nobody will be eating the kind of diet
I am, nor the kind in Asia (rich in coconut) that have been
studied by a few scientists who understood the importance of
doing so. And what will the results be? Because they lowered
SFA consumption slightly and raised PUFA consumption slightly,
they will say that "saturated fat causes heart disease," when
in fact nothing of the sort was demonstrated (and of course
they will not define "saturated fat" in a scientifically
precise way). Those who have reviewed all of the literature
realize that you need to control for things like HCAs
generated from the meat (rich in "saturated fat," relatively
speaking), the antioxidants, the cooking techniques, etc., not
to mention that they would still be determining "risk factors"
and not taking into account that one's serum cholesterol level
is fine up to at least 220, as long as it is not getting
oxidized. They have created such a mess that most people don't
have thte patience that I do to go through all of the
mistakes, faulty assumptions, flawed experimental designs,
etc. in order to get at what is really going on here.
Fortunately, this is exactly what I was trained to do in
graduate school. Then there is the fact that these kinds of
people hardly ever address the evidence that exists and is
contrary to their claims. This is one of the first things we
were taught to do when making an argument (after studying the
evidence), and hese people don't even seem to be aware of the
existence of the literature with which they are supposed to
acquainted. If they were correct, the results of these studies
of peoples who consume a large amount of coconut (as well as
the raw demographic data, of course) would be impossible.
However, the results of their studies is explicable if one
takes all factors into account. It is a matter of basic logic:
their claims cannot be correct, but the fact that they don't
even try to explain the contrary evidence demonstrates a
severe lack of academic standards. There is no way they would
have graduated from the program I did with such sloppy
research skills and flawed methodology.

[Ron Peters]

monty1945@lycos.com wrote:
> Well, Ron, you are actually suggesting that the current
> dogma, that is, that "monounsaturates" are "heart healthy,"
> is totally wrong. In any case, this is where the shenanigans
> are often played, that is, when they say "saturated fat" did
> this or that, what do they mean?

The problem is that saturated fats, and transfats, are solid
at body temperature and hence incapable of being metabolized
once stored in fat cells. Try an experiment, take melted
coconut oil and pour it in your garbage disposer, turn on the
cold water and then turn on your garbage disposal.

--
Ron

[monty1945]

Yes, Mike, Ron is does not know some basic facts. I wish he
would at least read something like Bruce Fife's book,
"Saturated fat may save your life," though I don't agreee with
a few of Fife's points. However, my site has information that
is much more technical, and so many may be intimidated by much
of the evidence. Very long chain saturated fatty acids are
found in candle wax, and indeed it would not be a good idea to
eat candles. Coconut oil, on the other hand, is more easily
metabolized than anything else you can eat. Again, this brings
us to a point I've made many times on this NG, that is, the
abstract classification schemes invented by "nutritional
experts" in order to make "nutritional science" a discipline
in its own right (distinct from biochemistry, for example) has
led to this sad state of gross ignorance. If we were to ask
medical doctors some basic questions, many people (at least
those of us who understand the implications of the answers)
would be very concerned. For example, this was actually done
with a question: which is more susceptible to lipid
peroxidation, PUFAs or SFAs, and nearly 40% thought SFAs were,
which of course demonstrates an incredible stupidity (if they
had left the question blank, it would demonstrate terrible
ignorance instead).

[Ron Peters]

Mike Robinson wrote:
> On Sat, 12 Aug 2006 19:47:33 -0700, Ron Peterson wrote:

> > The problem is that saturated fats, and transfats, are
> > solid at body temperature and hence incapable of being
> > metabolized once stored in fat cells. Try an experiment,
> > take melted coconut oil and pour it in your garbage
> > disposer, turn on the cold water and then turn on your
> > garbage disposal.

> Coconut oil melts well below body temperature.

The major fatty acid of coconut oil is lauric acid which has a
melting point of 44 degrees celsius.

There is a small amount of monounsaturated and pufa in coconut
oil which lowers the melting point of oil.

--
Ron

[Ron Peters]

monty1945@lycos.com wrote:
> Yes, Mike, Ron is does not know some basic facts. I wish he
> would at least read something like Bruce Fife's book,
> "Saturated fat may save your life," though I don't agreee
> with a few of Fife's points.

His close alliances with the coconut oil industry make his
writings suspect. Do you know of any medical researchers
outside of the industry that advocate high saturated fat
consumption from any source?

