Re: Fats & Cholesterol

[Guest guest]

Hi

From the data I have seen, it is not conclusive that oxidized LDL is a direct

contributor to

the atherogenic process. I'd love to see any studies that you think prove

otherwise (not

simply association, but cause).

Here is Dr. Rory reporting on the HPS study I quoted earlier (in BMJ Nov

2001):

" There was no evidence of any benefit at all from antioxidant vitamins. On the

other hand,

there was no evidence of any harm. "

That study lasted five years and had ten thousand patients. I do not know if

the

antioxidants lowered the amount of oxidized LDL (I'd love to find out). But why

wouldn't

they?

In any event, it's probably not worth quibbling about because I agree that

causes of

oxidation in the diet should be avoided for other reasons in addition to the

possibility that

oxidized LDL is a causative factor in CHD.

As far as I've seen, the response to injury hypothesis hasn't been discredited.

I've seen

many, many studies that support it. I have not seen the study you mentioned

(would you

mind providing a reference?) I'm actually surprised that a study was approved

which

allowed purposeful damage to be done to the endothelium - sounds quite unethical

to me,

in light of the fact that many believe that kind of damage to be a major risk

factor for

CHD. Did the people who developed atherosclerosis after the injury have high

levels of

oxidized LDL, or just high levels of LDL?

There is just so much data that contradicts the popular hypothesis that LDL

(non-

oxidized) is a causative factor for CHD. I'd be happy to share some with you,

if you're

interested.

Best,

Chris

--- In , " Masterjohn "

<chrismasterjohn@...>

wrote:

>

> Hi

>

> > In addition, the theory that oxidized LDL causes atherosclerosis is also

> > incomplete and not

> > entirely supported by the data. Some studies have indicated an association

> > between high

> > levels of oxidized LDL and a significantly increased risk of heart attack,

> > regardless of total

> > LDL levels. (Holvoet P, et al. Arterioscler Thromb Vasc Biol.

> > 2003;32:1444-1448; Holvoet

> > P, et al. Diabetes. 20004;53:1068-1073)

>

> Yes, the total amount of oxidized LDL-associated phospholipids is a

> huge predictor of risk, about eight times greater than LDL.

>

> > Yet the Heart Protection Study (5 years, 10,000 patients) demonstrated " no

> > evidence of

> > any benefit from antioxidant vitamins " , which would be expected if

> > oxidization of LDL was

> > the cause of CHD (Kmietowicz, Z. Statins are the new aspirin, Oxford

> > researchers say. BMJ

> > 2001;323:1145)

>

> Were the antioxidants effective at reducing LDL oxidation? The study

> would not be meaningful to the theory at all otherwise.

>

> > If the endothelium had receptors for oxidized LDL, then oxidized LDL would

> > be absorbed

> > through all artery walls everywhere and we would not see discreet plaques

> > forming - just

> > general thickening of the artery wall. This is not the case.

>

> The issue is not what receptors the endothelium expresses, but what

> receptors the macrophages that embed themselves in the endothelium

> express. They take up oxidized LDL and glycated LDL at a rapid rate

> through scavenger receptors but do not take up non-oxidized LDL. The

> uptake of oxidized LDL by macrophages generates all kinds of

> inflammatory cascades characteristic of atherosclerosis.

>

> > The fact that plaques form in discreet locations lends credence to the

> > " response to injury "

> > hypothesis, which is becoming more widely accepted and is very well

> > supported by the

> > data. This theory suggests that it is an injury to the epithelial wall

> > (lining of the artery)

> > that causes plaques to form and promotes heart attacks.

>

> This was one of the first theories investigated and was set back by a

> number of early findings, such as that directly inducing injuries to

> the vessel walls did not produce atherosclerosis in the absence of

> hyperlipidemia, but aggravated atherosclerosis in its presence.

>

> > Proven risk factors

> > for such an

> > injury include: nutrient deficiencies, poor glycemic control (insulin

> > resistance), cigarette

> > smoking, homocysteine, nitric oxide depletion, high iron levels, microbial

> > infection,

> > dietary trans fatty acids, high PUFA intake, and excessive refined

> > carbohydrate intake

> > (which promotes poor glycemic control).

>

> Oxidized LDL causes nitric oxide depletion; poor glycemic control

> causes LDL glycation; high PUFA intake causes LDL oxidation. So these

> risk factors are not actually teasing out the response-to-injury

> hypothesis from the oxidized lipid hypothesis, but instead are showing

> the convergence of both hypotheses.

>

> > It is still of course wise to avoid foods and other factors that promote

> > oxidization, since

> > free radicals have many proven ill effects on the body. In spite of the

> > commonly held

> > belief, saturated fats are much better for heart health than PUFAs. I could

> > show you reams

> > of data on that (actually, if you're interested you can download my

> > presentation at

> > http://chriskresser.com/research/cholesterol_class.pdf), but based on your

> > presence here

> > I'm guessing you already know that.

>

> I certainly agree with that -- which is consistent with the oxidized

> LDL hypothesis as well, since PUFAs are the first target of oxidation

> in the LDL particle.

>

> Chris

>

[Guest guest]

I don't know if I asked this clearly in my last response, but I'm curious to

know what your

theory is on what causes CHD. Clearly you believe oxidized LDL is causative.

But wouldn't

damage to the endothelium be a necessary precondition in that scenario?

Otherwise, my

earlier comment about oxidized LDL causing arteries to thicken everywhere in the

body

rather than simply in discreet locations would seem to contradict the

hypothesis.

