Re: About cholesterol and fat

[Guest guest]

>> Rabbits given the daily caffeine equivalent of one cup of coffee

>> and fed a cholesterol-rich diet for 12 weeks suffered relatively

>> little

>> damage in their blood-brain barrier (BBB), which protects the central

>> nervous system from the rest of the body's circulation, new

>> research found.

The key word, I think, is this: rabbits. Rabbits are herbivores.

Herbivores fed a diet unsuitable for their natures are going to have

just as many problems as carnivores and omnivores fed diets unsuitable

to their own natures.

-

[Guest guest]

On 4/9/08, Idol <Idol@...> wrote:

> The key word, I think, is this: rabbits. Rabbits are herbivores.

> Herbivores fed a diet unsuitable for their natures are going to have

> just as many problems as carnivores and omnivores fed diets unsuitable

> to their own natures.

The main difference for rabbits is that their cholesterol levels shoot

through the roof, into the thousands (in mg/dl) when they are fed

cholesterol. The reaction to high blood levels of cholesterol, at

least with respect to atherosclerosis, is pretty much the same in all

species: without extra antioxidants, it leads to atherosclerosis; with

antioxidants, it doesn't.

Chris

[Guest guest]

Chris-

> The main difference for rabbits is that their cholesterol levels shoot

> through the roof, into the thousands (in mg/dl) when they are fed

> cholesterol. The reaction to high blood levels of cholesterol, at

> least with respect to atherosclerosis, is pretty much the same in all

> species: without extra antioxidants, it leads to atherosclerosis; with

> antioxidants, it doesn't.

Well, yeah, because they're not adapted to consuming it. But what

really constitutes " high " , anyway? I mean, the relationship doesn't

really show up in humans outside of familial hypercholesterolemia,

right? (IOW not considering issues of oxidized LDL and so on, just

absolute levels.)

-

[Guest guest]

I think we also need to ask what kind of cholesterol were the rabbits fed. Are

we talking the same old powdered eggs and dry milk?

And who funded this study, Starbucks?

[Guest guest]

--- Masterjohn <chrismasterjohn@...> wrote:

> The reaction to high blood levels of cholesterol, at

> least with respect to atherosclerosis, is pretty much the same in all

> species: without extra antioxidants, it leads to atherosclerosis; with

> antioxidants, it doesn't.

is the reaction also affected by the percentage of PUFA

incorporated into the lipo-proteins? My guess would be that diets

high in PUFA would tend to favor more cholesterol/lipoprotein that

includes PUFA and would therefore be more vulnerable to oxidation and

it's associated problems. I'm also guessing that with diets low in

PUFA, the cholesterol/lipoproteins would be made primarily with

saturated and monounsaturated fats and therefore would be less

vulnerable to oxidation problems.

[Guest guest]

,

> I think we also need to ask what kind of cholesterol were the rabbits fed.

> Are we talking the same old powdered eggs and dry milk?

The original experiments in the cholesterol-fed rabbits used foods

like ox brains, liver, egg yolks, and so on, in many cases dissolved

in liquid milk. This review covers the early experiments:

http://jn.nutrition.org/cgi/reprint/125/3_Suppl/589S

Unfortunately they are all in foreign journals in other languages so I

can't look at the originals, and in most cases this review does not

specifically state the foods were unprocessed. However, in some of

them it explicitly states that the food was powdered, defatted, or

otherwise processed, which leads me to believe that in the other cases

the foods were unprocessed.

Do you have information contradicting this, specifically with

reference to the earliest studies mentioned in this review, such as

those by Ignatowski?

Chris

[Guest guest]

,

> Well, yeah, because they're not adapted to consuming it. But what

> really constitutes " high " , anyway? I mean, the relationship doesn't

> really show up in humans outside of familial hypercholesterolemia,

> right? (IOW not considering issues of oxidized LDL and so on, just

> absolute levels.)

I don't know when the relationship turns up in humans because I

haven't gotten a chance to look critically at the data. I read

Ravnskov's book in which he asserts what you are saying, but I read it

years ago and without much of a critical eye to it.

But what I am saying is that in the experimental induction, they can

very easily get the same result in the cholesterol-fed rabbit in a

dog, so long as they can raise the blood level to an equivalent

degree. There are no experimental inductions of atherosclerosis in

humans, so we can't really say there. But across all species,

regardless of carnivory, omnivory, or herbivory, the experimental

induction is more or less the same result and dependent on the blood

level reached. The main difference with herbivores is that it is much

easier to raise their blood levels.