--
Ron

[monty1945]

Perhaps you would care to disclose these conflicts of interest
of which you speak? If not, then I will have to conclude that
you are inventing this, or that the "conflict" is of such a
minor quality that it is ridiculous. I can do my own
investigation, in any case, since that is what I was trained
to do. I found his book useful in terms of the evidence he
cites, which I then examined for myself. I did not assume that
his interpretation was accurate, and in fact, I found several
things that he misinterpreted (in my opinion, based upon all
the evidence I've reviewed).

As for coconut oil's melt point, if you hold a small amount in
your hand, it soon melts. Inside your body, it will melt even
quicker. Now Ron, why don't you tell us about how coconut oil
is metabolized in the body? Or are you unaware of this? You
seem to like to make accusations or cite the grand
pronouncements of "experts," but you never seeem to want to
answer any questions that I pose, even though they are the
kind that any reasonable person would ask in this situation.

As to what "experts" are advocating, are you aware of the
writings of biologist Ray Peat, for example? Are you only
interested in following the advice of an "expert" who you feel
"comfortable" with, or do you base your decisions on something
like those old TV commercials that stated that "four out of
five dentists recommend" that you use a particular tooth
paste? I do my own investigation. I examine any claim that is
made very closely, and I demand to see the evidence that the
claim is supposed to be based upon. How do you come to your
conclusions, Ron?

[Ron Peters]

monty1945@lycos.com wrote:

> As for coconut oil's melt point, if you hold a small amount
> in your hand, it soon melts. Inside your body, it will melt
> even quicker.

You're not looking at the melting point of the
consituent parts.

> As to what "experts" are advocating, are you aware of the
> writings of biologist Ray Peat, for example?

Look what coconut oil advocate Mary Enig has to say
about Ray Peat:

"Peat also asserts that polyunsaturated fatty acids become
rancid in our bodies. This is not true; the polyunsaturated
fatty acids in our cell membranes go through different stages
of controlled oxidation. To say that these fatty acids become
"rancid" is misleading. ..."

"Actually, Peat's argument that polyunsaturated fatty acids
become harmful in the body and hence cause cancer simply does
not make sense. It is impossible to avoid polyunsaturated
fatty acids because they are in all foods."

"EFAs are, however, harmful in large amounts and the many
research papers cited by Peat showing immune problems,
increased cancer and premature aging from feeding of
polyunsaturates simply corroborate this fact. But Peat has
taken studies indicating that large amounts of EFAs are bad
for us (a now well-established fact) and used them to argue
that we don't need any at all."

--
Ron

[monty1945]

I am not interested in what any particular "expert" has to
say Ron, in the sense that not matter what anyone claims I am
going to do my own investigation and examine the evidence
presented, though these days many "experts" don't seem too
interested in worrying about evidence at all. Why won't you
answer any of my questions? Let's get back to Fife: what
evidence do you possess that suggests that he is making big
profits from the sale of coconut oil? If you do not answer
this question, you will reveal yourself as someone who is not
interested in an objective investigation into these matters.
As to your other question, Ray Peat advocates and himself
consumes such a diet, as do I. I base my conclusions on the
evidence, which suggests in the strongest possible terms that
free radical mediated damage is the underlying cause of
"disease." If you go to my web site, you will see how much
evidence there is, and I just chose the most concise example
- there is much, much more that I did not cite, but that I
have saved up on my hard drive. And there are many other
studies that can be found by a simple google search, as I've
pointed out here over and over again (as well as pubmed.com
searches). The "bottom line" is simple: a fat source as
saturated as coconut oil will not cause free radical mediated
damaged, whereas the highly polyunsaturated oils will (in the
context of the typical Western diet). If you do not perceive
this, then you either have reading comprehension problems,
you have deluded yourself for whatever reason, or you don't
understand the basic biochemistry (or perhaps some
combination). I have been willing to "put my money where my
mouth is" on this for years, but of all the people who have
attacked my posts (usually in incredibly ludicrous ways, such
as for obvious "typo" errors, paragraphs that are too long,
etc.), not one has shown even the slightest interest in
taking me up on this offer.

As for you, Ron, if you do not answer my questions, I will no
longer address yours, and I think readers will understand
that you are incapable of a fair, on point discussion,
because you expect others to answer your questions yet you do
not answer theirs.

[monty1945]

Mary Enig is totally wrong on these points. I have tried to
contact her more than once, but she has never responded, even
though the web site's that listed her contact information said
that she would. Again, I have investigated these issues for
myself. The "lipid bilayer membrane" stuff is nonsense. Just
get any of Gilbert Ling's recent book and you will not only
learn about this topic, but you will also see how science
should be conducted. As to PUFAs, when they go rancid in your
body it is called "in vivo lipid peroxidation," and if she
wishes to disbelive this, that is her perogative, but just go
ahead and do a google or pubmed search for this. There are
3726 items that result on pubmed when you search for this
phrase, for example. You can go to my web site and see all the
evidence on PUFAs and free radical damage, and again, I just
put the "tip of the iceberg" up on my site.