Thanks,

Chris

--- In , " Masterjohn "

<chrismasterjohn@...>

wrote:

>

> Hi

>

> > In addition, the theory that oxidized LDL causes atherosclerosis is also

> > incomplete and not

> > entirely supported by the data. Some studies have indicated an association

> > between high

> > levels of oxidized LDL and a significantly increased risk of heart attack,

> > regardless of total

> > LDL levels. (Holvoet P, et al. Arterioscler Thromb Vasc Biol.

> > 2003;32:1444-1448; Holvoet

> > P, et al. Diabetes. 20004;53:1068-1073)

>

> Yes, the total amount of oxidized LDL-associated phospholipids is a

> huge predictor of risk, about eight times greater than LDL.

>

> > Yet the Heart Protection Study (5 years, 10,000 patients) demonstrated " no

> > evidence of

> > any benefit from antioxidant vitamins " , which would be expected if

> > oxidization of LDL was

> > the cause of CHD (Kmietowicz, Z. Statins are the new aspirin, Oxford

> > researchers say. BMJ

> > 2001;323:1145)

>

> Were the antioxidants effective at reducing LDL oxidation? The study

> would not be meaningful to the theory at all otherwise.

>

> > If the endothelium had receptors for oxidized LDL, then oxidized LDL would

> > be absorbed

> > through all artery walls everywhere and we would not see discreet plaques

> > forming - just

> > general thickening of the artery wall. This is not the case.

>

> The issue is not what receptors the endothelium expresses, but what

> receptors the macrophages that embed themselves in the endothelium

> express. They take up oxidized LDL and glycated LDL at a rapid rate

> through scavenger receptors but do not take up non-oxidized LDL. The

> uptake of oxidized LDL by macrophages generates all kinds of

> inflammatory cascades characteristic of atherosclerosis.

>

> > The fact that plaques form in discreet locations lends credence to the

> > " response to injury "

> > hypothesis, which is becoming more widely accepted and is very well

> > supported by the

> > data. This theory suggests that it is an injury to the epithelial wall

> > (lining of the artery)

> > that causes plaques to form and promotes heart attacks.

>

> This was one of the first theories investigated and was set back by a

> number of early findings, such as that directly inducing injuries to

> the vessel walls did not produce atherosclerosis in the absence of

> hyperlipidemia, but aggravated atherosclerosis in its presence.

>

> > Proven risk factors

> > for such an

> > injury include: nutrient deficiencies, poor glycemic control (insulin

> > resistance), cigarette

> > smoking, homocysteine, nitric oxide depletion, high iron levels, microbial

> > infection,

> > dietary trans fatty acids, high PUFA intake, and excessive refined

> > carbohydrate intake

> > (which promotes poor glycemic control).

>

> Oxidized LDL causes nitric oxide depletion; poor glycemic control

> causes LDL glycation; high PUFA intake causes LDL oxidation. So these

> risk factors are not actually teasing out the response-to-injury

> hypothesis from the oxidized lipid hypothesis, but instead are showing

> the convergence of both hypotheses.

>

> > It is still of course wise to avoid foods and other factors that promote

> > oxidization, since

> > free radicals have many proven ill effects on the body. In spite of the

> > commonly held

> > belief, saturated fats are much better for heart health than PUFAs. I could

> > show you reams

> > of data on that (actually, if you're interested you can download my

> > presentation at

> > http://chriskresser.com/research/cholesterol_class.pdf), but based on your

> > presence here

> > I'm guessing you already know that.

>

> I certainly agree with that -- which is consistent with the oxidized

> LDL hypothesis as well, since PUFAs are the first target of oxidation

> in the LDL particle.

>

> Chris

>

[Guest guest]

Hi

> From the data I have seen, it is not conclusive that oxidized LDL is a

> direct contributor to

> the atherogenic process. I'd love to see any studies that you think prove

> otherwise (not

> simply association, but cause).

Well I don't know if there are any studies that " prove " it conclusive,

since empirical science is not capable of proving anything, but

oxidized LDL inhibits nitric oxide production, is cytotoxic, attracts

and accumulates into macrophages and activates the transformation to

foam cells, which leads to an inflammatory cascade. So, these

mechanistic details in conjunction with strong correlation observed in

vivo in humans makes it very highly unlikely that oxidized LDL does

not make some causal contribution to the disease.

> Here is Dr. Rory reporting on the HPS study I quoted earlier (in BMJ

> Nov 2001):

>

> " There was no evidence of any benefit at all from antioxidant vitamins. On

> the other hand,

> there was no evidence of any harm. "

I don't know what your point is -- this is evidence regarding the

benefit of antioxidant vitamins, not evidence regarding the role of

oxidized LDL in atherosclerosis.

> That study lasted five years and had ten thousand patients. I do not know

> if the

> antioxidants lowered the amount of oxidized LDL (I'd love to find out).

Then you are citing a study that may well be completely irrelevant.

> But

> why wouldn't

> they?

Perhaps the doses weren't high enough, they didn't accumulate in LDL,

they weren't given in conjunction with needed cooperative

antioxidants, or they were given in a dose or ratio that led to

pro-oxidant activity. Or, there actually was a benefit but it was too

small to be statistically significant, it was compensated for by some

other adverse effect, it occurred at the wrong stage in the disease

process, etc.

> In any event, it's probably not worth quibbling about because I agree that

> causes of

> oxidation in the diet should be avoided for other reasons in addition to the

> possibility that

> oxidized LDL is a causative factor in CHD.

Ok.

> As far as I've seen, the response to injury hypothesis hasn't been

> discredited. I've seen

> many, many studies that support it.