Of course in experimental inductions you have something different than

what you have in humans, and that is a tightly controlled diet. " All

things being equal " more lipoproteins are going to mean more oxidized

lipoproteins. But all things are only equal, with a little luck, in

the lab.

Chris

[Guest guest]

,

> is the reaction also affected by the percentage of PUFA

> incorporated into the lipo-proteins? My guess would be that diets

> high in PUFA would tend to favor more cholesterol/lipoprotein that

> includes PUFA and would therefore be more vulnerable to oxidation and

> it's associated problems. I'm also guessing that with diets low in

> PUFA, the cholesterol/lipoproteins would be made primarily with

> saturated and monounsaturated fats and therefore would be less

> vulnerable to oxidation problems.

I agree. Diets high in PUFA do increase the vulnerability of LDL to

oxidation. The absolute concentration of LDL is relatively

irrelevant. It might have some very slight degree of influence, but

to the extent there are correlations it is mostly a marker for a)

other things that raise cholesterol levels like inflammation and

oxidized LDL. The latter has to exert at least some causal influence,

because in animal experiments hypercholesterolemia is basically a

prerequisite for atherosclerosis. So the inflammation studies, for

example, are mostly done in hypercholesterolemic models and probably

dependent on them to some degree. But if you make the animals

hypercholesterolemic and give them antioxidants, they don't get the

atherosclerosis. So it's no the hypercholesteroemia per se. It's the

high level of PUFA-rich LDL membranes floating around.

Chris

[Guest guest]

Chris-

> I don't know when the relationship turns up in humans because I

> haven't gotten a chance to look critically at the data. I read

> Ravnskov's book in which he asserts what you are saying, but I read it

> years ago and without much of a critical eye to it.

My recollection is that his assertion wasn't one of the weak parts of

the book, but that said, I'm sure I'd turn a sharper eye to it if I

read it today, so who knows.

> But what I am saying is that in the experimental induction, they can

> very easily get the same result in the cholesterol-fed rabbit in a

> dog, so long as they can raise the blood level to an equivalent

> degree.

I understand, but I think it's profoundly important that a rabbit is

an herbivore and simply isn't adapted to dietary cholesterol. It's

much, much harder to raise cholesterol levels to extreme heights in

carnivorous and omnivorous animals because they actually have

biological mechanisms for dealing with dietary cholesterol. So the

fact that feeding some cholesterol to rabbits causes problems is, IMO,

essentially meaningless for humans.

> Of course in experimental inductions you have something different than

> what you have in humans, and that is a tightly controlled diet. " All

> things being equal " more lipoproteins are going to mean more oxidized

> lipoproteins. But all things are only equal, with a little luck, in

> the lab.

Well, yeah, that's the other issue at hand, as points out. My

only point was that there's no practical take-home message for human

nutrition from a study involving feeding rabbits cholesterol-rich

foods or isolated cholesterol. The foods (or isolated cholesterol)

simply won't have the same effects on normal humans, and in fact you'd

have to cause a profound metabolic derangement to achieve the sort of

astronomic numbers required for anything like an apples-to-apples

comparison. Any dietary recommendations for people based on rabbit

experiments like these are just bunk.

-

[Guest guest]

,

> Well, yeah, that's the other issue at hand, as points out. My

> only point was that there's no practical take-home message for human

> nutrition from a study involving feeding rabbits cholesterol-rich

> foods or isolated cholesterol. The foods (or isolated cholesterol)

> simply won't have the same effects on normal humans, and in fact you'd

> have to cause a profound metabolic derangement to achieve the sort of

> astronomic numbers required for anything like an apples-to-apples

> comparison. Any dietary recommendations for people based on rabbit

> experiments like these are just bunk.

Yeah, I agree with that.

Chris

[Guest guest]

> I agree. Diets high in PUFA do increase the vulnerability of LDL to

> oxidation. The absolute concentration of LDL is relatively

> irrelevant. It might have some very slight degree of influence, but

> to the extent there are correlations it is mostly a marker for a)

> other things that raise cholesterol levels like inflammation and

> oxidized LDL. The latter has to exert at least some causal influence,

> because in animal experiments hypercholesterolemia is basically a

> prerequisite for atherosclerosis. So the inflammation studies, for

> example, are mostly done in hypercholesterolemic models and probably

> dependent on them to some degree. But if you make the animals

> hypercholesterolemic and give them antioxidants, they don't get the

> atherosclerosis. So it's no the hypercholesteroemia per se. It's the

> high level of PUFA-rich LDL membranes floating around.