And what about the 1948 experiments in which rats were given
not fat, yet lived without any problems? Enig and the other
"EFA" advocates never mention this, which is a violation of
basic academic standards. Do you really want to follow the
advice of such people blindly? And let's assume that Fife is
in fact making $200,000 a year off of coconut sales,
hypothetically (you still have supplied no evidence that he
makes even a dollar a year to this point), are you suggesting
that hardly anyone else in the biomedical and nutritional
estanblishments are not conflicted? I actually ignore such
possibilities, since so many people are conflicted, and I just
examine the evidence. Notice that I said that I examine the
evidence. I don't just assume that the interpretation of the
evidence that the researcher states afterward is accurate. I
have seen many, many examples where the interpretation of the
evidence is downright nonsensical.

In science, if two people or groups come to different
conclusions about the evidence, then the next step is to agree
on an experiment that will settle the issue. I have made the
experimental offer on this NG many times before, and no one is
interested in even negotiating terms. What does that tell you,
Ron? If you have an experimental idea in mind, why don't you
articulate it on this thread and perhaps we can work something
out and settle this the scientific way.

[Ron Peters]

monty1945@lycos.com wrote:
> Mary Enig is totally wrong on these points.

Her close association to the coconut oil industry leads me to
suspect her analysis.

> As to PUFAs, when they go rancid in your body it is called
> "in vivo lipid peroxidation," and if she wishes to disbelive
> this, that is her perogative, but just go ahead and do a
> google or pubmed search for this. There are 3726 items that
> result on pubmed when you search for this phrase, for
> example. You can go to my web site and see all the evidence
> on PUFAs and free radical damage, and again, I just put the
> "tip of the iceberg" up on my site.

OK, I did a search, and will continue looking.

A report by G. Spiteller says: "The deduction that consumption
of n-3 PUFAs protects against vascular diseases is based on
the observation that people living on a fish diet have a low
incidence to be affected by vascular diseases. Fish are rich
in n-3 PUFAs; thus, it was deduced that the protective
properties of a fish diet are due to n-3 PUFAs. Fish, fish
oils, and vegetables contain besides n-3 PUFAs as minor
constituents furan fatty acids (F-acids). These are radical
scavengers and are incorporated after consumption of these
nutrients into human phospholipids, leading to the assumption
that not n-3 PUFAs, but F-acids are responsible for the
beneficial efficiency of a fish diet."

Staprans I, Pan XM, Rapp JH, Feingold KR have a more serious
result with: "We hypothesize that diet-derived oxidized fatty
acids in chylomicron remnants and oxidized cholesterol in
remnants and LDL accelerate atherosclerosis by increasing
oxidized lipid levels in circulating LDL and chylomicron
remnants. This hypothesis is supported by our feeding
experiments in animals. When rabbits were fed oxidized fatty
acids or oxidized cholesterol, the fatty streak lesions in the
aorta were increased by 100%. Moreover, dietary oxidized
cholesterol significantly increased aortic lesions in apo-E
and LDL receptor-deficient mice. A typical Western diet is
rich in oxidized fats and therefore could contribute to the
increased arterial atherosclerosis in our population."

> And what about the 1948 experiments in which rats were given
> not fat, yet lived without any problems?

Jensen M, Groth L, Holmer G, Hansen HS, Fullerton A. say:
"Hairless rats were fed with a fat-free diet lacking linoleic
acid. The EFAD condition was established within 8 weeks. In
order to ensure that this condition had been established,
several parameters were measured and observed, i.e. animal
weight, water consumption, transepidermal water loss, clinical
skin symptoms, histology of the epidermis and fatty acid
analysis of serum and skin. "

> In science, if two people or groups come to different
> conclusions about the evidence, then the next step is to
> agree on an experiment that will settle the issue. I have
> made the experimental offer on this NG many times before,
> and no one is interested in even negotiating terms. What
> does that tell you, Ron? If you have an experimental idea
> in mind, why don't you articulate it on this thread and
> perhaps we can work something out and settle this the
> scientific way.

I assume that very few of the posters are researchers and any
reasonable experiment would take at least 2 years to complete.

I would like to know the optimal fatty acid balance for a
diet, but it would take a large number of test animals to get
any accuracy.