I didn't say it's been discredited. I said it ran up along problems

indicating that it isn't sufficient for atherosclerosis. The original

studies prior to the cholesterol-fed rabbit used mechanical injury,

adrenaline injections, injections of bacteria or their byproducts,

etc, and could not induce atherosclerosis, but could initiate or

aggravate it in the presence of hypercholesterolemia (which we now

also know involves high levels of oxidized LDL, and antioxidants such

as resveratrol reverse its effects without changing cholesterol

levels).

> I have not seen the study you mentioned

> (would you

> mind providing a reference?)

Which study do you mean?

> I'm actually surprised that a study was

> approved which

> allowed purposeful damage to be done to the endothelium - sounds quite

> unethical to me,

> in light of the fact that many believe that kind of damage to be a major

> risk factor for

> CHD. Did the people who developed atherosclerosis after the injury have

> high levels of

> oxidized LDL, or just high levels of LDL?

They did these in animals, not in people.

> There is just so much data that contradicts the popular hypothesis that LDL

> (non-

> oxidized) is a causative factor for CHD. I'd be happy to share some with

> you, if you're

> interested.

But I don't believe that non-oxidized LDL is a causative factor, and

most researchers don't either. The mainstream view is that oxidized

LDL, not non-oxidized LDL, plays a causative role.

Chris

[Guest guest]

Hi

> I don't know if I asked this clearly in my last response, but I'm curious to

> know what your

> theory is on what causes CHD.

I just gave a pretty succinct summary in the " heart attack " thread.

> Clearly you believe oxidized LDL is

> causative.

I believe it plays a causative role. What proportion of the total

causation, I have no idea, but I think it makes some causative

contribution.

> But wouldn't

> damage to the endothelium be a necessary precondition in that scenario?

Oxidized LDL does damage the endothelium because it is cytotoxic.

Also, in inhibits nitric oxide production, which is somewhat damaging

in and of itself.

> Otherwise, my

> earlier comment about oxidized LDL causing arteries to thicken everywhere in

> the body

> rather than simply in discreet locations would seem to contradict the

> hypothesis.

Not at all.

The location can be explained by the direction and pressure of blood

flow. Where blood flow is disturbed, there is less shear stress, and

nitric oxide production is downregulated. Less nitric oxide means

less blood flow and vessel dilation, more recruitment of white blood

cells and aggregation of platelets and migration of smooth muscle

cells, etc. Where the blood flow is not disturbed, there is lots of

shear stress which upregulates nitric oxide production and prevents

the development of atherosclerosis. The places of disturbed blood

flow correspond to the places where atherosclerosis develops.

Moreover, it is not the endothelial cells that take up the oxidized

LDL, but white blood cells called macrophages that infiltrate the

endothelium. Macrophages do not take up non-oxidized LDL but they

take up oxidized and/or glycated LDL. Moreover, oxidized LDL acts as

a chemoattractant to macrophages to cause them to migrate to a certain

location and then immobilizes them, and when it accumulates in

macrophages, it causes them to secrete adhesion molecules that further

the atherosclerotic process.

Nitric oxide prevents the oxidation of LDL, and oxidized LDL prevents

the production of nitric oxide, so they are interrelated.

So, we would not expect from the theory atherosclerosis to be

everywhere evenly, but wherever the macrophages accumulate, because it

is those cells that are taking up the oxidized LDL.

Chris

[Guest guest]

Thanks for your very clear and thorough explanation. I understand the role of

macrophages in the inflammatory cascade, and that part always made sense. What

I didn't

have an explanation for is why oxidized LDL only causes endothelial injury or

thickening in

some areas and not others. Your description of the hemodynamics involved

clarified that

for me.

Out of curiosity, are you working in this field?

Chris

--- In , " Masterjohn "

<chrismasterjohn@...>

wrote:

>

> Hi

>

> > I don't know if I asked this clearly in my last response, but I'm curious to

> > know what your

> > theory is on what causes CHD.

>

> I just gave a pretty succinct summary in the " heart attack " thread.

>

> > Clearly you believe oxidized LDL is

> > causative.

>

> I believe it plays a causative role. What proportion of the total

> causation, I have no idea, but I think it makes some causative

> contribution.

>

> > But wouldn't

> > damage to the endothelium be a necessary precondition in that scenario?

>

> Oxidized LDL does damage the endothelium because it is cytotoxic.

> Also, in inhibits nitric oxide production, which is somewhat damaging

> in and of itself.

>

> > Otherwise, my

> > earlier comment about oxidized LDL causing arteries to thicken everywhere in

> > the body

> > rather than simply in discreet locations would seem to contradict the

> > hypothesis.

>

> Not at all.

>

> The location can be explained by the direction and pressure of blood

> flow. Where blood flow is disturbed, there is less shear stress, and

> nitric oxide production is downregulated. Less nitric oxide means

> less blood flow and vessel dilation, more recruitment of white blood

> cells and aggregation of platelets and migration of smooth muscle

> cells, etc. Where the blood flow is not disturbed, there is lots of

> shear stress which upregulates nitric oxide production and prevents

> the development of atherosclerosis. The places of disturbed blood

> flow correspond to the places where atherosclerosis develops.

>

> Moreover, it is not the endothelial cells that take up the oxidized

> LDL, but white blood cells called macrophages that infiltrate the

> endothelium. Macrophages do not take up non-oxidized LDL but they

> take up oxidized and/or glycated LDL. Moreover, oxidized LDL acts as

> a chemoattractant to macrophages to cause them to migrate to a certain

> location and then immobilizes them, and when it accumulates in

> macrophages, it causes them to secrete adhesion molecules that further

> the atherosclerotic process.