Omega 3's are a PUFA. Should people be worried about omega 3's in seafood and in

supplements, like fish and krill oil?

[Guest guest]

-

> Omega 3's are a PUFA. Should people be worried about omega 3's in

> seafood and in

> supplements, like fish and krill oil?

Of course.

-

[Guest guest]

Chris-

> But if you make the animals

> hypercholesterolemic and give them antioxidants, they don't get the

> atherosclerosis. So it's no the hypercholesteroemia per se. It's the

> high level of PUFA-rich LDL membranes floating around.

So shouldn't there be a very visible effect on the correlation between

cholesterol levels and atherosclerosis from the amount of PUFA in the

diet? Have there been any experiments in which cholesterol (in one

form or another) was fed to rabbits (or other animals) in order to

raise their cholesterol levels to astronomical heights but very, very

little PUFA was fed?

-

[Guest guest]

,

> Omega 3's are a PUFA. Should people be worried about omega 3's in seafood

> and in

> supplements, like fish and krill oil?

Yes. I haven't seen Krill oil tested, but regular fish oils increase

lipid peroxides even when they are compared to a corn oil placebo, and

vitamin E does not protect against the effect.

Chris

[Guest guest]

,

> So shouldn't there be a very visible effect on the correlation between

> cholesterol levels and atherosclerosis from the amount of PUFA in the

> diet? Have there been any experiments in which cholesterol (in one

> form or another) was fed to rabbits (or other animals) in order to

> raise their cholesterol levels to astronomical heights but very, very

> little PUFA was fed?

I don't know; I've only seen these experiments described in reviews.

The original experiment with isolated cholesterol dissolved it in

sunflower oil, and most lab diets are high in PUFA. However, liver

was used in some of the earlier studies, and it is very low in fat; I

don't know what the basal diet was.

Still, even if low PUFA is fed, PUFA only declines so much in the

body. Even if no PUFA is fed, the body still makes PUFA from oleic

acid. A very high level blood cholesterol represents a transfer of

the PUFA from safer places to the blood, where it is more easily

oxidized, especially if it is in small LDL particles that can fit

through the spaces in the endothelium.

So you still need the antioxidants (especially and above all CoQ10,

also vitamin E, etc) to protect the PUFA in the LDL, no matter how

much you reduce dietary PUFA. If you just increase LDL, and you don't

increase antioxidants, you are decreasing the antioxidant:LDL ratio,

or the antioxidant:LDL-associated PUFA ratio.

Chris

[Guest guest]

--- In , " Masterjohn "

<chrismasterjohn@...>

wrote:

> > Omega 3's are a PUFA. Should people be worried about omega 3's in seafood

> > and in

> > supplements, like fish and krill oil?

>

> Yes. I haven't seen Krill oil tested, but regular fish oils increase

> lipid peroxides even when they are compared to a corn oil placebo, and

> vitamin E does not protect against the effect.

I have been overdosing on krill oil (and recently cod liver oil) after having a

test with low

HDL cholesterol and then reading a randomized trial showing krill oil reduces

LDL, raises

HDL and lowers triglycerides, but quite a substantial margin. (*) Only patients

with

hyperlidpidemia were in the trial.

I also reviewed surveys of evidence about fish oil and total mortality and/or

heart disease,

such as AHRQ's Evidence Report #94, " Effects of Omega-3 Fatty Acids on

Cardiovascular

Disease " , which conclude that fish oil reduces disease and has few adverse

effects. Again,

your position is that the beneficial effects of omega 3 supplementation accrue

only to

those already suffering from a disease, like cardiovascular disease?

In your thought-provoking PUFA report, you don't address the grass fed beef

issue.

Proponents of grass fed beef highlight its more balanced omega-6 to omega-3

ratio.

Would your position be that the PUFA ratio doesn't matter, eat all the grain fed

beef you

want (as long as its organic)?