--
Ron

[Mattlb]

monty1945@lycos.com wrote:
> Mary Enig is totally wrong on these points.

Which points?

> I have tried to contact her more than once, but she has
> never responded, even though the web site's that listed her
> contact information said that she would.

She can obviously spot a crank.

> I have investigated these issues for myself. The "lipid
> bilayer membrane" stuff is nonsense.

Prove it. Come up with a model of red cell ghosts, that
precludes a lipid bilayer, like I've asked you to many times.
You won't because you never do, and you can't because the
evidence is clearly stacked up to support their existence.

> Just get any of Gilbert Ling's recent book and you will not
> only learn about this topic, but you will also see how
> science should be conducted.

Via obscure books that haven't been peer reviewed?

> As to PUFAs, when they go rancid in your body it is called
> "in vivo lipid peroxidation,"

In vivo peroxidation isn't the same thing as going rancid due
to being left out of the fridge. There's no light and far less
oxygen in the body than in the kitchen.

> and if she wishes to disbelive this, that is her perogative,
> but just go ahead and do a google or pubmed search for this.
> There are 3726 items that result on pubmed when you search
> for this phrase, for example. You can go to my web site and
> see all the evidence on PUFAs and free radical damage, and
> again, I just put the "tip of the iceberg" up on my site.

> And what about the 1948 experiments in which rats were given
> not fat, yet lived without any problems?

Please list the experimental details so we can all examine
the evidence.

> I actually ignore such possibilities, since so many people
> are conflicted, and I just examine the evidence.

What is published as evidence you mean. Or are you saying
you visit their labs and observe? If you don't think
what's published follows the money in some cases, you're
seriously deluded.

> In science, if two people or groups come to different
> conclusions about the evidence, then the next step is to
> agree on an experiment that will settle the issue. I have
> made the experimental offer on this NG many times before,
> and no one is interested in even negotiating terms.

No, your experiment tests one thing: how long animals live
when given abnormal diets high in PUFA or coconut oil. This is
not surprising as you have a blinkered obsession that how long
an animal lives is the only thing that matters.

MattLB

[monty1945]

"MattLB" is on my "do not respond, as he is likely to be a
shill" list. Still, I would respond if he made a reasonable
point on one of these issues. For example, if one does not use
overall mortality, then what constitutes the "endpoint?" Is
there a diet that is tasty and satisfying and allows you to
live to an old age but make you feel terrible? If there is,
MattLB, then tell us why. He "pops up" now and then to attack
my posts, but never does so in a way that is academically
appropriate. I have challenged him to a form, moderated
debate, I have put forth various experimental offers, etc.,
but he continues to attack, ignoring evidence contrary to his
claims, citing evidence that contradicts his claims, etc. One
can search old posts and see him "at work," doing the work of
an apparent industry shill. He knows that few will read
Gilbert Ling's works, so that he can make baseless,
unscientific remarks. I know that Ling of another scientist
would be willing to debate MattLB on this issue of "lipid
bilayer membranes," but of course he won't take up the
challenge. I will point out that conclusive experiments have
be done on this point. Here are two:

1. Cells were cut and the cytoplasm allowed to "leak out"
into a fat-freee aqueous medium. Many globules formed,
just the way it is said that "lipid bilayer membranes"
form. The problem is that the surface area of these many
small globules is much, much larger than the amount of
fatty acids required to make all the "membranes." Thus,
this notion was demonstrated to be physically impossible.

2. Cells have had the surface fatty acids washed off and the
cells have "held together" without any problems. Again,
this alone makes the "lipid bilayer" claim, as it is
proposed in many textbooks, a physical impossibility. Ling
has much more evidence, along with his hypothesis, which is
not contradicted by any experimental data, in several of
his recent books.

MattLB talks of an "artificially high" PUFA or SFA diet, yet
many people have lived on both kinds of diets. In nations
like the USA today, consumption of oils rich in omega 6s in
particular has increased dramatically since the mid twentieth
century, and many "diseases" rarely seen before circa 1940
are now common or are reaching "epidemic" levels, as our
"experts" like to tell us. If anyone wants to verify this
information, you can read the National Research Council's
book, "Diet and Health."

With regard to Ron's points, I'm not sure what you are trying
to say about Enig at this point. You mentioned her, so I will
leave it to you to clarify your position. As I've said now a
few times just on this thread, I examine the evidence, and I
don't really care what one "expert" says. If Ling, Peat, Enig,
Spiteller, or anyone else appears to be incorrect, I will be
quick to point it out. I also don't know what your point is
about Spiteller. Again, please clarify.