>

> Nitric oxide prevents the oxidation of LDL, and oxidized LDL prevents

> the production of nitric oxide, so they are interrelated.

>

> So, we would not expect from the theory atherosclerosis to be

> everywhere evenly, but wherever the macrophages accumulate, because it

> is those cells that are taking up the oxidized LDL.

>

> Chris

>

[Guest guest]

> > I have not seen the study you mentioned

> > (would you

> > mind providing a reference?)

>

> Which study do you mean?

>

The one where they induced endothelial damage (in animals, as I understand now)

and

atherosclerosis only developed in the presence of hyperlipidemia. I'm guessing

that they

didn't measure oxidized LDL separately at that time, since if this study was

done before the

rabbits then we're talking about the early 50s right?

Chris

[Guest guest]

I read your post in the heart attack thread. I have a question about this part:

Inflammation also interferes with nitric oxide functioning.

Inflammation is correlated with cholesterol, so part of the

correlation with cholesterol reflects the role of inflammation. The

other part of the correlation reflects the causal participation of

oxidized LDL.

What is the correlation between cholesterol and inflammation that you mention?

I am a student at an acupuncture and integrative medicine college in Berkeley,

and I'm doing

a major research project on cholesterol, saturated fat and heart disease. Any

references you

could provide, or even general pointers on which journals/authors to look for if

you can't

remember the specific citation, would be appreciated.

Thanks again,

Chris

[Guest guest]

Hi

> Thanks for your very clear and thorough explanation. I understand the role

> of

> macrophages in the inflammatory cascade, and that part always made sense.

> What I didn't

> have an explanation for is why oxidized LDL only causes endothelial injury

> or thickening in

> some areas and not others. Your description of the hemodynamics involved

> clarified that

> for me.

You're welcome.

> Out of curiosity, are you working in this field?

No, but I learnt a lot of this when I did the research for my stroke

article that was in Wise Traditions the journal before the current

one. It isn't available online yet, but there is a condensed version

on my site under the " myths " section (www.cholesterol-and-health.com).

Also, a lot of it is covered in Steinberg's new book, which I

just did a review of:

http://www.cholesterol-and-health.com/-Steinberg-Cholesterol-Wars.html

I'm working on vitamin A stuff, though not really started with anything yet.

Chris

[Guest guest]

--- " chriskjezp " <chriskresser@...> wrote:

> I am a student at an acupuncture and integrative medicine college in

> Berkeley, and I'm doing a major research project on cholesterol,

> saturated fat and heart disease. Any references you could provide, or

> even general pointers on which journals/authors to look for if you

> can't remember the specific citation, would be appreciated.

(Kresser), have you read Colpo's book, " The Great

Cholesterol Con " ? He reviews all the studies and has references for

them. You can get his book on Amazon and his book has a five-star

rating from reviews there (search for " Colpo " in Amazon books). You

can also get an e-book copy from 's web site:

http://www.thegreatcholesterolcon.com/

[Guest guest]

Hi

> The one where they induced endothelial damage (in animals, as I understand

> now) and

> atherosclerosis only developed in the presence of hyperlipidemia. I'm

> guessing that they

> didn't measure oxidized LDL separately at that time, since if this study was

> done before the

> rabbits then we're talking about the early 50s right?

No, way before that. I haven't seen them first hand but Steinberg

discusses them in his book. I just gave a link to my review of it in

my other post. You could get the references from his book, and some

of them might be available online, since a lot of the old stuff in the

prestigious journals has been going up online in recent years.

Otherwise, you'd have to dig them out of a library.

Chris

[Guest guest]

Hi

> What is the correlation between cholesterol and inflammation that you

> mention?

I discuss it in my article on Rho Activation:

http://www.cholesterol-and-health.com/Rho-Activation.html

Inflammatory compounds such as TNF-alpha and certain interleukins, and

lipopolysacharide, which is derived from the breakdown of

gram-negative bacteria, stimulate HMG CoA Reductase. This increases

the pool of mevalonate, from which cholesterol and

geranylgeranylpyrophosphate (GGPP) are both made. They also, however,

inhibit squalene synthase, which shunts mevalonate from the

cholesterol synthesis pathway to the GGPP pathway (among other

pathways), causing a smaller increase in cholesterol levels and a

higher increase in GGPP levels. GGPP activates Rho, which induces a

stress response that powerfully inhibits nitric oxide synthase, the

enzyme that makes nitric oxide.

> I am a student at an acupuncture and integrative medicine college in

> Berkeley, and I'm doing

> a major research project on cholesterol, saturated fat and heart disease.

> Any references you

> could provide, or even general pointers on which journals/authors to look

> for if you can't

> remember the specific citation, would be appreciated.

There are some citations in that link that will lead you to more references.

Chris

[Guest guest]

Could I have the list again of the foods that are not good because of

PUFA' s (and yet another definition which I shall now copy over to a

permanent note on my desktop labelled " definitions " ) and oxydized

LDL's?

Thanks, it's hard to keep in my head. I want to really get it.

if you ever make a CD and in my case a tape, since that's all that will

play in my car and I HATE those cd players that plug in.

I want one. I want a series. Please if you make CD's have breaks

frequently so that I can find where I left off since I'm out in the

field and make frequent stops and the CD's just start over. That's

assuming I'm forced into CD's but I don't have a player and no hope of

getting one so PLEASE a TAPE.

They need to be affordable too.

Much to ask but everything you say is so important and I finally get it

if I hear it over and over. I've played Sally's 6 tape series from a

conference 4 years ago and need to have the reinforcement. Also it took

at least 100 times for me to hear them without hearing something I've

missed. Actually, I heard something the other day that I hadn't gotten.