Today, before reading your report, I ate about 0.5 pounds of grass fed beef

liver, which

would correspond (using the grain fed data on NutritionData) to roughly 1.3

grams of

PUFA, more than half linoleic (although with a good chunk of arachidonic) and

all omega

6. On the other hand, eating a 0.5 pounds of top sirloin steak (again grain fed)

would give

about 0.9 grams of PUFA. Because people like steak more than liver and tend to

eat more

of it, do you really need to eat liver to get enough PUFA? Maybe we should avoid

liver to

avoid getting too much PUFA, by the logic that oxidized cholesterol is a leading

cause of

chronic disease?

(*) Bunea, El Farrah, Deutsch (Alternative Medicine Review, vol 9 no 4 2004)

[Guest guest]

,

> I also reviewed surveys of evidence about fish oil and total mortality

> and/or heart disease,

> such as AHRQ's Evidence Report #94, " Effects of Omega-3 Fatty Acids on

> Cardiovascular

> Disease " , which conclude that fish oil reduces disease and has few adverse

> effects. Again,

> your position is that the beneficial effects of omega 3 supplementation

> accrue only to

> those already suffering from a disease, like cardiovascular disease?

I will be primarily addressing this in the PUFA Report Part 2 coming

out later this year. However, my preliminary look at the evidence

indicates that fish oils are primarily beneficial to people with

established heart disease subject to cardiac arrhythmia, and might be

harmful for other people.

> In your thought-provoking PUFA report, you don't address the grass fed beef

> issue.

> Proponents of grass fed beef highlight its more balanced omega-6 to omega-3

> ratio.

> Would your position be that the PUFA ratio doesn't matter, eat all the grain

> fed beef you

> want (as long as its organic)?

Well, I don't go in-depth, but I do note that grass-fed is a better

source of DHA. I think the ratio is unimportant if total PUFA is low,

at least if it is under 1% of calories, but it is difficult to

restrict it that low and the ratio might become more important above

it. Also, grass-fed has other benefits like vitamins and CLA and so

on.

> Today, before reading your report, I ate about 0.5 pounds of grass fed beef

> liver, which

> would correspond (using the grain fed data on NutritionData) to roughly 1.3

> grams of

> PUFA, more than half linoleic (although with a good chunk of arachidonic)

> and all omega

> 6.

Does nutritiondata have figures specifically for grass-fed liver?

>On the other hand, eating a 0.5 pounds of top sirloin steak (again grain

> fed) would give

> about 0.9 grams of PUFA. Because people like steak more than liver and tend

> to eat more

> of it, do you really need to eat liver to get enough PUFA? Maybe we should

> avoid liver to

> avoid getting too much PUFA, by the logic that oxidized cholesterol is a

> leading cause of

> chronic disease?

Well it is the oxidized PUFA in the lipoprotein, not so much the

cholesterol. Liver is very, very low in PUFA. The point is it has

plenty of arachidonic acid and B6, and when you get those, you don't

need that much PUFA. And of course liver is loaded with many other

nutrients. Grass-fed is better, and tends to be lower in fat.

Chris

[Guest guest]

--- In , " Masterjohn "

<chrismasterjohn@...>

wrote:

> I will be primarily addressing this in the PUFA Report Part 2 coming

> out later this year. However, my preliminary look at the evidence

> indicates that fish oils are primarily beneficial to people with

> established heart disease subject to cardiac arrhythmia, and might be

> harmful for other people.

As I have no heart disease that creates visible symptoms (at least before I

started taking

the supplements), I will discontinue the omega 3 krill oil and cut back the cod

liver oil to a

few times a week, at least until Part 2 comes out and I see your arguments in

detail.

> Does nutritiondata have figures specifically for grass-fed liver?

No, I used the figures for grain fed beef. I suspect the figures are mainly from

the USDA,

and the USDA does not seem to care about grass fed beef.

> Well it is the oxidized PUFA in the lipoprotein, not so much the

> cholesterol.

Sorry. I suppose Part 2 will go into more detail about disease.

> Liver is very, very low in PUFA. The point is it has

> plenty of arachidonic acid and B6, and when you get those, you don't

> need that much PUFA. And of course liver is loaded with many other

> nutrients. Grass-fed is better, and tends to be lower in fat.

I try to eat at home a lot, but the demands of work and being social otherwise

mean I eat

out several times a week. I suspect I get plenty of PUFAs from cooking oil at

these

restaurants. I agree liver has many other nutrients, although not Vitamin D. I

have heard

that leucine, a protein, helps maintain muscle mass.