You did not offer the citation information on that rat
experiment, but if the rats lived fine in 1948 on a fat-free
diet, that was conclusive, unless it was outright fraud. Rats
in the 1930 experiment did not get essential B vitamins. Thus,
what you cite is likely the result of some deficiency problem.
You need to provide the information or else I can't evaluate
it. In any case, if this "EFA" nonsense was true for humans, I
should have experienced deficiency symptoms back in 2001,
instead of only experiencing only benefits up to this point.
This is what all the recent literature makes clear, that is,
my diet should produce these symptoms is about 8 weeks or
less. What they are likely seeing, if they have done such
studies on people who were not gravely ill (which is the only
evidence I have been able to unearth on this subject), are
some phenomena that occurs when you are getting the
arachidonic acid out of your body. I didn't experience much of
a transition - I only noticed that I drank a little bit more,
but that may be because I was eating a lot of antioxidant-rich
foods. And I recommend that if one follows my diet, that he or
she eat such a diet for about two years at least, while the AA
is removed, to avoid the appearance of such "EFA symptoms."

[Mattlb]

monty1945@lycos.com wrote:
> "MattLB" is on my "do not respond, as he is likely to be a
> shill" list.

A very weak excuse for avoiding the scientific challenges I
make. I'm not involved with any industry in any way.

> Still, I would respond if he made a reasonable point on one
> of these issues. For example, if one does not use overall
> mortality, then what constitutes the "endpoint?"

Your big claim is that EFA aren't required. There are well
established symptoms of EFA deficiency, so there is no need to
wait for death (which could come from many causes). The other
point is that this would be better served by a dose-response
experiment whereby increasing levels of EFA are given to a
basically coconut oil diet. There should be a graded level of
health as a result, indicating a dosage effect of EFA (one way
or the other). Comparing all-coconut to all-EFA is very
unnatural and would be too much PUFA, which no-one disagrees
shouldn't be eaten to excess.

> I He "pops up" now and then to attack my posts, but never
> does so in a way that is academically appropriate.

Attacking the falsehoods in your arguments and challenging you
to defend them is what I do. What is inappropriate about that?

> I have challenged him to a form, moderated debate, I
> have put forth various experimental offers, etc., but
> he continues to attack, ignoring evidence contrary to
> his claims,

You don't provide such evidence.

> One can search old posts and see him "at work," doing the
> work of an apparent industry shill.

And see you failing time after time to address specific
scientific queries.

> He knows that few will read Gilbert Ling's works, so that he
> can make baseless,

No, based on scientific papers and direct scientific research.
I've made red cell ghosts and cell membrane preparations. You
can't convince me they don't exist.

> I will point out that conclusive experiments have be done
> on this point. Here are two:
>
> 1. Cells were cut and the cytoplasm allowed to "leak out"
> into a fat-freee aqueous medium. Many globules formed,
> just the way it is said that "lipid bilayer membranes"
> form. The problem is that the surface area of these many
> small globules is much, much larger than the amount of
> fatty acids required to make all the "membranes." Thus,
> this notion was demonstrated to be physically
> impossible.

It's a bit of a vague description, but it sounds like whoever
did it grossly underestimated how much membrane there is
inside the cell. Also the globules may not have been bilayer
vesicles, they may have been micelles.

> 2. Cells have had the surface fatty acids washed off and the
> cells have "held together" without any problems.

If they were growing on a support medium, in a suitable
buffer, you could use detergent to remove the lipids and leave
the proteins behind. These will predominantly be the
intermediate filaments which give the cell it's shape. You
can't do the same thing to red blood cells though, which is
why I keeping asking you for a model of them that doesn't have
a bilayer membrane.

> Again, this alone makes the "lipid bilayer" claim, as it is
> proposed in many textbooks, a physical impossibility.

It doesn't, it just makes your (or his) understanding of cells
look very naive.

> Ling has much more evidence, along with his hypothesis,
> which is not contradicted by any experimental data, in
> several of his recent books.

> MattLB talks of an "artificially high" PUFA or SFA diet, yet
> many people have lived on both kinds of diets. In nations
> like the USA today, consumption of oils rich in omega 6s in
> particular has increased dramatically since the mid
> twentieth century

Not to 30% and not of only one oil.

> You did not offer the citation information on that rat
> experiment,

And you never provide details of ones you cite. You keep
quoting this 1948 experiment that wasn't in a journal and that
I can't get hold of to see what was actually done. Tell me and
everyone else what the experiment was - or OCR the pages.
Until then you just have a fairly mythical golden proof that
can never be disproved.

MattLB