Our ears and minds don't absorb what we're not ready for. You who have

great absorptive powers wouldn't know what that's like.

On Feb 5, 2008, at 8:07 AM, Masterjohn wrote:

>> It is still of course wise to avoid foods and other factors that

>> promote

>> oxidization, since

>> free radicals have many proven ill effects on the body. In spite of

>> the

>> commonly held

>> belief, saturated fats are much better for heart health than PUFAs.

>> I could

>> show you reams

>> of data on that (actually, if you're interested you can download my

>> presentation at

>> http://chriskresser.com/research/cholesterol_class.pdf), but based on

>> your

>> presence here

>> I'm guessing you already know that.

>

> I certainly agree with that -- which is consistent with the oxidized

> LDL hypothesis as well, since PUFAs are the first target of oxidation

> in the LDL particle.

Parashis

artpages@...

portfolio pages:

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

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

[Guest guest]

What is your opinion of the role of HDL in heart disease? I've read a lot of

contradictory

information on this. Dr. Farr, whom I reference previously, believes it is

impossible

for HDL to actually remove LDL from atherosclerotic plaques:

" Again, it is true that HDL `picks-up' loose cholesterol from dead cells and

transports it

back to the liver, using the `reverse cholesterol transport system.' But if you

want to

explain how it manages to suck cholesterol out of an atherosclerotic plaque,

then you are

going to have to travel well past the realms of the improbable, and into the

zone of the

completely impossible.

HDL is travelling through an artery when, suddenly, it spots a cholesterol laden

plaque. It

stops at that exact point and transports itself through the endothelium.

Bravely, battling

against a concentration gradient, our plucky HDL locks onto the plaque, sucks

cholesterol

out, changes direction, reverses back through the endothelium and into the

bloodstream.

From there to the liver where it heroically unloads its package of `Bad

cholesterol.' File

under: Great Myths of the Western World.

Despite this, it has become another established truth that HDL is not just

associated with

a reduced rate of CHD; it is, in fact, an active protective factor. Oh, would

someone please

set up a university dedicated to teaching the difference between an association,

a cause,

and an effect. All researchers into CHD will be forced to attend, and beaten

with large

clubs until they finally understand that when you find factor X is raised in

condition Y, it

does not mean that factor X causes condition Y. Other explanations are possible

- thwack!

`Repeat after me, other explanations are possible.' Thwack! `And have another

Thwack for

good measure - you dolt.'

From this, you may be able to gather that I am not a great supporter of the

hypothesis

that HDL protects against CHD. So it came as no great surprise to me to find

that,

although HRT raises HDL levels and thus, according to accepted wisdom, should

protect

against CHD, when this was finally studied, guess what?

The rate of CHD in women on HRT went up. Despite the increase in HDL, (and a

decrease

in LDL). To quote from the conclusion of the heart and estrogen/progestin

study. "

His jocular tone aside, what he says makes sense to me. Is there another

explanation that

he is missing? In addition to the study he quotes, I've seen other studies that

indicate that

HDL levels are not protective - and I've seen studies which indicate that they

are. The HRT

study seems quite persuasive, though.

Chris

[Guest guest]

The other will weigh in I'm sure, but in short the main dietary source of

PUFAs is

vegetable oils - sunflower, safflower, cottonseed, soy and corn oils in

particular. Canola

oil is not as high in n-6 fatty acids as other vegetable oils, but should be

avoided because

of oxidization of its high content of n-3 fatty acids during processing.

The easiest way to avoid these things in the diet is to avoid eating processed

foods, and to

drastically reduce eating out at restaurants (which surely use inferior quality

vegetable oils

- this is true for even high end restaurants). If you start reading labels of

processed foods

you'll see that almost all of them have these vegetable oils in them. By

avoiding processed

foods, and cooking at home with saturated fats like butter, coconut oil, lard

etc. you will

be dramatically cutting back on your intake of PUFAs.

It should be pointed out that we do need a small percentage of our fat intake to

be from

healthy sources of PUFAs (Enig & Fallon and other researchers say about 4%).

This can be

done by eating salmon, raw egg yolks, butter, CLO, etc. or it can also be taken

in

supplement form using Udo's Oil or Yes Parent Essential Oils.

You'll also want to avoid eating foods that contain oxidized PUFAs. This means

foods that

contain PUFAs that have been heated, fried, hydrogenated or processed in such a

way that

they have become rancid. Again, if you avoid processed foods and restaurants

you'll be

eliminating most of these foods - presuming you're not using any offending oils

at home

in your cooking.

K.

>

> >> It is still of course wise to avoid foods and other factors that

> >> promote

> >> oxidization, since

> >> free radicals have many proven ill effects on the body. In spite of

> >> the

> >> commonly held

> >> belief, saturated fats are much better for heart health than PUFAs.

> >> I could

> >> show you reams

> >> of data on that (actually, if you're interested you can download my

> >> presentation at

> >> http://chriskresser.com/research/cholesterol_class.pdf), but based on

> >> your

> >> presence here

> >> I'm guessing you already know that.

> >

> > I certainly agree with that -- which is consistent with the oxidized

> > LDL hypothesis as well, since PUFAs are the first target of oxidation

> > in the LDL particle.

> Parashis

> artpages@...

>

> portfolio pages:

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

>

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

>

[Guest guest]

so does this mean that one should eat lots more eggs, meat and so on

compared to nuts?