I checked NutritionData about beef liver again. The amount of Vitamin A (21,600

IU) in just

one slice is twice was Enig and Fallon recommend for an adult on the WAPF

website. I had

several slices for dinner today.

[Guest guest]

Is fish oil the same as Cod Liver Oil? Sounds silly but I think there

might be a difference.

On Apr 13, 2008, at 5:27 PM, Masterjohn wrote:

>> Omega 3's are a PUFA. Should people be worried about omega 3's in

>> seafood

>> and in

>> supplements, like fish and krill oil?

>

> Yes. I haven't seen Krill oil tested, but regular fish oils increase

> lipid peroxides even when they are compared to a corn oil placebo, and

> vitamin E does not protect against the effect.

Parashis

artpages@...

portfolio pages:

http://www.flickr.com/photos/11468108@N08/

http://www.artpagesonline.com/EPportfolio/000portfolio.html

[Guest guest]

On 4/14/08, Parashis <artpages@...> wrote:

> Is fish oil the same as Cod Liver Oil? Sounds silly but I think there

> might be a difference.

Some people use fish oil to include cod liver oil, but I do not. They

are similar in that they are both high in EPA/DHA, but CLO is high in

vitamins too.

Chris

[Guest guest]

--- In , " Masterjohn "

<chrismasterjohn@...>

wrote:

It is interesting to note that Colpo mentions several studies in his book where

rates of

heart disease decreased with a reduction in oxidized LDL even when total LDL

cholesterol

stayed the same or went up.

For example, in a study of Japanese patients undergoing surgery to remove plaque

from

their arteries, blood levels of ox-LDL were significantly higher than those

measured in

healthy controls. However, there was no association between oxidized LDL and

overall LDL

levels.

This seems to indicate that the relationship between antioxidant status, total

cholesterol

and ox-LDL is more important than the level of each measurement on its own.

Perhaps

that's already obvious but I thought I'd point that out.

Also, if high total cholesterol by definition increases the amount of ox-LDL in

circulation,

then why do more than 18 studies indicate that high cholesterol not a risk

factor CHD,

stroke or mortality in elderly people?

Even Steinberg (leading supporter of the lipid hypothesis) admits " We

have all seen

myocardial infarction in patients with cholesterol levels <200; we have also

seen patients

with heterozygous familial cholesterolemia and cholesterol levels >300 who

somehow

survive into their 70s with no clinically evident CHD... patients with very

different LDL

concentrations can come into the catheterization laboratory with similar degrees

of

atherosclerosis. "

I'm not arguing that ox-LDL isn't a risk factor. But I am not completely

convinced that

high total LDL necessarily increases ox-LDL. If someone is following a whole

foods based

diet with low intake of PUFA and high antioxidant intake, and they test with

high LDL, I'm

not certain they have anything to worry about.

K.

[Guest guest]

> Also, if high total cholesterol by definition increases the amount of ox-LDL

> in circulation,

> then why do more than 18 studies indicate that high cholesterol not a risk

> factor CHD,

> stroke or mortality in elderly people?

Neither I nor anyone else siad that high total cholesterol " by

definition " increases the amount of ox-LDL. I said that elevating LDL

-- all things being equal -- will elevate ox-LDL. I also said that

all things are never equal, except, if you get lucky, in a laboratory.

> Even Steinberg (leading supporter of the lipid hypothesis) admits " We

> have all seen

> myocardial infarction in patients with cholesterol levels <200; we have also

> seen patients

> with heterozygous familial cholesterolemia and cholesterol levels >300 who

> somehow

> survive into their 70s with no clinically evident CHD... patients with very

> different LDL

> concentrations can come into the catheterization laboratory with similar

> degrees of

> atherosclerosis. "

Well I don't know in what context Steinberg said this, but I can't

imagine he was using it to contradict the idea that cholesterol levels

are important. Obviously the <200 level is arbitrary. According to

Castelli I think it is, as I believe Steinberg cites in several

places, in the Framingham study over decades they have not observed a

single heart attack in anyone with a total cholesterol level under

150.

> I'm not arguing that ox-LDL isn't a risk factor. But I am not completely

> convinced that

> high total LDL necessarily increases ox-LDL.

Again, I didn't say it did.

Chris