-jennifer

On Feb 6, 2008, at 11:33 AM, chriskjezp wrote:

> The other will weigh in I'm sure, but in short the main

> dietary source of PUFAs is

> vegetable oils - sunflower, safflower, cottonseed, soy and corn oils

> in particular. Canola

> oil is not as high in n-6 fatty acids as other vegetable oils, but

> should be avoided because

> of oxidization of its high content of n-3 fatty acids during

> processing.

>

> The easiest way to avoid these things in the diet is to avoid eating

> processed foods, and to

> drastically reduce eating out at restaurants (which surely use

> inferior quality vegetable oils

> - this is true for even high end restaurants). If you start reading

> labels of processed foods

> you'll see that almost all of them have these vegetable oils in

> them. By avoiding processed

> foods, and cooking at home with saturated fats like butter, coconut

> oil, lard etc. you will

> be dramatically cutting back on your intake of PUFAs.

>

> It should be pointed out that we do need a small percentage of our

> fat intake to be from

> healthy sources of PUFAs (Enig & Fallon and other researchers say

> about 4%). This can be

> done by eating salmon, raw egg yolks, butter, CLO, etc. or it can

> also be taken in

> supplement form using Udo's Oil or Yes Parent Essential Oils.

>

> You'll also want to avoid eating foods that contain oxidized PUFAs.

> This means foods that

> contain PUFAs that have been heated, fried, hydrogenated or

> processed in such a way that

> they have become rancid. Again, if you avoid processed foods and

> restaurants you'll be

> eliminating most of these foods - presuming you're not using any

> offending oils at home

> in your cooking.

>

> K.

>

>

>>

>>>> It is still of course wise to avoid foods and other factors that

>>>> promote

>>>> oxidization, since

>>>> free radicals have many proven ill effects on the body. In spite

>>>> of

>>>> the

>>>> commonly held

>>>> belief, saturated fats are much better for heart health than PUFAs.

>>>> I could

>>>> show you reams

>>>> of data on that (actually, if you're interested you can download my

>>>> presentation at

>>>> http://chriskresser.com/research/cholesterol_class.pdf), but

>>>> based on

>>>> your

>>>> presence here

>>>> I'm guessing you already know that.

>>>

>>> I certainly agree with that -- which is consistent with the oxidized

>>> LDL hypothesis as well, since PUFAs are the first target of

>>> oxidation

>>> in the LDL particle.

>> Parashis

>> artpages@...

>>

>> portfolio pages:

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

>>

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

>>

>

>

>

>

>

>

>

[Guest guest]

Hi ,

> Could I have the list again of the foods that are not good because of

> PUFA' s (and yet another definition which I shall now copy over to a

> permanent note on my desktop labelled " definitions " ) and oxydized

> LDL's?

Ay, my post got lost! I'll try again. For added fats and oils, it

should look something like this:

Use freely -- butter, coconut oil, ruminant fats (e.g. lamb and beef

fat), cocoa butter, macadamia nut oil.

Use in moderation -- palm oil, olive oil, lard

Avoid -- poultry fats, nut/seed/legume oils

Ideally all oils should be unrefined, virgin and grass-fed wherever

applicable. If using TT coconut oil, use gold-label rather than

green-label. Antioxidant-rich fruits and vegetables, especially

berries, red meat cooked medium or less, fresh foods in general, and

small amounts of unrefined palm oil should be useful.

Chris

[Guest guest]

On 2/6/08, chriskjezp <chriskresser@...> wrote:

> It should be pointed out that we do need a small percentage of our fat

> intake to be from

> healthy sources of PUFAs (Enig & Fallon and other researchers say about 4%).

> This can be

> done by eating salmon, raw egg yolks, butter, CLO, etc. or it can also be

> taken in

> supplement form using Udo's Oil or Yes Parent Essential Oils.

I don't think the actual requirement for PUFA is anywhere near 4% of

calories, but I'll be writing a Special Report on this soon and I'm

not completely done with my research. But basically I do not think it

is possible to develop essential fatty acid deficiency on a whole

foods diet unless you have enzyme deficiency that require some of the

elongated ones preformed and you don't have them in your diet from

eggs and liver and fish and so on.

Chris

[Guest guest]

> Avoid -- poultry fats, nut/seed/legume oils

>

Why do you suggest avoiding poultry fats and fats from nuts/seeds/legumes? Are

you

suggesting avoiding these foods entirely (since you can't avoid eating them

without their

fats)? If so, on what basis?

Thanks,

Chris

[Guest guest]

I'll be curious to see your Special Report, since I've seen that 4% number in

several studies

(Lasserre M, et al. Lipids. 1985;20:4:227). Enig suggests 1.5% of calories for

n-3, and

since she recommends a 2:1 or 3:1 ratio of n-6:n-3 the total amount would be

something

like 4.5% of calories.

Regarding the conversion of ALA into the longer chain derivatives, Udo Erasmus

PhD has a

very interesting article on that subject on his website:

http://www.udoerasmus.com/articles/udo/fish_oil.htm. He believes that the

conversion

process functions quite well, even in persons who are ill, and therefore it

isn't necessary

to supplement with derivatives (EPA, DHA, GLA, etc.).

I agree that supplementation is unnecessary (and even undesirable) in people who

are

eating a WAPF type of diet with eggs, butter, fish, etc. I've seen research

that excess

amounts of the fatty acid derivatives can cause problems.

Chris

>

> > It should be pointed out that we do need a small percentage of our fat

> > intake to be from

> > healthy sources of PUFAs (Enig & Fallon and other researchers say about 4%).

> > This can be

> > done by eating salmon, raw egg yolks, butter, CLO, etc. or it can also be

> > taken in

> > supplement form using Udo's Oil or Yes Parent Essential Oils.

>

> I don't think the actual requirement for PUFA is anywhere near 4% of

> calories, but I'll be writing a Special Report on this soon and I'm

> not completely done with my research. But basically I do not think it

> is possible to develop essential fatty acid deficiency on a whole

> foods diet unless you have enzyme deficiency that require some of the

> elongated ones preformed and you don't have them in your diet from

> eggs and liver and fish and so on.

>

> Chris

>

[Guest guest]

> Why do you suggest avoiding poultry fats and fats from nuts/seeds/legumes?

> Are you

> suggesting avoiding these foods entirely (since you can't avoid eating them

> without their

> fats)? If so, on what basis?

No, I'm suggesting avoiding the oils derived from them as added oils.

However, it would probably be good not to base ones diet around those

as staples but rather use them in moderation.

Chris

[Guest guest]

On 2/6/08, chriskjezp <chriskresser@...> wrote:

> I'll be curious to see your Special Report, since I've seen that 4% number

> in several studies

> (Lasserre M, et al. Lipids. 1985;20:4:227). Enig suggests 1.5% of calories

> for n-3, and

> since she recommends a 2:1 or 3:1 ratio of n-6:n-3 the total amount would be

> something

> like 4.5% of calories.

The 4% figure is the standard recommendation. It's based on

biomarkers rather than symptoms, and on feeding methyl and ethyl

esters of purified fatty acids rather than real foods, and it's done

in animals using experimental conditions that increase the need for

PUFA, which is why it's so inflated.

> Regarding the conversion of ALA into the longer chain derivatives, Udo

> Erasmus PhD has a

> very interesting article on that subject on his website:

> http://www.udoerasmus.com/articles/udo/fish_oil.htm. He believes that the

> conversion

> process functions quite well, even in persons who are ill, and therefore it

> isn't necessary

> to supplement with derivatives (EPA, DHA, GLA, etc.).

That's quite different from the information you find anywhere else

including textbooks and reviews in peer-reviewed journals, but I

suppose there is also a subjective component of what it means to

" function quite well. " Unfortunately the link came up as " file not

found. "

> I agree that supplementation is unnecessary (and even undesirable) in people

> who are

> eating a WAPF type of diet with eggs, butter, fish, etc. I've seen research

> that excess

> amounts of the fatty acid derivatives can cause problems.

Indeed.

Chris

[Guest guest]

I have a question along these lines. I have a friend who is a vegan

and trying very hard to convince me to become one. She and her family

are incredibly healthy. How can you be a vegan and keep PUFAs down to

the level you suggest? I'm really confused about all this. For the

last 8 months I've been doing no grains/no sugars/nothing processed etc

etc, free range meats. I try for 50% raw and eat a LOT of fermented

foods. I lost 50lbs in the first 4 months, the last 4 months I haven't

lost an ounce and haven't changed a thing. Got results of semiannual

lab work, basically total cholesterol down from 300 to 150. HDL 51,

LDL over 100 (can't remember exact number). From what ya'll have been

saying, I'm not worried about the numbers anymore. I am wondering if

going vegan will jumpstart the weight loss, but if I do, will I not get

things I essentially need and an overabundance of PUFAs. The only

things I haven't completely beat by changing my lifestyle are my

weight, an inflammatory arthritis, hypothyroidism and asthma. Thanks

for any suggestions and answers about the vegan issue.

Patty

[Guest guest]

Hi Patty,

> I have a question along these lines. I have a friend who is a vegan

> and trying very hard to convince me to become one. She and her family

> are incredibly healthy. How can you be a vegan and keep PUFAs down to

> the level you suggest? I'm really confused about all this.

I would not at all recommend going vegan. Just because your friend is

healthy does not mean veganism is healthy or the ideal diet. At the

very least, I would make some effort to consume shellfish, especially

oysters and clams, several times per month if you wish to reduce

animal products.

That said, coconut oil is the most saturated fat in existence and is

completely vegan. So by using coconut oil and/or macadamia nut oil as

the primary fats and using palm oil in smaller amounts, and, perhaps,

some olive oil, one could easily keep PUFAs down so long as one does

not try to get the bulk of one's protein from nuts.

> For the

> last 8 months I've been doing no grains/no sugars/nothing processed etc

> etc, free range meats. I try for 50% raw and eat a LOT of fermented

> foods. I lost 50lbs in the first 4 months, the last 4 months I haven't

> lost an ounce and haven't changed a thing. Got results of semiannual

> lab work, basically total cholesterol down from 300 to 150. HDL 51,

> LDL over 100 (can't remember exact number).

If your total cholesterol is 150 and your HDL is 51, I don't see how

your LDL could be over 100.

> From what ya'll have been

> saying, I'm not worried about the numbers anymore. I am wondering if

> going vegan will jumpstart the weight loss, but if I do, will I not get

> things I essentially need and an overabundance of PUFAs.

Why would going vegan jumpstart weight loss? Have you tried

introducing an exercise routine?

> The only

> things I haven't completely beat by changing my lifestyle are my

> weight, an inflammatory arthritis, hypothyroidism and asthma. Thanks

> for any suggestions and answers about the vegan issue.

Regarding the asthma, how are your vitamin A levels? Do you eat much

vitamin A (i.e. liver or cod liver oil)?

What do you do for exercise? Being healthy is more than what you eat.

Chris

[Guest guest]

Dr. Erasmus quotes several peer reviewed studies in his summary of the issue.

I'm not

sure why the link didn't work, because that is indeed the address. You can find

the article

by going to his site, clicking on " articles " and then " Humans turn ALA to

EPA/DHA " . Here's

an excerpt:

--------------------

Every year, more research confirms that n-3 conversion takes place effectively,

provided

that enough ALA is present in the diet and interfering factors are avoided. One

of the

main factors that interferes with n-3 conversion is too much n-6 in the diet,

which is the

case in the diets commonly eaten by people living in developed nations. N-6

slows down

the conversion of n-3.

While researchers still disagree on the exact rate of conversion (because the

rate is

affected by many nutritional and hormonal factors) and the optimum n-3/n-6

ratio, they

agree that substantial conversion does take place. Here are some of their

estimates (the

first three estimates below were given to Udo by Sam Graci from discussions Sam

said he

had with Holub, Sears, and Schmidt):

Dr. Bruce Holub (U. of Guelph): 10-15%;

Dr. Barry Sears (The Zone Diet): up to 18%;

Dr. Schmidt (Smart Fats): 10%;

Dr. EA Emken et al3 (research): 17%;

Dr. GC Burdge et al1,2 (research): 16%-men; 36%-women;

Dr. SM Innis7 (research): infants convert;

Dr. JT Brenna8 (research): all ages convert;

VP Carnielli et al9; C Billeaud et al10 'prematures' convert;

A few writers still claim that conversion is less than 5%, but more and more

studies report

much higher rates of conversion.

The fact of conversion is just common sense. The brains, eyes, and nervous

systems of all

animals, from insects up are rich in long chain n-3s. Many of these animals are

vegetarian, including rabbits, horses, and gorillas. They must be converting the

basic n-3

in their own body, because their foods supply provides only ALA, the basic n-3.

The long-

chain n-3 are important, so nature equipped creatures to make what they need,

and to

turn up production if long-chain n-3 are not present in the diet.

-------

The only reason this is relevant in my mind is regarding the debate on whether

derivative

supplementation is necessary/beneficial at all. Some (like UDO, and the people

who make

the YES Parent Essential Oil supplement that Dr. Cowan recommends) suggest not

taking

fish oils at all, and taking the n-3/n-6 fatty acids in the form of vegetable

and seed oils.

Others, like WAPF, are big on CLO and fish oils. Of course CLO has other

benefits, in

particular Vitamin A & D.

Chris

> > I'll be curious to see your Special Report, since I've seen that 4% number

> > in several studies

> > (Lasserre M, et al. Lipids. 1985;20:4:227). Enig suggests 1.5% of calories

> > for n-3, and

> > since she recommends a 2:1 or 3:1 ratio of n-6:n-3 the total amount would be

> > something

> > like 4.5% of calories.

>

> The 4% figure is the standard recommendation. It's based on

> biomarkers rather than symptoms, and on feeding methyl and ethyl

> esters of purified fatty acids rather than real foods, and it's done

> in animals using experimental conditions that increase the need for

> PUFA, which is why it's so inflated.

>

>

> > Regarding the conversion of ALA into the longer chain derivatives, Udo

> > Erasmus PhD has a

> > very interesting article on that subject on his website:

> > http://www.udoerasmus.com/articles/udo/fish_oil.htm. He believes that the

> > conversion

> > process functions quite well, even in persons who are ill, and therefore it

> > isn't necessary

> > to supplement with derivatives (EPA, DHA, GLA, etc.).

>

> That's quite different from the information you find anywhere else

> including textbooks and reviews in peer-reviewed journals, but I

> suppose there is also a subjective component of what it means to

> " function quite well. " Unfortunately the link came up as " file not

> found. "

>

>

> > I agree that supplementation is unnecessary (and even undesirable) in people

> > who are

> > eating a WAPF type of diet with eggs, butter, fish, etc. I've seen research

> > that excess

> > amounts of the fatty acid derivatives can cause problems.

>

> Indeed.

>

> Chris

>

[Guest guest]

At the very least, I would make some effort to consume shellfish,

especially oysters and clams, several times per month if you wish to

reduce animal products.

I'm seriously allergic to shellfish (iodine) and play Russian

roulette when I do eat them and have to make sure I have my inhaler

handy.

For the

> > last 8 months I've been doing no grains/no sugars/nothing

processed etc

> > etc, free range meats. I try for 50% raw and eat a LOT of

fermented

> > foods. I lost 50lbs in the first 4 months, the last 4 months I

haven't

> > lost an ounce and haven't changed a thing. Got results of

semiannual

> > lab work, basically total cholesterol down from 300 to 150. HDL

51,

> > LDL over 100 (can't remember exact number).

>

If your total cholesterol is 150 and your HDL is 51, I don't see how

your LDL could be over 100. I can't remember the exact numbers

except that HDL was up from around 30 to 51 and total way down from

300. I have to go to another building 40 miles away to get copies,

they wouldn't print them for me at the clinic (VA)

Regarding the asthma, how are your vitamin A levels? Do you eat much

vitamin A (i.e. liver or cod liver oil)?

I take CLO (3 caps 3x/day..NOW brand) Do I need more than that?

What do you do for exercise? Being healthy is more than what you eat.

I try to exercise with a Gazelle (cross country ski-ing). It's the

only thing I can remotely tolerate. I have had a hip replacement

which is unstable, a knee replacement, back and neck surgery, a

separated shoulder joint and have severe arthritis in my feet, so,

until I can beat the pain, I can't do a lot of exercise, but I try.

I very much appreciate the suggestions. I don't understand why no

fat from poultry because you get the fat if you eat it and I eat

poultry almost exclusively. The knowledge in this group is amazing.

Thanks again!